Clinical Avian Medicine - 2 Volume Set PDF

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Clinical
Avian
Medicine
VOLUME I
GREG J. HARRISON, DVM
Diplomate Emeritus American Board of Veterinary Practitioners (Avian)
Diplomate European College of Avian Medicine and Surgery (n.p.)
Palm Beach, Florida
TERESA L. LIGHTFOOT, BS, DVM

Diplomate American Board of Veterinary Practitioners (Avian)
Florida Veterinary Specialists
Tampa, Florida
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Spix Publishing, Inc.,

Palm Beach, Florida
Library of Congress Control Number: 2005922214
Clinical Avian Medicine (2-volume set) ISBN: 00-9754994-0-8
Production: Zoological Education Network
Cover Design: Jean Coffinberry
Cover photos: Mimi Walling, We Shoot Birds (cockatiel, black-capped lory, double yellow-headed Amazon, African grey
parrots, Quaker parrot, sun conure, budgerigar); Loro Parque, Tenerife, Spain (blue and gold macaws)
Proofreading: K. Stormy Hudelson, DVM, Dipl ABVP-Avian, Paul Hudelson
Indexing: Ann Truesdale, DVM
Administrative Assistants: Lesley Flahie, Patty Wolf
Technical Assistance: Chris Lane
Printing and Binding: Four Colour Imports
Advertising and Sales: HBD Intl Inc. www.harrisonsbirdfoods.com
©2006 Spix Publishing, Inc., Palm Beach, Florida

All rights reserved. No part of this book may be reproduced or used in any form or by any means, electronic or mechan-
ical, including photocopying, or by any information storage or retrieval system, without permission in writing from the
publisher. Address any inquiries to Spix Publishing Inc, 3610 South Ocean Blvd #601, Palm Beach, FL 33480-5877.
Last digit is the print number: 9 8 7 6 5 4 3 2 1

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CONTRIBUTORS
HEATHER L. BOWLES, DVM, Diplomate American Board of Veterinary Practitioners (Avian),
Certified in Veterinary Acupuncture (Chi Institute)
Hunt Valley Animal Hospital, Hunt Valley, Maryland
Evaluating and Treating the Reproductive System, Surgical Resolution of Soft Tissue Disorders
MARCELLUS BÜRKLE, DVM

Tierärztliche Praxis, Karlsruhe, Germany
Management of Zoo and Park Birds
GARY D. BUTCHER, BS, MS, DVM, PhD, Diplomate American College of Poultry Veterinarians
Poultry Medicine and Management, College of Veterinary Medicine,
University of Florida, Gainesville, Florida
Management of Galliformes
CARL D. CHENEY, PhD

Department of Psychology, Utah State University, Logan, Utah
Concepts in Behavior, Section I: The Natural Science of Behavior
PETER COUTTEEL, DVM

Dierenartsenpraktijk Trigenio, Nijlen, Belgium
Management of Canaries, Finches and Mynahs
LORENZO CROSTA, DVM

Avian, Exotic and Zoo Animal Consulting, Como, Italy
ROBERT D. DAHLHAUSEN, DVM, MS

Veterinary Molecular Diagnostics, Inc., Milford, Ohio
Implications of Mycoses in Clinical Disorders
BOB DONELEY, BVSc, FACVSc (Avian Health)

West Toowoomba Veterinary Surgery, Toowoomba, Queensland, Australia
Maximizing Information from the Physical Examination, Management of Captive Ratites
M. SCOTT ECHOLS, DVM, Diplomate American Board of Veterinary Practitioners (Avian)

Adjunct Professor, Texas A&M University College of Veterinary Medicine,
Westgate Pet and Bird Hospital, Austin, Texas
Evaluating and Treating the Kidneys
THOMAS M. EDLING, DVM, MSpVM

Director, Veterinary Medicine, Petco Animal Supplies, Inc., San Diego, California
Concepts in Behavior, Section I: The Natural Science of Behavior, Updates in Anesthesia and Monitoring
GWEN B. FLINCHUM, BS, MS, DVM

All Bird Clinic of Palm Beach County, Lake Worth, Florida
Clinical Practice, Emergency and Critical Care, Management of Waterfowl
SUSAN G. FRIEDMAN, PhD

Department of Psychology, Utah State University, Logan, Utah
Concepts in Behavior, Section I: The Natural Science of Behavior
MICHAEL M. GARNER, DVM, Diplomate American College of Veterinary Pathologists

Adjunct Associate Professor, Washington State University, Northwest ZooPath, Monroe, Washington
Overview of Tumors Section II: A Retrospective Study of Case
Submissions to a Specialty Diagnostic Service
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STACEY GELIS, BSc, BVSc (Hons), MACVSc (Avian Health)

Kingston Veterinary Clinic, Mentone, Victoria, Australia
Evaluating and Treating the Gastrointestinal System
PHOEBE GREENE LINDEN, BA, MA

Santa Barbara Bird Farm, Santa Barbara, California
Concepts in Behavior, Section II: Early Psittacine Behavior and Development
KENDAL E. HARR, DVM, MS, Diplomate American College of Veterinary Pathologists

Associate Director Aquatic Animal Health, Clinical Assistant Professor,
College of Veterinary Medicine, University of Florida, Gainesville, Florida
Diagnostic Value of Biochemistry
LORI DANIELLE HARRISON, DVM

Avian and Exotics at Central Animal Hospital, Eden, North Carolina
Evaluating and Treating the Liver
GREG J. HARRISON, DVM, Diplomate Emeritus American Board of Veterinary Practitioners (Avian),
Diplomate European College of Avian Medicine and Surgery (n.p.),
Avian Consultant, Palm Beach, Florida
Clinical Practice, The Companion Bird, Nutritional Considerations Section II: Nutritional Disorders,
Emergency and Critical Care, Maximizing Information from the Physical Examination, Surgical
Resolution of Soft Tissue Disorders
PETER HELMER, DVM, Diplomate American Board of Veterinary Practitioners (Avian),

Chief of Staff, Avian and Animal Hospital of Bardmoor, Largo, Florida
Advances in Diagnostic Imaging, Surgical Resolution of Orthopedic Disorders
CLAUDIA HOCHLEITHNER, Dr med vet

Private practitioner, Vienna, Austria
MANFRED HOCHLEITHNER, Dr med vet, Diplomate European

College of Avian Medicine and Surgery
Private practitioner, Vienna, Austria
JAN HOOIMEIJER, DVM

Clinic for Birds, Meppel, The Netherlands
Management of Racing Pigeons
K. STORMY HUDELSON, BS, DVM, Diplomate American Board of Veterinary Practitioners (Avian)
Private practitioner, Tucson, Arizona
Endocrine Considerations
PAUL M. HUDELSON, BA, MA

Tucson, Arizona
Endocrine Considerations
JACK J. KOTTWITZ, DVM

Underwood Animal Hospital, Heath, Ohio
Surgical Resolution of Soft Tissue Disorders
MARIA-ELISABETH KRAUTWALD-JUNGHANNS, Prof Dr med vet, Dr habil,

Diplomate European College of Avian Medicine and Surgery, German Veterinary Specialist for Birds/Reptiles
University Professor, Scientific Assistant, Clinic for Birds and Reptiles, University Leipzig, Leipzig, Germany
Evaluating and Treating the Cardiovascular System
ANGELA M. LENNOX, DVM, Diplomate American Board of Veterinary Practitioners (Avian)

Avian and Exotic Animal Clinic, Indianapolis, Indiana
The Companion Bird
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TERESA L. LIGHTFOOT, BS, DVM, Diplomate American Board of Veterinary Practitioners (Avian)
Florida Veterinary Specialists, Tampa, Florida
Concepts in Behavior Section II: Early Psittacine Behavior and Development, Concepts in Behavior
Section III: Pubescent and Adult Psittacine Behavior, Maximizing Information from the Physical
Examination, Emergency and Critical Care, Integument, Overview of Tumors Section I: Clinical Avian
Neoplasia and Oncology
MICHAEL LIERZ, Dr med vet, MRCVS, Certified Specialist Poultry (Avian Medicine),
Certified Species Conservation
Institute for Poultry Diseases, University of Berlin, Berlin, Germany
Diagnostic Value of Endoscopy and Biopsy
KEATH L. MARX, DVM

Seven Seas Veterinary Services, Blacksburg, Virginia
Therapeutic Agents
DEBRA McDONALD, PhD, BSc (HONS I)

Zoo Nutrition Advisory Group (NAG), Healesville, Victoria, Australia
Nutritional Considerations, Section I: Nutrition and Dietary Supplementation
Nutritional Considerations, Section II: Nutritional Disorders
ROBERT D. NESS, DVM, Certified in Chiropractic (American Veterinary

Chiropractic Association), Certified in Veterinary Acupuncture (Chi Institute)
Ness Exotic Wellness Center, Lisle, Illinois
Integrative Therapies
ESPEN ODBERG, DVM

Private practitioner, AviVet, Oslo, Norway
Surgical Resolution of Soft Tissue Disorders
JOANNE PAUL-MURPHY, DVM, Diplomate American College of Zoo Medicine

Associate Professor, School of Veterinary Medicine, University of Wisconsin, Madison, Wisconsin
Pain Management
MICHAEL PEES, Dr med vet, German Veterinary Specialist for Birds/Reptiles

Scientific Assistant, Clinic for Birds and Reptiles, University of Leipzig, Leipzig, Germany
DAVID N. PHALEN, DVM, PhD, Diplomate American Board of

Veterinary Practitioners (Avian)
Department Large Animal Medicine and Surgery, Texas A&M University College of
Veterinary Medicine, College Station, Texas
Preventive Medicine and Screening, Implications of Macrorhabdus in Clinical Disorders,
Implications of Viruses in Clinical Disorders
SIMON R. PLATT, BVM&S, MRCVS, Diplomate American College of Internal

Medicine (Neurology), Diplomate European College of Veterinary Neurology, RCVS Specialist in
Veterinary Neurology
The Animal Health Trust, Centre for Small Animal Studies, Kentford, Newmarket, Suffolk, United Kingdom
Evaluating and Treating the Nervous System
CHRISTAL G. POLLOCK, DVM, Diplomate American Board of Veterinary

Practitioners (Avian)
Department of Clinical Sciences, College of Veterinary Medicine,
Kansas State University, Manhattan, Kansas
Implications of Mycobacteria in Clinical Disorders
DIANA POST, VMD

Executive Director, Rachel Carson Council, Inc., Silver Spring, Maryland
Low-risk Pest Management
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MADELINE A. RAE, BS, DVM, MS, Diplomate American Board of Veterinary

Practitioners (Avian)
Amazon Veterinary Diagnostics, Salem, Oregon
Diagnostic Value of Necropsy
PATRICK T. REDIG, DVM, PhD

Professor and Director, The Raptor Center, College of Veterinary Medicine,
University of Minnesota, Saint Paul, Minnesota
Surgical Resolution of Orthopedic Disorders
JILL A. RICHARDSON, DVM

Associate Director, Consumer Relations and Technical Services, The Hartz Mountain
Corporation, Secaucus, New Jersey
Implications of Toxic Substances in Clinical Disorders
PETER SANDMEIER, Dr med vet, Diplomate European College of Avian

Medicine and Surgery
Private practitioner, Baden-Dättwil, Switzerland
Management of Canaries, Finches and Mynahs
JAIME SAMOUR, MVZ, PhD, Diplomate European College of Avian

Medicine and Surgery
Fahad bin Sultan Falcon Center, Riyadh, Kingdom of Saudi Arabia
Diagnostic Value of Hematology, Management of Raptors
ROBERT E. SCHMIDT, DVM, PhD, Diplomate American College of

Veterinary Pathologists
Zoo/Exotic Pathology Service, Greenview, California
Integument
MICHAEL STANFORD, BVSc, MRCVS

Birch Heath Veterinary Clinic, Tarporley, Cheshire, United Kingdom
Calcium Metabolism
JENS STRAUB, Dr med vet, German Veterinary Specialist for Birds/Reptiles

Scientific Assistant, Clinic for Birds and Reptiles, University of Leipzig, Leipzig, Germany
LINDA TIMOSSI, DVM

Avian, Exotic and Zoo Animal Consulting, Como, Italy
THOMAS N. TULLY, Jr., MS, DVM, Diplomate American Board of Veterinary Practitioners (Avian),
Diplomate European College of Avian Medicine and Surgery
Louisiana State University School of Veterinary Medicine, Baton Rouge, Louisiana
Update on Chlamydophila psittaci: A Short Comment
LIZ WILSON, CVT

Levittown, Pennsylvania
Concepts in Behavior Section II: Early Psittacine Behavior and Development, Concepts in Behavior
Section III: Pubescent and Adult Psittacine Behavior
Note to the Reader

The National Research Council (NRC) has not established standards for nutritional products fed to birds; therefore, claims of
nutritional completeness can not legally or ethically be made. Human medical textbooks and those of domestic animals have
established normal laboratory values, recommended treatment regimes and nutritional disease states — all based on individu-
als meeting minimum standards of nutrition. These are not available in avian medicine.
Disclaimer
The publisher, editors, authors, reviewers and distributors involved assume no legal responsibility for use and make no claims
or warranties regarding results that may be obtained from information in this text, nor necessarily endorse the procedures,
medications, medication dosages or their uses as offered in this work. The above parties shall not be liable to any party for any
damages, nor considered negligent for any misstatement or error obtained in this text.
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Foreword
I f you do something long enough, you will eventually be able to step back and observe
the real progress that has been made in your field of endeavor. After almost thirty years of
avian practice I am amazed and gratified how far we have come. When I started practicing
in 1976, in a given year, it was an easy task to read every thing published about clinical avian
medicine. That has obviously and dramatically changed. The formation of the Association of
Avian Veterinarians increased the generation of published materials considerably. Over the
years, as each major text neared the publication date, an excitement was generated. Greg
Harrison, with the assistance of co-editors Linda Harrison and Branson Ritchie with previous
texts, and Teresa Lightfoot with Clinical Avian Medicine, has learned to distill the massive
amount of material into a manageably useful and cohesive text.
Clinical Avian Medicine is predominantly written by clinicians for clinicians with a wonderful
degree of clinical relevance. The number of high quality color photos inserted into the body
of the text makes it easy to follow the ideas being presented. Thank you to doctors Harrison
and Lightfoot and the fifty international authors for their hard work and perseverance in gen-
erating this most current and comprehensive avian medical reference text.
Donald W. Zantop, DVM, Diplomate American Board of

Fallston Veterinary Clinic, Fallston, Maryland
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Preface
T
he future of avian medicine and stewardship is increasingly bright. Importation of
wild-caught birds has been largely curtailed, and the vestiges of unethical (yet legal)
loopholes as well as illegal venues for smuggling are being actively and more effec-
tively opposed.
With the cessation of mass importation, along with vastly improved nutritional provisions,
increased diagnostic and therapeutic techniques and a better understanding of the emotional
needs of our pet birds, we are privileged to observe the first generations of captive-born
psittacines that may survive to attain their optimal quality and length of life.
Clinical Avian Medicine offers knowledge gleaned from years of clinical experience, combined
with cutting edge research. New methods of prevention, diagnosis and treatment of various
diseases are included in the areas of virology, neoplasia, dermatology, neurology, necropsy
techniques, hepatic disease, pain management, behavior, soft tissue and orthopedic surgery,
anesthesia, endoscopy, reproductive disorders, nephrology, hematology, biochemistry,
endocrinology, gastroenterology, and therapeutics. Novel topics such as low-risk (i.e., environ-
mentally safe) pest control and integrative (alternative) avian medicine are provided. The
approaches and coverage of all these topics by contributing authors are both enlightening and
readily applicable to clinical practice.
Anecdotal, yet often invaluable, clinical information regarding avian disease syndromes, treat-
ment, husbandry and nutrition are included in Clinical Avian Medicine. The exclusion of these
essentials would be an impediment to the practitioner searching for information to provide
treatment for his or her avian patient. Anecdotal reports can create concern with efficacy and
safety if not appropriately identified. Therefore, throughout this text, we have attempted to
indicate the source of the stated information, allowing the individual veterinarian to deter-
mine its applicability. Unarguably, strict scientific methods are needed to document the valid-
ity of diagnostic and treatment protocols. Yet we must not squelch the introduction of innova-
tive and potentially life-saving techniques in clinical practice due to delays in the completion
of scientific validation. Our duty as authors and editors is to present the facts as they currently
stand. We believe this availability of information has the potential to enhance the quality of
avian medicine, surgery and husbandry when placed in the discriminating hands of veterinary
practitioners.
Greg J. Harrison, DVM, Diplomate Emeritus American

Board of Veterinary Practitioners (Avian),
Teresa L. Lightfoot, DVM, Diplomate American Board of

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Vision
T
he vision of clinical avian practice as stated in the Preface mirrors the history and
achievements of Dr. Greg Harrison. This book is first, last and foremost, the result of
his lifetime dedication to avian medicine and stewardship.
When Dr. Harrison began the practice of avian medicine in the 1970’s, he was one of a very
few individuals in this field. Nearly all of the accepted “facts” in avian medicine were extrapo-
lated (correctly or incorrectly) from companion animal medicine or poultry science. Dr.
Harrison’s early work precipitated the subsequent exponential increase in avian medical and
surgical innovations throughout the following three decades. The discoveries and improve-
ments in avian endoscopic techniques, microsurgery, radiosurgical modifications and applica-
tions, and a multitude of other current standard avian therapies are the direct result of his
early work in these fields.
The publication in 1986 of the textbook, Clinical Avian Medicine and Surgery (Harrison and
Harrison), provided practitioners with a much needed avian veterinary reference text.
Throughout the development of that book, Dr. Harrison enlisted colleagues within the USA
and abroad, involving some of the foremost authorities in this burgeoning field. The contribu-
tions of these authors, combined with Dr. Harrison’s vast experience (and due in no small
part to Linda Harrison’s unsurpassed organizational and editorial skills), created a text with a
depth of knowledge and information invaluable and previously unavailable to veterinarians in
avian practice.
This has been Dr. Harrison’s modus operandi throughout his career: to put forth ideas, solicit
input and encourage innovation in others, and to listen open-mindedly to alternative theories.
Dr. Harrison has consistently walked the difficult line between improving the application of
current techniques, while seeking alternative treatments and more fundamental data.
In recent years, Dr. Harrison has dedicated his time and energies to preventive avian medi-
cine, specifically in the area of nutrition. The outcome of this commitment has improved the
health, quality and length of life of untold numbers of beloved pet birds.
As is common in innovative persons of all fields, Dr. Harrison’s intense focus and drive have
created ardent followers and admirers, as well as skeptics. It is again to his credit that both
reactions are welcome. Advancements in avian medicine will be accelerated by those whose
research validates Dr. Harrison’s hypotheses, and by those whose work may contradict various
theories. Within Clinical Avian Medicine, Dr. Harrison’s third major avian text, the reader will
encounter this broad perspective in the presentation of contrasting ideas presented by various
authors.
Greg Harrison has been my role model, teacher, mentor and friend. I have been and will
remain awed by him. The world of avian veterinary medicine and the world in general is a bet-
ter place thanks to his contributions and his presence among us. This publication is a reflec-
tion of his life’s commitment.
Teresa L. Lightfoot, DVM, Diplomate American Board of

June 2005
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Acknowledgements
A
ny undertaking that involves 50 authors is touched by many others, all of whom,
unfortunately, may not be mentioned. So for all those who contributed in any way, I thank
you. I offer deep appreciation to all the authors for their patience and tenacity in repeat-
edly revisiting and reworking material to create this exceptional text.
Stormy and Paul Hudelson were very supportive, reviewing all and revising much of the text. Patty
Wolf was there for every chapter over and over. Vanessa Rolfe for doing a final read through. Heather
Bowles, Lori Harrison, Jack Kottwitz, Michael Lierz, Michael Pees and Michael Stanford stepped up to
work on subjects that offered challenges late in the process and came through in rapid fashion.
We welcome the breakthrough contributions in this text of Debra McDonald, Robert Ness, Diana
Post, Susan Friedman, Liz Wilson, Phoebe Greene Linden, Heather Bowles, Peter Sandmeier and
Peter Coutteel.
To our contributors whose first language is not English, including Espen Odberg, Michael Lierz,
Michael Pees, Peter Sandmeier, Manfred Hochleithner, Claudia Hochleithner, Jan Hooimeijer,
Marcellus Bürkle, Peter Coutteel, Maria-Elisabeth Krautwald-Junghanns, Jens Straub, Lorenzo Crosta,
and Linda Timossi: the extra skill and effort required to write in a non-native language is appreciated
and admired.
Teresa Lightfoot made the whole process possible. Her talent, brilliance, humor and tenacity were my
saving graces. I love her beyond words. Teresa enrolled the follow reviewers: Keeley McNeal, DVM;
Lisa Teske, DVM; Krysta Deitz, DVM; Benjamin Welbourne, DVM; Hugues Lacoste, DVM; Raimon
Duran-Struuck, DVM; Lisa Dixon, DVM; Valerie Sadler, DVM, Diplomate ACVR; Neil Shaw, DVM, Dipl
ACVIM; John Meeks, DVM, Dipl ACVIM (Neurology); Tracy LaDue, DVM, Dipl ACVIM (Oncology), Dipl
ACVR (Radiation Oncology); Mark Levy, DVM, Dipl ACVS; Eric Mears, DVM, Dipl ACVIM; Amy
Benedict, CVT; Brenda Fulcher, CVT; Lee Burstiner, DVM, Dipl ABVP. Teresa also wishes to thank
Florida Veterinary Specialists for the latitude and attitude to tap the knowledge and experience of the
above individuals, and most of all, never-ending thanks to her husband, Chris Lane — for everything.
Nigel Harcourt-Brown is acknowledged for his art work and review of portions of the text. Additional
reviewers to whom we are grateful are: David Rupiper, DVM; Jürgen P. Schumacher, Dr med vet, Dipl
ACZM; and Rebecca E. Gompf, DVM, MS, Dipl ACVIM (Cardiology). Thanks to Dr. Carolyn Cray for
contributions of the University of Miami to hematology and chemistry reference ranges. To others
who reviewed material without acknowledgement, I offer my thanks.
Thanks to Mimi Walling for her beautiful bird photos, to Scott Echols for the use of his surgery pho-
tos and to the following for their photographic support: Auckland Zoo, E. Alberti, Lucy Bartlett, Peter
Helmer, Chris Griffin, Nancy Boedeker, Carol Canny, Friedrich Janeczek, Judy St. Ledger, Eduardo
Nycander, Drury Reavill, Nico Schoemaker, Michael Walsh and Don Zantop. Special thanks to Jean
Coffinberry for promotional and cover concepts and to Ray Kersey, Chris Lane and Friedrich Janeczek
for cover and presentation ideas.
Thank you to Tanya Harrison-Coffinberry for assistance with the organizational and financial manage-
ment, production, legal issues and sale of this work. I appreciate the clients of The Bird Hospital and
Harrison’s Bird Foods who helped create a need for this information in the veterinary field.
My love and gratitude to Linda Harrison for encouraging me to spread my own wings with this book.
There is no greater communicator of practical veterinary information than you, Linda.
Greg J. Harrison, DVM, Diplomate Emeritus American

Board of Veterinary Practitioners (Avian),
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Clinical Avian Medicine

CONTENTS VOLUME I
1 Clinical Practice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .1
GREG J. HARRISON, GWEN B. FLINCHUM
2 The Companion Bird . . . . . . . . . . . . . . . . . . . . . . . . .29

ANGELA M. LENNOX, GREG J. HARRISON
3 Concepts in Behavior . . . . . . . . . . . . . . . . . . . . . . . . 45
Section I: The Natural Science of Behavior . . . . . . . . . .46
SUSAN G. FRIEDMAN, THOMAS M. EDLING, CARL D. CHENEY
Section II: Early Psittacine
Behavior and Development . . . . . . . . . . . . . . . . . . . . . . .60
LIZ WILSON, PHOEBE GREENE LINDEN, TERESA L. LIGHTFOOT
Section III: Pubescent and
Adult Psittacine Behavior . . . . . . . . . . . . . . . . . . . . . . . 73
LIZ WILSON, TERESA L. LIGHTFOOT
4 Nutritional Considerations . . . . . . . . . . . . . . . . . . .85

Section I: Nutrition and Dietary Supplementation . . . . 86
DEBRA M cDONALD
Section II: Nutritional Disorders . . . . . . . . . . . . . . . . . .108
GREG J. HARRISON, DEBRA M cDONALD
5 Calcium Metabolism . . . . . . . . . . . . . . . . . . . . . . . .141

MICHAEL STANFORD
6 Maximizing Information from the

Physical Examination . . . . . . . . . . . . . . . . . . . . . . .153
BOB DONELEY, GREG J. HARRISON, TERESA L. LIGHTFOOT
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7 Emergency and Critical Care . . . . . . . . . . . . . . . .213

GREG J. HARRISON, TERESA L. LIGHTFOOT, GWEN B. FLINCHUM
8 Pain Management . . . . . . . . . . . . . . . . . . . . . . . . . . .233

JOANNE PAUL-MURPHY
9 Therapeutic Agents . . . . . . . . . . . . . . . . . . . . . . . . .241

KEATH L. MARX
10 Integrative Therapies . . . . . . . . . . . . . . . . . . . . . . .343

ROBERT D. NESS
11 Low-risk Pest Management . . . . . . . . . . . . . . . . .365

DIANA POST
12 Evaluating and Treating the

Cardiovascular System . . . . . . . . . . . . . . . . . . . . . .379
MICHAEL PEES, MARIA-ELISABETH KRAUTWALD-JUNGHANNS,
JENS STRAUB
13 Integument . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .395
ROBERT E. SCHMIDT, TERESA L. LIGHTFOOT

Gastrointestinal System . . . . . . . . . . . . . . . . . . . . .411
STACEY GELIS
15 Evaluating and Treating the Liver . . . . . . . . . .441

MANFRED HOCHLEITHNER, CLAUDIA HOCHLEITHNER,
LORI DANIELLE HARRISON
Index
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CHAPTER
1
Clinical
Practice
GREG J. HARRISON, DVM, D ipl ABVP-A vian, Dipl ECAMS;
Avian medicine has seen dramatic growth and develop-

ment over the past several years. Veterinarians who wish
to incorporate avian medicine into their practices now
have numerous resources available to help them get
started. The Association of Avian Veterinarians (AAV) is
currently the most recognized avian veterinary profes-
sional organization in the United States, Europe and
Australia. AAV national conferences provide veterinarians
opportunities to share information and advice, along
with programs that reveal the latest innovations in avian
medicine. Other organizations in the USA include the
American Federation of Aviculture, Mid-Atlantic States
Association of Avian Veterinarians and statewide profes-
sional associations. The European Association of Avian
Veterinarians meets every other year on the odd years.
The Australian Committee of the AAV (AAVAC) meets
yearly (see Table 1.1).
Education
There are numerous journals and educational materials
that provide information about avian medicine. The
AAV’s Journal of Avian Medicine and Surgery is an inter-
national journal that provides information on the medi-
cine and surgery of captive and wild birds and publishes
scientific articles, book reviews and information regard-
ing upcoming AAV meetings in its accompanying
Newsletter. There are other resources listed in Tables 1.2
and 1.3.
Information sharing with veterinary colleagues is also

available on the Internet. Forums such as Veterinary
Information Network, Avian Medicine On-Line and
Exotic DVM Readers’ Forum (see Table 1.2) allow veteri-
narians from all over the world to communicate directly
concerning their cases and experiences.
2 C l i n i c a l Av i a n M e d i c i n e - Vo l u m e I
Fig 1.1a | A veterinary clinic’s heart is its staff, who ideally are Fig 1.1b | Educating one’s self and staff is much easier with
devoted, dependable, friendly, compatible and committed to access to current textbooks, references, newsletters, brochures
patient care, service and hospital quality from floors and plants and CDsl.
to attire. From record keeping to honesty and controlling costs,
a veterinarian’s dream can come true if everyone works at these
goals and the work is made enjoyable. meetings of these organizations will provide opportunity
for hands-on experience via wet lab attendance to
improve one’s practical skill, and direct interaction with
others in avian veterinary medicine. Ideally, a novice
avian practitioner would work directly with an experi-
enced avian veterinarian. When this is not possible, a
referral/phone consultation relationship with an experi-
enced avian veterinarian will allow one to comfortably
refer complicated cases, and to properly handle those
cases that are within one’s current skill level, while one’s
diagnostic and therapeutic abilities increase. Wild bird
rehabilitation organizations are often in need of veteri-
nary services. In exchange for these services, practition-
Fig 1.1c | Educating the public is the goal of a good staff.
ers will gain valuable experience in handling and will
Brochuresl, newsletters from the clinic or product distributors,
web sites, clinic-sponsored classes and guest lectures all con- build confidence in their surgical abilities without fear-
tribute to client education. ing the loss of a beloved pet bird. Ownership of birds of
various species will make the practitioner comfortable
For those veterinarians who are interested in specializ- with behavioral differences among species.
ing in avian medicine, The American Board of Veterinary
Practitioners (ABVP) has approved residency programs The goal of this text is to assist the veterinarian in
leading to board certification. Alternately, experienced becoming a competent avian practitioner. Knowledge of
practitioners may apply for ABVP-Avian certification with- one’s limitations regarding both equipment and experi-
out completing a residency. In either case, the current ence is part of this qualification.
procedure for becoming a Diplomate of ABVP-Avian
The American Animal Hospital Association (AAHA) 2003
Practice includes writing case studies, passing rigorous
written and practical examinations, as well as satisfying study on standards and patient care states that failure to
other required criteria. A similar but more academically educate clients is the leading reason pets do not receive
oriented credentialing system has been established in optimal care (this study is available on the AAHA web
Europe and is called the European College of Avian site, see Table 1.1)1 A knowledgeable staff and
Medicine and Surgery (ECAMS). appropriate educational support material is the under-
pinning of client compliance (Figs 1.1a-c).
KNOWLEDGE AND EXPERIENCE

The first challenge is to acquire the knowledge and
MARKETING SERVICES
experience necessary to practice avian medicine in a Once the decision has been made to incorporate avian
manner on par with other branches of veterinary medi- medicine into the practice, attracting prospective clients
cine. One needs to study the available reference materi- is a priority. This can be accomplished through advertise-
als, including the journals and proceedings from the ments in various modalities, including the telephone
professional organizations listed in Table 1.1. Attending directory, various Internet group listings, newspapers,
Chapter 1 | C L I N I C A L P R A C T I C E
3
pet stores and in the “veterinary services” section of bird

magazines. A guide to help locate additional advertising
venues is available.4
The following questions can be used to define specific

emphases within avian medicine. Some items may pres-
ent areas for future expansion of your knowledge and
the scope of your practice’s client services.
Jan Hooimeijer
What makes your practice distinctive?
Does your practice possess specialized equipment and
procedures (eg, endoscopy, laser unit, microsurgery)?
Does your veterinary or technical staff have specific Fig 1.2 | Bird expositions are a common source of sick birds in
the pet industry.
training in the areas of avian medicine, surgery, nurs-
ing or behavior?
Are classes or consultations offered to clients for Renting a booth and showcasing your clinic will allow
behavior disorders? you to meet hundreds of bird enthusiasts. Although this
Does your practice carry recommended diets, bird-safe is a high-visibility opportunity that may bring new clients,
and appropriate toys, perches or caging? there are disadvantages. The most obvious problem is
Are house calls offered? that the very presence of an avian veterinarian at these
Is emergency service for avian patients provided? shows implicitly condones their existence. (Fig 1.2).
Therefore, conflicts of interest may arise between sellers,
Colleagues who do not treat birds can be a good source buyers and veterinarians at such an event.
of referrals. Pet store owners and bird breeders may
refer their customers if a good relationship is developed Dr. Jan Hooimeijer of The Netherlands has developed a
with your practice. unique offering for bird owners who desire to share
their passion for their birds. He implements a strict
Bird marts, bird shows and bird fairs are very popular in client education program and regimented standards that
the USA. Educating the public of the inherent dangers of must be met by the clients. These include recommenda-
these bird fairs should be a goal of avian veterinarians, tion of an organic formulated diet, disease testing and
responsible bird breeders and bird clubs. Currently, such behavior classes. Log on to www.harrisonsbirdfoods.com
events involve bird traders, neophyte hobbyists (the latter for further information. Dr. Hooimeijer’s clients are then
group often having the best of intentions) and a number of invited to attend a “Bird Walk,” a yearly celebration held
uneducated individuals, who often purchase birds on in a local park, and the public and media are invited to
impulse. Birds at these fairs sometimes are poorly bred, attend. Some 400 clients and their family members
incorrectly fed and/or improperly raised. Husbandry prac- attended in 2002, and the event was covered by national
tices prior to the fair are unknown, and the co-mingling of television (Figs 1.3a,b).
species from various breeders that occurs at the fairs can be
a major source of disease exposure and transmission. If a Another modality for attracting clients is to offer free
bird is purchased from a bird show or bird fair, it should be educational classes after hours in the clinic, a local pet
quarantined from other birds in its new household, store, local university or other continuing education
although this seldom is accomplished. Sadly, the volume- facility. (Fig 1.4) The classes can cover topics such as
oriented, discount-minded pet store often is a similar choosing a bird, bird behavior, nutrition and first aid.
source of potentially diseased and compromised birds. Flyers for the classes can be placed in pet stores, univer-
Fortunately, awareness of these problems is increasing in sity bulletin boards, supermart bulletin boards, and
both the USA and the EU. In the interim, encouraging advertisements can be placed in local newspapers. The
clients to at least consider the methods of breeding, raising, classes can be also be promoted with flyers in the hospi-
feeding, testing and hygiene that are practiced by the seller tal, on the clinic’s web site and in the clinic newsletter.
prior to purchase will decrease the risk of acquiring a sick This will attract current clients as well as prospective
or debilitated bird. See Chapter 3, Concepts in Behavior for ones who are interested in becoming more knowledge-
comments on proper husbandry and raising techniques. able about bird care.
For guidelines on helping owners to choose a pet bird, see
Chapter 2, The Companion Bird. Client referral is an excellent method to increase clien-
tele, reflecting the satisfaction of an existing client and
Despite all these problems, avian and exotic animal expo- generating positive advance impressions in a new client.
sitions are an acknowledged source of potential clients. The extent of this “word of mouth” client referral will be
Jan Hooimeijer
Fig 1.4 | Classes at public meeting places and sanctioned by
clubs, schools and other public groups serve as the bedrock of
educated clients. This gathering at Pine Jog Environmental Center
in 1970 led to a university course on aviculture at Florida Atlantic
University. From this small group came leaders of aviculture,
founding secretary of Avian and Caged Bird Society of Ft.
Lauderdale, FL (Ellen Tannerhill); a president of the American
Federation of Aviculture (Tom Ireland); head curator of birds at
Sea World, Orlando (Sherry Branch); Harvard Botanical collection
director (George Staples); organizational president, AAV and HBD
(Greg Harrison); president of ZEN, editor, Exotic DVM (Linda
Harrison); owner, Palm Beach County, FL, oldest bird pet shop,
Fins, Furs and Feathers (Charlie Holland); four other pet shop
owners and a dozen avid aviculturists. One lady later became the
wife of the head of veterinary services at Busch Gardens, Tampa,
FL — she and her husband still breed birds some 20 years later.
Jan Hooimeijer
Fig 1.3a,b | Dr. Jan Hooimeijer has an annual “Bird Walk” to

proudly show off his clients and their family members. More
Mimi Walling/We Shoot Birds

than mere pets, Jan molds his patients into a cohesive unit.
Bicycle rides and family outings like this strengthen the clinic-
client bond. Clinic support of bird clubs or bird-oriented groups
concerned with parrot welfare provides opportunities for the
clinic to impact the bird world in a very important way.
Fig 1.5 | A client waiting room with a pleasant presentation of

based to a great extent on client satisfaction. Client satis- safe toys, educational materials and veterinarian-only dispensed
faction starts with a clean, comfortable, bird safe, well- bird foods makes a strong statement about the value of these
planned clinic with a friendly, knowledgeable staff and items. Selling only items endorsed by the staff reduces confusion
and improves client compliance.
minimal waiting time. When technicians and doctors
have ample time to spend discussing educational mate-
rial and answering questions, this reflects concern and Having photos of recommended pet birds at various
genuine interest in the patient, which pleases clients and locations throughout the clinic lets clients know of your
impresses upon them that the staff and doctors are com- special interests. A photo album containing photos
petent. Clients also are impressed with professional either solicited from your clients, or taken at your hospi-
achievement awards, certifications achieved by the hos- tal of the clients and their birds, is a very popular item
pital (eg, AAHA) or staff with advanced training. They in the waiting room.
appreciate knowing about areas of special interest and
the number of years that the staff and doctors have been FOOD, TOYS AND OTHER BIRD
involved in bird treatment. PRODUCT SALES
Let clients know about your continuing education efforts, Clinic service and income can both be increased through
any papers you publish or news items written about your the sales of recommended bird food, toys, books,
clinic. These items can be put on web sites, in newsletters perches, carriers and various other products. Toy selec-
or in waiting room binders for the client to see. tion should be based on bird-safe toys (Figs 1.5, 1.6a,b)
5
Fig 1.6a | Unsafe toys include clips like the one caught on this Fig 1.6b | Unsafe toys can trap a bird by the foot or leg. With
African grey’s beak. For more on safe toys, see Chapter 6, its owners in the next room, this Amazon was totally silent as it
Maximizing Information from the Physical Examination. chewed its leg free from being caught in a toy’s rings.
Fig 1.7 | Just because a toy is made Fig 1.8 | Staff at The Bird Hospital Fig 1.9 | This boarding facility offers an obser-
for a bird does not ensure it is safe. removes unsafe metal (galvanized clanging vation window from the reception area. Plants,
The Amazon in fig 1.6b mangled its metal bells and clips) and replaces them up-to-date periodicals, and a clean, fresh pres-
foot with this set of rings (top). Similar with stainless steel chain and chain “quick” entation attract clients.
metal circles are used on this key ring links. Avoid man-made fibers like nylon in
toy (bottom), which could easily trap a toys, and instead use natural cotton,
toe or foot. leather, sisal or hemp.
such as woven palm leaves, leather, wood and unbreak- once yearly to be eligible for after-hours emergency serv-
able plastic. Since many chains, mirrors and toy clips (Fig ices. The receptionist informs callers, shoppers, food
1.7) are made of unsafe metals, clips should be switched and toy buyers that a physical exam and current testing
to stainless steel C-clips (Fig 1.8). These can be bulk are required for eligibility for emergency service and
ordered and the cost can be incorporated into the price
boarding services (Fig 1.9). This maintains client commit-
of the toy.
ment to routine care for their birds and reassurance that
they have access to emergency services when needed.
AFTER-HOURS EMERGENCY
SERVICES Qualified veterinarians may give special training in avian
Service availability is another factor in client satisfaction. emergency medicine to local emergency clinic person-
Weekend and late-night office hours are a convenience nel. Such training should emphasize stabilization of sick
for clients who work during weekdays. An answering birds and include basic nursing care such as the admin-
service allows clients to talk to a real person after hours istration of injections, selection of medications fre-
when needed. Clinic brochures can be offered to give quently administered in avian emergencies, gavage-feed-
information on office hours, special services and direc- ing techniques and general supportive care. Avian veteri-
tions to the clinic.
narians in several major cities provide training programs
Offering a 24-hour emergency service is an advantage including procedure manuals for emergency clinicians in
that clients value and appreciate. One author (GJH) their area. This often allows the avian veterinarian to
employs a reasonable policy that requires clients to have consult on emergencies via telephone, decreasing the
physical examinations performed on their birds at least demands of providing 24-hour emergency care.
Fig 1.10a | House call kit. Fig 1.10b | Needles, blood collection tubes, styptic and materials
for record keeping.
Fig 1.10c | Suture, simple surgical instruments, heparin, slides Fig 1.10d | Rotary drill, stethoscope, culturettes, syringes and
for smears and injectable antibiotics. medications round out the kit. Fresh, clean towels and species-
specific equipment like nets are included as called for by the
house call.
COLLEAGUE RELATIONSHIPS requirements or permits that may be necessary when

house calls are added to your current practice.
Developing and maintaining a positive professional rela-
tionship with colleagues benefits everyone. Local veteri-
narians can be excellent sources of referral cases.
Lectures given at local veterinary associations will Practice Equipment
increase referrals from these colleagues.
The operating microscope is one of the most useful
tools in avian practice (Fig 1.13). A variety of types are
HOUSE CALLS
available, and some have automated pedal switches that
House calls are a convenience that clients appreciate. allow hands-free adjustment of focus, magnification
This is especially important for clients with numerous power and zoom-in view. Some operating microscopes
birds or birds that are too large (swans, geese) to trans- have photographic capabilities so that pictures can be
port. A house call kit (Figs 1.10a-d) can be easily made taken of the image seen through the microscope. The
using a tool kit from a hardware store. Significant data operating microscope greatly enhances visualization dur-
regarding husbandry and potential disease can be ing surgery. It is useful for physical examinations of
obtained with a visit to the home or aviary. (Figs 1.11a-e) smaller birds such as canaries and finches.
A video of the facility can be a useful alternative if a
house call is not possible. See Chapter 6, Maximizing Head loupes (Fig 1.14) are helpful for enhancing visuali-
Information from the Physical Examination for an ideal zation, and are less expensive and more portable than
psittacine aviculture setup. For an example of a mobile operating microscopes. A magnifying loupe allowing a
practice see Figs 1.12a-g. Be certain to check with your minimum of 4 to 8x magnification is needed for many
state regulatory authority regarding any additional avian surgeries. Various of types are available, with and
7
Fig 1.11a | House calls reveal a world one would not suspect Fig 1.11b | The husbandry of an aviculture facility is best
unless seen: several tens of thousands of dollars of champion- observed firsthand. Note the hardware cloth door. This type of
bred show canaries packed into 70 cages, stacked in one large wire is zinc coated and potentially toxic. The feeding of seeds
room of a physician’s home. An outbreak of polyomavirus and allowing debris to accumulate are not ideal practices.
allowed a rare visit into this private aviculture world. Infectious
disease will rapidly spread in this type of inadequate housing.
Fig 1.11c | Turtle eggs incubated in the Fig 1.11d | Housing mixed ages and species Fig 1.11e | Rodents leave a black
same room with parrots. Salmonella and together can potentiate disease outbreaks that a streak from body oil on the wall
other problems are invited by such meas- house call can identify and prevent. over this perch in the cockatoo
ures. facility of a prominent US zoo. The
heavy stain indicated a lack of
effective pest control measures.
without light sources. Head loupes make the field of Microsurgical equipment also should be a part of avian
view appear closer, rather than actually magnifying what practice. This is discussed in Chapter 35, Surgical
is seen. Endoscopy equipment is another essential in Resolution of Soft Tissue Disorders.
avian practice (Figs 1.15a-h). Currently (and since the
inception of avian endoscopy) the most commonly used AVIAN ANESTHESIA EQUIPMENT
endoscope is a rigid 2.7-mm with operating sheath (see In avian medicine a semi-open, non-rebreathing system
Chapter 24, Diagnostic Value of Endoscopy and Biopsy). is recommended. Supplemental heat capability is critical
Several types of biopsy forceps are available to use with for success in extended avian surgeries. For further
the operating sheath. Most endoscopes can be equipped information, see Chapter 33, Updates in Anesthesia and
with cameras and video monitors, and photographs can Monitoring. A mobile field units for endoscopy (Figs
be taken from the image seen through the endoscope. 1.16a-f) and anesthesia (Figs 1.16g) can be made.
These images can be recorded to a disc or printed as a
hard copy, which allows documentation of the endo- ULTRASOUND
scopic procedure. There also is a 1.2-mm semi-flexible
Ultrasound can be a useful diagnostic modality, although
endoscopea that is especially useful for endoscopy of the its use in birds is limited by patient size, conformation
trachea of small birds such as cockatiels and canaries. A and by the presence of air sacs.5 Ultrasound is particu-
flexible endoscopeb is available and comes equipped larly useful in differentiating abdominal swellings.7
with grasping forceps useful for gastrointestinal Further information on avian ultrasonography can be
endoscopy and foreign-body removal. found in Chapter 25, Advances in Diagnostic.
Thomas M. Edling
Fig 1.12a | A mobile house call practice allows the veterinarian an opportunity to bring
state-of-the-art technology to various clinics, malls, zoos, aviculturists and private owners.
Thomas M. Edling
Thomas M. Edling
Fig 1.12b | Miniature laptop computers and compact equip- Fig 1.12c | Intensive care cages with heat, humidity, oxygen
ment powered by generators, batteries or plugging into an out- and nebulizer capabilities in the mobile clinic.
side source allow all laboratory procedures to be performed.
Thomas M. Edling
Thomas M. Edling
Fig 1.12d | Treatment area in the mobile clinic. Fig 1.12e | Mobile clinic surgery.
Thomas M. Edling
Thomas M. Edling
Fig 1.12f | Storz endoscopy video monitoring equipment. Fig 1.12g | Isoflurane, sevoflurane, oxygen, monitors, scav-
engers and surgical support equipment in the mobile clinic.
9
Espen Odberg
Fig 1.13 | A complete surgical suite in The Bird Hospital, allowing Fig 1.14 | The General Scientific Corporation’so ergonomically
video from rigid or flexible endoscopes and operating microscopes. designed optical magnification system allows comfortable oper-
ating distance, lighting and magnification for microsurgery and
delicate examinations.
Fig 1.15a | A set of four rigid endoscopes in Fig 1.15b | Flexible endoscope, allow- Fig 1.16a | Steps to custom power an endo-
sizes to accommodate procedures on various ing flushing, suction and biopsy of sites scope for portability. The embedded magnifi-
size birds and a multiport sheath (top). difficult to reach with a rigid scope. cation focus lens is removed from over the
light of a Surgitel magnification scope.
Fig 1.16b | Close-up of removed lens Fig 1.16c | The modified light is ready to Fig 1.16d | Light source snapped onto
(left) and the custom-made adapter (right) be attached to the endoscope. the endoscope.
to allow this unit to power an endoscope.
Fig 1.16e | The final scope with battery pack for full mobile Fig 1.16f | Alternatively, an electrical plug can
endoscopy. The author (GJH) uses it for tracheoscopy without run the unit instead of battery power. The total unit
anesthesia on canaries. This is a portable, lightweight field unit price is several thousand dollars less than a tradi-
and it also produces more than enough light. tional light source and flexible fiberoptic cable.
Fig 1.16g | A field anesthetic setup. A plastic drink bottle is filled

with cotton wool and two straws or tubes are glued in place, one in
the opening of the bottle neck and the other in a hole made near the
neck. The neck tube is attached to a second bottle fashioned as a
facemask induction chamber. The bird is placed in the induction mask
and a towel seals around the neck. The anesthetist puffs (blows) on
the second tube in the bottle with the cotton that has had 10 cc of
isoflurane, halothane or ether added to the cotton. The anesthetic gas
enters the induction mask. No more “blowing” is done until the level
of anesthesia is so light that more gas is needed. Human exposure
to volatile anesthetic gases must be considered when using an
open system such as this without suction or exhaust. This semi-
closed system avoids the waste of a mask with cotton and anesthesia
in the mask itself. In a plain mask system it is difficult to control the
anesthetic depth. With the anesthetic generator chamber one has
more control, which in this case required covering the chamber with a
stocking cap to keep the chamber temperature lower, as the sun pro-
duced heat that was causing too much anesthetic in the air-gas mix-
ture, and birds were going down too fast and too deep.
Fig 1.17a | Metal toxicosis is seen commonly Fig 1.17b | The bird is placed in a bag Fig 1.17c | Bird in bag on the cas-
in avian practice. A “bag rad” technique is sealed with tape and the bag is placed on sette being exposed.
used as a preliminary scout film to make scout the cassette; the exposure is made.
films fast, affordable and safe.
Fig 1.18a | Heart-liver-coelomic area view of a cockatiel, with no Fig 1.18b | “Metal” density (arrow) in ventriculus area in left
metal densities. caudal lateral aspect, liver swollen, increased shadowing of
lungs and heart area.
RADIOLOGY GRAM’S STAINING

Radiology in avian medicine is discussed in Chapter 25, Laboratory sampling is discussed elsewhere; however,
Advances in Diagnostic Imaging. In cases where radiol- Gram’s staining will be mentioned here and in Chapter
ogy is used to identify metal-dense particles, anesthesia 4, Nutritional Considerations. In past decades, Gram’s
is not needed, since proper positioning is not required. stains of feces and choanal swabs were used as a major
Most birds can be safely placed in paper bags (Figs method of testing newly imported birds. The paucity of
1.17a-c) and placed directly on the cassette for radiogra- knowledge at that time regarding the methods of safe
phy. This allows a scout film to be safely made and metal venipuncture and subsequent interpretation of results
densities to be visualized (Figs 1.18a,b). made Gram’s stains and cultures the only available diag-
11
Fig 1.19 | A simple Gram’s staining rack that con- Figs 1.20a,b | Placing a wooden-stemmed match head into a bird’s cloaca
fines the stains to the sink area. stimulates the production of a fresh sample. Feces are usually produced
moments after placing the match in the cloaca.
Fig 1.21a | Small birds can be restrained as shown to Fig 1.21b | Lovebird being restrained using clamps to
make jugular venipuncture easier. It stretches the neck hold a towel around the neck like a whiplash collar,
out in an ideal fashion for small to medium-sized birds. immobilizing the bird.
One pulls the right wing caudally to be held with the leg
on the same side as the wing. At the same time the
head is held. A second person draws the blood sample.
Fig 1.21c | Pelican bill restraint. Fig 1.21d | A restraint device for positioning a bird
for radiography or surgery.
nostic tools. In retrospect, this use of Gram’s staining than of illness.

was less than optimal, and the results of the Gram’s
stain often were misinterpreted or over-interpreted. The procedure can be very messy, and various racks (Fig
1.19) make this more manageable. Gram’s stain solu-
Currently, in these authors’ practices, Gram’s staining of tions can be purchased in large-quantity containers,
fecal material is done routinely and prophylactically. making the cost per test minimal. Ideally, the client is
These authors have found that a bird’s intestinal bacter- instructed to bring fresh, voided feces as part of the
ial balance is an excellent reflection of its general nutri- patient evaluation (see Chapter 4, Nutritional
tional state and thus more of a determinate of wellness Considerations). If the client lives a long distance from
a b
c d
Fig 1.22 | a. Single-handed restraint to start a wing clip b-d. The foot and wing are restrained simultaneously.
Wing trim in a light-bodied bird.
Fig 1.23a | Capture of an Amazon in a Fig 1.23b | Positioning the wing for trim- Fig 1.23c | In an Amazon trim, secondaries
towel. ming in a heavy-bodied bird. only (distal to elbow) are clipped on one wing.
the clinic, there is a recommended method for getting a Small birds can be held for jugular bleeding as shown
fresh sample (Figs 1.20a,b). (Fig 1.21a). Towel clamps can be used to secure the
towel once the bird is wrapped (Fig 1.21b). Waterfowl,
RESTRAINT wading birds and water birds in general need the beak
controlled (Fig 1.21c) while raptors need foot restraint
The restraint of birds such as raptors and other birds of
that will prevent taloning or “footing” of either the han-
prey is discussed in the special species chapters. The
dler or of the bird itself. A plastic restraining boardc (Fig
towel restraint is discussed in Chapter 6, Maximizing
1.21d) is ideal for restraining birds for radiography and
Information from the Physical Examination. For groom-
certain other procedures under anesthesia.
ing, the towel makes single-person restraint and proce-
dural accomplishment possible. Old towels can be pur-
chased inexpensively at thrift or secondhand stores. AVIAN GROOMING
Washcloths work well for smaller birds such as budgeri- Grooming birds consists of wing trimming, nail cutting,
gars or parrotlets, hand towels are ideal for cockatiels beak trimming and bathing. Wing trimming for large
and lovebirds, and larger birds such as Amazons and birds involves taking off a variable number of the primar-
macaws need to be wrapped in full-sized bath towels. ies (see Chapter 6, Maximizing Information from the
13
Fig 1.24 | Number of feathers removed from a cockatiel to Fig 1.25a | Sternal ulcer from falling due to over-clipped
stop flight. The bird was flying after an incorrect wing trim. wings.
Fig 1.25b | After removing scab. Fig 1.25c | An African grey, a heavy-bodied bird, that was
falling and creating a sternal ulcer as seen in Fig 1.25a. The
bird is having trimmed feathers pulled under anesthesia to
speed feather regrowth. Use a firm grip with a needle holder,
pull gently and steadily to avoid ripping the follicle and sur-
rounding membranes.
Fig 1.25d | This photo shows the number of feathers pulled Fig 1.25e | Several weeks after the wing feathers have regrown,
from the bird in Fig 1.25c. This is a form of forced (non-drug) the bird regained stability and then flight. At this time, the wing
molt. New feathers will grow in over the following few weeks. should be properly trimmed. If additional sternal trauma can be
The bird must be kept on the floor or in a perch-less cage dur- avoided for several weeks, the ulcer will heal by second intention.
ing regrowth to avoid falling. Proper diet speeds up feather regrowth and healing.
Physical Examination and Figs 1.22a-d and 1.23a-c). The birds can usually be groomed by clipping both the pri-
primaries are cut as closely to their insertion as possible. maries and some of the secondaries. Since there are
Currently, the most popular method of wing trimming is many modifications to wing trims, it is NOT safe for
to remove a variable (4-7) number of distal primary birds to be carried free outdoors after ANY wing-trim-
feathers from both wings. In the authors’ practice, large- ming procedure. Fig 1.24 shows the limited mass of
bodied birds have primary feathers cut from their right feathers needed to achieve flight in a cockatiel that was
wing only, from the elbow to the tip of the wing. Small inadequately trimmed.
Fig 1.26a | Beak and nail trimming. Fig 1.26b | Positioning the upper beak (maxilla) Fig 1.27 | Nail trim in a small bird, sin-
The stone on this electric hand-held inside the lower beak (mandible) to accomplish a gle-person hold. Brace fingers against one
rotary toole has been “loaded” with controlled trim and avoid tongue damage. Note another for maximum control.
plastic or paint by grinding such a sur- the bracing of fingers one against another to
face in such a manner as to “load” the allow fine controlled motions.
stone, creating a smooth surface. This
smooth surface generates heat for
cautery if a beak or nail starts to bleed
during trimming.
Fig 1.28a | Grinding a baby macaw’s nails Fig 1.28b | Using the towel restraint (see Fig 1.28c | Changing angles and fin-
and accustoming it to the rotary tool. Older Fig 1.23), the foot and toes can be con- ger positioning to allow complete hon-
birds unaccustomed to this procedure should trolled. Note the leveraging of the fingers ing of each nail.
always be restrained to avoid biting or grabbing one against another to provide accurate
the drill or causing injury to the bird. control.
is overgrown due to underlying health problems or mal-

occlusion. Some clients will request the beak be dulled
Conversely, excessive feather removal in heavy-bodied to mitigate mutilation or the pain to themselves or oth-
birds can result in sternal ulcers from falling onto hard
ers from being bitten.
surfaces (Fig 1.25a-e). African greys (Psittacus erithacus)
and some macaws, cockatoos and Amazons develop Cement (concrete) perches are useful for providing a
necrotic ulcers of the skin over the distal wing that heal rough surface on which the bird can clean its beak. Even
when the cut feather stubs are pulled under anesthesia. birds that will not stand on a cement perch will often
Personality changes from the sudden instability created
utilize one for cleaning food debris and excess keratin
by a wing trim can occur, especially in sensitive species
off the beak. These perches can be hung vertically in the
such as African greys. It takes weeks for new feathers to
cage to provide the bird with better beak access. Some
emerge. In the authors’ experiences, sternal ulcers usu-
of the available commercial cement perches are too
ally heal successfully by avoiding further trauma (keep-
rough and can cause plantar surface irritation, especially
ing the bird from falling repeatedly) and allowing
if the cement perch is located where the bird elects to
feather regrowth. No medical or surgical (sternal keel
perch for prolonged periods of time. Other brands are
reduction) treatment is usually needed if recurrence of
the trauma can be prevented. too smooth and are therefore not effective in providing
an abrasive surface for the nails or beak (T. Lightfoot,
Beak trimming is not necessary in birds unless the beak personal communication, 2003). A hand-held rotary
15
Fig 1.29 | Close-up view of a nail. Simply cutting the parrot’s

nail tip does not address the two sharp edges of the nail that
are normally present (1,2). Controlled honing with a grinding or
filing device leaves a smooth-surfaced nail and provides weeks,
longer satisfaction for the client. Explaining this to the client and
keeping towels and rotary tools sterile justifies the additional
charges needed for a veterinary facility to provide grooming.
Fig 1.30a | Bathing of birds is a part of grooming. Fig 1.30b | Some “advisors” suggest blow-drying Fig 1.30c| The use of a
Thorough rinsing, towel drying and, in some birds, can be a cause of dry skin and that birds do not like feather cleansing solution
blow-drying may be used. blow-dryers. “Papagei,” a pampered Moluccan cock- provides a good vehicle for
atoo, thoroughly enjoys his bimonthly bath and topical medications (ie,
blow-dry. He moves on his own to get each spot dry. heparin, F10).
He does not have a dry skin problem.
toole is ideal for trimming beaks and nails because it files they remain sharp when only the tip of the nail is
the tissue back in a smooth, controlled manner. Further- removed (Fig 1.29). The rotary tool is ideal for smooth-
more, the heat generated by friction from the filing tip ing ridges so nails do not feel sharp. Again, as with wing
facilitates cauterization if bleeding occurs. A conical- trims, clients should be forewarned that the bird will be
shaped rasping tip (Fig 1.26a) works best for avian less able to maintain its balance after a nail trim and will
grooming. Caution must be used when honing the sides be more likely to fall from its cage or the owner’s shoul-
of the rhinotheca, as the final protective/germinal layer der when the nails are dull.
is very thin and can easily be ground through or burned,
creating a long-standing deficit. To facilitate shortening Giving birds a bath with soap and water is not a routine
of mandibular rhamphothecal length, the maxillary part of the grooming process as with cats and dogs.
rhamphotheca can be inserted inside the mandibular However, some birds really enjoy the process, as do the
rhamphotheca (Fig 1.26b). This positioning not only owners. The type of soap that is used for fine washable
makes the mandibular rhamphotheca more accessible, garments has been noted as safe and effective for bird-
but also helps prevent the patient’s tongue from making baths for the past three decades. It is recommended that
contact with the rotary bit. one drop of soap per 250 cc water be used for routine
bathing. Up to 3 cc soap in 250 cc water may be used to
Restraint for nail trimming is demonstrated (Figs 1.27, clean more heavily soiled feathers. The bird should be sub-
1.28a-c). As the rotary tool is held, fingers should be sequently rinsed in warm water, towel dried, then blow-
positioned to allow maximum dexterity. Birds have dried with an electric dryer (assuming the bird accepts this
sharp ridges on the sides of their nails, and this is why procedure) (Figs 1.30a-c), taking care not to burn the skin.
Fig 1.31a | An Fig 1.31b | If the band Fig 1.31c | Bring digit 1 Fig 1.31d | Continue Fig 1.31e | The band is
aluminum leg band. is too large it can be of the banded leg up to slip the band off. off. Reversing the process
easily slipped up over along the metatarsus and allows the band to be put
the ankle and removed slip the band down over back on for travel needs.
intact. that digit.
Fig 1.32a | Metal cutting pliers Fig 1.32b | To custom-make a very small bird Fig 1.32c | The flat grind wheel on a hand-
can cut only aluminum bands. band remover an Olsen-Hager needle holder held rotary toole can be used to remove the nee-
They will only slightly dent the on the left can have the needle holder plates dle holder’s tips and make the cuts shown in Fig
stainless steel band shown here. ground off as shown in Fig 1.32c. 1.32d. This makes an excellent band remover
for the fine plastic bands and some aluminum
bands used for birds like canaries.
b c
a
Fig 1.32d | Close-up of the cuts Fig 1.32e | A collection of tools used to remove vari- Fig 1.32f | Side cutters and needle-
made to create a band remover ous leg bands: Bolt cutter (a), vise or locking pliers (b), nose pliers are examples of tools used
from a needle holder. metal snips (c), modified needle holder (d), Kras to cut bands and hold metal for bend-
cutterf (e). ing or cutting.
17
b c
b a
a f
d
c
e g
Fig 1.32g | Close-up of band-cutter heads. Metal snip (a), Fig 1.33 | Three split bands (a,b,c): (b) A stainless steel band
modified needle holder (b), Kras cutterf (c). that requires a bolt cutter or a two-vise-grip twist to be
removed. (d,e,f) Aluminum bands: (d) and (e) can best be cut
with modified needle holders; (f) requires one of the two tools
shown in Fig 1.32e. (g) A solid stainless steel ring that requires
bolt cutters once or twice and then vise grips.
Espen Odberg
Espen Odberg
Fig 1.34a | A leg constricted by a band due to accumulation of Fig 1.34b | Malnutrition creates a proliferation of the scales
exfoliated skin under the band. that can accumulate under a band. Over time, a depression in
the leg’s structure is formed by the proliferating skin mounding
between the band and the leg. Pressure from this accumulation
under the band causes constriction of the leg vessels. The foot
can be lost due to necrosis. The custom-made needle holder
band remover usually works best on this problem if the band is
aluminum.
Espen Odberg
Espen Odberg
Fig 1.34c | A metal snip also can be used to cut aluminum Fig 1.34d | Pressure necrosis caused by tissue proliferation
bands constricting the leg. makes a deep groove that severely compromises circulation.
Fig 1.35 | A variety of mouth specula. Fig 1.36 | A mouth speculum cut to reduce beak cracking.
Fig 1.37 | Sections of plastic pipe used to make a Fig 1.38 | Various metal gavage Fig 1.39 | Silicone feeding tubesh.
speculum with a hole through which a gavage device tubes.
can be passed.
BAND-REMOVAL INSTRUMENTS mize this potential problem (Fig 1.36). Specula are also
made from tubular plastic material (Fig 1.37). Plastic
Oversized bands can be slipped off the foot. The band is
specula are commercially available and are found useful
slipped proximally over the tibiotarsal-tarsometatarsal
by some practitioners to obtain pharyngeal swabs for
joint (hock) as high as possible (Fig 1.31a-e). Digit 1 is
PCR tests or culture. Two pieces of gauze also can be
retracted along the joint as shown and the nail is placed
used to hold the beak open. For most procedures, a
under the band. If needed, a lubricant can be applied.
speculum is not necessary.
With light pressure the band slips off. It can be replaced
later if need be. Band cuttersf work well for removing
most small, closed bands. (Figs 1.32a-g) Bands that are Feeding Tubes
too small (Fig 1.33) or build up layers of keratin under Because they are indestructible and easily disinfected,
them from nutritional disorders can cause constriction stainless steel feeding tubesg (Fig 1.38) work best for
(Figs 1.34a-d). The larger steel bands are too strong to most pet birds. Disposable silicone tubesh (Fig 1.39) work
be cut with most band cutters and must be twisted off well for tube feeding neonates, waterfowl or other birds
using vise grips or split with heavy metal (bolt) cutters that cannot bite the tube. Red rubber cathetersg are ideal
(large red-handled device in Fig 1.32e). for long-necked birds such as seabirds. See Chapter 14,
Evaluating and Treating the Gastrointestinal System for
photos of damage avoidance and proper tube placement.
OTHER EQUIPMENT
Specula Microchipping Equipment
Stainless steel specula have the advantages of being Microchips are small electronic devices that can be
indestructible and easy to sterilize (Fig 1.35). However, if injected into the body. The left pectoral muscle is the
the bird bites down aggressively on the speculum, dam- accepted placement of microchips in psittacines. These
age to the mandibular beak can occur. Cutting one side devices contain a code that, when scanned with a reader,
of the speculum so that it is slightly moveable can mini- will provide identification of the bird. One disadvantage of
19
Fig 1.41 | Disposable paper bags make easy Fig 1.42 | A plastic tube perch in a cage.
restraint devices to weigh small birds and
require no cleaning.
Fig 1.40 | A Moluccan cock-

atoo on the perch on a scale.
microchips is that there is no industry standard, and one (Figs 1.43, 1.44; see Fig 1.51b), not on the owner’s
model of microchip reader cannot identify all microchips.6 shoulders (Fig 1.45). This is to prevent injury to bird or
The USA’s FDA and USDA have approved a combination owner. Restraint for assisting doctors, grooming or
AVID code and Fecava code 125-kHz chip reader.i,i1 In administration of treatments is most effectively achieved
Canada, Western Europe and Australia, the chips operate as previously discussed using a towel.
at 134.2 kHz. This ISO chip can be read with a global scan-
ner, but not by the USA 125-kHz scanner, which only reads
the corresponding chip.
Avian Practice Staff
Gram Scale Members
Pet birds need to be weighed in grams. Modern digital
All clinic staff should sign clinic confidentiality agree-
scales allow placing the bird on a perch (Figs 1.40). The
ments; professional staff should include this agreement
tare function on these scales will allow automatic deduc-
as part of their employment contract. Contracts should
tion of the weight of a box, bag or towel from the digital
have buy-outs and exit strategies well outlined and
readout. These digital scales can be fitted with an AC
should be renewed to keep them effective. Without
adapter to avoid constant battery replacement. Most pet
these procedures chaos is invited.
birds will sit on a perch to be weighed. For those that
do not, various bags (Fig 1.41) work and they are The delineation of duties within the course of an avian
replaceable without cleaning. appointment will vary between practices. The relative
experience of staff, technicians and doctors, as well as
Examination and Clinic Cage Perches the ratio of these and the current level of activity, makes
Acrylic perchesj (Fig 1.40) are ideal clinical perches for cross training and flexibility advantageous, as in any vet-
the exam room because they are relatively inexpensive erinary practice. In order to give concrete examples of
and can be easily disinfected. Plastic tube perches are how the various steps involved in a patient visit can pro-
inexpensive, easy to clean and the material with which ceed, the authors have assigned specific responsibilities
to construct these can be purchased at any local hard- to each staff member in the following examples.
ware store in multiple diameters. This plastic piping can
be cut to any length to be custom fit to cages (Fig 1.42). RECEPTIONIST
Wrapping these plastic (PVC) perches in removable self-
The demands of avian medicine are different from the
adhering bandage material (ie, VetWrap) offers the bird
demands of small animal practice; therefore, staff mem-
better traction while perching, and hygiene can be main-
bers should be appropriately trained. The receptionist is
tained by changing the wrap between patients.
the client’s first contact with your hospital and a major
representative of the clinic. The receptionist should make
PATIENT PRESENTATION clients feel welcome and comfortable and should be edu-
Birds should be presented to the clinic in travel cages cated enough to answer questions concerning general
Fig 1.43 | Bird in a carrier made Fig 1.44 | A plastic storage box used to transport Fig 1.45 | A hyacinth macaw on its owner’s
of hardware cloth, which is a birds and other small pets. shoulders. An improper presentation mode
potential source of zinc or lead. for a clinical visit.
Lead will will cause a wet test
strip j1 to turn red.
bird care. A competent receptionist should be able to able at special seminars or conferences, such as the
successfully complete paperwork and expedite clients as Association of Avian Veterinarians’ annual conference and
they move in and out of the waiting room. Other respon- the International Conference on Exotics (ICE). There
sibilities for the receptionist may include debt collection, also are programs available through technical colleges
retail ordering of food and toys, organizing reminder throughout the USA. A complete list of veterinary tech-
cards, initiating client callbacks and other communica- nology programs in the USA is available in the American
tion to be sent out to clients. A skilled receptionist can Veterinary Medical Association Directory and Resource
turn the telephone shopper into an appointment. Manual (Table 1.1). Although there currently are no tech-
nical programs that specialize in avian medicine, most
programs do cover exotic animal care. Following are
VETERINARY ASSISTANTS
descriptions of responsibilities that technicians can be
Finding certified technicians with avian experience often trained to perform.
is very difficult. Therefore, one is often forced to train
assistants to support the veterinarian in certain duties. Client Communication
While seldom competent in all areas taught to veterinary
There is a recognized lack of accurate information avail-
technicians, enthusiastic assistants can provide a great
able to pet bird owners. This can be overcome by training
deal of support. Assistants often can be taught many of
technicians to give short talks during appointments on
the technical duties: client questioning, performing fecal
dietary requirements, husbandry and home care. See
Gram’s stains, administering drugs, and assisting in radi-
Chapter 6, Maximizing Information from the Physical
ology and surgery. Assistants can perform procedures
Examination for a form that covers these topics.
but seldom understand all the ramifications or anatomi-
Technicians also can become involved with writing and
cal, physiological, pathological and pharmacological rea-
distributing educational handouts and presenting classes.
sons for their actions. Depending on the size of the hos-
pital and the presence and extent of avian boarding, the
Initial Examination
veterinary assistant and kennel assistant may have over-
lapping duties (see the following section on Kennel After reception, the technicians or assistants project the
Assistants). clinic’s second image to the client. They take the bird
into the exam room, review the case history and records,
Technicians, on the other hand, know why they are and verify that the paperwork is correct including name,
doing what they are doing. They often can support the phone number, bird’s name, age, sex, species and color.
veterinarian by offering suggestions based on practical They should present the clinic philosophy of wellness
understanding, demonstrating the huge difference and education, offer take-home educational material and
between assistants and technicians. start the medical record. (See Chapter 6, Maximizing
Information from the Physical Examination for a form
that can be completed by the support staff.) Procedures
VETERINARY TECHNICIANS are more readily understood and accepted by the client
Veterinary technicians are certified as to their special if visual educational material is presented. Diet, preven-
training. They often need further experience and guid- tive practices, and the physical exam are discussed and
ance to adapt to birds. Training opportunities are avail- performed. An information video on the value of proper
21
surgery. A new small steam generatork is available for

equipment cleaning and is efficient, effective and very
affordable. The steam sterilizes as it loosens debris and
reduces the need for chemicals (Fig 1.46).
Hospital inventory
Technicians should develop a rapport with several med-
ical supply company representatives, increasing the
chances of finding the best prices on drugs and hospital
supplies. In addition, a pharmacy inventory should be
kept so that stock can be kept up to date and reordered
when needed. Shelves should be checked on a regular
basis to remove expired food and drugs.
Fig 1.46 | A steam cleanerk makes

dried matter easier to remove.
KENNEL OR HOSPITAL ASSISTANTS
Kennel or hospital assistants are responsible for weigh-
ing birds daily, and for clinic sanitation including clean-
diet can be shown. A sample of fresh feces is Gram’s
ing cages and rooms. Assistants should be comfortable
stained in the laboratory. The veterinarian can then
around birds because cleaning often necessitates han-
come in to evaluate the records, complete the physical
dling birds without getting bitten, injuring the bird or
examination, record the clinical signs, and form and
permitting the birds to escape. Assistants should be
record a list of differential diagnoses. These are then dis-
astute enough to observe any abnormalities in feces,
cussed and the diagnostic tests necessary are explained
appetite or weight changes, so that technicians and doc-
to the owner. The technician records these and prints
out an estimate, including the diagnostic and treatment tors can be notified. These employees must be able to
protocols. This is explained to the client by the techni- recognize proper placement of perches, food and water
cian, then approved by the client. The owner can then bowls within the cage to make certain the bird is access-
sign treatment permission and price quotation forms. ing these. For example, a nervous bird may sit on a high
perch in an unfamiliar animal hospital environment and
Under veterinary supervision, technicians draw blood, not venture down to the level where the food and water
perform laboratory tests and collect, prepare and prop- are placed. Assistants also may be responsible for mak-
erly submit laboratory samples. Technicians also review ing sure that food and toy supplies are stocked on
cases daily with the veterinarian. shelves and ensuring that any such items offered to hos-
pital and boarding birds are safe and appropriate.
Technicians should monitor boarding and hospitalized
Individual items such as cups, toys and carriers should
birds on a daily basis noting and recording appetite, fecal
be marked with the owner’s name so that they are
production, weight and behavior. If any abnormalities are
returned when the patient leaves the hospital.
noted, these should be discussed with the doctor. In addi-
tion, technicians should become competent at performing
routine treatments, preparing medications to be dis- AVIAN BEHAVIORIST
pensed, administering injections, gavage-feeding, adminis-
Biting, screaming and feather picking are frequently
trating oral and topical medications, and performing radi-
encountered problems with pet birds. Owners often do
ography, cytology and blood collection. Technicians are
not know how to react correctly without reinforcing the
usually familiar with medical terminology so they can take
problem. It is ideal to have an in-house bird behaviorist
notes for doctors during exams, surgery and necropsies.
Taking radiographs, ordering medical and surgical sup- to work with clients to overcome these types of prob-
plies, contacting owners for follow-ups on laboratory lems. Behaviorists also can train birds (and their own-
reports and preparing instructions for patients being ers) to overcome such bad habits as refusal to perch and
released are tasks a technician often masters. A competent insisting on staying on the owner’s shoulders. Training
technical staff with such skills is irreplaceable. Technicians for behavioral work can be obtained by attending confer-
also assist in surgery, including preparing the operating ences and seminars and by consulting with behavioral
room for surgery, monitoring anesthesia and patient experts. For further information see Chapter 3, Concepts
recovery, and cleaning and sterilizing instruments after in Behavior.
Fig 1.47 | Padlock cage. Fig 1.48 | White butcher paper.
Fig 1.49 | Central vacuum. Fig 1.50 | Shredder toys.
Hospital Facilities Central vacuum access in the surgical preparation area is

also an advantage, allowing feathers to be immediately
vacuumed as they are plucked.
BOARDING
Fig 1.9 shows boarding birds that can be seen from the Preliminary Testing for Boarding Birds
reception area. The presence of a “clinic bird” in a The policies that are implemented for testing prior to
mixed small animal practice often serves to announce boarding should be tailored to the individual bird and
the practice’s interest in birds. its particular risk factors. For example, juvenile birds,
birds that are exposed to other birds at bird shows and
Boarding birds should be housed in an area located those that accompany their owners to pet stores, should
away from noise and excitement. This is easier to do in be tested more frequently. It is good policy to require
an exclusively avian practice versus a small animal prac- every boarding bird to have a physical examination and
tice, where birds must have a special area away from a minimum laboratory base-line, including a Gram’s
dogs, cats or other exotic animals. Stainless steel or stain, within 6 months of boarding. It may be prudent to
fiberglass cages, such as those used for dogs and cats, require a psittacosis PCR test at the same interval. This
work well for housing birds because they are indestructi- not only reduces the potential that sick birds will be
ble and easy to clean. Some stainless steel cages can be housed with healthy birds, but also provides client loy-
padlocked (Fig 1.47), which is useful to safeguard alty for the clinic. Birds that have not been tested or
“escape artists” and help ensure the security of very have test results pending must stay in an isolation room
expensive birds. Plastic pipe for perches can be cut to until the test results have been received. An extra daily
any size to fit in cages. White butcher paper (Fig 1.48) is fee is justified for housing in isolation.
non-staining and can be used for the cage lining. The
white paper allows quick visualization of fecal and urate
color and consistency, and this helps monitor the bird’s
TOYS FOR BIRDS
health. For smaller birds, cages can have the bottoms Many clients will purchase toys for their boarding and
removed and be placed directly on the butcher paper, recovering birds. This is good for the bird and also gen-
thus facilitating cleanup. erates income for the clinic. Alternatively, the clinic can
provide inexpensive toys such as native nontoxic woods
Central vacuum systems (Fig 1.49) make cleaning easier. or palm leaf pieces (Fig 1.50).
23
Fig 1.51a | A cockatiel in plexiglas container. Fig 1.51b | Acrylics are lighter Fig 1.51c | Hospital intensive care unitp with toys.
and more scratch resistant than
plexiglas.
top and replacing it with wire (Fig 1.52). It is convenient

to have hospital supplies, such as frequently used med-
ications, syringes, needles and electrolyte solutions,
located in the hospitalization room. Supplemental oxy-
gen should be located in the hospitalization room for
use with patients requiring oxygen therapy. Commercial
brooder-incubatorsp are available that allow control of
humidity and temperature. The authors have found it
easier to keep sick and recovering birds warm if air con-
Fig 1.52 | A plastic tub, its top replaced with ditioning vents are not installed in hospital rooms; this
wire and with a heating pad underneath,
makes a practical homecare unit.
also reduces air from these rooms circulating into well-
bird areas. A simple electric space heater can be used to
increase the temperature of bird rooms needing warmer
temperatures. Heating pads under cages for heat and
other forms of dry heat can cause dehydration. Humidity
should be added as needed.
ISOLATION
An isolation area is necessary for housing untested birds
or birds with unknown illnesses away from other birds
in the clinic. Ideally, the isolation room should have a
ventilation system that is separate from the main clinic
ventilation system. Staff should be instructed to strictly
adhere to precautionary measures associated with iso-
lated birds. These include treating isolated birds last and
Fig 1.53 | A shower stall is made into a cage having scrubs, gowns, gloves, shoe coverings and cold
by placing a flexible panel used to block doors
sterilization dishes that are to be used only for isolated
for toddlers. This makes a practical, easily
cleaned unit for water birds that need frequent birds. Staff also should be instructed on proper room
cleaning with large volumes of water. disinfection procedures.
The authors’ clinic uses a chemical autoclave that

HOSPITALIZATION employs a form of alcohol rather than water for vapor.
The hospitalization room should be a quiet environ- This machine is kept in the isolation room and birds are
ment, separated from the boarding and isolation areas. moved to a bathroom when autoclaving; thus, the fumes
Birds requiring supplemental heat should be housed in help keep this room sterile. Other than the bathrooms,
incubator-type enclosures. Many of these are equipped this is the only room with an exhaust fan in the clinic.
with a heat and humidity source. Most sick birds should The clinic’s isolation area contains a shower to house
be kept at a temperature of 26.7 to 29.4° C (80-85° F) large waterfowl such as pelicans and swans (Fig 1.53).
and humidity of 70% (Fig 1.51a-c). A plastic container This area can be hosed down as needed to help contain
can be used as a brooder by cutting a section out of the odor and mess.
Fig 1.55 | A locked safe is used to store controlled

drug and may be bolted to the floor.
Fig 1.54 | Necropsies should be performed as
often as possible in avian medicine to add to
both the individual veterinarian’s and the avian
veterinary community’s collective knowledge. A
wide selection of tissues must be collected for
histopathologic confirmation.
In larger hospitals and those that also offer hospitaliza- age, temperament and relationship with its owners, each
tion and/or boarding for dog and cat patients, physical visit may be accompanied by the discussion of a specific
distance can serve as additional separation between mul- behavioral concern. In addition, there are educational
tiple sick birds that need to be isolated. Fortunately, few newslettersm available for client distribution.
contagious diseases of birds are commonly contagious Development of a clinic newsletter can be a positive
to pet dogs and cats. Attention must then be paid to addition to client education, retention and recruitment.
appropriate temperature, humidity, and lack of stressful This can cover new innovations in bird health as well as
stimuli when traditional companion pets are present inform clients about new developments within the prac-
with clinically ill avian patients. tice. Newsletters can be placed on the clinic web site.
Educational brochures can be orderedm to place in the
CLIENT RELATIONS reception area. These contain information regarding var-
ious pet bird species, first aid, signs of illness, specific
Once a clientele has been established in the practice, it
diseases, nutrition and hand-feedingn. Bird species iden-
is important to make sure they return on a regular basis
tification books tend to be popular with clients. Having
for continued care of their birds. Appointment
both normal and abnormal feathers available will
reminders for semi-annual exams and laboratory test-
demonstrate to clients the difference (see Figs 6.57k,l)
ing, including Gram’s stains and other recommended
tests, should be sent out every 6 months. Client infor- between healthy and unhealthy conditions of their bird’s
mation foldersl (see Fig 1.1b) can be given to clients so feathering.
they have a record of body weights, health history and
Educational material is available through companies that
identifying characteristics of their bird. These are
manufacture pet bird products such as food, cages and
updated at each visit. Designing a client library that
toys. Furthermore, most of the companies have web
includes an avian veterinary medical text is also a good
sites, and clients can communicate directly with com-
idea (see Fig 1.1b), although avian textbooks contain
pany representatives via e-mail. With the advent of com-
medical terminology that clients might have difficulty
puter technology, web sites have become powerful tools
understanding.
for providing information to people all over the world.
Education and communication are important aspects of Setting up a clinic web site enables thousands of people
maintaining good client relations. Handouts with cur- to see pictures of clinic facilities and staff and to commu-
rent information on pet bird health and disease are use- nicate questions directly via e-mail. A hospital web site
ful in clarifying information that was covered during the with recommended links can also direct clients and
office visit. Topics that might be addressed include metal potential clients to reliable sources of information on
toxicosis in birds, importance of nutrition, safe diet con- the Internet, providing a counterpoint to misleading and
version and zoonotic diseases of concern. Behavioral inaccurate information that can be encountered else-
issues become more prevalent with increased length of where on the web. As a convenience, appointments can
ownership and are becoming more pervasive in our cur- be made via e-mail as well. E-mails can be sent to clients
rent pet bird population. Based on the bird’s species, for follow-up office visits, and appointment reminders
25
also can be sent via e-mail. A clinic web site can provide implications.
an opportunity for clients to download the clinic
newsletter, calendar of events or other educational infor- Additionally, the use of digital cameras for documenting
mation about pet bird health. necropsy findings can be invaluable. The complete
necropsy shown in Fig 1.54 involves opening the skull
Another aspect of client satisfaction is conveying the mes- and demonstrates the value of the camera while illustrat-
sage that the staff and veterinarians take a personal inter- ing a critical portion of the necropsy that is often omit-
est in the client. This can be accomplished by sending ted by many practitioners.
thank you notes for referrals and to thank new clients for
their business. Clients also are very appreciative of expres- For the highest quality pictures, digital cameras should
sions of sympathy such as cards, flowers or donations in have a built-in macro capability (to enable good close-
their bird’s honor when they have lost a beloved pet. ups) and should be capable of image densities of two
megapixels or greater.3
There are special adapters that allow cameras to be

Record Keeping mounted on microscopes to capture microscopic
images, while the addition of macro lenses and built-in
macro functions of some digital cameras will create
COMPUTER SOFTWARE exceptional images when placed directly onto one of the
Increased computer technology has brought many eyepieces of a microscope.
advances to veterinary medicine. One of the most impor-
tant has been the increased efficiency and accuracy of PAPERWORK
record keeping through computer software developed
Although increasing numbers of veterinary hospitals
for veterinary practices. Although there is no computer
have become virtually paperless, there are still several
program currently available specifically for avian prac-
situations that are best addressed by signature authority.
tice, it is possible to adapt small animal programs for
Authorization forms document the client’s understand-
use in avian practice. Estimates for future hospital serv-
ing of and consent to having a particular service or serv-
ices can be written and stored in the computer program.
ices performed and the terms of that service.
When an estimate is needed, the information can be eas-
Authorization forms are commonly used in avian prac-
ily accessed and modified, and presented quickly and
tice, as are forms that limit liability.
accurately. Photographs and radiographs can be loaded
into the patient’s record. This is an advantage when
records must be transferred or a patient is being SECURE ITEMS
referred, because the information can be electronically Keeping cash, controlled drugs and vital records in a
transmitted to another clinic, saving time and eliminat- fireproof safe is important for security. Fireproof con-
ing lost records. Computer programs are able to keep tainers have a lining that generates moisture upon heat-
track of each client’s visit and generate timely reminder ing, making combustion less likely (Fig 1.55). These con-
cards. Computer programs store billing history and high- tainers are guaranteed for only 5 years, as this function
light bills that are overdue, making billing more consis- deteriorates over time.
tent. Computer software also prints and records drug
labels, which precludes mistakes due to illegible hand-
CONTROLLED DRUG S
writing on labels, and allows directions for previous
therapeutics prescribed to be retrieved. In addition, soft- Controlled drugs, radiology monitoring, medical waste
ware allows auditing, individual access and monitoring and OSHA training are areas covered by federal and state
for security measures. laws in the USA. Such subjects need to be reviewed with
your national, state and local authorities.
DIGITAL CAMERA S
Another advance in record keeping is the development
of digital cameras. Digital images allow information to
General Information Avian
be shared quickly among veterinarians via the Internet. Practitioners Should Have
With digital cameras, it is possible to capture images of
the patient and any related conditions or procedures.
Available
Radiographs can be digitally recorded and the file sent
to another practitioner without concern for the physical TRAVEL FORMS
possession of the radiographs and associated legal On many occasions, people wish to take their pet birds
with them while traveling. In some situations, it is neces- PSITTACOSIS INFORMATION

sary to have travel forms that permit the bird to accom- The Committee of the National Association of State
pany the owner. Public Health Veterinarians has compiled a compendium
Travel by car within the USA requires Interstate Health of psittacosis control. The compendium discusses psitta-
Certificates. cosis infection among humans and birds, transmission,
When traveling by airplane within the USA: Form SA-B clinical signs and symptoms, case definitions, diagnosis,
(Official Certificate of Veterinary Inspection for treatment, and recommendations and requirements.
Interstate Movement of Dogs, Cats, and Other Non- Copies of the compendium can be accessed at the
livestock Species) must be filled out by an accredited Center for Disease Control web site (www.cdc.gov/
veterinarian. APHIS form 7001 (US Interstate and ncidod) and at the web site for the American Veterinary
International Certificate of Health Examination for Medical Association (www.avma.org).
Small Animals) also may be used for this purpose.
Travel by airplane outside the United States: An
IMPORT-EXPORT OF PET BIRDS
accredited veterinarian must fill out APHIS form 7001.
The bird owner must then mail or hand-carry this Most parrots are classified as endangered species, which
completed form to the designated USDA-APHIS office, require a special Conference on Endangered Species
along with a processing fee. The form will then be (CITES) permit to be imported or exported to or from
approved by a USDA veterinarian and sent back to the the USA. See Table 1.1 and the discussion on
owner to accompany the bird during travel. Because of Regulations in Chapter 2, The Companion Bird.
the time needed to process this form, owners should
be advised that planning ahead is imperative in order Products Mentioned in the Text
a. Karl Storz Veterinary Endoscopy-America, Inc, Goleta, CA, US,
to receive the completed paperwork in time for travel. 805-968-7776, www.karlstorz.com
Additionally, the country to which the bird is being b. Endoscopy Support Services, Brewster, NY, US, 800-fix-endo,
www.endoscopy.com
exported may have its own forms that must be com- c. Miami Vise, Veterinary Specialty Products, 800-362-8138,
pleted prior to exportation, and may have differing [email protected], www.vet-products.com
d. Poly Perches, 888-765-5971, www.pollyspetproducts.com
requirements regarding testing, vaccination and identi- e. Dremel, Racine, WI, US, 800-437-3635, www.dremel.com
fication. The owner should check with that country’s f. Kras Avian Leg Band Cutter, Veterinary Specialty Products, P.O. Box
812005, Boca Raton, FL, US, 33481, 800-362-8138, [email protected],
embassy in the USA prior to making travel plans. www.vet-products.com
Travel with poultry or hatching eggs for export: g. Feeding Tube and Urethral Catheter, Sovereign, Sherwood Medical, St.
Louis, MO, US
There is a special form for poultry, VS form 17-6. h. Silicone feeding tubes or human female catheters, Veterinary Specialty
Products, 800-362-8138, [email protected], www.vet-products.com.
Unless the birds are hatching eggs and newly hatched Also catheters and tubes A/S, DK-3540 Lynge Denmark or AUV Veterinary
poultry, the veterinarian must go to the premise to Surgeons Cooperative, The Netherlands (31)4855-3355-55
i. AVID, 3179 Hamner Ave, Norco, CA, US 92860, 800-336-2843,
inspect the birds in order to validate the travel form. www.avidid.com
i1.Home Again. Schering Animal Health,
www.homeagainid.com/vets/index.cfm
Contacts for Further Information j. Acrylic perches. Lyon Electric Company, Chula Vista, CA, US,
619-216-3400
Division of Animal Husbandry (850-488-8280) j1.Leadcheck Kit/Hybrivet Systems, Inc., Farmingham, MA
The United States Department of Agriculture k. Steamfast - a small steam generator available from appliance stores
l. Zoological Education Network, PO Box 541749, Lake Worth, FL, US,
(305-526-2926) 33454-1749, 800-946-4782, www.exoticdvm.com, [email protected]
www.Aphis.USDA.gov/travel/pets.html m.Avian Examiner, Harrison’s Bird Foods, HBD International, Inc.
Brentwood, TN, USA, 615-221-9919, www.harrisonsbirdfoods.com
www.Aphis.USDA.gov/us/sregs - US State and Territory n. Juvenile Hand Feeding Formula, Harrison’s Bird Foods, HBD
International, Inc. Brentwood, TN, USA, 615-221-9919,
Animal Import Regulations www.harrisonsbirdfoods.com
o. General Scientific Corp., 800-959-0153, www.surgitel.com
p. Lyon Electric Co. Inc., 1690 Brandywine Ave., Chula Vista, CA 91911-6021
US, www.lyonelectric.com
27
Table 1.1 | Avian Veterinary Medical Organizations and Web Sites

Organization Website
American Animal Hospital Association (AAHA) www.aahanet.org
American Board of Veterinary Practitioners (ABVP) www.abvp.com
American Veterinary Medical Association (AVMA) www.avma.org
Association of Avian Veterinarians (AAV) www.aav.org
Association of Avian Veterinarians Australian Committee (AAVAC) www.vet.murdoch.edu.au/birds/aav/join/htm
European College of Avian Medicine and Surgery (ECAMS) www.ECAMS-online.org
Mid-Atlantic States Association of Avian Veterinarians www.masaav.org/contact.htm
USDA-APHIS US State and Territory Animal Import Regulations www.aphis.usda.gov/vs/sreqs/
APHIS - US Fish and Wildlife Service www.permits.fws.gov (click on Import/Export)
Table 1.2 | Journals and Sources of Information on Avian Medicine

Information Contact
American Journal of Veterinary Research www.AVMA.org
Avian Diseases - Journal of the American Association of www.aaap.info/audis
Avian Pathologists
Avian Examiner www.avianmedicine.net
Avian Pathology (UK) www.tandf.co.uk/journals/tf/03079457.html
Veterinary Record - In Practice www.vetrecord.co.uk
Compendium of Small Animal Practice www.VetLearn.com
Exotic DVM Magazine and Exotic DVM Readers’ Forum www.exoticdvm.com
Journal of Avian Medicine and Surgery www.aav.org
Proceedings American Association of Zoo Veterinarians and www.aazv.org/aazv_001.htm
Journal of Zoo and Wildlife Medicine
Proceedings Association of Avian Veterinarians (AAV) www.aav.org
Proceedings Association of Avian Veterinarians www.vet.murdoch.edu.au/birds/aav
Australian Committee
Proceedings European College of Avian Medicine and Surgery www.ecams-online.org
Proceedings of the European Committee of the Association of www.eaav.org
Avian Veterinarians
Seminars in Avian and Exotic Pet Medicine www.us.elsevierhealth.com/product.jsp?isbn
+1055937X
Table 1.3 | Avian and Veterinary-oriented Web Sites

Subject Comments Contact
Avian Medicine On-line Password needed to enter www.avianmedicine.net
Birdmed Discussion List Password needed to enter www.vet.murdoch.edu.au
For veterinarians, students, /birds/birdmed.htm
technicians, free archives
Exotic DVM For veterinarians and veteri- www.exoticdvm.com
nary students only
Veterinary Information Password needed to enter www.vin.com
Network By subscription, access to
archives
Exotic Animal Network Free www.exoticanimal.net/
Avian and avian medicine- Part of Birdmed – see above www.vet.murdoch.edu.au
related links /birds/aav/avi-links.htm
References and Emergency Care: A Manual for book may be found at www.ama- Ritchie BW, Harrison GJ, Harrison
Emergency Clinics. Seattle, Assoc zon.com. LR (eds): Avian Medicine:
Suggested Reading of NW Avian Vet, 1991. 5. McMillan MC: Imaging techniques. Principles and Application.
1. Cantarzare TE: Compliance begins 3. Kramer M: Practical digital imaging In Ritchie BW, Harrison GJ, Brentwood, TN, HBD Int’l, Inc,
and ends with the veterinary team. for the exotic animal practitioner. Harrison LR (eds): Avian Medicine: 1994, pp 42-43.
DVM Best Practices Supplement of Exotic DVM 4(4):33-35, 2002. Principles and Application. 7. Zantop DW: Differentiating abdom-
DVM Magazine, July 2003, pp 4-7. 4. Herschell GL: Big Profits from Brentwood, TN, HBD Int’l, Inc, inal swelling in birds with ultra-
2. Johnson-Delaney CA (ed): Avian Small Budget Advertising. 1994, p 260. sonography. Exotic DVM 2(3):11-
Publishing information about this 6. Perry RA: The avian patient. In 12, 2000.
02_Companion Bird30.qxd 8/22/2005 1:10 PM Page 29
CHAPTER
2
The
Companion Bird
ANGELA M. LENNOX, DVM, Dipl ABVP- Avian and
GREG J. HARRISON, DVM, Dipl ABVP- Avian , Dipl ECAMS
More veterinarians than ever are willing to treat com-

panion birds. The quality of avian medicine has greatly
improved over the years as evidenced by the increase in
numbers of professional publications, scientists pursu-
ing companion bird research and continuing education
opportunities. In the United States, the Association of
Avian Veterinarians (AAV) began in 1980 as a group of
175 veterinarians. Today, membership tops 3300 veteri-
narians from 43 countries.5 The explosion of new infor-
mation, treatment and surgical protocols provides
opportunities to practice avian medicine at very high lev-
els. This also represents a double-edged sword, as those
wishing to provide veterinary care for companion birds
must be willing to practice at this advanced level and
stay abreast of the current standard of care. It is no
longer acceptable for veterinary professionals to pro-
claim the pet to be “just a parakeet” and inform the
owner there is not much that can be done.
In 1993, the American Board of Veterinary Practitioners

established a board specialty for avian practice, with
rigid requirements for certification. In 2002, there were
92 board-certified avian specialists in 22 states, and in
Canada and the Netherlands.1 Outside the USA, the
European College of Avian Medicine and Surgery
(ECAMS), established in 1993, and Australia’s avian vet-
Jan Hooimeijer
erinary specialist program provide similar advanced

degrees.8 Certified avian specialists should be viewed as
a valuable resource for those desiring second opinions
and referrals on difficult cases. As in any medical referral
situation, human or veterinary, referring veterinarians
should provide complete medical records including radi-
ographs and laboratory results to the referral veterinar-
ian and expect a timely response, written report and
complete follow-up recommendations.
Pet Bird Ownership Typical pet bird owners do not fit a general profile,
although a few statistical generalizations can be made.
in the United States More owners are couples rather than single, and the
majority have at least two children. Personal income
The popularity of pet birds, especially psittacines, does not seem to influence the likelihood of bird owner-
remains strong.2 However, an American Veterinary ship, but level of education apparently does. Persons
Medical Association (AVMA) survey covering 1991 to with advanced college degrees are much less likely to
2001 showed that the percentage of households owning own pet birds. Bird owners are slightly more likely to
pet birds and the actual numbers of birds kept as pets live in urban rather than rural areas. Therefore, the “typ-
had decreased. In that time period, numbers of birds ical” bird owner in the USA may be a young couple with
owned as pets decreased from 11 to 10.1 million.4 undergraduate college degrees, with two children, living
According to most recent statistics, more than half of in a large metropolitan area with a single pet bird.
USA households own a companion animal, and of these
households, approximately 4.6% own pet birds. Yet Companion bird ownership appears to be popular out-
another survey covering 2001 to 2002 by the American side the USA as well. In Australia, pet bird ownership
Pet Products Manufacturing Association (APPMA) showed apparently is even more popular as approximately 17%
6.9 million homes owned a bird. This survey conflicts of households own a bird, with an average of 8.7 birds
with data generated by AVMA and actually reports the per household (R. Doneley, personal communication).
number of households owning birds as slightly increasing.
Birds remain the most popular specialty or exotic pet,

second only to fish. As a comparison, less than 2% of Frequency of
households owned pet rabbits. All other exotic pets sur-
veyed, including ferrets and reptiles, were well below
Veterinary Care
one half of 1%. Practitioners seeing even modest num- The AVMA survey indicated both good and bad news for
bers of pet birds will affirm APPMA statistics proclaiming avian practitioners. On the negative side, pet bird own-
the cockatiel as currently the most popular pet bird ers overall are not likely to seek veterinary care. In 2001,
species in the USA (Table 2.1). only 11.7% of bird owners in the USA reported at least
one veterinary visit. In comparison, 83.6% of dog own-
Bird ownership was strongest in the Pacific and Mountain ers and 65.3% of cat owners reported at least one veteri-
regions of the USA in 2001, while the lowest percentage of nary visit in 2001. On the positive side, however, a 6-
bird owners lived in the West, North and Central regions. year survey indicated the average number of veterinary
visits for pet birds actually increased. An estimated 2 mil-
Table 2.1 | Numbers and Types of Avian Patients Seen lion avian veterinary visits occurred in 2001, compared
in 1 Year at a Busy Avian Practice16 to 1.6 million in 1996. This represents a solid increase in
Patient # Patient # Patient # demand for the services of avian veterinarians. More evi-
Blue-fronted 44 Nanday 9 Hybrid 14 dence for this conclusion can be seen in the fact that
Double Mitred 6 Bronze-winged 3 veterinary expenditures for bird owners increased dra-
32
yellow-headed
Sun 22 Maximillian 7 matically from 37 million dollars in 1991 to 135 million
Lilac-crowned 15
dollars in 2001.
Red-sided 11 White-capped 9
Orange-winged 8 Solomon 20 Budgerigar 99 It is interesting to note those veterinary services most

Red-lored 11 Grand 2 Cockatiel 240 commonly purchased for pet birds. Examinations are
Spectacled 10 Vosmaeri 9 Lovebirds 50 purchased most frequently, followed by laboratory tests,
Yellow-naped 40 Blue and gold 90 Senegal 33 then emergency care. In comparison, emergency care is
Goffin’s 38 Blue-throated 2
not even listed in the top five services most commonly
Indian ring-
necked
10 purchased by dog and cat owners. This does not suggest
Lesser sulfur- Green-winged 19
crested
10 that emergency care for dogs and cats is uncommon.
Hahn’s 11 Canary 20
However, it does support what many avian practitioners
Moluccan 46 Hyacinth 12 Congo A. Grey 122 already suspect. While many bird-owning clients appre-
Umbrella 59 Illiger’s 1 Timneh A. Grey 16 ciate the value of preventive medicine, far too many
Galah 15 Military 7 Chicken 18 others consult the avian veterinarian only in time of
Blue-crowned 20 Scarlet 13 Duck 16 medical crisis.
Green-cheeked 20 Severe 14 Dove 5
Slightly more than half of surveyed clients selected their
Jenday 7 Yellow-collared 8 Flock consult 39 regular dog and cat veterinarian to provide care for their
Chapter 2 | T H E C O M P A N I O N B I R D
31
interaction and typically do not bond to owners, like

finches and canaries, are less often seen by veterinarians
(Fig 2.1).16
Pet Loss, Grieving and

Euthanasia
Most owners bonded to their pets go through a grieving
Greg J. Harrison
process of variable intensity in the face of loss of their
pet. Many choose to be present with their bird during
euthanasia. This necessitates that the avian veterinarian
Fig 2.1 | While undoubtedly popular, birds like canaries and be competent and comfortable with an anxiety and pain-
finches are not presented as frequently for veterinary care as free euthanasia process. In 2000, AVMA published a
are birds more likely to bond with their owners.
guide to humane euthanasia techniques for many pet
species. Included in the list of acceptable techniques
avian pets. Encouragingly enough, 24.2% made their for birds was thoracic compression.15 The AAV responded
selection based on the fact that the veterinarian was a with an editorial requesting this technique be stricken
bird specialist. (Note that this survey does not distin- from the list. In most situations, euthanasia can be best
guish between veterinarians who are board-certified spe- accomplished by first inducing general inhalant anesthe-
cialists and those claiming a “special interest” in avian sia. Euthanasia solution can subsequently be adminis-
medicine). Discouragingly, just as many clients chose a tered by intravenous injection. This technique, per-
veterinarian based simply on location. formed in a quiet, private area with veterinary personnel
relating to the patient in a gentle, compassionate man-
It is obvious avian practitioners have a great deal of
ner, is usually gratefully accepted by grieving owners.
work to do to catch up to our fellow dog and cat practi-
tioners. While bird owners who do seek regular veteri- The same survey of pet bird owners mentioned above
nary care are generally seeking a higher quality of care indicated that the majority of owners would, in the
and more frequent visits for their pets, it is obvious the event of the death of their pet bird, choose private bur-
great majority of bird owners either are unaware such ial on their own property. A surprising number, how-
services are available or not convinced of their value.4 ever, stated they would select individual cremation with
return of ashes.11
Very few owners indicated they had provided for their pet
The Human-Bird Bond in a formal or legal will in the event of their own death.
The great majority of owners, however, said they had
There is no doubt that many owners develop a deep already discussed the possibility and made informal
attachment to their birds, due in part to their relative arrangements for continued care of their pet.11
longevity. A recent survey of bird-owning clients of a
busy avian practice revealed that most owners consider
their pets equal in importance to family members.11 This
must be contrasted, however, to the growing problem of History of Pet Bird
unwanted birds, to which organizers of parrot rescue
facilities can readily attest. Human-bird interaction stud-
Ownership
ies indicate that birds play many of the same roles for The literature is full of tantalizing, although not com-
people as do dogs and cats. Some significant differences pletely documentable, references to pet parrots in his-
between human-bird and human-dog/cat interactions tory. The earliest reference may be Ctesia’s Indica,
exists. More effort is required by the bird owner to elicit which contains a reference to a bird resembling a plum-
a positive response from their pet. Birds require more headed parakeet (Psittacula cyanocephala). Aristotle
time to train than dogs and cats and lose pet quality gave the name Psittace to a similar bird he described.
faster when there is no regular interaction. It has been Frederick II (1194-1250) was said to enjoy the company
theorized that birds may be a more consistent stimulus of an umbrella cockatoo given to him by the Sultan of
for calming interaction than other pets, as owners must Babylon. In 1492, Columbus brought back a pair of
approach birds in a quiet, non-threatening manner to Cuban Amazons to Queen Isabella of Spain. The first
maintain a satisfying relationship.6 Birds that require less sighting of an Australian bird by a European was said to
be on August 22, 1699, when William Dampier spotted a

flock of little corellas off the northwestern coast of
Australia.12 A reference on Aztec burial customs reports
the burial of a prince together with a macaw. It is fasci-
nating to consider the improbable relationship of the
stereotypical pirate and his pet parrot.
Regulations Concerning
Pet Birds
Greg J. Harrison
While regulations exist in the USA prohibiting the own-
ership of some native wild birds, there are few restric-
tions concerning pet bird ownership. Some communi- Fig. 2.2 | The solid aluminum breeder band is often inscribed
ties prohibit the keeping of birds that are considered to with letters (breeder and state) and numbers (year of birth and
ID number) The “TX” means this bird was bred in Texas.
be farm animals, such as geese and chickens. Some
apartment dwellings and condominiums include birds in
pet ownership restrictions. International trade in birds close-banded within weeks of birth. (Fig 2.2) Closed
for the pet trade, however, is regulated by the bands are difficult to remove. They have no legal mean-
Convention on International Trade in Endangered ing other than identification. Using one of these bands
Species of Wild Fauna and Flora (CITES). CITES is an to trace the origin of a bird is nearly impossible.
international agreement between governments to ensure
that trade does not threaten the survival of wild animals Although illegal importation exists, the proliferation of
and plants. CITES entered into force in 1975 and large corporate and small “backyard” parrot breeders
includes over 150 participating governments protecting supplies the pet trade with an ample number of birds at
approximately 5000 species of animals and 25,000 reasonable prices. Many breeders place a band on their
species of plants. Since the adoption of CITES, not a sin- birds when they are very young. Breeders may inscribe
gle protected species has become extinct as a result of bands with any combination of symbols. A typical
international trade. Protected species are classified into breeder band may contain a set of letters identifying the
three Appendices, listed I, II and III. Appendix I species breeder, a two-letter combination indicating state of
are threatened with extinction, and trade is prohibited hatch, and two numbers signifying year of hatch.
with exceptions made for specific circumstances, such as Interstate movement of any bird, including pet birds
scientific research. Appendix II species are not threat- vacationing with owners, requires a state-issued health
ened but may become so if trade is not restricted. Trade certificate completed by a licensed and accredited vet-
in these species must be approved and an export permit erinarian indicating the bird is free of signs of illness. In
granted. Appendix III species may be legally traded, but addition, the destination state may require additional
are listed in order to solicit cooperation of other coun- testing before the bird can cross state lines. Require-
tries to ensure trade is not unsustainable. Specific per- ments are obtained by phoning the destination state’s
mits also are required. Board of Animal Health, or looking up requirements on
each state’s individual web site. That being said, many
Under the classification Psittaciformes, 44 species are owners are oblivious to these regulations and do not
listed under CITES Appendix I, including 13 Amazon request health certificates when they travel.
and 6 macaw species. Within the USA, CITES is enforced
by United States Fish and Wildlife Service division of The destination country similarly determines require-
Management Authority.7 Legal importation of CITES I-, II- ments for entry into foreign countries. Most countries
and III-listed species to the USA officially ended in 1993 require the bird to be identified with a leg band or
with passage of the Wild Bird Conservation Act. Birds microchip. Requirements can be obtained by phoning
legally imported to the USA prior to this act still may the consulate office of the destination country. In the
bear an import band placed at the time of entry into a USA, international requirements can be obtained by call-
USA quarantine station. Quarantine bands are easily rec- ing the local US Department of Agriculture-Animal and
ognized and are imprinted with three letters and three Plant Health Inspection Service office (USDA-APHIS).
numbers. Once birds leave quarantine, there is no legal Alternatively, requirements are posted on the USDA-
requirement to retain the band, and most have since APHIS web site, which also contains information for trav-
been removed. Domestically bred birds are commonly eling with birds into the USA from foreign countries.17
33
Greg J. Harrison
Chris Migliore
Fig 2.3 | The Endangered Species Act forbids the keeping of Fig 2.4 | Moluccan cockatoos (Cacatua moluccensis) appreciate
Queen of Bavaria (or golden) conure (Aratinga guarouba) for human attention, even if it means wearing a costume.
commercial purposes. Feather picking is common in this species.
The movement of CITES-protected species is not regu- potentially zoonotic diseases, in particular, chlamydiosis
lated within the USA; however, international travel with (see Chapter 27, Update on Chlamydophila psittaci: A
these species requires a special permit. Information on Short Comment). Facility and health department person-
travel from the USA with CITES-protected species may nel, along with the veterinarian, must determine a rea-
be obtained from the United States Fish and Wildlife sonable amount and frequency of testing to minimize
Service (USFWS).9 health risk due to the presence of pet birds, especially in
the presence of persons with diseases compromising the
The Endangered Species Act was passed in 1973. This act immune system. New additions should be quarantined
is enforced by USFWS, which regulates commerce con- away from existing birds and residents for at least 45
cerning endangered species. Any bird listed as threat- days.9 Attention must be given to proper cage construc-
ened or endangered may not be traded in interstate com- tion, dietary requirements and cage additions, such as
merce. The Queen of Bavaria or golden conure (Aratinga perches and toys. Birds in care facilities occasionally are
guarouba) is listed as endangered as well as several subjected to multiple caregivers, or are in the care of
other species occasionally seen in pet practice (Fig 2.3). persons with no training or interest in their well-being.
Under the provisions of the Endangered Species Act, Caretakers must receive adequate training in all aspects
these species may not be sold in interstate commerce or of care of their charges and be familiar with common
kept for commercial purposes.9 Government regulations signs of illness.
concerning companion birds are further discussed in
Chapter 1, Clinical Practice.
Birds and Animal Welfare

Birds in Schools and Many well-known animal welfare groups have taken
Care Facilities stands for and against pet bird ownership. In 2002, the
American Society for the Prevention of Cruelty to
Birds are gaining in popularity in nursing homes and Animals (ASPCA) proclaimed January as “Adopt a
other care facilities. Birds most commonly seen in care Rescued Bird Month.” The ASPCA web site contains links
facilities are canaries, budgerigars, cockatiels and love- to a directory of birds available for adoption and worthy
birds (Fig 2.4).13 Many studies suggest the benefits of information on the pros and cons of pet bird
birds and other animals in care facilities. One experi- ownership.3 People for the Ethical Treatment of Animals
mental study documented better attendance and less (PETA), an organization known for aggressive animal
hostility in group therapy meetings of psychiatric rights positions, encourages formulated diets and regu-
patients in rooms containing finches.6 Local health lar veterinary care for pet birds. The same organization,
departments may require veterinary examinations and however, advises against any captive breeding of parrots
periodic testing for animals in contact with residents. and encourages owners to allow pet birds to select a
Veterinarians performing these exams must be aware companion bird of its own species and to free fly.14 The
they cannot certify that any bird is completely free of Humane Society of the USA, the largest animal welfare
Table 2.2 | General Guidelines for Recommended Pet Birds Based on General Pet Quality
Common name and/or representative General traits Potential concerns
species
African Grey - Congo The most demonstrably intelligent psittacine sp. Intelligent and emotionally sensitive; i.e., prone OW
(Psittacus erithacus) Greatest potential for range of vocalizations and to remember negative experiences and make
increasing vocabulary throughout their lives. associations with people and objects that may
Research has documented cognitive association develop into phobias/neuroses. Feather destruc-
between learned words and both actions and tive behavior is a very common condition in cap-
objects. tive African greys.
African Grey - Timneh (Psittacus e. timneh) Similar in appearance and characteristics to the Both positive traits (learning ability) and negative OW
(Darker grey and smaller than the nominate nominate species noted above. traits (neurosis, obsessive behavior) are usually
Congo species) somewhat reduced in this subspecies compared
to the nominate species.
Amazons (Amazona spp.) Active, fairly hardy. Tend to become bonded to Screaming, territoriality, and aggression are NW
• Yellow-naped (A.ochrocephala auropalliata) certain individuals and aggressive toward others. common. Learn quickly to use lunging or biting
• Blue-fronted (A.aestiva) Some are excellent talkers (eg, yellow-nape, to relay their negative opinions. Quieter species
• White-fronted (A.albifrons) double yellow-head, blue-fronts). include: spectacled (white-front) orange-winged,
• Orange-winged (A. amazonica) mealy, festive
• Mealy (A.farinosa)
• Festive (A.festiva)
Budgerigars Can be interactive, enjoyable pets. Genetic predisposition to many diseases and OW
(Melopsittacus undulatus) neoplastic conditions.
Caiques (Pionites sp.) Beautiful, small parrots, playful personalities Although difficult to locate, this genus is a NW
• Black-capped (P. melanocephala) favorite recommended species. Not known for
• White-bellied (P. lucogaster) their talking ability.
Cockatiels Intelligent, popular pets. Can become very Chronic egg-laying in some females. Aggression OW
(Nymphicus hollandicus) attached to the owner or to conspecifics. may develop in males as they mature (especially
toward children). Color mutations may be more
prone to illnesses.
Cockatoos general (Cacatua sp.) Enjoy physical contact. Vocabulary is limited but Screaming, mate aggression (conspecific or sur- OW
intelligible and often endearing. rogate) may be severe. Occasional unpredictable
severe biting episodes, even with humans to
which they are bonded. (Note: Powderdown pro-
duction is pronounced, and is not only a clean-
ing concern, but can cause allergic reactions in
some people and in some macaws)
Smaller Cacatua sp. More active than other, larger cockatoos. Can be hyperactive. Not as predictably accepting OW
• Goffin's (C. goffini) of cuddling and petting.
• Red-vented (C. haematuropygia)
• Bare-eyed (C. sanguinea sanguinea)
Larger Cacatua sp. Enjoy cuddling, petting, and prolonged physical Can develop behavioral and medical problems, OW
• Umbrella or white cockatoo (C. alba) contact. (screaming, feather destructive behavior, self-
mutilation, vent prolapse) related to their
demand for physical stroking and/or other psy-
chological captive abnormalities.
Moluccan or salmon-crested cockatoo As with umbrellas, but can be less predictable Often escape artists. Behavior problems, as with OW
(C. moluccensis) and even aggressive. umbrella cockatoos above, can occur. May be
very destructive with their beaks.
Conure (Aratinga sp.) Beautiful, intelligent birds. Loud, high resonance screams. Can become ter- NW
• Sun (A. solstitialis) ritorial. Not known for their talking ability.
• Jenday (A. jandaya)
• Gold-capped (A. auricapilla)
Conure Historically, were common imports and relatively Established feral colonies of nanday conures NW
• Nanday (Nandayus nenday) inexpensive. Captive-raised individuals can exist in parts of south Florida. May develop loud
make excellent pets. and persistent screaming behavior.
Conure Beautiful, larger conure. Relatively quiet. Historical documentation as carriers of Pacheco's NW
• Patagonian (Cyanoliseus patagonus) disease virus has made owners wary of introduc-
tion into their collection. This may still be a valid
concern in multiple-bird households.
Conure (Pyrrhura sp.) Smaller and generally quieter than Aratinga sp. NW
• Green-cheeked (P. molinae) conures.
• Black-headed (P. rupicola)
• Maroon-bellied (P. frontalis)
Doves, Pigeons (Columbiformes) Gentle, excellent pets. Although the degree of If raised by humans may have no fear or defense OW
interaction (vocal, body posturing) is limited, against dogs or cats NW
there is little or no danger of injury to humans
from bites.
Eclectus sp. (ten subspecies) Most pronounced sexual dimorphism of any Unless socialized early, may become alarmed by OW
• Red-sided (E. roratus) psittacine. “Pensive” when considering novel new situations or locations. Feather destructive
• Vos (E. vosmaeri) items or situations in a secure environment, behavior common. In breeding situations,
• Solomon Island (E. solomonensis) leading to the misconception that eclectus are females will often traumatize males.
dull-witted. Moderately good talkers. Males tend
to be more docile than females.
Finches, Canaries (Passerines) Easy to care for, quiet, pleasant vocalizations. Inbreeding has created genetic predispositions OW
Limited ability to interact with their owners as to multiple disease syndromes in some lines.
compared to psittacines.
35
Table 2.2 | General Guidelines for Recommended Pet Birds Based on General Pet Quality
Common name and/or representative General traits Potential concerns
species
Hyacinth macaw Largest psittacine. Beautiful bird. Temperament Possibly due to genetics or captive rearing limi- NW
(Anodorhynchus hyacinthinus) can be calmer than other macaws. The attending tations, this species can become neurotic/pho-
veterinarian needs to be aware of specific nutri- bic. Research into the parents’ temperament is
tional needs and pharmacologic sensitivities. recommended. Expensive.
Lories and Lorikeets Ring-necks and lories were previously considered Fruit and nectar diet makes droppings messy. As OW
• Rainbow (Trichoglossus haematodus) aviary birds, but can be quite tame when captive with Aratinga sp, their beak sharpness and their
• Red (Eos bornea) raised. Beautiful colors and brilliant sheen to speed make bites, if they occur, painful.
• Dusky (Pseudeos fuscata) feathers.
Lovebirds (Agapornis sp.) Can be very tame and bonded to people or other Can be very aggressive during breeding season. OW
• Fischer’s (A. fischeri) birds.
• Peach-faced (A. roseicollis)
Macaws (Ara sp.) Large, physically active, vocal birds. Intelligent, Need physical outlets for their abundant energy. NW
• Blue and gold (A. ararauna) highly interactive and energetic. Require frequent Loud; screaming can become a problem.
• Green-winged (A. chloropterus) training and structured play to focus their energies. Generally develop a limited vocabulary. Learn
• Scarlet (A. macao) tricks readily. Require a knowledgeable owner.
Mini-macaws Can be excellent, affectionate and intelligent pets. Common as imports in previous decades. Few NW
• Yellow-collared (Ara auricollis) were bred in captivity following cessation of
• Noble (A. n. cumanensis) importation. Therefore the current availability is
• Severe or chestnut-fronted low and the genetic pool is limited for many
(Ara severa) species.
Mynahs Excellent mimics. Have the same interactive limi- Stools are projectile and messy. Prone to iron OW
• Indian hill mynah (Acridotheres tristis) tations as the small passerines. storage disease.
Grass parakeets (Neophema sp.) Quiet, easily maintained birds, often kept in Not as readily bonded to people as many other OW
• Bourke's (N. bourkii) aviaries. parrots.
• Turquosines (N. pulchella)
Pionus sp. Parrots Usually gentle, smaller and quieter than the Generally, limited ability to mimic speech com- NW
• White-headed (P. seniloides) related Amazons. pared to Amazons. Produce a rapid “sniffing”
• Bronze-winged (P. chalcopterus) sound when frightened that is often mistaken for
• Dusky (P. fuscus) respiratory disease.
Poicephalus sp. Parrots Playful, active, usually gentle, fairly hardy. Can become territorial with sexual maturity. OW
• Senegal (P. senegalus)
• Myers (P. meyeri)
Quaker parakeet (Monk) Intelligent, feisty birds, with moderate talking Can become aggressive. Tendency to become NW
(Myiopsitta monachus) ability. Hardy, including tolerance of colder envi- obese and a relatively high incidence of pancre-
ronments. Colony breeders. atic problems. Illegal in some US states due to
their propensity for establishing feral popula-
tions, even in temperate climates.
Ring-necked Parrots (Psittacula sp.) Generally quiet, can be tame and personable. Few, except Old World species disease suscepti- OW
• Mustached (P. alexandri) Were previously thought to be “aviary birds” bility. Some new color mutations may be geneti-
• Derbian (P. derbiana) until captive breeding produced tame, human- cally predisposed to problems.
oriented individuals.
Toucans (Ramphastos sp.) Beautiful, fascinating birds. Recognize owners, Dietary requirements can be difficult to fulfill, NW
• Keel-billed (R. sulfuratus) but limited interaction (may “clack,” but do not including low iron and some live prey. Prone to
• Toco (R. toco) mimic speech or posture as do psittacines). iron storage disease. Voluminous, messy stool.
• Channel-billed (R. vitellinus)
Waterfowl Usually gentle, may be aggressive during breed- Require water for swimming/bathing/drinking. NW
• Geese (Anser sp.) (Branta sp) (Nettapus sp.) ing. Outdoor environment highly recommended. Voluminous stools OW
• Ducks, mallard (Anas platyrhynchos)
• Muscovy (Cairina moschata)
Waterfowl Swans (Cygnus sp.) Beautiful, but often aggressive. Not usually tame as adults
Note: Since disease susceptibility (eg, circovirus and sarcocystosis), nutritional needs and/or dietary sensitives may be dependent upon
the area of origin, Old World (OW) vs. New World (NW) is noted in the final species column.
organization in America, considers only canaries,

finches, budgerigars, lovebirds and cockatiels suitable as
Selective Breeding, Color
pets. Larger birds are not recommended, and reasons Mutations and the Future
stated against ownership include longevity, specialized
needs and demands for care.10
of Companion Birds
Selective breeding has produced a variety of desirable
physical and behavioral traits in many species of com-
The Ideal Pet Bird panion animals. Along with these desirable traits, how-
ever, come some that are less desirable or even detri-
While opinions vary on what constitutes the ideal pet mental to the health of the animal. So-called “puppy
bird, Table 2.2 lists commonly kept birds and some of mills” in the USA in the 1960-1970s produced large num-
their characteristics relating to pet qualities (Figs 2.5- bers of dogs for the pet market without regard to the
2.45). quality of animals produced. Practitioners are beginning
C l i n i c a l Av i a n M e d i c i n e - Vo l u m e I
36
to recognize this phenomenon in pet birds, particularly and docility and spends significant amounts of time rais-
cockatiels (Figs 2.36, 2.37), lovebirds (Fig 2.42) and ing and socializing young birds and feeds a formulated
budgerigars (Fig 2.45). Anecdotal reports indicate these diet (Fig 2.47). The ideal breeder consults with an avian
mass-produced birds have an increased incidence of dis- veterinarian and may offer birds that have been exam-
ease, unthriftiness and shorter life spans. In some cases, ined or even screened for underlying disease conditions.
mass-produced birds are given prophylactic antibiotic Table 2.3 summarizes the ideal characteristics of breed-
and antifungal medications without a medical diagnosis. ing facilities that produce parrots for the pet trade. In
Pathogen resistance is a clear risk with this practice. many cases, the only source of birds available locally
Many bird breeders are producing new and novel color may be those found in pet stores or bird fairs. Buyers
mutations of common species. Unusual varieties of cock- must be aware of the potential for disease when
atiels, budgerigars and lovebirds have been available for unweaned young birds from varying sources are mixed
many years. Avian practitioners now are seeing unusually together. Buyers should question bird vendors carefully
colored Quaker parrots and conures as well. Whether or and obtain a health guarantee. Not all health guarantees
not these mutations are less healthy than their normal are alike and should be examined carefully. Some guar-
counterparts remains to be determined. antees offer to pay veterinary bills if a health problem is
discovered within a certain time period. Some merely
An unusual color variation has been seen in African grey offer to replace the ill bird with another from the same
parrots. These birds fledge with or later develop pink or source, which often is unsatisfying to purchasers who
red contour feathers over various portions of the body (Fig may quickly bond to their new pet.
2.46). This coloration has been linked to circovirus or a
dietary imbalance (see Chapter 4, Nutritional Considera- Increased computer access has allowed people to search
tions, Section II and Chapter 13, Integument). Many of for and purchase parrots over the Internet. While pur-
these birds, however, do not appear to develop other clini- chasing birds in this manner has many advantages, dis-
cal evidence of illness. advantages include potentially shipping young birds
long distances and in some cases, the inability to fully
scrutinize the source.
Selecting Healthy Many commercial hatcheries produce healthy ducks,

Pet Birds chickens, geese and other exotic fowl that can be pur-
chased in small numbers for the pet trade. These facili-
The average pet owner has at least a few choices with ties tend to follow strict disease prevention protocols,
regard to selection of a pet bird. The ideal source is a and often are much safer sources than backyard breed-
breeder with limited numbers of hand-reared offspring ers or animal auctions (see Chapter 21, Preventive
of just a few species. For purposes of disease control, the Medicine and Screening).
ideal breeder does not raise larger psittacines in the
same premises as smaller birds such as cockatiels, love-
birds and budgerigars. The ideal breeder selects for char-
acteristics that maximize pet quality, such as calmness
Comments on Life
with Birds
Table 2.3 | Summary of Characteristics of Breeders of Sharing life with pet birds is not for everyone.
Parrots for the Pet Trade Experienced bird owners understand that birds can pro-
Ideal Not Ideal duce a great deal of dust, dander and mess, require con-
Raises small numbers of birds Raises many birds stant handling to remain tame and in many cases are
Specializes in a few species Many species intermixed at same
facility
long-lived. Many birds naturally tend to dunk food into
Does not mix larger parrots with Larger hand-fed parrots mixed
water bowls and shred toys into tiny bits. Some owners
small species, such as cockatiels, with smaller species can be frustrated by the demands of pet birds and end-
lovebirds and budgerigars
less cleaning routines. Overall, birds require more inten-
Selects breeders to maximize ideal Breeders selected for reasons
pet characteristics other than to maximize ideal pet sive training to remain social than do most dogs and
characteristics: only birds avail-
able, “bargain birds,” unwanted
cats. A well-cared-for parrot may live for many decades.
pets with problems such as
phobias and feather plucking All parrots make noise, and while this fact doesn’t seem
Sells only weaned, hand-fed parrots Sells unweaned young birds to bother parrot lovers, it can bother many neighbors.
Sells birds directly to clients, and Sells birds through venues where
not through pet stores or bird fairs young birds are co-mingled:
It’s important to find out in advance if the noise is likely
pet stores and bird fairs to cause problems. Sometimes the quiet but constant
Raises birds on pellets Raises birds on seeds beeping of a cockatiel may be more offensive than the
37
Greg J. Harrison
Fig 2.6 | Doves, such as this pied ringneck dove (Streptopelia
Jan Hooimeijer
risoria), are gentle and quiet.
Fig 2.5 | The human/avian bond can occur with

common birds, such as pigeons (Columba livia).
Greg J. Harrison
Angela Lennox
Fig 2.7 | Often overlooked as pets, some chicken breeds may Fig 2.8 | The rose-breasted cockatoo or
be good pets for children. galah (Eolophus roseicapillus) is considered
a pest in its native Australia, where free-
ranging birds are captured for the pet
trade.
Greg J. Harrison
Greg J. Harrison
Fig 2.9 | The black palm cockatoo (Proboscigar aterrimus) is a Fig 2.10 | These pied Bengalese (or society) finches (Lonchura
rare, expensive and endangered species that is uncommon in domestica), while commonly kept as pets, are also used as foster
captivity and seldom seen in clinical practice. parents to chicks of more exotic finch species.
Greg J. Harrison
Greg J. Harrison
Fig 2.11 | The appealing cordon bleu finch (Uraeginthus spp.) Fig 2.12 | The yellow-collared macaw (Ara auricollis) is one of
has become expensive due to bans on wild-caught birds and the so-called “mini” macaws that exhibits characteristics similar
aviculture challenges. to larger macaws but in moderation.

Fig 2.13 | Like most mini macaws, this
severe (or chestnut-fronted) macaw (Ara
severa) can be hard to find, because
breeders are often few in numbers.
Fig 2.14 | Although this white phase scarlet
macaw (Ara macao) is rare and valuable, muta-
tions like this are often less resistant to disease.
Greg J. Harrison
Loro Parque
Fig 2.15 | Green-winged macaws (Ara chloroptera) are beauti-

ful and gregarious, but they need special homes because of
their size, noise level, destructive habits and demand for atten- Fig 2.16 | The blue and gold macaw (Ara ararauna) is the
tion. most common macaw species kept as a pet in the United States.
39

Fig 2.17 | The caninde (or blue-throated) macaw Fig 2.18 | The spix macaw (Cyanopsitta spixii) is the rarest
(Ara glaucogularis) is smaller than the blue and gold macaw and likely no longer exists in the wild.
macaw and is rarely seen in captivity.

Fig 2.20 | The military macaw (Ara militaris) is often confused

with the Buffon’s macaw, but is slightly smaller and equally rare
Fig 2.19 | Despite the initial investment to purchase, it is in captivity.
not uncommon for the hyacinth macaw (Anodorhynchus
hyacinthinus) to be moved from home to home due to the
great demands of upkeep.
Friedrich Janecheck
Greg J. Harrison
Fig 2.21 | The white-fronted Amazon (Amazona alb- Fig 2.22 | The blue-fronted Amazon (Amazona
ifrons) is one of the few sexually dimorphic parrots; red aestiva) is probably the most popular Amazon
feathers are found on the wings of the mature male parrot because of its gregarious nature and ability
and not on the female. to mimic, but like the larger Amazons, is fre-
quently abandoned to a rescue facility.

Fig 2.25 | Some communities have banned
the Quaker (or monk) parakeet (Myiopsitta
monachus) because escapees have estab-
lished free-ranging breeding colonies even in
temperate climates.
Fig 2.23 | The double yellow-headed Fig 2.24 |Yellow-naped Amazons (Amazona
Amazon (Amazona ochrocephala oratrix) is auropalliata) are successfully bred in captivity
one of the least commonly seen Amazon par- and are popular pets because they are enter-
rots due to depletion in the wild and their taining talkers, singers and clowns.
aggressive personalities in captivity.

Greg J. Harrison
Fig 2.28 | Small Australian parrots, includ-
ing the superb parrot (or barraband para-
Fig 2.27 | The white-bellied caique keet) (Polytelis swainsonii), are usually
Fig 2.26 | While the black-headed caique (Pionites leucogaster) may be threatened with viewed as aviary birds. However, if an indi-
(Pionites melanocephala) is recommended as extinction in the wild and should not be kept vidual is hand-raised in a family environ-
a pet, it is relatively rare and hard to find. as a single pet. ment, it can be a good pet.
Greg J. Harrison
Fig 2.31 | The sun conure (Aratinga sol-

stitialis) is one of several conure species
Greg J. Harrison
that are commonly bred in captivity, but

even hand-raised individuals are loud
and somewhat aggressive.
Fig 2.29 | A dusky-headed conure (Aratinga

weddellii) is considered an ideal parrot Fig 2.30 | Maroon-bellied conures
because of its size, temperament, hardiness, (Pyrrhura frontalis) are smaller and gener-
lack of mutations and potential for human ally more acceptable as a pet than the
bonding. slightly larger Aratinga species.
41

Greg J. Harrison
Greg J. Harrison
Fig 2.34 | In the USA, African grey parrots
Fig 2.32 | Blue-headed pionus parrots Fig 2.33 | Although infrequently seen (Psittacus erithacus) are being domestically
(Pionus menstruus) are noted for their in practice, pionus parrots (Pionus spp.) bred and managed to eliminate negative
calm behavior and quiet nature, but represent ideal pet characteristics: pre- characteristics that are still prevalent in
are subject to stress-related disorders. dictability, reserved nature, quiet, tidy, imported greys in Europe: feather-picking,
gentle and tolerant. screaming and respiratory infections.
Greg J. Harrison
Loro Parque
Fig 2.37 | The popularity of cockatiel color

mutations brings an increase in disease and
Fig 2.36 | The cockatiel (Nymphicus unthriftiness. Lutinos (with reddish eyes) seem to
Fig 2.35 | Eclectus parrots (Eclectus roratus) hollandicus) is the most common have immune deficiencies and short lives,
are the most pronounced example of sexual patient seen by avian veterinarians. A whereas pieds (such as this pied white-faced
dimorphism: the female is red and the male male is shown. For best results a cock- cockatiel with dark eyes) have fewer health
is green. Eclectus appear to have some atiel should be purchased from a rep- problems.
unique disorders that are not yet fully under- utable breeder with less emphasis on
stood. developing color mutations.
Fig 2.38 | The meyer’s parrot, a member of the Fig 2.39 | Because of their bright colors and clown-like antics, lories
Poicephalus genus, can be an enjoyable pet. (Loricus and other species) in general are appealing, but their traditional
nectar diets result in loose, messy droppings. This particular species, the
black-capped lory, is rare and thus should not be kept as a pet.
Friedrich Janeczek
Greg J. Harrison
Fig 2.40 |The Bourke’s parrot (Neophema bourkii) has all the
same characteristics as other Australian small parakeets and is
becoming more popular as an aviculture bird because of muta-
tions, such as this rosy Bourke. Fig 2.41 |Toucans can be entertaining clowns but are not gen-
erally recommended as pets because of their special dietary and
large housing requirements.
Greg J. Harrison
Fig 2.42 |Lovebirds (Agapornis spp.) are best Fig 2.43 | The hardy Indian ring-necked para-
obtained from a reputable breeder who has not keet (Psittacula krameri) is a common pest bird
concentrated on developing mutations and has in its native India. It is dimorphic: the male has
paid more attention to their long-term health. a distinct ring around the neck, whereas the
Many breeding birds have endemic circovirus. female’s ring is not a full collar.
Fig 2.45 | The budgerigar (Melopsittacus undulatus) is the

most popular pet parrot in the world. Budgerigars bred for
Fig 2.44 | Creating color mutations, such as show are often grossly overweight and have reduced life
this lutino ring-necked parakeet, result in spans. The wild-type green color reflects sexual dimorphism:
weaker birds with more health problems. the cere is blue in males and brown in females.
43
Nico J. Schoemaker
Greg J. Harrison
Fig 2.46 | Unusual red-colored feathers in African grey parrots Fig 2.47 | Weaning a budgerigar to a formulated diet often is
may be linked to a dietary deficiency or circovirus infection. In easier using a mirror. Seed diets are the major cause of illness
many cases, however, these birds remain apparently healthy. in pet birds.
occasional yell from Amazons. Canaries, pigeons, doves, With the above in mind, many things must be consid-
finches, and even female ducks and chickens have been ered before acquiring a pet bird. The biggest birds do
found in homes where neighbors never suspected they not automatically make the best companions. Most of
lived. In many cases, as far as neighbors are concerned, the birds that these authors generally recommend are
the best bird is a quiet bird. medium to small birds, which are easier to manage,
house, feed and train than are large psittacines. While
Appropriately sized cages can take up considerable beauty is in the eye of the beholder, the finches and
space, especially for larger birds. Large cages, play gyms small parrots often are the most ornate. If song is most
and toys can be prohibitively expensive. Some owners inspiring, only one bird has held the title of “Elvis of
seek to cut costs by buying used cages, which may not Birds” for so long: the humble canary. In many cases, for
be safe if the previous inhabitant died of a communica- beauty, size and song, one has to look no further than to
ble illness. Wooden perches and porous items cannot be the tiniest birds to fulfill many desires.
properly disinfected and should not be reused.
So why does one choose to cohabit with a bird? It gener-
Pets often are restricted for owners living in apartments ally comes down to what seizes a person’s heart. For
or condominiums. However, one ingenious owner res- some people, birds fill the void in a way no other pet can.
cued a boisterous Moluccan cockatoo, took it to the
swimming pool and put it on the fence, declaring the
bird to be the condo mascot. While the condo had a no-
pet rule, regulations apparently did not cover mascots.
Conclusion
Avian companions clearly occupy more than just a niche
Medical care for birds tends to be less expensive than in their caregivers’ homes and lives. The importance and
that for other domestic species. An example was heard expertise of avian medical practice must continue to
on National Public Radio program update on veterinary expand to meet the demands of this multi-species disci-
costs for pets entitled, “How Much is that Doggie in the pline. Bird ownership increasingly embraces large and
Window?” The woman interviewed had just spent over small companions, where value often is not related to
$20,000 to treat her cat for cancer. Although many avian the cost of the bird. The proliferation of birds in other
vets have never come close to that sum with a sick bird, non-home settings, debates regarding animal rights and
the interviewee’s expenditure may have been due to her the wide variety of opinions generated by these issues
inability to let go of her pet and not reflective of an will continue to occupy avian medical practitioners and
expensive but successful treatment protocol. caregivers alike.
References and Association: US Pet Ownership and Management Authority web site: 14. People for the Ethical Treatment
Demographics Sourcebook. 2002. www.fws.gov. of Animals web site:
Suggested Reading 5. Association of Avian Veterinarians 10. The Humane Society of the www.peta-online.org.
1. American Board of Veterinary web site: www.aav.org. United States, Armstrong M, per- 15. Report of the AVMA Panel on
Practitioners web site: 6. Beck A: Bird-human interaction. sonal communication, web site: Euthanasia. J Am Vet Med Assoc,
www.abvp.com. J Am Vet Med Assoc 3:152-153, www.hsus.org. 218:669-696, 2000
2. American Pet Products 1980. 11. Independent survey, Avian and
16. Speer B: Bird Numbers, e-mail
Manufacturer’s Assoc. 2001-2002. 7. Convention on International Trade Exotic Animal Clinic of
from AVNVET 12/21/02, 1:45:48
National Pet Owner Survey. APPMA in Endangered Species web site: Indianapolis, 2002.
web site: www.appma.org. Jan PM EST.
www.cites.org. 12. McMillan RJ: The Parrot Society
2003. 8. European College of Avian UK web site: 17. United States Department of
3. American Society for the Medicine and Surgery web site: www.theparrotsocietyuk.org. Agriculture Animal and Plant
Prevention of Cruelty to Animals ecams.online.org/public/ 13. Orosz S: Veterinary management of Health Inspection Service web
web site: www.aspca.org. introduction/asp. birds in care facilities. Proc Assoc site: www.aphis.usda.gov.
4. American Veterinary Medical 9. Fish and Wildlife Division of Avian Vet, 2002, pp 369-374.
03_Concepts in Behavior I.qxd 8/22/2005 12:58 PM Page 45
CHAPTER
3
Concepts in
Behavior
Section I: The Natural Science of Behavior
Section II: Early Psittacine Behavior and
Development
Section III: Pubescent and Adult Psittacine
Behavior
Edwardo Nycander
Concepts in Behavior:
Section I
The Natural Science of Behavior
SUSAN G. FRIEDMAN, P hD; THOMAS M. EDLING, DVM, MS pVM;
CARL D. CHENEY, PhD
Of all the many facets of parrots’ total wellness sup-

ported by veterinarians, perhaps the most challenging of
What is Behavior?
all is behavior. Having adapted over eons for survival in Fundamental to all science is the task of explaining phe-
the free-range environment, many parrot behaviors run nomena by identifying observable, physical events that
counter to those necessary for success in our homes. produce them. This is true with behavioral science as
This challenge is intensified by parrots’ extraordinary
well, where the goal is to explain behavioral phenom-
ability to learn maladaptive behaviors from their often-
ena. In this scientific context then, behavior is anything
unwitting caretakers. Veterinarians also face educational
an animal does that can be observed and measured. This
challenges as their pursuit of a comprehensive and cohe-
includes overt behaviors that can be directly observed by
sive knowledge of behavior often is made difficult by the
others (such as preening and eating) as well as covert
fractured development of the science itself — the natural
behaviors, which can only be directly observed by the
science of behavior historically crosses two disciplines,
individual so behaving (such as thinking and feeling). As
zoology and psychology, each with its own purpose and
a result, covert behaviors are of limited use in our work
methods. Finally, among professionals and laypersons
with parrots due to their inaccessibility. And, considering
alike, there is a general lack of awareness that a science
the difficulty most of us have guessing what members of
of learning and behavior exists within the field of psy-
our own species are thinking in the absence of direct
chology. A sound understanding of this science, known
measures, accurate interpretation of parrots’ covert
as behavior analysis, is critical to successfully keeping
behaviors is all the more remote.
parrots as companions. These challenges contribute to
the current state of affairs in which too many pet parrots
Similarly, the practice of describing what an animal is
unnecessarily fail to thrive due to behavior problems.
rather than what it does is an obstacle to understanding
In this chapter, we provide the foundation for a compre- and changing behavior. Labels, such as “is territorial,” “is
hensive and cohesive understanding of behavior as it dominant,” and “is spoiled,” do not describe behaviors,
relates to facilitating the lives of companion parrots. To they describe ideas. These ideas, called hypothetical psy-
meet this goal, the following topics are discussed: free- chological constructs, are largely untestable theories
range behaviors as a basis for predicting and interpret- about mental processes believed to explain behavior.
ing the behavior of parrots in captivity, a simplified Focusing on constructs often gets in the way of identify-
model for systematically analyzing the functional rela- ing straightforward behavior solutions. To change behav-
tionships between behavior and environmental stimuli, ior, clients must work with behavior directly, and they
and the teaching technology based on the fundamental should be encouraged to move past inferences of covert
principles of learning and behavior. With this informa- behaviors and construct labels to observe and describe
tion, veterinarians will be able to better guide their what their birds actually do. For example, the frequently
clients to proactively teach their parrots successful com- used label “is territorial” often describes a bird that
panion behaviors and effectively analyze and resolve bites; “is dominant” often describes a bird that does not
behavior problems that inevitably arise. step up; and “is spoiled” often describes a bird that
Chapter 3 | C O N C E P T S I N B E H A V I O R : S E C T I O N I
47
screams for intolerable durations. Territoriality, domi- Some researchers reason that “flexible action patterns” is
nance and the degree to which the bird is spoiled can’t a more accurate description of species-specific behavior
be changed directly because they have no tangible form; chains.21 For example, fledglings’ flight skills certainly
however, biting, stepping up and screaming are all improve with practice, as does perching and climbing.
behaviors birds do, which we can do something about. Even simple reflexes can be modified through habitua-
tion26 (eg, cats28) and through sensitization (eg,
Behavior is the result of the indivisible blend of heredity blowflies9). These studies add to the evidence that
and learning. These two processes work toward the same heredity and learning are inextricably entwined. None-
end, ie, coping with environmental change through adap- theless, knowledge of the behavior patterns of free-range
tation. Adaptation through heredity, phylogenetic adapta- parrots, as well as the environmental conditions that
tion, occurs slowly over generations at the species level. elicit and shape them, greatly increases our ability to pre-
Through the process of evolution by natural selection, dict, interpret and manage many parrot behaviors in cap-
phylogenetic adaptation equips each species for common tivity. For these reasons, knowledge of the free-range
lifestyles in their natural habitat. Alternatively, adaptation behavior of parrots is important to improving the care of
through learning is an individual process that occurs captive birds.
within the short span of a lifetime. As defined by Chance,
learning is a change in behavior due to experience.8
SOCIAL SIGNALS
Learning is the astonishing mechanism that equips each
individual within a species to meet life’s ever-changing Among the many things we can learn from the behaviors
circumstances with rapid modifiability. of free-range birds, perhaps the most important are those
that serve a communication function among parrots. This
is a language very unfamiliar to many caretakers, to the
detriment of their birds and themselves. In an interesting
Observations from the Field study on cross-species communication, it was found that
dog pups only a few weeks old were more skillful at read-
Parrots are most brilliantly adapted for the free-range ing human social cues (such as pointing, looking and
environment. For example, the physiology of wings, touching) to locate hidden food than were chimpanzees
beaks and vocal structures prepares them well for the and wolf pups.13 The researchers theorize that dogs
natural behaviors of flight, nest carving and long-dis- uniquely possess this skill due to the process of domesti-
tance contact calls. Clearly these and many other behav- cation in which communication skills with humans were
iors are supported by parrots’ genes and are part of selected.
their natural history. From an evolutionary perspective,
the genes that enable these behaviors likely serve sur- Unfortunately, our parrots’ current lack of domestication
vival functions related to food gathering, courtship and leaves them unprepared to innately interpret human sig-
mating and protection from predators. It is worth not- nals. This puts the onus on us to accurately interpret
ing, though, that the evolutionary origins of many behav- their communications at the same time they are learning
iors often are easier to hypothesize than to prove. to interpret our signals. Observations from the field con-
firm that parrots have a rich and subtle communication
Ethology, a discipline within zoology, is the field of behav- system that involves nearly every feather on their bodies.
ior science most concerned with the study of behavior Head, eye and neck movements, body posture, wings
patterns characteristic of different animal species as they and tail and leg and foot gestures are all used as signals
occur in their free-range environments. More complex to communicate desires, intentions and general comfort
than reflexes, ethologists call these species-specific behav- or discomfort with current events and conditions.
ior chains “fixed action patterns.” Fixed action patterns
are displayed by nearly all members of a species under Caretakers often misunderstand the behaviors used to
similar environmental conditions, with very little variabil- communicate the boundaries of personal space, espe-
ity in the way in which they are performed across individ- cially those that function to back intruders away. Most
uals or instances. According to Gray, these behavior pat- species of parrots use threatening stances rather than
terns are fixed in the sense that the “controlling mecha- outright aggression to drive off perceived intruders in
nisms are ‘fixed’ in the animal’s nervous system by hered- the wild, and many of these behaviors are seen in captiv-
ity and are relatively unmodifiable.”12 In this sense, we call ity as well. These behavior patterns are made up of vari-
them innate behaviors. ous vocalizations and both overt and subtle movements
and postures. Depending on the species, such warnings
There is some debate about how unmodifiable fixed include raised nape feathers with wings slightly lifted, a
action patterns actually are, as few, if any, behaviors can raised foot held open at chest level, directed hacking
be said to be immutable or impervious to experience. motions with an open beak, and growling.18 By not
heeding these warnings, caretakers push parrots to esca- slowly), or contraprepared (in which case the course of
late their message to serious biting. As a result, stress is learning is slow and irregular).” Too often, unknowing
unnecessarily increased and trust is decreased for both caretakers simply expect too many behaviors for which
birds and humans. Learning to perceive, interpret and parrots are contraprepared. This occurs when, for exam-
respond to these signals is essential for building rela- ple, caretakers insist that parrots be petted by strangers
tionships with captive parrots. Veterinarians can help (or for some birds, petted at all), or when birds are left
caretakers become more astute observers of their par- in cages for interminably long durations with nothing to
rots’ “messages” by discussing social signals with them. do (from the birds’ perspective). Of course, the particular
limits of parrots’ behavioral preparedness to learn vary
ACCOMMODATING INNATE greatly across species and between individuals within
BEHAVIORS species; still, knowledge of species-typical behaviors
Other innate behavior patterns common to free-range observed in the free-range environment is an excellent
parrots, such as loud contact calls, wood chewing, food starting point for predicting and interpreting the behav-
flinging and territorial biting, can be challenging to deal ior of different species of captive parrots. It also is essen-
with in the captive setting. Changing the environment to tial to helping clients set reasonable expectations for par-
accommodate them to the greatest extent possible, rather rot behavior in their homes.
than attempting to change the bird, often best manages
these behaviors. For example, simply answering a bird’s
calls, even from another room, often deters parrots from
screaming. Arranging challenging body and brain activi-
Applied Behavior Analysis
ties provides alternatives to chewing household wood-
Ethology informs us about the behavioral norms of dif-
work. Offering smaller, more frequent food servings in
ferent parrot species in the free-range environment.
cages fitted with aprons reduces the mess and waste of
While this information is important to successful com-
food flinging. Allowing birds to climb out of their cages
panion parrot care, it is not sufficient to meet the chal-
when the door is opened, rather than insisting they step
onto intruding hands, reduces the opportunity for biting. lenges of living with captive parrots. It also is essential
By keeping natural behavior repertoires in mind and to have expertise in applying the fundamental principals
arranging the environment to manage them, caretakers of learning and behavior applicable to all species of ani-
can focus on engaging appropriate behavior rather than mals. This is true for several reasons. First is the extent
disengaging problem behavior. to which individuals of the same species are known to
vary from one another and from expected behavioral
norms: Any particular African grey (Psitticus erithacus
THE LIMITS OF LEARNING
erithacus) may exhibit the cuddly behaviors of the aver-
Another important reason for clients to understand par- age umbrella cockatoo (Cacatua alba); and, any particu-
rots’ free-range behaviors is to guide the general limits lar sun conure (Aratinga solstitialis) may be as quiet as
of what our parrots can reasonably be expected to learn.
the average dusky Pionus (Pionus fuscus). Second is the
A classic article on behavior, lightheartedly entitled “The
wide variability across captive environments in which
Misbehavior of Organisms,” reported the breakdown of
companion parrots are challenged to live: Ranging from
novel trained behaviors in favor of fixed action patterns,
quiet, routine lives with a single caretaker to noisy,
even though food reinforcement was contingent solely
unpredictable lives full of kids and other pets, no two
on the performance of the trained responses.3 The
home environments are alike. Third, parrots’ extraordi-
authors called this phenomenon “instinctive drift,” as
nary longevity means most birds will be confronted with
they observed that raccoons tended to rub coins with
decades of changing circumstances for which they need
their paws in a characteristic washing motion rather than
to be extremely flexible learners.
deposit them into a bank; pigs tended to toss coins with
their snouts in a characteristic rooting motion rather
When we change our focus from the species level to the
than carry them in their mouths; and chickens tended to
individual level and from innate responses to learned
scratch the floor with their feet in a characteristic wiping
responses, the natural science of behavior is (much like
motion rather than stand still.
veterinary practice itself) a “study of one.” The field of
Instinctive drift is consistent with Seligman’s continuum behavior science that most explicitly concentrates on the
of preparedness, described by Chance6: “An organism learned behavior of individuals is applied behavior
comes to a learning situation genetically prepared to analysis; it primarily is the applied science of teaching
learn (in which case learning proceeds quickly), unpre- and learning, which is why it is so very relevant to com-
pared (in which case learning proceeds steadily but more panion parrots and their caretakers.
49
ACCOUNTING FOR BEHAVIOR of antecedents that may be functionally related to these

behaviors in many situations:
For lack of knowledge about the fundamental principles
When I leave the bird room, then the bird screams.
of learning and behavior, many people are utterly baffled
When I offer an open hand, then the bird steps up.
by the things their parrots do. Caretakers often describe
When I pet the bird, then the bird bites.
their birds as inscrutable creatures that behave in com-
pletely unfamiliar and unpredictable ways. People don’t In these examples, leaving the bird room, offering an open
realize that many of their birds’ behaviors are the direct hand and petting are all antecedents that are functionally
result of the environments they provide and the pattern related to the specific behaviors that immediately follow
of interactions they have with their birds. A different them (eg, screaming, stepping up, biting). Antecedents sig-
problem is a general resistance to the idea of training nal to each individual which behavior to exhibit in any
animals. To some people, training carries the connota- given circumstance. Without the relationship between
tion of forcing an animal to succumb to the will of their antecedents and behavior, humans would indeed behave
human captors. They believe parrots should be taught as willy-nilly, tossing out behaviors without rhyme or reason;
little as possible so they remain “natural.” On the con- or we may just sit there doing nothing at all.
trary, parrots’ tendency to learn is as natural as their ten-
dency to eat and sleep. Learning enables parrots to In day-to-day conversation, the word “consequence”
adapt to life in captivity and in the wild. It also is the often is used to mean something punitive, as in, “Suffer
mechanism through which we can provide enrichment the consequences!” In behavior analysis, consequences
activities to our birds to improve what might otherwise are those events or conditions that affect the future rate
be a stultifying life in captivity. Concerns about force are of the behaviors they immediately follow. Consequences
immediately dispelled when people learn the teaching are outcomes produced by an individual’s behavior and
technology of applied behavior analysis, which facilitates provide environmental feedback about whether the
positive-first learning solutions. behavior just performed should be repeated or modified
in the future, when similar circumstances (antecedents)
The focus of applied behavior analysis is on the environ- next arise. Of course, consequences don’t always come
mental elements that account for behavior. By changing from people. For example, when a new fledgling bumps
what we do and the environments we provide, we can against a branch when it first takes flight, it will quickly
facilitate behaviors more suited to life in captivity and adjust the angle of its wings. No behavior emitted goes
reduce problem behaviors. This is the way to protect cap- without some consequence in return, and all learners
tive parrots from lives locked in cages, multiple homes actively sift through the feedback to discover how to
and eventual homelessness. To make the most of every make behavior “work.” We can add the following conse-
teaching/learning opportunity, clients need to know how quences to our examples of bird behavior from the pre-
behaviors are learned, how to functionally analyze behav- vious section:
ior, how to teach new behaviors, and how to reduce When I leave the bird’s room, if the bird screams, then
problem behaviors with effective, non-forceful behavior I return.
intervention plans. As veterinarians often are the first and When I offer an open hand, if the bird steps up, then I
only professionals parrot caretakers turn to for help, this praise it.
information is critical to providing the gold standard of When I pet the bird, if the bird bites me, then I
veterinary care and support to companion parrots. remove my hand.
Behaviors that produce valued consequences (such as

THE ABC s OF BEHAVIOR
our return to the bird room, praise and the removal of
Behavior doesn’t randomly spurt out of a behaving an unwanted hand) tend to be repeated or increased.
organism from some internal fount, nor is it performed Behaviors that result in consequences of no value or
in a vacuum or broadcast into a void. On the contrary, negative value tend to be modified, decreased or aban-
behavior has function. The function of any particular doned. In this way, individuals learn to operate on their
behavior is related to the environmental stimuli that pre- environment to produce certain outcomes. Skinner
cede and follow it, called antecedents and conse- called this process “operant” conditioning to emphasize
quences. Antecedents are those events or conditions that the learning process in which the learner is an active
immediately precede a behavior, which set the occasion participant.27 (This is in contrast to respondent or
for the behavior to occur. Not all preceding events or Pavlovian conditioning in which the animal is a passive
conditions are functionally related antecedents, just participant, responding reflexively to eliciting stimuli.)
those specifically related to the ensuing behavior. For
example consider three common parrot behaviors - As can be seen in the examples above, consequences
screaming, stepping up and biting. Below are examples also strengthen the antecedent-behavior relationship.
For example, if stepping up consistently produces some- Step 6: Evaluate the outcome, reanalyze and adjust the
thing of value to your bird, offering your hand will teaching program as needed. Ask: Was the desired out-
become a strong antecedent for stepping up, as it sig- come achieved?
nals the availability of a valued consequence.
Below are three examples of functional assessments for
These three terms, antecedent, behavior and conse- one very common problem, a bird that refuses to step
quence, comprise the ABCs of behavior. Skinner called up from the top of his cage:
this three-term contingency the smallest meaningful unit
of analysis. In other words, no behavior can be under- Functional Assessment #1:
stood in isolation of its related antecedents and conse- Parrot Refuses to Step Up from Top of Cage
quences. Focusing on our birds’ behavior alone has no Antecedent: Caretaker says, “Up!” and offers hand to
meaning because their behaviors are not performed in bird on top of cage.
the absence of antecedents and consequences. Behavior: Bird performs evasive maneuvers running
around the cage top.
FUNCTIONAL Consequence: Caretaker gives up chasing bird and walks
ASSESSMENT/ANALYSIS away.
The process of hypothesizing the functionally related Prediction: Bird will continue to run away from his care-
antecedent, behavior and consequence is called functional taker’s hand in the future to avoid being removed from
assessment. It is an important tool for understanding cage top.
problem behaviors and for devising specific plans to teach
new behaviors. With functional analysis, caretakers can Many people ascribe to hypothetical constructs to
determine exactly what leads to and maintains specific par- explain such “misbehavior.” One pervasive theory
rot behaviors by systematically making changes and evalu- repeated in many popular parrot magazines is that birds
ating the effect on behavior. Finally, caretakers can design are asserting dominance over their caretakers by refus-
new antecedents and/or consequences to facilitate success- ing to step up from the tops of their cages and are vying
ful behaviors — their own and their birds’. When caretak- for control of the human-parrot flock. Caretakers are
ers consider behavior in light of this behavior-analytic told that to solve this problem, they need to increase
approach, the causes of problem behaviors and workable their rank in the eyes of their birds and disallow them
solutions often become very clear. Functional assessment from making any important decisions about what they
and analysis reduce the likelihood that caretakers will do and when, and never allow their birds higher than
resort to unverifiable, hypothetical constructs to explain the caretaker’s heart level. Alternatively, a functional
their parrots’ behavior, which may lead them further astray assessment, which adheres to describing the observable
from practical solutions. relationships between antecedents, behaviors and conse-
quences, suggests a more plausible hypothesis, as
There are six basic steps to conducting a functional described below:
assessment/analysis:
Step 1: Operationally define the target behavior. A target Functional Assessment #2:
behavior is the response you want to maintain, increase Bird Willingly Steps Up When Requested
or decrease. To operationally define the target behavior, Antecedent: Caretaker says, “Up!” and offers hand to
describe it in clear, observable terms. Ask: What does the bird on top of cage.
bird actually do? Behavior: Bird steps up.
Step 2: Identify the antecedents that set the occasion for Consequence: Bird is returned to cage.
the target behavior. Ask: What event or condition immedi- Prediction: Bird will step up less in the future to avoid
ately precedes or “leads” the bird to exhibit this behavior? being returned to the cage.
Step 3: Identify the consequence that immediately fol-
lows the target behavior. Ask: What happens immedi- This functional assessment suggests that this bird has
ately after the behavior is exhibited? What do you do or learned to run away from the offered hand simply to
how does the environment respond? avoid being locked in its cage. It seems an intelligent
Step 4: Predict the probable future behavior that most choice from the bird’s point of view, given the conse-
likely will occur as a result of the current consequence. quences of complying with the request. Unlike the con-
Ask: Will the behavior likely be repeated, increased or struct explanation, this behavior-analytic explanation
decreased? meets the scientific criterion of a good hypothesis:
Step 5: Devise and implement a new antecedent and/or 1. We can test it by changing the consequence and see if
consequence to facilitate a different behavior. Ask: What the behavior changes;
can we do instead? 2. it is as simple as possible, but no simpler;
51
3. it allows us to predict future events; and, The relationship between behavior and reinforcers is
4. it is useful, as it implies workable, positive alterna- clear, as we see the effect of this principle all around us.
tives. For example, most parrots would be very When we fasten our seat belts and the buzzer stops, we
responsive to stepping up from their cage tops if they learn to fasten our seat belts more often to stop the
valued the consequence for doing so. A few moments buzzer; when the cat sits in front of the door and we let
of attention before being returned to the cage and a it out, the cat learns to sit at the door more often to be
treasured food treat after entering the cage are usually let out; when the parrot steps up and we take it out of
all it takes. its cage, the parrot learns to step up more often to be
removed from its cage.
Of course, human behavior also is a function of its con-
sequences. Below is a functional assessment of the care- Characteristics of Effective Reinforcement
taker’s behavior whose bird refuses to step up:
Less well considered are the characteristics of effective
reinforcement, the most important of which are clear con-
Functional Assessment #3: tingency, close contiguity and attention to individual dif-
Caretaker Leaves Bird in Cage
ferences. Contingency refers to establishing the depend-
Antecedent: Bird is playing on cage top. ency between a behavior and its reinforcing consequence.
Behavior: Caretaker says, “Up!” and offers hand to bird Some people refer to it as “Grandma’s Law,” which states,
on top of cage. “If this is your behavior, then this is your consequence.”
Consequence: Bird runs away. Thus, reinforcement is the process of delivering a rein-
Prediction: Caretaker asks bird to step up less often to forcer contingent upon the performance of a particular
avoid refusal. behavior. Consistency is important to establishing clear
contingency between a behavior and a reinforcer.
Chances are, in the long run, this caretaker either will
leave his bird in its cage more and/or become more Contingency also is clearer when reinforcers are deliv-
forceful when retrieving the bird. As a result, many birds ered with close contiguity, the second characteristic of
escalate their initial refusal to biting. All this caging, effective reinforcement. Contiguity refers to immediacy;
force and refusal are unnecessary when a simple positive that is, the shorter the interval of time between the
strategy like offering a food treat or a few minutes of behavior and the reinforcer, the more effective it will
uninterrupted attention before being returned to the be in increasing the future rate of that behavior. Lattal
cage can solve the problem of birds refusing to step up demonstrated the importance of contiguity in an interest-
from their cage tops. ing study with pigeons.19 In an effort to teach a pigeon to
peck a disk, Lattal arranged to deliver a food pellet each
Before considering how to change a behavior, caretakers time the pigeon moved toward the disk. However, he
should conduct a functional assessment to determine purposely delayed the delivery of the pellet for just 10
the function the behavior likely serves for the parrot. seconds after the target behavior was exhibited. After
The question is not, “Why is the bird behaving this way?” 40 days of 1-hour training sessions, the pigeon never
but rather, “What valued consequences result from per- learned to peck the disk. Subsequently, when the delay
forming the behavior for this particular bird in this situa- between the behavior and the reinforcer was reduced to
tion?” By changing antecedents and consequences, we 1 second, the bird learned to peck the disk in less than
change target behaviors. As antecedents and conse- 20 minutes.
quences most often are stimuli or conditions we control,
changing our birds’ behavior always is the direct result Reinforcers also are highly individual. Some people are
of first changing our own behavior. not reinforced by the cessation of the car buzzer and so
do not increase the behavior of buckling their seat belt;
some cats are not reinforced by going outside, thus, they
INCREASING AND MAINTAINING do not sit by the door; and some parrots are not rein-
BEHAVIOR forced by coming out of their cages, preferring instead to
When you think about it, consequences influence behav- drive away the caretaker with a serious bite. Reinforcers
ior in one of two basic ways: Consequences function to are not what we think “should” increase the frequency of
maintain/increase the frequency of a behavior or they a particular behavior; rather, reinforcers are those conse-
function to eliminate/decrease the frequency of a behav- quences that actually do increase the frequency of a par-
ior. In this section, we are concerned with consequences ticular behavior they contingently follow. The only way to
that function to increase behavior, called reinforcers, know for sure which consequences will be reinforcing
and with the process of delivering reinforcers, called for any particular bird is to try them and then observe
reinforcement. the future frequency of the behavior.
Developing New Reinforcers small step at a time, reinforcing calm behavior with the
word “good.”
Some consequences such as food, water and warmth are
inherently reinforcing to all animals from the moment
they are born. These consequences are called uncondi- Positive and Negative Reinforcement
tional reinforcers (also called unconditioned or primary Admittedly, distinguishing two types of reinforcement
reinforcers); they are unconditional in the sense that with the terms “positive” and “negative” is at best eso-
they are not dependent on prior experience (learning), teric and at worst utterly confusing. It is tempting just to
but they do require certain conditions or “establishing avert the discussion, define reinforcement precisely and
operations” to function as reinforcers, eg, hunger, thirst leave it at that. The distinction is pursued here because
and cold. Surely these unconditional reinforcers are part these terms are so commonly misunderstood and mis-
of nature’s clever plan to kick-start behavior at birth for used, and because positive reinforcement is the preferred
survival. strategy for changing behavior, as explained below.
As soon as an animal starts to interact with its environ- Foremost, reinforcement is reinforcement. That is,
ment, learning begins, and many different consequences regardless of type, positive or negative, reinforcement
become reinforcing by being paired with existing rein- results in an overall increase in the behavior it follows
forcers. These learned reinforcers are called conditional when next the occasion (antecedent) is set for the
reinforcers (also called conditioned or secondary rein- behavior to be performed. A positive reinforcer is some-
forcers); they are conditional in the sense that their rein- thing that an individual behaves in a particular way to
forcing properties are acquired and maintained by being produce (+, add to its environment). It is gaining the
paired with existing reinforcers. Praise, petting and toys reinforcer that functions to increase the behavior with
are examples of conditional reinforcers for many com- positive reinforcement. Alternatively, a negative rein-
panion parrots and have become reinforcing though forcer is something that an individual behaves in a par-
association with food or other valued stimuli. ticular way to remove (-, subtract from its environment).
It is the removal or escape from the reinforcer that func-
The more reinforcers an individual parrot has, the more tions to increase behavior with negative reinforcement.
tools we have to influence its behavior, as novelty and The example of increasing a bird’s calm behavior contin-
variety are essential to effective reinforcement.30 New gent upon the caretaker’s withdrawal is an example of
reinforcers can be conditioned throughout the lives of negative reinforcement, functionally analyzed below:
all animals, and caretakers can make use of this process Antecedent: Caretaker approaches cage.
by pairing existing reinforcers with new stimuli to build Behavior: Bird flails.
a rich pool of reinforcers with which to teach and enrich Consequence: Caretaker remains near cage.
their parrots’ lives. Providing a constant supply of new Antecedent: Caretaker remains near cage.
treats, toys and activities allows our birds to sample new Behavior: Bird stops flailing for an instant.
stimuli that may prove to be reinforcing. Consequence: Caretaker steps back 5 paces from cage.
Prediction: Perching calmly will increase to remove care-
Caretakers often complain that they have no way to
taker from cage.
teach their bird desirable behaviors because the bird has
no reinforcers. Of course if that were the case, their bird Below are additional examples of positive and negative
would have no behavior. It sometimes takes sharp pow- reinforcement to make this distinction clear. Notice two
ers of observation to notice what reinforces a particular things:
bird’s behavior. Subtle outcomes like being set down or 1. In all cases, the target behavior is increased or main-
returned to the cage, or a caretaker’s retreat, are often tained as these examples all describe reinforcement;
conditional reinforcers for poorly socialized birds. We 2. With negative reinforcement, an aversive stimulus has
can use even these reinforcers to increase their adaptive to be present in the environment in the first place in
behavior, and condition more positive ones by associa- order to increase behavior by its removal.
tion. For example, to teach a fearful bird to remain calm
in our presence, we might start by withdrawing our- Examples of Positive and Negative
selves from its cage for a few seconds contingent on Reinforcement #1:
quiet, still behavior. If our removal functions as a rein- Background: Beaker is a parrot that lunges at Grace’s
forcer, we will see calm behavior increase over several hand every time she puts her hand in or near Beaker’s
repetitions. Again, if our removal functions as a rein- cage. Grace has decided to teach (increase) Beaker’s
forcer, saying “Good!” at the same moment we retreat behavior of perching on the branch farthest from the
will result in the word “good” acquiring reinforcing food cups so she can replenish them without Beaker’s
properties for this bird. Eventually, we can advance one lunging.
53
Positive reinforcement solution: experience their environments as negatively reinforcing

Antecedent: Grace says, “Perch!” or outright punishing. Caretakers are encouraged to be
Behavior: Beaker perches. analytical about the approaches they employ when inter-
Consequence: Grace puts food and the food bowl in cage. acting with their birds, so that they can deliberately
Prediction: Beaker will go to the perch more often to decrease their use of aversive procedures. Positive rein-
add (+) the food to the environment. forcement occasions none of this “aversive fallout,”
clearly making it the preferred behavior change strategy.30
Negative reinforcement solution:
Antecedent: Grace herds Beaker to a particular perch in
SHAPING NEW BEHAVIOR
his cage with a stick.
So far, we have discussed using positive reinforcement
Behavior: Beaker perches.
for maintaining or increasing the frequency of behaviors
Consequence: Grace puts down stick.
that a bird already performs. Shaping, also called
Prediction: Beaker will go to the perch more to remove
Differential Reinforcement of Successive Approximations,
(-) the stick from the environment.
is a procedure to teach new behaviors. To shape a new
Examples of Positive and Negative target behavior, start by contingently reinforcing the
Reinforcement #2: response already exhibited by the bird that most closely
Background: Of course, Grace also has a problem getting resembles (approximates) the target behavior. Once mas-
Beaker to step up from inside the cage without lunging. tered (ie, performed without hesitation), reinforcement
then is withheld for that behavior. Withholding reinforce-
Positive reinforcement solution: ment for a previously reinforced behavior is called extinc-
Antecedent: Grace offers her hand. tion. Extinction results in an initial increase in respond-
Behavior: Beaker steps up. ing and effort, which offers natural variability in the way
Consequence: Grace praises Beaker enthusiastically and the behavior is offered. Careful observation of this vari-
sets Beaker on top of the cage. ability allows us to “catch” the next closer approximation
Prediction: Beaker will step up more to result in Grace’s with reinforcement. This process of ignoring one behav-
attention and cage-top location. ior (the mastered approximation) and subsequently rein-
forcing another behavior (the next closer approximation)
Negative reinforcement solution: is called differential reinforcement of successive approxi-
Antecedent: Grace holds a towel in one hand while mations. Differential reinforcement of successive approxi-
offering her free hand. mations is continued until the final target behavior is dis-
Behavior: Beaker steps up on free hand. played and reinforced.
Consequence: Grace sets down towel.
Prediction: Beaker will step up more to result in the Many new behaviors required of successful companion
removal of the towel. parrots can be simply shaped and different dimensions
of existing behaviors can be shaped, too. For example,
As can be seen with these examples, a condition of nega- proximity to a feared person or object can be increased;
tive reinforcement is the presence of an aversive stimu- duration staying on a play gym or under a shower can
lus in order for the animal to have something to work to be increased; and latency in responding to the requests
escape. Indeed, another name for negative reinforce- “step up” or “off there” can be reduced. With shaping,
ment is escape/avoidance learning. Research over an endless number and variety of adaptive behaviors can
decades with many different species of animals has be taught and problem behaviors solved, all with posi-
shown that procedures that rely on aversive stimuli, tive reinforcement, thus avoiding the negative side
such as negative reinforcement and punishment, tend to effects that occasion more forceful or coercive methods.
be associated with negative behavioral side effects. As
Here’s an example of the approximations that can be
you read the common types of side effects, consider
differentially reinforced to teach a parrot to play with
how well they describe the behavior of many unfortu-
foot toys:
nate parrots in captivity:
1. Look at toy;
1. escape/avoidance behavior,
2. aggressive behavior, 2. move toward toy;
3. response suppression, and, 3. touch toy with beak;
4. fear of people or things in the environment in which 4. pick up toy with beak;
the aversive stimuli are presented.2 5. hold toy with foot;
6. hold toy with foot and manipulate with beak;
The fact that these four general side effects are common 7. hold toy with foot and manipulate with beak for
descriptions of captive parrots suggests that many birds longer durations;
Table 3.1.1 | Intermittent Schedules of Reinforcement to prereinforcement levels. When human attention is the
Fixed (set) Variable (on average) reinforcer maintaining a particular behavior, extinction
Ratio FR - reinforcement occurs VR - the number or responses is synonymous with ignoring, ie, we withdraw attention.
(number) after every “nth” response. required before reinforcement
FR 3 means that every third varies unpredictably around Using extinction for the purpose of decreasing an
response will be reinforced. some average. VR 3 means unwanted behavior is not a simple procedure to prop-
the number or responses
required will average around erly implement. There is much to learn about the cor-
3 but will vary.
rect use of ignoring, which is briefly discussed in a sub-
Interval FI - reinforcement occurs VI - the period of time that
(time) after a fixed period of time must elapse before a sequent section.
elapses. response is reinforced varies
FI 6” reinforcement will occur unpredictably around some Somewhere between continuous reinforcement (1:1)
after 6 seconds elapse. average. In a VI 10” sched-
ule, the average period and extinction (1:0) is another category of simple sched-
required before the next
response is reinforced is 10”. ules of reinforcement known as intermittent reinforce-
ment schedules. With intermittent schedules, only some
8. repeat with other toys until the behavior is general- (as opposed to all or none) of the target behaviors are
ized to all toys. reinforced. There are two basic dimensions along which
intermittent schedules can be arranged: The first dimen-
Unfortunately, negative behaviors can unwittingly be sion regards what is being counted, either frequency of
shaped as well. We inadvertently teach our birds to bite responses (called ratio schedules) or time elapsed
harder, scream louder and chase faster through the sub- (called interval schedules). The second dimension along
tle mechanism of shaping. For better or worse, shaping which intermittent schedules can be arranged regards
is endlessly applicable to teaching our birds, limited the predictability of reinforcement, either fixed or vari-
only by our imagination and our commitment to practic- able. With fixed schedules, the ratio (frequency of
ing its use. responses) or interval (length of time) that must occur
for reinforcement to be delivered is predetermined and
SCHEDULES OF REINFORCEMENT unchanging, ie, it remains the same throughout the pro-
gram. With variable intermittent schedules, reinforce-
Schedules of reinforcement are the rules we follow to
ment fluctuates around a preset average and the learner
determine when a particular instance of the target
never knows how many responses, or how long they
response will be reinforced out of the many responses
must wait, for each reinforcer.
that occur. Several so-called simple schedules are rele-
vant here, as research demonstrates that different ratios Crossing the two dimensions of intermittent reinforce-
of “behavior-to-reinforcement” result in remarkably dif- ment schedules results in four basic types of intermittent
ferent, but extremely predictable, patterns of behavior. schedules of reinforcement: Fixed ratio (FR), variable
ratio (VR), fixed interval (FI) and variable interval (VI).
A continuous reinforcement schedule (CRF) is one in Numbers follow these acronyms to indicate the exact
which each and every occurrence of the target behavior is value of the unit of measure (Table 3.1.1). For example,
reinforced. With CRF, the ratio of “behavior-to-reinforce- FR 3 means every third response will be reinforced; VR 3
ment” is 1:1. Generally speaking, continuous reinforce- means the number of responses required for reinforce-
ment is the best reinforcement schedule to use with our ment will vary unpredictably around an average of every
birds, especially when the goal is to teach a new behavior third response. An FI 6” means 6 seconds must elapse
or increase the rate of an existing behavior.30 CRF is the between the first reinforced response and the next. In a
clearest way of communicating exactly what behavior we VI 10” schedule, the average period required before the
want to see again. Research also has demonstrated that next response is reinforced is 10 seconds.
individuals behave in proportion to the reinforcement
available for a given response.15 There is little doubt that Intermittent schedules of any kind are known to cause
the more you positively reinforce your bird’s desirable more persistent behavior than continuous schedules
behavior, the more frequently your bird will exhibit desir- under conditions of extinction or very lean reinforce-
able behavior. We get what we reinforce. ment. For example, many birds try to clamber out of
their cages when the door is opened. Every once in a
On the other end of the spectrum is a schedule called while they make it to the top of the cage. This intermit-
extinction (EXT), discussed previously as it applies to tent reinforcement maintains their persistent effort to
shaping. With an extinction schedule, no instances of “escape” every time the door is opened.
the behavior are reinforced, ie, the ratio of behavior-to-
reinforcement is 1:0. As the name suggests, when the The now classic analogy of the different rates of putting
particular reinforcer that maintains a behavior is with- coins in machines observed with a coke machine vs. slot
held, the rate of that behavior will predictably decrease machines is a sound demonstration of the effects of dif-
55
ferent schedules of reinforcement: With the continuous positive and effective solution to overcoming behavioral
reinforcement provided by the typical coke machine, resistance, much preferred over force.
most of us do not keep putting money in the slot if
nothing comes out. Yet, many people continue to drop
coins into slot machines with a very lean schedule of
reinforcement. All things considered, our birds benefit
Decreasing Behaviors
most from our ability to “catch them being good” at as Scientifically speaking, punishment is the process by
high a rate as possible and reinforcing them for it. One which a consequence decreases the behavior it follows
important benefit of this approach is that people who and the consequence itself is called a punisher. As you
deliver dense schedules of reinforcement are more likely can see, this simple, functional definition is quite differ-
to become valued reinforcers themselves. ent from common use, which often has more to do with
venting anger than actual behavior change. Just like rein-
OBSERVATIONAL LEARNING forcement, the effect of punishment depends on contin-
gency and contiguity between the behavior and the con-
Observational learning describes the process of learning
sequence, as well as the schedule with which the pun-
by observing the experience of another individual. As
isher is delivered. Also, just like reinforcement, punish-
described in Chance,7 it was not until the 1960s that
ment is a very individual matter. A consequence that is
research on observational learning really took off after
punishing to one bird may not be punishing to the next
initial results with monkeys were reported.32 Since that
bird. As always, the function of a consequence can be
time, research has demonstrated observational learning
demonstrated only by observing the future rate of the
takes place with many different species including cats,14
behavior. If the behavior doesn’t decrease over time, the
octopi,10 bats,11 children and adults.16,17
procedure is not punishment.
Irene Pepperberg’s work with Alex, the African grey par-
There also is a distinction between positive (+) and neg-
rot, suggests the effectiveness of observational learning.24
ative (-) punishment. Positive punishment is the process
Her work also confirms that observational learning has
of adding an aversive stimulus to the environment to
enormous relevance to increasing adaptive behaviors
decrease behavior; negative punishment is the process of
with parrots that display limited companion repertoires
removing something of value (ie, a reinforcer) from the
or seriously maladaptive behaviors.
environment to decrease behavior. Negative punishment
includes relatively mild behavior-decreasing techniques
BEHAVIORAL MOMENTUM such as extinction and time out from positive reinforce-
Nevin hypothesized that the physics principle of momen- ment, both of which are further discussed below.
tum is a good metaphor for behavior.22 He asserts that
Unfortunately, positive punishment is all too commonly
compliance to demanding or undesirable tasks can be
applied to birds. To reduce unwanted behaviors, people
increased by first requesting a series of easy or high-prob-
rely on what they know, their “cultural knowledge,” which
ability behaviors. He calls this procedure behavioral
is learned over a lifetime of personal experience with pun-
momentum. Behavioral momentum appears to be an
ishment. For lack of alternative information and skills, peo-
effective positive strategy for increasing parrots’ compli-
ple often force their birds out of cages in towels, squirt
ance to requests they initially balk at doing. For example,
them with water to move them off unapproved perches,
one author observed master trainer Phung Luu using this
and cover their cages to stop them from screaming. They
approach with a kea (Kea nestor) learning the husbandry
are unaware or skeptical that positive reinforcement solu-
behavior of entering a crate. Having a known negative
tions are readily available to influence these behaviors.
history with crates (learned during the initial transport to
the zoo), the kea ignored the cue to crate several times.
Rather than forcing the bird into the crate or accepting NEGATIVE SIDE EFFECTS OF
that it wouldn’t enter the crate, the trainer cued bird to PUNISHMENT
several different perches in rapid succession, something As with negative reinforcement, people must be made
the kea did without hesitation. Once the kea built up aware of the predictable side effects occasioned by pun-
behavioral momentum by complying with the easy cues, ishment. These devastating side effects are most likely to
the trainer asked it to crate at which point the bird actu- result from positive punishment procedures in environ-
ally leaped into the crate where a jackpot of food rein- ments with little opportunity for positive reinforcement.
forcers was delivered. Caretakers can use the same proce- The negative fallout of all aversive strategies is important
dure to build behavioral momentum with fun, easy enough to repeat here:
behaviors before asking their birds to do something they 1. escape/avoidance behavior,
are less than willing to do. Behavioral momentum is a 2. aggressive behavior,
3. response suppression, and, FUNCTIONAL MISBEHAVIOR

4. fear of people or things in the environment in which The example of a bird biting its caretaker’s hand to
the aversive stimuli are presented. result in the caretaker removing her hand from the cage
brings up an interesting point: Problem behavior is often
Notice that one of the problems with punishment is not a misguided attempt by our birds to communicate a
that it doesn’t work. Punishment works to decrease need and/or to get desired reinforcers such as our atten-
behavior when executed correctly. This fact results in tion. For example, birds sometime display more raucous
perhaps the most detrimental side effect of punishment vocalizations and increased nippiness communicating
— whenever punishment works to decrease an that they are tired and ready for sleep. If we teach our
unwanted behavior, the person delivering the punish- birds more acceptable ways to communicate with us, we
ment is reinforced for using it. Therefore, s/he is more can decrease their undesirable behavior. This strategy
likely to use punishment in the future. This is not only has been validated in several studies with children who
disconcerting, it explains at least one reason punish- were self-injurious, aggressive to others and otherwise
ment is so pervasive in our society, punishment often is disruptive.5 The problem behaviors the children exhib-
reinforcing to the punisher. ited served a valid communication function as evidenced
by the significant decrease in the problem behaviors
DIFFERENTIAL REINFORCEMENT
after the children learned more acceptable alternatives
OF INCOMPATIBLE/ALTERNATIVE
BEHAVIORS to gain objects, activities and attention.
Fortunately, there are effective alternatives to punish- With this hypothesis in mind, Alberto and Troutman1
ment for decreasing unwanted behaviors, which make developed three criteria for selecting incompatible and
use of differential reinforcement. Differential reinforce- alternative behaviors for DRI and DRA strategies that can
ment first was introduced in the section on shaping, be applied to solving behavior problems with our birds:
where continuous reinforcement was combined with 1. Always first analyze the inappropriate behavior to
extinction to advance from one approximation to the determine if it serves an important function for the
next closer approximation of the target behavior. In this bird. If it does, then a replacement behavior should
section, two differential reinforcement strategies to be found that serves that function, but in a more
decrease an unwanted behavior in favor of a desirable appropriate way.
alternative are discussed. 2. The alternative behavior should give the bird the
same amount or more reinforcement than the
With differential reinforcement of an incompatible behav- unwanted behavior or it will just revert back to the
ior (DRI), we reinforce a behavior that is incompatible or inappropriate behavior in the long run.
mutually exclusive with the unwanted behavior, which we
3. DRI and DRA strategies work best if the incompatible
ignore. For example, if continuous screaming is targeted
or alternative behavior already is something the bird
for reduction, we can reinforce talking because the two
knows how to do. In this way, the effort the bird
behaviors cannot occur at the same time. If biting people
expends can be on replacing an unwanted behavior
is targeted for reduction, we can reinforce chewing a foot
with a desirable behavior, rather than learning some-
toy because chewing a toy and biting a person are incom-
thing new.
patible. DRI allows us to decrease the frequency of the
undesirable behavior by increasing the frequency of an
incompatible behavior with positive reinforcement. In EXTINCTION
this way, we take a positive reinforcement approach to Extinction as it relates to shaping and differential rein-
decreasing undesirable bird behaviors. forcement of alternative behavior already has been dis-
cussed, but it also can be used as a procedure to decrease
Differential reinforcement of alternative behavior (DRA) an unwanted behavior by permanently withholding the
is another way to indirectly decrease an unwanted reinforcement that has maintained it in the past. When
behavior using positive reinforcement. With DRA, the human attention is the reinforcer maintaining a behav-
behavior that is reinforced is not necessarily incompati- ior, extinction is in effect when the behavior is ignored.
ble with the unwanted behavior, but is a more accept- Ignoring an unwanted behavior sounds easy enough,
able alternative. For example, a bird that bites to get you however, it actually is one of the most difficult tech-
to remove your hand instead can be reinforced for a niques to use effectively.
vocalization to make its protests known. Differential
reinforcement is a highly effective approach to decreas- First, many problem behaviors just cannot be ignored,
ing unwanted behavior without negative side effects and such as extreme biting, screaming or chewing on wood-
with all the benefits that positive reinforcement affords. work. Second, extinction initially produces a reliable but
57
temporary increase in both frequency and intensity of A functional analysis of this program might look like
the unwanted behavior during the beginning stages of this:
the procedure, called an extinction burst. Extinction Antecedent: Caretaker is holding bird.
bursts give new meaning to the phrase, “It’s going to get Behavior: Bird puts beak on button.
a lot worse before it gets any better.” Therefore, when Consequence: Caretaker removes bird to the nearby
considering using extinction, the critical issue is not counter for several seconds.
whether you can ignore current levels of the behavior, Prediction: Bird will bite button less to stay with
but whether you can ignore significantly escalated levels caretaker.
of the behavior until it finally begins to decrease.
Extinction is a relatively slow process and people often The most common way people fall short with this
inadvertently reinforce unwanted behaviors at these strategy is by not really removing access to reinforce-
escalated intensities, resulting in worse problems than ment at all.
before they began extinction.
For example, consider the following analysis:
Another challenge using extinction is that we are not Antecedent: Caretaker is busy preparing dinner.
always in control of the source of reinforcement that Behavior: Bird flies to newly reupholstered couch.
maintains unwanted behaviors. Parrots can derive rein- Consequence: Caretaker gets bird and walks down the
forcement from the feeling they get when they bite our hall, up the stairs, steps over the sleeping dog, passes
skin and from the reaction of other birds, pets or children the ringing phone, passes through the door of the bird
in the environment; even an echo in a particular room room and returns bird to its cage.
can reinforce screaming. In these cases, where “bootleg” Prediction: Bird will fly to newly reupholstered couch to
reinforcement is available to the bird, our efforts to pay get more time with the caretaker on the way to a
no attention to the behavior will have no effect. distant cage.
Finally, even after a behavior is successfully extinguished, At that point, the bird hardly could be aware of the con-
we can count on its sudden reappearance over time. If tingency between the misbehavior and the consequence
we prepare caretakers for this “spontaneous recovery,” meant to reduce it.
they will more likely reinstitute extinction immediately
rather than conclude the initial procedure failed. The Three additional ways TO is commonly used ineffectively
good news is that with each reapplication of extinction is when:
the behavior is less likely to reappear in the future. 1. birds are removed from reinforcing activities for too
Nonetheless, for these reasons, our best strategy for long,
reducing unwanted behavior is differential reinforcement, 2. birds are not given another chance to behave appropri-
ie, the combination of extinction of the unwanted behav- ately soon after the “infraction,” and,
ior and reinforcement of a more adaptive behavior alter- 3. the caretaker adds reinforcing emotional reactions
native. A sound axiom to guide caretakers in their choice including brusque movements, strained voices and
of managing difficult behavior is, “Replace rather than angry faces.
eliminate.” By following this rule, we teach the bird what
The effectiveness of TO is greatly increased by
to do instead of solely what not to do, we maintain a
following these suggestions:
higher level of reinforcement and we preserve the func-
1. Ensure clear contingency and contiguity by selecting a
tion for the bird that was served by the original unwanted
nearby TO location.
behavior.
2. Keep TO short, no more than a few minutes or the
bird likely will forget the connection between his
TIME OUT FROM POSITIVE behavior and the consequence.
REINFORCEMENT
3. After a short TO, bring the bird right back to the
Time out from positive reinforcement (TO) is another “scene of the crime” to earn reinforcement for doing
negative punishment procedure used to decrease it right.
unwanted behavior. With TO, behavior is decreased by 4. Let TO do all the work for you. There is no need for
temporarily removing access to desired reinforcers. For other consequences or histrionics, which likely will
example, birds can be taught to leave shirt buttons alone reinforce the unwanted behavior.
by setting the bird down for a few seconds contingent on
the bird moving toward or touching a button. If being Although TO is a punishment procedure, there is some
with the caretaker is reinforcing, removal from the care- evidence with children that suggests it can be used with-
taker will decrease the biting behavior given good deliv- out producing the negative side effects of positive pun-
ery of the consequence (ie, contingency and contiguity). ishment.25 In this sense, well-executed TO is a relatively
mild strategy for reducing negative behavior. Even so, or ignore cries of protest to get them into the tub. The
antecedent arrangements and positive reinforcement first step in solving behavior problems is to identify the
strategies should always be tried first before using any stimuli in the environment that set the occasion for and
other strategy. If strategies such as extinction or TO are reinforces resistance to a reasonable request. The next
used, special attention should be paid to arranging and step is to create an environment that sets the occasion for
reinforcing positive behaviors at a high rate to maintain and reinforces adaptive, cooperative behaviors.
a positive total environment.
A common criticism voiced by advocates of negative
reinforcement and punishment is that positive reinforce-
ment results in increased permissiveness. On the con-
Conclusion trary, the skills we want our captive parrots to exhibit do
not have to change with this urgent call to change the
Were it not for parrots’ extraordinary ability to adapt on
strategies we use to teach them. For example, with posi-
an individual level, one might conclude that at the
tive reinforcement, parrots can quickly and easily be
species level they are genetically ill equipped for the
taught to step up from all perching areas; with differen-
captive environment. Indeed, this may well prove to be
tial reinforcement of an alternative behavior, parrots can
the case for some species of parrots. Their high-decibel
be taught to voice their displeasure rather than bite; and
shrieking, ratchet beaking, food flinging, exclusive bond-
with shaping, parrots can be taught to play independ-
ing, wood remodeling and long-distance flying ways
ently for a reasonable duration rather than scream inces-
make them demanding animals to care for in our
santly for attention.
homes. Ensuring parrots’ success as companions will
require an increased awareness of their species tenden-
Over the course of decades researching and teaching
cies to set the behavioral context, and a sound working
about positive reinforcement, we have heard many
knowledge of how animals learn in order to teach them
unfounded trepidations. Countless times caretakers have
behaviors well adapted to our homes.
asked if teaching with positive reinforcement solutions
For years, the pervasive approach with companion par- diminishes intrinsic motivation, results in reward addic-
rots has been little more than a reflection of cultural tions, suppresses the root causes of behavior while
beliefs about behavior. The application of scientific infor- addressing mere symptoms, exchanges one symptom for
mation has been scarce. Based on these beliefs, many another, promotes bribery, works only with intelligent
people assume that behavior is caused by invisible forces learners, works only with simple behaviors, requires
originating inside the bird rather than the perpetual massive amounts of treats and takes too much work. We
interaction between the individual and the environment. are confident to report that given the extensive experi-
For example, one commonly advanced theory is that mental research base, combined with decades of suc-
parrots are driven by a desire for dominance. This is not cessful application in schools, zoos and other settings, it
a benign theory, as it predisposes people to interpret is clear that positive reinforcement increases our teach-
behavior as a struggle for position in some supposed ing efficacy in myriad ways and that these concerns are
hierarchy and, therefore, to advocate management prac- unfounded. And, we are heartened to observe among
tices designed for caretakers to win the struggle. Such the parrot-owning public that more and more people
practices often are forceful and coercive, relying heavily are questioning the drawbacks and limitations of using
on negative reinforcement and positive punishment, punishment.
both of which are defined in part by the presence of
aversive stimuli. Foremost among the many benefits of positive-first
teaching is that parrots are taught what to do rather than
As a result of this dominance-drive theory, caretakers not do, and they are empowered to operate on their
have been endlessly instructed how to take charge of environment in ways that result in competence and self-
their birds’ behavior, issue commands and establish their reliance. These benefits are especially important in light
superior rank. They’ve been encouraged to establish con- of the extensive research on learned helplessness, a class
trol by prying their bird’s toes off perches, threatening of behaviors that results from having little effect on
their birds with towels and ignoring their bird’s bites of one’s own outcomes when repeatedly exposed to aver-
protest. One of the most disturbing aspects of this dogma sive events.20 Not only does learned helplessness result
is the repeated use of an analogy to sound parenting in a loss of motivation to improve one’s condition when
practice so described: “You wouldn’t allow a small child improvement is possible, it is also associated with
to decide whether or not to take a bath, now would you?” deficits in learning, performance, and emotional prob-
No, we would not; however, the method of choice to lems. As this research has been replicated with cock-
facilitate children’s bathing would not be to pry, threaten roaches,4 dogs, cats, monkeys, children and adults,20,23 we
59
have every reason to believe that these effects also are approaches, as needed.
common among parrots.
Veterinarians often are in the position of being the first
Finally, applied behavior analysis not only empowers and most credible authority parrot owners turn to for
parrots but caretakers as well. Caretakers learn that guidance on the behavior of their birds. We could do no
behavior is functionally related to environmental better than to turn to the dual sciences of ethology and
antecedents and consequences, not some immutable applied behavior analysis to lead us into a new era of
force within. They know where to look to affect behavior understanding and skill with behavior. In this way, realis-
directly with positive-first solutions, one behavior at a tic expectations for companion parrots will emerge, as
time, and they understand that to change their birds’ will the commitment to apply scientifically validated, pos-
behavior, they must change what they do. With a begin- itive-first behavior management strategies. Veterinarians
ning knowledge of the principles of learning and behav- who are knowledgeable about species-level behavior and
ior, caretakers also are better able to make reasoned, individual learning will dramatically change the future of
informed decisions about alternative, less positive companion parrots and their caretakers.
Web Sites Recommended References and Science 256:545-547, 1992. 22. Nevin JA: The momentum of
11. Gaudet CL, Fenton MB: compliance. J Applied Behav Anal
by the Author Suggested Reading Observational learning in three 29:535-547, 1996.
1. www.avi-train.com 1. Alberto PA, Troutman AC: Applied species of insectivorous bats 23. Overmier JB, Seligman MEP:
2. www.naturalencounters.com Behavior Analysis for Teachers 5th (Chiroptera). Anim Behav 32:385- Effects of inescapable shock upon
3. www.thegabrielfoundation.org ed. Merrill-Prentice Hall, 1999, 388, 1984. subsequent escape and avoidance
4. www.groups.yahoo.com/group/ pp 287-288. 12. Gray P: Psychology 3rd ed. New responding. J Comp Physiol
Bird-Click 2. Azrin NH, Holz WC: Punishment. York, Worth, 1999, p 73. Psychol 63:28-33, 1967.
5. www.parrottalk.com In Honeg WK (ed): Operant 13. Hare B, et al: The domestication of 24. Pepperberg IM: The Alex Studies:
Behavior: Areas of Research and social cognition in dogs. Science Cognitive and Communicative
Books Recommended by Application. New York, Appleton- 298:1634-1636, 2002. Abilities of Grey Parrots.
Century-Crofts, 1966. 14. Herbert M J, Harsh CM: Massachusetts, Harvard U Pr,
the Author 3. Breland K, Breland M: The misbe- Observational learning by cats. J 2000.
1. Animal Training: Successful Animal havior of organisms. Am Psychol Comp Psychol 37:81-95, 1944. 25. Rortvedt AK, Miltenberger RG:
Management through Positive 16:681-684, 1961. 15. Herrnstein RH: Relative and Analysis of a high probability
Reinforcement, by Ken Ramirez 4. Brown GE, Hughs GD, Jones AA: absolute strength of response as a instructional sequence and time-
(1999). Effects of shock controllability on function of frequency of reinforce- out in the treatment of child non-
2. Clicking with Birds: A Beginners subsequent aggressive and defen- ment. J Exper Anal Behav 4:267- compliance. J Applied Behav Anal
Guide to Clicker Training Your sive behaviors in the cockroach 273, 1961. 27:327-330, 1994.
Companion Parrot by Linda (Periplaneta americana). Psychol 16. Higgins ST, Morris EK, Johnson 26. Sharpless SK, Jasper HH:
Morrow (available at Reports 63:563-569, 1988. LM: Social transmission of super- Habituation of the arousal reac-
www.avi-train.com/manual.html). 5. Carr E, Durand VM: Reducing stitious behavior in preschool tion. Brain, 79:655-680, 1956.
3. Clicker Training with Birds, by behavior problems through func- children. Psychol Rec 39:307-323, 27. Skinner BF: The Behavior of
Melinda Johnson. tional communication training. J 1989. Organisms. BF Skinner
4. Don’t Shoot the Dog: The New Art Applied Behav Anal 18:111-126, 17. Kanfer FH, Marston AR: Human Foundation, 1938.
of Teaching and Training (revised 1985. reinforcement: Vicarious and 28. Skinner BF: Science and Human
edition), by Karen Pryor. 6. Chance P: Learning and Behavior direct. J Exper Psychol 65:292- Behavior. New York, Macmillan,
5. Good Bird! A Guide to Solving 5th ed. California, Thomson 296, 1963. 1953.
Behavioral Problems in Wadsworth, 2003, 439. 18. Lantermann W: The New Parrot 29. Skinner BF: Selection by conse-
Companion Parrots! by Barbara 7. Chance P: Learning and Behavior Handbook. New York, Barron’s, quences. Science 213:501-504,
Heidenreich. 2004, Avian 5th ed. California, Thomson 1986, pp 91-94. 1981.
Publications, Minneapolis, MN, Wadsworth, 2003, 266. 19. Lattal KA: Contingency and 30. Sulzer-Azaroff B, Mayer GR:
www.avianpublications.com. 8. Chance P: Learning and Behavior behavior analysis. Behav Analyst Behavior Analysis for Lasting
6. The Power of Positive Parenting A 5th ed. California, Thomson 24:147-161, 1995. Change. Florida, Harcourt Brace
Positive Way to Raise Children, by Wadsworth, 2003, 24. 20. Maier SF, Seligman MEP: Learned Jovanovich, 1991, p 180.
Glen Latham. 9. Dethier VG, Solomon RL, Turner helplessness: Theory and evi- 31. Thorndike EL: Animal
LH: Sensory input and central dence. J Exper Psychol: General Intelligence: Experimental
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03_Concepts in Behavior II.qxd 8/22/2005 1:19 PM Page 60
Section II
Early Psittacine Behavior and Development
LIZ WILSON, CVT, PHOEBE GREENE LINDEN, BA, MA;
TERESA L. LIGHTFOOT, BS, DVM, D ipl ABVP-A vian
Ethologists have yet to map out the stages of develop- yet developed the physical coordination to consistently
ment for psittacine birds. As a consequence, the infor- walk without stumbling.
mation about companion psittacine behavior is predomi-
Generally speaking, small species like budgerigars (Melo-
nantly anecdotal and experiential. The wide variation in
psittacus undulatus) and cockatiels fledge around 3 to 4
maturation rates between species as well as between
weeks, wean around 6 to 11 weeks and enter puberty at
individuals within species, as exemplified in Table 3.2.1,
4 to 6 months. Medium-sized birds (Psittacus erithacus
further complicates this issue. As a general rule, the
and Amazona sp.) fledge at 10 to 12 weeks, wean
smaller the species, the faster an individual of that around 12 to 16 weeks and enter puberty at 3 to 4 years
species will mature. For example, most cockatiels of age. Larger psittacines such as Ara spp. fledge at about
(Nymphicus hollandicus) are sexually mature by 6 12 to 15 weeks, wean around 16 to 20 weeks and enter
months of age, whereas the average 6-month-old puberty at about 4 to 5 years. Table 3.2.1 presents more
hyacinth macaw (Anodorhynchus hyacinthinus) has not detailed information regarding representative species.
Table 3.2.1 | Stages of Development

Species Fledge Wean Puberty Sexual Geriatric** Life Span47
(weeks) (weeks) Onset Maturity (years) (years)
(years)
Budgerigar (Melopsitticus undulatus) 3-4 6-7 4-6 months 1 6-12 18
Cockatiels (Nymphicus hollandicus) 3-6 7-11 4-7 months 1 12-18+ 32
Sun conure (Aratinga solstitialis) 6-7 8-9 9-18 months 2 18-25 25
Green-cheeked conure (Pyrrhura molinae molinae) 4-6 6-12 9-18 months 2 12-15 25
Peach-faced lovebird (Agapornis roseicollis) 3-6 7-11 7-8 months 1 10-15 12
Yellow-naped Amazon (Amazona ochrocephala auropalliata) 11-13 15-18 4-6 years 7 35-45
Blue-fronted Amazon (Amazona aestiva) 10-12 12-16 3-5 years 6 25-35 80
Congo grey (Psittacus erithacus) 10-12 12-16 3-5 years 6 20-25 50
Eclectus parrot (Eclectus roratus) 10-11 14-16 3-5 years 6 15-20 20
Galah (rose-breasted cockatoo) (Eolophus roseicapillus) 8-10 11-18 1-2 years 4 18-20 20
Umbrella cockatoo (Cacatua alba) 10-12 12-18 3-4 years 8 20?
Moluccan cockatoo (Cacatua moluccensis) 12-15 16-25 3-5 years 10 25?
Yellow-collared macaw (Ara auricollis) 9-10 10-12 1-2 years 4-5 22-27
Blue and gold macaw (Ara ararauna) 10-12 14-22 4-6 years 8 30-40 50
Green-winged macaw (Ara chloroptera) 12-15 16-35 5-7 years 10-11 35-45
**True onset of “geriatric” in psittacines is subjective and requires several generations of captive-bred individuals of each species to determine.
Chapter 3 | C O N C E P T S I N B E H A V I O R : S E C T I O N I I
61
Behavior Development
and Changes
Alice J. Patterson, courtesy of Santa Barbara Bird Farm

The larger parrots are generally sexually mature by 3 to
5 years of age. This slow rate of maturation often con-
fuses those who assume that the behaviors displayed in
this prolonged babyhood will be permanent rather than
transient. For instance, a 2-year-old scarlet macaw (Ara
macao) is not yet an adult and remnants of youthful
behaviors exist. This scarlet macaw can be expected to
undergo significant behavioral changes in the future.
As a consequence, some owners are startled and upset

at the behaviors displayed as their parrots mature. Those
caregivers who are unprepared for avian adulthood rou- Fig 3.2.1 | Despite its blindness, this Moluccan cockatoo
hatchling is still exquisitely sensitive to its environment. At this
tinely complain to veterinarians and behavior consult- age, temperature is everything, both in environment and food.
ants that they “want their sweet baby back.” The concept
of neoteny is powerfully appealing to humans.5 How-
ever, the reality is that parrots continue to grow, mature prior to the next feeding. Several pitfalls are inherent if
and change. Psittacine behavior is readily influenced by this guideline is followed. Liquid food that is fed tends
positive interactions, so caregivers need not lament pass- to stretch the crop, and a small pendulous area of crop
ing babyhood, but instead embrace life-long learning. may retain liquid food for a prolonged period. Waiting
for this material to empty produces a hungry baby and
creates both emotional and physical stunting. (Ed. Note:
THE NEONATE
Retention of a desiccated portion of the hand-feeding
Parrots are altricial and are unable to thermoregulate, formula may indicate a poorly formulated product,
even in those species that are born with down feathers. improper temperature of the formula when fed, or pro-
Baby parrots are considered neonates from hatching longed crop-emptying related to illness.) Observation of
until their eyes open, and during that time their physical parent-fed babies demonstrates the normal state of
needs are simple but absolutely critical: a warm environ- marked crop distention.
ment and warm food (Fig 3.2.1).15
Chronically whining baby parrots (especially within the
Feeding cockatoo family) may be related to prolonged hunger.
Many breeders feed their babies on a rigid schedule of Breeders who no longer adhere to the rigid scheduled
every 1 to 4 hours, depending on their ages.24 Waking feeding style report neonates that sleep soundly for con-
baby birds to feed them or forcing hungry babies to wait secutive hours and awaken eager to eat. Rather than
for food until the next scheduled feeding is needlessly forcing babies to adhere to schedules tailored to human
stressful for young birds. The optimal feeding schedule convenience, feeding babies on demand is best for
is sensitive to the bird’s needs, including their rapid proper physical and emotional growth (Ed. Note: Recent
increases in weight and the concurrent increase in the research on African Greys (Psittacus erithacus) and
volume of food required at each feeding. Pionus spp., showed that many babies from parents fed
a seed-based diet had some degree of osteomalacia
Young budgerigars and cockatiels have been docu- radiographically. Figs 3.2.2a-b demonstrate an
mented to solicit feeding with typical baby cries only advanced case of bony deformation in a ring-necked
upon the entrance into the nest box of a parent bird. parakeet. In addition to physical malformations in
Occasionally a nestling will cry to solicit feeding from a severe cases of osteomalacia, chronic pain may be pres-
sibling. The only other vocalizations made are the hiss- ent in subclinical cases. Chronic pain at a young age
ing sound (made by cockatiels even at a young age) at may contribute to excessive crying and potentially to
the presence of an intruder in the nest box. Extrapolat- future behavioral problems. See Chapter 5, Calcium
ing this to captive bred nestling parrots would indicate Metabolism for further discussion and references.)
that healthy young psittacine hatchlings should not be
prone to indiscriminate or long-lasting crying binges.
Touch
Concern with the prevention of sour-crop has promoted Psittacines wild-caught as adults and not socialized to
the axiom that the crop should be completely empty humans may be adverse to touch. However, naturally
Bob Doneley
Bob Doneley
Fig 3.2.2a | An extreme example of osteomalacia from a Fig 3.2.2b | The radiograph of the bird in Fig 3.2.2a. Such
malnourished diet. birds are in pain based on similar problems in species that show
more of a pain response, such as monkeys.
occurring parental touch has been reported in many tally kicked apart when the parents leave the box, they
psittacine species. Aviculturist Katy McElroy collects will both stretch their necks out and lurch around in cir-
video nest box documentation of Moluccan cockatoos as cles until making contact” (K. McElroy, personal commu-
they lay, incubate, hatch and nurture a baby to fledging. nications/e-mail, 2002). The importance of physical con-
She and subsequent observers are impressed by the “lav- tact for neonates should not be ignored. The keeping of
ish attention” the parents paid to their baby, continu- multiple chicks together increases normal physical stim-
ously preening and touching their offspring all over its ulation. Incubator-hatched birds should have touch mas-
body between feedings. In one film, McElroy’s parent sage incorporated into their daily care.
birds are seen with their single baby; all three birds are
asleep in the nest box with the baby tucked under its Light
father’s wing, its head laid across his back. Like most
Prior to their eyes opening, neonatal parrots are respon-
animals, parrots are most likely adverse to rough han-
sive to light. Biologically designed to begin life in the
dling, but readily accept appropriate touching, especially
darkness of a tree cavity, baby parrots react adversely to
when raised to do so from an early age.20
strong light by flinching, hiding or trembling. As a conse-
There is an obvious positive reaction to touch, with quence, the popular practice of keeping babies in glass
neonates responding to soft stroking and wing tip mas- aquariums under fluorescent lights not only is poten-
sage by pushing their heads into the human hand. Prior tially detrimental to the developing eyes of neonates,
to the opening of their eyes, they also will respond to but also might cause psychological distress.15 Because
the sound of a familiar step and voice, popping their their eyes need time to develop slowly in a darkened
heads up on wobbly necks. One author (PL) has noted cavity, many aviculturists supply neonates with a dark-
the importance of duplicating the weight of the parent ened container in which to grow and develop. Hand-
bird’s wing when raising babies in incubators, especially raised psittacine babies actually gain weight faster when
when a single chick is housed alone. The baby or babies kept in the dark.25
should be placed into a secure container and covered
with towels that rest lightly on the neonates. Soft weight THE NESTLING
on the back quiets a baby after feeding.
After the neonatal psittacine’s eyes open, the baby is cate-
McElroy reports that her video has documented the gorized as a nestling. Psittacine birds with recently
extreme sensitivity of baby cockatoos to parental and opened eyes seem to be myopic, which is consistent with
sibling touch. “They sit upright on their bottoms a few most newborn animals. Certainly babies who are con-
hours after hatching and use their feet propped out like fined in a closed container have no need to see across
stabilizers to keep from tipping over. The slightest touch vast distances. If given the opportunity to do so too early
will cause them to spin around in that direction, using in the development process, nestlings will blink, recoil
one foot as a pivot as they search for food or a warm and seek a dark corner. They do, however, move toward
body. You rarely see a baby that isn’t snuggled up against and touch objects in close proximity, so boxes can be
a sibling or parent. If two blind neonates get acciden- enriched at this stage to encourage visual development.
63
Layne Dicker, courtesy of Santa Barbara Bird Farm

Fig 3.2.3a | This African grey baby was raised in a plastic Fig 3.2.3b | Baby blue and gold macaws benefit from an
incubator with its physiologic needs met. However, the excessive enriched cardboard box environment with a covered corner for
exposure to light, lack of parental or sibling weight, heat and hiding when needed.
support, are potentially psychologically devastating. Here the
baby is hiding after being frightened by a ringing phone.
As feathers develop and open, the need for supplemental Borrowing again from early development of more exten-
heat decreases, and young psittacines can be moved out sively studied species, it is fair to assume the existence
of brooders into unheated containers that allow more of a window of opportunity for the development of
movement but still resemble a nest. The limited space visual recognition, learning and acceptance in psitta-
has been demonstrated by Nigel Harcourt-Brown to be a cines. Therefore, to make the view more interesting, one
critical factor in the prevention of valgus deformities of can hang bright posters and add plants (either real or
the legs in neonatal birds.15a When the babies are fully artificial) to the nursery. People can wear bright colors
feathered, they can be housed at room temperature, (72- when working with babies. Colorful towels that cover
78° F, 22-26° C), which should be carefully monitored. the containers are simple enrichments. By rotating the
Various containment systems employ the judicious use of towels every couple of days, caretakers can ensure the
towels to provide darkness, privacy, traction and hiding babies become accustomed to different patterns and col-
places that appear to be critical to a stress-free environ- ors. In this manner, an early foundation is laid that
ment. For further comfort and physical and psychological encourages the birds to be receptive to change.
safety, food sources must continue in a dependable man-
ner and the environment must remain secure. Baby parrots raised in opaque plastic tubs receive no
visual stimulation. Cutting a notch in the side of the tub
(melting the edges so they are not sharp) so the babies
Visual Stimulation
can see out can counteract this lack of visual stimula-
Appropriately stimulating environments are vital to mention. Organic containers are more natural and stimulat-
tal development; the use of bright colors and accessible, ing: simple cardboard boxes (which can easily be cut to
touchable toys are enrichments that are simple to incor- provide a view and disposed of when soiled) or inex-
porate into young psittacine environments. Designs on pensive natural-colored baskets. Whatever the environ-
nursery walls and colorful mobiles are examples of visual ment, caretakers should cover most of the container
enrichment for birds at the peri-fledgling stage when they with towels throughout the day, and cover it completely
are perching intermittently on the edge of the nest box. at night. This provides privacy as well as darkness,
should a baby become overstimulated (Fig 3.2.3a). The
As the baby bird develops increased visual ability and towel coverings also influence thermoregulation and
physical mobility, increased opportunities for learning should be adjusted as needed (Fig 3.2.3b). Both the
must be provided. Fearless curiosity is characteristic of need to withdraw from stimulation and the need for
young animals,5 and this characteristic is best utilized in warmth decrease as the birds continue to develop.27
teaching the young bird to competently deal with the
world. In addition to the previously noted necessities of Most veterinarians use towels to restrain birds.
warmth, food and security, the neonates’ environment Acclimating a bird to being restrained in a towel will
needs increasing stimulation in terms of vision, touch, reduce the stress of veterinary visits and aid in grooming
sound and interaction. at home. Initially, cover the baby with the towel and let
it sleep. As the bird nears fledging, it can be carried

around in the towel. It can then be introduced to differ-
ent areas of the house, people, objects, and other pets,
using withdrawal into the towel for security. It is likely,
as is documented in dogs and cats, that if a bird is not
introduced to certain animal species by a certain age, it
will have difficulty accepting the presence of this species
in the future without fear. The positive and negative
results of creating this fearless state need to be consid-
ered (See Socialization and Co-parenting Section to fol-
Bob Doneley
low [Figs 3.2.4a-c]).
Parrots spend large amounts of time with their faces

Fig 3.2.4a | Picking a safe color towel and teaching a bird close to their babies. As the babies develop, visual con-
restraint will make veterinary exams and training easier as a tact — face-to-face and eye-to-eye — soon expands into
bird matures. Here a bird is introduced to a towel. vocal interactions post feeding, as the babies respond to
gentle murmuring of the hand-feeder. Introduction to
adult foods during the neonatal period will increase
acceptance and prevent the development of food rigidi-
ties in the future (Figs 3.2.5a-b).
Tactile Stimulation
Periodically stroking baby birds with warm hands simu-
lates parental attention. One author (PGL) has observed
the following regarding toenail sensitivity in baby birds:
“Touch the toenail clipper to the nail while holding the

baby securely. Some birds do not flinch at all, while oth-
ers react with varying degrees of withdrawal. Interest-
ingly, this relative sensitivity is consistent into fledging.”
Bob Doneley
Subsequent training exercises are used to desensitize the

tender-footed neonate at an early age, while continuing
Fig 3.2.4b | Slowly covering the bird with the
to increase the amount of reinforcement the less reac-
towel in a reassuring way. tive baby receives.
Aural Stimulation
Vocal communication between parents and chicks begins
early. Hand-feeders are encouraged to talk to the babies
in their care, accustoming them to human voices and
language. Varieties of other types of sounds also are
healthy and useful. The positive aspects of music have
been proven repeatedly with animals as well as people.
Reactive Attachment Disorder

Reactive attachment disorder involves children 5 years old
or younger. This condition was known in previous cen-
turies as orphanage baby syndrome and is better known
in the current lay literature as failure to thrive. Defined as
Bob Doneley
“a disturbance of social interaction and relatedness”, this

condition is associated with “grossly pathological care,
with persistent disregard for a child’s basic emotional
Fig 3.2.4c | Adding pressure and restraint slowly
needs for comfort, stimulation and affection, as well as
over time allows grooming and examination or
restraint whenever needed in a safe unfrightening repeated changes of the primary caregiver that prevent
way. the formation of appropriate bonds.”2 This severe absence
65
Greg J. Harrison
Greg J. Harrison
Fig 3.2.5b | An example of the proper kinds, amounts and types
of organic dry foods to teach a baby bird to accept, for macaw-
Fig 3.2.5a | Shown are examples of the most valu- sized birds on the left and Amazon-sized birds on the right. These
able types of moist foods to be offered to baby birds bowls show the amount of food offered to a pair of the respective
to teach variety. Starting at mid left going clockwise: birds mentioned. The limiting of seeds and nuts is vital; these are
organic acorn squash, lettuce, beets and beet tops, offered only to breeding birds until the babies are weaned. Then
broccoli, carrots, yams (sweet potatoes) and butter- the nuts and seeds should be stopped altogether for the babies
nut squash. and suspended until the next breeding period for the parents.
of care can result in serious psychological and physical Socialization and Co-parenting
problems in children, such as stunted growth, the inabil-
Socialization is a process by which an individual forms
ity to socialize appropriately and increased potential for
an attachment to other species.3 Time frames for social-
self-destructive behaviors later in life.13
ization in birds are not established as they have been for
dogs and cats. The hand-feeding of psittacine chicks cer-
Currently, many captive-bred, hand-fed parrots do not
tainly provides exposure to humans. Conversely, provi-
know how to play, accept appropriate touching, interact
or even how to eat a variety of foods. Perhaps as a result sion of all the natural elements outlined in this chap-
of improper or incomplete early development, increas- ter—feeding, warmth and tactile, visual and vocal stimu-
ing numbers of parrots engage in feather destruction lation—can be difficult for the human caregiver to pro-
and even self-mutilation as adults. Increasing numbers vide. Ongoing studies at the University of California-
of young domestically bred and hand-fed parrots seem Davis with co-parenting have shown great promise. Pairs
unable to form a healthy relationship with humans. The of orange-winged Amazons (Amazona amazonica) were
authors wonder if these increasing problems are related raised by their parents through fledging, with university
to psittacines being raised in an assembly-line fashion in students interacting with the young in the nest box for
a cold, clinical nursery. If this is the case, the produc- brief but regular periods of time. The study is ongoing,
tion-raising of psittacine birds is not the best technique but preliminary results show that limited handling by
for producing an emotionally and physically stable com- humans for short periods, several times a week, may
panion animal. Happily, the industry seems to be turn- produce offspring that are socialized to humans, but
ing away from production techniques, as evidenced by benefit from all the inherent advantages of parent-raised
the important work being done in large facilities such as birds. Extreme caution should be exercised in the selec-
the University of California-Davis and Texas A&M.26 tion of parents and young for this protocol to ensure
that parental infanticide, abandonment or abuse does
The dangers of creating “failure to thrive” are lessened not occur.
to an extent by raising neonates together rather than in
individual enclosures. When aviculturists have substanti-
THE FLEDGLING
ated the health of their babies (see Chapter 21,
Preventive Medicine and Screening), the young of cer- Prior to fledging, babies show increasing interest in the
tain species may be housed together; in these mixed- world outside their enclosure. A partial covering of tow-
species settings animation and interaction increase. Early els will enable the babies to see out of their container or
work on raising psittacines in mixed-species groups to retreat and hide. As they get braver, they will spend
yielded such good results — youngsters that seek touch- more time looking out of the container and less time in
ing, sleep readily, play with and seem curious about oth- concealment. There is often a great deal of wing flap-
ers — that the practice is widely accepted by many breed- ping that happens inside the nest as babies start build-
ers today. ing up their pectoral muscles.
As their foot and leg strength develops with exercise,
Lori Reilly Walton, courtesy of Santa Barbara Bird Farm

low perches should be added to the inside of the con-
tainer. In this way, babies can perch when they wish and
also stand flat-footed when they prefer.
As their distance vision improves, objects that stimulate

vision can be added to the nursery walls. When possible,
a view of the outdoors should be provided. Visual acuity
continues to increases as the bird spends more time
observing objects and movement outside of the nest
box. For instance, immediately after opening their eyes,
Eclectus nestlings will track food as it comes toward
Fig 3.2.6 | A blue and gold fledgling displays a partial wing
their eyes, but remain largely unresponsive to noiseless
clip that slows flight but does not curtail it. Graduated clipping
activities farther away. As the weeks progress, these birds done over a period of several days is recommended over a
track movements at greater distances. Just prior to fledg- severe clip that ends flight abruptly.
ing, birds can be seen scanning the horizon, (e.g., track-
ing an airplane’s progress in the distant sky), and then
quickly adapting their vision to objects presented at is normal at this stage, as the youngsters lose baby fat
close range. Play behavior increases with developing and slim down to a more streamlined, aerodynamic fig-
visual acuity. McElroy describes a 6-week-old Moluccan ure. Inexperienced hand-feeders often are confused by
chick that plays with a parent’s molted feather in the this phase if they assume that the lack of interest in
nest box, flapping her wings wildly and rolling around food indicates that fledglings are starting to wean. This
as if she had another bird as a playmate. is not the case. The process of weaning doesn’t begin
for another week or more after fledging, so caretakers
A fledgling is a young bird that is learning to fly. In
should continue to hand-feed appropriate foods at
nature, fledging happens prior to weaning, which is logi-
every possible opportunity. Although requiring a dedi-
cal when one realizes that a parrot baby must develop
cated area to avoid serious damage to the bird or one’s
the physical strength and dexterity to learn controlled
environment, fledging confers significant developmental
flight before it follows its parents to various and distant
advantages. The young psittacine’s coordination, mus-
food sources. Only then is it sufficiently developed to
cular structure and social skills increase as the fledgling
achieve the complex manual dexterity necessary to eat
learns to interact with a wider variety of flock members
on its own. Flight competence therefore precedes wean-
once flight is achieved.
ing in psittacine birds.
In the past, aviculturists automatically clipped the wings Should a new owner wish trimmed wings on his young
of baby parrots at their first attempt at flight. The popu- parrot, a gradual wing clip is preferable to the abrupt
lar belief was that the psittacines would not miss flight curtailment of flight. Instead of a drastic clipping of
if never allowed to fly. However, in the last few years it flight feathers, graduated clips, several days apart,
has been recognized that fledging can make a marked should be performed, gradually limiting flight (Fig 3.2.6).
difference in a bird’s physical and emotional develop-
ment, even when the wings are later clipped.17 Fledging THE WEANLING
is a normal part of psittacine development and allowing
“To wean” is defined as “to accustom to take food other
this stage to progress naturally makes the weaning
than by nursing” and second as “to detach from a source
process much easier.16 An excellent example of this phe-
of dependence.”22 A weaned parrot is capable of survival
nomenon is the African grey parrot. African grey babies
with little or no guidance in procuring adequate nutri-
formerly were perceived as being awkward and prone
tion. Weaned wild birds, therefore, find and supply
to falling. Actually, this species is amazingly adept at
themselves with a variety of nutritious foods in sufficient
flight and readily learns to maneuver in mid-air if given
adequate opportunity. After all, wild babies that fall fre- quantity.14 The best weaning process for psittacine com-
quently surely could not survive. The African grey’s rep- panions allows eating skills to develop gradually over a
utation for clumsiness has more to do with early wing period of several weeks. Unfortunately, many pet stores
clipping than with any inherent lack of coordination. and breeders consider a baby parrot “weaned” as soon
as it shows interest in eating on its own; which is a
The fledgling psittacine is a creature obsessed. Though regrettable and potentially fatal misconception. The
still food-dependent, the fledgling often loses interest weaning process is a gradual process wherein a baby
in eating. Flight becomes all-consuming and weight loss parrot learns where, what and how to eat. There are
67
Dissimilar environments might produce substantial dis-

parities in the urgency of achieving food-independence.
Development is faster in parrots from dry regions than
in those from rain forests. This is because the period in
which food is most abundant is shorter in an arid envi-
Laura Price, courtesy of Santa Barbara Bird Farm

ronment like the Australian hinterland than on an
Indonesian island where there is considerably more tree
cover.25 Differences in parental post-fledging feeding
have been noted among cockatiels, lovebirds, budgeri-
gars and Eclectus sp. (Kavanau 1987).
Reasons for these differences are still speculative. There-

fore, we must astutely analyze the circumstances associ-
ated with crying in the baby bird in order to respond
appropriately.
Fig 3.2.7 | A young female eclectus enjoys a meal of squash
and the novelty of new foods. Just as in human children, messy
eating and experimentation are part of the process of learning VOCALIZATION
to accept and enjoy foods of various textures, shapes and tastes.
During a specific developmental period, young psitta-
cine birds develop a loud, repetitive, plaintive call,
numerous motor skills necessary to accomplish this, and which would, in the wild, signal parent birds to locate
these take time to develop. those fledglings. Key developmental events collide at
this point: young fledglings learn to fly, navigate, land,
Psittacine parents assist in the weaning process by hold-
come and follow and practice independent eating skills.
ing food in their beak and feet for their babies. Human
Therefore, conscientious caregivers are challenged to
caretakers can assist parrot weanlings by finger-feeding
carefully observe crying fledglings to determine what the
warm, wet food. Ideal foods for this technique include
cries signal. Does this young psittacine need comfort,
chunks of cooked squash, carrots or yams and mango.
exercise or food?
Weaning pellets, or the type of formulated diet that is to
be fed when the bird is weaned, can be soaked and If comfort is needed, the bird should be held only until it
offered in this same manner (Fig 3.2.7). All foods are settles down. If the bird needs exercise, playtime can be
warmed and moistened in hot water or fruit juice. The initiated wherein the fledgling is encouraged to try new
temperature range is critical for maximum palatability physical skills such as flapping or climbing. If the bird is
and digestion. Foods should be warmed to 104 - 105° F hungry, it should be fed a moderate amount of food and
(38-38.5° C). Candy thermometers work well for this and then shown how to forage to find accessible foods.
are available in any kitchen supply store.
While some parent birds might actually let their babies
Using a camera in the nest box of a pair of wild-caught cry in order to have them practice making a verifiable
Moluccan cockatoos (Cacatua moluccensis), the process retrieval signal, this cry has a function separate from the
of raising a youngster was videotaped for 11 months. cry of a hungry youngster. In no case should young
Although the baby was noted to be typically noisy while fledglings be ignored or allowed to go hungry. Teaching
being fed, it was never noted to cry for food or to get a bird to whisper and to hum can be immediately
the parent’s attention (K. McElroy, personal communica- rewarding and contribute to acceptable vocalization for
tions, 2002). years to come.
Conversely, Harrison’s observation of a trio of black

Selling Unweaned Parrots and Force-weaning
cockatoos in Australia depicted the parents and their
young flying from tree to tree. While the parents located Avian veterinarians see a multitude of potentially serious
and ingested food, they ignored the crying of their medical problems when unweaned parrots are sold to
accompanying youngster for 30 minutes. The youngster inexperienced caregivers. Some cases of aspiration pneu-
finally chose and ingested food on its own. This was monia and crop burns are treatable but some are fatal,
obviously the final stage of weaning, as the baby was not and most are preventable through ethical breeding and
easily differentiated from the adults.10 sales practices. Many feel strongly that the practice of
selling unweaned birds should be made illegal, as it is
A possible explanation for variations of parental partici- with puppies and kittens. However, should that happen,
pation in feeding young after fledging may be reflected the fear is that baby parrots will be “force-weaned” in an
by the environmental conditions of the species. effort to expedite the weaning process.
Force-weaning entails withdrawing hand-feeding when

parrots are still begging for it, based on the belief that
hunger will force the babies to start eating on their own.
A multitude of behavioral problems may be associated
with forced or stressful weaning.16
Courtesy of Santa Barbara Bird Farm

Baby parrots that are force-weaned often later become
high strung, hyper-responsive to stimuli, prone to stress
and rigid in their eating habits. When eating skills are
not firmly in place and readily practiced, underlying
undesirable behaviors manifest. Force-weaned African
greys, for instance, seem much more prone to develop-
ing phobic behaviors later in life than do abundantly
weaned African greys.28 Cockatoos that are force-weaned Fig 3.2.8 | A juvenile Moluccan cockatoo in full display.
often become chronic whiners, which may contribute to Juveniles can be a challenge, but less so if clear, consistent con-
trols and limits are established for their behavior.
cockatoo prolapse syndrome. The large macaws, proba-
bly not truly “food-independent” in the wild until they
are at least 6 to 9 months old, often are the victims of enclosure in a bathroom with the shower running to cre-
force-weaning. When macaws are force-weaned, they ate high humidity, or exposure to actual, warm rainfall.
generally get into patterns of obsessive food begging, Increased humidity will soften the keratin sheaths of pin-
often with repetitive wing flicking and a typical macaw feathers and enable them to open more easily.
begging sound well into adulthood.4 Birds that are
weaned prematurely will exhibit chronic begging behav- Bathing Skills
iors. It is common for them to flap one wing and bob
their heads for food while crouched down.1 In contrast, Bathing skills are critical for good feather and skin health,
properly weaned birds will run to a food bowl, investi- and a thoroughly soaked parrot is inspired to healthy
gate its contents, and select a morsel and consume it, feather grooming. Many parrots are rain forest species
albeit wastefully. The aberrant behaviors of force-weaned that evolved in environments where annual rainfall is
birds are assumed to result from deprivation during a measured in feet, not inches. Even those from arid
critical period of their development. regions often are found within flying distance of water
pools or rain-drenched microhabitats where bathing
opportunities abound. With artificial heat and air condi-
THE JUVENILE OR PREADOLESCENT tioning, human environments are seriously dry, so peri-
The hallmark of this period of psittacine development is odic soakings are needed to counteract these conditions.
often the bird’s refusal to cooperate. Increased inde- Bathing skills are important for young parrots to learn,
pendence and increased athleticism both necessitate and caretakers must be patient and creative in discover-
training and learning that is critical to the future devel- ing an individual bird’s preferred bathing technique.
opment of the parrot and cohabitation with humans. Some parrots prefer pool bathing in a shallow dish, and
Most of the medium and large species of parrots listed some leaf bathe in wet kale, romaine and chard. Others
in the “Pets for Sale” section in local newspapers will be prefer rain bathing via a hand-held sprayer, the human’s
between 8 and 24 months of age (Fig 3.2.8). When prop- shower stall, a garden hose or natural rain on warm sum-
erly reinforced for desirable behaviors, this need not be mer days. It is important for caretakers not to frighten a
an overly stressful time for bird or owner (see Chapter young parrot with the introduction to bathing. This may
3, Behavior, Section I, The Natural Science of Behavior). create fears that can be difficult to overcome.11,12
Additionally, parrots who bathe or shower with vigor also
Juvenile Molt are adept at exercise because the two vital functions rein-
force each other. (Ed. Note: Some believe that blow-dry-
Juvenile parrots often experience a heavy and uncomfort-
ing should be vehemently discouraged, as this can
able molt that may make them irritable when touched.
negate the positive effects of bathing by drying out feath-
Molting parrots can be testy at any age, so one must
ers and skin. Others disagree, believing that blow-drying
assume that they are uncomfortable. Owners should be
is acceptable if it is tolerated by the bird and carefully
cautious when petting their birds, as it is easy for human
regulated to prevent burns or overheating.)
fingers to accidentally inflict pain. Gentle stroking with a
feather or toothbrush is suggested at these times, as this
may decrease the bird’s discomfort.6 Frequent bathing Exercise
also can help during this period; either self-bathing, Exercise is important to parrots of all ages, and it is
69
Layne Dicker, courtesy of Santa Barbara Bird Farm

Courtesy of Santa Barbara Bird Farm
Fig 3.2.9 | Under close supervision, wing-trimmed fledgling Fig 3.2.10 | Prey species like psittacines need the choice to be
macaws play in juniper bush while showering. Exuberant exer- visible or not, so providing hiding places can greatly decrease
cise is critical to physical and psychological health for psittacines stress for any age of psittacine. With his softened face feathers,
as well as functionally decreasing problems in the captive envi- this fledgling yellow-naped Amazon displays the comfort level
ronment. Tired parrots tend to be quiet parrots. allowed by providing such choices.
especially important for juveniles. Parrots evolved to fly caged in the middle of a high-traffic area, especially if the
many miles each day in the wild, and this inherent need bird is startled by people appearing without warning.
for exercise is critical for success in the captive environ-
ment. Flying and/or flapping exercises are a daily neces- The height of the cage also is important. Many parrots
sity, and caretakers should encourage these activities in appear comfortable when allowed to perch at human
their parrots. Exercise also is enhanced by the use of chest or shoulder level. If caged too low, an insecure
movable perches and the provisions of branches, rather parrot can become seriously frightened. If caged too
than the thick, stationary perches (Fig 3.2.9). high, headstrong individuals may be more difficult to
handle. Hiding places also are important, so parrots are
Juveniles should be encouraged to chew, shred and oth- allowed the choice of whether or not to be visible (Fig
erwise pulverize a variety of destructible toys. Natural 3.2.10). Hiding places can include branches wired to the
branches from non-toxic, non-sprayed trees, complete outside of the cage to produce a “thicket-like barrier”
with bark and leaves, are ideal for parrots, and caretak- (M.S. Athan, personal communications, 2000), a fabric
ers should be encouraged to find a constant source of cover over one corner or wooden boxes attached to the
such things as bamboo and willow for their birds. side of the cage.
Environmental Enrichment
The Human Environment Because of the psittacine’s need to forage and shred,
suitable objects are necessary components of the
and the Companion Parrot enriched environment. Destructible objects, such as safe
branches with leaves and bark intact, paper cups, tongue
Cage Placement depressors and cotton-tipped applicators, also can keep
The ideal area in which to place a bird’s cage is depend- parrots quietly and inexpensively absorbed.7 One
ent on the personality of the specific bird. Most parrots author’s own blue and gold macaw hen (Ara ararauna)
enjoy being in the center of human activity, but care methodically works its way through an old phonebook
should be taken to allow for the instinctive insecurities once or twice a year, spending several weeks of intensive
of a prey animal. Placing a cage against a solid wall pro- work to render the entire publication into thumbnail-
vides security, but many parrots enjoy a window view. sized pieces. This activity appears to diffuse aggression.23
Cages may be placed partially against a window and par-
tially against a solid wall to provide the advantages of Four categories of parrot toys have been described:
both security and stimulation. chew toys, climbing toys, foot toys and puzzle toys.9 A
small number of stimulating toys, rotated on a weekly
Extroverted parrots that are caged away from human basis, seems to hold a parrot’s interest. One toy from
activities often scream excessively. Anxious, skittish par- each category might satisfy most parrots’ need to play,
rots may start showing feather-destructive behaviors if investigate and destroy, and also leave sufficient room
for the bird to move around its cage. In a very large cage TRAINING THE YOUNG PSITTACINE
or aviary, toys might be placed randomly about in order Young parrots need reinforcement for appropriate
to encourage the parrots to use their entire territory. behavior. Parrots, like other animals, will perform best
for positive reinforcement and will soon discard behav-
Foraging iors for which they receive no reinforcement. Without
A recent study demonstrates the value of environmental training, parrots do not understand how to be good
enrichment in psittacine birds.21 The use of foods and companions and people do not understand how to be
toys for foraging activities and environmental enrichment good caregivers.
is a long-standing tradition in many companion and avi-
cultural situations. Foraging is encouraged when foods Activities appropriate for the young bird to learn include
are offered in new and challenging ways, such as stuffing physical lessons such as swinging, flapping and climb-
an empty tissue box with greens or hiding a food within ing. With these athletic adventures, young birds learn to
view but not within reach, eg, inside a puzzle toy. Parrot burn their calories in appropriate ways and don’t have
owners must devise methods to keep their birds occu- massive amounts of energy left over at the end of each
pied, especially during the long hours spent alone. day for screaming, pacing or hyperactivity. In addition to
physical activities, young birds should be encouraged to
Toys also are useful as deflectors of aggressive energy, develop social skills that allow them to take food from
especially with species like Amazons. These birds may human hands, to play with toys with various people, and
interact roughly with their toys, dissipating potentially to step up on either an offered hand or a hand-held
aggressive energy. perch. Vocal skills also benefit young psittacines who are
encouraged to modulate their contact calls with more
Adequate Sleep pleasing and less repetitive, less plaintive vocalizations,
such as soft chortling and whistles.
Sleep is another important consideration, especially with
a young parrot. The actual sleep requirements and the The owner should train the young parrot to accept han-
presence of active (REM) vs. slow-wave sleep have not dling that facilitates life as a successful companion, such
been determined in various psittacine species. In dogs as entering and exiting the cage and stepping up and
the “active sleep-quiet sleep,” or slow-wave (REM) sleep down upon request. Ideally, parrots should be trained to
cycle, is only 20 minutes as compared to 90 minutes in tolerate procedures such as grooming; this can greatly
humans. In the absence of controlled data on normal minimize stress but is difficult for most people to
sleep rhythms, extrapolation and observation must be accomplish with their pet bird.
used to tentatively determine a pet bird’s sleep require-
ments. As tropical and neotropical species, most com- Parrots that do not receive rudimentary training are apt
panion parrot species evolved in an environment that to lose their homes for two reasons: (1) caregivers tend
provided 12 hours of darkness and daylight, year-round. to lose interest in “unmanageable” birds; (2) untrained
parrots shape their own behaviors into less compatible
As previously mentioned, due to their social nature, par- actions such as screaming and biting.
rots often are caged in high-traffic areas. This places
them in locations with extended hours of noise and arti- Parrots should not be making decisions, such as whether
ficial light. When questioned about sleep, owners gener- or not they wish to go back in their cages or whether or
ally believe that covering the bird initiates sleep. More not they wish to get off of the owner’s shoulders. Parrots
accurate information would be derived from asking what that learn to respond to reasonable requests are those
time the noise ceases and the lighting is extinguished in that consistently benefit most from positive reinforce-
the evening.29 ment, and caregivers should be aided in finding positive
ways to teach their birds.
Rather than declare major rooms off limits past a certain
hour to give a parrot more sleep, veterinary ethologist It is also important to understand that parrots are inde-
Andrew Leuscher originated the concept of the “sleep pendent creatures. While parrots should step on the
cage.” A sleep cage is a small, sparsely equipped cage that human hand on command when they exit their cages,
is kept in a room that is unoccupied by humans at night, the act of compliance with this command should be
and it allows parrots to be put to bed at a reasonable made a positive experience. For instance, rather than
hour. This allows them to get the hours of dark and unin- wait until the last possible second to return birds to
terrupted sleep that they appear to need. Behavioral man- their cages when owners are stressed and pre-occupied
ifestations of sleep deprivation in parrots include hyperac- by being late for work, they will have greater success if
tivity, aggression, excessive screaming (especially after sun- they choose to re-cage their parrots earlier under more
set) and feather-destructive behaviors such as plucking. relaxed circumstances. For example, to remove a parrot
71
from its cage, the owner may approach the cage and ask Inappropriate behaviors become problems when they
the bird if it wants to come out. Observation of body are inadvertently reinforced, such as the baby that
language readily answers this question. If the answer is lunges at a stranger, only to be hugged and soothed
affirmative, the parrot generally moves forward, and/or (and therefore rewarded for aggression) by the owner.
picks up a foot. If so the owner opens the cage door and Some birds will hold onto their owner, or their cage
uses the “Up” command to which the bird has been door, as the owner attempts to return them to their
trained. A negative response is equally obvious — the cage. This should be recognized as early defiant behav-
bird moves away and/or turns its back. If the response is ior and addressed.
negative, the interaction is ended. No command has
been given, so no control has been lost.8
SUMMARY
Birds vary in their reaction to food as a motivator for Aviculture undoubtedly will continue to raise psittacine
behavior. Most owners cannot and do not wish to with- birds destined to become human companions as long as
hold food from their birds in order to stimulate food- humans demand them. Accordingly, the need continues
motivated behavior. However, some who manipulate for examination of psittacine development. Appropriate
delivery of a favorite food report surprisingly good diets, stimulation, security, regular and consistent sleep,
results. Therefore, rewards should be selected for their appropriate lighting and sufficient exercise are important
efficacy in eliciting and reinforcing desired behaviors.21 for the development of young parrots. Fledging should
be part of the optimal psittacine development. Training
Juvenile Behavior Problems techniques that enhance success in the human environ-
For detailed analysis of the various problem behaviors ment include basic handling skills (such as cage entrance
seen in companion parrots, refer to Section III of this and exit competence). When we properly educate our-
chapter. Many of the problems seen in older birds have selves, we can raise young psittacines that have an excel-
their foundation in mishandling of the youngster. lent basis for success in their captive environment.
References Bird Report 5-3(23)1995:30-32. impact of weaning, The Pet Bird 1997.
10. Harrison G: Perspective on par- Report, Vol 4 #6, Issue 20, 24. Schubot R, Clubb K, Clubb S:
1. Abramson J: The Large Macaws. rot behavior. In Avian Medicine: 1995:4-11. Psittacine Aviculture. Avicultural
Abramson, Speer and Thomsen, Principles and Application. 17. Linden P: The lasting behavioral
Raintree Publications, Fort Bragg, Breeding and Research Center,
Ritchie B, Harrison G, Harrison L effects of fledging. The Pet Bird
CA, 1995:205. Loxahatchee, FL, 1992.
(eds). HBD Int’l Inc, Brentwood, Report #29, 9/96:40-45.
2. American Psychiatric Association: TN, 1999:97. 18. Martin S: Lecture: Things That 25. Silva T: Psittaculture: The
The Diagnostic and Statistical 11. Hefton D: Showering your par- Make You Go ‘Hmm!’ Annu Conf Breeding, Rearing and
Manual of Mental Disorders rot. Pet Bird Report 25:14-17, Int Aviculturists Soc, Orlando, FL, Management of Parrots. Ontario,
Washington, DC, APA, 1994:116- 1996:14-17. March 1998. Canada, Silvio Mattacchione &
118. 12. Hefton D. The fine art of bathing 19. May D: Greys of the Congo basin. Co, 1991:63.
3. Beaver B: Feline Behavior: A the psittacine. Pet Bird Report Bird Talk Magazine, January 2002 26. Styles D: The Importance of
Guide for Veterinarians. 31:18-23, 1997. 20(1):37-47. socialization and flocking prac-
Philadelphia, PA, WB Saunders, 13. Kaplan H, Sadock B, Grebb J: 20. McElroy K: Parent-rearing tices in shaping psittacine behav-
1992. Synopsis of Psychiatry ed 7. Moluccan cockatoos and breeding ior in the home and aviary. The
4. Blanchard S: Handfeeding trauma Williams & Wilkins, Philadelphia, cockatoos outdoors in a northern
in young macaws. Pet Bird Report Gabriel Foundation, Parrots in
1994, chapter 45.3:1109. climate. Proc 9th Ann Conf
#17 9/94:46-47. the New Millennium 2002,
14. Linden, PG: Abundance wean- Midwest Avian Research Expo,
5. Budiansky, S: The Covenant of ing. Pet Bird Report 13(3) 5: 18- 1998:51-56. February 8, 2002, San Diego, CA.
the Wild: Why Animals Chose 22, 1993. 21. Meehan C, Millan JR, Mench J: Verbal presentation.
Domestication, Yale University 15. Linden PG: Teaching Psittacine Foraging opportunity and 27. Wilson L: The NEW and
Press, New Haven, CT, 1992:77- Birds to Learn. Sem Avian Exotic increased physical complexity IMPROVED Baby Parrot. The
78. Pet Med: Behavior. Alan Fudge both prevent and reduce psy- Watchbird, J Amer Fed Aviculture,
6. Cravens EB: The essence of (ed); Christine Davis (guest ed), chogenic feather picking by Vol XXVI No 2, Mar/April 1999:47-
touch. Parrots Magazine No 33 Oct 1999 8(4):154-164. young Amazon parrots. Applied 49.
April/May 200:22-24. 15a. Harcourt-Brown NH: Anim Behav Sci, 80(1):71-85,
28. Wilson L: Phobic Parrots: An
7. D’Arezzo C, Shannon-Nunn L: Development of the skeleton 2003.
Parrot Toys and Play Areas. Crow Increasing Phenomena? Proc
and feathers of dughy parrots 22. Merriam-Webster’s Collegiate
Fire Pub, Springfield, VA, 2000. (Pionus fusous) in relation to Dictionary 10th Ed, 2000,1334. Assoc Avian Vet 1998:125-131.
8. Davis C: Spring is in the air. Bird their behavior. Vet. Rec 154, 42- 23. Murphy J: Shadow boxing or play 29. Wilson L: Sleep: How Much Is
Talk 19(4)2001:80-83. 48. 2004. fighting in Amazon parrots. Enough For A Parrot? The Pet
9. Foushee D: Play therapy. The Pet 16. Linden PG: The developmental Amazona Quarterly (2):14-16, Bird Report, April 1999 43:60-63.
Recommended Reading Three centuries of research, the- 2000. Spectacled Parrotlets (Forpus con-
ory, and mere surmise. Can J 16. Pepperberg IM, Wilcox SE: spicillatus): Evidence for
1. Blanchard S (ed): The Psychol 1989 Sept 43(3):369-96. Evidence for a Form of Mutual Individual Voice Recognition.
Companion Parrot Quarterly (for- 9. Kavanau JL: Behavior and evolu- Exclusivity During Label Behav Ecol Sociobiol 1998
merly The Pet Bird Report). tion: Lovebirds, cockatiels and Acquisition by Grey Parrots 43(3):197-202.
www.companionparrot.com, budgerigars. Science Software (Psitticus erithacus). J Comp
Alameda, CA Systems, Inc, California, USA, Psychol, 2000 Sept 114(3):219-31. 22. Welle KR: Avian Obedience
2. Brown SD, Dooling RJ: 1987. 17. Ritchie BW, Harrison GJ, Harrison Training. Proc Annu Conf AAV
Perception of conspecific faces by 10. Lightfoot T: Avian Behavior. Proc LR (eds): Avian Medicine: 1997:297-303.
budgerigars (Melopsitticus undu- Assoc Avian Vet, 2002. Principles and Application. 23. Welle KR: Psittacine Behavior.
latus): II. Synthetic models. 11. Linden PG: Abundantly Avian, Brentwood, TN, HBD Int’l, Inc, Proc Annu Conf AAV 1998:371-
Comp Psychol 1993 Mar The Compiled Works of Phoebe 1994. 377.
107(1):48-60. Linden Green. Pet Bird Report, 18. Shields KM, Yamamoto JT, Millam
3. D’Arezzo C, Shannon-Nunn L: Santa Barbara, CA, 1999, JR: Reproductive Behavior and 24. Wilson L: Handbook of Avian
Parrot Toys and Play Areas. Crow www.santabarbarabirdfarm.com. LH Levels of Cockatiels Articles. www.upatsix.com/liz.
Fire Pub, Springfield, VA, 2000. 12. Linden PG: Behavioral (Nymphicus hollandicus), 25. Wilson L: Phobic Psittacines
4. Davis C: Basic considerations for Development of the Companion Associated with Photostimulation, Birds-An Increasing
avian behavior modification. Sem Psittacine Bird. Proc Annu Conf Nest-Box Presentation, and Phenomenon? Proc Annu Conf
Avian Exotic Pet Med (8)4:183- AAV, 1998:139-143. Degree of Mate Access, Hormones AAV 1998:125-131.
195, 1999. 13. Linden PG: Teaching psittacine and Behavior 23:68-82, 1989.
5. Davis CS: Parrot psychology and birds to learn. Sem Avian Exotic 19. Sibley DA: The Sibley Guide to 26. Wilson L: Restraint in the Animal
behavior problems. Vet Clin No Pet Med (8)4:154-164, 1999. Bird Life and Behavior, Hospital. Vet Clin NA-Exotic Sept
Amer Small Anim Pract (6):1281- 14. Pearn SM, Bennett AT, Cuthill IC: Chantilleer Press, NY, 2001. 2001, 4(3):633-640.
8, 1991. Ultraviolet Vision, Fluorescence 20. Styles, D: Captive Psittacine 27. Wilson L: Screaming and Biting in
6. Diamond J, Bond AB: Kea, Bird of and Mate Choice in a Parrot, the Behavioral Reproductive the Psittacine Pet Bird. Vet Clin
Paradox. The Evolution and Budgerigar Melopsitticus undu- Husbandry and Management: NA-Exotic Sept 2001, 4(3):641-
Behavior of a New Zealand Parrot lates, Proc R Soc Lond B Biol Sci Socialization, Aggression Control, 650.
Univ of CA Press, USA, 1999. 2001 Nov 7;268(1482):2273- and Pairing Techniques. Proc AAV,
7. Foster S, Hallander J: Cockatoos 2279. Selected Topics in Non-Infectious 28. Wright TF, Wilkinson GS:
and African greys: Phobic behav- 15. Pepperberg IM: The Alex Studies: Disease (Specialty Advanced Population Genetic Structure and
ior. The Pet Bird Report 8(4)42 Cognitive and Communicative Program), 2001:3-19. Vocal Dialects in an Amazon
:18-23. Abilities of Grey Parrots, Harvard 21. Wanker R et al: Discrimination of Parrot. Proc R Soc Lond B Biol Sci
8. Harris LJ: Footedness in parrots: Univ Press, Massachusetts, USA, Different Social Companions in 2001 Mar 22, 268(1467):609-616.
03_Concepts in Behavior III.qxd 8/22/2005 1:25 PM Page 73
Section III
Pubescent and Adult Psittacine Behavior
LIZ WILSON, CVT; TERESA L. LIGHTFOOT, BS, DVM, D ipl ABVP- Avian
The prevalence of captive-raised psittacines as pets and pating this energy. Daily flapping exercise, play with toys
the ensuing problem behaviors have become critical and showers consume natural energy and provide learn-
issues for veterinarians as well as aviculturists and parrot ing opportunities with inherent reinforcement. Once
owners. Ethological considerations should occupy a through puberty, the adult psittacine may display a more
large area of future study, concern and advancement. predictable pattern of behavior (Fig 3.3.2).
The terms adolescent and puberty in this chapter are

used to identify the period of development during
which hormonal changes play an active role in both the The Adult Psittacine
initiation of reproductive capacity and associated varia-
tions in temperament. Recognition of the role of sexual
Companion
hormones in psittacine behavior is critical to the inter- In the wild, constant challenges test the parrot’s athleti-
pretation and modification of behavior. cism, ability to avoid predation and to find food. To suc-
ceed in such a demanding environment, parrots must be
flexible, adaptable and continue to learn. It has been
Puberty estimated that the average parrot’s day is divided thusly:
50% of waking daylight hours spent locating and con-
As with other psittacine developmental stages, the onset suming food; 25% spent interacting with one’s mate
of puberty varies with the species and the individual (see and/or other flock members; and 25% spent in preening
Table 3.2.1 in Section II of this chapter). If erratic behav- (J. Harris, personal communication, 1996). In contrast,
ior is inadvertently rewarded it may continue after the there are few challenging activities in the human habitat.
sexual hormonal fluctuations of puberty have subsided.9 Alone in a cage all day, the monotony is pronounced.
Enrichments, especially ones that encourage foraging
Owners are often unprepared for the prolonged develop- behavior, will provide appropriate learning and athletic
mental changes that their pet psittacine will undergo. experiences for captive psittacines.
Clearly established behavioral boundaries will decrease but
not eliminate hormone-induced behavior. To aid in estab- Management issues can significantly contribute to prob-
lishing rules and guidelines, the types of behavior for lem behaviors. Inadequate diet or sleep and boredom
which the animal is reinforced must be examined. Pubes- can all be problematic. Cage size, location and height
cent parrots can learn to behave in ways that mitigate are also important. Refer to Chapter 2, The Companion
obnoxious behaviors, hormonal or not, and should be Bird, for discussions of these subjects.
appropriately reinforced for non-reproductive behaviors
if they are meant to be non-reproductive companions.
TRAINING
Increasing sexual hormone levels may lead to the first Psittacines should be trained to step on and off both the
instances of territoriality and perceived aggression (Fig hand and a hand-held perch and to enter and exit their
3.3.1).1 In the adolescent parrot, fluctuating hormones cages on command. They also should be trained to step
add to the inherently high energy level to produce a from one hand to the other, an exercise called “ladder-
bird that needs directed, acceptable methods for dissi- ing.” When training a parrot, it is preferable to work out
Greg J. Harrison
Greg J. Harrison
Fig 3.3.1 | Sexually hormonal female yellow-naped Amazon
parrot that is agitated. Note the erect neck feathers and
forward-leaning stance as she defends her position on a
cage door. Fig 3.3.2 | Umbrella cockatoo exhibiting
“alert” display. Species and individual varia-
tion dictate how a parrot in this “state”
should be approached.
of sight of a parrot’s perceived territory. Lessons should Physical Examination). Teaching of toweling to young
be short and upbeat, with rewards that are meaningful parrots can include playing “hide and seek” with towels
to the bird. Positive interactions and praise work well for of preferred colors, while gradually increasing the par-
parrots that already like their trainers. Correct responses rot’s acceptance of restraint.
should be instantly rewarded. The reward will vary with
the personality of the individual parrot. It may be praise,
EXERCISE AND PLAY
desired physical contact such as head scratching, or a
food treat (see Section I of this Chapter). The importance of exercise and play increases with the
adolescent parrot and continues to be an important skill
The species most prone to feather destruction and self- throughout psittacine life. Behaviorists have equated the
mutilation in domestic life often inhabit large flocks in amount of play in which the young engage with a species’
the wild, and these same animals may therefore have general adaptability. Studies of keas (Nestor notabilis) are
evolved extensive interactions within a social order. particularly compelling in this regard.23 Play behavior is
When social order is ambiguous or absent in the human consistently demonstrated in properly raised captive
habitat, high levels of stress may result.27 psittacines. According to one biologist, “The question of
‘play’ in animals is an intriguing one. We use the word to
connote activity that has no obvious use in daily life —
Color Preferences and almost a frivolous pastime. In fact, play has an important
function for the animals that engage in it, humans
Applications included, and particularly for their young. It is a way of
developing dexterity and motor coordination, and of dis-
Many birds have preferred colors and other colors that
cerning the boundaries of social behavior, skills that are
are associated with fear or avoidance. To evaluate an
critical to success as an adult. Play, as we know from
individual bird’s color preferences, place the parrot in a
confined area with six or seven identical children’s col- watching our children, is a form of learning.”15
ored wooden or plastic blocks or balls. Note the colors
the parrot avoids and those with which it plays. Remove
the objects in the colors it ignores or avoids. Repeat this
test several times to verify the preferences.
Problem Behaviors in
Captivity
The positive colors can be supplied in the form of other
items in the parrot’s environment. During training, uti- An understanding of normal psittacine behavior is neces-
lize these favorite colors in the selection of clothing, sary when attempting to address problem behaviors in
perches and food cups (Fig 3.3.3). This color selection captivity (Fig 3.3.4). For example, it is perfectly normal
can aid in the acclimation and acceptance of toweling in for a parrot to use its beak when climbing, even when
parrots (see Chapter 6, Maximizing Information from the climbing onto a human hand. If that hand jerks in
Chapter 3 | C O N C E P T S I N B E H A V I O R : S E C T I O N I I I
75
Greg J. Harrison
Fig 3.3.3 | This lovebird is well-adapted to toweling by its Fig 3.3.4 | This is a common species threat posture displayed
owner and prefers the color blue. by a nervous green-winged macaw willing to defend against
entry into its cage.
anticipation of a “bite,” and the parrot doesn’t reach its

destination, the next time it might try a different (harder,
perhaps) grip before it steps. It has been observed that
inexpert handling by humans fuels fear in young parrots.
Further, psittacines are normally loud, destructive and
messy animals. While these behaviors may distress the
people who live with them, they are not aberrant.
When one examines a “problem” behavior, the first

question to ask is; “What function does the behavior
serve?” Behavior has a function, which means that every
learning-based animal performs certain behaviors based
on what the animal gets as a result of that behavior (see
Section I of this chapter).
Greg J. Harrison
INAPPROPRIATE BONDS
Some birds are reinforced when they show aggression
Fig 3.3.5 | This yellow-naped Amazon has been
toward less-favored people. Their actions may be accom- sexually regurgitating its food to the owner, and it has
panied by screaming, laughing or crying, culminating in some of this food on its beak.
a rescue by the favored person. All this vocalization and
activity is positive reinforcement.
parrots perform these behaviors during courtship and
Owners can work with their parrots to prevent over- we therefore assume that companion parrots interpret
bonding to one person. A useful technique is this type of petting as sexual. Panting and masturbatory
Blanchard’s handling exercise called the warm potato behavior often follow such intimate touching.6 Serious
game.14 A neutral room is ideal for this purpose. The aggression may follow, when the bird attempts to drive
parrot is passed from person to person with each mem- all creatures except the perceived mate from its territory.
ber interacting positively (ie, praise, petting, treats) with When unable to reach the targets of its attack, this bird
the bird. This handling exercise should be continued for may displace its aggression, often in the form of a severe
the duration of the parrot’s life. To avoid alarming the bite, to the perceived mate or even to themselves.
timid parrot, the socialization process can begin by step-
ping onto the shoe of a less-favored person (sitting with
COCKATOO VENT PROLAPSE
one leg crossed), then be stepped back to the familiar
hand and rewarded.30 This syndrome is extremely common in adult umbrella
(Cacatua alba) and Moluccan (Cacatua moluccensis)
People may inadvertently allow their parrots to form a cockatoos. Generally, these parrots are strongly bonded
mate bond with them (Fig 3.3.5). Owners often stroke to a human. Several veterinarians38 (Van Sant, personal
their companion parrot’s back and tail.18 Breeding communication, 2002) have made the observation that
Fig 3.3.6 | Prolapsed cloaca on Fig 3.3.7 | Closer look at the prolapsed cloaca Fig 3.3.8 | After prolaspe is reduced, loss of
an umbrella cockatoo. in Fig 3.3.6. elasticity and dilation of the cloacal lips are
evident.
delayed weaning appears related to this phenomenon PROLONGED HORMONAL

(see below). Although the etiology is still speculative, STIMULATION
several characteristics have been noted in most of these Captive-bred parrots display sexual behaviors at earlier
cases. They: ages than their tree-ranging counterparts. Eclectus hens
Are hand-raised individuals of the noted cockatoo (Eclectus roratus), for example, may lay eggs in captivity
species. at 3 years of age. In the wild, eclectus hens generally
Experienced delayed weaning and/or continued beg- don’t begin to lay until about 6 years of age.18 Sexually
ging for food. mature companion psittacines are also developing what
some avian veterinarians call “hormone toxicity.” Instead
Are psychologically attached to at least one person.
of going into nesting behavior once a year, circum-
Have a tendency to hold stool in their vent for pro-
stances in the human habitat can cause parrots to
longed periods (ie, overnight) rather than defecating remain hormonally stimulated indefinitely. In the wild,
in their cage. This may be exaggerated by potty train- seasonal triggers, like changes in photoperiod, suitable
ing these parrots. nesting sites and ample food, initiate nesting behavior.
Similar triggers initiate nesting behavior in captivity
Prolonged begging for food causes straining and dilation
(Table 3.3.1), but the artificial environment provides not
of the vent. Misplaced sexual attraction to their “human”
only safety from predation but also confusing signals.
mate also will cause vent straining and movement.
Artificial light mimics the long days of summer, and sea-
Retention of stool in the vent for prolonged periods
sonal variations are lacking. The same is true of tempera-
stretches and dilates the cloaca. The vent lips in these
ture, as indoor parrots are protected from cyclic change.
birds are often distended and flaccid (Figs 3.3.6-3.3.8).
Food is abundant and some parrots are fed daily rations
that provide many times their caloric needs.18
Behavioral modification is difficult for owners to accom-
plish, since it involves altering the tight bond that they In parrots that become aggressive when in breeding
have with their parrot. Behaviors that increase this inap- mode, pupillary constriction, filoerection of the nape or
propriate bonding in affected cockatoos include stroking
the parrot, especially on the back (ie, petting), feeding
Table 3.3.1 | Foods that Encourage Breeding or Foods to
the parrot warm foods by hand or mouth, and cuddling
Avoid to Reduce Breeding Behavior
the parrot close to the body.
Item Description
High fat items • Seeds such as a sunflower, safflower, hemp, niger,
If the parrot perceives the owner as either its parent or thistle, spray millet
its mate, it will continue to strain and the prolapse will • Nuts
• Meats
likely recur despite surgical correction (see Cloacopexy • Oils
in Chapter 35, Surgical Resolution of Soft Tissue Sweet items • Immature items such as corn, beans and peas
• Apples
Disorders). Some veterinarians have found that a total • Grapes
• Citrus
change of environment and human companionship (ie, • Bananas
finding the parrot a new home, either temporarily or Refined • Pasta
permanently) is necessary to correct this problem. carbohydrates • Breads and other baked goods
77
crest feathers, or flexion of the joints of the wing will

convey a warning of the parrot’s agitation and potential Case Study: Excessive Screaming
reaction to further approach (Figs 3.3.1, 3.3.2). If these A 9-year-old male umbrella cockatoo (Cacatua alba)
warning signs are not recognized, both physical and was screaming for hours on end and neighbors were
emotional damage may occur.7 Some companion psitta- beginning to complain.
cine species become reproductively active once a year
and during the remaining months are not so frenetic.22 Through the process of taking a detailed history the
following information was discovered. The bird’s
In recent years, sexual hormone manipulation has been cage backed up to a half-wall that allowed visibility
attempted with compounds such as chorionic gonado- from all directions and the bird had no hiding place
tropin or a GnRH agonist.b These medications may tem- in its cage. The cockatoo was getting only 6 hours of
porarily ameliorate the problem behaviors of hormonal dark, uninterrupted sleep and was eating a high-
aggression, as well as physical problems like chronic egg sugar, low-nutrition diet. The owners also were
laying (see Chapter 19, Endocrine Considerations and unknowingly allowing sexual behaviors such as mas-
Chapter 9, Therapeutic Agents). However, if the parrot’s turbation and had little control over the cockatoo.
environment contains triggers for nesting behavior, sex-
ual hormone levels may remain high despite the admin- The approach to this problem was multifaceted. The
istration of these medications. Environmental triggers owners purchased a sleep cage and began putting the
must be eliminated before lasting relief can be found.28 bird to bed at a much earlier hour, enabling 10 hours
of sleep. A large towel was positioned over one end
One aviculturist cites the following example of “energy of the parrot’s cage, allowing the bird to withdraw
management.” He suggests redirecting psittacine energy from sight whenever he wished, and the owners dis-
into survival behaviors instead of reproductive behaviors. covered that the bird chose to spend a great deal of
In the case of one excessively hormonal female umbrella time behind the barrier. The diet was adjusted and
cockatoo, he randomly modified the heat and light in the the owners began having daily lessons to establish
parrot room, the amounts and types of food offered, and better control. Sexual behaviors were curtailed with
the bird’s perception of safety (by not covering the cage no punishment or drama. Within a couple of weeks,
every night). Paper was provided during the day to shred. the screaming had abated tremendously, and 2 years
Within a week, the hen had returned to normal behavior. later, the owners (and their neighbors) continued to
(G. Wallan, personal communication, 2002). be very pleased with the decrease in the bird’s vocal-
izations to expected levels.
CHEWING
Chewing is not something that parrots “grow out of,” as
Amazons and cockatoos normally will produce 15- to 20-
do puppies. Owners who complain that their psittacine
minute bursts of screams several times per day, espe-
is chewing the wall behind the cage should move the
cially morning and evening.
cage, supervise their parrots when out of their cages,
and teach their parrots to chew on well-designed toys or Incessant screaming is not normal behavior. Once again,
other appropriate items. Dried pine cones, natural fresh the first step to changing a behavior is to analyze its
branches from unsprayed trees such as apple, citrus, function: what does the parrot achieve by screaming?
melaleuca, Australian pine, ash, beech, and aspen are Does the screaming parrot yell to get the owner’s atten-
also ideal. Indeed, bark chewing and eating behaviors tion, to obtain food or to alleviate boredom? Many par-
have been observed in African greys in Africa.31 rots that scream excessively do so to liven up their
monotonous existence.43 See Section I of this Chapter
EXCESSIVE VOCALIZATION for more information on inadvertent reinforcement of
People frequently ask how to “teach their parrots how to excessive screaming.
be quiet.” Parrots are loud animals and they cannot be
When taking a behavioral history, ask the owners what
taught to be otherwise. When lay bird magazines tout a
they do when their bird screams. They may let the par-
particular species as being “quiet,” this does not mean
rot out of its cage, pick the parrot up, give it a treat to
that parrots of that species make no noise; it means they
quiet it or yell at the bird. Unfortunately, all these
make less noise than the species that are known to be
responses are rewards and reinforce the behavior.
very loud.
Normal noise levels vary from species to species, but Modifying Screaming Behavior
generally speaking, parrots tend to vocalize loudly sev- There are inherent problems with most cases of exces-
eral times a day for 5 to 15 minutes. The large macaws, sive screaming. First is duration, because the more time
parrots have been reinforced for screaming, the more some special treats hidden in a difficult-to-get-at toy.
ingrained is the behavior. It is also essential that all peo-
ple involved understand that changing screaming behav- There are exceptions to the rule of ignoring excessive
ior requires participation by all the humans in the area. screaming. When the human “flock” reunites, parrots
If one person in the environment continues to reward tend to celebrate this occasion with raucous noise.
the screaming, the behavior will not change. Owners should not ignore the bird in this situation.
Instead, they should greet their parrots and spend a cou-
The resolution of any behavior problem requires a step- ple of minutes interacting with them. Owners should
by-step approach (see Section I of this chapter for more then ignore any noise that happens after a parrot is suit-
information). Circumstances that precede the behavior ably greeted. A second exception has been termed the
should be documented. These may include: “contact call.”24 In the wild, a parrot’s flock represents
• Time of day the safety and protection of numbers. When other flock
• Day of the week members are not visible, for example, when a flock is
• Activity/mood/noise level in the household feeding in the heavy foliage of the rain forest canopy,
• The parrot’s body language they may use the contact call. Its function is to make cer-
tain they have not become separated from the flock.
• Relation to feeding time
Companion parrots also do this, and they are simply
Reactions that accompany or follow the screaming making certain they are not alone. When contact calls
should be recorded (as these may be the inadvertent are not answered, they often escalate to a scream. If a
reinforcers of the behavior). scream is required to receive a response, this inadver-
tently reinforces screaming.
Owners are instructed to collect but not interpret data
for 10 to 14 days. If a pattern is detected, steps can be African greys (Psittacus erithacus erithacus) have been
taken to change what leads up to the behavior and the described as learning human contact calls, such as the
response to the behavior, therefore changing the behav- ringing of the phone and the beep of a microwave. It is
ior itself43 (see Section I of this chapter for an in-depth postulated that they mimic these sounds when they are
discussion of this behavioral model). seeking contact with the members of their human
flock.26 Cage location also can influence levels of
To successfully decrease excessive screaming, owners psittacine vocalization.
must be consistent and patient. If a parrot screams while
caretakers are in the room, they can turn their backs and Without an area in which to hide, vigilance behavior may
momentarily withdraw their attention. This maneuver is be displayed as excessive vocalization.
classified as a “time out.” The second the racket quiets,
they can turn back to the parrot and gently, so as not to BITING
reignite a screaming fit, reward with smiles, praise or
Unlike excessive noise, biting may not be grounded in
acceptable food treats. If the screaming begins again,
instinct. According to observations made of parrots in
caretakers should turn their backs and leave the room,
the wild, the beak is used for eating, preening and social
leaving the parrot alone. They should not return until
interaction, not as a weapon against other flock mem-
the parrot has temporarily quieted.
bers. Wild parrots use complicated body language,
If they are not in the same room when a screaming feather position and voice to express themselves in situ-
episode begins, they are to do nothing until the parrot ations of conflict with others in their flock. When a con-
quiets briefly and preferably makes some acceptable frontation is not quickly resolved, they simply fly away
type of noise. Then they can reenter the room and rather than engage in actual combat.36,37,39
reward the parrot for either silence or acceptable vocal-
Most captive parrots are caged and have clipped wings,
izations. Extinguishing excessive screaming will not pro-
so instinctive responses such as flight are not an option.
duce a completely quiet parrot.25
Hence, biting becomes a common behavior in captivity.
Parrots often scream excessively when company arrives.
Owners can take the following preemptive steps: (1) Do The Functions of Biting
not feed the parrot for 4 to 6 hours prior to company As was previously mentioned, it is critically important to
arriving; (2) Encourage the parrot to engage in flapping analyze the function of a behavior before appropriate
session, followed by a drenching shower. Once accom- recommendations can be made. A detailed history must
plished, move them to a sleep cage in a separate room be obtained. There are wide varieties of stimuli that
(for more information on sleep cages, see Chapter 2, motivate a parrot to bite, and these need to be identified
The Companion Bird); and (3) Give the bird a meal and and analyzed.
79
Fear-based Biting As exemplified by the frequent springtime attacks of small

The issue of fear is a critical consideration with a parrot. songbirds on substantially larger predators, like raptors,
Psittacines tend to be frightened of novel objects or situ- dogs and people, parrots take their territoriality quite
ations, as their survival in the wild would be enhanced seriously. Owners who allow their parrots total freedom
by approaching new things with extreme caution. in the home unwittingly exacerbate this problem, as the
Owners may not realize this and become impatient with parrots may then defend wider areas from non-favored
their parrot, increasing rather than dissipating its fear. people.21 In extreme cases, parrots assume the entire
One needs to look for techniques to gradually desensi- house as their territory, attacking anyone who enters.
tize the parrot to fear stimuli.
By training parrots to enter and exit the cage on com-
mand, caretakers maintain control over the cage space,
Biting and Territoriality
preventing territorial aggression. This is easily accom-
Parrots, like most animals, have territorial impulses.3 If a plished by teaching parrots that they must step onto the
parrot starts to lunge when around any perimeter, it is offered hand or hand-held perch if they wish to exit the
labeled as “territorial.” Caregivers can alter the configura- cage.13 If parrots do wish to come out of the cage, own-
tion of that perimeter, preferably with enrichment, ers should not just open the cage door and walk away,
decreasing the territorial response. Preferred behaviors allowing the parrots to exit whenever they choose.
should simultaneously be reinforced. Commonly identi- Instead, parrots should be taught to politely step onto a
fied perimeters frequently include nest boxes, feeding perch or the hand prior to exiting the cage. Feeding
stations, play gyms, dark places, cage interiors and cage such a parrot away from the cage makes the effort of get-
doorways. The territory outside of these locations can be ting the parrot out of its cage easier.
made more enriching than the protected areas. For
example, the parrot that balks at leaving its cage can be Parrots that have a very small living area (cage) may have
shown, before the cage exit is requested, that the reward increased territorial instincts. Setting up a number of
it will get contingent upon removal from the cage is other play areas can decrease territorial instinct back to
greater than that of solitude. a more normal level.
Case Study: Fear-Based Biting: Case Study: Biting as a Learned Defense

Normally sweet and unaggressive, Lily, a 9-month-old An extremely polite and unflappable 3-year-old male
African grey (Psittacus erithacus erithacus) hen African grey had always been very sweet and easy to
abruptly started biting when her owner’s friends handle, so this author (LW) was quite startled when
tried to handle her. She became especially aggressive the owner recently complained that the grey had been
with her person’s new boyfriend, striking quickly biting her.
and biting hard.
When questioned regarding the circumstances, the
Lily was biting from fear-based aggression. owner revealed that the bird was biting only when
Frightened by non-flock members, she needed to be she was trying to pet him. Upon further questioning,
better socialized. If not identified and handled prop- the owner admitted that on each occasion, the bird
erly, a shy parrot like Lily can blossom into a deter- had pushed her hand away several times before it
mined fear biter. Lily’s person needed to reassure would bite. This was a clear example of biting as a
her that she was safe when interacting with others. learned defense. The bird obviously had tried to
communicate to the owner that it did not wish to be
Introducing her to other people in neutral territory petted, but the owner did not understand. When the
with patience and sensitivity, the owner taught Lily frustrated bird finally resorted to biting, the woman
that new people are fun and interesting. Initially, she ceased her attempts to fondle it.
expected Lily only to step onto the outsider’s hand
politely, and then step right back onto her trusted In this manner, the owner was very clearly sending
caretaker’s hand. Lily’s good manners were then lav- the message that nothing short of violence would
ishly rewarded with smiles and praise. Each time Lily get her to stop forcing herself on the bird. It was
did this successfully, she discovered that positive explained to the owner that the parrot had politely
things happened when she was compliant with new refused her attentions and that request should be
people. As a result, Lily learned to enjoy interactions honored. The domesticated dog is the only animal
with non-flock members. that is always in the mood to be petted, and a parrot
is not, after all, a dog with feathers.
SHOULDERING
Case Study: Territorial Aggression
A potentially dangerous but extremely popular practice
Clients complained that their 14-year-old male is allowing parrots onto people’s shoulders. A popular
yellow-naped Amazon (Amazona ochrocephala tradition over centuries of parrot ownership, this prac-
auropalliata) was lunging and biting at family mem- tice probably did not become especially dangerous until
bers as they walked by his cage. the advent of captive-bred parrots.
The location of cages and playgyms can strongly
It has long been understood by raptor specialists that
influence parrot behaviors. In this situation, ques-
there is a substantial difference between raptors that
tioning revealed that the Amazon’s cage was in the
have been captured and tamed and those that are
middle of a high-traffic intersection, on the same wall
domestically raised and socialized to humans. Birds of
with doors. The consultant explained that while
prey that have been socialized to humans have no funda-
these social creatures like being in the middle of the
mental fear of people and they can become extremely
action, they can get overstimulated by constant traffic
dangerous when in nesting season, aggressively attack-
flowing by their cages, as well as being startled
ing people who encroach on their territory (M.J. Stretch,
repeatedly by the abrupt appearance of humans.
personal communications, 2000). Imprinted hawks may
Owners need to remember that parrots are prey ani-
need to be tethered during nesting season to prevent
mals that often react aggressively when frightened.
them from attacking people. Due to their potential
This aggressive behavior was eliminated when the
aggression toward humans, these raptors cannot be
owners relocated the cage out of the middle of the
released into the wild. The similar reaction seems to
traffic flow over to a far wall where the Amazon
could see people coming. occur in captive-bred parrots. Allowing parrots on the
shoulder can be particularly hazardous.
Parrots are often not comfortable with strangers invad- Additionally, a psittacine on a human’s shoulder easily
ing their cage space. If interaction with a stranger is to can reach vulnerable parts of the owner’s anatomy (eyes,
be attempted, the parrot should be removed from the ears, noses, lips). Facial injuries can be severe and also
cage first and then introduced to the stranger. When the permanently damage the parrot-human bond. Parrots
protected territory is a person to which the bird is should not be allowed on a human’s shoulder. This is
strongly bonded, owners must be vigilant to prevent one of the few issues on which all experienced persons
injury to other persons, the bird or themselves (see involved in parrot behavior agree.4,10,19,20,40
Mate-bonding).
BEHAVIORAL MODIFICATION FOR
HEIGHT BITING
No true dominance has been documented in birds as Undesired behaviors often can be avoided by interpreta-
relates to their relative perching height. Ornithologist Jim tion of psittacine body language. Careful observation is
Murphy commented, “Height does have its advantages, the first step in this process. Once experienced in read-
and behaviors can and do change as a result of it. Height ing body language, people will find that it is easier to
alone confers a temporary advantage if there is the deter- anticipate and avoid a bite.
mination on the part of the involved individual parrot to
exercise that advantage.”34 Parrots that become incorrigi- A parrot most often resorts to biting when other poten-
ble when above eye level are already out of control, and tials for communication have been exhausted. It then
this becomes more obvious with the increased altitude.46 continues to bite because it has been reinforced for
doing so. For example, a parrot often will respond to
In some situations, a temporary easement of problems unwanted human attention by raising its foot to fend off
can result simply from raising the people. For example, the hand, or by pushing the hand away with their beak.
a footstool placed next to a high play gym can enable Humans will get bitten if they ignore these warnings.
shorter people to more easily reach and therefore have
better control over a parrot.20 Whether being at an Owners reaching for a parrot while they are on the
increased height changes a parrot’s perception of its sta- phone may trigger a biting reaction. Psittacines often
tus or decreases its perceived vulnerability is still under behave as if they dislike telephones. From the bird’s per-
debate. Regardless of the psychology behind it, most spective, the ringing telephone elicits an immediate
parrot species that are incompletely trained are more response. The owner holds the phone to their ear and
compliant on the floor than when perched on top of a interacts with it verbally. It is not surprising that parrots
tall cage. act so negatively to this apparatus.
81
An owner can often prevent a bite by making direct eye items, the definition of phobic would seem to apply.
contact and putting a hand or finger up as a counter-
point of attention, while quietly but firmly saying some- There are few situations as frustrating as dealing with
thing like, “Be good” or “Settle down.” Seldom will a the phobic or neurotic parrot. The classic signalment is
parrot break eye contact in order to bite. Other methods a high-strung young parrot that suddenly begins reacting
of prevention include giving the parrot something on to humans as if they are deadly predators. This is espe-
which to place its beak while stepping it onto the hand, cially upsetting when the formerly beloved owner is an
or approaching from behind instead of offering the hand object of their terror. The parrot may flail around its
from the front. cage, screaming and trying to escape when the owner
approaches. A “phobic” parrot is not simply afraid of
When a parrot attempts to bite while sitting on a hand new toys or new people, it also overreacts to noise,
or arm, there are two techniques that can be effective. movement, and even direct eye-contact from humans.
Athan’s “Wobble Correction” entails a tiny rotation of the These parrots often break multiple blood feathers, and
arm or hand.5 Davis’ “Little Earthquake” involves per- cause extensive soft tissue damage to their keel and
forming a slight drop of the hand or arm.10 If used con- wing tips.12
sistently, parrots soon make the connection between bit-
ing and losing their balance. Ordinarily, aggressive parrots are not phobic (J. Doss,
personal communications, 1997-1998). There has been
Laddering can be can effective deterrent to biting. This is discussion concerning whether these are two different
the exercise described previously in “Training” in this responses to the same stimulus. If so, insecure parrots
section. The technique is the same, but the handler’s that perceive themselves as threatened can become
facial expression and tone of voice is quiet and firm and either phobic or aggressive, depending on individual
the handler is frowning. When the parrot follows the personality type (P. Linden, L. Dicker, personal commu-
command, the owners tone turns positive, and the bird nications, 1997). Some species are particularly prone to
is then placed on a perch. Laddering works well with phobic behaviors, including small cockatoos like the
many cases of aggression when firmly implemented. rose-breasted (Eolophus roseicapillus), citron-crested
(Cacatua sulphurea citrinocristata) and triton (C. s. tri-
Some owners are not aware that parrots normally use
ton); small Poicephalus (Meyers [P. meyeri] and Senegal
their beaks as hands rather than weapons. Afraid of
parrots [P. senegalus]); African greys (especially the
being bitten, these people often pull away when a bird
Congo [Psittacus erithacus erithacus]); and eclectus
reaches for them with their beaks. Repetition of this
parrots (Eclectus roratus). These same species also are
exchange will teach young parrots that if they wish to
predisposed to feather-destructive behaviors.
climb onto a hand they must grab it quickly. At some
point the bird may grab the human hand with enough The etiologies of phobic behavior are unknown. A par-
force to cause pain. If this is rewarded with vocalization
ticular incident may precipitate phobic behavior, but the
by the person (such as “OW, BAD BIRD, NO BITE!”), the
actual underlying causes may be species-specific tenden-
bird has received positive reinforcement. Instead of ver-
cies and developmental problems (see Relative
bal reinforcement, a stern look and a quiet, firm, “No”
without withdrawing the hand is most effective. Once
Case Studies: The Non-Phobic Phobic
reprimanded, the parrot can be given a toy with which
to play, offering it a healthy outlet for exploration with Care must be taken to accurately diagnose phobics,
its beak. since they are handled so differently from the more
common problem behaviors seen in companion par-
rots. One author (LW) worked with a “phobic”
yellow-naped Amazon (Amazona ochrocephala
Neurotic Fears or Phobias auropalliata) that turned out to have an idiopathic
medical problem that predisposed the parrot to
According to human psychology, a phobia is defined as
falling from the hand because it could not grip prop-
“any unfounded or unreasonable dread or fear.”2 It is
erly with its feet. Multiple falls taught the parrot a
not unfounded or unreasonable for a prey animal such
direct correlation between handling and pain. The
as a parrot to be afraid of a predator such as a human,
result was a dramatic fear response when people
and this reaction would be expected in wild psittacines.
approached. Interestingly enough, the Amazon’s
However, most pet psittacines are acclimated to the
screaming and flailing was eliminated by the use of
human captive environment. When there is no precipi-
the dopamine antagonist, haloperidolc (D.
tating incident and the parrot is suddenly terrified of
Kupersmith, personal communications, 1997-1998).
people, noises, shadows, or comparable non-threatening
Table 3.3.2 | Sodium Contents in Foods

Food Sodium Food Sodium
Case Study: Feather Destruction
Serving (mg) Serving (mg)
A 3-year-old male African grey (Psittacus erithacus
Fruits/Vegetables Peanuts
erithacus) was boarded with this author (LW), and
Peppers (sweet) (1 cup) 3 Dry-roasted (unsalted) 0
Banana (one) 1 Oil-roasted (unsalted) 0
on presentation the bird had removed all its contour
Apples (one) 0 Roasted-in-shell (unsalted) 0 feathers on its chest, leaving only down.
Pineapples (fresh) (1 cup) 2 Sunflower seeds
The impetus for this behavior became obvious when
Raisins (1 cup) 17 Unsalted 0
Pumpkin (1 cup) 2 Popcorn (movie theater style)
the bird yanked out feathers whenever its wishes
Oranges (one) 0 Light (1 cup) 97 were frustrated. When the grey apparently realized
Cantaloupe (1/8) 6 Crackers that no one would acquiesce to its desires, the moti-
Strawberry (1 cup) 2 Crackers w/cheese 101 vation for the plucking was removed and the behav-
Bananas (one) 1 Whole wheat 105 ior ceased. The bird went home 3 weeks later with a
Papaya (1 cup) 4 Saltines® (4) 156 dramatic increase in contour feathers on its chest,
Grapes (European) (10) 3 Saltines® low salt (4) 75 and the owners were delighted. However, they
Watermelon (1 cup) 3 Chips - Bread
renewed their behavior of complying with the bird’s
Green beans (1 cup) 4 Chips (1 oz) 216
wishes whenever it touched a feather, so the bird
Romaine (1 cup) 4 Whole grain bread (1 slice) 127
promptly reduced its feather coat to only down again.
Olives (5) 192 Butter - Cheese
Yams (fresh no skin) (1 cup) 2 Butter (1 Tbsp) 117
The owners opted to do a consult at this point, and
Yams (canned heavy syrup) (1 cup) 76 Cheddar (1 oz) 176
learned how to avoid reinforcing the bird and the
Brussel sprouts (frozen) (1 cup) 36 American (processed) (1 oz) 405
behavior ceased once again. There were periodic
Cabbage (1 cup) 13 Mozzarella (whole milk) (1 oz) 150
Beet greens (1 cup) 347 Meat
episodes of plucking over the next few years (such as
Corn (cob) (1 cup) 8 Beef fresh (3 oz) 56 when the owners purchased a Great Dane puppy),
Corn (canned) (1 cup) 571 Beef (dried) (1 oz) 984 but when the owners did not reward the feather
Celery (1 cup) 104 Turkey (breast white) (3 oz) 54 destruction with attention, it ceased after a short
Carrots (1 cup) 39 Chicken (breast white) (1/2) 64 period. At this time, the bird is fully feathered.
Broccoli (fresh) (1 cup) 24 Bacon (3 slices) 303
Spinach (1 cup) 24 It is felt that success in a feather picker is that it does
Coconuts (1 cup) 24 not escalate, may cease, or does not mutilate. It has
Potatoes (french fries) (10) 15 been noted in many cases that during times of stress,
Mixed vegetables (frozen) 64 which varies from case to case (a storm, a new pet,
Mixed vegetables (canned) 243 new people, a new home or changes in the home)
Beans (canned) 700-
1000
the bird will revert at least temporarily to picking
* Products with 3 mg of sodium or more per serving should be avoided in
(G.J. Harrison, personal communication, 2003).
feather picking birds. Restrict foods to recommended yellow fruits and Guaranteeing a cure is seldom fulfilled.
vegetables (G.J. Harrison, personal communication, 2003).
Attachment Disorder in Section II of this chapter). tively good results in with several African greys using a
Potential exacerbating events may include physical or combination of diazepam and fluoxetine, or diazepam
psychological trauma such as aggressive capture and and amitriptyline. Conversely, haloperidol has worked in
restraint techniques.42 Ethologists agree that aggressive a number of Cacatua species, but the same dose caused
handling or “punishment” is not the only reason that excessive agitation in a male black-headed caique
parrots become phobic (A. Luescher, J. Oliva-Purdy, L. (Pionites melanocephalus), an eclectus (Eclectus
Seibert, personal communications, 2003). Often there is roratus) female and one eleanora cockatoo (Cacatua
no discernible history of abuse. eleanori) (see Chapter 9, Therapeutic Agents).
Rehabilitation of a phobic parrot can be a painfully slow

and difficult process. Misinterpretation and mishandling
of phobic behavior may increase the severity of the prob- Feather Destruction and
lem.44 Various psychotropic drugs may be used in con-
junction with behavioral modification to aid in the treat-
Self-mutilation
ment of phobic parrots. Many of these drugs are also Feather destructive behavior is a condition seen only in,
used for parrots with feather destructive behavior. and therefore caused in some manner by, captivity.17
Species specificities seem to exist but much of this infor- Species predilections exist, with African greys and cocka-
mation is still anecdotal. One author (TLL) has had rela- toos being over represented. Psychological as well as
83
physical etiologies contribute to feather-destructive

behavior.27
Feather-destructive behavior is a clinical sign, not a dis-

ease entity. Nutritional causes, including malnutrition
and food, pesticide, dye or preservative sensitivities, and
excess salt or sodium may be causative (Table 3.3.2).
Environmental factors including low humidity, inappro-
priate light cycles, and noxious aerosols, are all possible
potentiating factors. Primary dermatologic disease as well
as metabolic disease and parasitism may be causative.
The reader is referred to the appropriate chapters in this
and other references for more information. Fig 3.3.9 | Cataract in an older yellow-naped Amazon.
Cataracts may cause behavioral changes related to
The observation that “the best kept parrots often decreased vision.
develop feather-destructive behavior” is applicable, and
frustrated owners find comfort in this adage. With all
their food, attention and security needs met, some par- Gradual development of cataracts allows compensation
rots will redirect their energies. Normal preening then by the bird as long as its environment remains static.
becomes prolonged and exaggerated and may lead to Sudden onset of cataracts may cause behavioral abnor-
feather mutilation. Psychotropic medications seldom are malities that mimic aggression, lethargy, or even seizures
a complete answer but may be used as an aid during (Fig 3.3.9). Thousands of imported parrots that should
environmental and behavioral modification. be growing old in captivity have died of malnutrition
and husbandry related disease. Documentation of the
Additionally, owners often unconsciously reward parrots physical and behavioral changes of our current psitta-
for feather destruction. Psittacines may recognize the cine pets as they age will improve our understanding of
potential for feather picking or destruction to obtain their medical and emotional needs. Hopefully, we will
internal stimulation or external reinforcement. The first have an increasing captive geriatric parrot population
step in behavioral modification is to ignore this behavior.41 from which to learn.
The Geriatric Parrot Conclusion

Despite the USA having imported hundreds of thousands Psittacine birds have been sharing the human habitat for
of parrots in the 1970s and 1980s, there is little informa- hundreds of years. However, these are still not domestic
tion to be found on geriatric parrots. Additionally, the creatures. It will take additional research and application
physical and emotional health of these older import par- of existing knowledge to integrate parrots into the
rots may not equate to that of captive-bred psittacines that human environment. A growing number of owners, par-
will be reaching geriatric status in the coming decades. ticularly of cockatoos, are “donating” these parrots to
shelters and rescue organizations due to excessive
A study of the large macaws at Parrot Jungle (Miami, FL)
screaming, plucking or biting behavior.33 Other birds are
found their “functional breeding life-span” to be about
condemned to life in a cage due to the owner’s fear or
30 years, and their survival life-span was about 45 years.
inability to handle them. Early education of owners may
Physical signs in older macaws included increased scali-
prevent incompatible behaviors that lead to abandon-
ness of feet, thickening of the skin of the feet, thinning
ment or neglect.
of the facial skin, appearance of warts, cataracts and
other ocular color changes. It was noted the yellow iris
Products Mentioned in the Text
thinned so the dark retina could show through, produc- a. Chorionic gonadotropin, hCG, American Pharmaceuticals Inc., Los
ing a dark ring within the iris. Macaws over the age of 35 Angeles, CA, USA
b. GnRH agonist Depo-Lupron (Lupron Depot, leuprolide acetate), TAP
showed postural changes due to arthritis and degenera- Pharmaceuticals, Inc., Lake Forest, IL, USA
c. Haldol, Henry Schein, Melville, NY, USA
tive neurological disease. Causes of death in these older d. Prozac, Eli Lilly, Indianapolis, IN
birds included tumors, renal failure and other degenera-
tive diseases.16
References and Companion Parrot Handbook. Landsdowne Press, 1993, pp 423. 36. Shade R: Bronze-winged pionus
Oakland, CA, Abbey Press, 1999, 25. Friedman, S: Lecture 1, Intro- research project. Original Flying
Suggested Reading p 69. duction to behavior. Online Machine 2(42):42-45, 2000.
1. Abramson J: Captive breeding. In 14. Blanchard S: Maintaining flock course: Living and Learning with 37. Shindlinger M: Lecture: Tracking
Abramson J, Speer BL, Thomsen acceptance. Companion Parrot Parrots. www.ParrotTalk.com, Jan- the wild Amazons. D Grindol’s
JB: The Large Macaws. Fort Handbook. Oakland, CA, Abbey Feb 2003. Pet Bird Seminar, San Jose, CA,
Bragg, CA, Raintree Publications, Press, 1999, p 177. 26. Hallander J: Contact calls: The March 1999.
1995, p 150. 15. Burger J: The Parrot Who Owns communication link with our par- 38. Speer B: The clinical conse-
2. American Psychiatric Association: Me. New York, Random House rots. Pet Bird Report 42:62-65, quences of routine grooming pro-
The Diagnostic and Statistical Inc, 2001, pp 134-135. 1999. cedures. Proc Assoc Avian Vet,
Manual of Mental Disorders 4th 16. Clubb S: Geriatrics in macaws. 27. Jenkins J: Feather picking and 2001, pp 109-115.
ed. Washington, DC, APA, 1994, p Ann Conf Amer Fed Avicult, self-mutilation in psittacine birds. 39. Williams J: Steve Martin, trainer.
443. Baltimore, MD, 1998. Vet. Clini No Am: Exotic Ani Practi Bird Talk 3(25):25-28, 1985.
3. Ardrey R: The Territorial 17. Cooper JE, Harrison GJ: 4(3):656, 2001. 40. Wilson L: Behavior problems in
Imperative. New York, Kodansha Dermatology. In Ritchie BW, 28. Jenkins T: Lecture: Pet Bird adolescent parrots. Proc Assoc
America Inc, 1966. Harrison GJ, Harrison LR (eds): Information Council Conf, Avian Vet, Conf AAV, 1995, pp
4. Athan MS: The importance of Avian Medicine: Principles And Minneapolis, MN, May 2002. 415-418.
being “tall.” Guide To A Well- Application. Lake Worth, FL, 29. Lightfoot T: Captive-raised 41. Wilson L: Feather destruction: A
Behaved Parrot. Hauppauge, NY, Wingers Publishing Inc, 1994, pp psittacine birds and species differ- non-medical approach to the
Barrons, 1993, pp 64-66. 607-633. ences in the animal hospital envi- behavioral feather plucker. Proc
5. Athan MS: Beyond biting. In 18. Cravens EB: Early sexuality in ronment, Proc Assoc Avian Vet, Assoc Avian Vet, 1996, pp 3-9.
Guide To Companion Parrot captive psittacines. Birdkeeping 2002. pp 25-31. 42. Wilson L: Phobic psittacines: An
Behavior. New York, Barrons, Naturally. The Perch: Newsletter 30. Linden P: Bird Behavior Q&A. increasing phenomenon? Proc
1999, p 157. of the Peninsula Caged Bird Original Flying Machine 2:18-20, Assoc Avian Vet, 1998, pp 125-
6. Athan MS: Guide to Companion Society, Yorktown, VA, 12/2002. 2000. 131.
Parrot Behavior. Hauppauge, NY, 19. Davis C: New techniques in pet 31. May D: Lecture: Where the wild 43. Wilson L: What to do about biting
Barrons Pub, 1999, p 6. avian behavior modification. Proc greys are. Camelot, Atlanta, 2001. and screaming. Proc Assoc Avian
7. Bauck L: Growing pains. Bird 1989, pp 183-189. 32. Meehan C, Millan JR, Mench J: Vet, 1999, pp 71-76.
Times Magazine 8(1):10-11, 2000. 20. Davis C: Caged bird behavior, Foraging opportunity and 44. Wilson L: Behavior problems in
8. Bebe A: Seminar on dog and cat taming, and psychology with increased physical complexity pet parrots. In Olsen G, Orosz S
behavior, Harcum College, Bryn common behavioral problems both prevent and reduce psy- (eds): Manual of Avian Medicine.
Mawr, PA, 1997. and solutions. In Rosskopf W, chogenic feather picking by Philadelphia, Mosby, 2000, pp
9. Blanchard S: Games parrots play. Woerpel R (eds): Diseases of Cage young amazon parrots. Applied 124-147.
Bird Talk Magazine 9:48-54, 1991. and Aviary Birds 3rd ed. Anim Behav Sci 80(1):71-85, 45. Wilson L: The one-person bird:
10. Blanchard S: Problems with par- Philadelphia, Williams and 2003. Prevention and rehabilitation.
rots on shoulders. Pet Bird Wilkins, 1996, pp 19-29. 33. Murad JW: The sad reality: The Proc Assoc Avian Vet, 2000, pp 69-
Report 25(5):5, 1995. 21. Davis C: Today the sofa, tomor- need for avian humane facilities. 73.
11. Blanchard S: Sexual behavior in row the world! Bird Talk Proc Assoc Avian Vet, 2001, pp 46. Wilson L: Height dominance
companion parrots: Myths and Magazine 14(6):44-47, 1996. 429-436. revisited. Original Flying Machine
realities. Pet Bird Report 32:50- 22. Davis C: Spring is in the air. Bird 34. Murphy J: The above eye-height 5:11, 2001.
54, 1997. Talk Magazine 19(4):80-83, 2001. position. Amazona Quarterly 47. Zantop, D: Anafranil for prolaps-
12. Blanchard S. Phobic behavior in 23. Diamond J, Bond A: Kea: Bird of 13(1):9, 1997. ing cloacas. Exotic DVM
companion parrots. Proc Ann Paradox. Los Angeles, University 35. Parrot Education and Adoption 5(5):2003.
Conf Int Avicult Soc, Orlando, FL, of California Press, 1999. Center “Ask The Experts” round-
March 1998. 24. Forshaw J: Parrots of the World. table discussion. San Diego CA,
13. Blanchard S: Cage etiquette. Melbourne, Australia, November, 2002.
04_Nutrition I.qxd 8/22/2005 1:44 PM Page 85
CHAPTER
4
Nutritional
Considerations
Section I: Nutrition and Dietary Supplementation
Section II: Nutritional Disorders
Nutritional Considerations
Section I
Nutrition and Dietary Supplementation
DEBRA M cDONALD, P hD, BS c (HONS I)
Selection or formulation of appropriate diets for com- WATER REQUIREMENTS OF

panion and aviary birds is based on wild feeding ecol- PSITTACINE NEONATES
ogy, digestive anatomy and physiology, and nutritional The ratio of feed to water to maximize survivability in
requirements of related species. Research indicates that the growing chick is dependent on age; insufficient
requirements of some key nutrients for psittacines vary water within the first few days after hatch leads to high
from those of poultry. Apart from vitamin E, there is no mortality, and insufficient solids result in slow growth
evidence to suggest that vitamin and trace mineral rates.31 Studies of cockatiels indicate changes in the pro-
requirements for psittacines are greater than those rec- portions of solids to water from 7:93 for the first 4 days
ommended for poultry.54 While there are substantial dif- after hatch, increasing to 30:70 thereafter.65
ferences between production species and companion
bird species, dietary requirements of poultry remain the
NUTRITIONAL SUPPLEMENTATION
standard for estimating the needs of companion birds.
OF DRINKING WATER
Individual nutrient classes will be discussed with partic-
Supplementation of vitamins and minerals via the drink-
ular focus on recent research into the nutritional
ing water is not recommended. Water intake can vary
requirements of companion birds. See Nutritional
inter- and intraspecifically and is influenced by environ-
Disorders, Section II of this chapter for aspects of mal-
mental temperatures and diet. The high redox potentials
nutrition and nutritional diseases commonly diagnosed
of minerals, such as zinc, iron and copper, can destroy
in companion birds.
vitamins, and some vitamins are light-sensitive. It is
impossible to standardize intake of vitamins via drinking
water. Vitamin A and D toxicoses have been reported in
Water macaws and conures being supplemented with liquid
vitamins.7,67,78 Dehydration may result if the additives
Calculated water intake of adult Australian parrots does decrease water intake due to unpleasant taste or unfa-
not correlate with observed water intake (Table 4.1.1).37 miliar coloration.
Desert-adapted birds require less water intake than trop-
ical birds. Changes in diet or environmental tempera-
tures can alter water intake.
Energy
Table 4.1.1 | Water Intake Per Day of Various Birds When calculating energetic requirements of birds, the
Species Body Calculated Water Actual Water following equations are used:
Weight (g) Intake (ml) Intake (ml)
Budgerigar86 30-35 0.7-0.8 4 Passerine BMR
Canary85 18-24 0.4-0.6 4 kcal/day = 114.8 x kg0.726
Lovebird86 55 1.3 10 kJ/day = 480 x kg0.73
Cockatiel 86
100 2.4 13.6
Non-passerine BMR
Cockatoo86 300-900 7-22 15
kcal/day = 73.5 x kg0.734
Amazon/Grey86 350-600 8-14 17-35 kJ/day = kg0.73
Chapter 4 | N U T R I T I O N A L C O N S I D E R A T I O N S : S E C T I O N I
87
Basal metabolic rate (BMR) is calculated from energy tract (GIT) transit time than soluble fibers. Fiber also
expended when a bird is sleeping. Perching can increase increases excretion of bile acids and fat.
energy expenditure in budgies 2-fold; preening, eating
and shuffling locomotion cause 2.3-fold increase and ENERGETIC COSTS OF MOLT
flight increases as much as 11 to 20 times over BMR.10
Feather replacement requires energy and specific nutri-
Energy requirements of free-living birds are greater than
ents, as well as metabolic and physiological adapta-
those of their captive counterparts due to the increased
tions.24 Energy costs of the molt include the caloric con-
energy required for thermoregulation, food procure-
tent of the new feathers and feather sheath, the energy
ment and territorial defense. However, the daily needs
required in their synthesis, and the energy required to
for amino acids, minerals and vitamins are relatively con-
produce and maintain feather pulps. Approximately 3 to
stant regardless of energy expenditure.
10% of total body mass (20 to 30% total lean body mass)
Climate can influence BMR. Psittacines from temperate of passerines is replaced during a complete molt.24 Daily
climates have BMRs approximately 20% higher than energy expenditure of passerines undergoing a rapid
those of tropical species, with seasonal changes in ther- complete molt can increase from 3% (early and late in
moregulation varying from 3.07 times BMR in winter the molt) to 20% (at peak molt),52 with BMR doubling in
(5.9° C) to only 2.77 times BMR in summer (20.7° C).10 some passerines at peak molt.34 Increases in energy
expenditure due to rapid molt can be partly offset by
reductions in other activities such as locomotion or
ENERGY REQUIREMENTS singing.28,34
Daily consumption of calories must exceed daily energy
expenditure for a sustained period in order for over- Feathers grow throughout the day and night at similar
weight or obese body conditions to develop. A diet for rates,50 but the feather material deposited at night when
weight loss should be replete in all nutrients so that pro- most birds are fasting is of a slightly different quality.
tein, essential fatty acids, vitamins and minerals are pres- Feather synthesis at night requires complex and costly
ent in amounts sufficient to support normal physiologi- modifications to the metabolism of amino acids, com-
cal processes and to retain lean body tissue. Reducing pared to daytime synthesis, so the overall costs of molt
fat content of the diet too quickly or too far has led to may be lower in areas with relatively longer day length.51
obsessive eating behaviors in obese double yellow-
headed Amazons.22 Formulated calorie reduction diets
generally contain lower levels of fat with simultaneous
increase in indigestible fiber, air or moisture. Increased
Carbohydrates
levels of dietary fiber slow gastric emptying. Insoluble Carbohydrates (Fig 4.1.1) are used to produce energy in
fibers have a greater effect on slowing gastrointestinal the form of adenosine triphosphate (ATP) from glycolysis
Crude Fiber
Total Dietary Indigestible

Non-Fiber
Fiber Fiber
Insoluble Moderately Moderately Enzymatically Not Digested

Soluble Fiber Absorbed
Fiber Fermentable Fermentable Digested or Fermented
Rapidly Slowly Resistant Starch Mono- and

Pectin Lignin
Fermentable Fermentable Starch (polysacharides)
Disaccharides
Fructans, Galac-
tans, Mannans, Cellulose Hemicellulose
Mucilages
Pectin Hemicellulose
Fig 4.1.1 | Classification of carbohydrates.

species that lack the sucrase enzyme. Avoid feeding

Table 4.1.2 | In the Absence of Adequate Dietary
these birds fruits high in disaccharides such as mango,
Carbohydrate, Glucogenic Amino Acids are used to
Manufacture Carbohydrates apricot, nectarine and peach.
• Alanine • Glutamine • Serine
• Arginine • Glycine • Threonine POLYSACCHARIDES
• Asparagine • Histidine • Tryptophan
• Aspartic Acid • Methionine • Tyrosine While simple sugars such as the monosaccharides and
• Cysteine • Phenylalanine • Valine disaccharides are readily absorbed, the α-bonds of
• Glutamic Acid • Proline starches require further digestion. Heat from extrusion
processes gelatinizes the starch molecule, increasing its
digestibility. The ß-bonds of some of the complex carbo-
and the TCA (tricarboxylic acid) cycle, and produce heat
hydrates, such as those comprising the fibrous fraction
from the oxidation of glucose to CO2 and H2O. They are
of foods, require microbial degradation that may not be
also used to produce precursors of other nutrients, syn- sufficient in psittacines and passerines. Cellulose is com-
thesize glycogen or fat from glucose, decrease luminal posed of ß-bonds and is generally unavailable as a
pH through production of short-chain fatty acids, and source of energy, while hemicellulose consists of varying
increase the population of anaerobic flora. The proportions of α- and ß-bonds, depending on the
antibacterial properties of short-chain fatty acids may source. Hemicellulose is therefore partially digestible
decrease pathogenic intestinal bacteria and may be without microbial breakdown, but its close association
important in prevention of, and recovery from, intestinal with the polyphenolic lignin often makes it indigestible.
disorders. The carbohydrate content of psyllium fiber consists pre-
dominantly of hemicelluloses, so is partially digestible.
The central nervous system and erythrocytes require glu-
cose for energy, in contrast to muscles that can utilize
Fermentation of Polysaccharides
substrates such as fatty acids. In the absence of adequate
Postgastric microbial fermentation of polysaccharides
dietary carbohydrates, amino acids (glucogenic amino
occurs in nectarivorous, frugivorous and florivorous
acids via the gluconeogenic pathway) are shunted away
species. The process of enzymatic digestion taking place
from growth and production to be used for glucose syn-
prior to fermentation benefits species that feed on easily
thesis (Table 4.1.2).
digested foods such as nectar and fruit, as fermentation
of nutrient-rich foods is not energetically efficient. In
SUCRASE AND FRUIT SUGARS contrast, pregastric fermentation occurs in the hoatzin,
Sucrose, one of the predominant disaccharides of fruit which feeds on mature leaves, stems and branches.18
sugars (Figs 4.1.2, 4.1.3), is easily digestible. However, Such bulk foods are generally incompatible with flight.
some insectivorous passerines, such as thrushes that
feed on diets high in protein/fat and low in carbohy- Chitin
drate, lack the sucrase enzyme necessary for the diges- Chitin is a naturally occurring polysaccharide similar in
tion of these simple sugars. The differences in propor- structure to cellulose with an additional amino group. It
tions of fruit mono- and disaccharides are important for is the principal polysaccharide of cell walls of fungi and
* *
Fig 4.1.2 | Sugar content of fruits commonly fed to birds.

*Require sucrase for digestion
Fig 4.1.3 | Sugar content of stone fruits and berries.
*Require sucrase for digestion
89
Table 4.1.3 | Chitin physiological state, being highest in hatchlings and

Content of Various females laying large clutches, and lowest in adults at
Invertebrates and Fungi
maintenance. In granivorous birds protein requirement
Food Item Chitin Content
is correlated with body size,29 with larger species such as
Fungi 5-20%
Worms 20-38%
macaws possibly requiring more protein than smaller
Squid 3-20% birds. Preliminary studies with African grey parrots
Scorpion 30% (Psittacus erithacus erithacus) indicate a protein
Spider 38% requirement of 10 to 15% (dry matter).27 Protein require-
Cockroach 35% ment for the adult budgerigar is 6.8% (balanced protein
Crab 70% diet).14 Sunflower seeds, safflower seeds and peanuts are
deficient in the amino acids required by poultry.54
the primary constituent of the exoskeletons of crus-
taceans and invertebrates (Table 4.1.3). The digestion of High fiber diets can increase fecal nitrogen content due
chitin is considered low, but it still presents a useful to bacterial digestion, which can confound the results of
energy source for some species. While chitinase activity a protein digestion study.63 Nectarivorous and frugivo-
has been identified in starlings, raptors and a variety of rous species have lower obligatory protein losses.
seabirds, it is low in chickens and absent in African grey Rainbow lorikeets (Trichoglossus haematodus) may
parrots and pigeons. Measurements of crude protein require as little as 2.9% protein when fed high-quality,
may overestimate protein availability for birds that lack readily digested protein.16
chitinase enzymes.
While high dietary protein has been implicated in renal
dysfunction and gout in psittacines, studies of male
cockatiels (Nymphicus hollandicus) indicate that protein
Protein levels of 20, 30 or even 70% do not result in renal insuf-
ficiency.32 However, 70% dietary protein is not recom-
Proteins are composed of the nitrogen-containing mole-
mended, as excessively high protein is strongly corre-
cules, amino acids. They can be manufactured from
dietary precursors (non-essential) or are required as lated with a significant increase in liver lesions.32 Excess
dietary constituents (essential). Amino acids that are protein has been associated with overgrowth of beaks
deemed to be essential for birds include arginine, and nails.35 Introduction of birds to new diets with vary-
isoleucine, leucine, lysine, methionine, phenylalanine, ing levels of protein should be undertaken gradually, as
valine, tryptophan and threonine. In addition, glycine is sudden changes in dietary protein levels may result in
known to be essential for budgerigars (Melopsittacus nephritis and gout.32 Since birds are uricotelic, an over-
undulatus),79 and histidine and proline are essential for load of the excretory ability of the kidneys, caused by
chickens. It is presumed that the digestion of proteins by excessive intake of proteins or nucleic acids, may lead to
psittacines reflects that of poultry. Lorikeets digest only hyperuricemia. Dehydration exacerbates this problem
13.3% of complete protein (egg white).16 Digestion of and may produce visceral and articular gout even with-
proteins is more efficient in nestlings than in adult birds. out excessive dietary protein.35
MEASUREMENT OF PROTEIN PROTEIN REQUIREMENTS FOR

CONTENT OF FOODS REPRODUCTION
Protein values of food (crude protein) are measured using Protein requirements during egg production are influ-
the Kjeldahl technique with the assumption that all nitro- enced by clutch size/frequency and the protein composi-
gen in the food sample is present as protein and that all tion of eggs. There is little taxonomic variation in amino
proteins contain 16% nitrogen. Crude protein is calculated acid composition of avian eggs.39,49 Protein requirements
as follows: for species that lay only single eggs are similar to main-
CP (%) = g N/kg x 6.25 tenance requirements, but that may increase if essential
amino acids are lacking. Birds laying eggs require dietary
While this value is commonly used for converting nitro-
amino acids for maintenance, growth of the oviduct and
gen values to protein, it is not applicable to all foods,
accretion of egg proteins, at least a week prior to the
especially some seeds.
first oviposition.29,49 Budgerigars can maintain breeding
performance on 13.2% protein. However a diet of white
DIETARY REQUIREMENTS FOR millet, canary seed and hulled oats (13.4% protein) con-
PROTEIN AND AMINO ACIDS taining only half the necessary lysine, methionine and
The dietary requirement for protein varies with age and cysteine is not sufficient to support reproduction.1
PROTEIN REQUIREMENTS FOR the absorption of fat-soluble vitamins. In addition, they

CHICKS are precursors of many hormones and eicosanoids.
Protein requirements for growth are highest at hatch
and decrease over time as growth rate slows. Altricial CLASSIFICATION OF FATS
chicks have a higher fractional growth rate and may have Fats are described by the length of the carbon chain, the
higher total amino acid requirements. Protein require- number of double bonds and the exact position of the
ment for growth of cockatiels has been estimated at double bonds. Short-chain fats contain 2 to 4 carbons,
20%. In addition, the protein must include 0.8 to 1.5% medium-chain fats 6 to 10 and long-chain fats 12 to 24
lysine.64,65 Many birds in the wild supplement their diets carbons. Fatty acids with 4 to 12 carbons are found in
with insects, which will often provide additional protein; milks; those with 10 to 12 carbons are found in certain
however, some wild birds just increase their food intake. seed oils. Longer chain fatty acids are common in plants
While there is generally sufficient crude protein, lysine of marine origin.
and arginine in commercial hand-rearing mixes for
psittacines, most lack sufficient quantities of the sulphur
amino acids, methionine and cysteine, which leads to ESSENTIAL FATTY ACIDS
stunted feather growth.85 Saturated fatty acids (SFA) are those where all carbons of
the fat are satisfied with a single bond to another ele-
ment. If one double bond is introduced, they are
PROTEIN REQUIREMENTS FOR
monounsaturated fatty acids (MFA). Those with two or
FEATHERS
more double bonds are polyunsaturated fatty acids
Feathers comprise a large percentage of total body pro- (PUFA). The preferred nomenclature for fatty acids is
tein (22% lovebirds; 28% budgies) with approximately based on the position of the double bond from the
15% by mass contained in the sheath.50 However, the methyl end (Fig 4.1.4). For example, linoleic acid 18:2
amino acid composition of whole plumage differs from (n-6) contains 18 carbons with two double bonds,
that of the sheath and calamus. placed six carbons from the last double bond with refer-
ence to the terminal methyl end. Higher evolved animals
Dietary deficiencies in some of the sulphur amino acids
are unable to manufacture fatty acids of the n-3 or n-6
cause a pronounced curvature and periodic restriction of
families and must obtain these from dietary sources.
the rachis, abnormal persistence of the basal sheath, and
Fatty acid composition of seeds and nuts that are avail-
misshapen vanes.50 Feather strength is correlated with
able for companion birds may not resemble that of wild
adequate dietary lysine (0.203%).80 Cysteine is abundant
diets (see Fig 4.1.6).
in the epidermal structure and feather barbs.51 While cys-
teine is frequently cited as a potentially limiting nutrient PUFA profiles are not amenable to dietary manipulation.
in the growth of plumage, cysteine reserves may be suffi- Grains and seeds are generally rich in linoleic acid (n-6),
cient for keratin synthesis during overnight periods of grasses and leaves in α-linolenic acid 18:3 (n-3) and
fasting and short-term sulphur amino acid deficiencies. docosahexaenoic acid (n-3) (DHA). Fish and other
Dietary deficiencies of methionine result in dark, hori- aquatic insects are rich in 20:5 (n-3) or 22:6 (n-3).
zontal “stress lines” on feathers,38 while threefold
excesses are correlated with soft, weak feathers.80
Tyrosine is an important factor in melanogenesis, and a
FATTY ACIDS AND EICOSANOIDS
deficiency in phenylalanine also impairs melanogenesis.83 Certain membrane fatty acids have specific roles in the
regulation of cell functions. Arachidonic acid (AA), γ-
Production of sheaths during molt can increase protein linolenic acid and eicosapentaenoic acid (EPA) act as
requirements 4 to 8% per day above maintenance precursors for the synthesis of eicosanoids, an important
requirements.51 The additional energy required for ther- group of immunoregulatory molecules that function as
moregulation may increase food intake to provide suffi- local hormones and mediators of inflammation. Changes
cient protein for feather growth without increasing the in characteristics of fatty acids available to cells modify
proportion of protein in the diet. A number of products the fatty acid composition of the membrane phospho-
on the market promoted as supplements during periods lipids of those cells and may influence inflammatory
of molt are deficient in the required amino acids.87 processes (Fig 4.1.5).
Cis and Trans Fatty Acids

Lipids While most natural fatty acids occur in the cis form (car-
bons on same side), processing such as extensive heat or
Lipids supply energy, essential fatty acids and facilitate partial hydrogenation can convert fats to the trans form
91
Fig 4.1.4 | Structure of n-6 fatty acid.
Fig 4.1.5 | Production of eicosanoids from essential fatty acids.
(carbons on opposite sides), which affects their biologi- ored carotenoids such as ß-carotene.
cal activity. Although both cis and trans forms are metab-
olized for energy, trans isomers cannot function as Antioxidants help to counter the detrimental effects of
essential fatty acids. oxygen-free radicals. Oxygen-free radicals have been
implicated in the development of cancer, inflammatory
Antioxidants and Lipid Peroxidation conditions and heart disease. A deficiency of antioxidants
may promote peroxidation of membrane phospholipids.
Insufficient antioxidants such as vitamin E in the feed
also may enhance lipid peroxidation during storage.48
Diets high in PUFA require additional antioxidant protec- OBESITY
tion to prevent rancidity. There are a number of natu- Obesity can lead to congestive heart failure or hepatic
rally occurring substances in food that have antioxidant lipidosis and may predispose a bird to diabetes mellitus
properties including vitamins A, C, E, and yellow-col- or exacerbate this illness. Body weight relative to a bird’s
Table 4.1.5 | Fatty Acid Composition of Seeds of Wild Food

Plants of the Orange-bellied Parrot (Neophema chrysogaster)44
Linoleic α-linolenic AA EPA DHA
Acid Acid C20: C20: C22:
C18:2n-6 C18:3n-3 4n-6 5n-3 6n-3
Introduced Mainland
Atriplex prostrata 0.04 0.13 0.27 0 0.30
Cakile maritima 0.06 23.8 0 0 1.23
Chenopodium glaucum 0.06 5.28 0.14 0.02 0.06
Indigenous Mainland
Halosarcia pergranulata 0 1.6 0 0 0
Samolus repens 0 1.53 0 0 0
Sarcocornia quinqueflora 0 2.0 0 0 0
Suaeda australis 0.23 2.39 0 0 0.04
Indigenous Tasmania
Baumea tetragona 0 4.48 0 0 0
Fig 4.1.6 | Fat composition of nuts commonly fed to birds.
Gahnia grandis 0 0.37 0 0 0
Restio complanatus 0 3.55 0 0 0
Table 4.1.4 | Lipid Content of Egg Yolk
Commercial 0 1.42 0 0 0.08
of Various Birds
Species Chicken Gull Pigeon
Mode Precocial Semi-precocial Altricial
Triacylglycerol 71.4% 35.1% 58%
Phospholipid 20.7% 24.6% 30.7%
Cholesterol Ester 0.8% 1.1% 5%
Free Cholesterol 5.6% 5.9% 4.7%
optimal weight has been used as a defining criterion for diets are almost devoid of α-linolenic acid, while those
obesity because body weight is easier to measure than of the goose, pheasant and ostrich on similar diets have
body fat. Body weight in excess of optimal body weight high levels of this fatty acid, providing sufficient precur-
of 1 to 9% is acceptable, 10 to 19% is considered over- sors for conversion to DHA.
weight and greater than 20% is defined as obese.
SPERMATOZOA LIPIDS
DEPOSITION OF FATS IN EGG YOLK The high PUFA content of avian semen predisposes them
The yolks of precocial and altricial birds vary in lipid to lipid peroxidation. Susceptibility is increased in mem-
composition (Table 4.1.4). However, determination of branes high in DHA, which is present in duck spermato-
specific fatty acid dietary requirements has been under- zoa and can be exacerbated by low vitamin E. However,
taken only on granivorus species. In contrast to fatty similarities in lipid peroxidation of chicken and ducks
acid profiles of commercial grains, fatty acid composi- suggest the presence of high levels of antioxidant
tion of wild seeds on which the orange-bellied parrot enzymes. Age-related decreases in sperm output are
(Neophema chrysogaster) feeds is characterized by a dis- reduced with supplementation of 200 mg/kg vitamin E.
tinct lack of n-6 fatty acids (Table 4.1.5).44 Supplementation with longer chain essential fatty acids
is also beneficial.
BRAIN LIPIDS
There is a surge of brain growth in the second half of
the embryonic/early neonatal stage, with specific uptake
Vitamins and
of docosahexaenoic acid (DHA) by embryonic brain tis- Supplementation
sue. The selective depletion of yolk phospholipid DHA
results in a range of cognitive, behavioral and visual
Requirement
impairments. The high proportions of amino acids in
brain tissues imply a requirement for adequate levels of WATER-SOLUBLE VITAMINS
both n-3 and n-6 fatty acids in yolk lipids. While the Water-soluble vitamins include the B complex and vita-
avian embryo may be able to synthesize DHA from α- min C. As dietary requirements for B vitamins have not
linolenic acid, this ability may be species-specific. Yolk been evaluated for companion birds, further discussion
lipids of the domestic chicken maintained on formulated will be confined to disease entities that specifically impli-
93
cate imbalances in the B vitamins (see Section II FAT-SOLUBLE VITAMINS

Nutritional Disorders).
It is important to maintain an appropriate balance with
the fat-soluble vitamins as they all compete for sites of
Vitamin C uptake. Dietary excess of one vitamin can diminish
Vitamin C (ascorbic acid) is involved in the syntheses of uptake and availability of another, despite adequate
collagen, carnitine and catecholamine; in tyrosine, hista- dietary intake.
mine, steroid, fatty acid and drug metabolism; and in
the prevention of peroxidation. Birds under stress, Vitamin A
including the stresses associated with high temperatures,
Vitamin A is involved in vision, reproduction, immunity,
growth and reproduction may have increased require-
membrane integrity, growth, embryogenesis and the
ments for vitamin C.
maintenance of epithelial cells. Vitamin A is of animal
Sources of Vitamin C origin and does not occur in plant tissues. Some
carotenoids can be converted to vitamin A in the intes-
Most birds synthesize vitamin C in the kidney, liver or
both. Evolutionarily, enzymatic activity occurs in the kid- tinal wall via a specific enzyme.
neys of birds in older orders and becomes localized in
Forms of Vitamin A
the liver of more advanced Passeriformes. Some passer-
ines such as the vented bulbul (Pycnotus sp.) are unable The most active form (retinol) is susceptible to mois-
to synthesize vitamin C. Vitamin C is concentrated in ture, heat and light. The retinal aldehydes are incorpo-
fresh fruits, green leafy vegetables and animal organs, rated in rhodopsin and influence dim light vision.
with only small amounts in skeletal muscle. Retinoic acid supports growth and tissue differentiation
but not vision. Although retinoic acid appears to play a
Vitamin C Deficiency role in testosterone synthesis, it does not support the
Reproduction and growth increase the demand for colla- production of sperm.
gen. Supplementation of 100-200 mg/kg vitamin C
Dietary Requirement
improves growth, egg production and eggshell strength
of young chicks and hens exposed to high environmen- Vitamin A requirements vary among production species
tal temperatures.68 Dietary requirements also may vary (Table 4.1.6). Dietary requirements of cockatiels
with age, as willow ptarmigan (Lagopus lagopus) adults (Nymphicus hollandicus) at maintenance are 2000-4,000
are able to synthesize sufficient vitamin C, whereas IU/kg.30 Levels below 10,000 IU/ kg do not significantly
chicks require supplementation with 750 mg/kg.21 influence plasma levels in cockatiels.30 Dietary deficiencies
Berries that form part of the diet of the willow ptarmi- of vitamin A may not impact immunocompetence for up
gan during the breeding season can contain up to 5000 to eighteen months in birds previously maintained on suf-
mg/kg vitamin C.21 ficient dietary Vitamin A. Dietary vitamin A can be ade-
quately provided from 2.4 mg/kg ß-carotene in cockatiels.
Vitamin C is susceptible to destruction with handling Recessive white canaries (Serinus canaria) are unable to
and processing. While it is stable when exposed to boil- convert ß-carotene to vitamin A and require three times as
ing water for short periods, a greater proportion is much vitamin A as colored canaries.88
destroyed when heated at low temperatures for long
periods. Any form of processing that ruptures tissue Sources of Vitamin A
(such as freezing and thawing) exposes vitamin C to air The vitamin A content of animals varies. Vitamin A levels
losses due to oxidation, but vitamin C is generally stain invertebrates are extremely low (Table 4.1.7).4 Fish
ble during normal pelleting processes. store large amounts of vitamin A in the liver and fatty tis-
sue. Supplementation with cod liver oil is not recom-
Vitamin C Toxicity mended. Seeds and nuts are generally low in
Metabolites of L-ascorbic acid such as oxalic acid can carotenoids (Table 4.1.8), while some fruits can provide
bind calcium. Excesses of vitamin C also can bind cop- large quantities (Table 4.1.9).
per, resulting in growth deficiencies and increases in the
incidence of aortic rupture and decreases in elastin con- The vitamin A content of many formulated products,
tent of the aorta if diets are also deficient in copper. It is most parrot foods and nectar-replacement products (Fig
important to minimize dietary vitamin C content for 4.1.7, Table 4.1.10) exceed dietary recommendations for
species that are susceptible to iron storage disease, as poultry54 and cockatiels.30 While the vitamin A content of
vitamin C improves the absorption of iron by facilitating some products is higher than data reported by manufac-
the reduction of the ferric form to the more absorbable turers, poor packaging may result in breakdown of the
ferrous state. vitamin.41
Table 4.1.6 | Vitamin A Requirements of

Birds, Expressed as IU/kg of Feed Dry Matter
Growing Laying
Chicken54 1,670 4,440
Vitamin A IU/kg
Turkey54 5,550 5,550
Quail, Coturnix54 1,830 3,670
Duck, Pekin54 2,780 4,440
Goose54 1,670 4,440
Cockatiel (Maintenance)32 2,000
Table 4.1.7 | Fat-soluble Vitamin Content of Fig 4.1.7 | Vitamin A content of various commercial parrot foods.
Various Invertebrates Commonly Fed to Birds
Invertebrate Vitamin A Vitamin E Table 4.1.10 | Vitamin A Content of Various Commercial
(IU/kg) (mg/kg) Nectar Products41
Mealworm, larvae 811 30 Product name Vitamin A Vitamin E
Cricket, adult3 811 80 (IU/kg) (mg/kg)
Cricket, juvenile3 471 70 Aristopet* 5,994 6
Earthworm, wild-caught4 2400 70 Aves Nectar† 24,150 22
Earthworm, commercial4 328 230 Avione* 4,296 20
Fruit Fly4 0 23 Elliots Dry* 666 2.8
Waxworm4 150 500 Elliots Wild nectar* 666 1.3
HBD Adult Lifetime Fine (Maintenance)‡ 1,400 215
HBD High Potency Fine (Breeding)‡ 1,500 240
Lory Life Nectar§ 52,900 54
Table 4.1.8 | Table 4.1.9 | Carotenoid Lory LifePowder§ 10,130 11
Carotenoid Content of Content of Fruits41 Marion Lory¶ 8,500 250
Nuts/Seeds Nut/Seed Carotenoid Nekta Plus§ 12,470 12
Nut/Seed Carotenoid (RE/g)
Nekton Lori† 60,550 34
(RE/g) Apple 3.3
Nekton Lori and Gelb† 244,820 136
Flax 0 Banana 3.15
Noah’s Kingdom§ 330 25
Safflower 0.53 Cantaloupe 315.0
Passwells* 9,990 29
Sesame 0.09 Grape 3.76
Quicko Nectar§ 400 5
Sunflower 0.53 Honeydew 3.87
Rainbow Landing Lorikeet Nectar§ 22,467 45
Almond 0 Kiwi Fruit 10.32
Roudybush 15% Protein§ 19,500 33
Brazil 0 Mango 212.9
Roudybush 9% Protein§ 18,860 81
Hazel 0.71 Raspberry 9.68
Sheps Lori dry* 167 1.7
Macadamia 0 Strawberry 3.2
Sheps Wet*II 12,500 (333) 25 (1.8)
Peanut 0 Watermelon 43.11
Wombaroo Nectar†¶ 26,640 (28,740) 89 (27)
Walnut 1.29 Data reprinted with permis- 41
41 Data reprinted with permission from Elsevier Science
sion from Elsevier Science
*Independent laboratory analyses, §
Laboratory analyses (Graffam,
Australia 2002 1999)
†
Author’s laboratory analyses, 1999 ¶
Manufacturer’s data, 1999
‡
Independent laboratory analyses, II
Manufacturer’s data, 2002
USA 2002
Measuring Vitamin A The equivalencies are as follows:

Approximately 90% of total-body vitamin A is contained 0.6 µg ß-carotene is equivalent to 1 IU provitamin A
in the liver.46 Storage levels of 2-5 IU vitamin A/g liver are activity
deemed to be adequate.46 Plasma retinol does not 1 RE = 1 µg retinol = 6 µg ß-carotene or 12 µg of
change dramatically with marginal vitamin A status, and other provitamin A carotenoids
reduced levels are generally not detected until animals 1 RE = 3.33 IU retinol = 1.818 IU vit. A palmitate =
reach a severe deficiency. It is not adequate to evaluate 10 IU ß-carotene
vitamin A status from blood samples. Liver biopsies are
recommended. Data that is reported as µg/dl retinol can be converted to
SI units (µmol/L) as follows:
Interpreting Laboratory Data µg/dl x 0.0349 = µmol/L
Units are reported in international units (IU) for Approximately 10% of the more than 500 carotenoids have
vitamin A or retinol equivalents (RE) for provitamin A. provitamin A activity.
95
Signs of Vitamin A Deficiency Vitamin A Toxicity

Clinical signs of vitamin A deficiency often resemble In the wild, noncarnivorous birds are rarely exposed to
those of toxicity, and distinguishing between the two dietary excess of vitamin A. These birds probably
requires careful evaluation of dietary intake and other depend on the conversion of carotenoids to biologically
influencing factors. While turkey chicks exhibit signs of active vitamin A. Toxicities are avoided because the effi-
deficiency after only five weeks2 , cockatiels can be main- ciency of conversion of vitamin A from ß-carotene
tained on a diet devoid of vitamin A for up to two years decreases with higher levels of intake. Conversion effi-
before demonstrating clinical signs.30 Signs of vitamin A ciency in the chicken drops from a ratio of 2:1 to 5:1.46
deficiency can generally be classified into five categories: Studies of Japanese quail also indicate a saturation of
the retinol-transporting system, as birds supplemented
Vision with ß-carotene do not develop increased levels of
Retinol is utilized as the prosthetic group in iodopsin retinyl palmitate.60 Cockatiels at maintenance are more
(cones). Vitamin A deficiency results in a loss of opsin, the susceptible to vitamin A toxicity than deficiency.30
protein that converts vitamin A to rhodopsin, from the Perhaps ß-carotene would be a superior source of vita-
outer segments of the rods, leading to their eventual min A in some psittacine diets; however, ß-carotene
degeneration. Even in the late stages of vitamin A defi- may not be appropriate for hand-rearing mixes because
ciency, it is possible to regenerate rods, but cones eventu- chicks may not efficiently convert ß-carotene to vitamin
ally disintegrate and result in blindness. Vitamin A defi- A. Toxicities have been reported in cockatiels main-
ciency also results in decreased secretions of tear glands.40 tained at 10,000 IU/kg of vitamin A. Many commercial
diets exceed this level.30 Some hand-rearing diets have
Bone
levels in excess of 47,000 IU/kg.85 In lorikeets, commer-
A deficiency results in reduced activity of osteoclasts,
cial diets high in vitamin A and deficient in vitamin E
leading to excessive deposition of periosteal bone by the
are correlated with high rates of infertility, decreased
unchecked function of osteoblasts.
hatching and survivability of chicks.42 The author
Maintenance of Epithelial Tissue hypothesizes similar levels may contribute to the
Dietary deficiencies of vitamin A can alter the permeabil- increased incidence of iron storage disease in these
ity of lipoprotein membranes of cells and intracellular birds. Vitamin A toxicity causes epithelial damage and
particles. Low levels of liver vitamin A are correlated with keratinization of squamous cells.33 Epithelial damage
symptoms of focal metaplasia of the excretory duct as results from penetration of retinol into the lipid portion
well as the glandular epithelium of salivary glands. Loss of the membrane, causing it to expand. Weakening of
of membrane integrity also interferes with water reten- the membrane results from the inelastic protein portion
tion, and renal uric acid deposits can result. Coccidiosis of the membrane resisting expansion and increases
can lead to the destruction of vitamin A in the gut and access to pathogens and infection. Clinical signs of
injure microvilli of the intestinal wall, decreasing the Vitamin A toxicity include:
absorption of vitamin A.69 Vitamin A deficiency in chicks is
Vocalization Patterns
characterized by poor feathering on the head, neck and
breast regions, as well as facial dermatitis. Cockatiels maintained on excess dietary vitamin A
exhibit frequent stress calls of greater intensity and dura-
Reproduction tion.30 Vitamin A toxicities may contribute to behavioral
Defects in reproduction, including increased time problems in companion birds. Vocalization changes
between clutches, reduced hatchability, increased embry- were observed in psittacines maintained on diets that
onic mortality, decreased survival time of progeny, contained recommended levels of vitamin A.47,75
decreased testes size, failure of spermatogenesis and a
decline in sexual activity in males, are correlated with Iron Storage Disease
deficiencies of vitamin A. These may be associated with See Section II Nutritional Disorders for the potential
failure to maintain healthy epithelium.17 contribution of excess vitamin A to iron storage disease.
Splenic hemosiderosis has been correlated with excess
Immune Function vitamin A in cockatiels.30
Both deficiency and excess of dietary vitamin A suppress
immune function. Vitamin A deficiency in chicks leads to Pancreatitis
a rapid loss of lymphocytes. Diarrhea, pneumonia and Pancreatitis was diagnosed in cockatiels fed excessively
blunted immune response are characteristic of vitamin A high levels of vitamin A.33 Hypervitaminosis A increases
deficiency in cockatiels.33 Deficiencies lead to phagocytic the activity of sucrase and eliminates the duodenum’s
activity in macrophages and neutrophils, and impair ability to regulate this enzyme in the small intestine71
intestinal IgA response.33 which may lead to diabetes and digestive difficulties.
Table 4.1.11 | Ultraviolet Light Table 4.1.12 | Vitamin D and Calcium Content of Various
Type of light Distance UVA UVB* Commercial Foods*
(ft) (microwatts/cm2) (microwatts/cm2) Vitamin D3 Calcium
Product Manufacturer
Reptisun 5.0 1 23 10 (IU/kg) (%)
Vitalite 1 6 1.6 Avipels Blue Seal 4170 1.11
Blacklight 1 153 2.6 Bird of Paradise Zeigler 3970 1.34
Active UV Heat Bird of Prey (frozen) Animal Spectrum 3470 1.05
100 watt flood 1 400 50 Chick Starter Blue Seal 4000 1.19
100 watt flood 2 110 12.5 Crane Mazuri 10830 2.62
160 watt flood 1 640 85 Exotic Game Bird Mazuri 2500 0.89
160 watt flood 1.5 480 55 Flamingo Mazuri 6670 1.72
160 watt flood 2 320 25 HPC HBD International 150 0.69
160 watt flood 3 142 11 Nutribird Parrot Nutribird 1200 0.9
275 watt flood 2 720 66 Palm Cockatoo SSP 1900 1.1
275 watt flood 2.5 520 48 Psittacine Breeder Roudybush 1560 1.0
275 watt flood 3 320 30 Psittacine Handfeeder Roudybush 1560 1.0
275 watt flood 4 180 20 Psittacine Maintenance Roudybush 890 0.44
100 watt spot 2.5 1130 70 Scenic Bird Marion 1600 1.2
100 watt spot 3 562 40 Poultry NRC 200 0.99
100 watt spot 4 400 30 Turkey NRC 900 0.5
160 watt spot 3 1500 137 *From manufacturer’s published data 1999-2002.
160 watt spot 4 1200 100
Location Time Direct/ UVB
Shade (microwatts/cm3) dihydroxyvitamin D3 in the kidneys. Cholecalciferol can
Natural Sunlight be produced in the skin of most mammals from provita-
Equator noon direct sunlight 265 min 7-dehydrocholesterol via activation with ultraviolet
Germany noon direct sunlight 175 light in as little as 11-15 minutes daily. Vitamin D
Yucatan noon direct sunlight 250 enhances intestinal absorption and mobilization of cal-
Illinois noon direct sunlight 260 cium and phosphorus through the hormone 1,25-dihy-
Illinois 7:00 am direct sunlight 12 droxyvitamin D3. Circulating levels of 25-hydroxyvitamin
Illinois 7:00 pm direct sunlight 17
D3 are indicative of vitamin D status. One IU of vitamin
Illinois 1:00 pm shade 54
D activity is equivalent to the activity of 0.025 µg vitamin
Illinois 5:00 pm shade 22
*UVB is the biologically active ultraviolet light
D3. As vitamin D2 has only 1/10 the activity of vitamin D3
in chicks the International Chick Unit (ICU) is used with
Reproduction reference to vitamin D3 in poultry. Plasma half-lives vary
with the form of the vitamin ranging from 5 to 7 days
Excesses of vitamin A may interfere with uptake of vita-
(vitamin D) to 20 to 30 days (25-(OH)D3) (see Chapter
min E, compromising fertility, hatchability and survivabil-
5, Calcium Metabolism). In mammals and reptiles, acti-
ity of chicks.
vation depends on UVB radiation (290-320 nm) (Table
Antioxidant Status 4.1.11).
Vitamin A supplementation of laying hens increases liver,
Dietary Requirement
egg yolk and embryonic liver concentrations at the
The dietary requirement for vitamin D in poultry is 200
expense of vitamin E, compromising the antioxidant sta-
IU/kg. While higher dietary requirements are evident for
tus of progeny. High levels of vitamin A reduce uptake of
the turkey (900 IU/kg) and Japanese quail (1200 IU/kg),
astaxanthin, a powerful carotenoid antioxidant that pro-
optimum levels for companion birds have yet to be estab-
tects mitochondria from damage by Fe+2 catalysed lipid
lished. It has been suggested that dietary levels for poultry
peroxidation.
are adequate for breeding African grey parrots76 (Table
4.1.12), but many formulated foods exceed these levels.
Vitamin D
Vitamin D is a group of closely related compounds that Vitamin D Deficiency
possess antirachitic activity. They are obtained directly Vitamin D synthesis can be affected by liver malfunction;
from the diet or from irradiation of the body. The two intestinal disorders can reduce absorption of the vitamin
major natural sources (provitamins) are cholecalciferol and kidney failure can prevent synthesis of 1,25-(OH)2D3.
(D3 in animals) and ergocalciferol (D2, predominantly in Inadequate exposure to UVB radiation prevents produc-
plants). Both D2 and D3 forms also can be ingested and tion of vitamin D in the skin. Glass windows block the
further metabolized to 25-hydroxyvitamin D3 through penetration of UVB rays. The first signs of vitamin D defi-
hydroxylation first by the liver, and then again to 1,25- ciency include decreased egg production, thinning or
97
absence of eggshells, and an increased incidence of Table 4.1.13 | Vitamin K Table 4.1.14 | Influence of Heat
embryonic death. Inadequate maternal transfer of vitamin Content of Fruit on a Dry Treatment on Vitamin K Content
Matter Basis on a Dry Matter Basis
D3 and 25-(OH)D3 results in the failure of development of
Vitamin K Vitamin K Vitamin K
the upper mandible and failure to pip. Fruit
(mg/100 g) Vegetables (mg/100 g) (mg/100 g)
raw cooked
Apple peel, green 60.0
Vitamin D Toxicity Broccoli 205 270
Apple peel, red 20.0
Carrot 5 18
Vitamin D toxicity may arise from an excess of dietary vita- Apples, no skin 0.4
Cauliflower 5 10
min D or a deficiency in the other fat-soluble vitamins. Avocado, raw 40.0
Coriander leaf 310 1510
Toxicity leads to widespread calcification of soft tissue. Banana, raw 0.5
Mint leaf 230 860
Toxic levels can be transferred maternally to the embryo, Grapefruit, raw 0.02
Parsley 540 900
leading to abnormalities in chick development. Safe Grapes, raw 3.0
Kiwifruit, raw 25.0 Table 4.1.15 | Conversion of
upper limits in chicks less than 60 days old are 40,000 Carotenoids to Vitamin A
Melon, raw 1.0
IU/kg and 2800 IU/kg in birds older than 60 days.69 Relative Rat-biopotency46
Orange, raw 0.1
Carotenoid Biopotency
Peach, raw 3.0
Vitamin E Pineapple, raw 0.1
α-carotene 25
β-carotene 100
Vitamin E consists of tocopherols and tocotrienols in Plum 12.0
γ-carotene 14
four isomeric forms, α, ß, δ, and γ. α-tocopherol has the
Cryptoxanthine 29
highest vitamin E activity followed by ß, δ and γ, respec-
tively. Dietary requirements of vitamin E are dynamic,
with increased requirements with diets high in PUFA, oxi- bird foods. Choline can impact the activity of water-solu-
dizing agents, vitamin A, carotenoids, trace minerals and ble K3, destroying up to 80% within 3 months. γ-irradia-
decreased requirements in diets high in other fat-soluble tion of foods to increase storage life also inactivates vita-
antioxidants, sulphur-containing amino acids and sele- min K, while heat treatment can increase its bioavailability
nium. Vitamin E is one of the least toxic vitamins, how- (Table 4.1.14).
ever, high doses decrease absorption of vitamins A, D
It has been suggested that mortality from cerebral hem-
and K, resulting in reduced hepatic and egg yolk storage
orrhage in some species of fig parrots (Opopsitta spp.)
of vitamin A,77 impaired bone mineralization20 and coagu-
is the result of dietary deficiency of vitamin K.11 If fig par-
lopathies.53 Studies of pelicans indicate that 500-10,500
rots have developed a dependency on vitamin K2 pro-
IU vitamin E/kg result in decreased growth and coagu-
duced by the gut microbes of termites, they may be
lopathy.53 Japanese quail under heat stress (34° C) require
unable to process sufficient vitamin K1 from plant
250 mg/kg vitamin E and 0.2 mg/kg Se.66 Various
sources. Daily supplementation of 300 µg vitamin K1 per
researchers have recommended up to 60 mg α-toco-
pherol per gram of PUFA. Many formulated foods have fig parrot appears to alleviate clinical signs.11
less than 200 mg/kg of vitamin E. Vitamin E status can be
evaluated from single blood samples, but the magnitude
of body stores may not be reflected in α-tocopherol con-
centrations.45,81 High dietary concentrations of vitamin E
Nutritional Influence on
elevate vitamin E levels in the blood. Deficiencies affect Feather Pigmentation
the neuromuscular, vascular and reproductive systems.
The dietary pigments utilized by passerines for their col-
oration are referred to as carotenoids. Psittacines do not
Vitamin K
use carotenoids for feather pigmentation. Each
Vitamin K plays a major role in blood clotting factors and carotenoid produces a specific color. Carotenoids are
is involved in the synthesis of osteocalcin, with deficien- subdivided into carotenes and xanthophylls (Table
cies resulting in increased bleeding times and toxicities 4.1.15). Carotenoids may be used directly in the
resulting in kidney tubule degeneration. Vitamin K is plumage or modified to other forms prior to incorpora-
available as phylloquinone (K1) from plants, menaqui- tion into the feathers or skin (Fig 4.1.8, Tables 4.1.16-
none (K2) from bacteria and menadione (K3) which is syn- 4.1.18). Each carotenoid appears to have its own individ-
thetic. Vitamin K1 is present as the fat-soluble portion of ual pattern of absorption, plasma transport and metabo-
plant chlorophyll (Table 4.1.13). An energy-dependent lism. There are considerable species differences in the
process absorbs vitamin K1 from the intestine, whereas types of carotenoids that are preferentially absorbed and
vitamins K2 and K3 are passively absorbed. Estrogens stim- metabolized. Many carotenoids act as potent antioxi-
ulate the absorption of vitamin K1. Vitamin K3 has twice dants and stimulate the immune system.
the potency of natural vitamin K1 on a weight-to-weight
basis. Vitamin K3 is the most common form in commercial The yellow pigmentation of the helmeted honeyeater
β-carotene β-cryptoxanthin
Echinenone
3-hydroxy-echinenone
Canthaxanthin
Picofulvins
Adonirubin
Astaxanthin
Adonixanthin
Canary Xanthophyll B Papilioerythrinone
Canary Xanthophyll A α-doradexanthin
3-dehydrolutein
Zeaxanthin Lutein
Rodoxanthin
Rubixanthin 4-oxo-rubixanthin
Fig 4.1.8 | Metabolic pathways for various dietary carotenoids. Rodoxanthin and picofulvins are deposited directly from the food into
the feathers and are not metabolically transformed.
99
Table 4.1.16 | Metabolic Pathways of Various Carotenoids Responsible for Pink-col-

ored Feathers of Passerines
Species Common Feather Original Feather
Metabolism
Name Name Pigment Pigment Pigment
Aegithalos caudatus Long-tailed tit 3-hydroxy-echinenone oxid ß-crypto/ß-carot pink
Carduelis cannabina Common 3-hydroxy-echinenone oxid/hydrox ß-crypto/ß-carot carmine
redpoll red
4-oxo-rubixanthin oxid rubix
4-oxo-gazaniaxanthin oxid rubix
Carduelis flammea Linnet 3-hydroxy-echinenone oxid/hydrox ß-crypto/ß-carot carmine
red
Carpodacus roseus Pallas's 3-hydroxy-echinenone oxid/hydrox ß-crypto/ß-carot bright
rosefinch pink
Fringilla coelebs Chaffinches 3-hydroxy-echinenone oxid carots copper-
pink
4-oxo-rubixanthin
dehydrolutein
astaxanthin
Pyrrhula pyrrhula European α-doradexanthin oxid ß-carot pinkish-
bullfinch red
astaxanthin
adonirubin
Rhodospiza obsoleta Desert finch canthaxanthin oxid ß-carot pink
Oxid=oxidation, hydrox=hydroxylation, carots=carotenoids, ß-crypto=ß-cryptoxanthine,
ß-carot=ß-carotene, rubix=rubixanthin
Table 4.1.17 | Metabolic Pathways of Various Carotenoids Responsible

for Red-colored Feathers of Passerines
Metabolism
Bombycilla cedrorum American waxwing rodoxanthin direct rodox red
Carduelis carduelis Gold finch (face mask) canary xanthophylls B/C/D dehydrog lut/keratin red
Carduelis cucullata Red siskin α-doradexanthin oxid lut red
canthaxanthin red
Colaptes auratus Northern flicker astaxanthin oxid carots red
lutein/zeaxanthin direct lut/zea yellow
ß-cryptoxanthin direct ß-crypto yellow
Dendrocopos major Great spotted astaxanthin oxid lut/zea/carots red
woodpecker
α-doradexanthin
adonirubin
Hirundo rustica Swallow lutein direct lut red
zeaxanthin direct zea
3-hydroxy-echinenone oxid ß-crypto/ß-carot
Loxia curvisrostra Common crossbill (m) 3-hydroxy-echinenone oxid ß-crypto red
Loxia leucoptera White-winged 4-oxo-rubixanthin oxid rubix red
crossbill
4-oxo-gazaniaxanthin gazan
Luscinia calliope Siberian rubythroat astaxanthin oxid carots ruby red
α-doradexanthin
adonirubin
Pericrocotus flammeus Scarlet minivet (m) astaxanthin oxid carots red
α-doradexanthin
adonirubin
canthaxanthin
Picus viridis Green woodpecker α-doradexanthin oxid lut red
picofulvins lut/zea/ß-crypt green/yellow
Pinicola enucleator Pine grosbeaks (m) 3-hydroxy-echinenone oxid ß-crypt red
4-oxo-rubixanthin rubix
Pyrrhula erythaca Grey-headed bullfinch canary xanthophylls A/B dehydrog lut orange-red
Serinus pusillus Red-fronted serin canthaxanthin oxid ß-carot red
Trichodroma muraria Wallcreeper astaxanthin oxid zea red
Uragus sibiricus Long-tailed rosefinch 3-hydroxy-echinenone oxid ß-crypt/ß-carot red
Rodox=rodoxanthin, lut=lutein, zea=zeaxanthin, gazan=gazaniaxanthin
Table 4.1.18 | Metabolic Pathways of Various Carotenoids Responsible for Yellow-colored

Feathers of Passerines
Metabolism
Bombycilla garrulus Bohemian waxwing canary xanthophylls (tail) dehydrog lut/zea yellow
astaxanthin (wing patches) ß-caro
C. sinica/C. spinoides Asiatic finches canary xanthophylls direct lut yellow
Carduelis atrata Black siskin canary xanthophylls A/B dehydrog lut yellow
Carduelis carduelis Gold finch (wing bars) canary xanthophylls B/C/D dehydrog lut yellow
Carduelis chloris Greenfinch canary xanthophylls dehydrog lut yellow
Carduelis citrinella Citril finch canary xanthophylls A/B dehydrog lut yellow
Carduelis spinus Siskin finch canary xanthophylls A/B dehydrog lut yellow
Emberiza citrinella Yellowhammer lutein/zeaxanthin direct lut/zea yellow
E. melanocephala Black-headed bunting lutein/zeaxanthin direct lut/zea yellow
Fringilla coelebs Chaffinches (secondaries) lutein direct lut yellow tinge
Fringilla coelebs Chaffinches (rump) lutein direct lut
Leiothrix lutea Peking robin dehydrolutein dehydrog lut/zea yellow
α-doradexanthin oxid carots
astaxanthin oxid carots
Loxia curvisrostra Common crossbill (f) canary xanthophylls A/B dehydrog lut yellow
Motacilla flava Yellow wagtail lutein direct lut yellow
zeaxanthin zea
Oriolus oriolus Golden oriole lutein direct lut yellow
zeaxanthin direct zea yellow
oxo-carotenoids oxid lut/zea bright yellow
Parus ater Coal tit lutein direct lut yellow
zeaxanthin zea
Parus ceruleus Blue tit lutein direct lut yellow
zeaxanthin zea
Parus major Great tit lutein direct lut yellow
zeaxanthin zea
Pericrocotus flammeus Scarlet minivet (f) lutein/zeaxanthin direct lut/zea yellow
Pinicola enucleator Pine grosbeaks (f) lutein direct lut yellow
dehydrolutein dehydrog zea
Regulus regulus Goldcrest lutein direct lut yellow/green
zeaxanthin direct zea orange
Serinus mozambicus Yellow-fronted canary canary xanthophylls A/B dehydrog lut yellow
Serinus serinus Serin canary xanthophylls dehydrog lut yellow
(Lichenostomus melanops cassidix) (Fig 4.1.9) is from 1:1 to 2:1.61 Calcium availability can be influenced
replaced with near white pigmentation (Fig 4.1.10) when by solubility and particle size. Foods high in oxalic acid
maintained on commercial nectar mixes high in vitamin form insoluble calcium oxalates, while phytates bind
A. Feather structure and light refraction can influence phosphorus and decrease its availability. Additional
feather color. Carotenoids also can act synergistically oxalic acid can be produced from excesses of vitamin C.
with melanin pigments. Dark colors (black, brown, gray Fats can form insoluble calcium soaps.
and related tints) produced by melanin and porphyrin
pigments complexed with trace minerals are influenced The calcium content of nuts and seeds is variable (Fig
by amino acid nutrition. Stress can influence feather 4.1.11). Some green leafy vegetables and tubers that are
quality and color. high in calcium also are high in oxalic acid (Figs 4.1.12,
4.1.13), which decreases the calcium availability.
Invertebrates generally have poor Ca:P ratios (Table

Minerals 4.1.19). Crickets should be maintained on 80% poultry
mash and 20% calcium carbonate. Water should be pro-
CALCIUM AND PHOSPHORUS vided ad lib from produce (such as a slice of apple) or
Adequate dietary calcium can be negated by high phos- free water. If die-off of crickets occurs from constipation,
phorus content. The dietary ratio of Ca:P should range restrict gut loading to 48 hours prior to feeding. When
101
Fig 4.1.9 | Helemeted honeyeater, full pig- Fig 4.1.10 | Helemeted honeyeater, light pig-
mentation (in-house nectar mix). mentation (commercial nectar mixes).
% Dry Matter (as fed)
Fig 4.1.11 | Calcium and phosphorus content of nuts and seeds.
Fig 4.1.12 | Oxalic acid and calcium content of greens. Fig 4.1.13 | Oxalic acid and calcium content of tubers.
Table 4.1.19 | Calcium and Phosphorus Content of Invertebrates Table 4.1.20 | Calcium Content of Wild Food Resources of the
Calcium Phosphorus Orange-bellied Parrot44
Invertebrate Part Ca:P
(% DM) (% DM) Calcium Seed
Species Common Name
Bogong Moth Abdomen 0.64 (%) Weight (mg)
(Agrotis infusa) Mainland Indigenous
Wings 0.17
Whole 0.25 Halosarcia pergranulata Black-seed glasswort 0.1 0.3
Cricket Adult 0.21 0.78 0.27 Samolus repens Creeping brookweed 0.68 0.017
(Acheta domesticus) Sarcocornia quinqueflora Beaded glasswort 0.28 0.3
Pinhead 1.29 0.79 1.63
Fruit fly Pupae 0.77 2.73 0.28 Suaeda australis Austral seablite 0.08 0.4
(Drosophila melanogaster) Introduced Species
Larvae 0.59 2.3 0.26
Adult 0.1 1.05 0.10 Atriplex prostrata Hastate orache 0.08 1-3
Mealworm Larvae 0.11 0.77 0.14 Cakile maritima Beach rocket 0.16 7.4-9.6
(Tenebrio molitor) Chenopodium glaucum Goosefoot 0.07 0.4
Beetle 0.07 0.78 0.09
Pupae 0.08 0.83 0.10 Tasmanian Species
Baumea tetragona Square-twig rush 0.04 0.3
Gahnia grandis Brickmaker’s sedge 0.3 7.7
Restio complanatus Flat cord rush 0.2 0.5
antioxidants; the actions of vitamin E cannot be replaced

with selenium. Selenium toxicity decreases hatchability,
growth and reproductive success and results in deformed
embryos, diminished immune function, abnormal feather
loss, emaciation and liver lesions.23,74 Dietary selenium
affects whole blood levels.56 Mallards fed more than 10
mg/kg Se developed bilaterally symmetrical alopecia of
the scalp and dorsal cervical midline, broken nails and
necrosis of the tip of the beak.56 Chicks raised on diets
Fig 4.1.14 | Calcium and phophorus content of whole vertebrate
prey. depleted of both vitamin E and Se show signs of exuda-
tive diathesis on the superficial pectoral muscles.
Deficiencies of selenium are characterized by increases in
feeding whole vertebrate prey, it is not necessary to sup- heterophils and decreases in lymphocytes, basophils and
plement with calcium (Fig 4.1.14). hemoglobin. Selenium deficiency depresses plasma T3
concentrations.25 Dietary selenium up to 0.4 mg/kg
It has been suggested that optimum levels of calcium in appears to be adequate for large psittacines maintained
feed are between 0.3 to 0.7%.58 Many wild seeds provide on extruded diets with 200 mg/kg vitamin E.43
0.1 to 0.3% calcium (Table 4.1.20). Companies continue
to provide formulated feeds in excess of 0.7%. It is pos-
sible that the high calcium content of formulated foods
ZINC
contributes to the development of renal disease that is Zinc is involved in cell replication and in the develop-
observed in color mutation cockatiels. ment of cartilage and bone. Normal serum zinc concen-
trations reported for parrots range between 0.5 and 5.8
IRON ppm (7.65-84 µmol/L).82,45 However, plasma and serum
concentrations above 2 ppm (30 µmol/L) have been
Body iron is either hemal or non-hemal (Table 4.1.21).
considered diagnostic for zinc toxicity in most
Hemal iron forms part of the porphyrin group and com-
species.5,15,55,59,72,82 A lack of correlation between hepatic
prises 70 to 75% of total iron. Iron from animal sources
zinc levels and clinical diagnosis of zinc toxicity also has
is generally more available than that from plant sources.
been reported.12
Iron in soy isolates may be unavailable. Pectin, vitamins
A and C, and amino acids such as cysteine, histidine and
Zinc toxicosis usually arises from ingestion of zinc-
lysine enhance iron uptake. High levels of calcium
coated aviary wire or metallic foreign bodies.62 Clinical
and/or phosphate decrease iron absorption in chicks.
signs of zinc intoxication include anorexia, acute gas-
Cellulose and oxalate, as well as the heat and pressure
troenteritis, ataxia, lethargy, yellow-colored feces, vomit-
of food processing, increase the bioavailability of iron.
ing, extreme loss of plumage and hepatomegaly.72,85 It
(Tables 4.1.22-4.1.25).
can cause pancreatic cell necrosis.72 Excess dietary zinc
negatively impacts tissue concentrations of α-toco-
SELENIUM pherol.36 Zinc is more toxic in iron-deficient chicks than
Selenium (Se) and vitamin E function synergistically as in properly iron-supplemented birds.6,55 Liver biopsy is
103
Table 4.1.21 | Forms of Organic Iron Table 4.1.22 | Iron and Vitamin C Content of
Hemal Iron Non-hemal iron Native Australian Fruits
Hemaglobin Transferrin Iron Vitamin C
Fruits
mg/kg mg/kg
Myoglobin Ferritin
Lillypilly, Acmena smithii 15.15 303
Cytochromes Hemosiderin
Wild ginger, Alpinia caerulea 5.7 199
Cytochome oxidase Iron Proteinates
Davidson plum, Davidsonia pruriens 127.66 BDL
Catalase —
Quandong, Santalum acuminatum 108.61 BDL
Peroxidase —
Wild fig, Ficus platypoda 80.12 59.35
Native gooseberry, Physalis minima 265.82 63.29
Table 4.1.23 | Iron and Vitamin C Data reprinted with permission from Elsevier Science
41
Content of wild Australian Insects

(expressed as dry matter) Table 4.1.24 | Iron Content of Invertebrates
Iron Vitamin C Invertebrate Diet Iron mg/kg
Insect
mg/kg mg/kg
Mealworm wheat, grain, carrots 40
Honeypot ant, 35 15
Melophorus spp Mighty Mealy wheat, brain, supplements 26
Lerp scale, 78 100 Super Mealworm wheat, grain, carrots 50

Psylla eucalypti Cricket, adult cornmeal, wheat, soybean 110
Witchety grub, 102 127 hulls, meat meal
Cossidae spp molasses, fish meal
Bogong moth, 159 20 Cricket, juvenile shipped with raw potato 200
Argrotis infusa Wax Worm none 80
Green tree ant, 400 58 Fruit Fly commercial feed 450
Oecophylla smaragdina
Earth Worm, wild 11,100
Data reprinted with permission from Elsevier
41 Earth Worm, commercial peat humus soil 5,800
Science
Table 4.1.26 | Concentrations of Hepatic Zinc in Birds

Table 4.1.25 | Iron and Vitamin C Species
Zn (mg/kg) Zn (mg/kg)
Reference
Content of Fruits Commonly Fed to Physiological Status Intoxication
Birds Budgerigar 50.5 ± 12.7 153 7
(Melopsittacus undulatus) (37.6-70.5) n=10 250
Iron Vitamin C
Fruit Budgerigar (aviary bred) 64.7 ± 37 No clinical signs 12
mg/kg mg/kg
(Melopsittacus undulatus) (29-126) n=8 of toxicity
Apple, apricot,
banana, fig, — Low <1,000 Monk Parakeet 57.9 ± 34.5 179 ± 73.7 13
grape, raisin (Myiopsitta monachus) (28.1-156) n=14 (n=7)
Watermelon 20 1130 Lovebird 42.5 ± 8.9 75 62
(Agapornis roseicolli) (37.5-50.2) n=5 156
Canteloupe 21 4130
Macaws 38.9 ± 22 150 ± 37.0 13
Orange 9 4344 (Ara chloroptera, A. macao) (12.0-115) n=77 (n=3)
Papaya 9 5530 Rosellas and Lorikeets 74 ± 63 Wild-caught 12
Strawberry 45 6725 (27-166) n=4
Data reprinted with permission from Elsevier Galah 31.6 ± 5.4 Wild-caught 45
Science
41 (Eolophus roseicapilla) (24-45) n=16
Sulphur-crested Cockatoo 37.5 ± 7.8 Wild-caught 45
(Cacatua galerita) (25-59) n=21
Long-billed Corella 37.3 ± 9.8 Wild-caught 45
(Cacatua tenuirostris) (29-64) n=13
not definitive as a diagnostic tool (Table 4.1.26). Signs of (Table 4.1.27), while its digestibility is relatively low in
zinc deficiency include reduction in immune response, hummingbirds and lorikeets (4.5-6.6%).8 As the sugar
alterations to cell division, early embryonic death, fetal content of fruits increases, the volumetric intake and
abnormalities, weak chicks at hatching, retarded growth, passage rate decrease.84 The protein content of fig
alopecia, dermatitis, delayed sexual development, abnor- species is variable (4-25%).26
mal skeletal formation and feathering.
WHOLE PREY
Whole prey fed to birds in captivity can differ from that
Specific Diets available in the wild (Tables 4.1.28, 4.1.29; Figs 4.1.15,
4.1.16). and may require supplementation. Feeding
individual pieces of prey or eviscerated meat can con-
FRUIT AND POLLEN tribute to nutrient imbalances. Feeding high propor-
Nectarivorous birds feed on a variety of pollens, plants, tions of liver can result in hypervitaminosis A.
insects and their exudates.9,19,57,89 Pollen is high in protein Supplement meat-based diets with CaCO3, which has
Table 4.1.27 | Protein and Amino Acid Content of Pollen Sources in Australia73
Poultry Black
Pollen Onion Saffron
require- Eucalypts Banksias She-oak Hakea Wattles Almond /Spear Lavender
source weed thistle
ments thistle
Amino acids (% protein)
Threonine 3.77 3.66 4.06 3.67 4.26 3.97 4.58 3.25 4.17 3.27 4.05
(3.38-4.11) (3.81-4.3) (3.01-4.63) (4.47-4.7) (1.7-3.6)
Valine 3.47 4.94 4.92 4.07 4.78 4.70 5.21 4.33 4.54 11.08 5.69
(4.38-5.83) (4.7-5.4) (3.95-5.49) (4.83-5.4) (3.4-5.1
Methionine 1.68 2.14 2.24 2.44 2.04 2.58 1.77 1.78 2.21 1.30 2.55
(1.0-2.69) (2-2.273) (2.21-2.84) (0.7-2.57) (1.2-2.1)
Leucine 5.51 6.60 6.49 6.03 6.59 6.54 6.81 5.98 6.04 6.91 6.94
(5.97-7.63) (5.6-7.6) (5.35-7.28) (6.41-7.4) (4.6-6.4)
Isoleucine 3.35 3.97 3.89 3.34 3.93 3.89 4.3 3.98 3.59 4.56 5.03
(3.36-5.47) (3.5-4.5) (2.94-4.64) (4-4.7) (3.2-4.5)
Phenylalanine 2.99 3.94 4.43 3.29 3.81 3.76 3.57 3.55 4.11 3.38 4.18
(3.48-5.37 (3.71-5.4) (3.21-4.24) (2.3-4.9) (2.6-4.1)
Lysine 4.01 5.65 5.74 4.37 4.66 5.3 4.97 3.93 6.38 3.77 6.77
(5.17-6.34) (5.1-6.5) (4.66-6.19) (3.1-6.48) (1-6.8)
Histidine 1.44 2.31 2.58 1.73 2.4 2.05 1.95 2.7 3.67 1.64 4.43
(1.8-3.84) (2.37-2.98) (1.73-2.36) (1.82-2.1) (1.4-3.1)
Arginine 5.51 6.2 7.36 6.44 6.41 5.92 5.05 4.5 4.31 7.40 4.48
(4.13-7.18) (6.7-8.6) (4.66-7.2) (4.6-5.48) (3.7-6.5)
Crude 16.7 24.87 33.06 12.50 18.4 23.75 25.94 20.94 19.4 18.25 18.1
protein (%) (20.5-29.4) (31.2-36.9) (21.7-24.9) (23.3-30.7) (16.1-31.8)
Fat (%) 2.01 2.18 1.93 2.82 1.52 2.32 2.42 2.9 4.50 3.86
(0.48-3.9) (1.9-2.45) (0.9-2.52) (1.89-2.74) (2.25-2.59)
Note: Data in parentheses indicate ranges.
Table 4.1.28 | Mineral Content Table 4.1.29 | Fat-soluble Vitamin Table 4.1.30 | Calcium Content
of Whole Vertebrate Prey Content of Whole Prey of Various Supplements
Ca P Ca:P Mg Vitamin A Vitamin E Supplemental source Ca (%) P (%)
(IU/g) (mg/kg)
Mouse 3.0 1.7 1.7 0.16 Calcium borogluconate 8.32 0
Mouse (12weeks) 657 74
Rat 2.6 1.5 1.8 0.08 Calcium carbonate 40.04 0
Rat (adult) 335.3 152 (ground limestone,
Chicken 2.2 1.4 1.6 0.5
oyster shell, cuttlebone)
Chicken (6 weeks) 35.59 61
Frog 4.3 1.9 2.3 2.47
Frog, green 25.11 82.2 Calcium gluconate 9.31 0
Calcium glucobionate 23mg/ 0
Table 4.1.31 | Iron and Vitamin A Content of Invertebrates (4.6% Ca) ml
Iron Vitamin A Calcium lactate 18.31 0

Invertebrate Diet
(mg/kg) (IU/kg) Calcium phosphate 17.12 24.47
Mealworm Wheat, grain, carrots 40 810 (monobasic)
Mighty mealy Wheat, grain, supplements 26 160 Calcium phosphate 29.46 22.77
(dibasic)
Super mealworm Wheat, grain, carrots 50 970
Calcium phosphate 38.76 19.97
Cricket, adult Cornmeal, wheat midds, 110 810 (tribasic)
soybean hulls, meat meal,
molasses, fish meal Bone meal, steamed 31.74 15
Cricket, juvenile Shipped with raw potato 200 470 Table 4.1.32 | Calcium Content
Waxworm None 80 150 of Insects
Fruit fly Commercial feed 450 not Supplement Ca:P
detected
Mealworm nil 1:9
Earthworm, wild 11,100 2400
Cricket nil 1:16
Earthworm, commercial Peat humus soil 5800 330
Cricket Gut loaded 1:5
Cricket Gut loaded/dusted 1:3
the highest calcium content (Table 4.1.30). chemically similar to cellulose. Chitinase activity has
been identified in starlings, raptors and a variety of
seabirds. Vitamin E content of many insects is adequate,
INSECTS
but vitamin A content is relatively low or undetectable
There are limited varieties of invertebrates for captive (Table 4.1.31).4 Insects (especially from colder climates)
birds, with mealworms, earthworms and crickets form- contain high levels of polyunsaturated fatty acids.
ing the bulk of the available diet. Hard-bodied insects Insects generally concentrate a number of carotenoids
that contain up to 50% of their body weight as chitin that may be important for pigmentation or antioxidant
may be important sources of dietary fiber, as chitin is activity. Insects generally have poor Ca:P ratios (Table
105
Fig 4.1.15 | Vitamin A content of rodents at various stages of Fig 4.1.16 | Vitamin E content of rodents at various stages of
development. development.
4.1.32). Calcium content of termites is low, but

the content of their nest material (1.7%) pro-
vides a valuable source of calcium to birds,
such as fig parrots, that nest in termitaria.70
FISH
Fish must be stored below -18º C to maintain
nutritive value. Fish should be dry-thawed at
<4º C up to 48 hours before use, and emer-
gency thaws should be undertaken in plastic
bags under cold running water to prevent the
loss of nutrients. Supplementation of piscivo-
rous diets is required for some key nutrients,
depending on the species of fish fed and the
Fig 4.1.17 | Vitamin A content of fish stored in a frozen state (-10°C).
method of preparation. Feeding whole fish is
imperative to maintain proper Ca:P ratio.
Iodine content of marine fish is considered
adequate (0.9 mg/kg), while that of freshwater
fish may be as low as 0.03 mg/kg. Sodium levels
of marine fish are adequate if fish are not
thawed in fresh water. Heat stress may increase
a bird’s sodium requirement. Vitamin A content
of fish commonly fed to birds is adequate (Fig
4.1.17). Supplementation may be required if
eviscerated fish are fed. Vitamin E levels of
frozen fish are generally inadequate (Fig
4.1.18). Thawing of fish in water will deplete
water-soluble vitamins. However, there is no
data to support the supplementation of fish
Fig 4.1.18 | Vitamin E content of fish stored in a frozen state (-10°C).
with water-soluble vitamins other than thiamine
(B1) if they are dry-thawed. Many fish contain
thiaminase; these require 25 to 30 mg of thi-
amine per kg of fish fed.
Labeling Table 4.1.33 | Estimated Nutritional Requirements for

Psittacines
Nutrient Unit Maintenance Breeder
Most products will display information regarding only a
Protein
“guaranteed analysis.” This provides an indication of
Crude protein % 10-15 15-22
maximum or minimum levels of crude protein, fat and
Lysine % 0.8-1.5
fiber. However, there is no legal requirement for every
Lipid
batch to be chemically evaluated, rather these values Crude fat % 5 10-15
often are derived from calculated values and thus may Macrominerals
not be accurate. Furthermore, a value for “crude pro- Calcium % 0.3-0.7a 0.7-1.2
tein” provides no information about the digestibility of Magnesium % 0.15
the protein or the proportions of various essential Phosphorus % 0.3-0.7 0.5-0.8
amino acids. A crude protein value for products contain- Potassium % 0.7
ing invertebrates does not account for the proportion of Sodium % 0.2
Microminerals
nitrogen bound up in chitin. A crude fat content indi-
Copper mg/kg 4-12
cates neither whether the fats are saturated or unsatu-
Iron mg/kg 100b 100
rated, nor the proportions of essential fatty acids. A
Manganese mg/kg 65
crude fiber value does not delineate the proportion of Selenium mg/kg 0.30 0.4-0.5
soluble or digestible fiber, and provides no information Zinc mg/kg 40-50 50-80
about the lignin content. Vitamins
Vit A IU/kg 4000c 6000
Vit D3 IU/kg 200-1200 2000
SUMMARY
Vit E mg/kg 200-250 250-350
Nutrition is the single most important aspect of bird hus-
Vit K1 mg/kg 0.5d 0.5
bandry. Nutrition impacts the health, longevity, appear- a
Calcium requirements established for budgerigars, some species may
ance and behavior of birds in captivity. The complex bio- have higher requirements.
chemistry and interactions between levels of nutrients
b
Species susceptible to ISD may require less than 80 mg/kg.
c
Beta carotene 22.4 mg/kg.
coupled with the paucity of research in companion birds d
Supplementation of 300 μg daily for fig parrots susceptible to vitamin K
deficiency. Expressed on a dry matter basis. These values are estimates
make choosing an appropriate diet very difficult.
only and may not apply to all species.
Species differences between various psittacines makes

dietary recommendations even more complex. Table listed manufacturers, “crude” protein, fat, calcium,
4.1.33 offers current estimated nutritional requirements
etc., and knowledge of what method is used to
for psittacines. A summation of critical factors in the measure these levels.
selection of a diet should include: 4. Awareness, as in human, dog and cat nutrition of the
1. Consideration of any species — specific dietary potential dangers inherent in preservatives and addi-
requirements or sensitivities. tives.
2. Avoidance of excessive amounts of nutrients, as well 5. Recognition of the discrepancy between wild natural
as assuring adequate mineral levels. food sources and substitutions made by many com-
3. Analysis of the components and availability of the mercial manufacturers.
References and Philadelphia, WB Saunders, 1997, and aviary birds - “new wire dis- ates the development of repro-
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107
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04_Nutrition II.qxd 8/22/2005 2:56 PM Page 108
Nutritional Considerations
Section II
Nutritional Disorders
GREG J. HARRISON, DVM, D ipl ABVP-A vian , D ipl ECAMS
DEBRA M cDONALD, P hD, BS c (HONS I)
Nutritional disorders can result from malabsorption, a thread is the history of a basic seed and table food diet.
deficient diet, over-supplementation and/or overeating. Generally, at presentation of a “sick” bird, the IDC
Deficiencies and excesses of nutrients can both be harm- patient exhibits pansystemic clinical signs that often
ful to birds. include various behavioral problems. Typically though,
the earliest clinical signs are reflected in the integument,
Companion birds have been maintained for decades on followed closely by the digestive system. Often birds are
diets that, while nutritionally inadequate, support lim- not presented for evaluation until the reproductive or
ited breeding in a few species. While there are numer- respiratory system is affected. Behavioral problems can
ous publications regarding nutritional requirements of be the proximal cause of veterinary presentation when
agricultural species, captive passerine energetics and other clinical signs have been missed or ignored.
feeding ecology, there are few controlled scientific stud-
ies on aviary and companion birds or their wild con- The IDC can be initiated from a nutrient imbalanced
specifics. Variations in lifestyle and breeding ecology diet as well as from influences, such as improper hus-
result in differing nutritional requirements. Clinically, bandry, diet handling and storage or over-supplementa-
many health problems are correlated with nutritional tion of nutrients in formulated diets. Therefore, when
disorders. This chapter will provide an overview of these evaluating nutritional disorders, consider the composi-
conditions observed in companion birds, with reference tion of the diet eaten, as well as the stability or availabil-
to anecdotal observations in a clinical context and sum- ity of nutrients in that diet. Pathological influences such
maries of nutrient implications that have been predomi- as parasite infestation, metal toxicoses, malabsorption
nantly studied in agricultural species. Specific studies of syndromes, pancreatitis and gastroenteritis produce
companion and wild birds will be discussed. Parallels clinical signs similar to those seen in IDC, and therefore
may exist between the following description of the need to be ruled out (Table 4.2.2a).
improper diet cascade and the metabolic syndrome of
humans and rats.90b The IDC is the result of improper nutrient utilization,
usually from malnutrition that weakens the body
immunologically and structurally. This can allow inva-
sion of low level pathogens or commensals of viral, bac-
The Improper Diet terial, or fungal origin.
Cascade (IDC)
Recent research by Dr. M. Beck, University of North
The ‘improper diet cascade’ (IDC) (Table 4.2.1) has been Carolina15, showed that when the host is affected by a
postulated by the author (GJH) from decades of clinical nutritional deficiency, the invading pathogen is affected
experience, reports from pathologists and nutritionists, as well. By sequencing the viral isolates recovered from
as well as consultations with companies that produce selenium-deficient mice, she demonstrated mutations in
commercially formulated diets. The IDC expresses itself the viral genome associated with increased pathogenesis
in a highly individualistic fashion. The most common of the virus affected by nutrient deficiency. Bhaskaram
Chapter 4 | N U T R I T I O N A L C O N S I D E R A T I O N S : S E C T I O N I I
109
Table 4.2.1 | Improper Diet Cascade (IDC)
Nutritional Imbalance
MULTISYSTEMIC ABNORMALITIES
Cellular Structural Functional Immunologic

Impaired metabolism Metaplasia of columnar epithelium Goblet cells mucin production Commensal organisms normally
impaired bound to mucus are not excreted
Altered cell wall permeability Increased mucous viscosity Loss of cleansing ability of mucous Relationship with commensal
organisms disrupted
Cellular autointoxication Loss of normal collagen elasticity Normal glandular production of vari- Bone marrow suppression
Change in GI pH (less acidic) ous systems suppressed Decreased IgA, decreased
lymphocytes
Chronic: eg, Chronic: eg, Chronic: eg, Chronic: eg,

• Hepatic lipidosis, fibrosis, cirrhosis • Abnormal cilia • Diabetes mellitus • Secondary microbial infections
• Iron storage disease • Renal tubular nephrosis • Deposits of high density lipids in • Increased susceptibility to
• Irreversible degradation of retinal • Follicular atresia vasculature neoplasia
cones leading to blindness • Cataract formation • Exocrine pancreatic insufficiency
• Bone/muscle abnormalities • Infertility, decreased hatchability of
chicks
• Secondary hyperparathyroidism
ABNORMALITIES OF SPECIFIC SYSTEMS
Integument Gastrointestinal Respiratory Renal Endocrine Reproductive Cardiovascular

• Skin • Oropharyngeal • Nares • Glomeruli • Pancreatic • Ovarian • Vasculature
• Feathers • Pancreatic • Infraorbital sinus • Renal tubules • Thyroid • Uterovaginal • Myocardium
• Beak • Hepatic • Syrinx • Ureters • Parathyroids • Testicular • Air capillaries
• Nails • Intestinal • Air sacs • Urodeum • Intestinal • Cloacal • Pericardium
• Fat deposits • Gonadal • Egg abnormalities
Biochemical Hematological Behavioral
• AST, ALT • Increased WBC (see subsequent section)

• Bile acid
• Glucose • Altered total WBC
• HDL, LDL, Triglycerides
• Cytokines
Table 4.2.2a | Commonly Encountered Etiologies of Improper Nutrient Intake or Utilization
Congenital Individual Complicating Factors Rule outs that impair

Developmental digestion and/or
absorption
Improper parental diet Provision of improper diet Little or no sunlight Pancreatitis or organ failure
Improper handfeeding diet Consumption of improper Lack of bathing Malabsorption syndromes

diet
Weaned to improper diet Improper diet supplemen- Lack of exercise Viral, bacterial, fungal, or
tation parasitic gastroenteritis
Diet constituents interfere Improper food Metal toxicosis
with nutrient utilization packaging/handling or
storage
expanded this theory by showing that several micronu-

Table 4.2.2b | Nutrient Deficiencies of Seeds
trients such as vitamin A, ß-carotene, folic acid, vitamin
The seeds most commonly fed birds, such as oats, corn,
B12, vitamin C, riboflavin, iron and selenium could be sunflower, safflower and millet, are generally missing 32
involved in such a scenario in humans.17 These micronu- ingredients (from eight groups) needed to keep birds
trient-compromised viruses can lead to the emergence healthy. These include:
of new infections.17 This hypothesis was further • Vitamins - choline, niacin, pantothenic acid,
advanced by Lavender61, who showed that, at least for riboflavin (B2), cyanocobalamine (B12), biotin (H), D3, E, K,
and folic acid (M)
RNA viruses, host nutrient deficiencies and excesses can
• Minerals - calcium, phosphorous (70% tied up as non-
influence the genetic make-up of the pathogen. The digestible phytates in plant products, such as grains),
majority of viruses are RNA viruses.61 sodium
• Trace minerals - selenium, iron, copper, zinc, man-
The importation of wild caught psittacines has tradition- ganese, iodine, chromium, vanadium, bismuth, tin, boron
ally involved weeks to months of stress including severe • Pigments - chlorophyll, canthaxanthin
nutrient imbalance. Such birds imported into the USA in • Protein - (amino acids) lysine, methionine
• Fiber - (mucopolysaccharide) both soluble and insoluble
the 1970s and 1980s were a part of a pandemic of new
• Vitamin precursors - ß-carotene, converted to vitamin A
viral diseases. Psittacine beak and feather disease, in liver
proventricular dilatation disease and papillomatosis are • Omega 3 Fatty Acids
three that still plague us. The research community has
not adequately addressed the role of malnutrition in
viral pathogenesis. It is interesting to ponder this ciency not seen on other seed-based diets. The composi-
hypothesis in light of the new expressions of these same tion of commercially raised seeds differs dramatically
viruses occurring in the European Union countries that from wild seeds (see Section I of this Chapter).
still import wild-caught birds.
Birds do not exhibit nutritional wisdom when selecting
dietary ingredients; they show a preference for high-
IMPROPER DIET FORMULATION energy, lipid-rich seeds, high carbohydrate seeds and
There is a general perception that ‘fresh’ is best. fruits. The advent of formulated foods has diminished
However, presenting a bird with an array of fresh pro- the incidence of nutritional disorders in the author’s
duce, seeds and nuts does not necessarily provide a (GJH) practice. Yet not all formulated diets are created
nutritionally balanced diet. Commonly fed seeds are equal (Tables 4.2.2c-e). For example, products that offer
deficient in a number of nutrients (Table 4.2.2b). Much the opportunity for selecting favored food items are
of the produce is sold in its immature state of growth, poorly formulated and can be just as imbalanced as a
and even when mature, it does not have the equivalent seed-based diet in the end.
nutrient profiles of wild food items. Thus such produce
is unable to improve the nutrient profile of the diet. The Association of Avian Veterinarians (AAV) formed a
committee of nutrition experts who developed a list of
It is imperative that bird owners be informed of the recommendations to assist veterinarians and owners in
nutritional inadequacies of such diets. In the wild, feeding pet birds (Table 4.2.2f).
psittacines usually balance their diets by feeding on a
variety of seeds and other plant parts. Primary issues of While some essential nutrients are higher in organically
concern with captive diets are vitamin levels (vitamins A, certified plant products, a diet composed solely of
D, E, and K and the water-soluble vitamins—biotin and organic seeds will present as many nutritional problems
B12) and minerals. Seeds do not contain vitamin A and as a diet solely composed of non-organic seeds.
are generally low in the vitamin A precursor ß-carotene.
There are also the issues of diminished availability of
Hypovitaminosis A is particularly prevalent in birds on
some nutrients by interference from other nutrients and
all-seed diets. Mineral levels of seeds can vary among
potential breakdown of key nutrients.
plant species as well as geographically, depending on the
composition of the parent soil. Calcium is deficient in
most seeds and, while adequate phosphorous may OVER-SUPPLEMENTATION
appear to be present, up to 70% may exist in phytate Vitamin toxicity is an aspect of dietary management that
form that is generally indigestible. Fatty acid composi- is frequently overlooked, but can be responsible for a
tion will also vary among seed species and an imbalance number of clinical signs of a disease. Many commercially
can be an important cause of a number of health issues. formulated products contain excessive levels of the fat-
Many seeds provide adequate total protein but do not soluble vitamins A and D. The addition of vitamin sup-
contain the complete set of essential amino acids. A diet plements with high concentrations of these two vitamins
of predominantly millet seed will result in a lysine defi- compounds that excess. The generally low levels of
111
Table 4.2.2c | Provision of Improper Diet - Common Presentations

Excessive quantity of seeds or nuts Excessive percentage of fruits and Excessive quantity of "table foods" Improper/excessive vitamin-mineral
provided (minimal vitamin A precur- vegetables (deficient in essential such as the carbohydrate rich pastas supplementation
sors, lysine deficient, decreased vita- amino acids and essential fatty acids, and breads (in addition to the afore-
Potential toxicities Competitive
min E absorption, inverted Ca:P contain excessive sucrose) mentioned deficiencies, these pro-
eg, vitamin A,D3, nutrient absorp-
ratio, excessive calories) *Nutritional deficiencies vary widely vide a medium for yeast overgrowth
iron, selenium tion, eg, exces-
between fruits and vegetables - see in susceptible individuals)
sive fatty acids,
Figs 4.1.2, 4.1.3 and Tables 4.1.8,
phytates, and fat
4.1.9 in section 1)
soluble vitamins
Table 4.2.2d | Consumption of Improper Diet - Common Presentations

Formulated diet over-supplemented Diet provided requires bird to con- Supplements needed to balance diet
with vitamins (vitamin A) or minerals sume all components to achieve bal- are provided as a coating on food
(iron). Deficiencies: lysine, L-carnitine ance that is not entirely consumed
Table 4.2.2e | Preparation, Packaging and Storage Problems of Formulated Diets

Problems in Preparation Packaging Concerns Improper Storage
Inclusion of raw soybeans, oats or Use of oxygen- Continued mycotoxin production

brown rice. Cooking soybeans permeable packaging
improves the availability of methion-
ine & cystine14b & destroys trypsin Oxidation →
inhibitors. Oats & brown rice are
high in lipase [break down fats to Rancidity
free fatty acids & lipoxygenase (oxi-
dizes fatty acids to hydroperoxides)]43b
Inclusion of mycotoxin producing Exposure to light

agents
Poor quality control Insect contamination
Over cooking → Pesticide contamination Insect infestation (eg, transmission of

degradation of nutrients and Sarcocystosis)
conversion of cis to trans fatty acids
Addition of artificial coloring/dyes Soft plastics may act as Degradation of nutrients

long term effects unknown phytoestrogens
Preservatives (such as ethoxyquin) may be toxic or teratogenic. However, in the absence of preservatives, proper
packaging and storage are imperative to maintain quality and prevent rancidity.
vitamin E in both commercial diets and vitamin supple- quality control of source products is essential. The expo-
ments may exacerbate toxicity. Dietary supplementation sure to oxygen, moisture and heat act with the catalysts
should be undertaken only if there is an extensive naturally present in grains (iron, copper) to accelerate
knowledge of the nutrient composition of both the diet the deterioration process at all stages of grain handling
and the supplement. The common clinical practice of and product manufacturing.
injecting vitamins into sick birds may not be defensible,
especially if the bird has been on a formulated and/or These lipolytic enzymes act on lipids to release free fatty
supplemented diet. See Section 1, Nutrition and Dietary acids and triglycerides. In the presence of oxygen, heat
Supplementation for a more in-depth discussion. and moisture, these fatty acids and triglycerides are auto-
oxidized or acted upon by enzymes (primarily stored in
the germ) called lipoxygenases. Polyunsaturated fatty
RANCIDITY acids (oleic, linoleic, and linolenic) are the most likely to
Altering tissue structure mechanically (hulling, grinding, be oxidized, and they are usually the most abundant
and crushing in the case of vegetable matter or macera- fatty acids in nuts and seeds.43b This oxidation process
tion in the case of animal tissue) releases lipases. produces free radicals in a dark environment. A similar
but slightly different reaction occurs when exposed to
Grains damaged at harvest also allow this lipase release light. Both reactions end with the production of lipid
to occur. Similarly, micro-organisms (fungal contami- hydroperoxides which further break down, causing ran-
nants) contain lipases that cause hydrolysis of fats.43b So cidity. This process is often self perpetuating, starting
Table 4.2.2f | AAV Feeding Brochure
Association of Avian Veterinarians

Feeding Recommendations
FEEDING COMPANION BIRDS FEEDING TIPS·
Feeding of companion birds has been one of the most • Carefully monitor TOTAL food consumption during
challenging aspects of their care, primarily because of any diet change.
limited nutritional research on all species. However, • Introduce small amounts of a new food at a time.
based on studies of poultry and other animals, general- • Gradually reduce the total volume of seeds as you
izations can be made on adequate feeding practices for increase the volume of more nutritional foods.
companion birds. • Clean all food and water cups and remove old food
from the cage daily.
FORMULATED DIETS • Do not provide supplemental vitamins unless recom-
Formulated bird food products are available from the mended by your avian veterinarian.
pet food industry as a convenience to the owner and to
ensure a more nutritionally balanced diet than that BEHAVIORAL ENRICHMENT
offered by seeds alone. The current trend is toward A consistent daily feeding program contributes to physi-
specific formulations addressing age, activity, therapeu- cal and mental health as much as a varied diet. The
tic, and stress-related needs of the bird. For example, availability of natural items such as branches, empty
birds have special nutritional needs during molting, egg nutshells, leather pieces and coconut shells create a
laying, or raising young. However, improving a diet in stimulating environment.
the short term in anticipation of these life stages is not
effective; the feeding practices must be optimal year GRIT
round. Grit is small non-dissolvable rock. The necessity of grit
Commercial bird food products may be purchased as in the diet is debatable. Some birds, such as pigeons,
pellets, nuggets, crumbles, or hand feeding premixes. fowl, canaries and finches, appear to need the avail-
Converting a seed-eating bird to a formulated diet ability of grit. In psittacine species, an occasional grit
must be done with care because new items in the cage particle is harmless but it is not necessary for healthy
may not be immediately recognized as food. Your vet- maintenance of pet parrots, macaws, parakeets and
erinarian can recommend a commercial formulated similar species.
bird diet and help you with the conversion process.
SALT
ALTERNATIVE HOMEMADE DIETS Salt licks are not necessary for birds.
Where commercial diets are not available, attempts are
made to produce a homemade diet. While not ideal for DEPRAVED EATING HABITS
pet birds, these usually offer an improvement over an Birds that routinely eat inappropriate materials (eg,
exclusive seed diet. Overall, however, homemade diets feces, enclosure substrate) should be examined by a
are often lacking in calcium, iodine, selenium, protein, veterinarian. This behavior may be associated with dis-
fatty acid balance, fiber, pigments, and vitamins A, B ease or nutritionally deficient diets and is often pre-
complex, E, and D3 while providing an excess of carbo- vented by the feeding of a more balanced formulated
hydrates, and phosphorus. Additionally, homemade food product.
diets with moist ingredients tend to spoil easily and lose
nutrients if not stored properly or if made too far in SPECIAL REQUIREMENTS
advance of feeding. The time and effort involved in Lories and lorikeets require specialized diets in captivity.
preparing foods and the difficulty in balancing the These nectar diets attract insects and result in liquid
nutrients make homemade diets impractical for the pet and messy feces. Your avian veterinarian can recom-
bird owner. Owners choosing a fresh food plan tend to mend a diet for these species. Soft-billed birds, water-
offer too much variety and quantity of food each day, fowl, backyard poultry and gamebirds Commercial
permitting birds to pick out what they like. Birds will not foods are available for these birds. Some toucans and
choose a balanced diet if given free choice. Consult mynahs may have a special dietary requirement for a
your avian veterinarian for specific recommendations low-iron formula. Consult your avian veterinarian for
on items and quantities to feed. recommendations.
FRESH WATER
Fresh water must be provided at all times. Some avicul-
turists and companion bird owners have had success
using pet water bottles for birds, thereby limiting soiling © Association of Avian Veterinarians 2002
of water. Used with permission
113
slowly and increasing rapidly as reaction chemicals COOKING

become available. In the preparation of a formulated diet, cooking (roast-
ing, pelletizing or extrusion) is designed to stabilize oils.
Expressing the oil from seeds increases the surface area
However, depending on the condition of the products
being exposed to oxygen, which can increase the possi-
being mixed, some combinations may cause flash rancid-
bility of rancidity occurring.
ity (D. Jones, personal communication 2000). This is
The production of lipid hydroperoxides does not due to the presence of enzymes in items like grains and
appear to alter flavor. Lipid hydroperoxides deteriorate peanuts that cause natural fermentation when exposed
to aldehydes in the presence of oxygen.43b These do to warm moist air. The lipase concentration in some
alter flavor and finally palatability. Alcohols and hydro- grains is very high. Oats and brown rice are examples.43b
carbons are also produced. These latter products have Dehulling and milling these products causes rapid dete-
been reported to be mutagenic.16 Rancid fats can lead to rioration (rancidity) unless they are heat stabilized prior
selenium and vitamin E deficiencies implicated in to storage or further processing. When these raw prod-
encephalomalacia, pancreatitis, myocardial necrosis, ucts are combined under the heat of processing, this
hepatic necrosis and general myopathy. Biochemical flash rancidity can occur. For this reason, these ingredi-
analysis of affected birds’ blood may show anemia, ele- ents need to be roasted or other wise partially cooked
vated lactate dehydrogenase (LDH), aspartate amino- separately, then mixed with the other ingredients prior
transferase (AST), creatinine phosphate (CK) and phos- to final processing.
phorous levels. Many of these clinical conditions are
Raw soybeans contain trypsin inhibitors and can there-
not reversible.98
fore be difficult to digest. This enzyme is a critical part of
Chickens fed diets with increased rancidity parameters digestion in monogastric animals. Trypsin inhibitors are
(peroxide and aldehyde concentrations) experienced inactivated by heat.14b,70b Cooking also improves the avail-
increased mortality from fatty liver syndrome (FLS). ability of methionine and cysteine.14b Overcooking
Total blood proteins of affected chickens were elevated, destroys or makes unavailable certain amino acids
as were lipoproteins and total lipids.28 (lysine) and greatly reduces natural vitamin precursors
such as tocopherols and carotenoids.
HANDLING AND STORAGE
MOISTURE CONTENT
Wild birds naturally feed on an array of fresh foods while
their captive counterparts are provided with foods that Lowering the moisture content of a product also acts as
have been stored for extended periods. Nutritionally a stabilizer. Moisture plays a vital chemical role in most
imbalanced food supplies are not uncommon in wild sit- oxidation processes.43b Levels below 5% are often
uations. Agriculture produces seeds and nuts only at the required to deter degradation. The author (GIH) has
end of the growing season, usually in the fall. Storage shown that these low moisture levels cause minor
increases the potential for nutrient degradation. proventricular irritation evidenced by excessive regurgi-
Nitrogen flushing and storage under refrigeration are tation and minor weight loss in some pet umbrella cock-
steps that discourage oxidation. atoos. Even at these low moisture levels, over time non-
free ‘water’ is all lipases need to act. Non-free water can-
not be removed by drying.43b
COLD DARK STORAGE HELPS
PREVENT RANCIDITY
PACKAGING
Storing walnuts in the light at 21° C resulted in pro-
found oxidative changes.51 However, walnuts stored in Many bird foods are packaged in plastic, cellophane,
the dark at 5° C for 25 weeks, even in 50% oxygen, were coated paper or cardboard boxes. The latter two prevent
without a trace of rancid taste.51 However, it should be exposure to light. Airtight containers (plastic, cello-
remembered that rancidity, as determined by chemical phane) prevent moisture from evaporating, but many do
analysis, precedes taste detection. not stop oxygen from crossing into the food. The oxy-
gen then breaks down essential nutrients or changes
Storing corn oil at room temperature for 48 months their biological activity. An advertised vitamin A content
resulted in rancid oil, whereas storage in the refrigerator of 12,500 IU/kg may be reduced to as few as 1,500 IU/kg
did not.16 A specific strain of mice fed the rancid corn by inadequate packaging, with further deterioration
oil showed significantly increased expression of onco- once the package is opened. Even if one starts with a
genes in all major organs. The results demonstrated that nutritionally sound, preservative-free formulated diet,
rancid oils, rich in n-6 polyunsaturated fatty acids, could the lack of proper packaging and resulting rancidity can-
initiate tumors and promote tumor growth.86 cel its effectiveness.
Paper Polyethylene
Adhesive
Adhesive
Aluminum Foil Nylon

Adhesive
Fig 4.2.1 | Quadruple laminate packaging helps preserve the Fig 4.2.2 | A red-lored Amazon fed a seed and table food diet
freshness of fomulate diets and prevents rancidity. has an overgrown maxillary rhamphotheca that has been
recently honed down to a more normal shape.
Fig 4.2.3b | A yellow-naped Amazon fed a

seed and table food diet. The bird is obese, the
maxillary rhamphotheca is overgrown and the
Fig 4.2.3a | A green-winged macaw fed a feathers are abnormally pale green. The rectri-
seed and table food diet. The red feathers are ces are tattered. Structural abnormalities make
almost pink. Black pigment is co-mingled with the coverts of the wing and body contour feath-
green. The beak is hyperkeratotic. The breast ers lack the homogeneous interlocking appear-
and wing feathers are tattered and picked. ance of a normal bird.
To avoid oxygen deterioration, chemical preservatives inadequately packaged.

like ethoxyquin (originally used to soften rubber, later as
a herbicide) and propylene glycol have been used for For these reasons, all foods need to be smelled when
decades in dry animal foods. They have not been first opened. If they smell like old frying grease or lin-
deemed safe for human foods. Recent public demand seed oil they are rancid. A taste test should be observed
for more natural pet foods has led to a variety of newer when first offering a new bag of food to the bird. If the
techniques to avoid rancidity.
bird acts hungry but rejects the food it might be rancid.
Lipid peroxidation can particularly affect products com- Rancid foods should not be fed. Following the manufac-
posed of organic ingredients that lack synthetic preserva- ture’s directions for handling the food and shelf life will
tives but is no less an issue for any products that are usually prevent rancidity problems.
115
Table 4.2.3 | IDC and the Integument
Nutritional Imbalance
CLINICAL SIGNS
Feathers Skin Beak and Nails
• Frequent or incomplete molts • Flaky • Excessive length
• Retained feather sheaths • Dry • Exaggerated curvature
• Abnormal coloration • Pruritic • Friable texture
• Irritability due to feather discomfort • Hyperkeratotic • Splitting
• Deformities: • Loss of elasticity (tears readily) • Bruise readily
- Cysts • Plantar surface - loss of pattern • Chronic/Severe
- Loss of elasticity • Chronic/Severe - Marked deformity
- Barbules not interlocking - Pododermatitis - Secondary infections
• Chronic/Severe
- Feather destructive behavior
- Self-mutilation
INITIAL TREATMENT
Husbandry Medical Procedural Diet Conversion
• Increase UVB • Antipruritics: • Trim overgrown beak • Evaluate for the following:
• Increase outdoor exposure: - Systemic • Trim overgrown nails - Essential amino acids
- Humidity - Topical • Remove damaged feathers - Balanced fat and CHO
- Ventilation • Treat secondary infection if present • Trim rachis of feathers if irritating - Vitamins at physiologic levels (not
- Sunlight and significant bird excessive or deficient)
- Psychological stimulation • Psychotropic medications if self- • Mechanical barrier to self-mutila- - Free of dyes and preservatives
• Improve available perches, mutilating tion if needed - Need for supplemental essential
increased variety of sizes and tex- • Parenteral vitamin supplementation • Medicated padding and or band- fatty acids
tures for severe deficiencies aging for pododermatitis when • Formulated diet is often most con-
• Increase exercise, both • Blood work and other diagnostics if present venient and effective
physical and mental indicated • Monitor weight during
• Verify or improve hygiene conversion
EVALUATION OF THERAPY
• Dietary conversion is necessary for long-term treatment and control.
• Anticipate exacerbation of clinical signs for 3-9 months (pruritus, flaking of skin and molting) with integumentary regeneration.
• If clinical signs worsen, perform diagnostic work-up for systemic sequelae to IDC.
• At 9-12 months, marked improvement should be noted in initial clinical signs.
There are few natural oxidative inhibitors. Tocopherols (blocking light), a layer of nylon for puncture resistance,
(vitamin E) and rosemary leaves have been tried. In the a metal alloy as a barrier to oxygen and a polyethylene
author’s experience, preliminary studies of products layer to resist changes in moisture and retain oils, have
containing rosemary had less than ideal acceptance, and increased shell life of non-synthetically preserved prod-
the test subjects’ had lower than desired body weights. ucts by up to 14 months. However, once the seal is bro-
ken and exposure to oxygen and moisture increases,
The natural antioxidants found in whole cereal grains
these products are only viable for up to six weeks before
have not been fully exploited.
clinical signs produced in birds resemble those of birds
The development of quadruple laminate bags (Fig 4.2.1), maintained on diets depicted in Figs 4.2.2-4.2.3a,b. It is
consisting of a layer of poly-coated extruded paper important that clients adhere to the manufacturers’
Fig 4.2.4 | A blue and gold macaw that was fed a diet of pasta, Fig 4.2.5 | This blue and gold macaw hen died after laying a
crackers, cookies, pellets and vegetables. The feathers are tat- clutch of 5 infertile eggs. Note the pinfeathers after all the body
tered and lack symmetry. The blue feathers contain a black pig- and extremity feathers were removed. Also note the black pig-
ment. Under the contour body feathers, the bird had an excessive ment in the normally blue feathers. The bird had been fed a
number of pinfeathers. seed and table food diet.
Table 4.2.4 | Using a Formulated Diet INTEGUMENTARY SYSTEM

Shelf Life Use within 4-6 weeks of opening*
The integument is the site where clinical signs of dietary
Storage Store in manufacturer’s packaging
only if adequate** inadequacy often appear to be noticed first, but these
Express air to minimize oxidation early stages are so commonly encountered that they may
Feeding Frequency Offer fresh food 2-3 times daily dependent on not be perceived as abnormal (Table 4.2.3). The stratified
species
squamous epithelial (SSE) cells characteristic of skin are
Feeding Amount Ensure bird eats all food offered, including crumbs.
Amount fed should maintain normal body weight. involved in the production of integumentary compo-
Selective Feeding Don’t allow bird to favor individual particles nents such as the nails, beak, feathers, and feather folli-
Supplementation Follow manufacturer’s instructions as to types and cles. In addition to the integument, SSE cells are found
amounts of supplementary foods
in the rhinal cavity, mouth, salivary duct junctions, tear
Water Don’t allow birds to dunk food in water as this
degrades vitamins and pollutes water leading to ducts, ear canal, syrinx, air sac junctions to the lungs,
bacterial and fungal overgrowth bile duct, pancreatic duct, cloaca, renal tubules and
*Diets composed of nonorganic ingredients may have a longer shelf life vagina. Nutritional imbalance can influence the structure
due to synthetic preservatives.
**Many products are packaged in inferior packaging resulting in break- and function of any of these sites. While nutritional inad-
down of key nutrients before packaging is even opened. Quadruple
laminate packaging preserves nutrients for extended periods of time.
equacies are most often manifested in the integument,
the clinical presentation can be complicated by more
serious underlying illnesses. The development of nutri-
tionally balanced formulated diets has dramatically
storage directions, as even nutritionally adequate diets reduced the incidence of dermal disorders, but such
have a limited shelf life once opened (see Table 4.2.4). diets are far from successful in totally eliminating these
problems once they have developed.
The Physical Exam Form outlined in Chapter 6, Maximiz-

The IDC from a Systemic ing Information from the Physical Examination, is a use-
Point of View ful tool for identifying signs and common clinical pre-
sentations listed in Table 4.2.3. Minor integumentary
Although birds seldom present with only one system signs are often overlooked by the bird care industry. It is
affected by improper diet cascade, diagnosis, treatment important to establish a program of wellness with regu-
and prevention are best discussed by looking at a single lar checkups, especially for new birds, to identify prob-
system at a time. lems with nutritional inadequacies at an early stage.
Early recognition by the clinician of the effects of IDC on

various systems allows diagnosis and implementation of KERATINIZATION
dietary therapy. This is a key element in avian preventive Hyperkeratosis is characterized by failure of the new
health care. cells to differentiate beyond the squamous stage.
117
Table 4.2.5 | IDC and the Digestive System
Nutritional Imbalance→ Pathology of gastrointestinal organs, liver, pancreas
CLINICAL SIGNS
Body Condition Behavior Flora Digestive
• Obesity • Regurgitation • Total # gram-positives decrease • Bilestained urine, urates and stool
• Loss of muscle mass • Vomiting • Lower % gram-positive rods • Occult blood in stool
• Bleeding • Loss of appetite • Gram-negative bacteria increase • Undigested food and fiber
• Chronic • Listlessness • Yeast not budding in stool = pancreatic failure
- Emaciation • Aggression • Chronic • Liver shadow increases or
- Fatty liver - Gram-negatives predominate decreases
- Cirrhosis - Budding yeast • Chronic
- Hemochromatosis - Enterotoxemia (gram- - Ileus
positives explode) - Diarrhea
- Clostridial overgrowth
TREATMENT
Diagnostics for Medical Environmental Dietary
Secondary Infections Treatment Concerns Conversion
• Endoscopy and organ biopsy • Fluids • Heat • Same as Table 4.2.3
• Culture and sensitivity • Systemic treatment of secondary • Proper humidity • Formulated diet is often most con-
• Radiology infections venient and effective
• Hematology • GI stimulants
• Biochemistry • Bacteria, enzyme replacement
• Ultrasound • Lactulose
• Milk thistle
• SAMe
• Apple cider vinegar
• Chronic
- Ultra clear®f
- Hepasan®e
Dysfunctional, excessively keratinized cells replace nor- supplementation to treat hyperkeratosis. In rodents, oral
mal cells. This can result in epithelial lesions and an supplementation with vitamin A failed to raise serum
increased susceptibility to infection. If the imbalance is vitamin A levels in the absence of adequate vitamin E.6
severe and prolonged, columnar epithelium undergoes Therefore a mixture of both vitamin E and vitamin A
metaplasia to SSE. Keratinization can result in a loss of may be required to treat hyperkeratosis due to a vitamin
function of the tissues involved, including those of the A deficiency. Deficiencies of zinc and biotin have been
alimentary, reproductive, respiratory and urinary tracts. associated with hyperkeratosis. Biotin deficiencies,
which can result from excess of salt, are correlated with
Clinical signs of hyperkeratosis involving the integumen-
hyperkeratosis on the footpad and the plantar surfaces
tary system can manifest as overgrowth of the beak and
of the toes.7 Thus the caveat to not treat all hyperkerato-
nails, which retain their outer covering due to a prolifer-
sis with vitamin A injections is valid.
ation of basal cells. The keratinized outer coatings of
pinfeathers are thicker, less flexible and retained much
longer than normal. Retained coatings prevent pinfeath- GASTROINTESTINAL SYSTEM
ers from opening and such feathers appear to be painful
Secondary to the dermal system (and some behavioral
to the birds if the unopened feathers are manipulated.
traits), the avian clinician is likely to observe gastroin-
Clients commonly report that birds with chronically
testinal tract (GIT) dysfunction next in the unfolding of
retained pin feathers are irritable and vocalize as if in
the IDC (Table 4.2.5). Vitamin A deficiency may interfere
pain during preening (Figs 4.2.4 and 4.2.5).
with normal growth, rate by influencing functionality of
While hyperkeratosis is generally associated with dietary the small intestine by altering the proliferation and mat-
deficiencies of vitamin A, excesses of vitamin A are also uration of cells of the intestinal mucosa.104 Hyperprolifer-
correlated with hyperkeratosis. The percent of squa- ation of enterocytes, decreased number of goblet cells,
mous cells present in nasal flushes has been used as an decreased alkaline phosphatase activity, and decreased
indicator of vitamin A toxicosis.58 It is important to expression of brush-border enzymes are all correlated
obtain a full dietary history before prescribing vitamin A with vitamin A deficiencies.104
Table 4.2.6 | Techniques for Performing a Fecal

Gram's stain
1. Fecal samples should ideally be collected at home and

refrigerated until evaluated to prevent the proliferation
of saprophytic gram-negative bacteria that may be inter-
preted as pathogenic.
2. A small amount of feces should be applied to a pre-
cleaned glass slide using the wooden end of a cotton-
tipped applicator. The sample should be spread into a
uniform, thin, even film, using a single swath.
3. Heat fix
4. Place slide on staining tray:
Fig 4.2.6 | Improvement of fecal Gram’s stains over time with • Apply 3 drops of gentian violet to the sample and
only the use of an organic formulated diet.102 allow to stand for 30 seconds (stains all bacteria blue).
Key: • Rinse with water and drain excess water.
Seed = Initial assessment of 100 birds after 12 months of eating a seed- • Apply 3 drops of Gram’s iodine and allow to stand for
based diet
30 seconds (closes pores on gram-positive bacteria).
HPC = Samples collected 4 weeks after changing 80 birds to Harrison’s
High Potency Coarse (HPC) pelleted formulation • Apply 5 drops 95% ethyl alcohol to decolorize blue
HPC2 = Samples collected from same birds after 8 weeks on HPC stain from gram-negative bacteria.
HPC3 = Samples collected from same birds after 12 weeks on HPC • Rinse immediately with water and then add 5 drops
saffron to stain gram-negative bacteria red.
• Rinse immediately with water and blot dry with lens
The Fecal Gram’s Stain in Psittacines paper or tissue.
5. Scan slide under low microscope power for suitable eval-
While early studies of captive birds indicate that they uation site.
commonly have low levels of gram-negative bacteria in • Using the oil immersion lens, scan several fields for a
cultures of feces,5,9,18,21,54,99 other researchers maintain further idea of uniformity.
• Choose a uniform field and begin to estimate the total
that autochthonous flora in healthy parrots are not
number of bacteria, i.e., count 10 bacteria, assess the
gram-negative.37,38,45,46,47,102 Normal fecal flora of proportion of entire field occupied by those 10 bacte-
psittacines is comprised of 100% gram-positive, non- ria and then estimate the total bacterial population per
spore forming rods and cocci.37,38,45,46,47,102 One study of 1000x field.
6. Record results (see Table 4.2.7)
wild yellow-naped Amazon chicks showed 60% of cloacal
7. The presence of gram-negative cocci indicates improper
cultures had Enterobacteriacea.99 The author (GJH) has staining technique.
hypothesized that this group of nesting birds were
With experience, the entire process should take less than
under undue stress from poachers, the presence of
2-3 minutes to perform.
humans guarding the nests and a declining natural envi-
ronment. For 20 years, this author (GJH) has used fecal
Gram’s stains to evaluate the normal flora of pet birds.46
Table 4.2.7 | Recording Results of the
Studies of wild psittacines in a recent trial confirm the Fecal Gram’s Stain
absence of gram-negative bacteria.45.47 Gram-negative Date ____________________________________
bacteria were reduced to almost zero after conversion of Species __________________________________
African grey parrots from a typical seed-based diet to a Case ID __________________________________
nutritionally balanced one.102 (Fig 4.2.6) Glunder found Results:
(E. coli or Klebsiella spp.) it nearly impossible to colo- _______ total bacteria/1000x oil immersion
nize in the intestine of budgerigars on nutritionally bal- field
anced diets.38 Joyner54 whose MPVM thesis study looked _______ % G+ rods/field
at breeding pairs of aviary budgerigars on a seed-based _______ % G+ cocci/field
diet, reported a 60% cloacal presence of gram-negative _______ % G- rods/field
rods, and reported this as normal. This may be consid- _______ number yeast/field
ered normal for a seed-eating budgerigar in this study, _______ % budding yeast
but it should not be considered normal for a healthy _______ high fiber in feces
_______ undigested food
bird on a balanced diet.
_______ parasites
Normal resident microflora maintains an acidic environ- _______ clostridial organisms
_______ hyperkeratotic cells
ment that inhibits the proliferation of gram-negative
_______ normal intestinal cells
rods and yeast. An imbalance in the intestinal homeosta-
_______ RBC’s
sis results in alterations to the normal populations of
_______ WBC’s
microflora, and thus the distribution of bacteria in the
119
GIT. Normal intestinal flora of parrots, seen as gram-pos- • Decrease in percentage of gram-positive cocci
itive (blue) bacteria on a fecal Gram’s stain, represent • Increase in % gram-positive rods
both aerobic and anaerobic bacteria such as Bacillus,
Corynebacterium, Streptomyces, Lactobacillus, In the later stages of malnutrition and liver disease, the
Streptococcus and Enterococcus spp.,37 some of which Gram’s stain generally shows:
are not able to be cultured using standard techniques. • Increase in presence of gram-negative rods (generally
speaking, the more gram-negative rods, the more
Enterobacteriaceae are gram-negative (red) bacteria that pathologic the situation)
include pathogens (eg, Salmonella spp., E. coli, • Presence of yeast which are judged as to their clinical
Acinetobacter spp.) and non-pathogenic species. significance by the number of budding yeast per field.
Enterobacteriaceae are not normal components of The greater the percentage of budding yeast found,
unstressed parrots’ microflora37 and are not detected in the more likely that the immune system is compro-
preliminary studies of wild parrots.45,47 However, normal mised.
flora bacteria can become secondary pathogens depend-
ing on the functional state of the host defense system.37 The fecal Gram’s stain of the stool from pet passerines
Systemic disease, including septicemia and death, can should be free of bacteria, yeast and Macrorhabdus sp.
occur when bacteria leave the mucosal surface and pen- organisms.
etrate the intestinal wall, a situation that can be precipi-
Clostridia (gram-positive, anaerobic organisms), are
tated by an imbalanced diet influencing the integrity of
commonly associated with fetid stools in both cockatoos
mucosal surfaces. Parrot-specific Lactobacillusg (cur-
with cloacal prolapse and macaws with cloacal papillo-
rently only available in Europe) has been used success-
mas. Both the clostridial organism and the underlying
fully to treat chronic coliform infections, eliminating the
cause require treatment106 (Figs 4.2.16 and 4.2.18).
incidence of E. coli on culture.37 Techniques for per-
forming and recording a fecal Gram’s stain are outlined
Hepatobiliary System
in Tables 4.2.6 and 4.2.7.
Fatty Liver Syndrome
The fecal Gram’s stain is an important component of The following discussion is offered because the author
complete patient evaluation of psittacines. Although not (GJH) believes fatty liver hemorrhagic syndrome (FLHS)
definitive in making a diagnosis, it provides a visual of poultry is similar to a common clinical disease in
screen of the proportions of bacteria present in the GIT psittacines, which is primarily a result of malnutrition.71
at the time of sampling. When interpreted in conjunc- FLS, generally a consequence of an imbalance in energy
tion with a complete physical exam and diet history, it metabolism, is associated with an accumulation of exces-
can determine the next diagnostic step: whether to pro- sive abdominal and hepatic fat. Lipid infiltration weak-
ceed to a culture and aggressive therapy or to treat con- ens the hepatic cellular structure and results in
servatively with husbandry changes. hepatomegaly. Lipid deposits are also found in some
skeletal muscles, alimentary tract, autonomic ganglia,
Interpreting a Fecal Gram’s Stain CNS, pineal gland, kidney, heart and occasionally, small
Ideally, one should use a fecal Gram’s stain in conjunc- amounts are seen in the corneas, exocrine pancreas,
tion with culture and antibiotic sensitivity testing and adrenal medulla and epithelium of the thyroid follicles.
only then, antibiotic therapy. Figs 4.2.7-4.2.22 represent Endogenous hypercholesterolemia and cessation of egg
a range of fecal Gram’s stains commonly seen in clinical production are characteristic signs of a similar disorder
practice (1000x oil immersion field) from psittacines in poultry, fatty liver hemorrhagic syndrome (FLHS).100
maintained predominantly on seed-based diets. Figs
4.2.23-4.2.27 are representative of wild Australian
The numerous blood vessels of an enlarged friable liver
psittacines taken from birds in the December breeding are easily ruptured during egg laying. The rupture of
season when diets include a number of wild blossoms large blood vessels can result in death. This disease
(D. Brennan, personal communication). A healthy (FLHS) is most often seen in apparently healthy poultry
psittacine should have a predominance of gram-positive in a high state of egg production. It also affects young
rods and cocci, with an absence of gram-negative rods. birds, especially chicks from young parents, with 50%
higher mortality in females than males. Fatty liver syn-
Malnutrition and liver disease are characterized by drome is especially evident in older, overweight pet
changes in the number and distribution of bacteria on birds that are fed a diet of seeds or nuts, but can be seen
the fecal Gram’s stain. In the early stages, the change is in handfed chicks as well. Trauma associated with adult
reflected by: birds falling from a perch or being held for a routine
• Decrease in total bacteria clinical examination has caused hepatic rupture in FLS
Figs 4.2.7-4.2.12 | Fecal Gram's Stains (FGS) Commonly Observed in Psittacines in Clinical Practice (oil immersion 1000x).
Fig 4.2.7 | Budgerigar, 4-year-old male: Hx = Apparently Fig 4.2.8 | Cockatiel, 14-year-old male: Hx = Bird presented for board-
healthy bird, fed organic formulated diet.b Normal flora. Clinical ing, seed diet. CS = Dull feather color, retained pin feathers. FGS = 55
Signs (CS) = none. FGS = Normal distribution of organisms: bacteria per field; 90% gram-positive rods, 10% gram-positive cocci.
157 total bacteria per field, 70% gram-positive rods, 30% gram- Hyperkeratotic cell with characteristic straight sides suggests intestinal
positive cocci, 0 gram-negative bacteria, 0 yeast. Digestion of microflora imbalance, probably due to malnutrition, early liver disease.
food is complete. Rx = Conservative, diet change.
Fig 4.2.9 | African grey parrot, 4 years old, sex unknown: Hx Fig 4.2.10 | Psittacine: Iatrogenic gram-negative rods due to
= Intermittent vomiting or loose stool, not as playful. FGS = staining error. An error is suspected when the demarcation of
400 bacteria per oil field, 95% gram-positive short rods, 5% gram-positive and -negative is streaked and the groups are sim-
gram-positive rods, 0 yeast. Overgrowth of intestinal bacteria, ilar in shape and size, differing only in color. Note the presence
enterotoxemia, malnutrition. Rx = Aggressive, dietary change, of a normal intestinal epithelial cell, which is rounded and takes
antibiotics and supportive care. on a blue color. Compare this to the straight, pointed edges of
the hyperkeratotic cell in Fig 4.2.8. Rx = None.
Fig 4.2.11 | Amazon parrot, 8-year-old, female: Hx = Finicky Fig 4.2.12 | Severe macaw, 7 years old, sex unknown: Hx =
eater, occasionally grumpy. CS = Failure to molt correctly, bald- Depressed, not eating, weak. CS = Underweight, scant feces,
ing of feet, obvious layering of beak, overgrowth of nails, minor dark yellow urine and urates, malcolored feathers. FGS = 200
feather-picking. FGS = 40 bacteria per field, 90% gram-positive bacteria per field, 1% gram-positive rods, 0% gram-positive
rods, 0% gram-positive cocci, 10% gram-negative rods. (The cocci, 98% gram-negative rods. Rx = Aggressive for enteritis
normal binding of urates by protein is occasionally seen in fecal and septicemia.
gram’s stains). Rx = Conservative diet change.
121
Figs 4.2.13-4.2.18 | Fecal Gram's Stains Commonly Observed in Psittacines in Clinical Practice (oil immersion 1000x).
Fig 4.2.13 | Meyer’s parrot, 6 years old, sex unknown: Hx = Fig 4.2.14 | Ring-necked parakeet, 9-year-old male: FGS =
Diet of seeds and supplements, treated previously for “bacteria.” Scant gram-positive bacteria, occasional gram-negative, many
CS = Depressed, fluffed, poor appetite. FGS = Scant bacteria, apparent bacterial forms and colors; invasive filament of yeast
two budding yeast organisms, suggesting early malnutrition. Rx budding bi-directionally. Rx = Aggressive, antimicrobials, sup-
= Aggressive, antimicrobials, dietary change and supportive portive care, dietary correction.
care.
Fig 4.2.15 | Cockatiel, 8-year-old female: FGS = 80 bacteria Fig 4.2.16 | Umbrella cockatoo, 6-year-old female: Hx =
per field, 80% gram-positive rods, 20% gram-positive cocci; 20 Exposure to carnivorous pets, seed only diet. CS = Fetid stool,
non-budding, yeast-like structures (possibly from bakery prod- weight loss, passing undigested food. FGS = 200 bacteria per
ucts in diet, not clinically significant). Rx = None. field, 10% gram-positive rods of which 45% are Clostridium spp.,
45% gram-negative rods. Rx = Aggressive antimicrobials, sup-
portive care, dietary correction.
Fig 4.2.17 | Budgerigar, 4-year-old male: CS = Digestive Fig 4.2.18 | Moluccan cockatoo, 7-year-old male: CS = smelly
upset. FGS = 200 bacteria per field, 5% gram-positive cocci, stool. FGS = 50 bacteria per field, 90% gram-positive rods, 10%
95% gram-positive rods, of which half are large filamentous gram-positive cocci, 30 Clostridium spp. organisms. Rx =
rods. Rx = Aggressive. See Chapter 30, Implications of Aggressive (see Fig 4.2.16).
Macrorhabdus in Clinical Disorders.
Figs 4.2.19-4.2.22 | Fecal Gram's Stains Commonly Observed in Psittacines in Clinical Practice (oil immersion 1000X).
Fig 4.2.19 | Budgerigar, 3-year-old male: Hx = Frequent mas- Fig 4.2.20 | Psittacine: Various forms of gastrointestinal dis-
turbation. FGS = Presence of sperm. Rx =None. eases can be suspected if digestion of fiber or dietary ingredi-
ents is improper. Top slide = Normal fiber content of feces.
Bottom slide = Undigested fiber.
Fig 4.2.21 | Psittacine: FGS = Large amounts undigested fiber Fig 4.2.22 | Psittacine: FGS = 20 bacteria per field, 100%
(low microscopic power). gram-positive rods, lots of undigested food particles cluttering
field, suggesting some form of gastrointestinal disturbance.
123
Figs 4.2.23-4.2.27 | Fecal Samples from Free-ranging Australian Psittacines (oil immersion 1000x).
Fig 4.2.23 | Eolophus roseicapillus: 30 bacteria/field, 50% Fig 4.2.24 | Eolophus roseicapillus: 170 bacteria/field, 90%
small to medium gram-positive rods, 50% gram-positive cocci, large gram-positive rods, 10% gram-positive cocci, no gram-
no gram-negative rods, no yeast, slight debris, digested parti- negative rods, no yeast, moderate debris, digested particles.
cles, two yeast-like forms.
Fig 4.2.25 | Cacatua tenuirostris: 60 bacteria/field, 60% small Fig 4.2.26 | Cacatua tenuirostris: 90 bacteria/field, 70% small
to medium gram-positive rods, 40% gram-positive cocci, no to medium gram-positive rods, 30% gram-positive cocci, no
gram-negative rods, no yeast, moderate amount debris, gram-negative rods, no yeast, abundant debris (some not
digested particles, two circular non-cornified cells with nucleus, digested).
one pollen-like form.
Fig 4.2.27 | Cacatua tenuirostris: 15 bacteria/field, 50% large

gram-positive rods, 50% gram-positive cocci, no gram-negative
rods, no yeast, moderate amount debris (cellular and digested
particles).
Fig 4.2.28a | Fatty liver in a Mexican red-headed Amazon. Fig 4.2.28b | The feces from an obese bird will on occasion
The bird died while being restrained for grooming. The serum have a red cream-colored urate after restraint. The renal vessel
was lipemic. The veterinarian never realized long nails and beak fragility is a strong prognostic indicator of fatty liver disease.
were a sign of a problem.
Table 4.2.8 | Enzymatic Changes in Fatty

Liver Affected Birds.10,11,105
Enzyme FLHS-affected birds
Acetylcholinesterase ↑ activity
Aspartate aminotransferase ↑ activity
Aspartate transaminase ↑ activity
Glucokinase ↓ activity
Gluconeogenesis ↓ activity
Lactate dehydrogenase ↑ activity
Phosphofructokinase ↓ activity
Fig 4.2.29 | Fatty liver in a baby cockatiel fed
Sorbitol dehydrogenase ↓ activity
a commercial handrearing formula containing
excessive fat.
birds. A fatty, swollen liver that compromises the abdom- Nutritional Implications for Development of FLHS
inal and caudal thoracic air sacs can result in death from Dietary Fat
hypoxia (Figs 4.2.28a,b). Although there are some hered-
Liver fat and excess body weight (associated mainly with
itary tendencies towards the disease, nutrition plays a
an accumulation of abdominal fat) are believed to be two
major role in its development. There is little data on FLS
predisposing factors contributing to the onset of FLHS in
in caged birds and a plethora of references on FLHS (Fig
poultry.42 Unnecessarily force-feeding birds can increase
4.2.29). Because FLHS is on the decline in poultry as a
liver fat and plasma estradiol, producing FLHS.11,42 A simi-
result of such data, we offer the following discussion for
lar condition has also been observed in cockatoos and
consideration.
cockatiels fed improperly formulated diets (Fig 4.2.29).
Enzymatic Function and FLHS However, high liver lipid content alone may not be suffi-
A number of plasma enzymes increase with FLHS, such cient to cause FLS, as adequate dietary levels of lipid trig-
as AST, LDH and glutamate dehydrogenase (GDH). ger a feed-back mechanism, enhanced by dietary
These can be used as indices of the syndrome in laying starches, to prevent hepatic lipid accumulation.43a Long
hens27 (Table 4.2.8). chain fatty acids, especially those of the n-3 family are
beneficial in the diet as a preventative measure.44 Ground
Signs and Symptoms flaxseed (100 g/kg), flaxseed oil (40 g/kg) significantly
An overweight bird with a marked accumulation of fat is decrease hepatic fat.95 Safflower phospholipids decrease
a likely candidate for hepatic lipidosis. Typically these liver triglycerides (hepatic triglycerides increase with liver
birds may be considered behaviorally normal. Early signs hemorrhage score84), serum cholesterol and body
include bile pigments in the urine, changes in the fecal weight.3 Palm kernel oil at 2% of dry matter weight of
Gram’s stain and abnormal feather coloring. See Chapter diet decreases FLS.76 Palm oil is rich in vitamin E and
15, Evaluating and Treating the Liver for a further carotenoids. The vitamin E fraction (400 mg/kg) is in an
discussion. approximate ratio of 30:70 tocopherols:tocotrienols.
125
Tocotrienols have an unsaturated side chain rather than sulfhydryl groups passing through the stomach. The glu-
the saturated chain of the more common tocopherols. tathione compounds and taurine play important roles in
Tocotrienols more effectively lower cholesterol and show liver detoxification.
stronger antioxidant activity than tocopherols. See earlier
discussion under Rancidity for oxidation’s possible role SAMe production decreases with age. Dietary supple-
in FLHS in poultry. mentation may be required for older birds prone to fatty
liver disease. Without SAMe, the liver protective glu-
L-cysteine tathione cannot be synthesized. While increasing glu-
Deficiencies in essential amino acids can increase mor- tathione levels through supplementation is desirable,
tality from FLHS and may be prevented with supplemen- glutathione alone is not a substitute for the combined
tation of L-cysteine at 6 g/kg of feed.26 N-acetyl-L-cysteine actions of SAMe and glutathione.
(NAC) is the pre-crystallized form of the simple amino
acid cysteine. It is a powerful antioxidant and immune Betaine and SAMe
support substance that neutralizes the free radicals pro- Anhydrous betaine (trimethyl glycine, not to be con-
duced by normal metabolic activity. While both cysteine fused with the digestive aid betaine hydrochloride), is a
and methionine are precursors of glutathione, NAC is substance made from beet sugar that increases SAMe lev-
more effective. During digestion, approximately 85% of els. Impairment of SAMe synthetase may result in SAMe
the sulfur groups of L-cysteine are lost (these contribute being manufactured through the betaine pathway, an
to the active portions of glutathione), while only 15% alternative to the SAMe synthetase-dependent methion-
are lost from NAC, resulting in up to six times more sul- ine-plus-ATP route. Increasing levels of betaine reduce
fur groups after digestion (for detoxification). NAC is fatty infiltration and provide the precursors for the free
also a better source of glutathione than supplementation radical scavenger glutathione.
with glutathione itself, because less than half the supple-
mental glutathione leaves the digestive system for other It is recommended that SAMe supplementation in
organs. This greater efficiency is important since cellular humans for a diet comprising 16% protein range
glutathione levels tend to drop 30 to 35% with age. between 100 to 500 mg, with higher requirements in
females. Mild stomach irritation may result if not using a
S-adenosylmethionine (SAMe) product with an enteric coating. There have been no
S-adenosylmethionine (SAMe), a natural metabolite of clinical trials on the effectiveness of SAMe for birds with
the amino acid methionine, was discovered as a pharma- liver disease. Early empirical data is encouraging.
ceutical in Italy in the 1970s and has been available in
Europe for over 20 years. It is the most active of all Vitamins and SAMe
methyl donors arising from the amino acid methionine. Once a SAMe molecule loses its methyl group it breaks
While healthy livers synthesize sufficient methionine, down to form homocysteine. On its own homocysteine
liver disease can impair SAMe syntheses. On a cellular can be extremely toxic, but the presence of vitamins B6,
level SAMe maintains mitochondrial function, prevents B12 and folic acid convert homocysteine into glutathione
DNA mutations and, restores cellular membrane fluidity or re-methylate it into methionine. Deficiencies of any of
so that cell receptors become better able to bind hor- the active coenzyme forms of vitamins B2, B6, B12 or folic
mones and other factors. acid will disrupt SAMe production. Reciprocally, dimin-
ished SAMe production will impair conversion of folic
SAMe’s methyl groups make possible the production of acid and B12 to their coenzyme forms.
the “fat burner” carnitine; the neuro nutrient acetyl L-
carnitine; the primary ATP energy reservoir, creatine In order to maximize the effectiveness of the interlock-
phosphate; the stress hormone and neurotransmitter, ing SAMe pathways, the addition of the water-soluble
adrenaline; the neuro nutrient and chief membrane vitamins B2 (20 to 200 mg), B6 (40 to 400 mg), B12 (0.5
phospholipid, phosphatidyl choline; and the DNA bases to 5.0 mg) and folic acid (0.8 to 2.0 mg) is required.
methyl adenine and methylcytosine. Vitamins B6, B12 and folic acid also convert the toxic
homocysteine to glutathione or re-methylate it into
In addition to transmethylation, SAMe is involved in methionine.
transsulfuration, which begins with the by-products of
the transmethylation of S-adenosylhomocysteine (SAH). Biotin
SAH yields homocysteine, which can be converted to While low dietary protein predisposes chicks to develop
cysteine and then to a family of key sulphur biochemi- FLHS, high dietary protein can cause classical signs of
cals: glutathione, glutathione peroxidase, glutathione-S- biotin deficiency.11 Biotin is an essential coenzyme
transferase and taurine. As much as 80% of dietary cys- involved in the conversion of protein to carbohydrate
teine, low in many foods, can lose its bioactive and the conversion of protein and carbohydrate to fat.
Biotin enzymes are important in protein synthesis, whereas desthiobiotin and biotin sulfate are inhibitory
amino acid deamination, purine synthesis, and nucleic to bacteria. Biotinidase, present in pancreatic juice and
acid metabolism. Biotin itself is required for trans-car- intestinal mucosa, releases biotin from biocytin during
boxylation in the degradation of various amino acids; it the luminal phase of proteolysis. Physiological concen-
also plays an important role in maintaining normal trations of biotin are absorbed from the intestinal tract
blood glucose levels when dietary intake of carbohydrate by a sodium-dependent active transport process, which
is low. Biotin deficiency is most severe in young chicks is inhibited by desthiobiotin and biocytin.92
of heavier strain and greater rate of weight gain;8 pro-
moting higher growth rates in psittacines may predis- Cecal microorganisms do not supply chickens with sig-
pose birds to FLS. nificant amounts of biotin; they compete with the host
animal for dietary biotin, thereby increasing the require-
Many of the problems associated with biotin deficiencies ment. In poultry, polyunsaturated fatty acids, ascorbic
and FLHS result from biotin’s role as a cofactor for many acid, and B vitamins may influence the demand for
enzymes. These include: a decreased rate of lipogenesis; biotin. Biotin is rapidly destroyed as feeds become ran-
depressed gluconeogenesis from lactate and glycerol; an cid, with 96% inactivation occurring in as little as 12
increase in the activities of fatty acid synthase (FAS), cit- hours if linoleic acid of a high peroxide number is
rate cleavage enzyme (CCE) and phosphokinase11; added to the diet. Supplementary choline in biotin-defi-
abnormal fatty acid composition of infiltrated lipid, with cient diets decreases biotin status in chicks and increases
an increased proportion of monounsaturated fatty acids; mortality from FLHS.105 The use of sulfa drugs can also
severe hypoglycemia; and depleted hepatic glycogen.105 induce a deficiency. Conversely, α-tocopherol decreases
Low fat or protein levels that increase the metabolic rate inactivation of biotin.
of biotin-dependent enzymes (pyruvate, acetyl CoA car-
Minimum biotin requirements have been established for
boxylase) aggravate the condition. Biotin also serves as
a number of commercial species, with higher require-
part of the prosthetic group, a transient carrier of CO2,
ments for turkeys compared to chickens (NRC, 1994).
and is required for normal long-chain unsaturated fatty
The minimum dietary requirements of 120 µg/kg dietary
acid synthesis and is important for essential fatty acid
dry matter determined for poultry increases to 160 µg/kg
metabolism.59 FLHS is generally worsened by a high pro-
in order to prevent fatty liver development and as high
portion of long chain saturated fatty acids.48
as 240 µg/kg when sunflower seed meal is a dietary com-
ponent.75 Incorporation of 2% palm kernel oil can
Biotin deficiencies can result from a dietary deficiency of
reduce the prophylactic dietary biotin requirements
biotin or other factors that impact on the stability of
down to 120 µg/kg.76
biotin. The richest sources of biotin include: royal jelly,
liver, kidney, yeast, blackstrap molasses, peanuts and Choline
eggs, while poor sources include: corn, wheat, other Choline plays an essential role in fat metabolism in the
cereals, meat and fish. However, the chemical form of liver. Choline prevents abnormal accumulation of fat by
biotin (bound or unbound) as well as its overall content promoting fat’s transport as lecithin or by increasing the
in feed is important, as less than one-half of the biotin in utilization of fatty acids in the liver itself. While conver-
various feeds is biologically available. Starvation of birds sion to betaine is required before choline can be a
can lower liver biotin levels, leading to an increase in methyl donor, betaine itself fails to prevent FLHS. The
liver weight and lipid content.10 The addition of raw egg addition of choline can decrease the amount of fat in the
white also decreases biotin availability as the proteina- liver. Diets high in fat exacerbate choline deficiencies,
ceous avidin binds very tightly to biotin. While low mor- thus increasing the dietary requirement. This is particu-
tality is seen in broilers fed freeze-dried egg white at larly important for chicks, as they are unable to synthe-
11.8 g/kg, mortality is high if dietary concentrations size choline until approximately 13 weeks of age.68
exceed 17.7 g/kg. However, mortality increases in chickens that are supple-
mented with B vitamins (other than biotin), with higher
Not all forms of biotin are equivalent in their action; mortality if choline is also supplemented.105 Only 57% of
biotin contains three asymmetric carbonations, with biotin in multivitamin premixes68 is retained if the sup-
eight different isomers. Only the isomer d-biotin con- plement contains choline.
tains vitamin activity; the stereoisomer l-biotin is inac-
tive.59 Biotin is inactivated by rancid fats and choline 97 Normal dietary choline requirements for poultry range
and gradually destroyed by ultraviolet radiation. from 800 to 2,000 mg/kg. Choline is largely absent in
Structurally related analogues of biotin can vary in activ- fruit and vegetables and is low in corn. Wheat, barley
ity from anti-biotin activity, to no activity, to partial and oats have higher levels of choline. Peanuts are a
replacement.7 Oxybiotin has 1/3 biotin activity for chicks good source of choline as are cereal germs, legumes and
127
Table 4.2.9 | IDC and Iron Storage Disease

Nutritional Imbalance→ High iron content diet, presence of vitamin C and excess vitamin A
CLINICAL SIGNS
Insectivore/Frugivores Parrots
Early Early
• Listless • None - most common
• Respiratory wheeze or click • Found on necropsy
• Decreased exercise tolerance • Intestinal cellblock is saturated
• Sudden death Chronic
Chronic • Sudden death
• Swollen coelomic cavity
• Dyspnea with forward leaning posture
Diagnostics Diagnostics
• Radiology • Liver biopsy
- Pericardial effusion
- Hepatomegaly
• Ultrasound
• Endoscopy and biopsy (caution due to potential
coagulation disorders)
Treatment Treatment
• Low iron diet <80 mg/kg • Low iron diet <80 mg/kg
• Avoid vitamin C and excess vitamin A • Avoid vitamin C and excess vitamin A
• Iron chelator
• Black tea
• Phlebotomy
Table 4.2.10 | Avian Families Diagnosed

with ISD20,25,35,36,57,70a,91,107* antioxidants that increase levels of glutathione and pro-
Order Family Common Name tect the liver from oxidative damage. They may promote
Passeriformes Sturnidae Mynahs/starlings, tanagers growth of new, healthy liver cells.32,85 While clinical trials
Paradisaeidae Birds of Paradise in birds have not been undertaken to evaluate the effec-
Galliformes Cracidae Guans, currasows
tiveness of silymarin, it has proven effective empirically
Ciconiformes Ardeidae Bitterns
when administered twice daily to birds with liver disor-
Trogoniformes Trogonidae Quetzals
ders. See Chapter 10, Integrative Therapies, Chapter 9,
Piciformes Rhamphastidae Toucans, toucanettes, aracari
Ciconiformes Phoenicopteridae Roseate flamingos
Therapeutic Agents and Chapter 15, Evaluating and
Psittaciformes Loridae Lories Treating the Liver for further information.
Psittacidae Lorikeets
Parrot/cockatoos Environmental Influences
*See Chapter 4, Nutritional Considerations: Section I, Nutrition and
Dietary Supplementation for further discussion While nutritional imbalances are the main factors con-
tributing to both FLS and FLHS, stress alone can initiate
FLHS. When birds are subjected to mild stress and/or
oilseed meals. Choline needs of poultry fed wheat-based
short-term fasting, liver glycogen reserves become rap-
diets are much lower than those fed on other grains.
idly depleted and a progressive hypoglycemia develops
Wheat and sugar beets are high in betaine, which can
that can prove fatal. Stress-associated lipogenesis
spare choline for some reactions.
increases cholesterol synthesis and converts excess glu-
Vitamin E cose to fatty acids, which are stored as triglycerides.
Vitamin E powerfully combats the peroxidation of
Pesticides
polyunsaturated fatty acids in the liver. Daily supplemen-
While pesticide levels of individual ingredients may be
tation of 100 to 400 IU Vitamin E in conjunction with
deemed safe, a combination of a variety of pesticides or
low dietary vitamin A is recommended for birds suffer-
an accumulation of pesticides in tissues can result in
ing from FLHS. See earlier discussion of rancidity for
pesticide toxicity. Polychlorinated biphenyls (PCBs)
possible role of fat-soluble vitamin destruction and
increase liver and body weights of birds associated with
FLHS.
FLHS and can increase total cholesterol103. Many pesti-
Silymarin (Milk Thistle) cides have estrogenic actions; high estrogen levels are
Silymarin is a collective group of polyphenolic flavano- associated with FLHS.42 These estrogenic pesticides
lignans extracted from the seeds of the milk thistle mimic the action of normal endogenous hormones and
(Silybum marianum). The flavanoids are powerful influence ovarian function. A combination of estrogen
and excess dietary energy create sufficient fat deposition iron in various tissues, with the liver most frequently
in the liver for FLHS to occur.89 involved. In severe cases, iron pigment is found in the
liver, spleen, gut wall, kidney and heart; this leads to
Summary of Fatty Liver Disease subsequent development of ascites, heart failure and
multisystem pathology.25 Iron may be found within the
A variety of nutritional factors are implicated in the devel-
Kupffer cells in the liver36 and the macrophage cells of
opment of FLS and FLHS in chickens, but many are
the spleen, especially where concurrent diseases, such
avoidable by providing a nutritionally balanced diet.
as hemolytic anemia, septicemia, neoplasia or starvation,
Some factors are exacerbated by other dietary ingredi-
are present.25
ents, environmental stimuli or infectious diseases.19 While
the name of the disease, “fatty liver (hemorrhagic) syn- The syndrome of excessive iron overload in mynahs
drome,” implicates dietary fat levels as causative factors, shares most of the important histopathologic characteris-
there are many other dietary components that are impor- tics with idiopathic hemochromatosis in human beings.
tant and warrant further consideration. We feel this Iron storage disease has been correlated with immuno-
model may serve the captive parrot industry well, as logical stress,25,36 as well as crowded conditions.53
empirically the same corrections seem to apply. Reduced peristalsis or neuropathic gastric dilatation may
increase iron absorption.36 Stress increases lipid peroxi-
IRON STORAGE DISEASE dation and diminishes vitamin E levels, resulting in a
lower level of antioxidant activity. Iron and vitamin E are
Iron storage disease (ISD) is prevalent in many frugivo-
involved in electron transfer in reduction/oxidation
rous and insectivorous birds maintained on commer-
cycles; a dietary surplus of either iron or vitamin A
cially formulated foods (Table 4.2.9). Iron storage disease
decreases the α-tocopherol concentration. Therefore,
differs from one of its precursors53, hemosiderosis,
any impact on vitamin E levels may reduce the protec-
which is defined as the excessive accumulation of iron
tion of biological membranes against oxidation. In addi-
(hemosiderin) in hepatocytes or in free circulation in
tion, diets high in saturated fats increase iron absorp-
the blood, without alteration of normal tissue morphol-
tion.79
ogy or damage to any of the major organs. Various fac-
tors have been implicated in the development of this
disease, including genetic predisposition, immunological Nutritional Implications for ISD
stress, nutritional inadequacy and viruses; dietary iron Highly frugivorous or highly insectivorous birds have
content has been the main focus of nutritional investiga- adapted to foods low in iron (fruits and insects). The
tions. The causative factors of ISD have been addressed high vitamin C content of many fruits enhances iron
by several authors.29,36,70a Further studies on the interac- uptake from iron deficient diets. Consequently, high
tions of dietary sugars, copper and iron metabolism have dietary iron has been implicated in the development of
been proposed.87 The discussion here will be confined the disease and it is generally recommended that iron
to nutritional implications in the development of ISD. content of commercial diets be maintained below 100
There is a high correlation with commercially formu- mg/kg53, and in mynahs 19 to 25 mg/kg.29,94 However,
lated foods and ISD. Table 4.2.10 highlights a number of birds have been maintained on commercial foods that
avian families in which the disease has been reported. reflect the high values of iron in some dietary compo-
nents of wild toucans78 (150 mg/kg) with no evidence of
While iron is essential for fundamental cell functions, it iron storage disease. Diet is not implicated in the devel-
is also a catalyst for chemical reactions involving free opment of ISD in the Rothschild mynah.
radical formation that can lead to oxidative stress and
cell damage. Uptake of iron from the diet is regulated in
Vitamin A and Iron Uptake
the intestine, so acute intoxication is not observed
under natural conditions. Cellular iron levels are gener- Some commercially formulated products have high vita-
ally regulated to maintain adequate substrate levels min A content (see Chapter 4, Nutritional Considera-
while minimizing the pool of potentially toxic ‘free iron.’ tions, Section I Nutrition and Dietary Supplementation).
The main control of body iron homeostasis is in the These high vitamin A levels are in contrast to the low
duodenum where dietary iron is absorbed, but no con- vitamin A content of fruits and insects. Vitamin A from
trolled means of eliminating unwanted iron has evolved plants arises from conversion of carotenoids, a regulated
in animals. Consequently, chronic ingestion of large process that avoids potential vitamin A toxicity.
amounts of absorbable iron can lead to the storage of Productivity of psittacines increases when birds are
iron in the liver in many species. transferred to formulated diets low in vitamin A but high
in carotenoids.67 Additional vitamin A is either supplied
Iron storage disease results from the accumulation of from plant based carotenoids in the diet or else it may
129
Table 4.2.11 | IDC and the Respiratory System
Nutritional Imbalance → Squamous Metaplasia of Respiratory Epithelium
CLINICAL SIGNS
Oral/Rhinal Sinus Trachea/Lungs Air Sacs
• Blunting or loss of choanal papillae • Infraorbital swelling • Voice change or loss • Increased panting
• Increased mucus viscosity • Respiratory wheeze or click • Decreased exercise tolerance • Decreased exercise tolerance
• Serous rhinal discharge • Lacrimal duct infection or • Dyspnea with forward leaning • Mild, intermittent tail bob
• Sneezing, scratching nares impaction posture • Chronic
• Chronic • Chronic • Chronic - Secondary air sacculitis:
- Rhinolith formation: - Secondary sinusitis: - Tracheal obstruction: Aspergillus is commonly
Can be sterile, bacterial, or May be bacterial or fungal Often Aspergillus granuloma isolated
fungal. Dark discharge =
hemoccult+
TREATMENT
Diagnostics Medical Treatment Environmental Concerns
• Endoscopy (tracheal, coelomic for air sacs) • Debride rhinoliths • Proper humidity
• Cytology of respiratory exudate • Nasal/sinus flushes as needed • Adequate ventilation of enclosure
• Culture and sensitivity of exudate • Infraorbital sinus drainage as needed • Filtration of ambient air
• Radiology • Nebulization, this can be utilized for humidity, (medical grade filters)
• Hematology mucolytic agents, • Avoidance of exacerbating aerosols:
• Biochemistry or antimicrobial therapy delivery - cigarette smoke
• Serology (aspergillosis) • Systemic treatment of secondary - perfumes
infections - Aspergillus - cockatoo dust
• Diet correction - (see Fig 4.2.7: see diet conver- - pollens
sion challenges at end of chapter)
Recurrent or chronic respiratory infections are common with chronic IDC and marked changes in the respiratory epithelium.
be inferred that birds have an overall low requirement damage by Fe++-catalyzed lipid peroxidation during vita-
for vitamin A. The incidence of ISD is negligible in these min E deficiencies.62 It is two-fold more effective than ß-
birds. carotene in inhibiting production of lipid peroxidases.39
Peridinin, another carotenoid of marine micro algae,
Low serum retinol is associated with mild anemia in limits oxidative damage on iron-liposomes, possibly by
adult humans.30 Retinol also plays a role in increasing decreasing membrane permeability to initiators.12 While
levels of hemoglobin in children, especially those on
the direct benefits of the blue-green algae Spirulina
iron supplementation.2,63 Dietary iron also influences
platensis have not been evaluated in birds, the phyco-
conversion of ß-carotene to retinol by enhancing ß-
bilins (phycocyanins and allophycocyanin) of S. platensis
carotene 15,15’-dioxygenase activity in the small intes-
act as potent free-radical scavengers (hydroxyl and per-
tinal mucosa of rats.31 High levels of dietary vitamin A
oxyl) and inhibit microsomal lipid peroxidation in
may negatively influence availability of other fat-soluble
humans.88 Dietsb, low in vitamin A and containing micro
vitamins such as vitamin E.
algae, have demonstrated improvements in health and
In contrast to vitamin A, the presence of carotenoids in productivity of large psittacines.67
microsomal membranes partially inhibits the loss of
Canthaxanthin is a carotenoid compound that is supple-
α-tocopherol, especially during the late phase of oxida-
mented to promote feather pigmentation in flamingos
tive stress when ß-carotene decreases phospholipid
and scarlet ibis. A recent study suggests that canthaxan-
hydroperoxide production.73 However, despite its benefi-
thin can substantially alter the antioxidant status of
cial antioxidant activity, ß-carotene, like vitamin A, can
murine liver tissue in vivo. In mice, canthaxanthin
increase the absorption of iron by preventing the
reduces both cellular content of lipophilic antioxidants
inhibitory effect of phytate and tannins on iron absorp-
and the activity of enzymatic antioxidants, as well as
tion by forming complexes with iron that maintain solu-
increasing iron concentrations in the liver by up to 27%.
bility in the intestinal lumen.62
ISD has been diagnosed in flamingos.20 The addition of
The antioxidant activity of the different carotenoids is canthaxanthin to the diets of these birds may alter the
variable. The inhibitory effect of ß-carotene on the pro- protective ability of tissues against oxidative stress in
duction of lipid peroxidases is less than that of the vivo and increase iron storage in the liver. The
extremely potent antioxidant astaxanthin from marine carotenoid canthaxanthin is associated with eye and liver
micro algae. Astaxanthin protects the mitochondria from damage in humans.
Fig 4.2.30 | An old female budgerigar with IDC, Fig 4.2.31 | Liths in the bronchial syrinx area or the air ostium
chronic rhinorrhea and secondary rhinal infection to the lungs often become secondarily infected with yeast or fun-
with yeast and/or bacteria. gal spores. This lesion was taken from a free-ranging Major
Mitchell’s cockatoo.
Table 4.2.12 | IDC in Geriatric Budgeriagar with Goiter
History Clinical Signs Treatment
• Diet • Regurgitation • Dexamethasone
Seed based • Crop mucus accumulation (if severe)
• Dyspnea • Iodine
• Swollen thyroid • Diet change
Summary of ISD the cul-de-sacs of the infraorbital sinus or the layering of

the rhinal cavity under the operculum. In the case of the
While diets low in iron are advocated for birds susceptible
sinus, they may act as one-way valves causing the cervic-
to ISD, the high vitamin A content of commercially formu-
ocephalic air sac to hyperinflate. In the rhinal cavity, the
lated foods may also be implicated in the development of
accumulation leads to rhinitis or rhinorrhea (often con-
the disease. It is recommended that diets low in iron, vita-
taining blood). The liths in the bronchial syrinx area or
min A and saturated fats be presented to birds susceptible
the air sac junction to the lungs can become secondarily
to this disease in addition to supplementation with vita-
infected with yeast or other fungal spores (Fig 4.2.31).
min E. Furthermore, high levels of dietary ß-carotene may
Recent reports from Europe indicate this is a common
be detrimental. Vitamin A activity should be provided
respiratory sign seen in African greys with circovirus.
from other carotenoid sources, especially those present in
blue-green algae, such as Spirulina platensis. Frugivorous Liths are not confined to the respiratory tract. They can
species should be provided with fruits low in vitamin C to accumulate in the bile duct. When flecks of liths partially
minimize uptake of iron from commercial diets. Recent obstruct the duct in cockatiels, the duct balloons to
recommendations on the use of tannins from tea to tie up resemble a gall bladder. Liths in the kidney are often
iron have shown promise. It is evident that further associated with gout. In the uterus, they can form egg-
research on this topic is required. like structures of various sizes and shapes.
RESPIRATORY SYSTEM BUDGERIGAR GOITER

Loss of function of epithelial tissue is a problem in the It has been common knowledge since the 1950s, that
respiratory system because loss of cilia and mucus pro- budgerigars (Melopsittacus undulatus) develop goiter
duction decreases cleaning capacity (Table 4.2.11). In on a seed diet low in iodine. Table 4.2.12 shows the typ-
chronic cases, serum oozes from endothelial ulcerations ical scenario. The bird may only show obesity. Most com-
and provides a culture media for bacteria, yeast or other mon clinical presentations are “vomiting” (regurgitation)
fungi (Figs 4.2.30-4.2.31). The nares can reflect the inter- of a thick liquid (mucus) that accumulates on the feath-
nal condition. ers of the head. Respiratory sounds (squeaking) from
impingement on the syrinx by the swollen thyroid are
Liths that roll up to form “balls” can develop from also a frequent complaint. While diagnostic tests are
desquamated epithelial cells when proper cleaning func- possible, they are seldom used due to their expense and
tion has not been maintained. These balls may randomly the ease of diagnosis using response to treatment.
accumulate in such places as the connection between Dexamethasone may speed the response to injectable
131
Table 4.2.13 | Influence of Prostaglandins on Renal Function cause extensive renal damage, have also been associated
PGE2 Prostacyclin TBXA2 with vitamin A deficiency leading to gout.58
Vasodilation ↑ ↑
Vasoconstriction ↓ Dietary lipids have been implicated in the progression of
Renal blood flow ↑ ↑ ↓ chronic renal disease, especially in relation to a change
GFR ↑ ↑ ↓ in the balance of renal prostaglandins. A diet rich in
Platelet function ↑ ↓ arachidonic acid leads to a predominance of PGE2,
prostacyclin and thromboxane A2 (TBXA2), resulting in a
shift toward greater vasodilatation and less platelet
iodine by decreasing thyroid swelling and may be life aggregation (Table 4.2.13). For further discussion on this
saving in severely dyspneic birds. Complete recovery is topic, see Chapter 16, Evaluating and Treating the
insured by adding iodine to the water or seeds. Since Kidneys. The effects of excess vitamin A and/or D are dis-
other deficiencies will soon manifest on such a diet, only cussed in Section I of this chapter.
geriatric birds and birds that refuse to convert to formu-
lated diets are treated by iodine supplementation alone.
CARDIOVASCULAR DISEASE
INGLUVITIS Atherosclerosis
Baby psittacines from parents on seed-based diets com- Atherosclerosis is problematic for psittacines in captiv-
monly are plagued by ingluvitis. Seed-based malnutrition ity52 that are provided with high-fat diets and little exer-
is the primary cause and can be prevented with formu- cise compared to their free-ranging counterparts.
lated diets. Secondary invaders (yeast and Atherosclerosis involves the deposition of cholesterol
Enterobacteriaceae) may require specific antimicrobials within the innermost lining of the arteries and subse-
and resemble liver and gastrointestinal disorders caused quent inflammatory response and fibrosis. While choles-
by the same agents. In these latter conditions, crop terol-lowering agents and dietary changes are treatment
atony followed by ileus is not unusual, especially in mainstays in humans, the development of the disease
cockatiels. These birds are very difficult to cure and fre- may be prevented in birds with nutritionally balanced
quently suffer a prolonged wasting type malaise. See diets containing antioxidants.
Chapter 7, Emergency and Critical Care and Chapter 14,
Damage to the endothelial lining of the internal surfaces
Evaluating and Treating the Gastrointestinal System, for
of the heart increases permeability to lipoproteins and
further discussion.
macrophages. Increased endothelial permeability leads
to the accumulation of lipoproteins within the suben-
RENAL DISEASE dothelial space, which initiates the formation of athero-
Excesses of dietary protein and the accumulation of sclerotic plaques. The oxidation of lipoproteins retained
waste products derived from the catabolism of protein within the subendothelial space is responsible for the
result in uric acidemia and to a lesser degree, uremia, inflammatory response seen in atherosclerosis.
in birds. Excessive dietary protein is catabolized to uric Lipoprotein oxidation is a necessary step in the develop-
acid and other nitrogenous compounds normally ment of atherosclerotic plaques; the oxidation of low-
excreted by the kidneys. Decreased renal function leads density lipoprotein (LDL) is implicated in lesion forma-
to accumulation of these compounds. One goal of tion in the aorta. Vitamin A can attenuate the oxidation
nutritional therapy is to achieve nitrogen balance by of LDL and consequently minimize or even reverse aor-
proportionally decreasing protein intake as renal func- tic plaque development and endothelial dysfunction.
tion declines, except in cases of protein losing
nephropathy. Oxidants are produced by the normal metabolic functions
of the endothelium, macrophages, and smooth muscle of
Gout is associated with the deposition of a white chalky the arterial wall. Lipoproteins that accumulate within the
substance (urate) on body organs (visceral), in joints subendothelial space are exposed to these cellular oxi-
(articular) or in ureters (renal). Urates are the end prod- dants. Although a small degree of lipoprotein oxidation
ucts of protein metabolism in birds. Their accumulation may occur during circulation, most lipoprotein oxidation
impairs the function of key organs and can eventually be occurs within the arterial wall. It is therefore noteworthy
fatal. While excess dietary protein has been implicated in that lipoproteins are themselves enriched with antioxi-
the increase of serum uric acid, birds are usually able to dants such as vitamin E, coenzyme Q10 (ubiquinone) and
excrete excesses.58 However, fasting, dehydration or a carotenoids. Water-soluble antioxidants found in the
diet deficient in lysine may increase serum uric acid. plasma, such as vitamin C, may also be important in pre-
Alterations to normal elimination of uric acid, which can venting oxidation of lipoproteins in the circulation.
In a recent abbreviated study, two high fat and two low duction of commercial pet foods degrades B6.
fat diets were fed for periods of 24, 28 and 32 days.
Results showed that palm kernel oil (derived from the Coenzyme Q10 (CoQ10)
seed) produced significantly higher levels of plasma cho- Coenzyme Q10 is an antioxidant that plays a role in mito-
lesterol and phospholipid concentrations than did sun- chondrial function. A deficiency of CoQ10 is correlated
flower oil.13 No conclusions on the effect on atheroscle- with deterioration in heart function. CoQ10 is similar in
rosis could be drawn. The authors had previously shown structure to vitamin K and can interfere with the blood-
84% sudanophilic staining levels in aortas of parrots pre- clotting mechanism. Studies with humans indicate that
sented for necropsy.14a The authors recommended diets supplementation at 2 mg/kg body weight reduces symp-
of up to 10% fat on a dry matter basis. toms associated with cardiomyopathy and heart failure.
ß-blockers and cholesterol-lowering drugs from the
Nutritional Supplementation for the Treatment of statin family can interfere with the body’s production of
Atherosclerosis CoQ10.
In studies on humans, palm oil (derived from the fruity
coating outside the seed), which is distinct from palm Carnitine
kernel oil, has proven beneficial in the treatment of Carnitine is a small, water-soluble, vitamin-like quater-
atherogenesis. Palm oil is very rich in carotenes, vitamin nary amine found in high concentrations in mammalian
E and coenzyme Q10. The cholesterol lowering action of heart and skeletal myocytes. L-carnitine is synthesized
palm oil is attributed to its high vitamin E content, espe- primarily in the liver from the amino acids lysine and
cially the tocotrienol fraction. A typical palm oil vitamin methionine. Long-chain fatty acids are important for
E concentrate contains up to 30% α-tocopherol and 70% maintaining a constant energy supply to the heart.
mixture of different tocotrienol isomers (20% α- Carnitine is a critical component of the mitochondrial
tocotrienol, 20% γ-tocotrienol, 40% α-tocotrienol, 10% δ- membrane enzymes that transport activated fatty acids.
tocotrienol and 10% others).49 In addition to its role in fatty acid transport, free carni-
tine serves as a mitochondrial-detoxifying agent. Because
Cardiomyopathy of the high-energy requirements of the heart muscle, it
Cardiomyopathy has been associated with a number of is particularly vulnerable to carnitine deficiencies. A
disease entities including malnutrition, as the pathogen- recent report shows the potential for L-carnitine to
esis in birds is similar to mammals, it is possible that reduce the percent body weight and lipoma size in
similar nutritional inadequacies are implicated. While budgerigars.14c
supplementation levels have not been established for
birds, studies of mammals indicate that supplementation
OPHTHALMIC DISORDERS
with taurine, vitamin B6, coenzyme Q10 and carnitine are
helpful. Cataracts
Taurine While causative factors have not been identified clearly,

Taurine is an essential amino acid in cats as they have a cataracts have been described in aging macaws.24
limited ability to synthesize taurine from cysteine and Nuclear cataracts associated with aging occur in the cen-
methionine. Because there are many physiological simi- ter of the lens. The nucleus of the lens is particularly
larities between carnivorous birds and felines, it is possi- sensitive to nutrient deficiencies. Nuclear cataracts are
ble that taurine deficiency is implicated in the develop- associated with deficiencies in the fat-soluble vitamins A
ment of cardiomyopathy in carnivorous birds, especially and α-tocopherol and the water-soluble vitamins B2
those provided with commercial dog foods that are typi- (riboflavin) and B3 (niacin). Carotenoids have potent
cally low in taurine. Plasma taurine concentrations can antioxidant activity with marginal inverse associations
be influenced by food intake and food deprivation. between the carotenoids lutein and cryptoxanthine and
Whole blood concentration is a more reliable index of the development of nuclear cataracts. Riboflavin is
taurine status, as this only declines after prolonged peri- important in the production of glutathione peroxidase;
ods of depletion. While taurine levels for cats (plasma deficiencies in glutathione peroxidase have been corre-
<20 to 30 nmol/ml; whole blood <150 nmol/ml) are lated with cataracts. Selenium and vitamins C and E are
indicative of dietary deficiencies, similar data is not avail- also helpful in preserving glutathione levels. However,
able for carnivorous birds. supplementation with selenium is not recommended as
cataracts have been correlated with both deficiencies
Vitamin B6 and excesses of this trace mineral. Taurine deficiency
Mild deficiencies in vitamin B6 can interfere with taurine (particularly in animals fed heat-processed diets) has
conversion. The heat treatment associated with the pro- also been correlated with cataracts.
133
Table 4.2.14 | The IDC and the Reproductive System
History Signalment Diagnosis Treatment

Diet Eggs Blood • Treat specific disorder
• Seeds, nuts, produce, • No eggs, small clutches, • Increased cholesterol, Diet
supplemental vitamins, soft/rough-shelled eggs, hyperlipidemia • Nutritionally balanced formulated
table foods infertile eggs Diet Change organic foods, limit supplements:
Hatchlings • Response takes up to a year low sugar produce
• Failure to hatch, (need assistance), Reproductive Tissue - Breeding Birds: 5-10% high fat
early neonatal death, bent • Culture uterus, biopsy uterus/testis, items (sunflowers seeds, nuts)
legs/beaks, crop/digestive endoscopy (cystic ovaries) sugary fruits & vegetable (neces-
disorders, require hand raising Eggs sary for breeding stimulation)
(from day 1) • Necropsy, culture Genetics Cockatiels
Adults • Choose birds that are not chronic
• Egg binding, masturbation, regur- egg layers
gitation, nest building, mate muti- - Deplete body stores of nutrients
lation • Hormone therapy
Salpingohysterectomy
The cortical cataract occurs in the cortex of the lens and a Psittacine Behavior for a table of foods hypothesized to
subcapsular cataract starts as opacity under the capsule, be stimulatory.
usually at the back of the lens. The prevalence of cortical
cataracts is reduced in the presence of polyunsaturated Protein and Amino Acids
fatty acids. Insufficient n-3 fatty acids or excess saturated
Amino acid requirements increase at least one week
or ‘trans’ (hydrogenated) fats may impact on the progres-
prior to the first oviposition for growth of the oviduct
sion of eye disease. While high levels of α-tocopherol
reduce the risk of nuclear opacity, medium levels are asso- and accretion of egg proteins. While overall protein
ciated with a reduced risk of cortical opacities. requirements for birds laying small clutches may be little
more than maintenance requirements, a deficiency in
Macular Degeneration essential amino acids may increase overall protein
requirements. Budgerigars maintained on seed-based
While macular degeneration has not been reported in
diets that provided only half the lysine, methionine and
birds, there are different kinds of macular problems. In
cysteine required, produced fewer hatchlings, fledglings,
other animals the most common is age-related macular
fertile eggs, and total eggs.4
degeneration. Zinc deficiencies can exist in older birds
from poor absorption from food. Zinc is highly concen-
trated in the eye, particularly in the retina and tissues Vitamins
surrounding the macula. Zinc is necessary for the action Fat-soluble vitamins can influence breeding potential; a
of over 100 enzymes, including chemical reactions in the reduction in vitamin A and E reduces antioxidant func-
retina. While zinc supplementation may be beneficial if tion and increases exposure of lipid-rich tissues to per-
there is a dietary deficiency or malabsorption problem, oxidation. Both deficiencies and excesses of Vitamin A
excess zinc may also interfere with other trace minerals influence epithelial integrity. The resulting hyperkerato-
such as copper. The xanthophylls lutein and zeaxanthin sis can influence mucin production as well as proper
selectively accumulate in the macula, providing what is tone and elasticity of reproductive tissue. Vitamin A defi-
known as the macular pigment. Singlet oxygen produc- ciencies can result in failure of spermatogenesis,
tion in the eye can be increased by UV light exposure,
decreased size of testes and decreased sexual activity in
but this is yet to be established in birds. It is assumed
males.
this increased oxidative damage is due to increased free
radicals in the retina. Lutein and zeaxanthin are scav- Dietary excesses of vitamin A may negatively influence
engers of these free radicals. Anti-oxidants (vitamin A, C reproductive output of birds. Improved productivity has
and E) may also help slow down macular degeneration been recorded in a variety of larger psittacines main-
and other aging factors associated with activated oxygen
tained on diets low in vitamin A and high in vitamin E.67
from exposure to light, but this has yet to be established.
A study of blue and gold macaws (Ara ararauna) high-
lights the importance of maintaining breeding birds year
REPRODUCTIVE SYSTEM round on nutritionally balanced diets. Productivity sig-
Various reproductive problems can be caused by a nutri- nificantly decreased when birds were transferred to
tionally imbalanced diet (Table 4.2.14). A high fat and seed-based diets during the nonbreeding season.67
sugar based diet is strongly suspected to be involved in Maternal diets can influence nutrient transfer to
the overly stimulated breeding bird. See Chapter 3, embryos, as well as the antioxidant status of the devel-
Concepts in Behavior, Section III Pubescent and Adult oping embryo and hatchlings.
Table 4.2.15| Action of Pesticides at a Cellular Level whelmed by the inoculum.64 This is another area that, if
Action Result Pesticide proven, shows the value of the microflora to the body.
Altered membrane Interferes with fluid and DDT
integrity electrolyte movement Pyrethrins
Altered cell volume Alters energy metabolism, Dinitrophenol ADVERSE FOOD REACTIONS
regulation reducing energy availability Chlorophenol
to drive active transport fungicides
systems, synthesis of Arsenates
Food Allergies
macromolecules and main- Tin fungicides
tenance of osmotic balance
The bird should undergo a complete physical examina-
Results from Abnormal accumulation of industrial tion including appropriate diagnostics to look for any
metabolic defects lipids and pigments estrogenic wastes underlying pathology, which may be exacerbated by or
Alteration of protein Denaturation or inactiva- Oxalic acid
in addition to the suspected food allergy. Not all dermal
synthesis tion of enzymes Fluoroacetate problems are related to nutritionally imbalanced diets as
Organophosphates
Carbamates some birds, like cats and dogs, have allergic reactions to
Disturbance of DNA damage that is not Damage certain dietary ingredients. Advanced stages often result
growth regulation properly repaired or documented but
exceeds homeostatic control not the cause
in feather picking and self-mutilation. While early signs
of these food allergies are yet to be described, failure of
nutritional therapy may warrant skin allergy testing
Lipids and/or a simplified organic dieta where ingredients such
While obesity can be detrimental to breeding birds, an as corn and sunflower seeds are eliminated. While these
imbalance of essential fatty acids is also problematic. ingredients have been incriminated in the development
Linoleic acid (n-6) typically reduces liver fat and of dermal disorders65, they are regularly included in both
improves egg production.42,43a It is preferentially retained formulated and homemade diets as primary ingredients
by laying hens. Conversely, high levels of linolenic acid with no reports of digestive disorders. Organic formu-
reduce egg production in laying hens.1 lated diets are free from pesticide residues and preserva-
tives that could be potentially allergenic. Common aller-
Typical fatty acid profiles of chicken spermatozoa display gens for mammals (wheat, gluten, egg and dairy prod-
considerable resistance to manipulation by dietary ucts) should also be eliminated from sensitive birds,
means.56 Dietary supplementation of docosahexaenoic although no proof exists they are a problem. A commer-
acid (DHA) may inhibit synthesis of n-6 fatty acids in the cial organic mash dieta is composed of the following
testes23 resulting in an accumulation of DHA, a concur- ingredients: buckwheat, hulled gray millet, hulled white
rent decrease in vitamin E concentrations, and increased (proso) millet, spirulina, chia, alfalfa, clay, sea kelp,
susceptibility to lipid peroxidation. While supplementa- anise, natural sources of vitamins, minerals and trace
tion with n-3 fatty acids may be beneficial for the treat- minerals. (Can be wrapped in thin slices of banana for
ment of inflammatory diseases (see Chapter 16, feeding). This mash has been clinically correlated with
Evaluating and Treating the Kidney), it may influence the abatement of pruritis in several birds suspected to
fertility by impacting the integrity of the component fatty be suffering from food allergies. Once the mash has
acids in the spermatozoa’s phospholipid membranes. been accepted, the proportion of banana can be gradu-
ally decreased until eliminated. However, a bird could
Sperm output generally decreases with age, but this potentially be allergic to any dietary ingredient.
decrease can be prevented by supplementing diets with
oils rich in either arachidonic acid or DHA, in conjunc-
tion with vitamin E (200 mg/kg). Testes mass can also be
DIETARY ANTIFEEDANTS AND
increased up to 1.5 times in aging birds when supple-
XENOBIOTICS
mented with essential fatty acids. However, supplemen- As the practice of organic farming diminishes the detri-
tation with linoleic acid in the absence of vitamin E can mental impact of pesticides on wildlife and their habitats,
result in 50% reduction in spermatozoa per ejaculate in the consumption of organic products minimizes the need
aging birds. for animals in captivity to modify and detoxify
antifeedants in their diet. Evaluating the potential burden
The cloaca can transmit microbes retrograde into the that residual pesticides in non-organic ingredients place
reproductive tract. The hypothesis that there is a passage on a bird requires understanding the biochemical com-
of beneficial microbes at the time of copulation is plexities of detoxification mechanisms that enable ani-
intriguing. It has been hypothesized that females copu- mals to process these potentially harmful chemicals. This
late with multiple males to gain microfloral advantage can apply equally to foodstuffs with high concentrations
for the offspring from flora transmitted at copulation.64 of antifeedants, such as alkaloids, cardiac glycosides and
The female is thought to benefit by protection from phenolic compounds, that require detoxification.
future as well as present infections that become over- However, pesticide tolerance has not been evaluated in
135
Fig 4.2.32 | Phase I and II detoxification of xenobiotics.
companion birds. Clinically significant improvements in carried out by a suite of non-specific microsomal
health and productivity have been reported for birds enzymes referred to as mixed function oxidases (MFOs)
maintained on organic diets.67 that act primarily in the endoplasmic reticulum. The
detoxification process converts a lipophilic compound
Actions of Chemical Contaminants into a highly water-soluble product that is suitable for
Most toxicological injury results in cellular damage. The excretion in urine or feces. The two phases of detoxifica-
toxic response to any specific chemical is the result of tion place different demands on nutrient stores in the
dysfunction of relatively few basic biologic processes. body. Therefore, the ability to digest and process foreign
Normal processes can be suppressed or stopped com- chemicals may vary from one individual to another,
pletely, or they can be enhanced beyond normal physio- depending on species, feeding ecology, gender and
logic limits and, in turn, affect other systems dependent developmental stage. If liver function is diminished from
on their controlled functions. Cellular responses to any other disease process, detoxification capability may
chemical toxins occur through both structural and meta- also be affected.
bolic mechanisms in the cell. A single response or a
number of actions can be elicited from an individual Nutritional Requirements for Detoxification
pesticide (Table 4.2.15). Dietary nutritional deficiencies, such as minerals (cal-
cium, copper, iron, magnesium, zinc), vitamins (E, C
Detoxification of Xenobiotics and the B complex) and proteins, can limit the chemi-
Xenobiotics are pharmacologically, endocrinologically, or cals necessary for the synthesis of enzymes or conjugat-
toxicologically active substances not endogenously pro- ing agents. Energy deficits induced by fasting decrease
duced and therefore foreign to an organism. Pesticides the activity of xenobiotic metabolizing enzymes. Protein
acting as estrogens (xenoestrogens) are a common sub- malnutrition may also impair enzyme synthesis, MFO
ject of discussion at wild bird disease seminars33,34,40,41,103 activity and hepatic glutathione concentration.
(Fig 4.2.32).
Detoxification may also have an impact on ascorbic acid
The detoxification of xenobiotics is a biphasic process (vitamin C) levels, as glucuronate is a precursor in the
Table 4.2.16 | Behavioral Traits Attributed to Nutritional Inadequacy
History Signalment Individualistic Treatment

Overly permissive owners Distrustful Formulated Diet
Behavior Obsessive/Compulsive • Nutritionally balanced
•Craves sweets/fats Depressed, Separation Anxiety Environment
Diet Reproductive • Adjust, move/redecorate cage
• Poorly balanced 30-60% • Masturbation, hiding, nest building, egg laying Medication
warm table foods and numerous treats Feather Picking, Mutilation • Human chorionic gonadotropin
• Seed based Biting, Screaming • Lupron, dexamethasone
Husbandry Sweet/Lovable Clinging Behavior
• Poor Aggression • Modification, tolerance training, exercise
biosynthesis of ascorbate in most animals. Deficiencies while studies on the effects of individual pesticides may
of ascorbate reduce the ability to detoxify foreign chemi- not indicate any detrimental actions, a combination of
cals. Stress may also increase the rate of ascorbate two or more pesticides may enhance toxic actions.
metabolism. Any changes in environmental attributes Potentiation occurs when one chemical enhances the
(structural or nutritional) may impact on levels of ascor- toxicity of another, even though the toxicity of the
bate and thus a species’ ability to detoxify antifeedants potentiator is minor or nonexistent. See Chapter 11,
in its diet. Low-risk Pest Management for actions one might con-
sider in avoiding pesticides.
By consuming several different plant foods, and so using
various rate-limiting detoxification pathways, an animal
Pesticides and Behavioral Abnormalities
can ingest larger amounts of food per unit time enabling
them to obtain more energy and nutrients. While varying Levels of pesticide contamination in bird foods com-
the diet may be beneficial to some animals, there is the posed of non-organic ingredients have yet to be evalu-
risk of exposure to a greater variety of biologically active ated. Behavioral abnormalities associated with pesticide
compounds. If more than one xenobiotic is absorbed exposure include: reduction in courtship behavior33,34,74,
there can be an additive, synergistic or antagonistic inter- reluctance of females to take food from males, changes
action between them. Therefore, the ability to utilize a of activity patterns in males40, reduced levels of nest
single food substrate or to incorporate various plant defense33,34,41, alterations of incubation behavior,
species into the diet will be based on the individual. decreased parental attentiveness resulting in increased
embryonic mortality33,41,82, decreased time feeding young,
Implications for Pesticide Residues in Avian Diets fewer sorties to feed young and increased time away
Birds maintained in captivity are confronted with a dif- from nests.33,34,82
ferent set of stresses than their wild counterparts. In
addition to adjusting to the stress of being maintained in Eggshell thinning induced by dichlorodiphenyldichloro-
a confined environment, they are generally supplied ethylene (DDE) is species specific. Organochlorines
with foods that have been domesticated for the human reduce levels of androgens in males and estrogen and
palate or formulated foods composed of foreign ingredi- progesterone in females. Levels of thyroxine in both
ents. There are various natural antifeedants in foods that sexes decrease in a dose-related fashion. There are also
the avian system must detoxify, and the addition of resid- links between hyperthyroidism, PCB’s and dichlorodi-
ual pesticides in non-organic foods adds to this burden. phenyltrichloroethane (DDT).41 Chlorinated hydrocar-
Tannins differ in their actions. Condensed tannins have bons induce changes in the metabolism of steroid hor-
the potential to bind to proteins, rendering them insolu- mones by mixed function oxidases (MFO).82
ble and unavailable for assimilation; hydrolysable tan-
nins do not bind to proteins, but require detoxification, BIRD BEHAVIOR
placing a drain on nutrients associated with the detoxifi-
A range of behavioral traits can be attributed to nutri-
cation system. A nutritionally balanced diet is still not
tionally imbalanced diets, inappropriate dietary ingredi-
optimal if levels of feed contaminants require extensive
ents, and dietary exposure to pesticides (Table 4.2.16).
detoxification.
These include changes to vocalization patterns and
The toxicity of certain pesticides may be underestimated, breeding behavior. Behavioral traits of birds also need to
as cumulative effects or delayed toxicity can occur long be evaluated when converting birds to formulated diets
after exposure. This confuses the interpretation of signs (see Chapter 3, Concepts in Behavior, Section III
credited to pesticide exposure. Synergistic effects may Pubescent and Adult Psittacine Behavior). The subjects
also be observed, if one chemical affects the solubility, of high-fat and high-sugar diets along with elevated
binding, metabolism or excretion of another. Therefore, sodium are presented.
137
Dietary Influences on Vocalization Patterns problematic. Even if provided with surplus food, birds
Changes in vocalization patterns have been reported in can starve to death if they don’t consume the food
cockatiels maintained on diets with deficient or exces- offered. Therefore, it is imperative to immediately return
sive levels of vitamin A.58 Excessively high levels of vita- a bird to its original diet if it refuses to eat the new diet.
min A (100,000 IU/kg) increase the number of vocaliza- The following guidelines should be given to owners
tions and reduce the peak frequency of vocalizations, when a diet conversion is being initiated.
while moderately excessive levels of vitamin A (10,000
IU/kg) result in a reduction in peak amplitude and total Tips for Converting Birds to a Formulated Diet
power. These changes may influence breeding behavior, • Visit the avian veterinarian for a general health exam
social interactions and responses of adults to begging to decide if the bird is healthy enough to undergo a
behavior of chicks. diet change at this time.
• Discuss which formulated product is best for the bird.
Diet and Behavioral Changes • Determine the goal body weight that is appropriate
Reproductive behavior, normally regulated by photope- for the bird.
riod, can be influenced by dietary components. • Purchase a gram scale and learn how to use it
Additional seeds stimulate breeding behavior in African correctly.
grey parrots.69 Endocrine malfunction has been impli- • Weigh the bird at the same time every morning for a
cated in anecdotal studies of male budgerigars on all- week to establish normal fluctuations in weight.
seed diets that display continuous feeding behavior Report any serious fluctuations (10% or more) to the
towards a mirror. Reducing the synthetic vitamin A con- avian veterinarian.
tent of food fed to lorikeets reduced defecation in nest • Mix half formulated diet and half the old diet. Expect
boxes (Unpublished data, D. McDonald). See Chapter 3, the bird to exhibit negative behavior by throwing the
Concepts in Behavior, Section III Pubescent and Adult pellets/nuggets at owner, screaming, yelling, and hav-
Psittacine Behavior. ing tantrums. Talking to the bird may soothe it. As the
bird starts to eat the formulated diet, gradually
reduce the amount of the old diet and increase the
DIET CONVERSION CHALLENGES
proportion of the new diet.
Modifying a bird’s diet is one of the biggest behavioral
• Remove all perches from cage so the bird is forced to
challenges. Most issues can be overcome with patience
sit on the food dish or put the bird in a plastic or
and perseverance. Educating the owner about the bene-
glass box (aquarium) and sprinkle food on the floor.
fits of a formulated diet versus a seed-based diet is the
Provide a small water container—no toys.
first challenge. Feeding the new dietary items early in
• Place formulated food on a mirror located on the
the morning when the birds are most hungry is benefi-
floor (Figs 4.2.33a,b).
cial, but dietary changes should be undertaken gradually.
• Place the bird in a cage with another bird that is
If birds continue to have problems with acceptance of
already consuming a formulated diet. Do not provide
new dietary items, placement near birds that are already
any seed and separate birds at night. If the bird has
feeding on similar foods is beneficial as birds usually
not consumed any of the formulated food by evening,
mimic feeding habits of other birds. Mixing the new diet
provide it with seed.
with a favorite fruit can be helpful; mushy fruit works
• Once it starts to eat, place a bowl of formulated food
best as it sticks to the formulated food. Remove the fruit
near the highest perch.
after 4 to 6 hours to avoid consumption of spoiled food.
• Feed the old diet for 30 minutes in the morning,
An important concern is the bird’s refusal to eat or signifi- remove and replace with formulated food for remain-
cant weight loss. Although weighing the bird in grams on der of the day. Feed the old diet for 30 minutes at
a daily basis is the best method of monitoring adequate night if formulated diet is not eaten.
food consumption, monitoring droppings can also indi- • Grind formulated food in a blender (or purchase a
cate if the bird is eating enough. Prior to the diet change, mash product) and mix crushed millet in with the
note the number and character of the droppings (color, mash.
amount, liquid, form, shape, lack of odor, staining). See • Using a less palatable seed (hulled white millet),
examples in Chapter 6, Maximizing Information from the break the seeds up in a blender with the pellets. After
Physical Examination. Any change in volume and number a few days use less ground millet.
of droppings, usually a dramatic decrease in amount, • Thoroughly mix bird’s favorite fruit into formulated
indicates insufficient consumption. Character of drop- diet so bird gets a mouthful of new diet with fruit.
pings will change as the bird consumes more formulated • Under the guidance of an avian veterinarian, try
diet. Weight fluctuations greater than 10% are considered returning to hand feeding a juvenile formula with a
Fig 4.2.33a | Budgerigar that has become infatuated with its Fig 4.2.33b | Cockatiel in a container with only a mirror. Food
image in a mirror. is placed on the mirror. Return the bird to its own cage at night
for regular diet and water. Replace in mirror box next day after
having at least 30 minutes to eat regular diet and drink.
Diminish the time with seeds daily until weaned.
syringe and then wean to formulated food. While problems associated with the integument can pre-
• Very small particles of formulated foods seem more cede breakdown of other systems, they are seldom rec-
acceptable to small birds ognized in the early stages of the IDC. Therefore, diges-
tive upsets associated with gastroenteritis and ileus are
If patience and persistence doesn’t pay off, it is best to
more likely to instigate an investigation into yeast or col-
board the bird under clinical supervision. The veteri-
iform bacterial infection rather than dietary history. A
narian can convert the bird to the new diet while care-
proliferation of meetings, publications, investigative con-
fully monitoring weight and health of the bird. Most
sultancies, analytical laboratories and therapies aimed at
birds switch diets very quickly when removed from the
the presenting problems over the past 30 years have all
“comfort” of the home environment. Avian veterinari-
contributed to a better understanding of illnesses in pet
ans generally have more experience with dietary birds. While secondary problems associated with any
changes. Birds should be left for a sufficient period of one of dozens of common, yet serious, secondary
time to ensure conversion is complete ie, held for 2 to pathogens still warrant attention, preventive medicine
10 days. Wait until the bird maintains body weight for remains the most effective therapy.
at least two days after normal diet has been totally
removed. It is best that the bird is not returned to the
same routine at home (ie, move cage, redecorate cage,
don’t place in kitchen at mealtime).
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139
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drome. Biotin-mediated restora- 24. Clubb SJ, KarpinskiL: Aging in organophosphate pesticide. 58. Koutsos EA, Klasing KC: Vitamin
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The effect of biotin deficiency on fatty liver-hemorrhagic syn- cide. J Appl Ecol 19(2):327-335, metabolism in rats. J Nutr
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psittacines fed organic formu- commonly ingested by keel Calcium and its relationship to naped Amazon (Amazona
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1992 pp 78-82. naturally incubated dove eggs. J 93. Sayle R: Evaluation of droppings. carp from Saginaw Bay, Lake
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deficiency interferes with prolif-
Inhibition of beta-carotene and Environmental temperature as a tion of Indonesian pregnant
eration and maturation of cells
astaxanthin of NADPH-depend- factor in the aetiology of fatty women benefits vitamin A status
in the chicken small intestine. Br
ent microsomal phospholipid liver-haemorrhagic syndrome in of their infants. Br J Nutr
peroxidation. J Nutr Sci the fowl. Res Vet Sci 25(2):133- 86(5):607-615, 2001. Poult Sci 41(4):410-415, 2000.
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71:378-398, 1978. Ember I: Effect of rancid corn oil orrhagic syndrome in laying 106. Wilson GH, Fontenot DK,
75. Oloyo R A: Studies on the biotin on some onco/suppressor gene hens. Br Poult Sci 41(4):465-472, Greenacre, CB, et al: Enteric
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76. Oloyo RA, Ogunmodede BK: transport and the hemochro- ticular attention to the iron con- 107. Worell AB: Further investigations
Effect of dietary palm kernel oil matosis gene. Am J Physiol tent. Tijdschr Diergeneeskd in rhamphastids concerning
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kidney syndrome in broiler 282(3):G403-414, 2002. 97. Scott ML Nesheim, MC et al: Avian Vet, 1993, pp 98-107.
05_Calcium.qxd 8/22/2005 2:46 PM Page 141
CHAPTER
5
Calcium
Metabolism
MICHAEL STANFORD, BVS c, MRCVS
Calcium plays two important physiological roles in the

avian subject. First, it provides the structural strength of
the avian skeleton by the formation of calcium salts.
Second, it plays vital roles in many of the biochemical
reactions within the body via its concentration in the
extracellular fluid.3 The control of calcium metabolism in
birds has developed into a highly efficient homeostatic
system, able to quickly respond to increased demands
for calcium required for both their ability to produce
megalecithal eggs and their rapid growth rate when
young.2,3 Parathyroid hormone (PTH), metabolites of
vitamin D3 and calcitonin, regulate calcium as in mam-
mals, acting on the main target organs of liver, kidney,
gastrointestinal tract and bone.2,3,11,24 Estrogen and
prostaglandins also appear to have an important role in
calcium regulation in the bird.2,3
There are distinct differences between the mammalian

and avian systemic regulations of calcium. The most dra-
matic difference between the two phyletic groups is in
the rate of skeletal metabolism at times of demand. The
domestic chicken will respond to hypocalcemic chal-
lenges within minutes compared with response to simi-
lar challenges in mammals that can take over 24 hours.11
This is best demonstrated by an egg-laying bird where
10% of the total body calcium reserves can be required
for egg production in a 24-hour period.10 This calcium
required for eggshell production is mainly obtained
from increased intestinal absorption and a highly labile
reservoir found in the medullary bone, normally visible
radiographically in female birds. The homeostatic con-
trol of the medullary bone involves estrogen activity.2
Due to the rapid metabolic responses in the avian skele-
ton, it has become a common model for skeletal studies
concerning the regulation of calcium.
Abnormalities of calcium metabolism are common in the VITAMIN D3

poultry industry, leading to poor production and growth The vitamin D3 metabolism of birds has been extensively
defects, in particular, tibial dyschondroplasia in broiler reviewed.1,3,4,24,25 Following the identification of vitamin
chickens kept indoors. Due to the economic status of D3 metabolic pathways, vitamin D3 now is considered to
the poultry industry, calcium metabolism has been well be a steroid hormone exhibiting feedback relationships
researched in production birds, including the assess- in response to calcium requirements.8 The main role of
ment of the importance of dietary calcium, vitamin D3 vitamin D3 is in the control of bone metabolism by
and their interaction with ultraviolet light, especially in strictly regulating mineral absorption, but more recently
the UV-B spectrum (315-280 nm).1,4,14,24 it has been found to have profound effects on the
immune system, skin and cancer cells.1 Due to the
In captive pet birds, disorders of calcium metabolism
importance of the vitamin’s role in bone development
also are common, ranging from osteodystrophy in young
and the requirement for UV light in the metabolic con-
birds (due in part to the greater calcium requirement in
version of provitamin D3 to vitamin D3, the commercial
young growing birds) to hypocalcemic seizures and egg
availability of dietary vitamin D3 has been essential to
binding in adults.5,6,7,16 Although African grey parrots
allow the indoor production of poultry.4 Vitamin D
(Psittacus erithacus) are considered to be especially sus-
occurs naturally in plants as ergocalciferol (vitamin D2)
ceptible to disorders of calcium metabolism, problems
and this will function in mammals as well as vitamin D3,
have been reported in a variety of captive species. The
but birds do not respond well to dietary vitamin D2. This is
husbandry requirements with respect to calcium have
due to increased renal clearance of vitamin D2 rather than
been poorly researched in pet birds in the past, and
lack of intestinal absorption.10
much of our present knowledge is extrapolated from
work with poultry. It has been established that the domestic chicken
secretes 7-dehydrocholesterol (provitamin D3) onto the
featherless skin. It has recently been shown that there
Calcium Regulation in Birds are ten times more provitamin D3 on the featherless leg
skin than on the back, indicating the importance of this
area for vitamin D3 metabolism.25 Conversion of the
CALCIUM provitamin D to cholecalciferol (vitamin D3) occurs by a
Calcium exists as three fractions in the avian serum: 1) UV-B light-dependent isomerization reaction. Cholecal-
the ionized salt, 2) calcium bound to proteins, and 3) as ciferol is a sterol prohormone that is subsequently acti-
complexed calcium bound to a variety of anions (citrate, vated by a two-stage hydroxylation process.
bicarbonate and phosphate). Ionized calcium is the
physiologically active fraction of serum calcium, with a Cholecalciferol is initially metabolized to 25-hydroxy-
role to play in bone homeostasis, muscle and nerve con- cholecalciferol in the liver; 25-hydroxycholecalciferol is
duction, blood coagulation and control of hormone transported to the kidney via carrier proteins and con-
secretions such as vitamin D3 and parathyroid hormone. verted to either 1,25-dihydroxycholecalciferol or 24,25-
The majority of the protein-bound calcium is bound to dihydroxycholecalciferol, the active metabolites of chole-
albumin and considered to be physiologically inactive. calciferol in the domestic fowl. The most significant
Any change in serum albumin levels will directly affect active metabolite of vitamin D3 in domestic chickens is
the total calcium level. The binding reaction is strongly 1,25-dihydroxycholecalciferol, which displays a hypercal-
pH-dependent, so an increase or decrease in pH will cemic action.9,21 While not significant in mammals, 24,25-
respectively increase or decrease the protein-bound cal- dihydroxycholecalciferol is thought to have a special
cium fraction. The significance of the small, complexed active role in the laying hen.2 The synthesis of 1,25- dihy-
calcium fraction is unknown at the present time, but any droxycholecalciferol is tightly regulated by PTH, depend-
disease state that affects the levels of the binding anions ing on the calcium status of the bird. The metabolite
would be expected to significantly alter calcium levels.8,21,22 regulates calcium absorption across the intestinal wall by
inducing the formation of the carrier protein calbindin-
The ionized calcium level appears to be maintained D28k. The presence of this protein reflects the ability of
within a tight range in the normal individual compared the intestine to absorb calcium. Calbindin-D28k also is
with the total calcium level, which fluctuates with serum found in the wall of the oviduct, and levels rise during
protein concentrations, and any major change in the egg laying, although this process is not directly related
serum ionized calcium level is likely to be of pathologic to the actions of 1,25-dihydroxycholecalciferol. Bone for-
significance. Ionized calcium concentrations are regu- mation is stimulated by 1,25- dihydroxycholecalciferol,
lated by the interaction of PTH, vitamin D3 metabolites which induces osteoclastin production from osteoblasts.
and calcitonin in response to changing demands. In egg-laying birds, 30 to 40% of the calcium required
Chapter 5 | C A L C I U M M E T A B O L I S M
143
for eggshell formation is acquired from medullary bone. is poor.8 This may explain why PTH has appeared diffi-
The control of this highly labile pool of calcium involves cult to measure in the avian subject and is poorly
both 1,25- dihydroxycholecalciferol and estrogen activity. researched at the present time, although circulating lev-
The function of vitamin D3 is reliant on the presence of els are believed to be low compared with mammals. An
normal vitamin D3 receptors. The receptors have been inverse relationship has been found between PTH con-
found in bone, skin, skeletal muscle, gonads, pancreas, centrations and ionized calcium levels in the laying
thymus, lymphocytes and pituitary gland.2,3,4,8,11,14,24,25 chicken, indicating that PTH has at least an important
role in calcium regulation during this period. This
If vitamin D3 is supplied in the diet, it can be absorbed response is very efficient during egg production, with
with 60 to 70% efficiency. In most situations, there is a PTH levels increasing due to the greater demand for cal-
compromise between the amount of dietary vitamin D3 cium. A recent study in African grey parrots investigating
administered (on the basis of economy and toxicity) and hypocalcemia has used a mammalian 1-34 PTH enzyme-
UV light provided for natural vitamin D3 formation.10 linked immunosorbent assay with consistent results.18
PARATHYROID HORMONE (PTH) PARATHYROID HORMONE-RELATED

The parathyroid glands produce PTH from the chief cells PEPTIDE (PTHRP)
in response to a low ionized calcium level.8,10 As in mam- PTHrP is a second member of the PTH family, originally
mals, PTH has an essentially hypercalcemic action in discovered as a cause of hypercalcemia in malignancy in
birds, and if a parathyroidectomy is performed in quail, man and now the subject of much clinical research.
the birds respond with severe hypocalcemia unless cal- PTHrP has three isoforms of 139, 141 and 173 amino
cium is given in the diet.3 Birds appear more sensitive to acids, all with identical sequences through to amino acid
PTH than mammals, reacting to intravenous injections of
139. The hormone has distinct structural homology with
the hormone within minutes with a rise in blood cal-
PTH, suggesting a common ancestral gene. There is dis-
cium levels.2,3,11 The blood ionized calcium level feeds
tinct homology between the structure of mammalian
back on the chief cells in the parathyroid gland to tightly
and avian PTHrP in the 1-34 segment, as has been found
control secretion of the hormone. The hormone uses
with PTH. PTH and PTHrP share a common receptor.
the kidney and the bone as its main target organs in
Many tissues in the chicken embryo contain levels of
birds.3 In the bone, the hormone has rapid effects meas-
PTHrP. In chickens as in man, PTHrP is thought to play
urable within 8 minutes of administration compared
many regulatory and developmental roles in a variety of
with hours in mammals, so PTH is probably at least par-
tissues. Concentrations of PTHrP have been shown to
tially responsible for the speed of calcium metabolism in
rise in the shell gland of the chicken during the calcifica-
the bird.2
tion cycle, affecting smooth muscle activity in the gland.
PTH directly stimulates osteoclasts to resorb bone. The Levels of PTHrP return to normal once the egg has been
hormone also will actively stimulate osteoblast activity, laid. PTHrP has been shown to have effects on bone
and it is thought that PTH-stimulated osteoblasts regu- resorption in the chicken embryo.3
late osteoclast activity, providing the precise control sys-
tem necessary in avian skeletal turnover.2,3 ULTIMOBRANCHIAL GLANDS
PTH binds to osteoclasts, increasing bone resorption by The ultimobranchial gland in birds produces calcitonin.
stimulating their metabolic activity and division. PTH It is a 32-amino acid hormone that exerts an essentially
also has direct influence on both calcium and phospho- hypocalcemic effect in response to rising serum ionized
rus excretion in the bird. Calcium excretion is increased calcium levels.3 The levels of circulating calcitonin in
and phosphorus decreased following parathyroidectomy. birds, amphibians and possibly sub-mammals are high
These changes can be reversed by injections of PTH. and readily detectable compared with PTH. The bioactiv-
ity of calcitonin also varies among phyletic groups, with
PTH has a different structure in birds than in mammals. fish calcitonin exhibiting the most potent effect. In the
It consists of an 88-amino acid chain, compared with 84 bird, calcitonin levels increase following injections of
in mammals, and there is a lack of homology between calcium. There is a direct correlation between calcitonin
the two molecules. The greatest similarity is found in the levels and dietary calcium concentrations (and, hence,
1-34 segment of the chain, which also is responsible for serum calcium levels). Although calcitonin has been
much of the activity of the hormone.3,8 Unfortunately, shown in man to exert its hypocalcemic effects mainly by
this segment has a short half-life, and mammalian assays inhibiting osteoclastic bone resorption, its biological
tend to assess the middle and carboxyl-terminal regions action in the bird remains surprisingly unclear despite
of the amino acid chain where homology with avian PTH the high circulating levels of the hormone in this group.
PROSTAGLANDIN calcium levels. Therefore, a patient with metabolic aci-

Prostaglandins are powerful facilators of bone resorp- dosis would be expected to show an ionized hypercal-
tion, with hypercalcemic effects similar to PTH and vita- cemia level due to decreased protein binding. With an
min D3 metabolites. The osteoclast appears to be the site alkalotic patient, an ionized hypocalcemia would occur
of action for prostaglandin. Injections of prostaglandin as the protein-binding reaction increases. Ionized cal-
into chickens will produce hypercalcemia, and the use cium levels are therefore considered a far more accurate
of prostaglandin antagonists will produce hypocalcemia.3 reflection of the patient’s calcium status, especially in a
diseased animal. In mammals, positive correlations have
been found between albumin and total calcium levels.8,26
ESTROGEN This enables formulae to be developed that “correct”
Estrogens promote the formation of the vitellogenins total calcium levels for fluctuations in albumin levels.
from the liver. These are lipoproteins that are incorpo- Recent research has suggested these corrected estimates
rated into the egg yolk. They bind calcium, and their of free calcium are inaccurate in 20 to 30% of cases in
production is followed by a rise in serum calcium levels. mammals.8 In mammals, the relationship between total
This estrogen-controlled hypercalcemic effect is not seen calcium and albumin diminishes with the severity of the
in mammals and is thought to be due to the need to disease, and the correction formulae are now thought to
produce large calcified eggs, requiring a rapidly mobi- be less useful. Previous research in psittacine birds
lized source of calcium. Estrogens also influence the found a positive correlation between albumin and total
mobilization of medullary bone during the egg-laying protein in African grey parrots, but not Amazons
cycle (and also during the nocturnal fast). The effect of (Amazona spp.);12,13 more recent research in healthy
estrogen on avian medullary bone is a large research African grey parrots has not indicated a significant rela-
area due to the importance of estrogen in maintaining tionship.21,22 In the majority of cases, the measurement of
bone mass in postmenopausal women.2,3 ionized calcium is preferred in both mammals and birds.
Ionized calcium levels are measured by ion-specific elec-

trodes. Analyzers using ion-selective electrodes are
Investigating increasingly available for use in veterinary clinics. The
Abnormalities of methodology employed by the analyzers is based on the
Calcium Metabolism ion-selective electrode (ISE) measurement principle to

precisely determine the ion values. The analyzers are
normally fitted with ISE electrodes to assay the elec-
CALCIUM trolytes sodium, potassium and ionized calcium. Each
The measurement of serum ionized calcium provides a electrode has an ion-selective membrane that undergoes
more precise estimate of an individual’s calcium status a specific reaction with the corresponding ions con-
than does total serum calcium, especially in the diseased tained within a particular sample. The membrane is an
patient.8,26 Unfortunately, the majority of veterinary ion exchanger reacting to the electrical charge of the
pathology laboratories at the present time report only a ion, causing change in the membrane potential or meas-
total calcium value measured by spectrophotometer, uring voltage, which is built up in the film between the
reflecting the total combined levels of ionized calcium, sample and the membrane. A galvanic measuring chain
protein-bound calcium and complexed calcium. This can within the electrode determines the difference between
lead to misinterpretation of calcium results in birds, as the two potential values on either side of the membrane
any change in protein-bound calcium levels is not of the active electrode. The potential is conducted to an
thought to have any pathophysiological significance.22,26 amplifier by a highly conductive inner electrode. The ion
Measurement of total calcium in an avian patient with concentration in the sample is then determined by using
abnormal protein levels or acid-base abnormalities a calibration curve produced by measuring the poten-
would not truly reflect the calcium status of the animal. tials of standard solutions with a precisely known ion
Any state affecting serum albumin values in the blood concentration. Blood samples for ionized calcium assays
will affect the total calcium concentration, leading to an should be drawn into heparin and analyzed as soon as
imprecise result. In laying female birds, the serum albu- possible after venipuncture, as changes in the blood pH
min levels may rise by up to 100%. This would produce of the sample will affect the accuracy of the ionized cal-
an inflated total calcium concentration due to an cium levels (ie, contact with carbon dioxide in the air
increased protein-bound calcium fraction, while not will reduce the pH of the sample). Despite this, a study
affecting the ionized calcium level. The binding reaction in dogs suggests that samples will not be adversely
between the calcium ion and albumin is strongly pH- affected if not assayed for up to 72 hours, so it is possi-
dependent, so acid-base imbalances will affect ionized ble to use external laboratories.17 This has been the
145
Fig 5.1 | Effect of sample handling delay on ionized calcium concentrations.

There was no significant difference between ionized calcium concentrations
in the same sample despite delays of up to 48 hours. The samples were
stored at 3-5° C prior to analysis.22
Fig 5.2 | Serum ionized calcium concentrations in 80 healthy captive African grey parrots. The
ionized calcium concentrations are all within a tight range. The normal range was found to be
0.96-1.22 mmol/L.
author’s experience with avian samples, but it is advis- normal total calcium concentrations, suggesting that
able to fill the sample tubes to minimize contact with hypocalcemia is potentially under-diagnosed in this
the air22 (Fig 5.1). It also is important to chill the samples species.22 In mature female birds, hypercalcemia might
immediately to reduce glycolysis by the red blood cells, be over-diagnosed due to increased protein-bound cal-
which continue to produce lactic acid as a byproduct, cium producing a high total calcium level, but ionized
reducing the pH of the sample. levels would not be affected. Due to the potentially large
fluctuations in albumin levels in adult birds compared
A recent study in healthy African grey parrots indicated a with mammals, it is considered essential wherever possi-
narrow normal range for ionized calcium levels, but a ble to measure ionized calcium levels.
wide variation in total calcium levels due to protein fluc-
tuated among birds21,22 (Figs 5.2, 5.3). The study did not VITAMIN D3
reveal any significant correlation between albumin levels The measurement of 25-hydroxycholecalciferol is consid-
and total calcium levels in healthy birds. It was shown ered the best assessment of vitamin D3 status in the
that using total calcium values in isolation would lead to avian subject due to a longer half-life than other vitamin
misdiagnosis of disorders of calcium metabolism in this D3 metabolites.8 There are assays available for the other
species. Of 394 samples submitted from African grey par- metabolites of vitamin D3 and it is important to ensure
rots into the practice laboratory in 2001, 54 samples that any assay has been optimized for the metabolite of
(13.17%) had a low ionized calcium level despite having interest. Until recently, radioimmunoassays were the
Fig 5.3 | Serum total calcium levels in the same 80 healthy captive African grey parrots as Fig
5.2. The total calcium concentrations were outside the normal range (2.0-3.0 mmol/L) in several
birds despite normal ionized calcium levels. This fluctuation in the total calcium concentration was
due to protein variations in individual birds and has no pathological significance. This demon-
strates the importance of measuring ionized calcium wherever feasible rather than total calcium.
Fig 5.4 | 25-hydroxycholecalciferol concentrations in seed-fed African grey parrots. There was
a wide variation in vitamin D levels. It is postulated that this is due to both fluctuations in UV-B
levels received by individual birds and low dietary vitamin D.
only commercial assays available for both 25-hydroxy- psittacine birds has suggested that serum vitamin D3 lev-
cholecalciferol and 1,25-hydroxycholecalciferol. An els can be affected by both varying levels of dietary vita-
ELISA test for 25-hydroxycholecalciferol has recently min D3 and UV-B light exposure.23 Blood should be
been developed with the advantages of both conven- drawn into heparin and preferably frozen immediately
ience and economy. This assay has been shown to corre-
after venipuncture until the assay can be performed. The
late well with the radioimmunoassays.8 This has allowed
use of vitamin D3 assays will have an increasing use in
research to be carried out in the Psittacus species. A
avian medicine due to the common presentation of cal-
recent study in African grey parrots (a genus known to
cium disorders, both in terms of clinical disease and
suffer from hypocalcemia) indicated a wide variation in
25-hydroxy-cholecalciferol levels in seed-fed birds19,20 (Fig poor reproductive results. Vitamin D3 assays could possi-
5.4). Any 25-hydroxycholecalciferol results should be bly be useful for reptiles — another group that suffers
interpreted within the context of the diet and the levels problems with calcium metabolism, in many cases due
of UV light received by the bird.20 Recent research in to poor husbandry.15
147
Fig 5.5 | A 5-week-old African grey parrot with severe nutritional Fig 5.6 | Lateral radiograph of a 12-week-old African grey par-
osteodystrophy. There was radiographic evidence of pathological rot with severe osteodystrophy. There is severe deviation of both
fractures in both tibiotarsi and humeri with severe spinal malfor- tibiotarsi with marked deviation of the spine. The chick had
mation. The bird was euthanized. Histopathology of the parathy- been parent-reared by adults fed an unsupplemented seed-
roid glands confirmed vacuolated hypertrophic chief cells sugges- based diet. The bird was humanely euthanized.
tive of nutritional secondary hyperparathyroidism. The bird had
been parent-reared by adults fed an unsupplemented seed mix.
ASSAY FOR PTH supplied. If domestic poultry are receiving no UV light,

then all the cholecalciferol must come from the diet.10
PTH is very labile and any assay requires exacting sample
The domestic fowl does not have a dietary requirement
handling to produce good results. Blood should be
for vitamin D3 if it receives adequate UV-B radiation.10
drawn into EDTA and either assayed immediately or
frozen to -70° C within 1 hour of venipuncture. The
Unfortunately, caged birds have not been extensively
majority of human measurements involve a two-site
researched, but most would be expected to receive a
radioimmunoassay in an attempt to reduce the interfer-
poor diet with inadequate UV light. Seed-based mixes
ing effect of the many cleavage products of PTH that
traditionally used for feeding captive parrots have low
have long half-lives. Most human assays concentrate on
levels of both vitamin D3 and calcium.5,16,20,21 In addition,
the middle and terminal segments of the PTH molecule
they can contain high levels of phosphorus that can bind
due to the very short half-life of the biologically active 1-
the calcium in phytate complexes.10 Chronic deficiency
34 section. A human research kit for 1-34N section PTH
of vitamin D would be expected to lead to hypocalcemia
has been used to assay PTH in African grey parrots with
and secondary hyperparathyroidism. Vitamin D is
consistent results. This study indicated that as ionized
obtained by birds directly from the diet and by the
calcium levels rose in a group of 40 African grey parrots,
action of UV-B on vitamin D precursors in the cutaneous
PTH levels fell. Unfortunately, the assay for PTH 1-34N is
tissues. Either a deficiency in dietary vitamin D or lack of
too intricate for routine use at the present time and, in
available UV-B light would be expected to produce a
the author’s opinion, intact 1-84 PTH assays are not use-
vitamin D-deficient bird, potentially leading to subse-
ful in psittacine birds.8,13,18
quent problems with calcium metabolism.3,10 Hypo-
calcemia is a common syndrome in avian subjects, with
African grey parrots (Psittacus erithacus) in captivity
Effects of Husbandry appearing particularly susceptible, although the etiology
is still unconfirmed.5,6,7,16 Affected birds present clinically
on Calcium Metabolism with a variety of neurological signs, ranging from slight
in Psittacine Birds ataxia to seizures, which respond to calcium therapy.21,22
In adult females, egg binding or poor reproductive per-
The effects of altering dietary vitamin D3, calcium or formance is a common presentation. In young African
exposure to different levels of UV light have been well grey parrots, osteodystrophy also is a common present-
researched in poultry.3,4,10,14,24 Deficiencies in any of these ing clinical sign5 (Figs 5.5-5.8). The growing birds can be
parameters will lead to poor production and skeletal dis- affected by bony deformities that range from subtle radi-
orders such as tibial dyschondroplasia.3 Extensive ographic changes to obvious gross deformities in both
research has produced published results, enabling the the long bones and spinal column. Radiography has
poultry industry to select varying levels of dietary vitamin been routinely used to demonstrate juvenile osteodys-
D3 and calcium in accordance with the amounts of UV trophy in many other species of birds. In a recent study,
Fig 5.7 | An adult African grey with osteo- Fig 5.8 | Ventral dorsal radiograph of the
dystrophy. The bird has characteristic bend- bird in Fig 5.7. There is severe deviation in
ing in the tibiotarsi. The condition was suc- both tibiotarsi with folding pathological
cessfully corrected by osteotomy and fixation fractures. There also is evidence of abnor-
of both legs. mal skeletal development in both wings.
16 of 34 feather-plucking birds examined radiographi- available to captive birds. Initial work by the author with
cally as part of a normal work-up revealed evidence of South American species has shown that they do not
osteodystrophy.5 The condition will be permanent and appear to be as dependent as African grey parrots on
deteriorates as the birds increase in weight, which puts UV-B light for maintaining adequate vitamin D levels
increased pressure on the deformed bones and fre- (M. Stanford, unpublished data). This might explain the
quently requires corrective surgery. prevalence of disorders of calcium metabolism in African
grey parrots compared with other psittacine birds. South
A recent study in African grey parrots has shown that it
is possible to produce changes in calcium parameters by American rain forest has a dense canopy compared with
varying husbandry conditions as in poultry.21,23,25 The African forests, reducing the UV-B light levels reaching
study has demonstrated the effects of feeding a formu- the birds, so their vitamin D metabolism would be
lated nugget dieta with increased levels of vitamin D3 and expected to be different from those of African birds.
calcium compared with a seed-fed control group. The
nugget diet produced a statistically significant increase These studies show that it is important that breeders
in both the ionized calcium levels and 25-hydroxychole- feed their birds a diet that contains adequate calcium
calciferol levels over the seed-fed group21,25 (Figs 5.9, and vitamin D. It also is important to supply adequate
5.10). This was reflected in improved breeding perform- UV-B radiation to captive birds kept indoors. This would
ance in the nugget-fed group. These young birds devel- be expected to help prevent the many expressions of
oped without radiographic evidence of osteodystrophy. hypocalcemia seen specifically in African grey parrots
and other susceptible species. This includes the parent
In the same study, both the seed- and nugget-fed groups
birds, because the female birds lay down medullary
revealed a significant increase in 25-hydroxycholecalcif-
bone starting about 6 weeks prior to laying eggs. The
erol and ionized calcium concentrations when they were
nutrition of female birds appears to affect the early
exposed to artificial UV-B radiation23 (Figs 5.11, 5.12).
development of the chicks. In a recent study in African
The nugget-fed group under the same UV levels revealed
significantly higher concentrations of vitamin D3 and grey parrots, parent-reared juveniles showed radi-
ionized calcium over the seed control group.23 The initial ographic evidence of osteodystrophy at 8 weeks if the
observations from this study suggest that UV light levels parents were fed seed-based diets. The young from
also are important factors in the vitamin D metabolism nugget-fed parents had no radiographic signs of osteody-
of captive birds in addition to diet. In the future, it will strophy at 12 weeks 21,25 (Figs 5.13, 5.14). See Chapter 4,
be possible to supply diets with varying amounts of vita- Nutritional Considerations, Section I Nutrition and
min D depending on the ambient supply of UV-B light Dietary Supplementation.
149
Fig 5.9 | Effect of diet on ionized calcium concentrations in African grey parrots. There was a
significant increase in the serum ionized calcium concentrations in birds fed a formulated
nugget dieta compared with the same birds fed a seed-based diet.
Fig 5.10 | Effect of diet on vitamin D concentrations in African grey parrots. There was a signif-
icant increase in the 25-hydroxycholecalciferol concentrations in birds fed a nugget dieta com-
pared with the same birds fed a seed-based diet.
Fig 5.11 | Effect of UV-B supplementation on ionized calcium concentrations independent of diet fed.
There was a significant increase in ionized calcium concentrations in both the seed- and nugget-feda
groups exposed to 12 hours of UV-B light in every 24 hours.
Fig 5.12 | Effect of UV-B supplementation on 25-hydroxycholecalciferol concentrations in

African grey parrots independent of diet fed. There was a significant increase in 25-hydroxy-
cholecalciferol concentrations in both seed- and nugget-feda groups exposed to 12 hours of UV-
B light in every 24 hours.
Fig 5.13 | Lateral radiograph of a 12-week-old African grey

parrot with normal skeletal development. The bird was parent-
reared until weaning by adults fed a formulated parrot fooda
until weaning.
Fig 5.14 | Ventral dorsal radiograph of a

12-week-old African grey parrot with nor-
mal skeletal development. The bird was
parent reared until weaning by adults fed a
formulated parrot fooda .
151

a. Harrison’s High Potency Coarse, HBD International, 7108 Crossroads
Blvd, Suite 325, Brentwood, TN 37027 USA, 800-346-0269
[email protected],
www.harrisonsbirdfoods.com
References and Avian Examiner Special Suppl. 1993. parrots: The effect of diet. Proc
HBD International Ltd, Spring, 14. Mahout A, Elaroussi, et al: Euro Assoc Avian Vet, 2003.
Suggested Reading 1997. Calcium homeostasis in the laying 21. Stanford MD: Measurement of
1. Aslam SM, Garlich JD, Qureshi MA: 8. Hollis BW, Clemens TL, Adams JS: hen. Age and dietary calcium ionised calcium in grey parrots:
Vitamin D deficiency alters the In Favus MJ (ed): Primer on the effects. Poult Sci 73:1581-1589, The effect of diet. Proc Euro
immune responses of broiler chicks. Metabolic Bone Disease and 1994. Assoc Avian Vet, 2003.
Poult Sci 77(6):842-849, 1998. Disorders of Bone Metabolism. 15. Mitchell M: Determination of 22. Stanford MD: Measurement of
2. Bentley PJ: Comparative Vertebrate Philadelphia, Lippincott, Williams plasma biochemistries, ionised ionised calcium in grey parrots
Endocrinology. Cambridge, UK, & Wilkins, 1997. calcium, vitamin D3 and haemat- (Psittacus e. erithacus). Vet Rec
Cambridge Univ Press, 1998, pp 9. Hurwitz S: Calcium homeostasis ocrit values in captive green igua- 2004. In Press.
269-301. in birds. Vitam Horm 45:173-221, nas (Iguana iguana). Proc Assoc 23. Stanford MD: The Effect of UVb
3. Dacke GC: In GC Whittow (ed): 1989. Reptile Amphib Vet, 2002, pp 87- supplementation on calcium
Sturkie’s Avian Physiology 5th ed. 10. Klasing KC: Comparative Avian 95. metabolism in psittacine birds.
London, UK, Academic Press, 2000, Nutrition. New York, CAB Intl, 16. Rosskopf WJ, Woerpel RW, Lane Vet Rec 2004. In Press.
pp 472-485. 1998, pp 290-295. RA: The hypocalcemic syndrome 24. Taylor TG, Dacke CG: Calcium
4. Edwards JR, et al: Quantitative 11. Koch J, et al: Blood ionic calcium in African greys: An updated clini- metabolism and its regulation. In
requirement for cholecalciferol in response to hypocalcemia in the cal viewpoint. Proc Assoc Avian Freeman BM (ed): Physiology and
the absence of ultraviolet light. chicken induced by ethylene gly- Vet, 1985, pp 129-132. Biochemistry of the Domestic
Poult Sci 73: 288-294, 1994. col-bis-(B-aminoethylether)-N,N’- 17. Schenck PA, Chew DJ, Brooks CL: Fowl Vol 5. London, UK,
5. Harcourt-Brown NH: Incidence of tetra-acetic acid: Role of the Effects of storage on serum Academic Press 1984, pp #125-
juvenile osteodystrophy in hand- parathyroids. Poult Sci 63:167- ionised calcium and pH values in 170.
reared grey parrots (Psittacus 171, 1984. clinically normal dogs. Am J Vet 25. Tian XQ, Chen, et al:
erithacus). Vet Rec 152, 438-439, 12. Lumeij JT: Relationship of plasma Res 56:304-307, 1995. Characterisation of the transloca-
2003. calcium to total protein and albu- 18. Stanford MD: Development of a tion process of vitamin D3 from
6. Hochleithner M: Convulsions in min in African grey (Psittacus parathyroid hormone assay in the skin into the circulation.
African grey parrots in connection erithacus) and Amazon (Amazona grey parrots. Proc Brit Vet Zool Endocrinology 135(2):655-6121,
with hypocalcemia: Five selected spp.) parrots. Avian Pathol 19:661- Soc, 2002. 1994.
cases. Proc 2nd Euro Symp Avian 667, 1990. 19. Stanford MD: Measurement of 25 26. Torrance AG: Disorders of calcium
Med Surg, 1989, pp 44-52. 13. Lumeij JT, Remple JD, Riddle KE: hydroxycholecalciferol in grey metabolism. In Torrance AG,
7. Hochleithner M, Hochleithner C, Relationship of plasma total pro- parrots (Psittacus e. erithacus). Mooney CT (eds): BSAVA Manual
Harrison GJ: Evidence of tein and albumin to total calcium Vet Rec 153:58-61, 2003. of Small Animal Endocrinology.
hypoparathyroidism in hypocal- in peregrine falcons (Falco pere- 20. Stanford MD: Measurement of 25 Cheltenham, UK, BSAVA
cemic African grey parrots. The grinus). Avian Pathol 22:183-188, hydroxycholecalciferol in grey Publications, 1995, pp 129-140.
06_Physical Examination.qxd 8/22/2005 4:40 PM Page 153
CHAPTER
6
Maximizing Information from the
Physical
Examination
B O B D O N E L E Y , B V S c, FACVS c ( A v i a n H e a l t h ) ;
GREG J. HARRISON, DVM, Dipl ABVP- Avian , Dipl ECAMS;
TERESA L. LIGHTFOOT, DVM, Dipl ABVP-Avian
The last ten years have seen amazing advances in diag-
nostic testing capabilities in avian medicine. Tests that
were not even considered a decade or two ago are now
commonplace. However, the cornerstone of good avian
medicine is still the careful evaluation of the patient.
Diagnosis
Diagnostic tests are an important part of that evaluation,
but they are not the whole evaluation. Their use is only
a part of a continuum that starts with a careful anamne-
Diagnostic Testing sis and concludes with a diagnosis. This can be illus-
trated by the diagnostic pyramid shown (Fig 6.1).
Astute clinicians will move carefully through these levels,

refining their differential list through careful history tak-
Physical Examination
ing, physical examination and selection of diagnostic
testing until a final diagnosis (or at least a much short-
ened list of differentials) is reached.
Anamnesis
Understanding the
Fig 6.1 | The Diagnostic Pyramid
Masking Phenomenon
A common misconception held by many bird owners
and veterinarians is that birds are not very resistant to
illness. To the novice it often appears that birds show
signs of illness one day, are at the bottom of their cage
the next, and dead the day after. This misconception has
stemmed from two sources.
First, many of the birds seen in practice are only a few

generations descended from wild birds. As such, they
retain many of the protective instincts inherited from
their forebears. Many avian species kept as companions
are relatively low on the food chain. These protective
instincts have been developed to avoid drawing the
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 6.2c | This canary’s illness has wasted

away all the pectoral muscle. One must
observe the bird in a quiet situation — waiting
a few minutes for the masking behavioral
Fig 6.2a | The bird’s natural masking Fig 6.2b | Observing a caged bird is defense to wane and the fluffing to recur. A
phenomenon misleads owners and an art well worth perfecting. Outwardly, history of a small bird that has not eaten in a
many veterinarians. They think the bird this dead canary appeared fine to the day and has scant feces denotes a very sick
is fine, until the bird decompensates owner who brought the bird to the bird. See discussion under Fig. 6.42a-d prior
and shows overt signs of illness. This veterinarian. The bird died moments to handling such a sick bird.
blue budgerigar is showing the signs of after examination.
the latter stages of illness and is “sleep-
ing” and “fluffed up.” In the same envi-
ronment, the yellow bird is keenly alert.
attention of predators. One such instinct is often known and the ease with which early clinical signs can be over-
as the “masking phenomenon.” Predators are naturally looked highlight the importance of regular health exami-
drawn to prey that look or behave differently from oth- nations for the companion bird. Long-standing condi-
ers. Unusual coloring, weakness or lameness can single tions such as malnutrition can be detected and cor-
out a bird and make it attractive to a predator. A natural rected before the bird begins to decompensate and
instinct is therefore to avoid appearing “different.” A sick shows overt signs of illness.
bird will make a determined effort to look healthy, even
in the absence of predators. The classical “sick bird
look” we usually associate with illness — fluffed feathers,
closed eyes, lethargy — only develops when the bird is
History Taking
incapable of masking these signs (Fig 6.2a). Therefore, The collection of an accurate and thorough history of a
many of the patients presented to veterinarians are past patient is as crucial to making a diagnosis as is the physi-
the initial stages of their illness and are now decompen- cal examination and comprehensive diagnostic testing. A
sating rapidly. good history can alert the clinician to likely problems
and allow him/her to refine the diagnostic approach.
Secondly, due to lack of experience, most owners and
many veterinarians may miss subtle changes in a bird’s
behavior or appearance that are indications of a health SIGNALMENT
problem. Overlooking these early signs, combined with The first step in obtaining a history is to gain as much
the bird’s efforts to mask obvious clinical signs, invari- information about the bird itself as possible. A good
ably leads to the delayed detection of illness and the receptionist or technician can often obtain such informa-
presentation of the bird in extremis (Figs 6.2b,c). It is tion. The clinician should be familiar with avian taxon-
important that veterinarians learn to recognize early omy, sexual dimorphism, and species-specific behaviors.
signs of illness, and educate their clients, so that ill- Clients are often unaware of some basic facts about their
nesses can be detected before becoming too advanced. A bird (such as species, sex and age). Veterinarians intend-
physical examination form, used routinely by veterinari- ing to see avian patients regularly need to acquire a
ans and support staff, allows thorough and methodical working knowledge of commonly kept bird species and
documentation of the essential parameters of the physi- their physical characteristics. Such knowledge, while
cal examination (Fig 6.2c). The “masking phenomenon” available in some publications, is generally acquired
Chapter 6 | M A X I M I Z I N G I N F O R M A T I O N F R O M T H E P H Y S I C A L E X A M I N A T I O N
155
through experience and through being proactive and PATIENT HISTORY

inquisitive. This may require visiting other veterinarians,
How long have the clients owned this bird? (Fig 6.5)
aviaries, avian pet stores and zoologic collections and
Birds that have been in the owner’s possession for many
will take some time to acquire.
years, with no recent exposure to other birds, are less
The species of the bird is the first key piece of informa- likely to have infectious diseases (Fig 6.6) and are more
tion. Many clients are unaware of the correct identifica- likely to be suffering from underlying chronic conditions
such as malnutrition or inadequate exercise. Recently
tion of their bird, or may refer to it by a local name unfa-
obtained birds are more likely to have been in close con-
miliar to others. The cockatiel (Nymphicus hollandicus) is
tact with other birds and, as such, have possibly been
known all over the world as the cockatiel or ‘tiel, except
exposed to infectious diseases (Figs 6.7-6.9).
in Australia (the bird’s native land), where it is more com-
monly known as the Quarrion or, in Western Australia, as
Where did the owner obtain the bird?
the Weero (Figs 6.3a-f). The clinician needs to be able to
With experience, the clinician will be able to identify
recognize common species and have access to illustrated
“problem sources” of birds in the local area (ie, a certain
literature that will enable the clinician to confirm the sci-
breeder with a history of circovirus, bird fairs or a pet
entific name and to identify unfamiliar species (see
shop renowned for chlamydial problems). Developing a
Chapter 2, The Companion Bird for selected photos).
working knowledge of the quality of the sources of pet
Knowledge of the species can offer the clinician vital clues
birds in your area can be a key element of patient evalu-
to likely differential diagnoses for the sick bird and appro-
ation in your practice (Fig 6.10) (see Chapter 2, The
priate preventive medicine and husbandry during well-
Companion Bird).
ness examinations. For example, black cockatoos (Calyp-
torhynchus spp.) and some macaws require more fat in Is the bird aviary bred or wild-caught? (Fig. 6.11)
their diet than many other psittacines. The same diet fed Wild-caught psittacines, although less common in recent
to galahs (Eolophus roseicapillus) and budgerigars (Melo- times, are still coming into the pet market in certain
psittacus undulatus) can result in obesity, atherosclerosis parts of the world, such as in Europe. In countries such
or hepatic lipidosis. Species-specific behaviors, such as the as Australia, Africa and South America, it is reasonably
alarm “snuffing” typical of Pionus spp., is often mistaken easy to obtain a bird from the wild. The challenge of tam-
by new owners and veterinarians unfamiliar with this ing a wild-caught bird can be daunting. Paradoxically,
behavior as a pathologic respiratory condition. wild-caught (and therefore parent-raised) parrots that
survive the rigors of capture and have adapted to interac-
The age of the bird, while usually difficult to determine
tion with humans, are much less likely to demonstrate
once adult plumage has been attained, is another impor-
the common behavioral problems of our domestically
tant part of the anamnesis. Juveniles are more suscepti- raised parrots. Feather plucking, vent prolapse, inappro-
ble to conditions such as rickets, polyomavirus, circo- priate screaming, and learned biting are all more preva-
virus and bacterial infections, while adult birds are more lent in captive-raised African greys, Cacatua spp., and
likely to suffer from neoplasia, chronic malnutrition and macaws (Ara spp.) Fortunately, improved techniques for
degenerative conditions. While owners may not be sure raising these birds are being implemented, and both vet-
of the exact age of their pet, they usually know how long erinary and client awareness of the need for continued
they have owned it, and that may be sufficient for estab- attention to the emotional well-being of our parrots is
lishing an age-specific list of differential diagnoses. increasing. As veterinarians, our responsibility is to
inform the owners of the need for attention to and mod-
Many psittacines are sexually monomorphic — or at least
ulation of behaviors in their newly-acquired psittacine
appear that way to their owners. Knowing the sex of a
pet prior to the onset of problems. Suggesting and pro-
bird can be vital. For example, abdominal hernias are viding a contact for a knowledgeable parrot behavioral
almost non-existent in male birds, while being relatively consultant can make the difference between a decades-
common in females; yolk-related peritonitis and cystic long rewarding human-pet bond and years of frustrated
ovarian disease are obviously seen only in hens; cocks and dissatisfied co-existence (see Chapter 2, The
do not become egg bound. Do not accept the owner’s Companion Bird and Chapter 3, Concepts in Behavior).
assertion of their bird’s sex unless they have proof of sex
identification (ie, a history of egg laying or a certificate Parasitic infections (both gastrointestinal and hematoge-
of sex identification that can be correlated with this nous parasites) are more common in wild-caught birds.
bird). If such proof is not available, or the sex cannot be However, areas with outdoor aviaries in the USA often
positively diagnosed by physical characteristics, surgical have significant and occasionally fatal super infections
or DNA sexing may be required (Figs 6.4a,b). from various nematode species.
Fig 6.3b | These birds, if mature (over

9-12 months of age) represent the typi-
cal coloration of females of this species
and color type. Females are lacking the
bright yellow head in the normal gray
colored cockatiel. Today’s birds are sel-
dom pure, but rather hybrid mutations.
Coloration is not as dependable a factor
in determination of gender in these
mutation cockatiels. The bird on the left
has some yellow on the head and would

be said to be a hybrid — demonstrating
normal grey female markings like the
bird on the right but with the additional
yellow of a pied. Females of the normal
color have horizontal striping on the tail.

When compared to the male in Fig 6.3a
the body color is not the usual gray. This
Fig 6.3a | Knowing the species, the sex
is a sign of a split. The coloration illus-
and the name of the color mutation,
trated is likely to be “split” to cinnamon
such as in this cockatiel, makes an owner
as well as lutino in order to demonstrate
more comfortable with the avian veterinar-
these colors.
ian’s knowledge. While most immature
cockatiels resemble each other, mature
cockatiels are usually sexually dimorphic.
A mature gray male is shown here.
Greg J. Harrison
Greg J. Harrison
Fig 6.3c | This yellow-headed cockatiel was thought to be a Fig 6.3d | Young pearl-colored cockatiels (pearlies) have this
male until “he” laid an egg. color pattern. The males revert to being very similar to Fig 6.3a,
(normal grey), while the females retain the pearl pattern at
maturity.

Greg J. Harrison
Fig 6.3e | Yellow (in this case) or white wing bars are present Fig 6.3f | Pied-colored cockatiels are not as distinctly sexually
on the ventral surface in both cockatiel sexes until maturity. In dimorphic as normal grey cockatiels. Behavior may aid in gen-
immature females, these bars are present from the axillary der determination in these mutations. Male cockatiels carry a
region to the distal wing; in immature males they are present melody while females usually produce only one or two notes.
from the elbow joint to the distal wing. The bars are lost in
mature males during their first adult molt.
157
Jan Hooimeijer
Greg J. Harrison
Greg J. Harrison
Fig 6.5 | Some bird species, when prop-
erly cared for by the avian veterinarian
Fig 6.4a | Mature budgerigars are Fig 6.4b | A mature female budgerigar and the owner, can be safely co-mingled,
sexually dimorphic in the nominate with normal brown hypertrophy of the cere. especially in spacious outdoor housing.
green birds and most color mutations. Note the lack of hyperkeratosis, despite her
The male shown here has the charac- being an egg producing hen for several
teristic male blue cere. years.
Fig 6.6 | Boarding facility at an avian veterinary hospi-

tal. Proper testing prior to boarding is critical. Testing for

infectious diseases helps prevent disease outbreaks. A
complete history and physical examination at the time
of admission allows underlying disease, such as chronic
malnutrition, to be detected, brought to the owner’s
attention and addressed. This protocol minimizes the
chance that a bird will expire during boarding, and the
subsequent assumption by the owner that the boarding
was causative. Trained staff and attention to proper
husbandry and monitoring of the birds are essential.
Greg J. Harrison
Greg J. Harrison
Fig 6.7 | A free-flying Amazon in an Fig 6.8 | Wild birds at feeders outside
English aviculture facility is exposed to bird facilities can be a source of infection.
untested budgerigars and cockatiels. In this Wild lories at Currumbin Bird Park in
environment, this Amazon may serve as a Australia (see Chapter 21, Preventive
carrier, intermediate host or mechanical Medicine and Screening).
USDA
vector between the untested budgerigars

and cockatiels and the balance of the
aviary. As such, it poses as much or more Fig 6.9 | A cap, mask, coveralls or
danger to other aviary birds as exposure to gown, boots, disposable containers and
wild birds or infestation with rats or air filtration with HEPA-filters are used
roaches. at a USDA pet bird quarantine facility.
This demonstrates measures that must
be taken to impose a true quarantine
and limit disease transmission.
158
Friedrich Janeczek
Greg J. Harrison
Friedrich Janeczek
Fig 6.10 | These pet store birds have Fig 6.11 | Dr. Jan Hooimeijer exam-
been properly tested and are kept housed ines a confiscated Jamaican parrot
as a single species. Individuals for display, that was headed for the black market. Fig 6.12 | Perches over a fish pond and
sale and breeding are maintained in the Such birds are a constant source of rock substrate over drains facilitate cleaning.
store. When a collection is kept closed and diseases in the pet bird market and of The natural perches, artificial plants, and
is disease-free for several years, the inci- diseases potentially devastating to the reed walls are difficult to sterilize. However,
dence of disease will be much lower than poultry industry. in a properly managed, disease-free collec-
in birds from pet stores with mixed, tion, disinfection is not required.
untested, open collections.
Old World species of psittacines are also particularly sus- birds. Birds sold prior to weaning, often to inexperi-
ceptible to infection and death from sarcocystosis. enced owners, are predisposed to develop aspiration
pneumonia. Behavioral problems are also common in
In Australia, the probability of a wild-caught cockatoo babies hand-fed with the traditional methods (see
being affected with psittacine beak and feather disease Chapter 3, Concepts in Behavior).
(PBFD) is much higher than that of an aviary-bred bird.
The same is true of African greys imported into the Although incubator hatched eggs, when harvested by
European Union (EU) from the wild. In the USA and the knowledgeable aviculturists, have a far less chance of
EU, captive African greys, eclectus, lories, sun conures and accidental breakage or parental destruction, several
assorted other species can be infected with proventricular negative consequences arise. Inappropriate incubator
dilatation disease (PDD) (see Chapter 32, Implications of temperature or humidity can cause congenital deformi-
Viruses in Clinical Disorders). Macrorhabdosis is common ties. The lack of antibodies from initial crop feedings by
in captive-raised budgerigars and lovebirds (see Chapter the parents may create an increased susceptibility to
30, Implications of Macrorhabdus in Clinical Disorders). many diseases, some of which can prove fatal. Addition-
ally, the consequence of deprivation from parental con-
Is the bird hand-reared or parent-reared? If hand- tact during the first days and weeks of life is not docu-
reared, at what age was it pulled from the nest, or mented in birds, but extrapolation from other species
was the egg incubator hatched? would make it likely that a serious negative impact may
The health of juvenile birds is dependent largely on the arise from this isolation.
health and nutrition of the parents (Fig 6.12). Hand-
reared birds are dependent upon the quality of the Does the client have other birds? Are they in contact
hand-rearing formula being fed and the skill of the per- with each other? Are any of these birds affected with
son performing the hand-feeding. Parent-reared birds similar clinical signs?
tend to be more difficult to tame, unless they are han- Other birds in the household may have many effects on
dled on a regular basis before fledging. Hand-reared the environment of the presenting patient. These could
birds on the other hand, while usually more closely be a source of infection or susceptible to infection from
bonded to people, often have behavioral disorders asso- a bird presenting to the practitioner with a contagious
ciated with poor socialization, especially if reared in iso- disease. It would be significant if a blue and gold macaw
lation. If a large number of chicks from different sources (Ara ararauna) presenting for dyspnea was being kept
are reared in one facility, there is a higher probability of in the same room with a powderdown-producing
the spread of diseases such as polyomavirus and chlamy- species, such as an umbrella cockatoo (Cacatua alba).
diasis. All of these factors need to be assessed during the With feather destructive or self-mutilation behaviors, the
history collection, especially when examining juvenile presence or absence of other birds may affect (positively
159
Greg J. Harrison
Greg J. Harrison
Fig 6.13a | Birds are exposed to natural sunlight yet protected Fig 6.13b | Fluorescent lights may have cyclic flickering that is
from over-exposure in this aviculturist’s facility. potentially harmful, both physiologically and psychologically.
or negatively) the emotional state of the affected bird. Is the bird able to remove itself from view?
Is it supplied with a hide box or comparable visual
Previous Medical History screen? Is it kept isolated, away from family activities, or
The avian patient’s previous medical history should be in the middle of constant activity?
determined to the extent possible.
Is the bird permitted to get adequate sleep at night?
• Has the bird been ill before?
A common owner misconception is that covering a
• If so, what were the clinical signs, tests performed,
bird’s cage, while that cage is located in a room with the
results of those tests, diagnosis and therapy
lights and television on, is providing the bird with an
administered?
environment conducive to sleep. Whether covered or
• What was the bird’s response to this therapy?
not, the number of hours that a bird is supplied with
• Has the bird recently been treated with remedies sufficient darkness and quiet is critical to health — both
purchased at a pet shop or supplied by a breeder? emotional and physical.
If so, what medication and for what period of time was
or is it being administered? Does the bird have access to direct, unfiltered sun-
• If the bird is presented for a second opinion or as a light on a regular basis? (Figs 6.13a,b)
referral, may we request copies of the previous Increased calcium absorption and metabolism from
medical record? ultraviolet (UV) light exposure is beneficial to birds as it
is for many other species. Recent research shows that
HUSBANDRY some species may have an absolute requirement for UV
light (see Chapter 5, Calcium Metabolism). In the appro-
Is the patient an aviary bird, a companion bird, or a
priate climates or seasons, regular outdoor exposure to
zoological specimen?
sunlight can have many additional benefits, both physi-
The husbandry of aviary birds and zoological specimens cal and psychological. Increased humidity, the sounds
are discussed elsewhere in this book, and the reader is and sights of nature, breezes and changes in barometric
referred to the appropriate chapters. Assessment of a pressure all promote emotional well-being in birds
companion bird’s husbandry must include the cage, the when these are provided with adequate thought for the
environment around the cage, and the bird’s interaction bird’s safety and comfort. This leads to the next point:
with its environment.
If the bird is kept outside, is it safe from predators
Is the cage in which the bird was transported the and diseases?
bird’s permanent cage? Are there potential disease vectors such as mosquitoes,
If it is not, ask the owner to describe the permanent roaches or rats that can access the bird’s cage? If the bird
cage, using the guidelines contained in the following is brought into the house at night, is the food and water
paragraphs. removed and replaced to prevent contamination of the
cage contents overnight and subsequent exposure to
Where is the cage located in the house? diseases such as sarcocystosis? (Note: Additional hus-
In the kitchen, living room, individual’s bedroom, or bandry issues are covered in Figs 6.14-6.17a-c.)
screened porch? Predators such as raccoons are notorious for reaching
into cages and severing legs and wings from parrots. common thread of malnutrition. For many generations,
bird owners have accepted as fact that seed is a complete
Does the bird come out of its cage? Is it supervised diet for birds (Fig 6.25-6.41). This is reinforced by adver-
when out of the cage? tising from many producers and vendors of bird seeds.
Remember that “supervision” is subjective. Many birds Historically, there has been a lack of readily available
with heavy metal toxicity ingest the inciting material information on the deleterious effect of all-seed diets.
while being supervised. Owners are often adamant prior Birds, as many other animals, often prefer high fat diets.
to the radiographic diagnosis that their bird has no Given a choice between seed, vegetables, formulated
access to metal. diets and fruits, nearly all birds will consume the seed
first. Given this preference, it is not surprising to hear
Answers to questions concerning time out of the cage
many bird owners state, “All he will eat is the seed, so
will also help establish the degree of interaction
that is all that I give him.” Chapter 4, Nutritional Consid-
between the bird, its environment and its owners.
erations, gives more details on nutrition and nutritional
Are the bird’s wings clipped or is it free-flighted? Is disorders. The reader is urged to study this carefully.
the bird exposed to potentially dangerous situations?
How much food is being consumed?
Sinks full of water, ceiling fans, open toilet bowls and
sliding glass doors are among the potentially injurious, if An important part of history taking is to ascertain not what
not fatal, environmental hazards to which a bird may be the owner offers the bird, but more importantly, what the
exposed. bird actually consumes. The clinician needs to be aware
that there are major species differences in dietary require-
Different injuries and exposures occur in flighted and ments. For example, some species may have a higher
non-flighted birds. For example, heavy-bodied birds with requirement for fat than others. There is no single diet
severe wing clips are prone to beak and keel trauma. that is appropriate for all avian species any more than
While keel and beak tip trauma may be obvious due to there is one diet suitable for all mammalian species.
the presence of blood, the dislocation or straining of the
quadrate bone and associated muscles may present only In addition to the type of food offered and consumed,
as depression and lack of appetite. feeding practices need to be reviewed. Some birds, even
when provided with an excellent diet, will consume an
Conversely, concussive force to the head is most com- excessive quantity and become obese.
mon in fully flighted birds that fly into glass doors or
mirrors, as are ceiling fan injuries, burns from stovetops Is the food prepared fresh daily? Are dishes cleaned
and drowning from accessible water sources. each day? Does the bird dunk food into its water dish?
This last practice of dunking food creates a nutrient-rich
Does the bird interact with other animals or birds?
broth ideal for bacterial contamination. Sterilization is
Dogs and many other pets may carry clostridial bacteria not necessary in the healthy home environment, but rea-
normally, while pet birds often develop digestive disor- sonable cleanliness should be employed.
ders from exposure to such bacteria (see Chapter 4,
Nutritional Considerations, Section II Nutritional Does the bird get any treats?
Disorders). Also, cat claws and bites may cause penetrat- Treats can supply sufficient calories to pet birds that any
ing wounds that do not leave obvious external marks attempt at weight control is sabotaged. Also, certain
but often cause internal damage and/or infection. foods, such as guacamole dip, are not always perceived
by the owner as potentially toxic. Other foods, such as
Is the bird subject to potential exposure to toxins?
snacks containing excessive sodium, may cause or exac-
Burning plastic, non-stick cooking pans, cigarette
erbate feather-destructive or mutilation behaviors (see
smoke, aerosol sprays or household plants are some of
Chapter 2, Concepts in Behavior Section III p82).
the common substances causing toxicity in pet birds.
Additionally, the metal wicks of candles may contain
Are vitamin and mineral supplements being
lead. Smoke (including cigarette, incense, candles and
administered?
barbeque grills) and other strong smells are potentially
If so, what are the contents of the supplement and in
hazardous to pet birds, and exposure to these should be
what form is it provided (ie, in the water or on the food)?
avoided (see Chapter 31, Implications of Toxic
Vitamins administered in the water may decrease a bird’s
Substances in Clinical Disorders [Figs 6.18-6.24]).
water consumption, discolor the urates or feces, and
either be ineffective due to dilution and lability, or cause
DIET hypervitaminosis if administered in conjunction with vita-
Underlying many health problems in pet birds is the min-enriched seeds and/or formulated diets.
161
Greg J. Harrison
Fig 6.14 | Cage with natural perches. This bird’s cage is too Fig 6.15 | Here sand is used as a cage substrate. Note the
small to allow for flight. Note that two sources of calcium (min- accumulation of feces and food indicating poor husbandry and
eral blocks) are provided in addition to a formulated diet. This potential microorganism overgrowth. Sand can be used but
may lead to nutritional imbalance due to excess calcium (see needs to be raked clean often and replaced when dirty.
Chapter 4, Nutritional Considerations).
Greg J. Harrison
Greg J. Harrison
Fig 6.17a | Cement and sandpaper perches. Sandpaper

perches are generally ineffectual and may cause or add to plan-
Fig 6.16 | Newspaper is a good substrate if changed daily. tar surface abrasion. Overgrown nails are a sign of metabolic
The number and character of droppings can be determined disease and require addressing the underlying problem. Sharp
readily, yielding information reflecting the state of the bird’s nail points are normal and necessary in the wild. Owners often
health. These “popcorn” droppings are not normal. request trimming of these tips to prevent discomfort to their
skin. Some blunting may be necessary to prevent trauma to the
owner, but the bird will be less stable when perching and the
owners must be forewarned of this. In some cases cement
perches can work to keep the tips blunted when the proper type,
size, texture and placement in the cage is accomplished.
Greg J. Harrison
Greg J. Harrison
Fig 6.17b | Plastic perches with ridges to allow a better grip Fig 6.17c | Natural hard woods like manzanita make long
can be wedged into stainless steel cages. They are easy to clean lasting perches. However, these do not offer a rough surface on
and sterilize. which the birds can clean their beaks, nor is such a hard slick
surface the ideal perch.
Greg J. Harrison
Greg J. Harrison
Fig 6.18 | Some dog and cat flea products can be a danger to Fig 6.19a | “Hardware cloth” is galvanized iron. The galva-
birds. nized coating is usually predominately zinc and may also con-
tain lead. While usually safe for non-chewing birds like this
Tragopan sp., it is not safe for members of the psittacine family.
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 6.19b | Toys are frequently made of Fig 6.19c | Toys can have the galvanized
polished galvanized metal. Here a mag- hook replaced with brass, the chain
net is used as a diagnostic tool — if it replaced with stainless steel, leather or nat- Fig 6.20 | A decorative palm tree is a safe
attaches, the underlying metal is iron. ural fibers (hemp, sisal or cotton), and the house plant but items in the soil such as
This is a common metal that is galvanized link replaced by one of stainless steel. fertilizer beads and other slow release items
to prevent rust. Galvanization is primarily can be toxic.
zinc. The circular shaped magnet has
attached to a chain and anchor screw,
indicating galvanization is likely and
these objects should be removed.
Greg J. Harrison
Greg J. Harrison
Fig 6.21a | Lead weights used to balance car Fig 6.21b | Curtain weight made of Fig 6.21c | Lead soldered galvanized
tires and sink fish bait. These are extremely toxic, lead. water dish.
being rapidly dissolved in the ventriculus and
absorbed into the blood stream.
163
Greg J. Harrison
Greg J. Harrison
Fig 6.22 | A dangerous toy’s clip has gotten Fig 6.23a | While tobacco can be
stuck on this African grey’s beak. toxic if ingested, smoke from cigarettes
is the product’s greatest danger to
birds. Contact with nicotine has been
considered as a cause of dermatitis.
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 6.23b | Shelled nuts often get rancid Fig 6.23c | Seeds infested by insect Fig 6.23d | Chocolate contains dangerous
unless refrigerated or stored in glass or foil larvae that hatch often become “webby” levels of theobromine and caffeine.
bags. due to a fungus (usually Aspergillus) Chocolate containing less sugar generally
and can produce mycotoxins. Do not contains a higher level of toxic substances.
freeze webby seed and then feed it. The
larvae from a grain moth has pene-
trated this sunflower seed.
Greg J. Harrison
Greg J. Harrison
Fig 6.23e | Although pothos is considered Fig 6.24 | Mineral blocks, especially
poisonous in small animals, it has never when provided to birds on formulated
been a proven cause of systemic toxicity in diets, could add toxic levels of calcium
healthy pet birds. (see Chapter 4, Nutritional Considera-
tions).
Greg J. Harrison
Greg J. Harrison
Fig 6.25 | Palm nuts are eaten by wild hyacinth macaws.
Cattle consume and digest the sticky, fleshy outer coating.
The seed on the left has been passed out in feces; birds Fig 6.26 | Animal protein (meat, egg, cheese) has been removed
prefer to eat the nut in this form. from pet bird diets for 15 years with excellent results. Whether
adding scientifically formulated amounts of animal protein to the
diet of breeding birds is warranted is still unknown. Vegetable pro-
tein diets have been empirically proven to be sound.
Greg J. Harrison
Greg J. Harrison
Fig 6.27 | Offering excessive amounts of unbalanced foods Fig 6.28 | An aviculture diet used commonly in the 1980’s.
allows the bird to choose its diet and nutritional disorders result. Birds on sunflower seeds, apples, oranges, grapes, pound cake
The amount of food shown was offered twice a day. The imma- and bread rapidly developed nutritional disorders, especially the
ture corn (sweet corn), baby beans, zucchini, and squash are of breeding females. Nutritionally deprived parent birds were
little nutritional value. The broccoli, kale and carrots are difficult unable to raise their young. Incubation of the eggs and hand-
to digest. While no sunflower seeds are offered, safflower is just feeding from hatching had to be employed. The associated
as imbalanced, being even higher in fat than sunflower seeds. developmental problems in the young disappeared when a for-
Peanuts are also high in fat, and when fed without the shell, mulated diet was instituted.
often become rancid. Peanuts are a common source of myco-
toxins. If they are fed at all, a human grade of peanuts certified
free of mycotoxins should be used.
Greg J. Harrison
Greg J. Harrison
Fig 6.29a | Sunflower seed, millet and canary seed are the Fig 6.29b | Since no standards have been officially declared,
historic staples of the bird food industry. Only one current man- diets such as the one pictured above are incorrectly marketed as
ufacturer of formulated diets uses these century-old ingredients “complete diets” in many pet stores. Colored seed is the largest
and improves their nutritional balance with appropriate addi- part of the pet bird food market in the USA. Newer versions of
tives. This has improved acceptance and avoided potential prob- these colored seed diets have added shaped and colored pellets
lems that one may get when attempting to incorporate novel but empirically are not nutritionally superior to plain seeds.
ingredients. New, untested ingredients can create unforeseen
problems that may take decades to discover.
165
Edwardo Nycander
Fig 6.29d | Free-ranging scarlet macaws hand-raised on an
organic formula in Tambopata, Peru. Notice the tight feather
structure and brilliant colors compared to Fig 6.29c.
Fig 6.29c | A scarlet macaw taken from
a USA pet store magazine ad for a prod-
uct that claims to have been developed by
their researchers “to make a new all nat-
ural... treat (sic) premier supplement for
all caged birds — and better than all
other brands.” The abnormal color and
physical characteristics of the bird’s feath-
ers would indicate the company, their
researchers and/or advertisement person-
nel are uninformed as to the desired
physical attributes of a healthy bird.
Greg J. Harrison
Greg J. Harrison
Fig 6.30 | An aviculturist’s food bowls for macaws and large Fig 6.31 | Twenty-five grams of whole grain (dense) organic
cockatoos on the left and Amazons and African greys on the right. nuggets (on the right) compared to an equal weight of traditional
The organic formulated nuggets are a high potency formula. extruded brand made from refined flours that expand more read-
During the non-breeding season the seeds and nuts are stopped ily. The fiber and other ingredients in whole grain flours lack the
and for some species the nuggets are changed to a maintenance refined carbohydrates necessary to get the extrusion-induced
product. After ten years of this diet, the common avicultural prob- expansion (fluff) attained with extrusion of these less-nutritious
lems of infertility, incubation, raising, hand-feeding from day one, refined flours. These less expensive refined flours are by-products
congenital and developmental conditions and chronic “infections” of the oil industry. The end product produces larger, lighter bags
are no longer encountered. The parents incubate and raise the of food at a reduced cost. Such products require more additives
babies until a week or so prior to weaning, when hand feeding is than whole grains to establish balanced nutrition.
initiated to assure tameness. With production increased and prob-
lems decreased, profits at this aviary have soared.
Greg J. Harrison
Greg J. Harrison
Fig 6.32 | Quantity of pellets consumed in a day by a cockatiel Fig 6.33 | While many theme parks’ cage labels state that the
for $.01 (USA). Many owners waste food as they are not prop- birds eat a formulated diet, the bowls are often full of a seed
erly educated on proper food volumes. mix with colored pellets. Nutritional disorders are commonly
observed in such a facility. Incentives such as free foods, cash
donations and revenue sharing may be given to the facility for
reciprocal endorsements that have little to do with the actual
food fed or its nutritional value.
Greg J. Harrison
Greg J. Harrison
Fig 6.34 | Seeds top-dressed with a powdered mineral/vitamin Fig 6.35 | Veterinarians in the USA often recommend a pressed
supplement show the powder on the bottom of the food cup, seed cake. The waste in this bird’s cage shows that most has
which is subsequently disposed of with the seed hulls. been discarded except for the oat hearts. The food coating (egg,
minerals, and vitamins) was discarded untouched. This bird had
liver, respiratory and orthopedic problems that improved when
switched to an organic formulated nugget that could not be
selectively consumed.
Greg J. Harrison
Greg J. Harrison
Fig 6.36 | Organic formulated nuggets are low in synthetic Fig 6.37 | Vitamins in this bird’s water color it
vitamins and have natural sources of nutrients (alfalfa and spir- yellow. Many birds will not drink freely from
ulina for carotinoids, kelp for iodine and trace minerals, sea water with this color and taste, and dehydration
salt, natural clay with naturally chelated minerals, high soluble can result. Bacterial and fungal growth is also
fiber from digestible hulls and psyllium). These nuggets are free encouraged in this medium. Finally, the dilution
of pesticides, food coloring, by-products and preservatives. The of the vitamins and exposure to water, air, heat
absence of preservatives requires cool, dry, dark storage in air- and light degrade many of the labile vitamins.
tight containers to prevent rancidity or loss of nutrient value (see
Chapter 4, Nutritional Considerations, Section II Nutritional
Disorders).
167
Greg J. Harrison
Greg J. Harrison
Fig 6.38 | Water is often contaminated by improperly designed Fig 6.39a | Plastic pipe and water hoses have been incrimi-
purifiers. Many allow bacterial proliferation or fail to remove nated in chronic Pseudomonous spp. infections.
pollutants. In the USA, reverse osmosis (blue and white canis-
ters), bottle and tap water are commonly provided. Only water
labeled “USDA drinking water” is regulated and must meet gov-
ernment standards.
Greg J. Harrison
Greg J. Harrison
Fig 6.39b | Inadequately cleaned plastic bowls are potential Fig 6.40 | Salt/mineral spool, mineral block, powdered cal-
sources of bacterial infections. Crock and stainless steel are less cium, grit and oyster shell are not necessary for birds fed formu-
porous and thus less likely to be a problem. Water bottles are lated diets, and can be harmful (see Chapter 4, Nutritional
best constructed of non-porous glass. Considerations).
Fig 6.41 | Male cockatiel on a seed and

table food diet. Note the bent tail, ruffled
feathers, and excessive pin feathers over
the shoulder and crown. The same bird is
shown in Fig 6.3a 6 months after conver-
sion to an organic formulated diet.
Pediatric Patients feeding patterns of these birds. This technique has been
Concerns with babies still being hand-fed add additional extensively used by Phoebe Linden, of Santa Barbara
elements to the anamnesis. Bird Farms, with promising results.
What hand feeding formula is being used? Is the for- Inexperienced hand feeders often cause aspiration or
mula being prepared according to the manufac- inadvertent starvation of birds while hand feeding.
turer’s recommendations? Is anything extra being Generally, a baby bird can accept roughly 10% of its
added to an already balanced diet? body weight per feeding. The frequency of the feedings
It is common to see a hand-feeding formula designed for and the quantity of each feeding will vary with the age,
macaws used on a baby Cacatua spp., with resultant species and individual.
hepatic lipidosis. Likewise, additives such as peanut but-
Common problems to look for in the history and physi-
ter, macadamia oil and sunflower seeds can add addi-
cal examination of hand-feeding baby birds include:
tional fat and detract from other necessary nutrients.
1. Insufficient calories being given. Often a new bird
Conversely, many prepared formulas for hand-feeding owner will adhere to guidelines that state a bird
have insufficient calories per unit volume for some should have a reduced number of feedings per day at
species of psittacines, notably macaws. a given age. The owner may fail to understand that
this is based on the supposition that the bird is start-
What is the temperature of the food when fed? What ing to eat on its own at this age. Some birds have not
are the quantity, frequency and method (syringe, yet even been offered food, but the frequency of feed-
tube, spoon, cup, weaning pellets) of feeding? ings has been severely reduced, leading to weight loss
Using a microwave to heat the formula can lead to crop and debilitation.
burns. What is not commonly understood is the follow- 2. Over-distention of the crop. This can have many
ing: food heated in a microwave oven can have hot spots causes, but over-distention may be obvious on physi-
due to uneven heating. When water is heated in a cal examination and may be associated with a history
microwave oven and then poured into another con- of feeding an excessive volume at a given feeding.
tainer to be mixed with the formula, the temperature of
the resulting formula will be more uniform. The temper-
BEHAVIOR
ature of the formula should still be accurately assessed
A behavioral history is becoming increasingly important
with a thermometer.
as pet birds move out of their cages and into their own-
However, if the same container in which the water is ers’ lives. Just as countless dogs and cats are euthanized
heated is used to receive the powered formula, and mul- every year because of behavioral problems, many birds
tiple syringes are extracted over several minutes from suffer a similar fate or are transferred from household to
this container, disaster often occurs. Many containers household.
hold heat from the microwave, and gradually transfer
this heat into the formula, causing the subsequent As psittacine behavior is determined largely by the inter-
syringes that are delivered to be much hotter than the action between the bird, its owners and its environment,
initial temperature reading indicated. Severe crops questioning must focus on these areas. Who is the pri-
burns can result from this practice. mary caretaker? Whom does the bird seem to prefer?
Does the bird dislike anyone? How many hours per day
Conversely, baby birds may refuse formula that is not does the bird spend alone? What does the bird see and
warm, and cold formula can delay crop emptying. hear when it is alone? Does the bird spend time with
other birds or other pets?
Various methods of administering the formula are used.
Most common still is the use of a syringe, which allows Many factors that may influence pet psittacine behavior
an accurate determination of the quantity of formula are yet to be determined. For example, recent work has
being consumed. Spoon and cup feeding are also used indicated that fluorescent lights are perceived as a con-
successfully by some. Soft plastic or rubber tubing can stant flickering by the eyes of birds, and both physio-
be used, and this method does decrease the mess pro- logic and behavioral problems may arise from previously
duced by bobbing, but carries the inherent risk of acci- unrecognized sources such as these. Also, there is
dental ingestion of the tube if it becomes detached from increasing concern that our traditional methods of hand-
the syringe. It also may not be as psychologically satisfy- feeding may by laying the groundwork for the develop-
ing as having food that can be tasted. ment of behavioral problems later in life (see Chapter 3,
Concepts in Behavior).
The use of soft, warm, solid foods for feeding and wean-
ing is advocated to more closely approximate the natural It is important to clarify the bird’s interaction with its
169
owners (human flock). How tame is the bird? Does it turbing the bird until it has settled, otherwise valuable
readily step up onto a proffered hand? Does it always try clinical signs may be overlooked. The practitioner
to move up onto a person’s shoulder? Is this allowed or should be seated in order to remove any predatory
encouraged? Does the bird talk? Does it like to be pet- threat to the bird. This will expedite its relaxation and
ted? Where? How does it react to different family mem- therefore accelerate the demonstration of clinical signs.
bers? How does it react to strangers? For the potential
significance of the answers to these questions, see Observe the bird’s respiration (Fig 6.42a). Once the bird
Chapter 3, Concepts in Behavior. has settled in its cage in the examination room, there
should be no open-mouthed breathing, marked tail bob-
bing, increased respiratory effort or audible respiratory
noise. The presence of these signs should alert the clini-
The Presenting Complaint cian to potential respiratory compromise. Respiratory
compromise may be due to true respiratory disease, car-
Once the bird’s background has been established, it is
diac disease, space-occupying mass or fluid within the
time to assess the reason(s) the bird has been presented.
coelom, anemia or severe debilitation. Care must obvi-
Ask the client to describe the problem. Do not interrupt
ously be taken with handling patients that are demon-
the client other than to seek clarification of details. You
strating respiratory distress.
may need to repeat back to the client what they have
said to ensure that a mutual understanding and clarifica- The bird’s posture should be observed (Figs 6.42b-d).
tion of the owner’s concerns are reached. For example, Sick birds that are hypothermic will fluff their feathers in
many birds presented by their owners for “diarrhea” are an attempt to conserve body heat. They sit still to con-
actually polyuric. An explanation of the difference serve energy and, as they weaken, they sleep more (Fig
between diarrhea and polyuria, and a determination of 6.42e). Such signs are the classic “sick bird look,” but
which is actually present, should be made prior to the not all sick birds will display these signs.
physical examination and diagnostic testing.
Evidence of a wing droop, lameness or reluctance to
Once the practitioner has identified the problem(s), bear weight on one leg may indicate a musculoskeletal
appropriate questions must be asked of the client to problem or a central or peripheral neurologic affecta-
determine duration, severity, progression, previous diag- tion. Spinal deformities can often be detected by an
nostics if known, previous therapeutics, and response to abnormal positioning of the tail. An upright position
prior treatments. When did it start? Is this the first time with a wide-legged stance may indicate egg binding or a
it has happened? Have other treatments been tried? Who similar space-occupying mass in the coelom or cloaca.
prescribed these treatments? Did they work? Is this con- Birds that hold both wings away from their body and
dition static, progressive, or resolving? Are other birds pant are usually heat stressed or severely oxygen
affected? deprived.
The history taking as described above is not comprehen- The bird’s plumage can be cursorily examined prior to
sive. As one gains information, areas of concern will restraint. Normally the plumage should be sleek, well
become apparent, and additional questions may be groomed and clean. Untidy or dirty plumage may indi-
needed for clarification. The clinician must not domi- cate that the bird is not grooming itself, or that there is
nate the conversation — rather, he or she should ask some type of feather abnormality. Discolored feathers
short questions and listen carefully to the client’s reply. can reflect a variety of problems, including PBFD,
However, the clinician must be prepared to guide the chronic liver disease, excessive handling with oily hands
discussion, to ensure that the maximum amount of use- or malnutrition. Closer examination of the feathers is
ful information is obtained. warranted when the bird is removed from its cage.
Note the condition of the beak and toenails. Overgrown

or flaky beaks or overgrown and twisted nails may be
The Distant Examination associated with PBFD, poor husbandry, chronic liver dis-
ease or malnutrition.
During the history taking, the clinician should be observ-
ing the bird and noting its behavior prior to restraint. Watch as the bird defecates, looking for signs of strain-
ing or discomfort and listening for any accompanying
Most birds, no matter how ill, will make an effort to flatulence or vocalization. Birds do not generally pass
mask their clinical signs when first brought into the any gas and should be able to defecate effortlessly.
examination room. The clinically ill bird will be unable
to maintain this pose for any length of time. Avoid dis- Observe the bird’s behavior, assessing how tame the bird
Greg J. Harrison
Greg J. Harrison
Fig 6.42a | Prior to handling this dyspneic female cockatiel Fig 6.42b | The owner noted that this pearl female cockatiel
oxygen is warranted (see Chapter 7, Emergency and Critical was fluffed and not eating its seed diet.
Care).
Greg J. Harrison
Greg J. Harrison
Fig 6.42c | The same bird as in Fig 6.42b is shown preening. Fig 6.42d | A 20-year-old lutino cockatiel is shown
Physical exam demonstrated an egg in the reproductive tract. after having the jugular vein wet with alcohol for
This exemplifies the ability of a bird to mask symptoms. venipuncture. At this age, geriatric considerations
are pertinent. Even this minor restraint has caused
the bird to appear listless and sleepy. Geriatric (or
otherwise stressed) birds may require more gentle
handling and for shorter periods of time. Geriatric
birds may benefit from the addition of fatty acids
and herbs to the diet (see Chapter 10, Integrative
Therapies). Geriatric pet birds are becoming more
commonly seen in practice.
THE CAGE
Greg J. Harrison
The cage must be of sufficient size to allow the bird to

extend and flap its wings and to turn around without
Fig 6.42e | This finch (or any bird that is motionless and on damaging feathers. The bird should ideally be able to
the bottom of the cage) is a high risk patient. The clients need express its normal behaviors within its cage, unless the
to be informed in advance of the danger of handling such a sick cage is used only as a roosting space while the bird has
bird. Heat and oral electrolytes, glucose and caffeine are often
the best first steps. The prognosis for such birds is guarded, and access to a larger environment. The cage should be con-
a simple breast muscle evaluation will determine if emaciation is structed of materials that are safe and appropriate for the
present. This commonly encountered finding confirms the size and power of the bird’s beak. Small gauge wire,
chronicity and severity of the bird’s condition (see Fig 6.2c).
while suitable for smaller psittacines, is readily chewed
and eaten by larger birds, often leading to heavy metal
toxicity. Similarly, poorly galvanized cheap wire often has
is and whether it is showing any overt sexual display tags of zinc on it that are easily picked off and swallowed
towards the owner, objects in its cage or other people by psittacines of all sizes. Unsealed wooden cages are
present in the room. Note the owner’s interaction with inappropriate, not only because many birds will chew the
the bird, as this may reveal valuable clues to relation- wood, but also because wood is impossible to disinfect,
ships at home. making it difficult to maintain adequate hygiene.
171
The floor of the cage should not be covered with grit, ODORS
sand or wood shavings. The substrate of a cage is rarely Birds that are exposed to significant cigarette smoke will
changed with sufficient frequency, and ingestion of sub- absorb the odor of smoke onto their feathers. Problems
strate material can lead to blockage of the gastrointesti- ranging from respiratory disease to feather destructive
nal tract. Newspaper is a non-toxic and readily available behavior have been linked to excessive exposure to
substrate. It is also inexpensive, which encourages fre- smoke.
quent changing.
The feces of birds with enteritis, especially due to
Many cages are sold with plastic or wooden dowel clostridial species overgrowth, have a distinctive, fetid
perches. These are rarely suitable, since the smooth, odor. This seems to be most prevalent in cockatoos with
unchanging surface and diameter offer little exercise for fecal retention and cloacal prolapse and in birds with
the feet and toes, and the symmetry can create constant extensive and restrictive cloacal papillomatosis, although
pressure on selected areas of the feet, leading to podo- it may occur in any bird. The detection of this odor in a
dermatitis. The uninformed owner may be reluctant to bird’s stool should be pursued diagnostically, usually by
discard these perches, assuming that since they were first performing a Gram’s stain on the feces.
supplied with the bird cage that they are appropriate. Owners may present their bird, commonly an Amazon,
Just as variation in diameters and surfaces of perches are for “bad breath.” This is usually the natural smell of
important for the individual bird, birds of various sizes these species, and not related to disease.
and species require different ranges of perch diameters.
The positioning of the perches within the cage is also

important. Birds tend to sit on the higher perches, so Examination Room
the diameter and texture of these perches may need to
be alternated. Perches should not be placed so that a
Equipment
bird will be defecting into its food or water dish. A bird Appropriate equipment for use in the examination room
may be encouraged to sit on a concrete perch if a food includes:
dish or treat cup is placed so that access to this cup is • A supply of freshly laundered towels of different sizes
achieved by perching on the desired surface. (or paper towels) for restraining birds.
• Scales capable of weighing in grams, preferably with a
Dishes should be constructed of a material appropriate detachable T-perch (to allow birds to perch on while
to the species using them, and free of contaminants being weighed), and a container in which to weigh
such as lead, which has been used as a solder to repair smaller, fully flighted birds.
cheap galvanized dishes. Galvanized dishes should not • A training perch for the bird to perch on while being
be used, as the zinc in the galvanized coating may leech examined.
into the food or water. Dishes should be cleaned daily • Clinical equipment, such as stethoscope, a focal light
and positioned where they are unlikely to be soiled. source, magnifying loupes, needles and syringes,
Food and water dishes should not be placed alongside blood collection tubes and culture swabs.
each other, as many birds will drop their food into the
The use of heavy gloves to catch and restrain birds
water, producing a broth within a few hours. Birds that
should be discouraged. With these gloves on, the clini-
tend to dunk their pellets into their water may need to
cian cannot be sensitive to small movements of the bird,
have the water and food dishes placed on opposite sides and can easily hurt or even kill the patient. Additionally,
of the cage. these gloves cannot be cleaned or sterilized.
Toys should be appropriate for the bird, and should not Ensure that the room is escape proof, and that clinic
be so numerous as to restrict the bird’s movement staff will not enter the room unexpectedly. Avoid stress-
within the cage. Cheap toys, especially bells, are a com- ful sights and sounds such as dogs, cats and other
mon source of lead or zinc. Metal items that can be potential predators.
attached to a magnet are iron based. Shiny silver-appear-
ing metals are often galvanized and polished and are a
potential source of zinc toxicity (see Figs 6.19a-c). Toys
should be made of natural materials, such as rope and
Handling and Restraint
wood, and should be replaced as soon as they become Once a thorough history has been obtained and the bird
frayed. Bathing or misting should be available on a regu- observed in its cage, the next step is to examine the
lar basis (see Chapter 3, Concepts in Behavior). patient more closely. In order to do so, the bird will
need to be handled and restrained. In the case of aviary is potentially a very intimidating experience for a pet
birds, this should be done with a view of minimizing bird. Keep talking in a friendly voice, and maintain eye
stress to the bird, while at the same time, avoiding injury contact (see Chapter 3, Concepts in Behavior).
to the handler. Many companion birds, on the other
hand, have learned to trust humans and regard them Birds that are not tame can be caught using a towel as
affectionately. Destroying this trust through aggressive described above. These birds will rarely stay still during
catching and handling techniques can adversely affect capture, so a quick capture is the best approach. The
the bond between owner and bird. This relationship most dangerous part of the bird’s body should be immo-
must be preserved, and handling techniques for closely bilized first (ie, psittacines = the head and beak; raptors
bonded birds should emphasize minimal stress and fear = the feet). Once the dangerous areas are immobilized,
the bird is wrapped in the towel and removed from the
(see Chapter 3, Concepts in Behavior).
cage.
As the oils on human skin can be detrimental to the
When the bird has been removed from the cage, the
feathers of many species, a light dusting of unscented
next step will be determined by the bird’s tolerance of
talcum powder on the clinician’s hands is appropriate
handling. Very tame birds can be placed on scales to be
before beginning an examination.
weighed, while less tame birds may need to be exam-
Be aware that the scrubs or other clothing worn by the ined first while still restrained and weighed just before
technicians and practitioner will be exposed to powder being returned to their cage.
down and fecal material during handling and restraint. At all times the clinician must be aware of the bird and
The potential for disease transmission to subsequent how it is handling the stress of restraint and examina-
patients should be considered and clothing changed tion. Many birds are presented for evaluation of an ill-
when appropriate. ness, having been ill for a period prior to the owner’s
recognition of disease, and the stress of restraint can
By the time the clinician is ready to examine the bird,
exceed their ability to compensate. Collapse and death
the general temperament of that bird should have been
are, unfortunately, not uncommon with critically ill
established. If the cage is the bird’s home, its territorial
birds. If there is any doubt as to the bird’s ability to cope
instincts may drive the bird to protect its cage from the
with the stress, it should be immediately returned to a
intrusion of strangers. In many cases, therefore, it may
perch or the cage and allowed to regain its composure
be appropriate to ask the owner to remove the bird
before proceeding. Critically ill birds should not be han-
from the cage. If the owner is unwilling (or unable) to
dled initially (see Chapter 7, Emergency and Critical
do so, the clinician should study the cage to determine
Care).
the best means of removing the bird. Tame birds may
simply step through an open door. At other times, the
cage may need to be dismantled rather than trying to THE “PUT IT DOWN” LIST
catch and remove a bird through a small door. If the Panting and increased respiratory rate while being exam-
bird is friendly, the clinician should gently introduce a ined warrant attention. It may be that these are normal
hand into the cage, with the back of the hand to the compensation techniques for a stressed or obese bird,
bird. If there is no aggression, the forefinger is extended but during restraint, it is difficult to determine the extent
and placed under the bird’s chest. A tame bird will usu- of the stress without reducing the effectiveness of the
ally step onto the finger. Restrain the foot or a toe by restraint.
gently pressing on it with a thumb against the finger, 1. If the bird is panting or breathing rapidly, first alter the
keeping the bird steady, and gently bring it out of the grip on the head so the head is free to move. The bird
cage. During this procedure, the clinician should be talk- should immediately begin to turn its head in search of
ing to the bird, praising it, and maintaining eye contact. something to bite. If it doesn’t, PUT IT DOWN.
Once the bird has been removed from the cage, con- 2. A paper towel or a corner of the towel being used to
tinue to praise it and, depending on the species and restrain the bird can be placed into its mouth. It should
individual, scratch its head, its axilla, or simply continue immediately begin to bite at this, demonstrating that it
talking to it while raising it to a height at which it has sufficient oxygen reserves to do so. If the bird lets
appears comfortable. If the bird has to be physically the material lay limply in its mouth, PUT IT DOWN.
caught, it is usually best to use a small hand (or paper) 3. Have the bird grasp your hand or finger with both of its
towel to gently envelop and then restrain the bird. Show feet. (This should be part of the physical exam anyway,
the bird the towel and let it become accustomed to its to determine symmetry and strength of grip). If the
appearance. If possible, the clinician should envelop the bird’s grip is weak or non-existent, PUT IT DOWN.
bird in the towel from below — an approach from above 4. If the bird’s eyes close during the physical exam, PUT
173
Greg J. Harrison
Greg J. Harrison
Fig 6.43 | Disposable paper bags provide a dark area for
restraint for all but the largest of birds. This can be used to
obtain a body weight on untamed birds.
Fig 6.44 | For birds that will perch a
digital scale with an easily disinfected perch
stand is ideal. In this case, the wooden
perch is coated with an epoxy sealer.
IT DOWN. Conversely, do not be reassured if the bird Traditionally a bird’s body condition was determined by
has its eyes open — many birds have held their eyes palpation of the pectoral muscles and allocating a body
open as they drew their last breaths. score based on the muscle and fat coverage of the ster-
5. If in doubt, PUT IT DOWN. Return the bird to the num. Although useful as a cursory determination of
location (cage, owner) where it is most comfortable, emaciation, this technique fails to take into account that
and observe it while talking to the owner. most birds do not store fat in their pectoral region and
can be carrying significant fat deposits while still having
an apparently normal body score. Wetting the feathers
over the abdomen, flanks, thighs and neck with alcohol
The Physical Examination allows visualization of subcutaneous fat deposits, seen as
yellow fat under the skin rather than pinkish-red muscle
“You will miss more by not looking, then you will ever (Figs 6.45a,b-6.47a,b).
miss by not knowing.”
The combination of body-weight recording, pectoral
The old veterinary adage expressed above is as true for muscle palpation and examination of subcutaneous fat
avian medicine as it is for any other species. A thorough, allows an accurate assessment of body condition.
systematic physical evaluation of the patient is essential
to obtaining information regarding the bird’s problem
BLEEDING
and diagnosis. Clinicians should develop a thorough
examination protocol with which they are comfortable, Bleeding or bruising may be encountered during or pro-
and use it for every (stable) patient, regardless of the duced by the physical examination. Excessive, prolonged
reason for presentation. A physical examination form or abnormal bleeding or bruising in birds is often
may be useful in ensuring that nothing is overlooked. related to one or more manifestations of malnutrition.
The following is a brief list of the most common presen-
tations and associated etiologies:
BODY CONDITION • Conjunctival hemorrhage or “red tears” are commonly
All birds should be weighed during each visit to the vet- seen in African greys and Quaker parakeets (see Fig
erinarian, and at the same time each day while hospital- 6.47a2 for information on potential etiologies).
ized. Monitoring an individual bird’s weight will often • Denatured blood in the nasal debris of psittacines.
detect potential disease prior to the demonstration of This seems particularly prevalent in mutation cock-
clinical signs. The veterinarian will also develop an atiels (see Fig 6.47b2). Malnutrition causing squamous
appreciation for the normal body weight ranges of vari- metaplasia and secondary bacterial and fungal infec-
ous species. The weight should be recorded in grams, as tions is a likely cause in many birds. In these cock-
this allows accurate monitoring (Figs 6.43, 6.44). atiels, however, there may also be a decrease in
Greg J. Harrison
Greg J. Harrison
Fig 6.45a | Body condition scores on simple Fig 6.45b | Same bird as in Fig 6.45a at a dis-
pectoral profiling are not accurate. This blue and tance. Note the appearance of the feathers. They
gold macaw is 1300 g and has cleavage in the appear as a unit, not a collection of individual
area of the keel’s carina. When the bird’s feath- feathers. The colors are clear and crisp. The
ers are wetted down with alcohol, no fat in the feather margins are smooth and sharp. The
sub-cutaneous tissues is evident. However, on feathers are strong and straight. The skin is rep-
the commonly proposed body score technique, tilian and boldly patterned. The nares, facial skin,
this bird would be called obese because the eyes and nails are all exemplary. Max has been
breast muscle exceeds the keel’s carina in depth. on a high fat organic formulated nugget for 10
Obese birds are considered high risk birds. This years with limited fruits and vegetables. Natural
is a large blue and gold, but it is not obese. sunlight and showers are frequently provided.
Note the lack of flaking or layering of the beak.
No flaking is present on the facial skin and no
debris has accumulated in the nares.
intrinsic clotting factors. Verification and etiology of Attention should be paid to the following areas (Figs
this coagulopathy have not been determined, but mal- 6.57a-z-6.59c):
nutrition and hepatopathy, as well as genetic predispo- • Color of the Feathers. Abnormal coloration of feathers
sition, should be considered. can be due to a multitude of causes. PBFD can cause
• Facial skin bruising is often noted in macaws and green feathers to turn yellow and blue feathers to turn
African grey parrots (see Fig 6.47c2). This can be the white. It will also lead to a generalized dirtiness of the
result of restraint that is too aggressive or an inherent feathers, especially in cockatoos. Chronic liver disease
bleeding dyscrasia. The same condition likely occurs and/or malnutrition can cause darkening of feathers
in other species, but the presence of feathers in the and a decrease of powderdown production in applica-
periorbital area prevents observation of the bruising. ble species. Frequent handling of birds by the owner
Malnutrition is likely to be the major underlying cause can leave a deposit of oil on the feathers, which then
of overly fragile dermal tissue and decreased coagula-
encourages fungal overgrowth. This causes a black dis-
tion factor production.
coloration on these feathers. This is not seen in birds
• Beak injuries (Fig 6.47d2).
with powderdown, presumably because the powder
• Broken blood feathers (Fig 6.47e2).
keeps the feathers clean.
• Blood from the cloaca.
• Tidiness of the Plumage. Birds generally keep their
• Blood in the urine.
plumage well groomed and tidy. If the plumage is
• Bite wounds (Fig 6.47f2).
untidy, with no immediately obvious cause (eg, recent
PLUMAGE handling), the clinician should suspect that either the
Normal feather development in a baby cockatoo is bird is unable to groom itself properly, or a general-
shown in Figs 6.48a-g. Normal adult feathers are seen in ized feather dystrophy (eg, PBFD) is present.
Figs 6.49-6.56a-e and Chapter 2, The Companion Bird. • Evidence of Feather Damage. Chewed and/or broken
175
Greg J. Harrison
Greg J. Harrison
Fig 6.46b | This young budgerigar has a bulging fat
mass at the furculum (area one).
Fig 6.46a | Alcohol can be used to part the
feathers to ascertain the absence or presence of
body fat. This bird has an accumulation in area
three (the abdomen, just anterior to the vent).
Other areas should be observed.
Greg J. Harrison
Fig 6.46c | This euthanized blue-crowned conure has had its feathers removed to show the three fat
areas coalescing. 1 is area one. 2 is area two. 3 is area three. Area two, the axilla, is still discrete. Note
the fat is deposited subcutaneously to the feather tracts.
Greg J. Harrison
Fig 6.46d | Dorsal view of bird in 6.46c. Fat depositions con-

tinue in feather tracks over the wing, scapula and pelvis.
Greg J. Harrison
Greg J. Harrison
Fig 6.47a | A very ill conure is barely able to keep its eyes Fig 6.47b | Same conure as in Fig 6.47a. When the feathers
open and maintain its balance. Despite the presence of are wet with alcohol, there is obviously little remaining breast
strangers it remains fluffed during clinical presentation. musculature. This severe emaciation carries a grave prognosis.
This implies a grave prognosis. Handling such a bird without ascertaining its tolerance for
restraint via proper distance observation will often precipitate a
crisis. If the bird dies, the crisis will be with the owner. The
owner will assume the bird died due to inappropriate veterinary
care. Proper evaluation can avoid such a crisis. Most birds in this
condition will not survive, but a few, when gradually and cau-
tiously approached with treatment and diagnostics, will respond.
In either case, the owner must be informed in advance of the
severity of their bird’s condition.
Greg J. Harrison
Fig 6.47a2 | Quaker (monk) parakeet with a drop of conjucti-

val blood post-examination. This phenomena is commonly
observed in African greys when restrained. A nutritional disorder
is usually involved. Subclinical rhinitis and sinusitis have been
Peter Coutteel
incriminated in this production of bloody tears from conjunctival
hemorrhage, Squamous metaplasia of the respiratory system is
likely underlying the respiratory disease. The degree of blood
pressure elevation that restraint creates may also be a factor in Fig 6.47b2 | Cockatiel with black rhinal discharge that is
more sensitive species (see Chapter 4, Nutritional hemoccult positive. Secondary invaders are common and often
Considerations). require therapy. This therapy often includes nutritional correction.
Greg J. Harrison
Greg J. Harrison
Fig 6.47d2 | Budgerigar with beak bleeding after trimming. A

Fig 6.47c2 | Facial erythema and subsequent scabs like those nutritional disorder is likely. Budgerigars and other parrots do
shown in this African grey are often seen in macaws following not normally require beak trimming. The vessels in a nutrition-
restraint. While the immediate cause is the handling, the under- ally imbalanced bird’s beak grow closer to the tip and bleed
lying skin fragility usually responds to nutritional correction. more profusely. Styptics will usually control the bleeding.
177
Greg J. Harrison
Greg J. Harrison
Fig 6.47e2 | Mealy Amazon with a fractured primary remige. Fig 6.47f2 | According to the owner, this lovebird was mouthed
Pulling the feather is no longer recommended. Damage to the but not bitten when “picked” up by their dog. Wetting feathers to
delicate structure of the feather follicle (see Fig 6.56c,e) may examine for hematomas associated with tooth penetrations is an
occur. Clip off the distal portion and apply baking flour to the easy technique. The owner’s assumptions were proven wrong in
stub until bleeding stops. Birds that bleed excessively may this case and antibiotics are indicated.
respond to injections of vitamin K. Nutritional disorders need to
be addressed. In a well bird the feathers are less likely to fracture
and if they do, the subsequent bleeding is generally self-limiting.
feathers should lead the clinician to suspect over- tion, hepatic disease, genetic mutations (notably in
grooming, self-mutilation, cage mate trauma or malnu- cockatiels) and circovirus in Cacatua spp.
trition. Saw-toothed edges can indicate a failure to • Molting Patterns. Most birds will molt heavily twice
molt normally; hence, old, worn feathers are being yearly, in spring and autumn — the so-called “pre-
retained. It should be noted in cases of feather nuptial” and “post-nuptial” molts. Outside of these
destructive behavior, whether the feathers have been annual molts, there is a steady and progressive
bitten off level with the skin, plucked out, or if the turnover of old feathers. The end result in psittacines
shaft is being chewed. is that each feather is normally replaced once a year.
• Evidence of Feather Dystrophies. Retained feather Continual heavy molts or the sudden loss of many
sheaths, retained pulp, hemorrhage in the shaft of feathers is abnormal, as is the failure to molt (seen as
feathers, strictures of the calamus and twisted feathers the retention of worn and broken feathers).
are indicative of feather dystrophies, often of nutri- • The Presence of Stress Lines or Stress Bars. Stress or
tional, genetic, traumatic or viral origin (ie, polyoma- disease at the time a feather is growing will lead to a
virus, circovirus).
transverse “break” in the vane of the feather. The pres-
• Wing Clipping (if present). The wings should be exam- ence of many feathers with such stress lines is indica-
ined to determine if the bird’s wings have been clipped tive of a problem in the bird’s recent past.
and, if so, if that clip is appropriate to the species and
• The Condition of the Skin. The presence of erythema,
temperament of the bird. The degree of lift that the
excessive scale or areas of skin trauma should be
bird is achieving with the current clip should be deter-
noted. This can be done by parting the feathers with a
mined by asking the owner and by a “test flight” in a
cotton-tipped applicator, or gently blowing on the
safe area, if needed. The owner’s satisfaction and the
feathers.
effectiveness of the last clip should be determined. The
clip should be examined to determine if the cut ends • Areas of Trauma. The skin should be thoroughly
of feathers could be bothering the bird. examined for areas of trauma, especially on the wing
tips, sternum, cere, ventral pygostyle and axillae.
• Absence or Presence of Powder Down. Powderdown is
produced by the powderdown feathers on the thighs • Flexibility of the Feather (Figs 6.58a-c). The shaft of
of many species of birds, particularly cockatoos and the feathers of a healthy bird on a good diet should
African grey parrots. It is easily recognized by the pres- flex rather than break when the tip is drawn down
ence of a fine white powder on the clinician’s hands towards the base; the feather should spring back to a
and clothing after handling the bird. A lack of powder- normal position when released.
down leads to staining of the feathers and a shiny • Parasites. The presence of parasites on the feathers
appearance to the beak and feet. The most common should also be noted; microscopic examination may be
causes of loss of this powderdown include: malnutri- necessary for detection (Figs 6.59a-c).
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 6.48a | Baby Umbrella cockatoo at Fig 6.48b | At 2 weeks of age this bird Fig 6.48c | At 4 weeks of age. The
day 2. shows a minor prognathism developing organic hand-feeding formula has over-
and crooked toes. This was likely a result come the beak and toe problems.
of the seed-based diet fed to the parents.
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 6.48f | Ten weeks of age.
Fig 6.48d | At 6 weeks of age the slight Fig 6.48e | Eight weeks of age.
weakness of the abductor muscles in previ-
ous figures has been corrected and the
baby is standing.
Greg J. Harrison
Fig 6.48g | Twelve weeks of age. Fig 6.49 | A perfectly feathered goffin cockatoo in a defense
(attack) posture stimulated by the toy owl.
179

Fig 6.50 | A Moluccan (salmon-crested) Fig 6.51 | Two grey-eyed (immature) Fig 6.52 | This citron-crested cocka-
cockatoo displays a greeting feather erec- African grey parrots. Color tones and too is normal except for a mild unzip-
tion and reaches out with the foot to be feather scalloping on these birds are ping of the crest feathers.
picked up. The bird has been fed an ideal.
organic formulated diet since hatching,
8 years ago. A healthy bird can normally Fig 6.53a | This severe macaw is
separate its feathers in this manner. showing a defensive posture. The
Observe the beak, skin around the eye feathers are of poor color and
and the feet. Note the strength and structure. Such feathers often dra-
vibrance of the feathers. The bird’s atti- matically respond to diet change.
tude is upbeat and active. These are some
determinations one needs to master in
avian medicine. This requires either seeing
normal specimens, such as this bird, or
transferring in one’s mind’s eye the char-
acteristics seen in most wild birds. If only
Jan Hooimeijer
seed-eating pet birds are seen in practice,

normal is not appreciated.
Fig 6.53b | Approximately 1 year later, the bird in Fig 6.53a has been guided
by Jan Hooimeijer into the specimen seen here. Owners were instructed in an
hour long office consultation on nutrition, husbandry and behavior. The diet was
changed to an organic nugget. Periodic evaluations were scheduled to assure sec-
ondary problems were not becoming clinically significant. When an avian practi-
tioner has repeatedly seen improvement in these cases with only dietary correc-
tion, recommendations for diagnostics in future cases are often altered. A CBC
may be warranted to determine if concurrent infection is present. Serum
chemistries with bile acids may be performed. However, abnormalities in hepatic
enzyme levels, calcium levels and other parameters are often a reflection of the
effects of chronic malnutrition. In the absence of clinical disease, the practitioner
may elect to institute a wellness program, with the primary emphasis on dietary
correction. In this case an organic formulated diet, lactulose and milk thistle were
administered. This is a particularly judicious approach if the bird is stable but
likely suffering from malnutrition-induced decreased hepatic function. These birds
are not ideal candidates for venipuncture due to potential clotting deficiencies.
Even more significant, hepatic biopsy, although it may be diagnostic, can be a
Jan Hooimeijer
fatal procedure in the presence of hepatic insufficiency (see Chapter 4, Nutritional

Considerations).
Greg J. Harrison
Fig 6.54 | A 17-year-old seed-eating cockatiel shows hyperk- Fig 6.55 | A wild-caught sulfur-crested cockatoo (Cacatua
eratotic follicles, generalized weakness, worn feathers and galerita galerita) which is fed a seed diet, displays poor feather-
retained pin feathers. ing. Note the fluffed appearance, unzipped crest feathers and its
position on the bottom of the cage. The physical examination
revealed a retained egg. Malnutrition was addressed over the
next few visits.
1
5
2
Greg J. Harrison
Fig 6.56a | Plumage of the extended right wing. Dorsal view. 1. Primary remiges 2. Secondary
remiges 3. Primary coverts 4. Secondary coverts 5. Upper marginal coverts of the propatagium and
manus.
181
Greg J. Harrison
Fig 6.56b | Plumage of the extended right wing. Dorsal view. Upper marginal coverts of the propatag-
ium and the manus removed. 1. Major primary coverts 2. Major secondary coverts 3. Propatagium
4. Alular remiges.
2
4
3
1
Greg J. Harrison
Fig 6.56c | Plumage of the right wing. Dorsal view. Major primary and secondary coverts removed.
1. Secondary remex inserting on dorsal surface of ulna 2. Follicles of insertion for covert feather
3. Alular digit 4. Postpatagium.
Greg J. Harrison
2
Fig 6.56d | Plumage of right wing. Ventral view. 1. Under wing primary coverts 2. Under wing second-
ary coverts 3. Under wing marginal coverts of propatagium.
5 6
1 3
5a
123456789
Secondary Remiges
Greg J. Harrison
X IX VIII VII VI V VI III II I

Primary Remiges
Fig 6.56e | Plumage of right wing. Ventral view. Under wing primary and secondary coverts and the mar-
ginal coverts of the propatagium have been removed. 1. Axial secondary pin feather inserting on the dorsal
ulna. 2. Upper primary covert 3. Ulna 4. Postpatagium 5. Minor metacarpal III 5a. Major metacarpal II
6. Propatagium. I-X Primary remiges. (I - VI insert on metacarpals; VII the minor digit; VIII-X the major digit)
1-9. Secondary remiges (several additional ones were pulled).
183
Greg J. Harrison
Greg J. Harrison
b
Fig 6.57a | Four-year-old female umbrella cockatoo Fig 6.57b | Same bird as in Fig 6.57a demonstrating
fed a seed and table food diet. The crest feathers are tattered and broken tail feathers compared to a normal
failing to shed the keratin surrounding the underlying umbrella’s wing feather (b).
pin feathers. The bald crown area is normal.
Greg J. Harrison
Greg J. Harrison
Fig 6.57c | This close-up demonstrates the difference Fig 6.57d | These wing feathers show a lack of opacity
between stained feathers developed by a bird fed a and have a soiled appearance when compared to a per-
seed and table food diet compared to a perfect feather fect feather.
being held for comparison.
Greg J. Harrison
Greg J. Harrison
Fig 6.57e | Poor quality rump and tail feathers in a Fig 6.57f | Budgerigar on a seed diet with tail feathers
blue and gold macaw fed only seeds and table foods. unzipped. The lateral rectricies are a dull off-brownish-
The feathers lack a sharp vane margin (unzipped white compared to those they cover, which are pure
appearance). The feather color lacks uniformity and normal white but still unzipped.
many transverse (stress) lines are present.
Greg J. Harrison
Greg J. Harrison
Fig 6.57g | The parents of this palm cockatoo were fed seeds, Fig 6.57h | Same bird as in Fig 6.57g 2 months after being
vegetables and rancid pine nuts soaked in chlorine bleach to removed from described diet. The bird was placed on an
remove molds. This baby was raised on a high protein commer- organic high fat diet. The head, neck and some wing coverts
cial hand rearing product making up 70% of the diet with the have molted and regrown in normal texture and color. The
other 30% consisting of 20 g of sunflower seed kernels, 40 g bird’s timid and nervous attitude was replaced with a jolly play-
apple and 40 g broccoli. In addition to abnormal plumage there ful one. Fecal bacteria were returning to normal.
was a deficiency of normal flora in the fecal Gram’s stain.
Greg J. Harrison
Greg J. Harrison
Fig 6.57j | A rectrice with retained sheath and pulp material

that is normally shed. This is due to improper nutrient availabil-
ity to the feathers and a resultant hyperkeratosis. Seed and
table food based diets are the major cause (see Chapter 4,
Fig 6.57i | Same bird as in Fig 6.57g 6 months post-diet
Nutritional Considerations).
change. The color is uniformly normal. The beak has shed much
of its retained keratin. The normal red cheek patch took three
more months to appear.
Greg J. Harrison
Greg J. Harrison
Fig 6.57k | The two lateral feathers are from a bird with a nutri-
tional disorder. The bird was fed a seed and table food diet.
Compare these to the central feather of a bird with normal devel-
Fig 6.57l | Dorsal views of three normal and three abnormal
opment on a proper diet. Color, texture, strength, and structure
feathers from the same dietary situation(s) as described in Fig 6.57k.
(width of vein) are compared on the feathers’ ventral view.
185
Greg J. Harrison
Greg J. Harrison
6.57m | A sun conure and a gold-capped conure fed the same Fig 6.57n | Normal lilac-crowned Amazon fed an organic
formulated diet. The sun conure developed yellow primary formulated diet.
remiges. The addition of red palm oil, high in carotinoids and
vitamin E, allowed the development of new blue feathers. The
addition of wheat germ for vitamin B did not produce this
coloration, nor did other omega 3-6 oils, including fish, flax,
borage, evening primrose, corn and sunflower.
Greg J. Harrison
Greg J. Harrison
6.57o | Lilac-crowned Amazon fed a seed and table food diet.
Fig 6.57p | Sulfur-crested cockatoo picks at its neck feathers
The overgrown beak and black pigmentation of the feathers has
and is able to pull its crest feathers with feet to chew them. Diet,
empirically been associated with advancing liver disorders (see
behavior and integrative therapies (Chapter 10, Integrative
Chapter 4, Nutritional Considerations and Chapter 15,
Therapies) are often of benefit. A total cure is rare in such
Evaluating and Treating the Liver).
feather disorders unless caught at an early stage.
Fig 6.57q | This yellow-naped Amazon with a

history of an all seed, nut, table food diet has
keratin accumulating on the feet and beak.
While fungus (usually Aspergillus) can be cul-
tured from the black feathers, correcting the
diet has treated hundreds of birds under the
author’s (GJH) care with no specific therapy
instituted for the fungus. Supportive care is
often used, such as milk thistle and lactulose,
for regeneration of the liver.
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 6.57r | Budgerigar fed a vitamin-enriched seed
only diet. While liver disorders in budgerigars are com- Fig 6.57s | A pied/lutino cockatiel in the later stages of dis-
mon, this blue budgerigar has black in the blue rump ease. The dark yellow color is associated with a suspected hered-
feathers, which is rare. Most budgerigars with liver dis- itary liver disease. While too late for this bird, a formulated
orders do not show any indications in their feather color. organic diet and liver support in the form of lactulose and milk
thistle may be curative if diagnosed early.
Greg J. Harrison
Greg J. Harrison
Fig 6.57u| An 8-year-old lutino pied with advanced gold color-

ing of the feathers. This bird was fed a seed diet.
Fig 6.57t | A lutino cockatiel with staining of
the tail from being dipped in vitamin water,
oiled seeds top dressed with vitamins and feces,
as the perch was too low. A fungus is growing in
the black feather coating but the problem
cleared when the sources of contamination of
the tail feathers were removed.
Greg J. Harrison
Fig 6.57w | Budgerigar with oiled ventral body feathers. Such

Greg J. Harrison
birds become hypothermic and suffer digestive disorders from

preening the oil. Bathing, drying and placing in an incubator at
86° F is minimum therapy.
Fig 6.57v | A lutino cockatiel four months after therapy for

liver disease showing a return to white feathers.
187
Greg J. Harrison
Greg J. Harrison
Fig 6.57x | An 27-year-old yellow-naped Amazon with
abnormal yellow coverts developed while being fed a
seed, table food and nut diet. Fig 6.57y | Same bird as in Fig 6.57x with malcolored yellow
primary remiges.
Greg J. Harrison
Phoebe Linden
Fig 6.57z | Same bird as in Fig 6.57x 6 months after correct- Fig 6.58a | Healthy feathers are flexible with uniform color
ing the diet. The abnormal yellow areas are gone. and structure.
Greg J. Harrison
Greg J. Harrison
Fig 6.58b | Holding the feather by the tip, the feather is slowly Fig 6.58c | A narrow veined feather that broke (fractured) at
flexed tip to shaft. It should rebound to a normal position as in the mid-shaft on the flex test. Such easily damaged feathers
(a). indicate a nutritional disorder.
Greg J. Harrison
Peter Coutteel
Fig 6.59a | Feather lice eggs (“nits”) in a canary’s tail feathers. Fig 6.59b | A single louse on a finger. A few drops of alcohol
are safe on a healthy bird to obtain lice to show the owners.
Debilitated birds should not have alcohol used on them. (20x)
Table 6.1 | Uropygial Gland by Author

Observations (GJH)
Uropygial Gland Absent Uropygial Gland Present

• Argus pheasant • African grey
• Bustards • Blue and gold macaw
• Cassowary • Budgerigar
• Cormorant • Cockatiel
• Citron cockatoo • Eclectus
• Double-headed Amazon • Goffin cockatoo
• Yellow-fronted Amazon • Gold-capped conure
Greg J. Harrison
• Green-winged macaw • Indian ringneck

• Grey-cheeked parakeet • Moluccan cockatoo
• Hyacinth macaw • Most Psittacines
• Red-cheeked conure • Red-masked conure
Fig 6.59c | Louse under magnification (100x).
• Emu • Rose-breasted cockatoo
• Ostrich • Severe macaw
• Tailless domestic fowl • Sun conure
• White carnean and • Umbrella cockatoo
Abnormalities of the feathers and skin should be
rumples pigeon • Rock dove (wild pigeon)
recorded in a detailed manner. Veterinarians should • Woodpeckers
familiarize themselves with the descriptive terminology
used for the external anatomy of a bird. Such precise
terminology is essential for later comparisons of pro-
gression or resolution of lesions and for describing a
THE HEAD
case to another veterinarian (see the physical exam form The head should be first visualized in profile from a
at end of chapter). number of different angles, looking for asymmetry. Such
asymmetry may arise from exophthalmus, enophthal-
The uropygial (or preen) gland is located on the dorsal mos, sinus swelling or depression of the skin over the
base of the tail. It is bilobed and is not present in all sinuses. Pupillary size, iris color, lens clarity, feathers sur-
species (it is absent in many Columbiformes and rounding the external acoustic meatus (ear) and relative
psittacines, notably Amazona spp. and hyacinth macaws size of the ears, asymmetry of the cere, size of the nares,
but prominent in budgerigars, cockatoos and waterfowl) appearance of the nasal opercula, rhinothecal or gnath-
(Table 6.1). othecal deviations or overgrowth all need to be noted
(Figs 6.60a,b) (see physical examination form). Loss of
The uropygial gland should be assessed for evidence of feathers on the head can be due to a variety of condi-
enlargement or inflammation. Impaction, abscessation tions. Some cockatiel mutations, especially lutinos, have
and neoplasia, all of which may be followed by self- a bald spot behind the crest. Feather loss in other
trauma, are potential causes of uropygial gland abnor- species can be associated with fungal or bacterial derma-
malities. titis, infestation with ectoparasites, allergic dermatitis,
189
PBFD or excessive grooming by a cage mate. Feather • Food is present (ie, Is the bird eating?)
loss around the eyes can indicate facial rubbing associ- • It feels doughy or fluid-filled, indicating that crop
ated with conjunctivitis or sinusitis. Matting of the feath- stasis may be present
ers over the crown and nape may indicate the bird has • Ingluvioliths or other foreign objects are present
been regurgitating or vomiting. • The crop mucosa is thickened
• There is excessive water present
The conformation of the beak should be assessed (Figs
• The crop is overly distended
6.60c-6.61e) for the presence of congenital or acquired
abnormalities such as scissor (wry) beak, prognathism Care must be taken, especially in debilitated birds, that
and bragnathism. Trauma to the beak or localized sinus fluid or ingesta is not propelled retrograde from the
infections can result in anatomical abnormalities (eg, crop into the oropharynx and aspirated by the bird.
longitudinal grooves in the keratin). Excessive keratin
flaking of the beak can reflect poor nutrition or simply a
THE BODY
lack of opportunity to rub the beak on a suitably abra-
sive surface (ie, a cement perch). Overgrowth of the Palpation of the skin over the trunk occasionally reveals
beak can occur with PBFD, Knemidocoptes spp., con- the crackling or air-filled distention caused by subcuta-
genital or acquired malalignment of the upper and neous emphysema. While this is normal in species such
lower beaks, chronic liver disease or malnutrition. It is as pelicans, in most species it is the result of trauma or
rarely the result of a lack of objects to chew on. It is infection in the air sacs that allow the escape of air
important to note that some species, such as the long- under the skin.
billed corella, Cacatua tenuirostris, naturally have elon-
The abdomen in the normal bird is concave between the
gated beaks. This should not be mistaken for an over-
end of the sternum and the pubic bones. If this area is
grown beak.
convex, then distention is present. The clinician needs to
distinguish between internal and external distension of the
The cere (Figs 6.62a-c), the fleshy skin at the top of the
abdomen. Internal distension of the abdomen can be due
beak, is not present in all species. In the normal green
to fat, organ enlargement, ascites or the presence of an
budgerigar (Melopsittacus undulatus) cere color can be
egg. External distension can be due to subcutaneous fat,
used to sex the bird, with cocks having a blue cere and
neoplasia (especially lipomas), xanthomas or hernias.
hens a brown cere. However, this will vary with the age
Radiology may be required to distinguish between internal
of the bird, the color mutation, and the degree of
and external abdominal distension and between different
health. Cere hypertrophy — a thickening of the brown
etiologies of both. The use of GI contrast material (bar-
cere in the budgerigar hen — may reflect a normal or
ium) may help determine whether herniation is present
pathologic hyperestrogenic state.
and what structures may be incorporated into the hernia
(Figs 6.64a,b). Abdominal pain or discomfort can occasion-
ORAL EXAM (Figs 6.63a-f) ally be elicited by careful palpation. In passerines and juve-
Examination of the oropharynx can be accomplished by nile psittacines, wetting the ventral abdomen with alcohol
using roll gauze, plastic or metal speculums to open the may allow visualization of internal organs. The liver should
mouth. In many birds equipment is not needed, as the not extend pass the caudal border of the sternum in adult
approach of a light source toward the oral cavity will birds. If it does, liver disease should be suspected (eg,
produce a wide open-mouth reaction and allow visuali- atoxoplasmosis in canaries).
zation. The choana (the slit in the roof of the orophar-
ynx) should be free of excessive mucus or discharge and If ascites is suspected, careful abdominocentesis may be
fringed with well-defined papillae. There should be no indicated. After disinfecting the skin over the abdomen, a
abscesses or diphtheritic membranes present. In larger 23-27 g needle is gently introduced along the midline. If
birds, the infundibular cleft can be visualized in the hard the needle is inserted lateral to midline, ascitic fluid may
palate of the choana. In some cases of severe sinusitis or then communicate with the abdominal air sacs. In larger
otitis media, the infundibular cleft will be dilated and psittacines, a suitably sized intravenous catheter can be
contain purulent debris (see Chapter 26, Diagnostic used. Negative pressure with a syringe is applied, and the
Value of Necropsy). fluid obtained is processed for cytology, culture and pro-
tein analysis. Care must be taken when abdominocentesis
is performed that the loss of protein and/or the sudden
THE CROP change in abdominal pressure do not cause serious or
The crop can be palpated in most birds at the base of fatal results. See Table 6.2 for a cursory list of fluid charac-
the neck, just cranial to the thoracic inlet. It should be teristics and causes. A more complete discussion is avail-
carefully and gently palpated to assess if: able in other texts.
Table 6.2 | Abdominocentesis Abbreviated Results elasticity, trauma or scarring and for the presence of a tat-
Nature of Fluid Diagnostic Possibilities too (indicating the bird has been surgically sexed).
Yellow-pink, turbid fluid. Cytology shows Yolk-related peritonitis
fat droplets, proteinaceous material,
meso-epithelial cells, macrophages,
occasional heterophils.
THE LEGS AND FEET
Light colored, clear fluid. Cytology shows Ovarian cyst Each leg should be carefully palpated to detect abnor-
few cells of any description. Ascites malities, such as fractures, healed bony calluses, or
Various neoplasias
Dark brown fluid. Cytology shows meso- Renal or hepatic cyst
angular deformities of the long bones. Soft tissue
epithelial cells, occasional erythrocytes, Degenerating ovarian swelling may be palpable or be suspected by the bird’s
heterophils and macrophages. follicles
reaction to palpation. Suspicious areas should be exam-
Thick, gelatinous fluid. Salpingitis
ined for bruising. Each joint should be extended and
Fluid of variable color and consistency. Intestinal perforation
Cytology shows macrophages, erythro- Serositis flexed to assess mobility and range of motion. Joints
cytes and heterophils, possibly bacteria.
should also be examined for swelling or the presence of
subcutaneous and intra-articular deposition of chalky
white uric acid crystals (ie, articular gout). This condi-
The back should be carefully palpated for evidence of
tion is extremely painful and the bird will often be lame
scoliosis, lordosis or kyphosis. As the thoracic and lum-
and react violently to digital pressure applied to the
bar vertebrae are predominantly fused, flexibility of the
affected areas. All aspects of the legs should be com-
spine cannot be assessed as it is in dogs and cats.
pared with the contralateral side for symmetry, length,
strength of grip and degree of muscling (Figs 6.66a-d).
The carina of the sternum should be palpated for evi-
dence of distortion, trauma or congenital defects such as The toes should be examined for abnormalities including:
splitting. Distortion of the carina, often indicating a his- • Missing digits or nails
tory of rickets or other metabolic bone disease, should • Annular constrictions
lead the clinician to recommend radiographic evaluation • Swelling of interphalangeal joints, occasionally with
of the rest of the patient’s skeletal system. the deposition of uric acid crystals
• Avascular necrosis
The ventral area between the cloaca and the tail should
• Excessive thinness, especially in neonates
be assessed for splitting of the skin (avulsed pygostyle).
• Abnormal position and conformation of the toes
This condition may be mistaken for a cloacal prolapse
• Excessively long or twisted nails
on initial examination, until it is noted that the vent is
present cranial to the red, protruding tissue that is actu- The skin of the foot is an ideal reflection of the rest of
ally muscle. This condition is commonly seen in pet the dermis (Figs 6.67a-k). The plantar surface of each
psittacines and is associated with a poor diet, obesity foot should be examined and the condition of the
and/or excessively clipped wings. Obesity and an exces- metatarsal pads and digital pads noted (Figs 6.68a-g).
sively severe wing clip can cause the bird to land awk- Abnormalities seen here include: loss of definition of the
wardly, avulsing the tail from the pygostyle. Malnutrition epidermis (seen as a shiny, reddened surface), swelling,
causes the skin to lose its elasticity. The result is that the erosions, ulcers and scabs. Pododermatitis (bumblefoot)
skin and underlying muscle in this area split. The initial is common in captive raptors (bumblefoot is never seen
injury may not be noticed by the owner, but the subse- in wild, even one-legged birds - S. Hudelson, personal
quent bleeding and picking at the affected tissue usually communication, 2004), but can be seen in any bird. A
alert the owner to a problem. unilateral lameness causes increased weight-bearing on
the unaffected leg. This in turn can lead to pressure
THE WINGS (Figs 6.65a-e) necrosis, infection and subsequent pododermatitis.
Consequently, in cases of a unilateral lameness, the
Each wing should be carefully extended and flexed to
opposite leg should always be closely examined.
assess mobility and should be compared to the contralat-
Bilateral pododermatitis is frequently encountered in
eral wing. The bones and joints should be palpated for
older, obese psittacines with a history of poor diet,
swelling or crepitus. Recent trauma may be evident as inadequate exercise and/or unsuitable perches. Note the
greenish discoloration of the soft tissue. This is bruising discussion under Figs 6.67f-i for evaluating nails.
and should not be mistaken for infection or tissue death.
If the cause of a wing droop is not detectable after care- Occasionally, due to the nature of the injury or the dis-
ful palpation, radiology is required to assess the pectoral position of the bird, a full examination may require gen-
girdle. The bones of this girdle are covered by strong eral anesthesia. If this is the case, radiographs can be
muscles, and fractures are often not detectable by palpa- taken at the same time, minimizing handling of the con-
tion alone. The patagium should be evaluated for loss of scious (and therefore stressed) patient.
191
Respiratory/Cardiovascular these birds. In cockatiels, tracheal obstruction may be

due to seed or seed hull aspiration, especially when the
illness is truly acute in nature (as judged by the presen-
AUSCULTATION tation of a well-fleshed bird). In other cases, cockatiels
When to auscult is the prerogative of the clinician but may demonstrate a loss of voice and/or a squeaky sound
may be better performed before the bird has been produced for several days to weeks prior to the onset of
extensively restrained. The heart rate is usually rapid, more pronounced dyspnea. These cases are more likely
although that of some pet birds can be surprisingly to be due to a granuloma (eg, Aspergillus spp.) located
slow compared to wilder birds. Murmurs, arrhythmias, at the syrinx, but endoscopy may be necessary to differ-
muffled heart sounds from pericardial effusion, severe entiate between these etiologies.
tachycardia and bradycardia are occasionally detectable.
Older and larger birds (African greys, macaws and cocka-
Lung and air sac noises can be auscultated, and occa-
toos) often suffer from chronic malnutrition with accom-
sionally friction rubs associated with air sacculitis can be
panying vitamin A deficiency. This leads to squamous
detected. Since the avian lung is basically motionless,
metaplasia and a respiratory environment conducive to
the typical mammalian auscultation parameters do not
Aspergillus spp. propagation and granulomas of the tra-
extrapolate well.
chea and/or syrinx. The eventual prognosis for these
birds is guarded at best due to the long standing pathol-
CLINICAL PRESENTATIONS ogy and the potential for systemic disease.
Open-mouthed breathing, abdominal movements and
tail bobbing are due to respiratory distress but may also Upper respiratory disorders tend to show inspiratory
be due to the presence of space-occupying coelemic dyspnea. Lower respiratory tract disorders tend to show
masses, ascites, anemia, cardiovascular disease, poly- expiratory dyspnea that rarely have audible sound.
cythemia, obesity, egg binding and other non-respiratory
conditions. The nares, which are normally covered by feathers in
many species, are the openings into the rhinal cavity
Thyroid disorders in budgerigars can resemble either located at the top of the beak. The nares should be sym-
respiratory or crop/gastric disorders. Dyspnea is not metrical, open and dry. The normal opercula should not
uncommon.
be mistaken for rhinoliths. Blockage of the nares or an
The avian respiratory system is commonly affected by area of communicating cul de sacs of the infraorbital
subclinical chronic disease. This is usually due to compli- sinus may result in a subtle inflation and deflation of the
cations from stress disorders. Malnutrition is the most infraorbital sinus. This causes the up and down motion
common cause (see Chapter 4, Nutritional Considerations, of the skin over the infraorbital sinuses with respiration
Section II Nutritional Disorders). A common presenta- (see Chapter 4, Nutritional Considerations, Section II
tion is mild nasal discharge that stains the feathers over Nutritional Disorders).
the nares (Figs 6.69a,b). The discharge usually starts out
serous in nature and may progress to mucoid in nature.
This tendency seems to be species related. For example,
budgerigars tend to be more serous, Amazons are more
Neurologic Sensory
mucoid. African grey parrots and lovebirds seldom have Assessment
nasal discharge but build up debris and form rhinoliths
(Fig 6.69c). This can lead to atrophic rhinitis. A cursory evaluation of the nervous system should be
part of the physical examination. Birds presented for
If the nasal condition is not treated, the lower respira- neurologic problems require a thorough neurologic
tory tract may be affected (see Fig 6.69d). Sinusitis with assessment (see Chapter 17, Evaluating and Treating the
resulting ocular discharge may occur (Figs 6.69e,f). If it Nervous System):
is confined to sinuses of the head a sinus flush is benefi-
• Abnormal conformation or posture
cial for diagnosis. Sinus infections may present with
swelling over the infraorbital sinus. There is no simple • Paresis or paralysis of any or all limbs
method to evaluate this diverse air sac system. • Fractures of limb bones
• Weakness or inability to grip with one or both feet
Generally, tracheal obstruction can be differentiated
• Head tilt, opisthotonos, torticollis
from lower or generalized respiratory disease by the
sound of the respiration (tracheal noise) and the for- • Altered mentation
ward-leaning, neck-extended posture that is assumed by • Decreased visual acuity
Greg J. Harrison
Greg J. Harrison
Fig 6.60a | Normal beak in a blue and gold macaw. Fig 6.60b | Gray-cheeked conure with amputated maxilla. This
will not likely regrow due to the proximal location of the ampu-
tation. The excessive pin feathers indicate that a diet or nutrient
assimilation evaluation is needed.
Greg J. Harrison
Greg J. Harrison
Fig 6.60c | Close-up view of beak flaking. It may take a year Fig 6.60d | Amazon four weeks post-diet change from seeds
after diet correction for this flaking to abate. This bird is and table food to a formulated diet. New yellow head and
deceased and is demonstrating post-mortem prognathism, a green neck feathers and the flaking beak are positive signs that
common occurrence, which has no clinical significance after the bird is responding to the nutritional therapy. Sneezing and
death. itching often accompany this period. A higher fat and protein
diet speeds this recovery.
Greg J. Harrison
Greg J. Harrison
Fig 6.60e | Cockatiel with overgrown maxilla. Such gross over- Fig 6.60f | Overgrowth of the rhamphotheca and interlaminal
growths may be the result of symphyseal fractures of the hemorrhage are common in budgerigars fed seed diets with
mandible and the lack of normal wearing of the maxilla. liver disorders. Grinding or trimming is only a temporary solu-
Nutritional deficiencies and trauma may also result in severe tion. Diet change and liver therapy are needed.
maxillary beak overgrowth.
193
Greg J. Harrison
Fig 6.60g | Cockatoo with PBFD, necrosis of the maxilla and Fig 6.60h | Peafowl chick traumatized by clutch mates.
exposure of the periosteum under the rhamphotheca. Euthanasia
is strongly recommended for this presentation of circovirus.
Greg J. Harrison
Fig 6.60i | If not detected early, this traumatized bird will likely Fig 6.60j | Scissor beak in a stunted Alexandrine parakeet.
be further attacked and killed by its clutch mates. Harrison feels this is a form of rickets and myositis from an
unhealthy oral epithelium and facial muscle infections, often
emanating from nutritional disorders.
Greg J. Harrison
Greg J. Harrison
Fig 6.61a | A wild rehabilitating starling shows ideal head Fig 6.61b | Another passerine (warbler) shows the model beak
structures. This bird demonstrates a glass smooth rham- and nares, but at this magnification demonstrates retained pin
photheca, impeccable nares and pristine facial plumage. feathers over the crown. This presentation is common in wild birds
with toxic substance-related debilitation.
Greg J. Harrison
Fig 6.61d | This 20-year-old toucan was fed a toucan pellet for
a decade and then an organic low iron nugget for the second
half of his life. He had free flight and ate 1/4 of a raw organic
papaya daily. Two years after this he died of a pancreatic carci-
Friedrich Janeczek
noma.
Fig 6.61c | Long beaks are normal for a

species like the little (slender-billed) corrella.
Greg J. Harrison
Fig 6.62a | The cere of a mature egg-laying
budgerigar fed a seed diet. Compare this to the
Greg J. Harrison
normal cere in Fig 6.4b. The cere is dry, flaky and

lacks turgidity. The forehead feathers are predomi-
nately immature and have retained sheaths.
Malnutrition and other systemic disorders should
Fig 6.61e | Delaminating beak in this Toco toucan is a reflec- be on the differential diagnostic list (see Chapter
tion of a metabolic disorder as it is in other species. 4, Nutritional Considerations, Section II Nutritional
Disorders for the Improper Diet Cascade).
Greg J. Harrison
Fig 6.62b | Cere of a yellow-fronted Amazon. These Fig 6.62c | Scaly face (Knemidocoptes spp.) mites cause a
swellings in the cere tissue resemble sebaceous cysts of powdered look to the beak and a raised honeycomb mass,
mammals. They may decrease in size with dietary improve- either on the cere, eyelids, beak, feet or other body locations.
ment and weight loss if the bird is obese. They can be Magnification shows pinpoint tunnels in these powdery masses.
expressed but they tend to refill, or they can be surgically This is where the mites live. The tunnels are pathogomonic and
removed. Often no treatment is necessary since progres- help differentiate this from other causes of similar lesions.
sion of the cysts is usually halted after a diet correction. Scrapings may be negative even when mites are present.
195
Greg J. Harrison
Fig 6.63a | The “gape” in a nighthawk. Note the lack of a Fig 6.63b | Female eclectus with palatine and sublingual hyper-
choanal slit. There are leukoid plaques in the oropharnyx. keratotic salivary “abscess.” While usually sterile, the condition is
Candidiasis or trichomoniasis is suspected. reported to be due to hypovitaminosis A. Therapy with vitamin A
and dietary correction containing sufficient vitamin A precursors is
appropriate treatment. (Some cases of “foot stomping” in eclectus
parrots eating spirulina in the diet improve on dilution of the diet,
while others find a correlation with PDD. If not PDD then the
“stomping” may decrease over time with no therapy.)
Greg J. Harrison
Greg J. Harrison
Fig 6.63c | The intermandibular space found in all parrots. Fig 6.63d | A swelling of the sublingual salivary gland on the
left side of the intermandibular space. This lesion is usually a col-
lection of amorphous cellular debris. Surgical resection may be
necessary if these sterile abscesses interfere with tongue move-
ment.
Susan Kelleher
Susan Kelleher
Fig 6.63e | An oral speculum in an Amazon Fig 6.63f | The same Amazon as in Fig 6.63e after therapy
with a fungal infection. and dietary correction. While the choanal papillae are reduced
in stature and depigmented, they have regrown their pointed
characteristic tips.
Greg J. Harrison
Greg J. Harrison
Fig 6.64a | Anesthetized female budgerigar with an early
abdominal hernia. Hernias are correlated with fat accumulating
in the hernia area, xanthoma of the hernia sac’s skin, ovarian Fig 6.64b | Budgerigar hernia — see Fig 6.64a. A simple skin
cystic accumulation of estrogen laden fluids and nutritional dis- removal several weeks post-diet change aids in correction.
orders. Nutritional and hormone therapy should be instituted However, if the tissue is xanthomatous, it will not hold sutures
prior to considering surgery (see Chapter 18, Evaluating and well.
Treating the Reproductive System).
Peter Coutteel
Greg J. Harrison
Fig 6.65a | Dermatophytosis in a finch. Skin and feather
fungal infections that cause lesions are very rare in birds. Most
finches are fed a primarily seed diet. Combine that with crowd- Fig 6.65b | Patagial dermatitis is not uncommon in birds. In
ing, poor air quality, lack of sun and inability to bathe, and the birds with nutritional disorders, the skin (and all tissues) lose elas-
bird’s defenses may succumb. Topical and systemic medications ticity. As a result small tears can occur. While viruses have been
are needed, and the primary husbandry issues need to be suspected in lovebirds with similar lesions, none have been
addressed. reported in most other parrots. Treating for fungal and bacterial
infections, topical dressing and splinting to stop motion while
changing the diet and husbandry may be curative.
Fig 6.65c | Sternal ulcers are

seen in large bodied birds that
have had their wing(s) clipped too
short and are housed over hard
surfaces. The resultant falls cause
pressure necrosis (see Chapter 13,
Integument and Figs 1.25a-e).
Greg J. Harrison
197
Greg J. Harrison
Espen Odberg
Fig 6.65d | Xanthomas may be seen in birds with nutritional Fig 6.65e | Lovebird with polyfolliculitis. Multiple feathers form
disorders. If treated early, they may respond to dietary correction. in a single follicle. A necrotizing dermatitis is also present (see
Hormonal therapy may be of value in reproductively active hens Chapter 13, Integument).
with xanthoma. In advanced cases, surgical resection is often
required.
Greg J. Harrison
Greg J. Harrison
Fig 6.66a | Bruising from vascular injury associated with a tib- Fig 6.66b | Peafowl chick hock shows bruising from post-
ial fracture can be accessed if the feathers are wet or removed. traumatic repair. Subcutaneous blood in birds is often green
(biliverdin).
Greg J. Harrison
Greg J. Harrison
Fig 6.66c | Peafowl chick with a dislocated Fig 6.66d | A wild passerine in rehabilitation shows the
Achilles tendon. Providing an improved diet, sur- normal nail length, with the nail tapered and needle sharp.
gical repair and providing the enclosure with a This bird has a toxic neuropathy.
substrate that is not slick may be curative.
However, the prognosis is progressively guarded
as the species size increases.
Greg J. Harrison
Greg J. Harrison
Fig 6.67a | Normal Amazon dorsal foot skin patterns. Fig 6.67b | Dorsal surface of the foot of a free-ranging slender-
billed corrella. A severe drought led to water holes drying up and
very low natural food sources. The feet are dry but the patterns
remain bold. This is believed to be a temporary phenomenon as
a result of environmental stress.
Greg J. Harrison
Greg J. Harrison
Fig 6.67c | Acute phase of Amazon foot necrosis can occur in Fig 6.67d | Peracute phase of Amazon foot necrosis. The skin
a matter of minutes. The condition usually affects just Amazons will slough over several weeks. No therapy is effective at this stage,
(see Chapter 13, Integument). but prevention of self trauma and secondary infection may be nec-
essary (see Chapter 13, Integument).
Greg J. Harrison
Greg J. Harrison
Fig 6.67e | Permanent pigmental scars 3 months after the Fig 6.67f | A free-ranging slender-billed corrella shows the
initial lesions of Amazon foot necrosis. natural nail length and tapering needle points of the nail. Note
that while the foot has dry skin, the plantar patterns are still
bold. One would expect the dry skin to be replaced in a few
weeks if the drought is broken.
199
Greg J. Harrison
Greg J. Harrison
Fig 6.67g | This Amazon’s nails are thickened and overgrown Fig 6.67h | Nails of a captive canary on a seed-based diet. In
(see Chapter 4, Nutritional Considerations, Section II Nutritional addition to being long and twisted with no tapering, or sharp
Disorders). point, the feet scales are hypertrophic and dry. This could indi-
cate metabolic, parasitic or bacterial disease and/or malnutrition
(eg, Knemidocoptes spp., staphylococcal or fungal infection).
Greg J. Harrison
Peter Coutteel
Fig 6.67i | Finch supplied with synthetic nest material (nylon) Fig 6.67j | Papillomatosis of both feet of a finch.
has a strangulated digit that needs to be amputated. Natural
fibers or nest pads avoid this unnecessary calamity.
Greg J. Harrison
Greg J. Harrison
Fig 6.67k | Gout tophi is a painful collection of uric acid crys- Fig 6.68a | Normal Amazon plantar foot skin patterns.
tals in the joints and subcutaneous areas of the feet.
Greg J. Harrison
Greg J. Harrison
Fig 6.68b | This warbler shows the normal Fig 6.68c | Plantar surface of a slender billed corrella. As pre-
bold but delicate pattern of a small passer- viously mentioned, the skin is dry but the bold pattern is undis-
ine’s plantar foot surface. turbed.
Greg J. Harrison
Greg J. Harrison
Fig 6.68e | The degree of development

Fig 6.68d | Tarsal pad loss of epithelial pattern is common in of bald patterns on the plantar surface
parrots with nutritional disorders. As they become physically inac- can be an indication of nutritional disor-
tive, their tendons seem to weaken and they perch on their hocks. ders. Abrasive perches can exacerbate the
Dietary correction and supportive care, correction of husbandry problem, but these surfaces do not gener-
issues, and alteration of perches may improve this condition. ally cause plantar excoriation, ulceration
or pododermatitis in healthy birds. Large
bodied birds may be an exception.
Greg J. Harrison
Greg J. Harrison
Fig 6.68f | Advanced bumblefoot in a female lutino cockatiel. Fig 6.68g | Mynah bird with bumblefoot and massive tarsal
Anecdotally females develop bumblefoot more often than males scale proliferation indicative of a metabolic disorder. Nutritional
in several species (cockatiels, swans, flamingoes and chickens). and husbandry issues must be addressed and any secondary
Nutritional and hormonal disorders need to be addressed. infection treated.
201
Greg J. Harrison
Greg J. Harrison
Fig 6.69a | A 20-year-old male cockatiel fed a seed based diet Fig 6.69b | Budgerigar female with discharge from nares accu-
shows accumulation of discharge over the left naris and around mulated in frontal feathers. The cere is dry and appears to have
the eyes, which is typical of sinusitis. fungal growth around the right naris. The bird was old and had
obstructive bowel problems that lead to its demise. It was pre-
sented for panting.
Greg J. Harrison
Michael Walsh
Fig 6.69c | Lovebird rhinolith. Nutritional correction and nasal Fig 6.69d | Latex injection mold of the cervicocephalic air sac
flushes, systemic antibiotics and antifungals are often required. and the infraorbital sinus (red latex under eye, around naris and
The addition of hyaluronidase to the flush can expedite the the cranial aspect of the beak). A section of a wooden applicator
breakdown of caseated debris (see Chapter 9, Therapeutic is being used to prop open the oral cavity. (Some latex has run
Agents). down the rhamphotheca from the nares and more has run into
the oral cavity at the commissure of the mouth and on the lead-
ing edge of the beak).
Gwen Flinchum
Peter Coutteel
Fig 6.69e | Budgerigar with an extensive accumulation of Fig 6.69f | Canary with infraorbital sinusitis. Mycoplasma was
infraorbital sinus serous fluid. This is a very difficult problem to isolated.
correct. Mycoplasma has been incriminated in some cases.
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 6.70a | The iris of an immature blue Fig 6.70b | The iris of a mature blue Fig 6.70c | The iris of an immature
and gold macaw. and gold macaw. African grey.
Greg J. Harrison
Greg J. Harrison
Fig 6.70d | The iris of a mature African Fig 6.70e | The iris of an immature
grey. umbrella cockatoo. This appears the same
as one would see in a mature male
umbrella cockatoo.
EYES This is not as prevalent in the umbrella and Moluccan

cockatoos as it tends to be in the yellow or citron
The eyes should be bright and clear. Ocular discharge
crested members of this genus. Additionally, it is not a
and loss or matting of the feathers around the eye indi-
guarantee of gender, and a DNA determination of sex
cates either conjunctivitis or sinusitis. Conjunctival
should be made if the gender is questionable (Figs
hypertrophy is common in chronic conjunctivitis, espe-
6.70a-e).
cially in cockatiels. Mycoplasma has been implicated in
this syndrome in cockatiels. Focal light, magnification Both nuclear sclerosis and true cataracts occur in birds.
and fluorescein stain is needed for a detailed ocular In larger psittacines, cataract removal can be accom-
examination. Severe or non-responsive ocular disease plished by selected veterinary ophthalmologists. As in
should be referred to an ophthalmologist familiar with dogs and cats, the degree to which the bird is affected
the avian eye when possible. by the decreased or lost vision will often dictate whether
attempting surgery for cataract removal is warranted.
Determination of the integrity of the globe and neuro-
logic pathways necessary for vision can be difficult. Various congenital and acquired diseases of the eyelids,
Consultation with or referral to an ophthalmologist cornea, iris, and fundus exist in birds as in other species.
familiar with the avian eye may be necessary. Again, there are increasing numbers of veterinary ophthal-
mologists who are knowledgeable regarding avian ocular
Iris color can indicate sex and/or age. Young birds tend
anatomy and disease, and a referral may be indicated.
to have a dark iris that lightens as the bird matures. This
is true for blue and gold macaws and African grey par-
rots among others. In many white cockatoos the dark EARS
iris lightens to brownish red or even reddish orange in The ears can be examined by parting the ear coverts with
the mature female, while in the male it remains dark. the wooden end of a cotton-tipped applicator or similar
203
Greg J. Harrison
Greg J. Harrison
Fig 6.71a | Cloaca everted in a green-wing macaw in order to Fig 6.71b | Speculum in the cloaca of an anesthetized
check for papillomatosis. The small raised area at 9:00 needs to umbrella cockatoo. The hypertrophied opening of the ductus
be tested with acetic acid and/or biopsy. Blanching, in response deferens onto a prominent papilla is indicative of a male.
to the application of vinegar, is reportedly diagnostic.
appliance. The ears should be open and free of discharge bird, the fecal portion should be formed and homoge-
or erythema. Visualization of the tympanic membrane is nous, with little odor (except for poultry, waterfowl and
difficult in most species without the use of an endoscope carnivorous birds). The color should be various shades
(see Chapter 24, Diagnostic Value of Endoscopy and of brown when the bird is fed a pelleted diet. Seed diets
Biopsy). Note that the tympanum of birds is normally will cause the stool to be a more greenish color. Various
convex, as opposed to the normal concavity that is found fruits, especially those with strong pigments such as
in mammals. cranberries and blueberries, and artificially colored foods
including colored pellets, may affect the stool color
(Fig 6.72c).
DIGESTIVE AND URINARY SYSTEM
The cloaca can be assessed externally for enlargement The urates should be a crisp white and slightly moist. If
and dilation (often indicative of reproductive behavior in the bile pigments are not adequately resorbed from the GI
a hen), prolapse, ulceration or inflammation around the tract and reused by the liver, the excess of bile pigments,
mucocutaneous junction, and the presence or loss of mainly biliverdin, will leach out of the feces and into the
sphincter tone. Moistened cotton-tipped applicators can urates, causing the urates to develop a greenish tinge.
be introduced into the cloaca and used to isolate and Diet, species, and state of excitation may alter the ratio of
evert the cloacal mucosa. The mucosa is normally thin, urine to feces present in a dropping. Do not confuse
pink and smooth (Figs 6.71a,b). Gently everting the true polyuria with “excitement polyuria,” the excess
cloaca allows a cursory examination of the mucosa, pos- urine produced by an excited or nervous bird. See
sibly revealing papillomas in susceptible species. These Chapter 16, Evaluating and Treating the Kidneys, for
may be obvious pedunculated protrusions or more sub- information on polyuria and further diagnostics.
tle thickenings with a cobblestone appearance to the tis- Lorikeets, due to their liquid diet, will normally produce
sues. Suspicious areas can be painted with dilute acetic large amounts of urine. A close examination of the drop-
acid; blanching indicates the presence of a papilloma. A pings is a valuable and non-stressful starting point for
more thorough evaluation of the cloaca requires the clinical examination. Examination of the droppings
endoscopy. in the bird’s cage that have been collected from the past
24 hours will yield more information than limiting the
REPRODUCTIVE SYSTEM examination to stress droppings produced enroute to or
in the hospital.
Refer to the physical examination form, Chapter 4,
Nutritional Considerations, Section II Nutritional Some abnormalities commonly encountered in the avian
Disorders and Chapter 18, Evaluating and Treating the dropping include:
Reproductive System for in-depth discussions of repro- • Diarrhea — unformed fecal portion (Figs 6.72c,f2)
ductive anatomy, physiology and disease (Figs 6.72a,b,g). • Undigested food in feces (Fig 6.72f)
• Very bulky droppings — maldigestion; malabsorption;
Fecal Examination reproductively active hens; abdominal growth; pel-
Birds’ droppings are made up of three components: leted diet (Figs 6.72a2,d,e)
feces, urates and urine (Figs 6.72a2,b2). In a healthy • Melena
Greg J. Harrison
Fig 6.72a | Prolapsed uterus in a finch. Fig 6.72a2 | Normal Amazon dropping
seen when the bird consumes an organic
formulated diet.
Greg J. Harrison
Fig 6.72b2 | Normal passerine
dropping.
Fig 6.72b | Prolapsed uterus in a budgerigar.

Greg J. Harrison
Greg J. Harrison
Fig 6.72c | Passerine droppings with

artificially colored food items and mild Fig 6.72d| An elderly malnourished
enteritis. female budgie with an obstructive
Greg J. Harrison
cloacal condition from a uterine tumor.

When the obstruction was manipu-
lated, 8 cc of feces were expressed.
The owner elected euthanasia.
Fig 6.72e | The normal stress changes
observed in the droppings of a parrot that
traveled a long distance prior to examina-
tion. Droppings at home (bottom); drop-
pings at the clinic (top). The dark color at
home (a sign of melena) is not normal.
205
Greg J. Harrison
Greg J. Harrison
Fig 6.72f | Passing whole seeds in feces. Various causes of Fig 6.72f2 | A dropping from a parrot
proventriculitis, ventriculitis, and pancreatitis must be considered. with diarrhea is a rare observation.
Greg J. Harrison
Greg J. Harrison
Fig 6.72g | Egg-bound pearly cockatiel passes Fig 6.72h | A parrot’s droppings show excess urates with the
a loose liquid dropping after having the egg beginning of biliverdinuria.
removed. Biliverdinuria reflects the liver stress of
the situation.
Greg J. Harrison
Greg J. Harrison
Fig 6.72i | Loose feces from polydipsia in a large parrot. Fig 6.72j | Polyurates with biliverdinuria and feces typical of
enteritis.
Greg J. Harrison
Greg J. Harrison
Fig 6.72k | Parrot dropping with PU/PD and biliverdinuria. Fig 6.72l | The droppings from a cockatiel with PU/PD.
Hyperglycemia is a common cause of PU/PD, especially in obese
adult cockatiels on poor diets.
Greg J. Harrison
Greg J. Harrison
Fig 6.72m | A car in Florida (USA), parked under a tree where Fig 6.72n | Polyurates in a bird recently switched to an organic
roosting passerine birds have been eating a local tree’s sea- high fat and high protein diet. The pansystemic repair occurring
sonal fruit, demonstrates that they pass large amounts of urates requires massive tissue replacement leading to an increased
on such a diet. nitrogen load.
Greg J. Harrison
Greg J. Harrison
Fig 6.72o | Polyurates with fat. Fat in the urine is rare. Severe Fig 6.72p | Passing whole blood in the urine after the bird ate
kidney damage has occurred, and this bird did not survive. the back of an old mirror (mercury). Similar presentations have
been seen in lead toxicosis.
207
• Malodorous droppings — bacterial (clostridial or understanding of the species in question and the results
other) or fungal overgrowth of a thorough history taking and physical examination
• Aerated droppings — also called “popcorn stool” seen that enable the practitioner to develop an abbreviated
most commonly in cockatiels with giardiasis (see Fig list of differential diagnoses.
6.16)
• Green urates — often indicative of liver disease and Before proceeding with diagnostic tests, the clinician
biliverdinuria (Figs 6.72e,f,j,k) should first ask:
• Yellow urates — associated with anorexia and liver • Is the patient sufficiently stable to undergo diagnostic
bilirubin excess (Fig 6.72h) testing, or does it require supportive care prior to
sampling?
• Pink/red urates — blood, hemoglobin or denatured
hemoglobin that may be associated with renal disease. • Are the physical risks to the patient justified by the
Some species, such as Amazons, eclectus and galahs likely clinical value of the results?
will demonstrate pink to brown urates with lead • Are the test(s) appropriate to the patient (ie, species,
poisoning age, sex) and its clinical signs?
• Orange urates — may be due to vitamin B injection in • Has the test been validated to ensure that the result
the last few hours or artificial colors in the diet obtained is likely to be both accurate and meaningful?
• Thick, pasty urates — dehydration
If the answer to these questions is ‘yes,’ then diagnostic
• Polyuria — multiple etiologies, including: heavy metal
testing should proceed.
toxicity, renal disease, sarcocystosis, diabetes mellitus,
and pituitary adenoma (Figs 6.72i-l) Diagnostic testing should be done in steps, with the
• Polyurates (Figs 6.72m-o) results of each test allowing interpretation and reevalua-
• Anuria — etiologies include: tion of the subsequent diagnostic procedure. Where
Obstruction: Fecoliths or uroliths, egg-binding, appropriate, the clinician should endeavor to start with
cloacal prolapse, papillomatosis minimally invasive tests (ie, fecal wet smears, fecal flota-
Functional: Renal disease, severe dehydration tions and Gram’s staining) before moving on to more
• Fresh blood — cloacal pathology (Fig 6.72p) invasive tests. As each tier is passed, the information
gained should allow the clinician to narrow the differen-
A fresh fecal sample should be collected for a fecal tials and perform tests leading to a definitive diagnosis.
Gram’s stain (see Chapter 4, Nutritional Considerations:
Section II, Nutritional Disorders), flotation and wet The practitioner should be aware that the “normal” val-
smear evaluation. If there is polyuria, a urine sample can ues provided by laboratories for serum chemistries,
be collected for urinalysis. hematology and other parameters are generalizations
and are not species-specific. Some of these values are
Urine evaluation and the urinary system in general is inaccurate and are extrapolated from canine or feline
covered in depth in Chapter 16, Evaluating and Treating values. The practitioner should be familiar with normals
the Kidneys. for the species in question, or have a reputable refer-
ence text available (see also Appendix).
Clinicians also need to be familiar with the advantages,

Diagnostic Testing disadvantages and accuracy of the diagnostic test(s) they
Veterinarians treating birds (and other exotic species) employ. There is controversy and healthy debate within
are faced with challenges often not encountered by their avian medicine concerning many of the tests that are
colleagues treating dogs and cats. Many birds are pre- currently in use. Examples include:
sented to veterinarians only when near-terminally ill, • Are fecal Gram stains an appropriate diagnostic test to
and a rapid tentative diagnosis is often the difference use on healthy patients (see Chapter 4, Nutritional
between life and death. Birds are often limited in their Considerations, Section II Nutritional Disorders)?
range of expression of clinical signs and many clinicians, • What is the significance of yeast in a Gram’s stain?
through no fault of their own, lack the experience to • How should one interpret cloacal and choanal cul-
conduct a thorough physical examination. The combina- tures? Should these cultures be routinely performed?
tion of these factors has led to an increasing tendency in • Should zinc levels be assessed in patients not showing
avian medicine to conduct exhaustive diagnostic tests on clinical signs consistent with zinc toxicosis?
patients, often with scant attention paid to a complete • Can a diagnosis of zinc toxicosis be made from a sin-
history and a careful physical examination and with little gle blood level evaluation?
attempt to refine or focus the diagnostic efforts. The • Can aspergillosis be diagnosed or ruled out in a
selection of diagnostic tests should be based on a solid patient based solely on serologic tests or culture?
2
1
3
5
4
22
7 20
6
8
23 24
9 25
11
10 21
14 19
12 15
16
13 18
17
Ventral Dorsal
1. Front 6. Mandible 11. Breast (pectoral) 16. Claw (foot) 21. Hand
2. Crown 7. Gnathothea 12 Abdomen 17. Tail 22. Neck
3. Nape 8. Axilla 13. Vent 18. Uropygial gland 23. Wrist
4. Ear 9. Area of crop 14. Thigh (shank) 19. Flank 24. Forearm
Harcourt-Brown
5. Rhamphothea 10. Sternal carina (keel) 15. Shin (metatarus) 20. Alular digit 25. Upper arm
Fig 6.73 | Physical Exam
• How accurate is the differentiation between species of textbook. As with all non-peer reviewed information,
Mycobacterium via serology? What is the true zoonotic accuracy may be in question. It is important to trace
potential of Mycobacterium avium? Should birds diag- information to the original source to adequately evaluate
nosed with this disease be treated? the material. Journals, educational CDs, wet labs, annual
• Can disease be diagnosed from a positive DNA or PCR conferences and regular discussions with colleagues also
test on an asymptomatic patient? contribute to the maintenance of current knowledge.
• What is the appropriate interpretation of plasma elec- Conversely, a solid knowledge of the basics of avian
trophoresis? anatomy, physiology and disease generally requires more
• In what cases are biopsies (eg, renal, hepatic, and pan-
in-depth study than can be obtained through the above
creatic) warranted? What is the risk/benefit ratio?
sources. A combination of core textbook study, experi-
• Should crop biopsies be obtained for potential diagno-
ence, and Internet and journal-based current informa-
sis of PDD?
tion will yield the optimal breadth and scope of knowl-
• Is skin testing for birds sufficiently advanced to yield
edge necessary for avian practice.
clinically useful information?
As we move into the 21st century, it may no longer be Once again, “you will miss more by not looking than
sufficient to just have a textbook as a reference on these you ever will by not knowing.” It is only by a careful
issues and others. Access to discussion lists on the evaluation of the patient’s history, a thorough physical
Internet is an invaluable tool for keeping abreast of cur- examination, and the judicious use of appropriate diag-
rent issues. Topics are often discussed on the Internet nostic tests that the clinician can arrive at the correct
several years before they appear in even the most recent diagnosis and implement successful treatment.
209
Physical Examination Form

©Spix Publishing Inc, Adapted from Harrison GJ, Lightfoot TL: Clinical Avian Medicine, 2005.
MAP OF FINDINGS
Harcourt-Brown
B O DY C O N D I T I O N Occult blood in urine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Body weight ________ g “Chocolate milk” methemoglobin in urine . . . . . . . . . . . . . . . . . . . yes no

Hydration: Normal
Dehydration: <5% >5-10% >10% FEATHERS
Emaciation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Clipping of Wings
Underweight. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no IS BIRD CURRENTLY FULL-FLIGHTED? . . . . . . . . . . . . . . . . . . yes no
(percent or by how many grams? ______% _____ g
Owner declines clipping . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Amount of body fat: None Trace Light Obese
Wing clipped: Now . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Lipoma(s). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Previously . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Where located? _____________________________________ (see diagram)
Wing clipped: Right . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
BLEEDING Left . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
IF BLEEDING IS OR HAS BEEN PRESENT Both. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Bleeding/bruising of Feather Structure/Color

Sternum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Abnormal molt . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Describe _____________________________________________________
Distal wing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
(note: bleeding from wing tips may be from skin tears, bruising or damaged Chronic pinfeathers that fail to open . . . . . . . . . . . . . . . . . . . . . . . yes no
blood feathers and these must be differentiated) Retained keratin in the feathers of head . . . . . . . . . . . . . . . . . . . . yes no
Skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Feathers of body . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Location: _____________________________________________________ Saw-toothed edges to feathers (failure to zip) . . . . . . . . . . . . . . . yes no
Beak . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Broken, malformed or bent feathers . . . . . . . . . . . . . . . . . . . . . . . yes no
If yes from beak tip, trauma? . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Bite wound . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Lack of powder down when applicable . . . . . . . . . . . . . . . . . . . . . yes no
Skin at commissure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Dull appearance to feathers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Blood feathers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Stained or dirty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Cloacal blood Generalized Localized
Frank red blood in feces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Stress lines/bars . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Occult blood in feces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Flexibility of feather at 180° tip to base: (test of feather integrity)
Black feces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no • Breaks when bent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
• Bends and remains bent . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Frank blood from cloaca independent of droppings . . . . . . . . . . . yes no • Indents when flexed . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Hemolyzed blood in urine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no • Straightens back to normal when released . . . . . . . . . . . . . . . yes no
Are there malcolored feathers (abnormal for species, i.e., black on ABAXIAL SKELETON
normally green or blue feathers, pink or red feathers; yellow color-
ation to normally blue, green or white feathers; white discoloration Wings
of hyacinth feathers; red pigment in grey feathers). . . . . . . . . . . yes no Symmetrical at rest (i.e., no wing droop) . . . . . . . . . . . . . . . . . . . yes no
If yes, describe (color, location, onset): ____________________________
Bilaterally symmetrical on extension . . . . . . . . . . . . . . . . . . . . . . . yes no
Over-preening, picking, or other feather
Symmetrical range of motion . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
destructive behavior . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Pain on palpation, extension or flexion . . . . . . . . . . . . . . . . . . . . . yes no
Feather dystrophy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Swelling or thickening of any joints . . . . . . . . . . . . . . . . . . . . . . . . yes no
Multiple feathers in follicles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Skin of patagium healthy and elastic. . . . . . . . . . . . . . . . . . . . . . . yes no
BEAK Legs
Is beak symmetrical. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Tibiotarsal length ____________
If no, describe abnormality (scissors beak, prognathism, Symmetry of legs when extended . . . . . . . . . . . . . . . . . . . . . . . . . yes no
beak trauma, groove in beak from naris, previous rhinitis, other) ___________ Range of motion of leg joints - bilaterally symmetrical . . . . . . . . . yes no
______________________________________________________________
Pain on extension or flexion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Overgrown . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Weakness of grip when perched . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Friable . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Symmetrical grip strength . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Hyperkeratinization . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Favoring one leg when perched or ambulating . . . . . . . . . . . . . . . yes no
Small scratch abrasions from concrete perch evident on beak. . . . yes no
Feet abnormally warm. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
NAILS Posture (erect, drooped, unstable) . . . . . . . . . . . . . . . . . . . . . . . . yes

If yes, describe: _______________________________________________
no
Missing nails . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no

List: _________________________________________________________ Toes
Toes missing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Abnormally curled . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Which one(s): _________________________________________________
Otherwise deformed . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Toes deformed/luxated . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
If so, describe: ________________________________________________
Which one(s): _________________________________________________
SKIN Sternum
Carina of keel - smooth, straight . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Flaking . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Breast muscle bilaterally symmetrical . . . . . . . . . . . . . . . . . . . . . . yes no
Pruritic . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Other lesions (erythema, excoriations, scabs, lacerations, necrotic areas)
List and see diagram: ____________________________________________ A B D O M I N A L PA L PAT I O N
Normal or increased sterno-pubic distance. . . . . . . . . . . . . . . . . . . yes no
______________________________________________________________
Palpable fluid in sterno-pubic area . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Cutaneous or subcutaneous masses . . . . . . . . . . . . . . . . . . . . . . . yes no
Severity/extent of fluid? _________________________________________
Describe: ____________________________________________________
Masses palpable in sterno-pubic area. . . . . . . . . . . . . . . . . . . . . . . yes no
Loss of normal foot patterns (thin shiny skin) . . . . . . . . . . . . . . . . . yes no
Where located: ________________________________________________
Pododermatitis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no RESPIRATORY/CARDIOVASCULAR
Where located and degree _______________________________________ Nares
Self-cannibalized (mutilation). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Dirty feathers over nares . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Where located: ________________________________________________
Nasal discharge. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Burn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Character: ____________________________________________________
Where located: ________________________________________________
Nares asymmetrical. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Bite wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Describe: ____________________________________________________
Where located: ________________________________________________
Dry (lith), hard mass in nares . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
(Note: with a history of an encounter with a dog or cat, one should assume
that a bite wound has occurred whether or not a wound is detected) Infraorbital sinus swollen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Describe: ____________________________________________________
UROPYGIAL GLAND Excessive sneezing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Is a uropygial gland normally present or absent in this species?. . . yes no Dyspnea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

yes no
If present, is the uropygial gland normal in size and symmetry. . yes no If yes, characterize the dyspnea: ____________________________________
______________________________________________________________
Able to express small amount of sebum from papilla . . . . . . . . . . . yes no
Is neck extended and does the bird vocalize
with inspiratory dyspnea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
AXIAL SKELETON Is there increased abdominal movement . . . . . . . . . . . . . . . . . . . yes no
Is the spine completely immobile . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Open mouth breathing. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
If mobile, identify areas of bruising: _________________________________
Tail-bobbing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
_______________________________________________________________
Panting with exercise. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
_______________________________________________________________
Cessation of panting within 2-3 minutes . . . . . . . . . . . . . . . . . . . . yes no
211
Auscultation Submandibular space abscess . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no

Respiratory Rate ________ Heart Rate ________ Wounds . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Describe: ____________________________________________________
Cardiac murmur. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Arrhythmia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Regurgitation
Describe: ____________________________________________________ Passive or active regurgitation noted . . . . . . . . . . . . . . . . . . . . . . yes no
Air sacs audible . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Passively regurgitates water when handled . . . . . . . . . . . . . . . . . yes no
Describe: ____________________________________________________
Delayed crop emptying . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Lung sounds audible . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Food retained in crop/crop distention . . . . . . . . . . . . . . . . . . . . . . yes no
Describe: ____________________________________________________
Odor to crop contents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Nasal or tracheal noise/fluid/wheeze. . . . . . . . . . . . . . . . . . . . . . . yes no
Describe: ____________________________________________________ Lesions/burns/fistulas on crop skin . . . . . . . . . . . . . . . . . . . . . . . . yes no
Droppings
NEUROLOGIC - SENSORY Odor to feces. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Ears Decreased/increased amount . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Presence of symmetrical openings . . . . . . . . . . . . . . . . . . . . . . . . yes no
Yellow or green in urine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Discharge or matting of feathers . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Yellow or green in urates . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Pruritus, excessive scratching at ears. . . . . . . . . . . . . . . . . . . . . . yes no
Change in feces color . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Fluid or material visible beneath tympanic membrane . . . . . . . . . yes no
Increased liquid in urine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Head tilt . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Increased powdered urates. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Eyes White, fluffy droppings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Symmetrical size when viewed head-on . . . . . . . . . . . . . . . . . . . . yes no
Undigested food in feces. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
(If not, R/O glaucoma, exophthalmos, sinusitis,
microphthalmia, retrobulbar mass) Dark brown, black tarry or coffee ground-colored feces . . . . . . . . yes no
Redness or hyperplasia of conjunctiva . . . . . . . . . . . . . . . . . . . . . yes no Parasites (correlate with laboratory fecal exam for eggs) . . . . . . . yes no
Blepharospasm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Bubbly, gaseous droppings . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Corneal opacity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Scant feces . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Clarity of lens. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Diarrhea. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Iris color consistent with age, species and sex . . . . . . . . . . . . . . . yes no Pasting of vent. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Pupillary light response . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Gram’s Stain of Droppings
(Note: consensual response is not present in birds, and Normal numbers of digestive bacteria
voluntary constriction can occur, so interpret carefully.) (100-150/high power field) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Eyelid margins normal. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Decreased number of bacteria . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Does the bird appear visual . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no (______/field)
Egg-yolk stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no High % of gram-positive rods (>90%) . . . . . . . . . . . . . . . . . . . . . . yes no
Neurologic exam - use special form not included Low % of gram-positive cocci (<10%) . . . . . . . . . . . . . . . . . . . . . . yes no
Gram-negative rods. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
REPRODUCTIVE SYSTEM >1% >10% >30% >90%
Female More than 5-10 yeast per field . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Abdominal palpation suggestive of egg retention . . . . . . . . . . . . . yes no More than 10% budding yeast . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Evidence of cystic ovarian disease . . . . . . . . . . . . . . . . . . . . . . . . yes no Clostridium spp. present. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Egg-yolk peritonitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Undigested fiber . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Male RBCs in Gram’s stain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Is the vent irritated. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no WBCs in Gram’s stain . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Change in cere color (budgerigars). . . . . . . . . . . . . . . . . . . . . . . . yes no Megabacteria (macrorhabdosis) in Gram’s stain. . . . . . . . . . . . . . yes no
DIGESTIVE SYSTEM
Fungal or yeast hyphae in Gram’s stain . . . . . . . . . . . . . . . . . . . . yes no
Cloaca
ORAL EXAMINATION
Vent lips normal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Choana
Choanal papilla normal . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Diameter of vent and tone normal. . . . . . . . . . . . . . . . . . . . . . . . . yes no
Papillomas in oral cavity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Mucosa of cloaca normal thin, clear tissue. . . . . . . . . . . . . . . . . . yes no
Presence of plaques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Irritation, ulceration, cobblestone appearance
or papillomas noted . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no
Abscesses near glottis at base of tongue . . . . . . . . . . . . . . . . . . . yes no
Infundibular cleft visible . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Acknowledgements
Infundibular cleft swollen or discharge present . . . . . . . . . . . . . . . yes no Spix Publishing Inc acknowledges the following veterinarians
Mucous membrane color appropriate for species . . . . . . . . . . . . . yes no for their input into the physical examination form:
Sublingual area abscess/masses . . . . . . . . . . . . . . . . . . . . . . . . . yes no Drs. Greg J. Harrison, Teresa Lightfoot, Bob Doneley,
Tongue symmetrical and mobile . . . . . . . . . . . . . . . . . . . . . . . . . . yes no Nigel Harcourt-Brown, Jan Hooimeijer and Thomas Tully.
07_Emergency and Critical Care.qxd 8/22/2005 3:09 PM Page 213
CHAPTER
7
Emergency and
Critical Care
GREG J. HARRISON, DVM, D ipl ABVP-A vian , D ipl ECAMS;
TERESA L. LIGHTFOOT, DVM, D ipl ABVP-A vian;
Emergency Stabilization
Avian emergencies are typically more challenging than
dog and cat emergencies.10 This is because birds tend to
hide illness such that by the time they are brought in to
be examined they are in an advanced state of debilitation.
At this point, handling or other stress may be fatal. Some
birds will have such grossly severe clinical signs that han-
dling for examination is contraindicated (see the “Put It
Down” List in Chapter 6, Maximizing Information From
The Physical Examination). Such clinical signs include
pronounced dyspnea (Fig 7.1), prolonged panting or
gasping for air, inability to grasp with feet, weakness,
inability to bite, closing the eyes during the examination
Fig 7.1 | This dyspneic female cockatiel was unresponsive to (listlessness), lack of normal response to stimuli and inco-
stimuli and had flexed claws. This bird died shortly after ordination (see Fig 7.3), marked abdominal swelling,
presentation.
frank blood in feces (Fig 7.2) and fluffed appearance. A
lack of fecal material in the droppings (Fig 7.4) and
anorexia, especially in smaller birds, can foreshadow
impending death, which may be hastened by handling.
For this reason, these clinical signs have been referred to
as a “put it down” list.21 If such signs are noted during the
examination, the bird should be released immediately
back into its cage. Very critical patients, especially those
that are dyspneic, often will benefit from oxygenation
prior to handling. This is especially important with inhala-
tion toxicosis or in cases of tracheal obstruction. The least
stressful method of oxygen administration is to place the
patient in a chamber connected to an oxygen source to
create an environment of 40 to 50% oxygen concentra-
tion.31 When possible, the bird should remain in the car-
rier in which it is presented, and the carrier with the bird
inside is placed into an oxygen chamber (Fig 7.5). The
bird should remain in the chamber until it is stabilized.
Oxygen toxicity from prolonged exposure has been
recorded and should be avoided.
Fig 7.2 | Frank blood in the urine portion of the droppings is Fig 7.3 | In an emergency situation with a dyspneic bird, mini-
frequently an indication of renal disease. Mercury and lead toxi- mal handling is required to avoid further stress. Placement of
coses have been reported etiologies for hematuria. Blood from the bird into a container and then placing that container into a
the cloacal mucosa may be confused with blood in the urine. plastic bag will allow for direct delivery of oxygen.
Fig 7.4 | Psittacine and passerine birds seldom pass pure urates
and urine coated by mucous. Excessive fruit consumption,
increased water consumption due to heat, or stress may produce Fig 7.5 | Covering the cage of a dyspneic bird
such a dropping in an otherwise healthy bird. Passing such multi- with a plastic bag and flushing with oxygen can
ple droppings often indicates prolonged anorexia. Also note the be life saving.
yellow-colored bile pigment stain in the urates, indicating hepatic
disease. All these indicate a grave prognosis.
In these critical cases it is best not to handle the patient AIR SAC TUBE PLACEMENT
immediately. Explain to the client possible differentials,
In some cases, emergency placement of an air sac tube
prognosis and a plan of action. During this conversation, (Fig 7.6a-c) in the caudal thoracic or abdominal air sac is
the client will have time to comprehend the severity of necessary. This should be done in cases of tracheal or
the bird’s condition. Also, the owner may add information syringeal obstruction. Clinical signs of upper respiratory
to the history that will alter the list of differential diag- obstruction include gasping for air, often with the neck
noses, preliminary treatment or the prognosis. It is essen- extended (see Fig 7.1), and/or making “squeaking”
tial that the owner have a clear understanding of the sounds with each breath. Air sac tubes are not indicated
prognosis and cost estimation before treatment is begun. for respiratory disease below the syrinx or for non-respi-
ratory origins of dyspnea (ascites or organomegaly). For
Once the owner has agreed to hospitalize the bird, a example, primary lung disorders, such as polytetrafluo-
plan of action should be formulated. Severely ill birds roethylene (PTFE) toxicity, will not be improved by the
may die from handling, and one must proceed in a step- placement of an air sac tube, since the air capillaries will
wise fashion. One treatment or procedure is performed, still not be able to absorb and exchange oxygen.
and the bird is then placed back in its enclosure and Abdominal air sac tube placement is contraindicated in
allowed to recover prior to attempting the next diagnos- lower respiratory conditions such as air sacculitis. These
tic or therapeutic step. birds may present with whole-body movement during
respiration and/or crackling sounds on lung auscultation.
Chapter 7 | E M E R G E N C Y A N D C R I T I C A L C A R E
215
a b c
Gwen Flinchum
Gwen Flinchum
Gwen Flinchum
Fig 7.6 | Air sac tube. a) Non-cuffed tubea and retention disk that is sutured to the skin. b) The tube inserted anterior to the leg (or in
the left paralumbar fossa). c) A down feather plucked and used to detect airflow through the tube.
The approach to lacement of an air sac tube is similar to

preparation for lateral laparoscopy (see Chapter 24,
Diagnostic Value of Endoscopy and Biopsy). The patient
is placed in right lateral recumbency with the dorsal leg
pulled caudally. The caudal edge of the eighth (last) rib is
palpated and the skin over this site is surgically prepped.
A small skin incision is made behind the eighth rib. Using
mosquito forceps, the muscle wall is bluntly dissected
and the body wall is penetrated. A small tube is placed
into the hole (Fig 7.6b). To check if the tube is properly
seated, place a down feather over the tube opening. The
feather should move with each breath (Fig 7.6c). Keep a
tight hold on the feather so it is not sucked into the air
Fig 7.7 | A commercial incubatorb that allows regulation of
sac. Care must be taken to avoid iatrogenic organ dam-
temperature and humidity. Oxygen can be attached if needed.
age caused by pushing the tube in too far. The diameter
of the tube should be the approximate diameter of the
patient’s trachea. Modified red rubber catheters work FLUID THERAPY
well for air sac tubes, as do endotracheal tubes for
medium to larger birds. Avian air sac surgical cathetersa Oral Administration
are ideal because there is a retention disc attached to the Oral administration is the ideal method of giving fluids.
tube that makes suturing the tube to the skin easy and This method is more commonly used in mildly dehy-
secure (see Tracheal Obstruction later in this chapter). drated birds or in conjunction with subcutaneous (SC)
or intravenous (IV) therapy. Oral rehydration (30 ml/kg
PO q 6-8 h) also may be used in larger birds (eg, water-
fowl) that are difficult to restrain for parenteral fluid
Supportive Care therapy.
SICK-BIRD ENCLOSURES Subcutaneous Administration

Sick birds are often hypothermic and should be placed Subcutaneous fluid therapy is probably the most com-
in heated (brooder-type) enclosuresb (Fig 7.7) in a quiet mon method of administration, although administration
environment (see Chapter 1, Clinical Practice). A tem- in very critical patients must be done judiciously. With
perature of 85° F (29° C) with 70% humidity is desirable experience, warm fluids can be given over the dorsum in
for most sick birds. If brooders are not equipped with a very depressed birds without restraint or altering of the
humidity source, placing a small dish of water in the bird’s position within its incubator. Studies have shown
enclosure will often supply adequate humidity. A moist that adding hyaluronidasee to fluids (150 IU/L fluids)
towel that is heated and placed on the bottom of a cage greatly facilitates the absorption of these fluids.17 Subcuta-
or incubator rapidly humidifies the environment, as indi- neous fluids are most commonly given in the intrascapu-
cated by the fogging of the acrylic cage front. lar area, the flank, and the area over the pectoral muscles
Fig 7.8b | A butterfly catheter (24-gauge) and a much larger

Fig 7.8a | Materials needed for placement of an intravenous 22-gauge, three-quarter-inch catheter for larger birds are possi-
catheter in a bird: isotonic warm fluids, syringe and needle for ble alternative indwelling catheters for birds.
administering flush, heparin flush (not pictured), plastic-coated
intravenous catheterff (24-gauge pictured here), a catheter adapter
set (extension), bandage scissors, cotton wool, porous tape, stretch
fabric tapez, flexible bandage materialaa (Note: needle and catheter
sizes are based on medium to large psittacine patients).
or the axilla. Maintaining fluids on a heating pad or in an Intravenous plastic-coated catheters (IVC) (Figs 7.8a,b)
incubator, so they are available at the correct tempera- and the related plastic tubing and various rubber
ture for emergencies, is important. Warm fluids are both adapters — all derived from human pediatric medicine
an adjuvant treatment for hypothermia and less painful — have made catheter placement in small birds possible
on administration. However, as in mammals, a severely (Figs 7.9a-g). Anesthesia may be required for catheter
debilitated or dehydrated bird will not absorb SC fluids. placement and proper securing of the catheter and line.
Once placed, the security of the adhesive materials
Intravenous Administration incorporated into these devices, combined with the
severe debilitation of the patients in which these
Intravenous administration of fluids is necessary in cases
catheters are utilized, makes additional restraint or
of severe debilitation or severe hypovolemia. However, mechanical barriers usually unnecessary.
when dealing with critical cases in avian medicine, diffi-
cult decisions must often be made. For example, some With the advent of the use of hyaluronidase in subcuta-
patients may die from the stress of being restrained for neous fluids the IVC is seldom required. The multidose
injection or catheter placement. On the other hand, IV IV fluid technique also works on most cases in which
therapy may be imperative in saving a bird’s life. Careful subcutaneous fluids with hyaluronidase are inadequate.
consideration must be given to the bird’s history and The disadvantage to bolus IV fluids is that they cause
physical condition. Intravenous hetastarch (10-15 ml/kg hypervolemia with subsequent polyuria; therefore, less
q 8 h for 1 to 4 treatments) is indicated for hypopro- fluid is retained than with a constant rate infusion IV
teinemic patients (total solids <2.0 g/dl). drip. This drawback is minimized by the use of a syringe
pump that will deliver as little as 1 cc of fluids over peri-
Intravenous Catheter Placement ods of up to 1 hour.
Intravenous catheterization facilitates fluid administra-
tion; however, catheterization can be challenging due to Other Fluid Therapy Methods
the small size of bird veins. Avian veins also are more An alternative to IV catheterization is intraosseous (IO)
subject to rapid hematoma formation than are mam- catheterization of the distal ulna or proximal tibia. This
malian veins. This is especially true with the basilic method is very useful during the first 24 to 48 hours of
(wing) vein. Catheter placement may be more easily initial hydration and shock therapy. It also is used to
accomplished with the bird anesthetized, although the maintain hydration and IV access during prolonged pro-
risk of anesthesia must be considered. Furthermore, cedures, such as complicated orthopedic repairs. In the
catheter maintenance may be difficult, especially if the latter case, the IO catheter can be placed after the patient
bird is prone to chew at the site. Elizabethan collars can is anesthetized, avoiding the pain and stress related to
be placed to prevent this, but often result in further its placement. Insertion of IO catheters tends to be
stress to the patient. painful and often necessitates anesthesia for placement.
217
Fig 7.9a | Placing an indwelling catheter in the medial Fig 7.9b | A 24-gauge catheter needle has entered the
metatarsal vein on a lovebird’s leg. The vein is occluded at the metatarsal vein. Note the entry site is just the distance of the
proximal tibial-tarsus. catheter hub length proximal to the hock. This creates maximum
catheter stability when the taping snugs the hub into the depres-
sion proximal to the tibioltarsus’ distal condyles.
Fig 7.9c | The catheter is advanced to the hub. The hub is Fig 7.9d | A small tuft of cotton wool is wrapped around the leg.
taped with a 3- to 4-mm-wide and a 4- to 5-cm-long piece of
waterproof adhesivebb tape in the fashion shown.
Fig 7.9e | An extension with an injection Fig 7.9f | A layer of cohesive flexible ban- Fig 7.9g | The site is wrapped with stretch
port has been attached to the catheter and dageaa is wrapped over the catheter, exten- fabric tape. Fluids can now be administered
it is folded along the skin and covered with sion and injection port. by bolus as often as desired, or an IV pump
cotton wool. can be attached and a continuous drip
administered.
however, this again adds additional weight to the collars

and makes them more cumbersome.
Regardless of the material used, E. collars can be applied

facing one of two directions. Applying them with the
wide portion forward (cranial) allows for better balance
and does not interfere with wing movement; however, it
is more likely to impede eating and drinking, and the
visual presence of the collar surrounding the bird’s head
often frightens the bird. If the collar is applied facing
backward (with the wide end caudal), the bird can more
readily access food and water and can see its surround-
Fig 7.10 | An intraosseous needle and the insertion handle.
ings without visual impairment; however, with the collar
in this position, the wings cannot be extended for bal-
This may be too stressful for critically ill birds. An IO ance. In some cases, the collar must be left long enough
needle with a handlea1 (Fig 7.10) is available and makes to prevent the bird’s access to its legs and feet. In these
catheter placement easier and more precise. cases, the length of the collar is often significant and the
bird will tend to trip on it as it attempts to ambulate.
Rectal fluids also may be effective. Posturetal urine can
be modified in the rectum after retrograde movement Plastic disks that provide a neck ring of harder plastic or
from the coprodeum and subsequently be reabsorbed. metal are available. These neck rings may break and
In an experimental study, four out of six pigeons were some of these devices have a screw-type clamshell neck
rectally infused with a hypotonic solution, which suc- portion that is very difficult to apply without anesthesia.
cessfully maintained hydration.23
Various custom-made, padded cervical collars have been
utilized (Fig 7.11e). These are measured from the tho-
PROTECTIVE DEVICES racic inlet — with the neck fully extended — to the
Various traumas, postsurgical patients and cases of self- mandible. A compressible material consisting of a rubber
mutilation may require the placement of a mechanical or plastic foam, such as a swimming pool float or the
barrier to prevent self-trauma. Some birds require little insulation used to encase refrigeration piping and cov-
physical distraction (Fig 7.11a). Historically, circles of ered with an elastic tape, has worked well in this
exposed radiographic film were designed to encircle the author’s (GJH) experience. Disposable baby diapers or
neck, forming a type of Elizabethan (E.) collar. Various similar human pads used to absorb urine and feces also
types of padding used in conjunction with these collars can be shaped into lightweight, flexible neck collars
creates a safe and effective barrier to self-mutilation. (Figs 7.11f,g).
Such devices have several drawbacks, however: they are An additional device is a plastic “lego”-like, locking,
time-consuming to custom make; one must ensure that ballooned out collarf (Fig 7.11h). Care must be taken to
the collar itself does not abrade or otherwise injure the avoid entrapping the bird’s feathers in the device, pre-
bird; if the padding is not properly applied, the film’s venting it from locking. If the bird falls or hits this
sharp edge may cause abrasions or lacerations circum- device it may snap open and fall off.
scribing the cervical area; additionally, the collar must
be designed such that the bird does not destroy it. Regardless of the protective device selected, a primary
Radiographic film is not very durable and is challenging concern is that the application of the collar does not
to apply (Fig 7.11b). cause injury to the patient. Various combinations or
devices and alternating applications may be necessary.
Plastic disks are commercially available, but many are
heavy and cumbersome (Fig 7.11c); birds may stumble Removing the collar for a period of time each day so the
and fall, have difficulty perching and/or accessing food bird may preen will decrease the stress to some birds
and water (Fig 7.11d). These collars may become during prolonged use of a collar.
entrapped in the cage or on cage items. Almost all birds
will go through a period of agitation in response to The use of collars for feather-destructive behavior is sel-
application of these “collars.” Flapping in a circular, dom warranted, although their use in cases of self-muti-
spastic manner for a prolonged period is not uncom- lation can be life saving. This is where the clinical dis-
mon. Additional padding can be applied to avoid dam- tinction between feather destruction and self-mutilation
age to the propatagium during these violent episodes; becomes critical.
219
Fig 7.11a | This cockatiel needed only the Fig 7.11b | A severe case of Amazon foot Fig 7.11c | Plastic circular disks use a
minor distraction of the decorative portion necrosis that occurred prior to the advent of plastic clamshell shape to envelop the neck.
of a child’s sock to discourage picking. newer treatment techniques. Such cases The sleeve comes in two parts and is joined
faced months of collaring. This collar was by metal screws. Variations of this collar
reinforced with a heavy-duty fabric tape have a padded, rubber-like cervical edge
used in the construction industry. Note that and metal snaps.
the bird managed to pull in the disk’s edge
and remove part of the tape. This collar
also produced a weight burden for the bird.
Fig 7.11d | An Amazon is collared to prevent Fig 7.11e | A cervical brace-type protection
feather-destructive behavior. The bird’s nutri- device made from a padded material. While still
tional disorders, hormonal imbalances and requiring a period of adjustment, this variation
behavior problems were not being addressed. seems superior to the extensive Elizabethan col-
The use of a collar without addressing the under- lar for comfort and rapid return to normal func-
lying problem is inhumane. tion.
Fig 7.11f | A section of black refrigeration Fig 7.11g | Human diaper pads can be used as Fig 7.11h | A plastic clamshell
pipe insulation that can be cut into various padding material that is taped to offer durability and protective devicef with a soft bub-
lengths to fit the cervical area and prevent attached for a custom-made cervical brace protective ble section shaped to prevent the
mutilation. Elastic fiber tape makes a durable device. bird from reaching its body. The
coating. manufacturer reports faster adap-
tion and a higher rate of comfort.
Birds that have E. collars applied should be kept in the the extended period of time involved, the lack of labora-
hospital until they have acclimated to their presence. tory support for such studies and the lack of a wide-range
Some birds have an initial reaction of constant flipping of therapeutic choices. Gram’s stain results, such as bud-
and flailing. These birds should be placed in a padded ding yeast or fungal hyphae, or confirmation of asper-
but otherwise empty incubator and observed. The use of gillosis or other fungal infection through cytology or
a medication such as medazolam prior to the application histopathology will help confirm a diagnosis. Antifungal
of an E. collar may aid in its acceptance. Acclimation here medications also may be indicated during antibiotic ther-
is defined as being able to move around a normal cage apy to decrease the risk of secondary yeast infections,
and access food and water. The collar may require modi- especially in immunosuppressed birds. Birds with a his-
fication or reinforcement, either to facilitate ambulation tory of malnutrition and chronic respiratory disease may
or to provide a more extensive barrier to self-mutilation. benefit from prophylactic use of antifungal medications
Chewing at the collar may persist to some degree until a diagnosis can be made. Aspergillosis secondary to
throughout the period it is worn. chronic vitamin A deficiency and subsequent squamous
metaplasia may be an underlying problem in these birds.
Applying a protective barrier to a bird without considera- Among pet birds, Amazons (Amazona spp.),1,14 African
tion for and treatment of the underlying etiology is both grey parrots (Psittacus erithacus)1,25 and macaws (Ara
poor medicine and potentially cruel. If a less cumber- spp.)6 appear to be especially susceptible to aspergillosis.
some device can be used, it should be applied. Antifungal medications exhibit diversity in their mecha-
nisms of action, toxicities and cost. An understanding of
ANTIBIOTIC THERAPY these properties will enable intelligent decisions as to
The unnecessary use of antibiotics in veterinary medicine which drug is appropriate for a particular situation.
is a current concern. When practical, diagnostic testing
should be done prior to the initiation of therapy. Mini- MISCELLANEOUS MEDICATIONS
mally, confirmation of the need for antimicrobial therapy
should be determined by response to treatment. Com- Corticosteroids
plete blood counts should be performed if collecting Corticosteroids have been widely debated due to the
blood will not endanger the patient. Culture and sensitiv- potential complications arising from their use.26 These
ity tests can identify infective organisms and the appro- side effects include immunosuppression, adrenal sup-
priate medication choices; however, it may take several pression, delayed wound healing and gastrointestinal
days to get culture results, which is unacceptable for ulceration. Most of these side effects are seen following a
emergency therapy. Fecal, throat or crop Gram’s stains prolonged course of administration of corticosteroids,
can be done quickly, are relatively non-invasive and can although reports of potential glucocorticoid-induced
be useful in making therapy decisions. Although indis- adrenal suppression after topical use have been cited.
criminate use of antibiotics is discouraged, prophylactic
However, single doses of corticosteroids have been
use may be indicated on the basis of clinical signs and
reported to improve the prognoses in cases of shock,
history for birds that cannot undergo further testing.
trauma and toxicity31 without the occurrence of clinically
Antibiotics are commonly given intramuscularly (IM). observable adverse side effects. The use of corticosteroids
Although this route is quick and effective, recently there is not recommended in birds that have had a history of
has been concern about muscle necrosis and pain associ- immunosuppression or fungal disease. Dexamethasone
ated with IM administration. It has been suggested that sodium phosphate (2 mg/kg IM or IV once) is the pre-
medications be given SC, especially in smaller birds with ferred steroidal anti-inflammatory for birds.4 Prednisolone
less muscle mass. Controlled studies are needed to see if sodium succinate (0.5-1.0 mg/kg IM or IV once) has been
absorption from this location will provide adequate reported to be most effective in cases of neurologic
blood levels of antimicrobials. emergencies (see Stress in Chapter 19, Endocrine
Considerations).
Many critically ill or septicemic birds require IV injec-
tions. This requires repeated venipunctures or catheter Glucose Therapy
placement. Disadvantages of IV injections include the
Hypoglycemia may be present in cases of malnutrition
possibility of extravasation, hematoma formation and
or starvation, sepsis or hepatic dysfunction. This is seen
stress to the patient.
most often in passerines, but seldom in psittacines and
occasionally in raptors. Blood glucose levels can be
ANTIFUNGAL THERAPY determined on a laboratory panel, and levels will fall to
Ideally, antifungal therapy is based on culture and sensi- below half of the normal for the species in hypoglycemic
tivity testing. This is almost never done in practice due to patients.5 Severe cases must be treated immediately, as
221
symptoms may include seizures, weakness and depres-

sion. Treatment includes IV administration of 25% dex-
trose (1-2 ml/kg slowly to effect), although dextrose
alone should not be used in dehydrated patients.5 Oral
solutions such as honey or Karo® syrup also can be used
in birds that are not prone to aspiration. The underlying
cause, if hypoglycemia, must be subsequently deter-
mined and corrected.
o,p’-DDD
Mitotane, or o,p’-DDD, is an adrenal-blocking drug that
has been shown to inhibit stress-induced hypersecre-
tions of corticosteroid, thus bolstering immunocompe-
Fig 7.12 | Hand-feeding a sick bird using a warmed
tency during stressful situations.13 Adrenal blockers also hand-feeding product may be attempted prior to
have been shown to arrest tumor growth and inhibit tube-feeding. Hand-feeding will be more time-con-
stress-induced tumor metastasis.11 o,p’-DDD is used in suming but less stressful for the patient if accepted.
cases of suspected immunosuppression and for neoplas-
tic conditions. Its use should be avoided in cases of sus-
thin consistency of the carbohydrate supplement mixture
pected pesticide toxicity.
is more digestible than regular hand-feeding formulas. It
also is useful for hypoglycemic patients or those with pri-
ORAL NUTRITIONAL SUPPLEMENTS mary liver disease. Another similar productk is recom-
Below are listed some of the oral nutritional supple- mended for patients with primary hypoglycemia or for
ments that can be gavage-fed to debilitated birds. Various birds needing additional calories provided as highly
hand-feeding formulas are on the market and, as a digestible carbohydrates.
whole, are far superior to the homemade formulas used
decades ago that contained monkey biscuits, peanut but- Following rehydration in sick birds, the liver needs ade-
ter and ground seeds. Commercially available hand-feed- quate carbohydrates to carry out its functions, so carbo-
ing formulas for baby birds are often utilized in the treat- hydrates are next in line as nutriceuticals for ill birds.
ment of sick and debilitated adult birds. The quantity Carbohydrates are generally followed by a more complex
that can be fed at one time to a sick bird is greatly oral nutritional formula within 24 to 48 hours.
reduced from that of baby birds. On the average, a baby
parrot can accommodate 10% of its body weight per Carbohydrate Metabolic Detoxifierh
feeding due to the elasticity of the crop and its rapid Based on a rice protein concentrate, this product works
emptying. Adult birds have a greatly decreased crop as a metabolic detoxifier for the liver while also providing
capacity, averaging 3% of their body weight. Additionally, calories. This is useful in cases of chronic liver disease
sick birds are less tolerant of food in the crop and care and when severe biliverdinuria is present. It is used for
must be taken to avoid regurgitation and/or aspiration. several days following the initial use of the carbohydrate-
only formula. This is usually followed by the use of the
A sick or debilitated bird should always have its
hand-feeding formula or a sick-bird support formula.
hydration corrected prior to attempting to initiate
oral gavage-feeding.
Sick-bird Support Formulas
Some formulas that are used and the indications for
Medical and surgical patients are often undergoing pan-
these are summarized below. None of these formulas is
systemic debilitation. A productl with simple proteins
indicated in the presence of ileus. Many ill birds are cap-
(isolated soy protein) and simple familiar fats (hi-oleic
tive-raised and were hand-fed, and these patients may
sunflower oil) is added to the carbohydrate supplementa-
respond to hand-feeding techniques (Fig 7.12). This facil-
tion listed above to further meet the bird’s nutritional
itates both feeding and medication administration.
requirements. See the discussion on carbohydrates in
Chapter 4, Nutritional Considerations for the raffinose
Carbohydrate Supplement
values of soy.
A simple carbohydrate powderi (fructose and malt dex-
tran) can be mixed with water, Tyrode’s solutionj or Many surgical and medical patients have been fed a seed
Normosol-R to make a non-viscous tube-feeding solution. diet and need the additional nutritional support gained
This is useful for birds to resolve crop stasis because the from the administration of a balanced formula.
The method of administration of the supplemental for-

mula will depend on both the patient’s condition and
the experience of the person administering the food.
1. Hand-feeding can be an ideal way to supplement birds
that revert to baby begging and feeding behavior when
ill. However, the administration of a sufficient quantity
of supplement at each feeding requires that the patient
be strong enough to demonstrate an adequate feeding
response, and that the person feeding be experienced
enough to avoid causing aspiration of the material.
2. Gavage-feeding also requires experience. When gavage-
feeding is performed, the experienced person will be
capable of avoiding the following inherent dangers:
a) Mechanical damage to the oropharynx with the
metal crop feeder
b) Damage to the beak with inappropriate use of oral
speculums Fig 7.13 | A formulated diet designed for
c) Accidental tracheal gavage hand-reared psittacines. The psyllium in this
d) Reflux of the formula from the crop into the productd cleans the digestive system, improves
hydration and helps restore electrolytes while
oral cavity reducing toxins and cholesterol. This product
(See Chapter 1, Clinical Practice). delivers 1.5 Kcal/ml when reconstituted.
Precautions: Feeding sick birds should not be attempted

by inexperienced persons. Do not attempt to hand-feed tered and resulted in the death of one bird. Another bird
birds that are not aggressively feeding. Do not use formu- had complications at the site of administration. No fur-
las that are too cold or too liquid. Feedings must be ther reports are currently available. Financial constraints
accomplished promptly to avoid appetite loss. Failure to may be an additional reason that parenteral nutrition is
heed these cautions could result in aspiration and death. not being administered to avian patients. A recent e-mail
(TPN January 9, 2003 [email protected] on exoticdvm@
Hand-feeding Formulad (Fig 7.13) yahoogroups.com) stated that the cost of having a phar-
Although originally formulated for hand-feeding juvenile macist compound a TPN formula was $100 Canadian for
birds, these formulas have been ideal for nutritional sup- 300 ml, and the shelf life was very short (several days).
port of malnourished birds or as a tube-feeding formula
for sick birds. The average dose for psittacines is 30-60
FREQUENTLY SEEN EMERGENCIES
ml/kg per day, divided and dosed q 6-8 h for an adult
bird, in addition to parenteral fluid administration, assum- Liver Failure/Malnutrition
ing normal gastrointestinal motility. Malnutrition is a major cause of liver disease in birds eat-
ing seed-only diets. This is due to the high fat and low
TOTAL PARENTERAL NUTRITION nutrient content of seeds. As with many diseases in birds,
(TPN) no clinical signs may be apparent until the patient is in
Total parenteral alimentation is the IV administration of an advanced stage of decompensation. Clinical signs may
all essential nutrients. Indications for use include gastro- include lethargy, inappetence, diarrhea with loose green
intestinal stasis, severe head trauma that precludes oral feces and green or gold urates (Fig 7.14) (see Chapter 4,
alimentation, and malabsorption or maldigestion.31 Nutritional Considerations, Section II). There may be no
Although parenteral alimentation has been described,9,30 abnormalities on the serum chemistries of these patients,
it is not routinely utilized in avian medicine. There can although elevations in either the hepatic enzymes or bile
be difficulties in placing and maintaining a catheter, and acids may be present.16 Hepatic disease with malnutrition
sepsis and bacteremia can occur if the catheter becomes as the underlying cause may present commonly as
contaminated. The constant monitoring of the electro- hepatic lipidosis, fibrosis and cirrhosis.
lyte and acid/base blood values for adjustments to this
formula is blood volume-prohibitive in pet birds. Routine dorsoventral and lateral radiographs can be
helpful in identifying hepatomegaly or decreased liver
Total parenteral nutrition given intraosseously (TPN/IO) size. Bag radiographs (see Figs 1.17a,b,c, 1.18a,b) are
was reported in 1995 and was tried experimentally on non-invasive and can be done by placing the bird in a
pigeons. Hyperglycemia and glucosuria were encoun- paper bag for radiography. This technique is useful for
223
Fig 7.14 | Bilirubin in the urates, an indication of hepatopathy. Fig 7.15 | Milk thistlem with a
vegetable glycerin base is used
as an oral supplement to aid
hepatic regeneration.
screening for the presence of heavy metal densities, may be “constipation.” A retained egg may be palpated
but not reliable for determination of hepatic size (see in the abdomen, although care should be taken not to
Chapter 1, Clinical Practice for information on bag radio- confuse a caudally displaced ventriculus for an egg dur-
graphs). ing palpation of the sterno-pubic area. Radiographs are
recommended to help identify soft-shelled eggs or dou-
Response to treatment for malnutrition-induced hepatic ble eggs, as well as secondary problems such as an
disease depends on the duration of the disease and the enlarged liver shadow or coelomic fluid accumulation.
extent of organ dysfunction. Treatment includes par-
enteral fluid administration, treatment of any concurrent Treatment includes parenteral calcium supplementation
infection and gavage-feeding with an appropriate for- (if the shell is soft), SC fluids and supplemental heat
mula. In one author’s (GJH) practice, this is more specifi- (see Chapter 5, Calcium Metabolism). Oxytocin (5 IU/kg
cally defined as the administration of subcutaneous flu- IV or SC once) has been recommended to help in egg
ids, and tube-feeding with sick-bird support formulasd.l expulsion. It has been reported that oxytocin can have
If recovery is possible, a response to treatment should adverse side effects and should be used only if the
occur within 24 to 48 hours. In the presence of a leuco- uterovaginal sphincter is well dilated and the uterus is
cytosis, with or without hepatic enzyme or bile acid ele- free of adhesions. However, since oxytocin is not the pri-
vations, antimicrobials are routinely used by one author mary hormone of uterine contraction in birds, it is only
(TLL). These are empirically based on the CBC differen- partially effective, and the effect of exogenous adminis-
tial and fecal Gram’s stain and may often include both tration is diminished. Both prostaglandin F-2 alpha and
antibiotic and antifungal agents. prostaglandin E are reported to be effective in cases of
egg binding. Prostaglandin F-2 alpha is more readily
Milk thistle (silymarinm,12,34,37) has been shown to improve
available, although it also carries the concern of oviduct
liver function and enhance regeneration of damaged
rupture if the utero-vaginal sphincter is not dilated.
liver cells (Fig 7.15).
Prostaglandin E is used in human obstetrics. Egg extrac-
Various other medications may be added to aid in tion via the cloaca is the least invasive method and can
hepatic function (see Chapter 15, Evaluating and be utilized in most cases (Fig 7.16). When dealing with
Treating the Liver). soft-shelled eggs, eggs adhering to the oviduct or uterus,
or cranially located eggshell fragments, laparotomy may
A diet change from seeds to a formulated diet is impera- be necessary. Collapsing the egg with a syringe and nee-
tive in long-term successful treatment. dle (implosion) may facilitate removal. When the egg
cannot be visualized via the cloaca, this may be due to
Egg Binding complications such as an impacted uterus or mummified
Egg binding is common in lovebirds, budgerigars, cock- egg. During egg extraction all shell material must be
atiels, eclectus parrots and older Amazon parrots (10 removed. If left in the uterus, shell fragments tend to
years or older) that are usually fed seed-based diets. migrate proximally, making retrieval very difficult. The
Clinical signs include swollen abdomen, fluffed appear- use of delivery forceps, feeding needle, syringe, and cot-
ance and lethargy. Often, birds will act as if they are try- ton-tipped swab facilitates egg or egg fragment removal
ing to defecate but cannot; therefore, the client concern (Figs 7.17a-c). The collapsed egg can occasionally be
Fig 7.16 | An egg-bound bird with the eggshell adhered to the Fig 7.17a | Equipment pictured here may be useful in treating
uterus. This is typical in birds with nutritional disorders. egg-bound birds; a syringe for flushing the uterus with normal
saline, an ophthalmic speculum, metal feeding needles for
flushing, and a curved-tip forceps for dilating the uterus and
grasping the shell of a collapsed egg.
Fig 7.17b | Anesthetized female positioned over a towel to aid Fig 7.17c | A lateral view of the forceps dilating the cloaca and
in proper cloacal inspection. The tail is perpendicular to the the feeding needle in place to puncture the egg, aspirate the
spine. contents or flush out shell fragments.
Fig 7.18 | Expressing a collapsed egg after it has been aspi- Fig 7.19 | A retractorn makes cloacal examination much easier.
rated transabdominally.
225
Gwen Flinchum
Fig 7.21 | A semi-flexible endoscope for examining the salpingo-
uterine area in an egg-bound bird.
often includes primarily a seed diet, with subsequent vita-

min A deficiency. Clinical signs include open-mouthed
breathing with a high-pitched squeaking noise emitted
each time the bird breathes. The bird will often have a
Fig 7.20 | A ruptured uterus allowed the egg forward-leaning posture as it attempts to increase air
to become retro-coelomic, causing death in this intake (see Fig 7.1). Flexible and rigid endoscopes can be
cockatoo. used for oral approaches to the larynx and trachea. A 1.2
mm x 20 cm semi-flexible endoscopeo (see Fig 7.21) is a
valuable tool for visualizing and identifying the tracheal
removed intact (Fig 7.18). Use of a retractorn (Fig 7.19)
obstructions in birds under 100 g. Nebulization can be
makes visualization much easier. (See Chapter 35,
used to soften obstructive material. A needle can be
Surgical Resolution of Soft Tissue Disorders for more on
placed through the trachea to prevent distal migration of
retractor use. See Chapter 18, Evaluating and Treating
the material. The bird is then held upside down and suc-
the Reproductive System for forceps and procedures).
tion is applied until the obstruction is resolved. With
Occasionally the uterus will rupture and the egg will be
cockatiels, a tom cat catheter can be utilized to provide a
free within the coelomic cavity (Fig 7.20). tube of appropriate diameter for aspiration of the mate-
rial. A surgical approach to the thoracic inlet has been
The rigid, semi-flexibleo (Fig 7.21) or flexible endoscope
described and may be used to remove foreign material,
for egg delivery is useful. Warm saline/air flushing and
but the surgical risk is significant.2 A final option is to
insufflation with the endoscope can make visualization
push the foreign body into one main-stem bronchus and
and subsequent egg particle removal much less stressful
into the lung, and follow up with aggressive antibiotic
than blind forceps delivery. This is especially true for
and antifungal therapy. Air sac tube placement (discussed
eggs that have migrated proximally and for retrieval of
earlier in this chapter) will likely be necessary for any
eggshell fragments. Once the egg has been removed and
attempted treatment. Without an air sac tube, the bird’s
the bird is stabilized, a series of leuprolide acetate (500-
respiration may be severely compromised by the presence
1000 µg/kg IM q 2 weeks, 3 times)3,38 or chorionic
of equipment in the trachea (see Chapter 24, Diagnostic
gonadotropin (HCG) (500 IU/kg IM on days 1, 3, 7, 14 Value of Endoscopy and Biopsy and the previous section
and 21);22 injections have been recommended. One of this chapter regarding air sac tube placement).
author (GJH) has found diet change from seeds to a for-
mulated diet mandatory for full recovery and prevention
Vomiting and Regurgitation
of recurrence. Dexamethasone has empirically improved
the response to HCG injections (see Chapter 18, Differentiation must be made between behavioral and
pathologic regurgitation. Behavioral regurgitation is usu-
Evaluating and Treating the Reproductive System for an
ally done in a controlled fashion and directed at an
excellent review).
object in the cage or the owner. Pathologic regurgitation
is not controlled and the patient will often sling its head
Tracheal Obstruction
as it regurgitates. Causes for regurgitation include toxic-
Tracheal obstruction is frequently seen in cockatiels ity, especially heavy metal, foreign body ingestion, bacter-
subsequent to seed inhalation. In larger species of ial, fungal or protozoal gastrointestinal infection, inges-
psittacines, tracheal obstruction is often due to the pres- tion of oral irritants (ie, biting into a common houseplant
ence of tracheal granulomas or aspergillomas that of the Pothos sp.), goiter in budgerigars, rancid food
impinge on the tracheal lumen. The history of these birds ingestion, gastrointestinal obstruction, pancreatitis, renal
failure, hepatopathy, septicemia, dehydration, polydipsia, (*Ed. Note: The authors have performed tests on 15 clin-
motion sickness and proventricular dilatation disease. ically normal boarding birds: no blood was grossly or
Diagnostic tools include radiography (plain film and bar- microscopically noted in the stools and all were nega-
ium series), blood metal level tests, Gram’s stains of tive on the occult blood test. It has been stated that all
fecal, crop or regurgitated material, and culture and sen- birds’ stools test positive for occult blood, however, we
sitivity. Determining and correcting the underlying cause did not find this to be true. Positive blood on a fecal in
is necessary for long-term treatment. Initial therapy may a normal bird may be found when the diet includes
include parenteral fluid administration, metoclopramide meat products.)
parenterally, crop flushing, frequent gavage-feeding of
small amounts of a non-viscous formula. Melena is the passage of black, tarry feces containing
blood that has been acted upon by the digestive system.
Gastrointestinal Stasis This is commonly seen in advanced liver disease, gastro-
intestinal ulceration and starvation. It also may be seen
The most important aspect of resolving gastrointestinal
with gastric and hepatic adenocarcinoma and pancreati-
stasis is to identify the underlying cause. Differential diag-
tis. Treatment should include treatment for the underly-
noses include proventricular dilatation disease, bacterial
ing cause, vitamin K1 injections (0.2-2.5 mg/kg IM as
or fungal crop infection, foreign body ingestion, sep-
needed) and parenteral fluid administration. Tube-feed-
ticemia, gastrointestinal obstruction, toxicity or other
ing with barium sulfate suspension concentration (0.05
underlying disease. The first step in treatment of gas-
ml/g body weight PO as needed) provides a protective
trointestinal stasis is to remove excessive material from
and anti-inflammatory coating to the gastrointestinal
the crop if present. A Gram’s stain or culture and sensi-
tract, assuming no perforation exists.
tivity of the flush contents will help yield a diagnosis if
primary crop infection is present. Rehydration must be Hematochezia is the passage of frank blood in the feces.
accomplished via parenteral fluids prior to initiating gav- Causes include foreign body ingestion, reproductive dis-
age feeding. Once this is accomplished and the crop is ease, neoplasia, papillomas, cloacitis and gastroenteritis.
empty, the bird should be tube-fed small amounts of a The appearance of frank blood that is separate from the
dilute solution such as non-lactated multielectrolyte solu- fecal portion and the urine portion when multiple drop-
tion and 5% dextrose or carbohydrate substitute.j,k If pings are examined is generally either reproductive or
obstruction is not suspected, gastrointestinal stimulants cloacal in origin. In South American psittacines, the pres-
such as cisapridep (0.5-1.5 mg/kg PO q 8 h) or metoclo- ence of cloacal papillomatosis should be suspected and a
pramide (0.5 mg/kg IM q 8-12 h as needed) may improve cloacal examination done to rule out this disorder. Frank
motility. Although cisapride has been taken off the mar- blood or hemoglobinuria may be seen in the urine in
ket in the United States, it is still available through com- some cases of lead and other heavy metal toxicosis.
pounding pharmacies. It also is important to note that
metoclopramide has been shown to cause seizures in Cloacal Prolapse
macaws at 0.5 mg/kg; however, when given at 0.1 mg/kg
Cloacal prolapse has been associated with behavior
both PO and IM, no hyperexcitability or seizures have
problems (see Chapter 3, Concepts in Behavior, Section
been noted by one author (TLL). As gastrointestinal
III, Pubescent and Adult Psittacine Behavior), poor nutri-
motility improves, tube-feedings can be made more con-
tion, neoplasia, papillomatosis, infection and reproduc-
centrated until normal consistency is tolerated (see Oral
tive complications. Prolapsed tissue should be inspected
Nutritional Supplements in this chapter). Identification
for necrosis or tears. Viable tissue can be gently replaced
and treatment for the underlying cause of gastrointestinal
using a gloved finger or blunt swab lubricated with acti-
stasis must be accomplished (see Chapter 14, Evaluating
vated yeast gelr. In this author’s (GJH) experience, when
and Treating the Gastrointestinal System).
there is severe tissue inflammation, the topical applica-
tion of a dexamethasone-dimethyl sulfoxide (DMSO)
Blood in Droppings
solution (4 mg:10 ml) will help reduce swelling with no
It is important to note whether blood in the droppings apparent clinical adverse effects; however, inflamed tis-
originates from the urine, feces, reproductive tract or sue in addition to DMSO may allow systemic uptake of
cloaca. Blood in the urine (see Fig 7.2) is a sign of kidney these drugs causing potential adrenal suppression.
disease and is commonly caused by toxicity or tumors. Hyaluronidase also can be utilized to reduce tissue
Some birds will pass blood in the urine transiently after swelling. Its effect is assumed to last for several days, as
restraint. This vessel’s fragility is not normal and, like has been documented in people (TLL).
occult blood in the feces, may be a sign of liver or gas-
trointestinal disease. A fecal testq will identify blood ver- Suture placement to reduce the cloacal opening has been
sus artifact.* described to maintain reduction of a prolapse; however,
227
if the underlying cause is not corrected, this will be only Metal Toxicities
a temporary solution. In recalcitrant cases (ie, sexual
Toxicities are frequently seen in birds, especially in those
behavior/masturbation), 2-0 nylon may be necessary, as
that are allowed to roam freely in the house. Metal toxic-
smaller sutures will not hold. Care must be taken to
ity is common, with zinc toxicosis seen most often in the
avoid damage to the innervation of the vent. Do not
USA. Clinical signs may include general malaise, polyuria
place sutures directly within the vent lips. Do not inhibit
and diarrhea, and polydipsia with subsequent passive
defecation by having excessive restriction of cloacal out-
regurgitation of water. Neurologic signs are more com-
flow. Cloacal atony associated with these conditions has
been reported to respond to cisapride.p,39 mon with lead toxicosis than with zinc toxicity. Radio-
graphs can be helpful in identifying metal particles, how-
Many birds with cloacal prolapse may present for foul- ever, metallic foreign bodies will not be seen in some
smelling diarrhea. A Gram’s stain will often demonstrate zinc-toxic birds.36 Conversely, not all ingested metal is
overgrowth of clostridial organisms when this fetid diar- toxic. Placing a bird in a paper bag for radiography facili-
rhea is present in association with cloacal prolapse and tates screening for metal densities with minimal stress.
straining. Although the clostridial overgrowth is likely Blood metal concentration testss are dependable for the
secondary to irritated cloacal mucosa and fecal retention, diagnosis of metal toxicosis;35 however, significant blood
it still requires treatment when encountered. Gram-nega- elevations of metal may not always occur in clinically ill
tive overgrowth also can occur, and a culture and sensi- birds.15 Furthermore, there is disagreement as to what
tivity of stool would then be indicated. constitutes accurate reference levels for metal toxicities.28
Cases are best diagnosed and treated after careful consid-
More persistent or recurrent prolapses may require a
eration of history, clinical signs and test results.
cloacopexy. When the cloacal margins have been exces-
sively stretched, surgical reduction may be necessary to
Treatment for metal toxicity involves removal of the metal
reduce the diameter of the opening (see Chapter 35,
pieces from the gastrointestinal tract and/or chelation of
Surgical Resolution of Soft Tissue Disorders).
metal ions in the bloodstream. Cathartics, such as lactu-
The owner should be forewarned that there is danger of lose or 1% psyllium in a hand-feeding formula,d speed
stricture and/or impediment to defecation or urination elimination of smaller metal pieces. Oils such as peanut
when a cloacopexy is performed, and unless underlying butter are much less effective. Magnets are used in larger
causes are addressed and corrected, the prolapse is birds for removal of sizable iron pieces that have been
likely to recur. galvanized with lead or zinc. For chelation therapy, the
following drugs are commonly used:
Uterine Prolapse 1. Injectable edetate calcium disodium injection, USPt,
Uterine prolapse may occur as a sequel to egg binding or (CaEDTA) (35 mg/kg IM or IV q 12 h for 5 days, then
in conjunction with cloacal prolapse. Frequently, an egg repeat as needed) is an effective chelator. Its disadvan-
will be visualized within the prolapsed tissue. Prolapsed tages include expense, pain at the injection site and
tissue must be carefully flushed with sterile saline and potential nephrotoxicity (although this has not been
examined for tears and necrotic areas. Treatment documented in birds to date). The advantage of
includes supplemental heat, warm SC fluid administra- CaEDTA is that its parenteral formulation allows
tion, parenteral calcium and broad-spectrum antibiotics. administration even in birds that are regurgitating.
Secondary yeast infections are commonly seen in these 2. Succimer (30 mg/kg PO q 12 h for 14 days) is an oral
cases, so antifungal medication also may be indicated. chelating compound that is safe and effective, espe-
Once tissue has been debrided and inspected, it can be cially for lead. It is usually made by a compounding
gently replaced using a gloved finger or sterile swab. pharmacy into a 25-mg/ml suspension.36
However, the suspensory ligament has usually been dam-
3. D-penicillamineu is the author’s (GJH) drug of choice
aged by the prolapse, and suturing the cloaca to hold the
(55 mg/kg PO q 12 h for 1 to 2 weeks, off 1 week,
uterus as it involutes or performing a cloacal hysterec-
then repeat as needed). It is an oral chelating com-
tomy may be the best approach. Severely necrotic uterine
pound that is safe and effective. However, it is avail-
tissue may require resection. Subsequent ovulation
able only as an oral medication, and therefore may
would, therefore, potentially allow intracoelomic follicle
deposition and egg-yolk peritonitis in some species and not be used for the initial therapy if the patient is
individuals. Birds with uterine prolapses frequently have regurgitating. Also, it has been reported to cause
poor prognoses, since they are often malnourished and regurgitation in some birds. Prolonged use may create
may have advanced liver disease or other underlying a copper deficiency.
health problems. 4. DMSA and dimercaprol.
Airborne Toxicities The bird may present for clinical signs such as decreased
Superheated, Non-stick Plastic Fume Toxicity appetite, hesitancy to climb or failure to preen and his-
Superheated, non-stick plastic fume toxicity, or polytetra- tory of a fall or other trauma. When digital pressure is
fluoroethylene (PTFE) gas poisoning, can be rapidly fatal. applied to the rostral portion of beak, the distal damaged
Clinical signs include severe dyspnea, weakness and fragment may shift.
coma. Treatment should include supplemental oxygen,
One method of correction is to use an electric grinding
SC fluids, aminophylline (10 mg/kg IV q 3 h, after initial
tool and hone off the fractured tip. If bleeding occurs,
dose, other doses can be given PO), dexamethasone
the practitioner may use the grinding stone’s heat, or
sodium phosphate (0.8 mg/kg IV once), heparin (40-50
other cautery method, to cauterize the tip of the newly
IU/kg IV once) and nebulization with heparin, lactated
exposed beak. Soft foods may be used for a short period
Ringer’s solution and dexamethasone. The prognosis for
to encourage the bird to eat. It may be best to perform
severely affected birds is extremely poor (see Chapter 31,
this procedure under a light plane of inhalation anesthe-
Implication of Toxic Substances in Clinical Disorders).
sia. Damage to the beak tip is painful, and the anesthesia
Air Fresheners will prevent elevation of the bird’s blood pressure and
Clinical symptoms similar to PTFE toxicity have been associated increase in bleeding.
observed in smaller birds (budgerigars, canaries) after
Broken nails are a concern if they bleed excessively.
exposure to plug-in or wick air fresheners. Treatment is
Cutting off any remaining distal portion and cauterizing as
the same as for PTFE toxicity.
discussed above is usually corrective. Similarly, applying
Scented Candles flour as a first aid measure may be palliative until attended
Sneezing and nasal discharge may occur after exposure by a veterinarian. Telephone advice for this condition
to lighted, scented candles. Some scented candles con- includes suggesting that the owner place flour in the bot-
tain wicks made with lead. When these are lit, the result- tom of a shoebox or other container and place the bird
ing odor can be poisonous to birds as well as humans. inside. This way, the bird’s nail will come in contact with
the flour without the increased blood pressure (and subse-
Candy Cooking Flavoring quent increased bleeding) that can occur with restraint.
Flavorings such as peppermint and spearmint used in
candy cooking while birds were present in the kitchen Broken and bleeding feathers are handled similarly to the
caused death in two budgies that were located 10 feet beak and nails. Distal fragments can be removed, and if
from the stove in an open cage (K. Marx, personal com- still actively bleeding, place flour directly on and in the
munication, 2003). follicle. Ligating the proximal portion of the feather may
be necessary. Caution must be used in advising clients to
It is likely that other aerosolized agents may be toxic to attempt chemical cautery at home. Inadequate restraint
birds. Limiting the exposure of psittacines to any and insufficient application of hemostatic agents com-
aerosolized substance is a reasonable precaution. bined with the increased blood pressure generated by
the restrained bird often result in prolonged and
General Recommendations for Toxicity repeated bleeding episodes.
When toxicity is suspected, a complete anamnesis should
Cautery or pulling the broken feather is best avoided if
be collected to determine the substance that is most
possible. Pulling the feather may result in damage to the
likely responsible. If the bird is not regurgitating, acti-
feather follicle’s generative tissue, resulting in a crooked
vated charcoal solutionv can be given (10-20 ml/kg PO) to
or cystic feather.
prevent or reduce toxin absorption in the gastrointestinal
tract. Subcutaneous or IV fluid administration encour- Excessive bleeding from any source should be investi-
ages the elimination of toxins through urination. If gated. Hepatic disease is frequently an underlying cause
cholinergic toxicity is suspected, atropine (0.1-0.2 mg/kg of coagulopathy.
IM or SQ q 4 h PRN) is indicated.
More severe beak injuries are discussed in Chapter 14,
Poisoning by plants is infrequently seen; other references Evaluating and Treating the Gastrointestinal System.
including human and veterinary poison control centers
are recommended if such a case is encountered.
TRAUMA
BEAK, NAIL AND FEATHER TRAUMA Head Trauma
The tip of the upper beak may be cracked without any This is most often seen in free-flying birds encountering a
blood or obvious displacement of the rostral fragment. ceiling fan or sliding glass doors. Cranial trauma may
229
solution and gavage-fed prior to surgery. This

decreases blood loss in surgeries where excessive
bleeding may occur (GBF).
5. Vitamin K1 injection and evaluation for hepatopathy.
Once bleeding is controlled and the patient is stable,

wounds should be debrided and cleaned. Any feathers
that are sticking in the wound should be cut or removed.
Wounds can be flushed with 50% dextrose for its bacteri-
ocidal properties.19 Sterile saline also can be used. If
there is dirt and dried blood caked in the wound, gentle
Fig 7.22 | Micro-encapsulated ammonia solutionw for postsur-
gical or traumatic pain, burns and swelling. It is the author’s
cleaning with gauze and 0.5 to 1.0% povidone-iodine is
(GJH) observation that the solution also aids in preventing bac- helpful. In birds, many wounds will heal very well by sec-
terial overgrowth. ond intention without sutures. Patients that pick at their
wounds may require a collar.
cause neurologic clinical signs. Prednisolone sodium suc-
cinate is a rapid-acting steroid that helps decrease central BANDAGING
nervous system swelling. Dexamethasone sodium phos- Modern gel-type dressings (Figs 7.23a-d) have made
phate also can be given (2 mg/kg IM once). Head trauma bandaging of bird injuries much easier and more success-
cases should be placed in quiet, dark places with no ful. When combined with the improved properties of
heat. Minor cases usually recover within 24 to 48 hours. adhesive tapes (see Figs 7.9f,g), bandage removal has
been made difficult to impossible for the bird and rela-
Limb or Body Trauma, Bites, Lacerations tively easy for the veterinarian.
Non-penetrating traumas can be greatly aided by the use
If needed, protective neck devices or collars can augment
of a topical ammonia solutionw (Fig 7.22). This product
the bandage for additional safety. The bandages can usu-
reduces pain, swelling and the incidence of infection.
ally be left on for 2 days. The hydroscopic or gel dressing
(GJH)
can be reapplied at the time of bandage change.
In the case of fractures and deep penetrations, stabiliza-
Wounds that are deep, extensive or obviously contami-
tion of the patient is the first priority. If there is no active
nated require parenteral antibiotic administration as well
or severe bleeding, warm, quiet and oxygenation may be
as topical debridement. Puncture wounds, often from
the logically provided emergency care. While the bird is
dog or cat bites, may appear minor but have a great
stabilizing in the warm, humidified oxygen chamber, the
potential for infection and septicemia.
practitioner can be collecting information from the client
that will aid in subsequent determination of the location
Split Vent or Ruptured Pygostyle
and extent of the injuries, and in their treatment.
This condition is commonly seen in malnourished cock-
If significant active bleeding is present, this must be con- atiels and other psittacines, and results from trauma to
trolled. The application of direct pressure to the wound the region caudal to the vent during a fall (Fig 7.24).
for several minutes may accomplish this. Remember that When the bird’s tail feathers strike the floor, the skin
a bird’s blood pressure can undergo a threefold increase and connective tissue surrounding the vent is stretched
in response to painful stimuli. Therefore, if the bleeding to the point of tearing. The skin in malnourished birds is
has stopped, it may be wise initially to refrain from not flexible and it tears easily. These wounds often have
exploring the injured area until the patient is stable (see significant exposure of the subcutaneous tissue and
earlier portion of this chapter). Repeated manipulation muscle. Treatment includes debridement and flushing of
and restraint may cause the resumption of bleeding. the wound. Transecting the tail feathers so that they do
not touch the floor as readily helps minimize repeated
If bleeding persists, however, one or more of the follow- stretching trauma. The bird must be housed so that
ing steps should be taken: repeated trauma does not occur. If the wings were
1. Application of a pressure wrap. severely clipped, they should be allowed to grow out to
2. Radiosurgical cautery. allow some glide and decrease the severity of impact.
3. Application of ferric subsulfate. Amazingly, these wounds may heal very well without
4. The use of Yunnan Piaox, a Chinese herb that also is an sutures by second intention. In selected patients, sutur-
excellent hemostatic agent.24 It can be used as a topical ing may be indicated. Critical to the long-term preven-
agent or mixed with a non-lactated multielectrolyte tion of recurrence of this condition is changing the
Fig 7.23a | An example of a gel dressing with a biosynthetic Fig 7.23b | A hydroactive dressingdd is soft and spreads out as
absorbent coatingcc that helps to maintain wound hydration. it absorbs serum from a wound and molds to the area. This
This type of dressing does not adhere to skin and is ideal for “gel” is an excellent debriding agent and also forms a matrix in
wounds without appreciable necrotic debris. which cells can grow. If there is copious serum production, the
bandage should be changed daily. To apply, the protective back-
ing of the dressing is removed and the yellow-brown gel side is
applied to the wound. A flexible bandageaa is then applied over
the dressing.
Fig 7.23c | A section of the gel dressingddd has been cut into Fig 7.23d | The H-shaped dressing is placed on the plantar
the desired shape and the protective backing is removed. The surface of the claw. The four legs of the H fold around the meta-
red necrotizing tissue of Amazon foot necrosis is readied for the tarsus and the third digit, covering all surfaces of the wound. A
bandage with the bird under anesthesia. coating of a cohesive, flexible bandageaa and an over-covering
of elastic-cloth tapez is applied as shown in Figs 7.9 f,g.
bird’s diet to correct the malnutrition and obesity that

were contributing factors.
ACUTE BLOOD LOSS AND ANEMIA

Acute blood loss is more rapidly life threatening in mal-
nourished birds because they frequently have decreased
liver function with associated coagulopathies. Severely
anemic birds will appear pale on the skin covering the
nares and feet, and have pale mucous membranes of the
cloaca and oral cavity. Tachypnea and tachycardia also
Fig 7.24| A cockatiel with a split in the tissue just caudal to the
may be present.
cloaca’s yellow feathers. This is a sign of a nutritional disorder
that has diminished the skin’s elasticity. Improvement of the
As with other species, the administration of oxygen will bird’s diet, preventing the bird from falling on hard surfaces and
increase the efficiency of the remaining red blood cells. treatment as an open wound are indicated.
231
Transfusions are indicated when the packed cell volume reserve, and treatment that causes stress with increased
(PCV) is below 20%. Homologous transfusions, from the oxygen demand may prove fatal.
same genus and species, yield the best result.7,8 Trans-
fusion volume should be 10 to 20% of the patient’s calcu-
FRACTURES
lated blood volume.
In cases of fractured limbs, it is a priority to stabilize the
Studies showed that using washed RBCs (no plasma) in patient before attempting fracture repair. Birds will die
conures the same genus as a donor was as efficacious as from stress, anesthesia, debilitation or septicemia rather
homologous transfusions (white-eyed conure to sun than from the fractured limb. Topical analgesicw (Fig 7.23)
conure, sun conure to sun conure) for a single transfu- helps reduce soft tissue swelling and pain. Analgesics
sion.8 In another study, however, cockatiels received such as butorphanol are indicated for systemic pain relief
Amazon blood (a heterologous transfusion), and these in fracture patients (see Chapter 8, Pain Management).
washed and labeled RBCs were short-lived.7
For emergency care of fractures, bandaging, and fracture
Other alternatives for blood transfusions have recently
repair see Chapter 34, Surgical Resolution of Orthopedic
become available. Hemoglobin glutamer-200 (bovine)
Disorders.
(Oxyglobiny) (30 ml/kg IV once) has been shown to be
effective in the resolution of clinical signs in dogs, cats,
sheep, rats, horses and a number of exotic animals.27 Its Products Mentioned in the Text
use in avian medicine has been investigated,20 although a. 20 Fr Non-cuffed Tube with Retention Disk, Cook Veterinary Products,
Bloomington, IN, USA, 1-800-777-222, [email protected]
it is not labeled for use in birds. Hemoglobin glutamer- a1. Intraosseous Needle and Handle, Cook Veterinary Products,
200 is expensive due to the lack of availability of small Bloomington, IN, USA, 1-800-777-222, [email protected]
b. Animal Intensive Care Unit, Lyon Electric Company, Chula Vista, CA, USA,
packaging, but it is potentially useful in treating avian 619-585-9900, [email protected]
anemia. c. Tyrode’s solution, Zoological Education Network, www.exoticdvm.com
d. Juvenile Formula, Harrison’s Bird Foods, Brentwood, TN, USA, 615-221-
9919, www.harrisonsbirdfoods.com
Hetastarch e. Wydase, Wyeth Laboratories Inc, Philadelphia, PA, USA, 1-800-934-5556,
Hetastarch (10-15 ml/kg IV q 8 h up to 4 treatments)4,20 is www.wyeth.com
f. Spherical cervical collar, Gary Nelson, DVM, [email protected]
used primarily for intravascular volume restoration;
g. Epogen (epoetin alfa), Jansen C.lag. Agmen-Roche
however, it can be used in anemic patients when blood h. UltraClear Plus, UltraBalance Medical Foods, Gig Harbor, WA, USA, 1-800-
products are unavailable.29 843-9660, www.ultrabalance.com
i. Ultrafuel, Twin Laboratories, Ronkonkoma, NY, USA
j. Tyrode’s powder to make solution, Zoological Education Network,
Erythropoietin g
800-946-4782, www.exoticdvm.com
k. Critical Care; Nutri-Support; Carbo-Boost, Lafeber Co, Cornell, IL, USA, 1-
Erythropoieting (100 IU/kg SC 3 times per week until 800-842-6445, www.Lafeber.com
desired PCV is attained) has been reported to improve l. Recovery Formula, HBD International, 7108 Crossroads Blvd, Suite 325,
success in treating chronic anemia by stimulating ery- Brentwood, TN 37027, [email protected],
throcyte production in some mammals.29 m. Milk thistle, Zoological Education Network, www.exoticdvm.com
n. Lone Star Medical Products, Inc, 713-796-0505, www.LSMP.com
Erythropoieting is a hormone that stimulates erythro- o. Karl Storz, 1-800-955-7832, www.karlstorzvet.com
poiesis in severely anemic patients. Avian erythropoietin, p. Propulsid, Janssen-Cilag, www.janssen-cilag.com. Must be obtained in the
US from a compounding pharmacy
which is stimulated and released following hypoxia and
q. Hemoccult Fecal Test, SmithKline Diagnostics, San Jose, CA, USA
suppressed by induced polycythemia, is structurally dif- r. Preparation H Gel, Whitehall-Robins Healthcare, Madison, NJ, USA
ferent than the mammalian type. Whether or not mam- s. Louisiana Veterinary Medical Diagnostic Laboratory, Baton Rouge, LA,
USA, 1-504-346-3193
malian erythropoietin acts to stimulate RBC production
t. Calcium versenate, 3M Pharm, Northridge, CA, USA 91324
in birds is not documented. u. Cuprimine, Merck, www.Merck.com
v. Toxiban, Vet-A-Mix, Shenandoah, IA, USA
Interferon and F10 w. Penetran, Zoological Education Network, www.exoticdvm.com
x. Mayway Corp, Oakland, CA, USA, 1-800-2-Mayway, www.mayway.com
In the United Kingdom, preliminary results of clinical y. Oxyglobin, Biopure Corp, Cambridge, MA, USA
trials on circovirus-positive African greys with precipi- z. Elastikon, Johnson & Johnson Medical, www.jnj.com/home.htm
tous decreases in WBC and RBC counts show promise aa. Equi-flex, Burns Vet Supply Inc, Rockville Centre, NY 11590
bb. Nex-care Waterproof adhesive tape, 3M Healthcare, St. Paul, MN, 55144-
using interferon, F10ee, and Oxyglobiny injections (M.
1000
Stanford, personal communication, 2003). cc. BioDres, DVM Pharmaceuticals, Miami, FL, USA www.dvmpharmaceuti-
cals.com/about_dvm.html
As with all critical conditions in birds, the stress of treat- dd. DuoDERM, ConvaTec, Bristol-Myers Squib, PO Box 4000, Princeton, NJ
08543-4000, USA
ment must be considered prior to initiating intensive
ee. F10, Health and Hygiene (Pty), Ltd, Sunninghill, South Africa,
therapy. Birds with severe anemia have little oxygen www.healthandhygiene.co.za/products-select.asp
References and 10. Degernes LA: Trauma medicine. GJ, Harrison LR (eds): Avian 2001.
In Ritchie BW, Harrison GJ, Medicine: Principles and 29. Plumb DC: Veterinary Drug
Suggested Reading Harrison LR (eds): Avian Application. Brentwood, TN, Handbook 3rd ed. Ames, Iowa
1. Bauck L: Mycoses. In Ritchie BW, Medicine: Principles and HBD Int’l Inc, 1999, p 151. State Univ Press, 1999, pp
Harrison GJ, Harrison LR (eds): Application. Brentwood, TN, 19. Kelleher S: Wound and abscess 284,376.
Avian Medicine: Principles and HBD Int’l Inc, 1999, p 42, Fig 7. management in rabbits. Exotic 30. Pollock C: Practical total parental
Application. Brentwood, TN, 11. Deguchi M, et al: Usefulness of DVM 2(3):49-51, 2000. nutrition. Proc Assoc Avian Vet,
HBD Int’l Inc, 1999, p 1001. metyrapone treatment to sup- 20. Lichtenberger M, et al: 1997, pp 263-276.
2. Bennett A: Approach to the tho- press cancer metastasis facilitated Administration of Oxyglobin and 31. Quesenberry KE, Hillyer EV:
racic cavity of birds. Exotic DVM by surgical stress. Surgery 6% hetastarch after acute blood Supportive care and emergency
1(3):71, 1999. 125(1):120, 1995. loss in psittacine birds. Proc therapy. In Ritchie BW, Harrison
3. Bowles H: Update of manage- 12. Duke JA, duCellier J, Beckstrom- Assoc Avian Vet, 2001, p 15. GJ, Harrison LR (eds): Avian
ment of avian reproductive dis- Sternberg S: Western herbal medi- 21. Lightfoot TL: Avoiding disaster in Medicine: Principles and
ease with leuprolide acetate. Proc cine: Traditional materia medica. the critical patient. Proc Assoc Application. Brentwood, TN,
Assoc Avian Vet, 2001, pp 7-10. In Schoen AM, Wynn SG (eds): Avian Vet, 1998, pp 265-271. HBD Int’l Inc, 1999, pp 393,396.
4. Carpenter JW, Mashima TY, Complementary and Alternative 22. Lightfoot TL: Clinical use and pre- 32. Romagnano A, et al: Treatment of
Rupiper DJ: Exotic Animal Veterinary Medicine, St. Louis, liminary data of chorionic a hyacinth macaw with zinc toxic-
Formulary 2nd ed. Philadelphia, Mosby, 1998, pp 323,351.12. gonadotropin administration in ity. J Avian Med Surg 9(3):185-
WB Saunders Co, 2001, pp 161, 13. Flinchum GB, Harrison GJ: psittacines. Proc Assoc Avian Vet, 189, 1995.
221. Observations on the effect of 1996, pp 303-306. 33. Romagnano A: Avian obstetrics.
5. Clippinger TL, Platt SR: Seizures. adrenal-blocking drugs in termi- 23. Lumeij JT, Ephocrti C: Theory and Sem Avian Exotic Pet Med 5:180-
In Olsen GH, Orosz SE (eds): nally ill pet birds. Exotic DVM practice of rectal fluid therapy in 188, 1996.
Manual of Avian Medicine, St. 2(3):71-75, 2000. birds. Proc Europ Com Assoc 34. Saller R, Meier R, Brignoli R: The
Louis, Mosby, 2000, p 173. 14. Forbes NA: Respiratory problems. Avian Vet, London, 1997, p 101. use of silymarin in the treatment
6. Clubb SL: Psittacine pediatric In Beynon PH, Forbes NA, 24. McCluggage D: Holistic medicine of liver disease. Drugs
husbandry and medicine. In Lawton MPC (eds): Manual of in exotic species practice. In 61(14):2035-2063, 2001.
Altman RB, Clubb SL, Dorrestein Psittacine Birds. British Small Schoen AM, Wynn SG (eds): 35. Tully T, Hoefer H, VanSant F:
GM, Quesenberry KE, et al (eds): Anim Vet Assoc, 1996, p 152. Complementary and Alternative Heavy metal toxicosis. J Avian
Avian Medicine and Surgery. 15. Fudge AM, Speer B: Selected con- Veterinary Medicine, St. Louis, Med Surg 11(2):115-118, 1997.
Philadelphia, WB Saunders Co, troversial topics in avian diagnos- Mosby, 1998, pp 655,658. 36. VanSant F: Zinc and clinical dis-
1997, p 94. tic testing. Sem Avian Exotic Pet 25. McMillan MC, Petrak ML: ease in parrots. Proc Assoc Avian
7. Degernes LA, et al: Autologous, Med 10(2):97-98, 2001. Aspergillosis in pet birds: A Vet, 1997, pp 387-391.
homologus homologous and het- 16. Fudge AM: Avian clinical pathol- review of 45 cases. Proc Assoc 37. Wellington K, Jarvis B: Silymarin:
erolgus heterologous red blood ogy: Hematology and chemistry. Avian Vet, 1988, p 35. A review of its clinical properties
cell transfusions in cockatiels In Altman RB, Clubb SL, 26. Orcutt C, Flinchum G: Contrasting in the management of hepatic dis-
(Nymphilus hollandicus) J Avian Dorrestein GM, et al (eds): Avian views on corticosteroid use in orders. Biodrugs 17(7):465-489,
Med Surg 13(1):2-9, 1999. Medicine and Surgery. birds. Exotic DVM 3(5):43, 2001. 2001.
8. Degernes LA, et al: Autologous, Philadelphia, WB Saunders Co, 27. Orcutt C: Oxyglobin administra- 38. Zantop D: Using leuprolide
homologus homologous and het- 1997, p 149. tion for the treatment of anemia acetate to manage common avian
erologous heterologous red 17. Griffin C, Snelling LR: Use of in ferrets. Exotic DVM 2(3): 44- reproductive problems. Exotic
blood cell transfusions in conures hyaluronidase in avian subcuta- 46, 2000. DVM 2(3):70, 2000.
of the genus Aratinga. J Avian neous fluids. Proc Assoc Avian 28. Osofsky A, et al: Determination of 39. Zantop D: Cisapride Use in birds.
Med Surg 12(1):10-14, 1999. Vet, 1998, pp 239-240. normal blood concentrations of HBD’s Avian Examiner - The 4-
9. Degernes LA: A preliminary 18. Harrison GJ, Ritchie BW: Making lead, zinc, copper and iron in Year collection, 1998, p 35.
report on IV TPN in birds. Proc distinctions in the physical exami- Hispaniolan Amazon parrots. J Available online at
Assoc Avian Vet, 1995, p 25. nation. In Ritchie BW, Harrison Avian Med Surg 15(1):31-36, avianmedicine.net.
08_Pain management.qxd 8/22/2005 3:42 PM Page 233
CHAPTER
8
Pain
Management
JOANNE PAUL-MURPHY, DVM, D ipl ACZM
What is Pain?
The International Association for the Study of Pain
(IASP) defines pain as an unpleasant sensory and emo-
tional experience associated with actual or potential tis-
sue damage.2 The IASP also includes under this defini-
tion an important note: The inability to communicate
in no way negates the possibility that an individual is
experiencing pain and is in need of appropriate pain-
Greg J. Harrison
relieving treatment (Fig 8.1). This is a very important

statement that gives credibility to pain experienced by
non-verbal populations of species, including humans as
well as all animal species.
Fig 8.1 | With such a devastating lesion, pain would seem
obvious, but the canary did not show evidence of pain until this All animals have neuroanatomical and neuropharmaco-
band was removed.
logical components required for nociception: transmis-
sion, perception and response to noxious stimuli. But
when does nociception become pain? This is not easily
determined, but for the purposes of this chapter it will
be accepted that not only do birds perceive and respond
to noxious stimuli, but also that birds feel pain. Pain is
always subjective and the emotional component is diffi-
cult for us to translate because birds do not share a ver-
bal language with humans. In humans, we accept that
pain is what the patient says it is, but in birds as well as
other animal species, it is what people think it is.
RECOGNIZING PAIN
The challenge is to recognize avian behaviors that occur
with painful stimuli, both acute and chronic. Perhaps
birds have evolved behaviors to minimize painful dis-
plays as a way of minimizing the attention of predators.
We are not yet fully capable of recognizing when a bird
is affected by pain; therefore, it may be best to err on
the side of over-estimation and assume that conditions
that would be painful to humans also are painful to
birds. Nonetheless, having an identified behavior or set actions with the owner. This is often manifested by a
of behaviors that correlate with pain provides a means decrease in vocalizations or chattering that birds often
to monitor response to pain treatment. It is difficult to do with the owner or reluctance to seek stroking or pet-
say we have effectively treated something if we cannot ting from the owner. Guarding behavior to protect a
measure it before and after therapy. But there is no reli- painful body part is seen in birds and can subtly manifest
able measurement or gold standard for the assessment in similar antisocial behaviors. Aggression has been linked
of pain in animals, including birds, either for research in individual birds to painful conditions because often
subjects or clinical patients. Assessment of pain must the aggressive behaviors dissipate once the clinical prob-
give consideration to species, gender, age, strain, envi- lem is resolved. A behavioral change in feather grooming
ronment and concurrent disease. Significance must be is common to both solitary and social birds. The change
given to the type of pain, such as acute, chronic, can be either an increase or decrease in grooming.
somatic, visceral, clinical or neuropathic. Decreased self-grooming is a withdrawal behavior that
occurs when a bird’s focus is on pain and not daily activ-
Behaviors that occur with acute noxious stimuli are the ities. Increased grooming behavior to themselves or
easiest to identify. There is an immediate cause-effect rela- other birds in their environment can be an intentional
tionship between activation of nociceptors (a receptor distraction. Studies using chickens with induced sodium
preferentially sensitive to a noxious stimulus), withdrawal urate arthritis demonstrate that shifting attention can
reflexes and behaviors that correspond to conscious per- reduce the severe pain and potentially reduce peripheral
ception of the stimulus.12 Noxious stimuli that have been inflammation.13 Alternatively, grooming and feather pick-
used to study avian pain are similar to those used in ing may increase over a specific area, often directly
mammalian studies, such as electrical stimulation, thermal related to the region of discomfort or painful stimulus.
stimulation and pressure, but other studies have
employed noxious stimuli unique to birds, such as feather Decrease in appetite and weight loss often accompany
removal, beak amputation and comb pinching, as well as painful conditions. In a study of rats observed postoper-
research models for chronic pain using intra-articular atively, dehydration and weight loss due to decreased
injection of sodium urate.12,18 Physiological measurements food and water consumption was significantly lower in
are not always consistent or specific to painful stimuli and rats given adequate perioperative analgesia.9 Unfortu-
are not useful for assessment. Respiratory rate, heart rate nately, dehydration and weight loss can occur under
and blood pressure will increase during painful stimuli numerous stressful conditions, from something as sim-
but also can be affected by light, sound, temperature, ple as changing the perches in a bird’s cage to a variety
restraint and other external stimuli. Avian withdrawal of known diseases. Weight loss is not unique to pain,
behaviors to acute painful stimuli include escape reac- but because it can be quantified it is very valuable to
tions (foot lifting, wing flapping), vocalizations, decreased record a bird’s daily weight. If weight gain or stabiliza-
head movements or extreme movements (jumping). tion occurs following administration of analgesia, then it
When parrots were given a mild electrical stimulus to the was a useful gauge.
foot using a specially designed test perch, the expected
response was foot withdrawal with a reluctance to place Tonic immobility is an innate fear response characterized
the foot back on the perch; but there also were several by a profound and reversible state of motor inhibition.
individual parrots that did not lift the foot, but began flap- In chickens, crouching immobility has been associated
ping their wings when a stimulus was delivered.31 with prolonged pain, stress and fear responses. Studies
Chickens can display a distinctive behavior termed using chickens demonstrated that repeated feather
crouching immobility, which occurs experimentally when plucking caused an initial agitated response, which
they are exposed to repeated noxious stimulation.12,14,37 progressed to sustained crouching immobility of the
chicken.12,14 A later study using chickens with ulcerated
How do we know when a bird is experiencing prolonged oral lesions placed an irritating substance on the lesions,
pain or chronic pain? It is generally accepted that when which caused several birds to go into a crouch-like pos-
a bird is in pain there is a change in or absence of one ture, with the head held close to the body and a signifi-
or more normal behaviors. To accurately assess pain, the cant reduction in head movements.11 The immobility
observer must be familiar with normal and pain-associ- reaction is prolonged when fear is present and reducing
ated behavior of a given species of bird as well as that of the fear component decreases the time of immobility.
the individual bird. Social species of birds will decrease Companion birds may display similar tonic immobility
their social interactions. This may be as subtle as a postures postoperatively or under chronically painful
reduction in social grooming behaviors or as obvious as conditions. It has been suggested that tonic immobility
perching away from the flock. For social species of birds evolved as a response of a prey species to reduce poten-
housed as single pets, there may be a reduction in inter- tial damage produced brought on by struggling. In
Chapter 8 | P A I N M A N A G E M E N T
235
guinea pigs, it has been demonstrated that tonic immo- scious. All other types of pain are considered clinical or
bility induces an endogenous analgesia involving opioid pathological, often involving tissue damage with inflam-
synapses, which increases the animals’ threshold to nox- mation or nerve damage. Pathological pain can originate
ious stimuli.21 from a gentle tactile stimulus, causing an exaggerated or
prolonged pain response, or can persist in the absence of
The correlation of elevated corticosterone has been noxious stimuli.
studied in its relationship to pain. It is a hormonal indi-
cator known to become elevated with ACTH (adrenocor- Peripheral sensitization occurs when inflammation at the
ticotropic hormone) release and stress in birds and site of injury creates an increased response to a normally
other animals.24 Pain can induce both acute and chronic painful stimulus. Cell damage and leakage leads to a
stress. Fecal corticosterone levels may offer a measurable series of responses resulting in increased sensitivity of
response that can be collected without interfering with the peripheral receptors and may even activate “silent”
the bird’s normal activities.22 Studies are currently in nociceptors, which magnify the pain response. In addi-
progress to determine if measurable amounts of corti- tion to sensitization at the peripheral tissue and pain
coids in avian feces correlate to painful stressors. receptor environment, the central nervous system can be
sensitized as well. Central sensitization is an increase in
the excitability of spinal cord neurons and a recruitment
PAIN ASSESSMENT SCALES
of neurons not involved in pain perception under nor-
Pain assessment scales are used in human medicine for
mal circumstances. When stimulation from the peripheral
verbal as well as non-verbal segments of the population.
nociceptors to the spinal cord continues for an extended
Pain scales can be sensitive and repeatable, and a similar
time period, a wide range of spinal neurons become sen-
process could be used to develop pain scales for birds
sitized and hyper-responsive. The response to additional
with the understanding that each would have to be
noxious stimuli becomes heightened and prolonged.
species-specific. As an example, a recent study with
Stimulation from the periphery that was previously non-
pigeons noted that body trembling consistently occurred
noxious, such as a tactile stimulus, becomes painful.
for several hours after recovery from general anesthesia,
orthopedic surgery and opioid analgesia, but it did not Understanding the mechanism of peripheral and central
occur with controls given the same period of general sensitization helps to explain why prevention of sensiti-
anesthesia and opioid, but without orthopedic surgery. zation is critical and provides multiple places in the
Additionally, all pigeons received the opioid after sur- process that could be altered by different classes of anal-
gery, but the group of pigeons that also received opioids gesic therapy. When sufficient analgesia is provided at an
prior to surgery stopped trembling earlier in the recov- early stage of tissue trauma, such as with surgery, it can
ery period than the other surgical group (J. Paul-Murphy, greatly reduce the degree of postoperative discomfort.33
unpublished data). Body trembling may be specific to Although this has not been experimentally demonstrated
pigeons or it may be specific to orthopedic surgery, or it in birds, animal and human studies have demonstrated
may be specific to some other variable not measured in that when analgesics are given prior to a painful event
this early attempt to develop a pain scale for pigeons. rather than after the start of the stimulation, the spinal
There are currently more than 26 published pain scales excitability can be dampened.35,36 The earlier pain is
for children, each trying to manage variables that may treated, the less total drug will be required to maintain
confound pain assessment.23 A pain scale can be a very analgesia both during and after surgery. It has been
useful assessment tool under consistent conditions, and shown in mammalian species that a shorter period of
it may be necessary to develop numerous species-spe- analgesia is needed in the postoperative period when
cific scales until a more accurate method is found to analgesics are given in the preoperative period.33 A study
assess pain. of pigeons undergoing orthopedic surgery showed that
the pigeons receiving butorphanol before and after
PHYSIOLOGY OF PAIN orthopedic surgery returned to normal behaviors sooner
than those pigeons receiving butorphanol only in the
The physiology of pain in all animals involves the periph-
postoperative period (J. Paul-Murphy, unpublished data).
eral process of detecting a noxious stimulus (mechanical,
thermal or chemical) and transmission of the impulses to
the spinal cord. Here they are modulated and projected RELIEF OF PAIN
to the brain for central processing of the information, Pain is a combination of both peripheral inputs and neu-
which determines the perception of the noxious stimu- rophysiological processes within the central nervous sys-
lus. Nociceptive pain involves the activation of the pain tem. Diagnosing the cause of pain can be difficult at
receptors, is usually localized and transient, and usually times, but identifying the disease process or site of tis-
activates a withdrawal response, both reflexive and con- sue damage will influence the choice of analgesic drugs
and supportive care. Therapy should be directed at mg/ml), and the formulation without epinephrine is rec-
resolving the disease process or injury as well as reduc- ommended. The commercial preparation should be
ing pain signals coming from the periphery and its diluted 1:10 with sterile water or diluted further to the
effects on the central neural processing of the pain. For volume required for the block. The total dosage should
example, immobilizing a bird’s fracture maximizes bone not exceed 2 to 3 mg/kg. For example, a 500-g cockatoo
healing, but it also reduces micromovement irritation can receive 1 mg lidocaine; 0.05 ml is diluted to 1 ml
and inflammation, thus reducing noxious stimuli pro- and this solution is used to block a 2-cm surgical skin
jected from the site of trauma. Analgesia therapy may incision. The commercial preparation of bupivacaine is
include an opioid plus an NSAID, but the immobiliza- prepared as 0.25% (2.5 mg/ml), 0.5% (5 mg/ml) or
tion itself greatly reduces the pain. Conversely, we may 0.75% (7.5 mg/ml) solution. No bupivacaine dosage has
recognize the signs of pain in a patient before we actu- been established for birds, but 1 mg/kg total dose has
ally diagnose the cause, and in these cases, treatment of safely been administered to large birds.
the pain becomes part of the symptomatic approach to
therapy. Selection of analgesic drugs should be done Local anesthetic dosage recommendations for birds are
conservatively in situations where the cause of pain is lower than for mammals because birds may be more sen-
still under investigation. sitive to the effects of the drug. Systemic uptake of the
drug may be rapid in birds, increasing the potential for
Supportive care is very important to the management of onset of systemic reactions. There can be acute toxic
pain. This includes keeping the avian patient warm, dry effects if these drugs are accidentally injected intra-
and clean. Environmental stressors should be kept to a venously. Toxic side effects can include fine tremors,
minimum by providing a quiet, soothing hospital envi- ataxia, recumbency, seizures, stupor, cardiovascular effects
ronment away from barking dogs or strong smells of and death. Chickens were injected with high doses of
“predators,” such as cats and ferrets. If the bird is a pet, bupivacaine (2.7-3.3 mg/kg) and showed immediate
provide human contact and speak in a soothing voice. signs of toxicity such as drowsiness and recumbency.18
The duration of action of local anesthetics depends on

the molecular properties of each drug, especially the
Pharmacological Approach lipid solubility of the drug. Neither the time to effect nor
to Pain Control duration of action has been determined for these drugs
in birds. In mammals, bupivacaine lasts much longer (4-
10 hours) than lidocaine (1-3 hours).
LOCAL ANESTHETICS
Local anesthetics are used to produce regional anesthesia Intra-articular administration of bupivacaine (3 mg in 0.3
and analgesia by blocking the transmission of noxious ml saline) was studied for its analgesic effects in chick-
impulses. Local anesthetics such as lidocaine and bupiva- ens with experimentally produced acute arthritis. Chick-
caine block sodium channels in the nerve axon, which ens given bupivacaine were able to feed, peck and stand
interferes with the conduction of action potentials (pain on the affected limb similar to birds without arthritis.18
impulses) along the nerve. Reducing the number of pain
impulses reduces the nociceptor sensitization, which has Topical benzocaine has been used for minor wound
the beneficial effect of minimizing central sensitization. repair in small birds.3 Topical bupivacaine has been stud-
Local anesthetics do not need to be distributed systemi- ied when applied to the amputation site in beak-
cally for the analgesic effect, but will slowly be absorbed trimmed chickens and provided 4 hours of analgesia.16
by the vasculature in the region being blocked. In mammals, local anesthetics also are used in the form
of transdermal patches and transdermal creams, but the
Regional infiltration or a local line or splash block are use of these patches and creams has not been studied
among the most common methods used. A 25-gauge with birds. Local anesthetics also are used in mammalian
needle is used to make several subcutaneous (SQ) injec- medicine for epidural infusions, spinal blocks, intra-
tions of small volumes of dilute solution into the opera- venous blocks and peripheral nerve blocks and as an
tive area. A line block follows the course of the intended antiarrhythmic agent, but none of these applications has
incision by injecting a modicum of dilute anesthetic SQ, been reported for use in birds.
then withdrawing the needle and reinserting it at the
edge of the raised area. Another modicum is delivered
OPIOIDS
under the skin and the process is repeated until the
length of the incision is blocked. Opioids reversibly bind to specific receptors in the cen-
tral and peripheral nervous systems. There are three
Lidocaine has a commercial preparation of 2% (20 major classes of opioid receptors associated with analge-
237
sia: mu, delta and kappa. Chickens have similar propor- Hispaniolan Amazon parrots.30,31 Plasma concentration of
tions of each receptor type as do humans.7 The distribu- 2 mg/kg butorphanol in African grey parrots has a mean
tion, number and type of opioid receptors are conserved residence time of less than 2 hours (J. Paul-Murphy,
across species in the brainstem and spinal cord but vary unpublished data). Buprenorphine at 0.1 mg/kg IM in
substantially in the forebrain.27 In mammals, mu and African grey parrots did not show an analgesic effect
kappa receptors primarily are associated with pain relief, when tested by analgesimetry, but recent pharmacoki-
with mu receptors being widely distributed in the fore- netic analysis suggests that this dose may not achieve
brain, midbrain and hindbrain, whereas, delta and effective plasma levels, and the mean plasma residence
kappa receptors are numerous in the spinal and supra- time is only 1 hour (J. Paul-Murphy, unpublished data).
spinal regions of the central nervous system (CNS). Higher doses of buprenorphine using different avian
Autoradiography was used to identify mu, kappa and species may help to clarify if buprenorphine is an effec-
delta opioid receptors in the forebrain of rats, mice and tive analgesic for birds. Clinical use of buprenorphine
humans, and kappa receptors represented 9, 13 and suggests it has an analgesic effect.
37% of the total opioid receptor population, respec-
tively. In contrast, the forebrain of pigeons has a rela- Fentanyl was evaluated using cockatoos and, although
0.02 mg/kg provided plasma levels similar to the concen-
tively high proportion (76%) of kappa receptors.27
tration found to be analgesic in cats, it did not affect the
All drugs in the opioid classification have morphine-like withdrawal response of the cockatoos.30 A ten-fold
effects, which may be mediated primarily by an increase increase in the dosage of fentanyl (0.2 mg/kg SQ) did
in serotonin synthesis. Given at appropriate dosages, produce an analgesic response, but many birds were
opioids do not cause a loss of consciousness but can hyperactive for the first 15 to 30 minutes after receiving
cause sedation and respiratory depression. Opioids vary the high dose.30 The duration of analgesic effect from
in their receptor specificity and efficacy at different fentanyl has not been established, but 0.02 mg/kg given
receptors, which results in a wide variety of clinical IM to cockatoos maintained a plasma concentration con-
effects in different mammalian species, and is influenced sidered analgesic in people for 2 hours.
by the commercial preparation of opioid, the dose and
Butorphanol (1-3 mg/kg IM) is the current recommenda-
the species receiving the drug. It stands to reason that
tion for opioid analgesia in parrots. Butorphanol is a
the opioid and the dose also will have a wide range of
mixed agonist-antagonist with primarily kappa agonist
clinical effects in different avian species.
action. This supports the one study finding of a high
percentage of kappa receptors in the forebrain of
Physiological and analgesic effects of opioids have been
pigeons. The dosage of butorphanol for effective analge-
studied in parrots using the isoflurane-sparing technique.
sia needs to be balanced with sedation and respiratory
This method anesthetizes healthy birds with isoflurane
depression, which may vary with other avian species and
and determines the minimum anesthetic concentration
need further evaluation.
(MAC) by using a noxious stimulus (toe pinch) and
observing a withdrawal response with a cognitive body
movement. Each bird then is injected with an analgesic NSAID s
and the MAC is redetermined. If the concentration of Non-steroidal anti-inflammatory drugs (NSAIDs) are
isoflurane can be lowered, then this “sparing effect” is among the most commonly used classes of drugs in
considered due to the analgesic effects of the drug being small animal medicine. NSAIDs interfere with eicosanoid
tested. Butorphanol (1 mg/kg) was administered to three synthesis by the inhibition of cyclooxygenase (COX)
species of parrots, and the isoflurane MAC could be sig- enzymes. COX enzymes initiate a cascade of reactions
nificantly lowered in cockatoos and African grey parrots that results in polyunsaturated acids being converted to
but not Amazon parrots.5,6 The addition of butorphanol eicosanoids such as prostaglandins and thromboxane.34
also caused lowering of the heart rate, tidal volume, and These are released at sites of tissue injury and cause
inspiratory and expiratory times. A similar type of study inflammation and sensitization of nerve endings.
compared mu and kappa opioids in chickens, and both
drugs had isoflurane-sparing effects.4 Reduction of prostaglandins and thromboxanes
decreases inflammation at the site of injury and also has
The effect of different opioids on conscious parrots was a modulating effect within the CNS. The physiological
evaluated by studying the change in withdrawal thresh- mechanisms involving prostaglandins, their role in
old from noxious electrical and thermal stimuli before inflammation and their ability to sensitize sensory neu-
and after receiving an opioid. Butorphanol, 1 and 2 rons to physical or chemical stimuli in birds are similar
mg/kg IM, had an analgesic effect on African grey par- to those in mammals.29 The COX-1 enzyme is part of nor-
rots, and 1 and 3 mg/kg had an analgesic effect on mal cell composition in numerous tissue types and the
238
concentrations are fairly stable, keeping prostaglandin tive in one species and range from ineffective to toxic in
levels at homeostatic levels. In mammals, COX-2 concen- another species.
trations increase when stimulated at sites of inflamma-
tion, but both COX-1 and COX-2 are expressed in the Combining analgesics that act by different mechanisms
CNS and participate in spinal pain transmission. The rel- can maximize the analgesic effect. Administration of two
ative expression of COX-1 and COX-2 enzymes varies or more analgesics frequently produces a synergistic
among species, and both enzymes are important in avian effect, such as a local anesthetic at the surgical incision
pain at the site of peripheral inflammation as well as in or site of recent trauma, a NSAID plus an opioid. This
spinal pain transmission. However, more information is combination of drugs usually allows the dosage of each
needed to differentiate their physiological effects in drug to be reduced, thereby reducing the side effects.
avian species. Additionally, opioids such as butorphanol will reduce
the concentration of inhalation anesthetic needed for a
NSAIDs can be used to relieve musculoskeletal and vis- surgical plane. Adjunctive drugs, such as tranquilizers
ceral pain, acute pain (trauma or surgical) and chronic used in conjunction with analgesic drugs, can potentiate
pain such as osteoarthritis. The most common NSAIDs the analgesic effects by reducing anxiety. The most com-
used in avian medicine are piroxicam, carprofen, keto- mon sedatives used in avian medicine are the benzodi-
profen and meloxicam. These compounds vary in their azepines, which calm the bird and may reduce anxiety.
structure, but all inhibit COX enzymes. Generally, the
current NSAIDs are safe drugs but should be monitored
CHRONIC PAIN
and evaluated in each individual patient. Increased moni-
toring may be indicated with high-risk patients: establish- Treatment of chronic pain in birds opens more ques-
ing a base-line set of hepatic enzymes and uric acid prior tions than there are answers. How to treat chronic pain
to NSAID administration and reevaluating these parame- in a non-verbal patient such as the bird is the ultimate
ters at fixed intervals (see Chapter 16, Evaluating and challenge. It is difficult to evaluate response to treat-
Treating the Kidneys). NSAIDs should not be used if ment when the condition itself may be progressive, such
there is any indication of renal impairment, hepatic dys- as chronic degenerative joint disease or neoplasia.
function or severe hypovolemia or if gastric ulceration is Response to analgesic therapy is based on evaluation of
present. Only one NSAID should be used at a time, but a set of behaviors particular for each individual bird.
in cases of chronic pain, frequently review the response
NSAIDs are the first course of therapy for chronic disor-
to therapy and change to a different formulation NSAID if
ders. Carprofen is the current drug of choice because of
response is poor or diminishing. For treatment of mild to
its widespread use and low incidence of reported toxici-
moderate chronic pain, NSAIDs can be given on an as-
ties. Carprofen is an orally administered drug and can
needed basis. The dose and frequency of administration
be initiated at the low-end dosage and monitored for
has not been determined for any clinical NSAID use in
response to treatment. As pain gradually increases over
birds. Ketoprofen (5 mg/kg IM) administered to ducks
time, the dosage of carprofen can be increased, and mon-
anesthetized with isoflurane had an analgesic effect 30 to
itoring the renal and hepatic serum values every 2 to 4
70 minutes after administration.25 Carprofen given to rap-
months is recommended, especially in an older bird. If
idly growing chickens with chronic lameness improved
pain recurs over several months of treatment, the next
their ability to walk and navigate a maze.28 Carprofen (1
set of options includes changing to another NSAID, such
mg/kg SQ) given to chickens raised their threshold to
as meloxicam or piroxicam. There is a risk when switch-
pressure pain for at least 90 minutes.8 Peak plasma levels
ing NSAIDs that the side effects can be potentiated, so a
occurred at 1 to 2 hours after SQ administration of
no-drug period of 7 to 10 days is recommended. Piroxi-
carprofen to chickens.28 Plasma levels do not provide suf-
cam may have synergistic action with anticancer drugs
ficient information to indicate physiological activity of the
and also is an effective NSAID for degenerative joint dis-
NSAID because NSAIDs tend to accumulate in areas of
ease in birds. Piroxicam is noted for renal toxicity and
inflammation. In mallard ducks, 5 mg/kg flunixin and 5
gastric ulceration in mammals, but its long-term use
mg/kg ketoprofen suppressed thromboxane B2 levels for
(months of treatment) in cranes with chronic degenera-
12 hours, indicating a prolonged physiological effect.26
tive joint disease has not caused clinical problems. If pain
persists or increases, especially with neoplasia, opioid
MULTIMODAL THERAPY therapy may be indicated. Unfortunately, most parenteral
Information specific to birds is minimal, and many cur- forms of opioids reach “effective” plasma levels rapidly,
rent therapies for birds are extrapolated from species in but these levels are maintained for only a few hours. No
a different class of vertebrates. Some drugs are handled information is available regarding oral opioids in birds,
similarly across species lines and other drugs may have but in mammals much higher dosages are required for
very different mechanisms of action; they may be effec- oral administration to reach effective plasma levels.
239
References and (buprenorphine jello) for post- 19. Jenkins JR: Postoperative care of lates release of substance P in
operative analgesia in rats: A clini- the avian patient. Sem Avian Exot avian sensory neurons. J Neurosci
Suggested Reading cal trial. Lab Anim 33(2):169-74, Pet Med 2:97-102, 1993. 12:1917-1927, 1992.
1. Beynon PH, Forbes NA, Harcourt- 1999. 20. Johnson-Delany CA: Exotic 30. Paul-Murphy J, Ludders J: Avian
Brown NH: BSAVA Manual of 10. Gentle MJ: Pain in birds. Animal Companion Medicine Handbook analgesia. Exot Anim Prac 4(1):
Raptors, Pigeons and Waterfowl. Welfare 1:235-247, 1992. for Veterinarians. Lake Worth, FL, 35-45, 2001.
Ames, Iowa State Univ Press, 1996. 11. Gentle MJ, Hill FL: Oral lesions in Zoological Education Network, 31. Paul-Murphy JR, Brunson DB,
2. Merskey H, Bogduk N (eds): the chicken: Behavioral responses 2000. Miletic V: A technique for evaluat-
Classification of Chronic Pain, 2nd following nociceptive stimulation. 21. Leite-Panissi CR, et al: Endogenous ing analgesia in conscious perch-
ed. IASP Task Force on Taxonomy. Physiol Behav 40(6):781-7833. opiate analgesia induced by tonic ing birds. Am J Vet Res
Seattle, IASP Press, 1994, pp 209- 1987. immobility in guinea pigs. Braz J 60(10):1213-1217, 1999.
214. 12. Gentle MJ, Hunter LN: Med Biol Res 34(2):245-250, 32. Paul-Murphy JR, Brunson DB,
3. Clubb SL: Round table discussion: Physiological and behavioural 2001. Miletic V: Analgesic effects of
Pain management in clinical prac- responses associated with feather 22. Ludders JW, et al: Fecal corticos- butorphanol and buprenorphine
tice. J Avian Med Surg 12(4):276- removal in Gallus gallus var. terone reflects serum corticos- in conscious African grey parrots
278, 1998. domesticus. Res Vet Sci 50(1):95- terone in Florida sandhill cranes (Psittacus erithacus erithacus and
4. Concannon KT, Dodam JR, Hellyer 101, 1991. (Grus canadensis pratensis). J Psittacus erithacus timneh). Am J
PW: Influence of a mu and kappa 13. Gentle MJ, Tilston VL: Reduction Wildl Dis 37(3):646-652, 2001. Vet Res 60(10):1218-1221, 1999.
opioid agonist on isoflurane mini- in peripheral inflammation by 23. Paul-Murphy J, et al. The need for 33. Roughan JV, Flecknell PA: Effects
mal anesthetic concentration in changes in attention. Physiol a cross-species approach to the of surgery and analgesic adminis-
chickens. Am J Vet Res 56:806-812, Behav 66(2):289-292, 1999. study of pain in animals. Mar tration on spontaneous behavior
1996. 14. Gentle MJ, Jones RB, Woolley SC: 1;224(5):692-697, 2004. in singly housed rats. Res Vet Sci
5. Curro TG: Evaluation of the isoflu- Physiological changes during 24. Lumeij JT, et al: Action of ACTH 69:283, 2000.
rane-sparing effects of butorphanol tonic immobility in Gallus gallus upon plasma corticosterone con- 34. Vane JR, Bakhle YS, Blotting RM:
and flunixin in Psittaciformes. Proc var. domesticus. Physiol Behav centrations in racing pigeons. Cyclooxygenases 1 and 2. Annu
Assoc Avian Vet, 1993, pp 17-19. 46(5):843-847, 1989. Avian Pathol 1:199-204, 1987. Rev Pharmacol Toxicol 38:97-120,
6. Curro TG, Brunson D, Paul- 15. Gentle MJ, Hunter LN, Wadding- 25. Machin KL, Livingston A: 1998.
Murphy J: Determination of the ton D: The onset of pain-related Assessment of the analgesic 35. Woolf CJ: A new strategy for the
ED50 of isoflurane and evaluation behaviors following partial beak effects of ketoprofen in ducks treatment of inflammatory pain:
of the analgesic properties of amputation in the chicken. anesthetized with isoflurane. Am Prevention or elimination of cen-
butorphanol in cockatoos Neurosci Lett 128:113-116, 1991. J Vet Res 63(6):821-826, 2002. tral sensitization. Drugs 47(Suppl
(Cacatua spp.). Vet Surg 23:429- 16. Glatz PC, et al: Analgesia therapy 26. Machin KL, et al: Pharma- 5):1-9, Discussion:46-47, 1994.
433, 1994. of beak-trimmed chickens. Aust codynamics of flunixin and keto- 36. Woolf CJ, Chong MS: Preemptive
7. Danbury TC, Hudson AL, Vet J 69(1):18, 1992. profen in mallard ducks. J Zoo analgesia: Treating postoperative
Waterman-Pearson AE: Saturation 17. Graham J, et al: Pharmacokinetics Wildl Med 32:22-29, 2001. pain by preventing the establish-
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8. Danbury TC, et al: Self-selection of protocol for determining the carprofen on lameness in broiler Physiological and behavioral
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146(11):307-311, 2000. experimentally induced articular 29. Nicol GD, Klingberg DK, Vasko lation. Comp Biochem Physiol
9. Flecknell PA, Roughan JV, Stewart pain in the domestic fowl. Res Vet MR: Prostaglandin E2 increases 88A(1):27-31, 1987.
R: Use of oral buprenorphine Sci 63(3):263-267, 1997. calcium conductance and stimu-
09 Therapeutic agents.qxd 8/22/2005 5:22 PM Page 241
CHAPTER
9
Therapeutic
Agents
KEATH L. MARX, DVM
Editors’ Disclaimer:
Every attempt has been made to ensure accurate citation

of dosages and references. However, the reader must
assume ultimate responsibility for the use of any medica-
tion. Indications and usage listed are as per the refer-
ence(s) cited, and may not bear pharmacodynamic data
verifying efficacy or safety.
Dosages that vary significantly (by a factor of 50x or

greater) from other empirical or pharmacokinetic stud-
ies may be omitted from the table, but may be found in
the references.
No claims to efficacy or safety are intended or implied.
See abbreviations key at the end.

DRUG NAME SPECIES DOSAGE (mg/kg ROUTE DOSAGE C.I.** REFERENCE COMMENTS (see references for
242
unless otherwise INTERVAL duration, precautions and

stated) contraindications)
Acepromazine Maleate Avian 0.5-1 IM QD E 53, 704 Add ketamine
Acepromazine Maleate Cassowary, Double-wattled 0.63 IM PRN G 447 Add etorphine
Acepromazine Maleate Hawk 2.0 NL PRN D 1401 Add ketamine
Acepromazine Maleate Ostrich 0.16-0.19 IM PRN B 447 Add etorphine
09 Therapeutic agents.qxd
Acepromazine Maleate Ostrich 25 MG TD NL PRN D 1401 Add etorphine + xylazine

Acepromazine Maleate Owl 2.0 NL PRN D 1401 Add ketamine
Acepromazine Maleate Raptor 2.2 IM PRN E 1386 Add ketamine
Acepromazine Maleate Ratite 0.25-0.5 IM PRN G 418

Acepromazine Maleate Ratite 0.1-0.2 IV PRN G 418
8/22/2005
Acetylcysteine Amazon, Red Lored 22 mg/ml Nebulize QD G 700 10% concentration

5:22 PM
Activated Charcoal Avian 52 PO Once E 1526 Give after first dose of fluids for oiled birds
Activated Charcoal Avian 2-8 g/kg PO NL E 1554, 1745

Activated Charcoal Psittacine 2-8 g/kg PO PRN E 1240 Absorb ingested toxins
Activated Charcoal Raptor 2-10 g/kg PO PRN E 1400 Antidiarrheal, absorbs toxins
Page 242
Acyclovir Avian 1 g/L water Drink NL A 435

Acyclovir Avian 400 mg/kg food Feed Once A 435
Acyclovir Avian 80 PO TID E 1470, 1473 For herpesvirus, (also ref # 1560, 1650)
Acyclovir Avian 25 IM NL G 435
Acyclovir Avian 40 IM TID G 1306 For Pacheco's disease
Acyclovir Avian 80 PO TID G 1306 For Pacheco's disease
Acyclovir Avian 330 Gavage BID G 1352
Acyclovir Avian 0.4 g/L Drink QD G 1352
Acyclovir Chicken 10 IM QD B 435
Acyclovir Macaw 80 PO TID A 435
Acyclovir Parakeet, Quaker 40 IM TID A 1060
Acyclovir Parakeet, Quaker 1 g/L feed Feed QD A 1060 Change feed BID
Acyclovir Psittacine 0.4 g/L water Drink NL E 763
Acyclovir Psittacine 80 PO TID E 1365 For Pacheco's virus
Acyclovir Raptor (Peregrine falcon) 80 PO TID G
Acyclovir Raptor 333 PO BID G 94 Juvenile dosage
Albendazole Avian 100 PO Once E 1526 For nematodes and Capillaria

Albendazole Avian 50 PO QD E 1526 For nematodes and Capillaria
Albendazole Bird, Aquatic 100 PO Once E 1503 For nematodes and Capillaria
Albendazole Bird, Aquatic 50 PO QD E 1503 For nematodes and Capillaria
**A = Pharmacokinetic research; B = Clinical efficacy trial; C = Manufacturer’s recommendation; D = Published with reference; E = Published without reference; F = Extrapolation from other species; G = Anecdotal
Albendazole Crane 20 PO QW E 1361 For trematodes
Albendazole Emu 10 NL NL G 1471 For fascioliasis

Albendazole Penguin 50 PO QD E 1478 For nematodes and flukes
Albendazole Penguin 100 PO Once E 1478 For nematodes and flukes
Albendazole Ratite 0.264 PO BID E 1240 Repeat in 2 weeks, antiprotozoal
8/22/2005
Alfaxalone + Alfadolone Avian 10-36 IM-IV-SC PRN E 704
Alfaxalone + Alfadolone Avian 5-10 IV PRN E 1181 Short duration, may be apnea
5:22 PM
Alfaxalone + Alfadolone Avian 36 IM-IP PRN E 1181 Short duration

Alfaxalone + Alfadolone Buzzard (Augur, Lizzard) 10 IV PRN B 1610
Alfaxalone + Alfadolone Chicken 10 IV PRN B 1610
Alfaxalone + Alfadolone Crane 4-8 IV PRN E 1240 May cause transient apnea, surgical anesthesia
Page 243
for 8 to 10 min
Alfaxalone + Alfadolone Eagle (African Fish, Hawk, Tawny) 10 IV PRN B 1610
and Falcons
Alfaxalone + Alfadolone Flamingo 4-8 IV PRN E 1240
Alfaxalone + Alfadolone Goshawk, African 10 IV PRN B 1610
Alfaxalone + Alfadolone Owl, Great-horned 6-12 IV PRN B 1174
Alfaxalone + Alfadolone Pelican 5.4 IV PRN G 595
Alfaxalone + Alfadolone Pigeon 5-7 IM-IV PRN G 232
Alfaxalone + Alfadolone Psittacine 5-10 IM-IV PRN E 1240
Alfaxalone + Alfadolone Raptor 10 IV PRN B 1568 For wild injured raptors anesthesia induction
Allopurinol Avian 10-15 IM, PO QD G 58, 704

Allopurinol Budgerigar 0.33 g/L Drink NL G 111
Allopurinol Budgerigar 0.67 g/L Drink NL E 763 For gout
Allopurinol Psittacine 10 PO QD B 1035 For hyperuricemia
Allopurinol Psittacine 0.33 g/L Drink NL E 1240 To treat gout
Allopurinol Psittacine 10-30 PO BID E 1756
Aloe Vera Avian 16 ml/L Drink QD G 1682

Aloe Vera Avian 30 ml/L Drink QD G 111
Amantadine HCl Avian 0.001 g/L Drink NL E 1650 For orthomyxoviruses

Amantadine HCl Avian 25 PO NL E 1650 For orthomyxoviruses
Chapter 9 | T H E R A P E U T I C A G E N T S
Amantadine HCl Poultry 2 PO NL G 435

Amantadine HCl Turkey 10 PO QD G 435
243
244

Amikacin Sulfate Amazon, Blue-fronted 10-15 IM BID-TID A 697
Amikacin Sulfate Amazon, Orange-winged 13-20 IM/IV BID A 736
Amikacin Sulfate Avian 10-15 IM-IV-SC BID-TID A 1473, 111
Amikacin Sulfate Bird, Aquatic 18-20 IM BID E 1478, 1559
Amikacin Sulfate Chicken 20 IM TID A 1058 For hens

Amikacin Sulfate Cockatiel 15-20 IM BID-TID A 32, 697, 879
Amikacin Sulfate Cockatoo, Goffin 15-20 IM BID-TID A 697
Amikacin Sulfate Crane 10 IM-SC BID E 629

Amikacin Sulfate Fowl, Domestic 10-20 IM QD-TID A 1631 For salmonellosis
8/22/2005
Amikacin Sulfate Gull 15 IM BID E 1357

Amikacin Sulfate Ostrich 7.6 IM TID A 747
Amikacin Sulfate Parrot, Grey 10-20 IM BID-TID A 112, 692
5:22 PM
Amikacin Sulfate Penguin, African 15 IM BID G 1353 Monitor hydration

Amikacin Sulfate Pigeon 15-20 IM-IV BID G 590
Amikacin Sulfate Psittacine 15-40 IM QD-BID E 565
Amikacin Sulfate Raptor 15-20 IM QD G 1314
Amikacin Sulfate Ratite 7.6-11 IM BID G 1308
Page 244
Amikacin Sulfate Stork, Saddle-billed 10 IM BID G 1645
Aminoloid Raptor 0.25-0.75 IM q2w E 111 Induce molting
Aminonitrothiazole Raptor 20-40 PO NL E 1463 For trichomoniasis
Aminopentamide Sulfate Avian 0.05 IM-SC BID E 111, 1240. 1473 Control vomition
Aminophylline Avian 0.5 Nebulize BID-TID G 1199 Add acetylcysteine, antibiotic, 5 ml NaCl
Aminophylline Avian 10 IV-PO q3h E 1151
Aminopromazine Avian 6.75 IM NL F 1209
Aminothiazole Pigeon 5 ml/L Drink QD E 1240
Amitriptyline HCl Psittacine 1-5 PO B-QID D 1446, 111, 1240 For behavioral feather picking
Ammonia Solution Avian 10 ml/L Topical PRN G 111 Add aloe vera + 4 drops sulfonate detergent,
control skin pruritis
Amobarbital Sodium Anseriformes 2 PO PRN G 4 Soak food in solution

Amobarbital Sodium Duck, Mallard 3.6 g/L feed Feed Once G 1398
Amoxicillin Avian 150-175 PO QD-BID E 111

Amoxicillin Avian 250 IM QD E 704 Long-lasting preparation
Amoxicillin Avian 0.2-0.4 g/L Drink QD E 704 Soft feed
Amoxicillin Avian 167 PO QD-BID E 741
8/22/2005
Amoxicillin Avian 150 IM-PO NL E 924 Broad spectrum

Amoxicillin Avian 100 PO BID E 1431
Amoxicillin Avian 150-175 PO QD-BID E 1473
Amoxicillin Avian 100-150 SC QD E 1526 Broad spectrum
5:22 PM
Amoxicillin Avian 100-150 IM NL G 1618 For open fractures

Amoxicillin Bustard 100 IM-SC BID E 1240
Amoxicillin Canary 0.3 g/L Drink NL A 1139
Amoxicillin Canary 0.5 g/kg feed Feed Once A 1139
Page 245
Amoxicillin Chicken 16 PO QD B 1006

Amoxicillin Currawong, Pied 25-50 PO BID G 1609 Post-surgical
Amoxicillin Duck 20 Drink QD C 705
Amoxicillin Falcon 100 Parenteral q2d G 1128
Amoxicillin Galliformes 0.17 g/L Drink QD E 704
Amoxicillin Goshawk 10 PO BID G 127 Precede with ticarcillin
Amoxicillin Gull 100 PO QD-BID E 1357
Amoxicillin Penguin, African 200 PO TID G 1353
Amoxicillin Pigeon 20-90 PO QD-BID A 493 Use capsules
Amoxicillin Pigeon 100 PO QD-BID A 565 Gram negative bacteria
Amoxicillin Pigeon 50 IM QD-BID A 565 Gram positive bacteria
Amoxicillin Pigeon 18-91 PO QD-BID A 733 Use high dosage for Enterobacteriaceae
Amoxicillin Pigeon 1.5 g/L Drink NL A 800 For Streptococcus bovi s
Amoxicillin Pigeon 150 IV-PO NL A 800 For Streptococcus bovis
Amoxicillin Pigeon 0.2 g/L Drink NL A 993
Amoxicillin Pigeon 75-100 PO BID A 1066
Amoxicillin Pigeon 20 Drink QD C 704
Amoxicillin Pigeon 25-50 PO QD G 47
Amoxicillin Poultry 15-20 Drink QD C 705
Amoxicillin Poultry 55-110 PO BID-TID G 585
Amoxicillin Psittacine 150-175 PO QD-BID E 565
Amoxicillin Psittacine 250 IM QD E 1140
Amoxicillin Psittacine 100 SC NL G 1613
Amoxicillin Raptor 150 IM-PO BID E 1400 Bacterial infections
Amoxicillin Raptor 50 IM BID E 1612

Amoxicillin Ratite 15-22 PO BID G 1308
245
246

Amoxicillin + Tylosin Avian 10 g/L Drink QD E 1492 For flock treatment of bacterial and
mycoplasmal infections
Amoxicillin + Tylosin Avian 3000 PO QD E 1492
Amoxicillin + Tylosin Avian 10 g/L Drink QD E 1650
Amoxicillin + Tylosin Avian 3000 PO QD E 1650
Amoxicillin Depot Bustard 100-250 IM-SC q3-7d A 1127, 1240

Amoxicillin Depot Pigeon 150 IM q2d A 493 Long-lasting formulation

Amoxicillin Depot Pigeon 150-200 SC QD A 991 Long-lasting oil based susp.
8/22/2005
Amoxicillin Sodium + Amazon Parrot 125 NL TID A 1491

Clavulanate Potassium
5:22 PM
Amoxicillin Sodium + Avian 125 PO QID E 704 Dosage based on amoxicillin

Amoxicillin Sodium + Avian 100 PO, IM BID E 1431 Useful in young birds
Amoxicillin Sodium + Avian 50 IM BID-QID E 1470 For bacterial infection with liver disease
Page 246
Amoxicillin Sodium + Avian 150-175 IM-PO BID E 1474 For neonatal septicemia
Amoxicillin Sodium + Bird, Aquatic 125-150 IM, PO BID E 1478 Pre- and post-operative
Amoxicillin Sodium + Canary 125 Gavage BID G 1139 For GI infection
Amoxicillin Sodium + Chicken 0.5 g/L Drink NL A 801
Amoxicillin Sodium + Hawk, Red-tailed 50 PO BID G 1626 Post-operative
Amoxicillin Sodium + Owl, Great-horned 125 PO BID G 173
Amoxicillin Sodium + Passerine 200 NL TID G 1489 For frostbite associated skin infection
Amoxicillin Sodium + Pigeon 125 Gavage BID B 751 For localized gut infection
Amoxicillin Sodium + Psittacine 100 PO BID D 1446 For staphylococcal dermatitis
Amoxicillin Sodium + Raptor 150 PO, IM BID E 1400, 1433 Can be nephrotoxic
Amoxicillin Sodium + Raptor 125 PO BID G 234
Amoxicillin Sodium + Ratite 11-15 IV-PO TID G 1308
Amphotericin B Amazon, Yellow-naped 50-75 mg TD IT QD G 740

Amphotericin B Avian 1 IT TID E 625 Add flucytosine + IV amphotericin B,
8/22/2005
aspergillosis therapy
Amphotericin B Avian 1.5 IV TID E 625, 674 See above
Amphotericin B Avian 100 PO BID E 1492 For macrorhabdosis (formerly megabacteria
or avian gastric yeast)
5:22 PM
Amphotericin B Avian 0.83g/ L Nebulize BID E 1526 For aspergillosis therapy. Must use sterile
water - NaCl inactivates Amphotericin
Amphotericin B Avian 1 IP QD G 861

Page 247
Amphotericin B Bird, Aquatic 100-200 PO TID-QID E 1503 For GI candidiasis

Amphotericin B Bird, Aquatic 1.5 IV-SC QD E 1503 For aspergillosis therapy
Amphotericin B Budgerigar 109 PO BID B 589 For macrorhabdosis (formerly megabacteria
or avian gastric yeast)
Amphotericin B Crane 0.33-0.67 g/L Nebulize TID G 1361
Amphotericin B Gull 1 IT BID E 1357
Amphotericin B Gull 1.5 IV TID E 1357
Amphotericin B Psittacine 1.5 IV BID-TID E 111, 745
Amphotericin B Psittacine 1 IT BID-TID E 111, 741, 1309
Amphotericin B Raptor 1.5 IV TID B 1178 Add IT amphotericin B + flucytosine +
rifampin for aspergillosis
Ampicillin Amazon Parrot 150-200 PO BID-TID A 567 May give combination of both oral and
parenteral
Ampicillin Anseriformes 100 IM q4h E 1318, 1358
Ampicillin Avian 0.25g/kg Feed QD E 741
Ampicillin Avian 1.041 g/L Drink QD E 741
Ampicillin Canary 1-2 g/L Drink QD G 49
Ampicillin Canary 2-3 g/kg food Feed QD G 49 In soft food
Ampicillin Crane 15-20 IM-SC BID A 596
Ampicillin Crane, Greater Sand Hill 20 IM BID A 847
Ampicillin Emu 20 IM BID A 847
Ampicillin Falcon 100 IM-PO BID E 1027
Ampicillin Parrot, Blue-naped 150-200 PO BID-TID A 567 May give combination of both oral and
parenteral
Ampicillin Pigeon 25-120 PO QD-BID A 493 Use capsules
Ampicillin Pigeon 100 IM q2d A 493 Long-lasting formulation
247
248

Ampicillin Poultry 55-110 Parenteral BID-TID G 585
Ampicillin Psittacine 100 IM q4h E 111
Ampicillin Psittacine 100-200 PO QID E 1240 Poorly absorbed
Ampicillin Raptor 100-250 IM NL E 1463
Ampicillin Sodium Amazon Parrot 50-100 IM q4-8h A 567 May give combination of both oral and
parenteral
Ampicillin Sodium Pigeon 150 IM QD-BID A 493

Ampicillin Sodium Pigeon 773 IM QD-BID A 733 For Enterobacteriaceae
8/22/2005
Ampicillin Sodium Pigeon 155 IM QD-BID A 733

Ampicillin Sodium Ratite 0.1 - 0.2 g/L Drink NL G 418 Clostridial treatment
5:22 PM
Amprolium Avian 0.048-0.096g/L Drink QD E 111

Amprolium Avian 0.08 g/L Drink QD E 1492 Coccidiostatic, overdose reversed by
administration of vitamin B complex
Amprolium Chicken 40-250 mg/kg food Feed QD E 564 No slaughter withdrawal
Amprolium Crane 0.06 g/L Drink QD E 1361 For coccidiosis
Page 248
Amprolium Pigeon 0.2 g/L Drink QD G 232

Amprolium Poultry 1.25 cc/L Drink QD G 585 Use 20% powder formulation
Amprolium Psittacine 0.25 g/L Drink QD E 1365 For sarcocystosis
Apramycin Chicken 0.5 g/L Drink QD B 881 For colibacillosis
Arecoline Hydrobromide Pelican, Brown 1-1.6 PO QH B 1089 Give thiabendazole previous day
Arsanilic Acid Poultry 0.1 g/kg food Feed QD E 564 Nutritional use, 5-day slaughter withdrawal
Ascorbic Acid Avian 20-40 IM QD-QW E 1473
Ascorbic Acid Avian 20-50 IM-PO NL E 924 For viral infection, liver disease, stress
Ascorbic Acid Avian 20-40 IM QD-QW E 1473
Ascorbic Acid Ostrich 20-50 mg TD IM q2d G 401 For chicks
Ascorbic Acid Raptor 250 PO QD E 1359 Antioxidant therapy, administer during lead
chelation therapy
Asparaginase Avian 0.4 KIU/kg IM QW E 1470

Asparaginase Owl, Great-horned 1.7 KIU/kg SC Once F 125
Aspirin Amazon, Red Lored 0.5-1 PO QD-BID G 1756 Add fatty acid omega 6:omega 3 < 6:1 ratio,
use until renal histology normalizes for renal
disease
Aspirin Amazon, Yellow-naped 0.5-1 PO BID G 1033
8/22/2005
Aspirin Avian 5 PO TID-QID D 1533

Aspirin Avian 1.2 g/L Drink QD E 1650
Aspirin Avian 5 PO TID G 1341, 1671
Aspirin Psittacine 0.5-1 PO QD-BID E 1756
5:22 PM
Aspirin Stork, Saddle-billed 1 PO QD G 1645
Astragalus Avian 10 drops/kg PO TID E 1205 Chronic GI problems and infections

Astragalus Avian 33-66 drops/kg PO QD E 1435 Immune stimulant
Page 249
Atipamezole
Atipamezole Anseriformes 0.25 IV PRN D 1503 Add flumazenil to reverse ketamine +
medetomidine + midazolam
Atipamezole Avian 0.25-0.38 IM PRN E 1181 Reverse ketamine + xylazine or ketamine +
medetomidine
Atipamezole Duck, Mallard 0.25 mg TD IV PRN B 764 Add flumazenil
Atipamezole Pigeon 0.5 IM PRN B 1588 Reverse medetomidine
Atipamezole Psittacine 0.25-0.38 IM PRN E 1240 Reverse xylazine or medetomidine
Atropine Anseriformes 0.1 IM-IV q3-4h D 1150 For anticholinesterase poisoning

Atropine Avian 0.04-0.1 IM-SC Once G 1309 Preanesthetic
Atropine Avian 0.1-0.2 IM-SC q4h E 1151 For cholinergic toxin
Atropine Avian 0.2-0.5 IV q3-4h E 1554 For anticholinesterase toxicity
Atropine Avian 0.01-0.02 Parenteral q3-4h E 1650 For organophosphate toxicity
Atropine Avian 0.1-0.2 IM-SC PRN G 1309 For organophosphate poisoning
Atropine Canary 0.2 Parenteral q4h G 1714 For convulsions possibly caused by
organophosphate toxicity
Atropine Pigeon 0.27 IM-IV q4-8h G 590
Atropine Psittacine 0.05 IM-SC QH E 1240 For acetylcholinesterase poisoning
Atropine Psittacine 0.5 IM-SC NL E 1688
Atropine Raptor 0.5 IM-IV PRN G 61 [May thicken secretions and increase risk of
airway obstruction - KLM]
Atropine Raptor 0.1 IM-IV q3-4h E 1240, 1400 For acetylcholinesterase poisoning
Atropine Raptor 0.02-0.05 IM-IV PRN E 1359 For organophosphate toxicity
Azamethiphos Poultry 5-20 g/L Topical NL E 1479 Apply to animal facilities, insect spray
249
250

Azaperone Ostrich 4-6 IM PRN B 522 Add metomidate, chick dosage

Azaperone Ostrich 3.3-6.6 IM PRN G 283 Add metomidate
Azaperone Ratite 0.5-2 IM Once G 1226 Add ketamine + diazepam after 10 to 15
minutes, sedation
Azithromycin Avian 50-80 PO QD G 702 For chlamydophilosis

Azithromycin Avian 43 PO QD G 1154 Add ethambutol + rifabutin for

mycobacteriosis
8/22/2005
Azithromycin Falcon 40 PO QW F 1157 For chlamydophilosis
Bach flower Avian 1 drop Drink QID G 912 For calming effect, also apply topically as
5:22 PM
spray
Bach flower Avian 45-75 drops/L PO QID G 912 See above
Bacitracin Poultry 110-220 mg/kg feed Feed QD E 564 Nutritional use, no slaughter withdrawal
Page 250
Bacitracin Ratite 0.4 g/L Drink NL G 418 Clostridial therapy
Bambermycin Chicken 3.3 mg/kg feed Feed Once B 400

Bambermycin Ostrich 0.07 mg/kg feed Feed Once C 283 Growth promotant
Barium Sulfate Avian 50 ml/kg PO NL E 1151 G.I. protectant and antiinflammatory

Barium Sulfate Avian 10-20 ml/kg PO NL E 1482 Mix 50:50 with hand-feeding formula for GI
contrast rads
Benzyl Benzoate Pigeon 25% solution Topical PRN E 704 Apply to lesion
Benzyl Benzoate Raptor 10% solution Topical QD E 1612 For Knemidocoptes
Betamethasone Avian 0.1 IM NL D, E, 201, 1533, 1573

G
Betamethasone Bird, Aquatic 0.1 IM NL E 1503
Betamethasone Pigeon 1 IM Once E 704 Anaphylaxis
Biotin Raptor 0.025 PO QD E 1068 During regrowth of claw

Biotin Raptor 0.05 PO QD E 1240 Aid in beak and claw growth
Bismuth Subsalicylate Avian 35 PO BID E 1240 May help remove ingested toxins
Bismuth Subsalicylate Avian 35-88 PO Once E 1526 Enteric coating for oiled birds
Brewers yeast Anseriformes 75 g/kg feed Feed QD E 1358 For niacin deficiency with leg deformities,
weakness, poor growth
Bromhexine HCl Avian 3-6 IM NL E 704, 1434

Bromhexine HCl Avian 1.5 IM QD-BID E 1526, 1617 Liquefy respiratory mucus
8/22/2005
Bromhexine HCl Raptor 1.5 IM QD E 1612 Mucolytic
Bunamidine HCl Raptor 25 PO NL E 1463 Anthelmintic

5:27 PM
Bupivacaine HCl Parrot, Grey 2 IM PRN A 1339 Maintain plasma concentration for less than 2
hours
Buprenorphine HCl Avian 0.01-0.05 IM-IV-SC BID E 1167

Page 251
Buprenorphine HCl Pigeon 0.5 IM q5h B 1656
Butorphanol Tartrate Amazon, Hispaniolan 1-3 IM NL A 1339

Butorphanol Tartrate Cockatoo 1 NL PRN B 1678 Isoflurane sparing
Butorphanol Tartrate Parrot, Grey 1-2 IM NL A 1339 Plasma levels maintained less than 2 hours at
2 mg/kg
Butorphanol Tartrate Parrot, Grey 1 IM NL B 586, 1339
Butorphanol Tartrate Pigeon 4 IM q3h B 1656
Butorphanol Tartrate Psittacine 3-4 IV-PO NL E 111, 1249
Butorphanol Tartrate Psittacine 3-4 IV-PO TID E 1240 Also analgesic
Butorphanol Tartrate Raptor 2-4 IM-SC QD E 1359
Butorphanol Tartrate Rhea 0.7 IM PRN G 1628 Add ketamine + medetomidine
Butorphanol Tartrate Toucan, Toco 2 IM Once G 1379 Post-surgical pain
Calcitriol Avian 0.000025 (0.025ug/kg) Gavage QD G 1183 Add calcium source to gavage for
hypocalcaemia
Calcium Borogluconate Avian 200 IM-IV QD E 1431 Used during egg laying problems, often with
oxytocin
Calcium Borogluconate Avian 100-500 IM-SC NL E 1434 For egg binding and hypocalcemic tetany
Calcium Borogluconate Goshawk 300 IV NL G 234

Calcium Borogluconate Pigeon 100-500 IM-SC NL E 1432 For egg binding and hypocalcemic tetany
Calcium Borogluconate Psittacine 100-200 IM-IV NL E 1240

Calcium Borogluconate Raptor 100-500 IV-SC Once E 1240
251
252

Calcium Borogluconate Raptor 10-50 IV-SC Once E 1400 For egg binding or hypocalcaemia, give IV
slowly
Calcium Carbonate Raptor 10 g/kg food Feed Once D 1612 For osteodystrophy
Calcium Glubionate Avian 0.44 g/L Drink NL E 1492 For egg binding and calcium deficiencies
Calcium Glubionate Avian 150 PO BID G 54
Calcium Glubionate + Avian 363 PO QD E 1617

8/22/2005
Calcium Lactobionate
Calcium Gluconate Avian 100-300 IM-SC NL E 1480 Add phytonadione for bleeding syndrome
5:27 PM
Calcium Gluconate Avian 5-10 IM-SC BID E 1473

Calcium Gluconate Avian 50-100 IV NL E 1473 Slowly to effect
Calcium Gluconate Avian 5-10 IM NL E 1474
Calcium Gluconate Avian 50-100 IV NL E 1474 Give slowly, follow with oxytocin or
Page 252
dinoprostone for egg binding, may add

vitamin E + selenium
Calcium Gluconate Avian 100-300 SC NL E 1481
Calcium Avian 5-10 IM-SC NL E 1570 For egg binding

Glycerophosphate +
Calcium Lactate
Calcium Glycerophosphate Avian 0.5-1 IM QW G 54
+ Calcium Lactate
Calcium Glycerophosphate Lory, Red 7 IM NL G 1621 Add oxytocin for egg binding
+ Calcium Lactate
Calcium Glycerophosphate Parrot, Grey 5-10 IM-SC BID G 88 Acute therapy

+ Calcium Lactate
Cambendazole Avian 60-100 PO QD G 57 Avoid during breeding season

Cambendazole Pigeon 75 PO QD E 1051 For ascarids and capillaria
Caprylic Acid Avian 270 PO NL E 111 Adjunct to aspergillosis therapy
Carbaryl Avian N/A Topical NL E 111 5% mixture, powder formulation

Carbaryl Avian N/A Topical NL E 1240 5% mixture, lightly dust feathers for
ectoparasites
Carbenicillin Disodium Avian 150 IM-PO NL E 924 Gram negative, Pseudomonas

Carbenicillin Disodium Avian 100 IM TID G 55
8/22/2005
Carbenicillin Disodium Avian 100-200 IM BID G 861 Freeze small portions indefinitely
Carbenicillin Disodium Crane 100 IM-IV BID-TID E 629, 1361
Carbenicillin Disodium Owl, Great-horned 150 PO BID G 173
Carbenicillin Disodium Pigeon 100 IM BID-TID G 260
5:27 PM
Carbenicillin Disodium Psittacine 100-200 IM TID-QID E 565

Carbenicillin Disodium Psittacine 100 IM BID E 763
Carbenicillin Disodium Raptor 100-200 IM TID E 1240
Carbenicillin Disodium Raptor 100 IT QD E 1240 For Gram negative bacteria, synergistic
Page 253
w/aminoglycosides
Carbenicillin Disodium Raptor 100-200 IM TID E 1400
Carbon Dioxide Gas Avian N/A IH NL E 1564 Euthanasia
Carboplatin Amazon, Yellow-naped 125 mg/m3 IV q2-3w G 1033 Dilute with 5% dextrose
Carboplatin Budgerigar 5 IV QM G 1259 Dilute 1:10 with sterile water
Carboxymethylcellulose Avian 0.1% solution Drink QD G 1457 Add amphotericin B, mix fresh daily, allow to
Sodium stand overnight, dissolve drug in the AM
Carfentanil Citrate Ostrich 3 mg TD IM PRN B 521 Add xylazine

Carfentanil Citrate Ostrich 0.024 NL PRN G 465
Carnidazole Avian 33 PO Once E 1526 For trichomoniasis, no food/water night

before treatment plus no water 2 to 3 hours
after treatment
Carnidazole Avian 20-30 PO Once E 1554 For trichomoniasis and giardiasis
Carnidazole Bird, Aquatic 33 PO Once E 1503
Carnidazole Bustard 20-25 PO Once E 1240
Carnidazole Dove 30 PO NL G 61
Carnidazole Falcon 25 PO Once B 1420 For Trichomoniasis, less effective than
multiday dimetridazole
Carnidazole Finch 20-30 PO Once E 1572

Carnidazole Pigeon 20-30 PO Once D 1221 For trichomoniasis
Carnidazole Pigeon 200 PO Once E 111, 1473
253
254

Carnidazole Pigeon 12.5-25 PO Once E 1240 Use lower dosage for juveniles
Carnidazole Pigeon 20-30 PO QW-q2w E 1364
Carnidazole Psittacine 20-30 PO Once E 1240 For trichomoniasis, hexamitiasis,
histomoniasis, use lower dosage for juveniles
Carnidazole Raptor 30 PO QD G 61
Carprofen Amazon, Orange-winged 4 IM BID G 1377 Post-surgical

Carprofen Anseriformes 4 SC QD E 1190
8/22/2005
Carprofen Anseriformes 5-10 IM NL G 1345

Carprofen Avian 1-2 IM-PO BID D 1533
Carprofen Avian 4 IM-IV-PO NL E 1167
5:27 PM
Carprofen Avian 5-10 IM QD E 1431 Pre-operative painkiller

Carprofen Bird, Aquatic 1-2 IM-PO BID E 1503
Carprofen Pigeon 5-10 IM NL G 1345
Carprofen Psittacine 2-10 IM-IV-SC QD E 1240 Post-surgical pain
Carprofen Raptor 1-2 IM-IV-PO BID D 1400
Page 254
Carprofen Raptor 2-10 IM-IV-SC QD E 1240 Post-surgical pain
Cefadroxil Pigeon 100 PO BID G 260
Cefazolin Sodium Crane 25-30 IM-IV TID E 629

Cefazolin Sodium Poultry 11-55 NL BID-TID G 585
Cefazolin Sodium Raptor 100 IM Once E 1359 Perioperative, use amoxicillin/clavulanate
post-operative
Cefotaxime Sodium Amazon Parrot 75-100 IM q4-8h A 697
Cefotaxime Sodium Amazon, Blue-fronted 100 IM TID A 748
Cefotaxime Sodium Avian 75-100 IM-IV TID-QID A 1473
Cefotaxime Sodium Bird, Aquatic 100 IM TID-QID E 1478 For hock joint pressure sore infections
Cefotaxime Sodium Crane 50-100 IM-SC TID E 629
Cefotaxime Sodium Hawk, Red-tailed 100 IM NL G 1626 Intra-operative
Cefotaxime Sodium Pigeon 100 IM BID-TID G 260
Cefotaxime Sodium Psittacine 50-100 IM TID E 565
Cefotaxime Sodium Psittacine 50-100 SC TID E 632 Neonate dosage
Cefotaxime Sodium Psittacine 100 IM BID E 763 Frozen reconstituted drugs lasts 12 weeks in
freezer, 10 days in refrigerator
Cefotaxime Sodium Raptor 100 IM-IV Once E 1359 Perioperative, use amoxicillin/clavulanate
post-operative
Cefotaxime Sodium Ratite 25 IM TID G 1308 For young birds
Ceftazidime Psittacine 75-200 IM-IV BID-QID E 1756 For bacterial nephritis
Ceftiofur Sodium Amazon, Orange-winged 10 IM BID-TID A 788

Ceftiofur Sodium Avian 50-100 IM QID E 1240
Ceftiofur Sodium Chicken 0.16 mg TD IM QD A 788
8/22/2005
Ceftiofur Sodium Cockatiel 10 IM q4h A 788

Ceftiofur Sodium Psittacine 100 IM TID E 1756 For bacterial nephritis
Ceftiofur Sodium Ratite 10-20 IM BID G 1308
5:27 PM
Ceftriaxone Sodium Amazon Parrot 75-100 IM q4-8h A 697

Ceftriaxone Sodium Avian 75-100 IM-IV TID-QID E 111
Celecoxib Avian (Macaw) 10 PO QD G 1750 For proventricular dilatation disease

Page 255
symptoms
Cephalexin Avian 35-50 PO q4-6h E 111

Cephalexin Avian 40-100 IM-PO TID-QID E 1240 For E. coli and Proteus
Cephalexin Avian 35-50 PO q4-6h E 1473
Cephalexin Avian 35-50 PO QID E 1492
Cephalexin Bird, Aquatic 35-50 PO QID E 1503
Cephalexin Bustard 40-100 IM-PO TID-QID E 1240 For E. coli and Proteus
Cephalexin Crane 35-50 PO QID A 596
Cephalexin Crane 100 IM QID A 697
Cephalexin Crane 100 PO q4-6h E 111
Cephalexin Crane 35-50 PO QID A 457, 847
Cephalexin Duck 35-50 PO q2-3h A 457
Cephalexin Duck 100 IM BID-TID A 697
Cephalexin Duck 35-50 PO QID A 847
Cephalexin Emu 35-50 PO QID A 418, 457, 847
Cephalexin Emu 100 IM QID A 697
Cephalexin Pigeon 35-50 PO QID A 847
Cephalexin Pigeon 100 PO BID-TID G 260
Cephalexin Poultry 55-110 NL BID G 585
Cephalexin Psittacine 35-50 PO QID E 763
Cephalexin Psittacine 100 PO TID G 697
Cephalexin Quail 100 IM BID-TID A 697
Cephalexin Quail, Bobwhite 35-50 PO q2-3h A 457
Cephalexin Quail, Japanese 35-50 PO QID A 847

Cephalexin Raptor 40-100 IM-PO TID-QID E 1240
Cephalexin Raptor 50-100 IM-PO TID E 1400
255
256

Cephalexin Raptor 50 PO QID G 234
Cephalexin Ratite 15-22 PO TID G 1308
Cephalothin Sodium Avian 100 IM-IV QID A 1473

Cephalothin Sodium Avian 100 IM-IV QID E 111

Cephalothin Sodium Avian 100 IM q2-6h E 565
Cephalothin Sodium Avian 100 IM QID E 741 No gastrointestinal absorption
Cephalothin Sodium Ratite 30-40 IM-IV QID G 1308

8/22/2005
Cephradine Avian 35-50 PO q4-6h E 111, 1473

Cephradine Crane 100 PO q4-6h E 111
Cephradine Emu, pigeon 100 PO q4-6h E 1473
5:27 PM
Chitosan Avian < 50 Topical q3d-q2w B 1633 Rinse and apply sparingly to wound surface
or pack suppurating wound, promote wound
healing
Page 256
Chloral Hydrate Avian (budgerigar, canary, chicken, 106.5 IM PRN B 1084 Add magnesium sulfate + pentobarbital
crow, crane) sodium, reduce dose 15 to 20% in debilitated
birds
Chloral Hydrate Eagle, Golden 80.9 IM PRN B 1086
Chloral Hydrate Falcon, Prairie 64 IM PRN B 1086
Chloral Hydrate Gull (California, Laughing, 106.5 IM PRN B 1084
Herring)
Chloral Hydrate Hawk (Marsh, Red-tailed, 64-68 IM PRN B 1086
Swainson's)
Chloral Hydrate Owl, Saw-whet 106.5 IM PRN B 1084
Chloral Hydrate Pea Fowl, pheasant 106.5 IM PRN B 1084
Chloral Hydrate Pigeon, sparrow, toucanet 106.5 IM PRN B 1084
Chloral Hydrate Rail, Wood 106.5 IM PRN B 1084
Chloralose Anseriformes 0.4-0.48g/L bait Feed Once G 1230 Add diazepam for anesthesia
Chloralose Bird, Seed-eater 2 g/kg grain Feed Once E 4
Chloralose Blackbird, Red-winged 0.02-0.025 mg TD Feed Once G 1230 Add secobarbital
Chloralose Crane 1.54-1.79 g/L corn Feed Once G 1361
Chloralose Duck 0.4-0.5 g/L bait Feed Once G 1386 Add diazepam
Chloralose Duck, Mallard 15 Feed Once B 1095
Chloralose Duck, Mallard 40 PO PRN D 1401
Chloralose Turkey 8 g/L corn Feed Once E 1386 Sedation in 40-60 min, 9% mortality
Chloramphenicol Avian 50-100 PO QD E 704
Chloramphenicol Avian 200 mg Nebulize TD E 704 Dilute in 15 ml 0.9% saline solution

Chloramphenicol Avian 50-100 Parenteral QD E 704
Chloramphenicol Budgerigar 50 IM BID A 394
Chloramphenicol Canary 0.1-0.15 g/L Feed QD E 695 In soft food
8/22/2005
Chloramphenicol Chicken 50 IM BID A 394

Chloramphenicol Conure (Nanday, Sun) 50 IM QID A 394
Chloramphenicol Crane 100 SC TID A 596
Chloramphenicol Duck, Chinese 100 IM-IV QID A 508
5:27 PM
Chloramphenicol Duck, Chinese 25 IM-IV q3h A 508

Chloramphenicol Duck, Chinese 240 IM-IV TID A 508
Chloramphenicol Duck, Muscovy 50 IM BID A 394
Chloramphenicol Eagle 50 IM QD A 394
Page 257
Chloramphenicol Goose, Egyptian 50 IM BID A 394

Chloramphenicol Hawk 50 IM BID A 394
Chloramphenicol Macaw 50 IM QID A 394
Chloramphenicol Ostrich 10 IM BID G 401 Double dosage for birds below 5 kg
Chloramphenicol Owl, Barred 50 IM BID A 394
Chloramphenicol Pea Fowl 50 IM QD A 394
Chloramphenicol Pigeon 95 PO QID E 111 With grit in diet
Chloramphenicol Pigeon 50 PO TID E 704
Chloramphenicol Pigeon 30 PO QID E 1473 Without grit in diet
Chloramphenicol Pigeon 80 IM BID E 1650 For salmonellosis
Chloramphenicol Psittacine 50 IM-IV TID-QID E 111
Chloramphenicol Raptor 50 IM TID E 1240
Chloramphenicol Ratite 35-50 IM-IV-PO- TID G 1308 Not for food animals
SC
Chloramphenicol Avian 80-100 Gavage BID E 741

Palmitate
Chloramphenicol Palmitate Avian 50 PO TID G 55
Chloramphenicol Palmitate Avian 150-200 PO TID-QID G 739 For large birds
Chloramphenicol Palmitate Psittacine 100 PO BID-QID E 741
Chloramphenicol Palmitate Turkey 50 PO QID E 741

Chlordiazepoxide HCl Cowbird, quail 150 g/kg food Feed Once B 1094 Anesthesia
257
258

Chlorhexidine Gluconate Avian 2.5 ml/L of 2% Drink NL E 741 For candidiasis or antimicrobial prophylaxis
solution/L
Chlorhexidine Gluconate Avian 2.5-7.5 ml of 2% Drink NL E 1240 Prevent or treat mild intestinal candidiasis
solution/L
Chlorhexidine Gluconate Avian 0.5% solution Flush NL E 1240 Wound flush
Chlorhexidine Gluconate Avian 0.005 g/L Drink QD E 1492 For candidiasis
Chloroquine Avian 0.4 g/L Drink QD E 1180 For blood parasites

8/22/2005
Chloroquine Avian 10 PO TID G 57 Usually in combination with primaquine

Chloroquine Avian 10 PO QD G 61 Add primaquine phosphate
Chloroquine Falcon 10 PO Once B 1177 Add primaquine, follow 1st dose with 5
5:27 PM
mg/kg at hours 6,18 and 24

Chloroquine Passerine, Small 2.1 g/L Drink NL E 1187 Therapeutic but not curative for Plasmodium
Chloroquine Penguin 5 PO QID E 111, 1240 Loading dosage 10 mg/kg

Chloroquine Penguin, African 5 PO QD B 262
Page 258
Chloroquine Raptor 5 NL NL D 1612

Chloroquine Raptor 25 IM QD E 1400 Plasmodium and Leucocytozoon
Chloroquine Raptor 10 PO QD G 61, 94 Add primaquine phosphate
Chlorpromazine Avian 0.0125 g/L Drink NL E 1492, 1650 For feather picking and anxiety
Chlortetracycline HCl Amazon, Blue-fronted 2.5 g/kg corn Feed QD A 230 For therapy less than 2 weeks duration
Chlortetracycline HCl Amazon, Green-cheeked 2.5 - 5.0 g/kg food Feed Once B 1062 For Chlamydophila
Chlortetracycline HCl Amazons 5 g/kg food Feed QD B 1079 For Chlamydophila
Chlortetracycline HCl Avian 1 g/L Drink QD E 704 Prophylactic dosage
Chlortetracycline HCl Avian 5 g/L Drink QD E 704 Therapeutic dosage
Chlortetracycline HCl Avian 100 PO QID E 704
Chlortetracycline HCl Avian 0.5 g/L Drink QD E 741 For chlamydophilosis initial therapy
Chlortetracycline HCl Avian 100 IM-PO NL E 924
Chlortetracycline HCl Avian 34 IV NL F 1209
Chlortetracycline HCl Budgerigar 5 g/kg seed Feed QD A 731 Hulled medicated millet
Chlortetracycline HCl Budgerigar 500 mg/kg food Feed QD E 565 Antichlamydophilial
Chlortetracycline HCl Canary 1.5 g/kg food Feed QD E 695
Chlortetracycline HCl Chicken 2.5 g/L Drink NL A 802 Add chlortetracycline feed also
Chlortetracycline HCl Chicken 2.5 g/kg food Feed Once A 802 Add chlortetracycline drinking water also
Chlortetracycline HCl Chicken 20-60 PO NL C 705

Chlortetracycline HCl Chicken 220 mg/kg food Feed QD E 564 No slaughter withdrawal
Chlortetracycline HCl Cockatiel 2.4 g/kg food Feed QD A 738 Hulled millet + oats for chlamydophilosis
Chlortetracycline HCl Cockatoo, G Sulfur-crested 4.4 g/kg food Feed QD B 1079 For chlamydophilosis
Chlortetracycline HCl Conure (Maroon-bellied, Nanday) 2.4 g/kg food Feed QD A 738 Hulled millet + oats for chlamydophilosis
8/22/2005
Chlortetracycline HCl Finch 1 - 1.5 g/L Drink QD E 1572

Chlortetracycline HCl Finch 1.5 g/kg food Feed QD E 1572
Chlortetracycline HCl Galliformes 30 Drink QD E 704
Chlortetracycline HCl Lorikeet 0.5 g/kg fruit Feed QD A 1077 For chlamydophilosis
5:27 PM
Chlortetracycline HCl Lorikeet 0.5 g/L liquid food Feed Once A 1077 For chlamydophilosis
Chlortetracycline HCl Lory (Ornate, purple-naped) 0.5g/kg liquid food Feed Once A 1077 For chlamydophilosis
Chlortetracycline HCl Lovebird, Abyssinian 2.4 g/kg food Feed QD A 738
Chlortetracycline HCl Macaw, Buffon's 10-15 g/kg Feed Once A 781
Page 259
Chlortetracycline HCl Parakeet (Bourke's, red-front, ring- 2.4 g/kg food Feed QD A 738 Hulled millet + oats for chlamydophilosis
necked)
Chlortetracycline HCl Passerine 1.5 g/kg soft food Feed QD E 1437 Add drug to drink at the same time, use for
30 days for chlamydophilosis
Chlortetracycline HCl Passerine 1.0 - 1.5 g/L Drink QD E 1437 Add drug to food at the same time, use for
Chlortetracycline HCl Pigeon 40-50 PO B-TID A 565 Without grit in diet
Chlortetracycline HCl Pigeon 100 IM QD G 232
Chlortetracycline HCl Pigeon 50 PO TID-QID G 260 With or without tylosin
Chlortetracycline HCl Pigeon 0.5 g/L Drink QD G 590 Change daily
Chlortetracycline HCl Poultry 0.106-0.264 g/L Feed QD C 564 Prophylactic
Chlortetracycline HCl Poultry 110-550 mg/kg feed Feed QD C 564
Chlortetracycline HCl Psittacine 2.5-10 g/kg food Feed QD A 693 Dosage based on weight of food
Chlortetracycline HCl Raptor 33 PO TID E 1612 For chlamydophilosis
Chlortetracycline HCl Ratite 15-20 PO TID G 1308
Chlortetracycline HCl Turkey 2.5 g/L Drink NL A 802 Add chlortetracycline feed also
Chlortetracycline HCl Turkey 10-30 PO NL C 705
Choline Avian 500-1300 Feed QD E 1470 For hepatic lipidosis
Chromium Picolinate Avian 10 drops/kg PO QD E 1435 Stock solution 1 pill per 30 ml lactulose for
diabetes
Chromium Picolinate Avian 0.1 PO BID E 1205
Cimetidine Penguin, African 35 PO QD G 128

259
260

Ciprofloxacin HCl Avian 80 PO QD D 1470, 1571 Add ethambutol + rifampin for liver
mycobacteriosis
Ciprofloxacin HCl Avian 20 PO BID D 1571 Add clofazimine + cycloserine + ethambutol
for avian mycobacteriosis
Ciprofloxacin HCl Avian 10-15 PO BID G 1319

Ciprofloxacin HCl Canary 20 PO BID G 48
Ciprofloxacin HCl Chicken 5 PO NL A 797
Ciprofloxacin HCl Cockatiel 30 PO BID G 44

Ciprofloxacin HCl Gull 20 PO QD E 1357
8/22/2005
Ciprofloxacin HCl Hawk, Red-tailed 50 PO BID A 168

Ciprofloxacin HCl Ostrich 20 NL BID E 628 For oviduct infection
Ciprofloxacin HCl Pigeon 0.25 g/L Drink QD G 590 Change daily
5:27 PM
Ciprofloxacin HCl Pigeon 5-20 PO BID G 590

Ciprofloxacin HCl Psittacine 20-40 PO BID E 111
Ciprofloxacin HCl Toucan, Toco 10 PO BID G 1379
Cisapride Avian 0.5-1 PO TID E 1151 To improve GI motility

Page 260
Cisapride Psittacine 1 NL BID G 1263 For ileus

Cisapride Raptor 0.25 PO TID E 1400 Increase gut motility
Cisplatin Macaw, Blue and Gold 0.3 mg/cm3 Parenteral QW G 1369 Intralesional-fibrosarcoma
Citric Acid Avian 0.5 g/L Drink QD E 704 Add oxytetracycline

Citric Acid Passerine, Small 1.0 g/L Drink NL E 1187
Clanobutin Psittacine 0.2 PO QD G 1722 Liver support
Clarithromycin Avian 85 PO QD G 1154 Add ethambutol + rifabutin, dose

allometrically for mycobacteriosis
Clazuril Anseriformes 5-10 PO q3d D 1150 For coccidiosis

Clazuril Pigeon 5-10 PO QD G 57 Repeat after 2 days
Clazuril Pigeon 6.5 PO Once G 109
Clazuril Pigeon 5 PO NL G 109
Clazuril Poultry 5-10 PO QD G 57 Repeat after 2 days
Clazuril Psittacine 7 PO QD E 1240 Wait 2 days then repeat for coccidiosis
Clazuril Raptor 5-10 PO q3d E 1240 For coccidiosis
Clindamycin HCl Avian 100 PO QD D 1221 For clostridiosis

Clindamycin HCl Avian 150 PO QD E 1431 For osteomyelitis
Clindamycin HCl Eagle, Little 40 PO BID G 1568 For post-operative orthopedic surgery
Clindamycin HCl Goshawk, Brown 40 PO BID G 1568

Clindamycin HCl Gull 100-150 PO QD E 1357
Clindamycin HCl Owl, Barn 40 PO BID G 1568
Clindamycin HCl Owl, Great-horned 12.5 PO BID G 173 Add enrofloxacin
8/22/2005
Clindamycin HCl Pigeon 100 PO QD A 1473

Clindamycin HCl Pigeon 100 PO QD E 111
Clindamycin HCl Psittacine 100 PO QD E 1240 For osteomyelitis and tendon sheath
infections
5:28 PM
Clindamycin HCl Psittacine 50 NL BID F 1170 Used to treat anaerobic osteomyelitis

Clindamycin HCl Psittacine 25 NL TID F 1170
Clindamycin HCl Raptor 30-40 PO BID B 1568
Page 261
Clofazimine Avian 6 PO QD D 1470 Add ethambutol + rifampin for liver

mycobacteriosis
Clofazimine Avian 1.5 PO QD D 1571
Clofazimine Psittacine 1.5 PO QD E 1240 For mycobacteriosis
Clofazimine Raptor 1-5 PO QD E 1240, 1154
Clomipramine HCl Avian 0.5-1 NL QD-BID D 1475 Control of self-mutilation, mixed results
Clomipramine HCl Cockatoo 3 PO BID G 1278 Cloacal prolapse
Clomipramine HCl Psittacine 0.5-1 PO BID B 43
Clomipramine HCl Psittacine 0.5-1 PO QD-BID E 111 Gradually increase dose over 4 to 5 days
Clopidol Chicken 125-250 mg/kg food Feed QD E 564 5-day slaughter withdrawal, prophylactic
Clopidol Poultry 0.25 g/kg food Feed QD C 564 Prophylactic
Clorsulon Anseriformes 20 PO q2w D 1150 For cestodes and nematodes

Clorsulon Avian 20 PO q2w G 818 For tapeworms
Clorsulon Psittacine 20 PO q2w E 111
Clorsulon Raptor 20 PO q2w E 1240 For trematodes and cestodes
Clotrimazole Crane 10 g/L Nebulize TID E 1361 Antifungal

Clotrimazole Raptor 70-100 g/L Nebulize BID E 1359
Cloxacillin Sodium Avian 100-200 IM QD E 565

Cloxacillin Sodium Avian 250 PO BID E 1234 For bumblefoot

Cloxacillin Sodium Avian 100 PO QD E 1470
Cloxacillin Sodium Raptor 250 PO BID E 1240
261
262

Cloxacillin Sodium Raptor 100-250 IM NL E 1463 For bacterial infections
Coenzyme Q10 Avian 1 PO QD-BID E 1205, 1435 For heart, geriatric, diabetic, immune
deficient birds
Colchicine Avian 0.04 PO QD D 1470 For hepatic fibrosis

Colchicine Macaw 0.01 PO BID G 45
Colchicine Psittacine 0.2 PO BID E 111, 1473

Colchicine Psittacine 0.04 PO QD-BID E 1756
8/22/2005
Corticotropin Avian 16 IU TD IM Once B 88, 532

5:28 PM
Crotamiton Psittacine 10% Topical NL E 1240 For knemidocoptic mites
Cupric Sulfate Avian 51% powder Topical PRN E 1240 For ulcerative dermatitis
Cupric Sulfate Ostrich 0.5 g/L Drink QD G 1254, 283 For candidiasis, use acidified copper sulfate
Page 262
Cupric Sulfate Psittacine 1:2000 dilution Topical q2w D 1446 For dermatomycosis
Cyanocobalamin Avian 0.25-0.5 IM QW E 111
Cyclophosphamide **Check current literature prior to use

Cyclophosphamide Owl, Great-horned 25 PO Once F 125 Maximum dosage listed
Cyclophosphamide Psittacine 200 mg/m2 IO QW E 1470 Lymphosarcoma
Cycloserine Avian 5 PO BID D 1571 Add ciprofloxacin or enrofloxacin +

clofazimine + ethambutol for avian
mycobacteriosis
Cycloserine Raptor 5 PO BID E 1240, 1154
Cyclosporine Duck, Pekin 60 IV QD A 835

Cyclosporine Duck, Pekin 10 IV TID-QID A 835
Cypermethrin Pigeon 0.05% solution Topical QD E 704 Apply as spray

Cypermethrin Psittacine 2.0% solution NL NL E 1240 Spray premises for Dermanyssus , avoid contact
with skin
Cypermethrin Raptor 2% solution NL NL E 1240
Danofloxacin Mesylate Chicken 0.05 g/L Drink NL A 837 For Mycoplasma gallisepticum
Danofloxacin Mesylate Chicken 5 PO QD B 893, 990 For colisepticemia
Decoquinate Chicken 30 mg/kg food Feed QD E 564 No slaughter withdrawal, prophylactic

Decoquinate Pheasant, Ring-necked 0.03 g/kg food Feed QD B 895 For coccidiosis
Deferiprone Toucan 50 PO BID G 1280 For iron storage disease, zinc

supplementation may be required
8/22/2005
Deferoxamine Mesylate Avian 100 SC QD D 1470 To reduce liver iron levels

5:28 PM
Deferoxamine Mesylate Avian 20 PO Once G 87 Continue IM q4h as needed

Deferoxamine Mesylate Mynah 40 IM QD G 340 Repeat qow for series of 10 treatments
Deferoxamine Mesylate Toucan 100 SC QD G 1280 For iron storage disease
Deferoxamine Mesylate Toucan 1.28 mg/kcal IM QD E 1180 Iron chelation
Page 263
Delmadinone Acetate Avian 1 IM NL E 1434

Delmadinone Acetate Pigeon 6.67 IM NL E 1432
Detomidine HCl Avian 0.3 IM NL G 1320

Detomidine HCl Chicken 0.3 IM PRN E 1573 Sedation
Detomidine HCl Ostrich 0.3 IM PRN E 1573 Sedation
Dexamethasone Avian 1-2 IM NL D 1533

Dexamethasone Avian 2-4 IM QD E 1431 Use sparingly
Dexamethasone Avian N/A Topical NL E 1151 Add dimethyl sulfoxide for cloacal or uterine
prolapse
Dexamethasone Crane, Sarus 0.5 IV Once G 1087
Dexamethasone Falcon 2 IM-IV Once E 1027 For shock, trauma, toxic conditions
Dexamethasone Heron, Great Blue 0.5 IV Once G 1087
Dexamethasone Pigeon 0.15-1.5 IM-IV BID E 1432
Dexamethasone Pigeon 0.3-3 IM-IV BID E 1432 For shock
Dexamethasone Psittacine 2-4 IM QD-BID E 1240
Dexamethasone Psittacine 4 IM-SC NL G 632 Neonate dosage, shock or sepsis
Dexamethasone Raptor 2-4 IM QD E 1433 Use with great care
Dexamethasone Raptor 0.3-3 IM q2d E 1240 Long-lasting formulation, reduce
inflammatory response and shock
Dexamethasone Sodium Amazon, Yellow-naped 1 IM q3-7d G 1033

Phosphate
Dexamethasone Sodium Anseriformes 2 IM QD E 1240
Phosphate
263
264

Dexamethasone Sodium Avian 2 IM-IV Once E 1151
Phosphate
Dexamethasone Sodium Bustard 2 IM QD E 1240
Phosphate
Dexamethasone Sodium Psittacine 2-4 IM-IV NL E 1688

Phosphate
Dexamethasone Sodium Raptor 2 IM QD E 1240
Phosphate
8/22/2005
Dextrose Avian N/A Topical PRN E 1151 For flushing wounds

Dextrose Avian 50 IV-PO-SC NL E 1240 Isotonic for hypoglycemia and dehydration,
IV slowly
5:28 PM
Dextrose Avian 50-100 IV NL E 111 Give slowly

Dextrose Avian 50 IV-PO-SC NL E 1240
Dextrose Avian 50-100 IV NL E 1473 Give slowly
Dextrose Avian 1 IV NL G 1311 For hypoglycemia, 50% solution, may be
deleted
Page 264
Dextrose Psittacine 2 ml/kg IV NL G 632 Neonate dosage, use 50% solution, slow
bolus
Dextrose Raptor 500-1000 IV Once E 1400 Give slowly for hypoglycemia
Diatrizoate Meglumine Budgerigar 0.2 ml TD IP NL G 95 Goiter therapy
Diatrizoate Meglumine + Amazon, Double Yellow-head 400 IV Once D 1756 For IV excretory urography
Diatrizoate Sodium
Diazepam Anseriformes 1 NL PRN D 1403 Add ketamine

Diazepam Anseriformes 1.2-1.6 g/L bait Feed Once G 1230 Add chloralose
Diazepam Anseriformes 0.5-1 IM-IV BID-TID E 1240 Control seizures
Diazepam Avian 0.5-1 IM NL E 1120, 1492 For seizures related to lead toxicoses
Diazepam Bird, Aquatic 0.6 IM-IV PRN E 1503
Diazepam Bird, Aquatic 0.5-1 IM-IV PRN E 1559 For lead poisoning to control convulsions
Diazepam Crane 0.5-1 NL PRN E 1189 For tranquilization 4 to 6 hours

Diazepam Crane 0.2-0.5 NL PRN E 1189 Add ketamine for anesthesia
Diazepam Duck 1.3-1.7 g/kg bait Feed Once G 1386 Add chloralose
Diazepam Emu 0.6 IV PRN G 283 Add pentobarbital after 1 hour
Diazepam Emu 5 IV NL E 4 Sedation
Diazepam Falcon 1.2 IV PRN D 1401 Add ketamine
Diazepam Hawk, Rough-legged 1-1.5 IV PRN G 1092 Combine with ketamine
Diclofenac Sodium Pigeon 12.5 mg/TD PO NL E 1240 For arthritis
Diethylcarbamazine Raptor 50 PO NL E 1463 Anthelmintic

Citrate
Diethylstilbestrol Avian 0.025-0.075 IM NL E 111

Diethylstilbestrol Avian 0.1-0.3 IM NL E 1473
Digoxin Amazon, Yellow-naped 0.02 PO BID G 1033

8/22/2005
Digoxin Avian 0.02 NL NL D 1470

Digoxin Avian 0.01 PO QD-BID E 1152
Digoxin Avian 0.02-0.05 PO QD-BID E 1152
5:28 PM
Digoxin Avian 0.0033 g/L Drink QD G 1323 Change daily

Digoxin Budgerigar 0.02 PO QD A 882
Digoxin Sparrow 0.02 PO QD A 882
Dimercaprol Avian 2.5 IM q4h E 1120, 1236 Continue BID for 10 days (or longer if
Page 265
needed) for lead toxicoses

Dimercaprol Avian 25-35 PO QD-q2d E 1240, 1473 Give 5 days per week for lead toxicosis
Dimethyl Sulfoxide Avian

Dimethyl Sulfoxide Avian 5 ml Nebulize NL E 704 Add tylosin + 10 ml 0.9% saline solution
Dimethyl Sulfoxide Avian 10 ml/L Nebulize TID-QID E 1650 Add appropriate antimicrobial, adjunct to
parenteral therapy for air sacculitis
Dimethyl Sulfoxide Avian Ointment Topical NL E 1650 For prolapsed phallus
Dimethyl Sulfoxide Avian 1 ml/kg 50 % solution PO NL G 1717 Also apply topically
Dimethyl Sulfoxide Avian 20 IM BID-TID G 861 For heavy metal poisoning

Dimethyl Sulfoxide Chicken Mix 50:50 Topical NL B 1342 Add bupivacaine, prepare 50:50 solution
Dimethyl Sulfoxide Raptor N/A Topical NL E 1240 Reduce swelling, vehicle to carry drugs
through skin particularly on legs
Dimethylglycine Avian 5 PO TID E 1205 Brain disorders

Dimethylglycine Avian 2-4 PO QD-BID E 1435 Immune and energy booster
Dimetridazole Avian 50 PO QD E 704

Dimetridazole Avian 1.25lmllpowder/LlllllllllDrink NL E 741 For trichomoniasis, giardiasis and
histomoniasis
265
266
Dimetridazole Avian 50 PO NL E 924 For protozoa
Dimetridazole Avian 30 Gavage Once E 1650 For trichomoniasis, giardiasis and

histomoniasis
Dimetridazole Finch 0.1 g/L Drink QD G 1334 For cochlosomiasis
Dimetridazole Lorikeet 0.1 g/L Drink QD E 1479

8/22/2005
Dimetridazole Pigeon 0.4 g/L Drink NL A 791

Dimetridazole Pigeon 50 PO QW E 1432
Dimetridazole Pigeon 20 PO QD G 232
Dimetridazole Poultry 500 mg/kg food Feed QD C 564 Prophylactic
5:28 PM
Dimetridazole Poultry 0.5-1.0 g/L Drink QD G 585

Dimetridazole Raptor 125 PO NL D 1612 For trichomoniasis
Dimetridazole Raptor 100 PO NL E 1463 For trichomoniasis
Page 266
Dinitolmide Chicken 40-187 mg/kg food Feed QD E 564 No slaughter withdrawal, prophylactic
Dinoprost Tromethamine Anseriformes 0.02-0.1 IM-Topical Once D 1150 Apply to cloacal mucosa topically, egg
(Prostaglandin F-2a) binding
Dinoprost Tromethamine Anseriformes 0.02-0.1 IM Once E 1240 For egg binding

Dinoprost Tromethamine Avian 0.02-0.1 IM Once E 1473 Also intracloacal
Dinoprost Tromethamine Ostrich 5 mg TD Parenteral Once G 1224 For caseous salpingitis, add appropriate
antimicrobials for 1 week
Dinoprost Tromethamine Psittacine 0.02-0.1 Vent Once E 1240 Apply to cloacal mucosa for egg binding
Dinoprost Tromethamine Psittacine 0.02-0.1 IM Once E 1240 For egg binding
Dinoprost Tromethamine Raptor 0.02-0.1 Vent Once E 1240
Dinoprostone Avian 0.2 Vent NL E 1474 Precede with calcium gluconate for egg
(Prostaglandin E) binding, apply into cloaca, may add vitamin E
+ selenium
Dinoprostone Cockatiel 0.02 Vent Once G 1699 For egg binding
Diphenhydramine HCl Avian 2 IO NL E 1470 Give before asparaginase and doxorubicin to

minimize anaphylaxis
Diphenhydramine HCl Avian 4 IM TID E 1554 For anticholinesterase toxicity
Diphenhydramine HCl Avian 2-4 PO BID D 1475 Control of self-mutilation
Diphenhydramine HCl Avian 2-4 NL BID E 1477 For feather, suture and bandage picking
Diphenhydramine HCl Psittacine 2-4 PO BID E 1473
Diphenhydramine HCl Raptor 4 IM TID G 50
Diprenorphine Cassowary, Double-wattled 2 mg/mg etorphine NL PRN D 1401 Etorphine antagonist

Diazepam Kestrel 2.2 IV PRN D 1401 Add ketamine
Diazepam Ostrich 1 IV PRN D 1401 Smooth anesthesia recovery

Diazepam Ostrich 5 PO PRN E 4 Standing sedation
Diazepam Ostrich 1-2 IV PRN G 481 Give just prior to recovery from
tiletamine/zolazepam
8/22/2005
Diazepam Owl 1 IV PRN D 1401 Add ketamine

Diazepam Passerine 0.5 PO NL E 1439 Anxiolytic and hyperphagic for wild fractious
species
Diazepam Pigeon 2.5 IM PRN E 1432 Add ketamine, 20 to 30 minutes deep
5:28 PM
sedation
Diazepam Pigeon 0.5-1 IM-IV PRN G 590 Add ketamine
Diazepam Psittacine 2.5-4 PO PRN E 1473
Diazepam Psittacine 0.5-1 IM-IO-IV PRN E 1688
Page 267
Diazepam Psittacine 1-1.5 IM-IV PRN G 824

Diazepam Raptor 1 IM PRN D 1401 Add ketamine
Diazepam Raptor 1-1.5 IV PRN D 1533 Add ketamine
Diazepam Ratite 1 NL PRN D 1403 Add ketamine
Diazepam Ratite 0.1 IM PRN E 4 Add ketamine
Diazepam Ratite 0.2-0.3 IV PRN E 243 Add ketamine
Diazepam Ratite 0.3 IV PRN G 418 Tranquilization particularly during anesthesia
recovery
Diazepam Rhea 5 IV NL E 4 Sedation
Diazepam Swan 1.3-1.7 g/kg bait Feed Once G 1386 Add chloralose
Dibutyltin Dilaurate Chicken 200 mg/kg food Feed QD E 564 10 day slaughter withdrawal
Dibutyltin Dilaurate Poultry 374 mg/kg food Feed QD C 564
Dichlorophen Pigeon 100 mg/TD PO q10d G 232
Dichlorvos Avian N/A IH QD E 704 Impregnated strip, 30 m³ minimum

Dichlorvos Strip Kakariki N/A IH QD G 1609 For Knemidocoptes
Diclazuril Chicken 0.5-1.0 mg/kg food Feed QD G 564

Diclazuril Crow 10 PO QD D 1438 Dose on days 0, 1, 2, 4, 6, 8 and 10 for
toxoplasmosis
Diclazuril Partridge, European grey 0.366 Feed QD B 891 For Eimeria
Diclazuril Passerine 10 PO QD G 1334 Give on days 0, 1, 2, 4, 6, 8 and 10
Diclazuril Pheasant, Ring-necked 0.369 Feed QD B 891 For Eimeria

Diclazuril Quail, Japanese 0.29-0.56 Feed QD B 891
267
268

Diprenorphine Ostrich 0.05-0.06 IV PRN B 447 Opioid antagonist
Diprenorphine Ostrich 4.5-24 mg TD IM PRN G 481 Reverse etorphine
Docusate Sodium Psittacine 0.3 g/L Drink NL E 763 To aid in expelling lead or prevent
constipation following cloacal surgery
Doxapram HCl Anseriformes 10 IV Once D 1150 Stimulant

Doxapram HCl Avian 5-10 IM-IV Once E 111, 1473

Doxapram HCl Avian 5 IM-IO-IV NL E 243
8/22/2005
Doxapram HCl Avian 6 IV NL G 496

Doxapram HCl Avian 20 IM-IO-IV NL E 1183 Also drop onto tongue for cardiac arrest
Doxapram HCl Falcon 10 IM-IV Once E 1027
5:28 PM
Doxapram HCl Ostrich 0.5-1.5 IV PRN G 522

Doxapram HCl Psittacine 20 IM-IO-IV NL E 1688
Doxapram HCl Raptor 10 IM-IV Once E 1240
Doxapram HCl Raptor 5-20 IT-IV Once E 1359 For anesthetic emergencies
Page 268
Doxepin HCl Avian 0.5-1 PO BID E 111 Control feather picking

Doxepin HCl Avian 0.5 PO BID E 704 Or add to drinking water
Doxorubicin **Check current literature prior to use

Doxorubicin Avian 30 mg/m2 IO q3w E 1470 Give 30 mg/m² of body surface for
lymphosarcoma
Doxycycline Amazon Parrot 1 g/kg food Feed QD A 693

Doxycycline** References Avian 100 IM QW A 55 European formulation. For
followed by ** are based chlamydophilosis, may be spaced 5 to 7 days
on the long acting for first 4 weeks
formula)
Doxycycline Amazon Parrot 40-50 PO QD-BID E 111
Doxycycline** Amazon Parrot 100 IM q5d-QW A 230 For chlamydophilosis
Doxycycline** Amazon 50 IM q4-5d B 1062
Doxycycline Anseriformes 0.24 g/kg food Feed QD D 1150
Doxycycline Anseriformes 50 PO BID D 1150 For chlamydophilosis
Doxycycline** Avian 100 IM q10d B 583
Doxycycline Avian 15 Drink QD C 705
Doxycycline** Avian 75-100 IM-SC q5d-QW E 565 Antichlamydophilial
Doxycycline** Avian 75-100 IM q5d E 703 For chlamydophilosis, may be spaced 5 to 7
days for first 4 weeks
Doxycycline Bird, Aquatic 25-50 PO QD E 1503 Broad spectrum, food for respiratory
infections, treat for 45 days for

chlamydophila
Doxycycline Bird, Aquatic 10 g/L Drink QD E 1503 See above
Doxycycline** Bird, Aquatic 75-100 IM QW E 1503 See above
8/22/2005
Doxycycline** Bustard, Houbara 100 IM QW A 1240 See above

Doxycycline Bustard, Houbara 22-44 IV Once A 1240 Continue therapy with IM or PO dosage for
severe chlamydophilosis
Doxycycline Chicken 20 PO QD A 762
5:28 PM
Doxycycline Chicken 0.1 g/L Drink NL A 803

Doxycycline Chicken 10 Drink QD B 1009 For fowl cholera
Doxycycline Cockatiel 0.83 g/L Drink QD A 1638 For chlamydophilosis
Doxycycline Cockatiel 0.5 g/kg seed Feed QD A 1638 For chlamydophilosis, may cause toxicosis
Page 269
Doxycycline Cockatiel 1 g/kg mash Feed QD A 1638 For chlamydophilosis

Doxycycline** Cockatiel 100 IM q10d A 1638 For chlamydophilosis, may not maintain
adequate drug plasma levels
Doxycycline Cockatiel 40-50 PO QD E 111, 703 For chlamydophilosis
Doxycycline Cockatoo 1 g/kg food Feed QD A 693
Doxycycline Cockatoo, Goffin 25 PO BID A 697
Doxycycline Cockatoo, Goffin 0.4 g/L Drink NL A 749
Doxycycline Cockatoo, Goffin 1 g/kg mash Feed QD A 1639
Doxycycline Macaw 25 PO BID A 697
Doxycycline Macaw, Blue and Gold 1 g/kg corn mash Feed QD A 730 Each bird fed 100 g mash
Doxycycline Ostrich 10 NL BID E 628 Oviductal infection therapy
Doxycycline Parrot, Grey 25 PO BID A 697
Doxycycline Parrot, Grey 0.4 g/L Drink NL A 749
Doxycycline Parrot, Grey 1 g/kg food Feed QD A 1639
Doxycycline Passerine 0.25 g/L Drink QD E 1437 Add drug to food at the same time, use for
Doxycycline Passerine 1 g/kg food Feed QD E 1437 Add drug to drink at the same time, use for
Doxycycline Penguin 10 NL QD G 1353 For babesiosis
Doxycycline Penguin, African 20 PO BID G 1353
Doxycycline ** Pigeon 75 IM Once A 379
Doxycycline** Pigeon 75-100 IM-SC q5d-QW A 565
Doxycycline Pigeon 25 PO BID A 565 With grit in diet
Doxycycline Pigeon 15 Drink QD C 704

Doxycycline Poultry 0.05 g/L Drink QD C 564
Doxycycline Poultry 0.25-0.5 g/L Drink QD G 585 Add tylosin, antimycoplasmal
269
270

Doxycycline Psittacine 25-50 IV NL E 111
Doxycycline** Psittacine 100 IM QW E 632 Neonate dosage
Doxycycline Psittacine 50 PO QD E 632 Neonate dosage
Doxycycline ** Psittacine 20 IV Once E 632 Neonate dosage
Doxycycline Raptor 50 IM NL B 1568

Doxycycline Raptor 25 PO BID G 94 Juvenile dosage
Doxycycline Ratite 2-3.5 PO BID G 1308 For chlamydophilosis
Doxycycline Hyclate Avian 0.4 g/L Drink QD A 703 For chlamydophilosis

8/22/2005
Doxycycline Hyclate Avian 200-400 mg/kg food Feed QD E 565 Antichlamydophilial
Doxycycline Hyclate Cockatiel 0.2-0.4 g/L Drink QD A 703 For chlamydophilosis

5:28 PM
Doxycycline Hyclate Cockatoo, Goffin 0.8 g/L Drink QD A 703

Doxycycline Hyclate Parrot, Grey 0.8 g/L Drink QD A 703
Doxycycline Hyclate Pigeon 55 PO BID G 47
Edetate Calcium Anseriformes 10-40 IM-IV BID D 1150 For lead poisoning
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Disodium
Edetate Calcium Disodium Avian 30-50 IM-IV QID D 1221 For lead or zinc toxicosis, may use in
conjunction with penicillamine
Edetate Calcium Disodium Avian 20-40 IM-IV BID D 1470 To reduce liver lead and zinc
Edetate Calcium Disodium Avian 20-40 IM BID-TID E 111
Edetate Calcium Disodium Bird, Aquatic 35 IM BID D 1478 Give 3 to 4 days per week for lead poisoning
Edetate Calcium Disodium Crane, Sand Hill 35 IM BID B 1088 Repeat 4 days later for lead poisoning
Edetate Calcium Disodium Lory, Chattering 30 SC BID G 42
Edetate Calcium Disodium Macaw 35 IM BID G 40
Edetate Calcium Disodium Pigeon 30 IM BID G 590
Edetate Calcium Disodium Psittacine 10-40 IV BID E 1240 Lead and heavy metal poisoning
Edetate Calcium Disodium Raptor 35-50 NL BID E 1188 For lead toxicity
Edetate Calcium Disodium Raptor 10-40 IM-IV BID E 1240 Lead and heavy metal poisoning
Enilconazole Avian 2 g/L NaCl Topical NL E 924 For skin mycosis

Enilconazole Psittacine 2 g/L NaCl Nebulize BID G 1034 Dilute 100 mg/ml 1:50 in normal saline
Enilconazole Psittacine 0.1-1% solution IT NL E 1240
Enilconazole Raptor 5 IT QD E 1240 Dilute 1:10
8/22/2005
Enilconazole Raptor 0.2% solution Topical BID E 1240

Enilconazole Ratite 10% solution Flush NL G 1224 For mycotic dermatosis
Enrofloxacin Amazon Parrot 7.5-15 IM-PO QD-BID A 1473

5:28 PM
Enrofloxacin Amazon 15 IM QD A 749

Enrofloxacin Amazon, Blue-fronted 0.5 mg/kg food Feed Once A 858 For chlamydophila
Enrofloxacin Amazon, Red Lored 10 IM BID G 700 2.5% concentration
Enrofloxacin Anseriformes 10-15 IM-PO BID D 1150, 1358
Page 271
Enrofloxacin Aracari, Black-necked 10 PO BID G 1367 Pre-surgical

Enrofloxacin Avian 5-15 IM-PO-SC QD-BID A 916
Enrofloxacin Avian 30 PO NL E 1492 For Mycoplasma, Chlamydophila
Enrofloxacin Avian 10 g/L Nebulize TID-QID E 1650 Add dimethyl sulfoxide, adjunct to parenteral
therapy for air sacculitis
Enrofloxacin Avian 0.25-1 g/kg food Feed QD F 916
Enrofloxacin Avian 0.05-0.5 g/L Drink NL F 916
Enrofloxacin Avian 15 PO QD G 580 Add ethambutol + rifampin,
antimycobacterial
Enrofloxacin Bird, Aquatic 30 IM BID E 1478 Post-trauma infections
Enrofloxacin Budgerigar 30 Feed Once A 920 For chlamydophilosis
Enrofloxacin Bustard, Houbara 15-30 IM-IV-PO BID A 790
Enrofloxacin Chicken 10 Drink NL A 811
Enrofloxacin Duck, Muscovy 15 Drink QD B 842 Pulse dose for 4 hours each day
Enrofloxacin Duck, Pekin 10 Drink QD A 854 For Pasteurella and coliforms
Enrofloxacin Gull 10 IM BID E 1357
Enrofloxacin Hawk, Red-tailed 5 IV QD A 978
Enrofloxacin Hornbill, Great 10-20 PO BID G 1587
Enrofloxacin Lory, Red 15 PO BID G 1621
Enrofloxacin Ostrich PO TID G 418
Enrofloxacin Owl, Great-horned 5 IM-PO BID G 173 Add clindamycin or cephalothin
Enrofloxacin Parrot, Grey 0.5 g/L Drink QD A 921 For salmonellosis
Enrofloxacin Parrot, Grey 0.5 g/kg food Feed Once A 921 Higher blood levels in neonates
Enrofloxacin Penguin, Rockhopper 9 PO QD G 1646
Enrofloxacin Pheasant 20 IM-PO NL G 678

Enrofloxacin Pheasant, Chinese Ringneck 7.5 IM QD G 1296 Continue therapy orally
Enrofloxacin Pigeon 15 IM-SC QD A 179
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272

Enrofloxacin Pigeon 10 PO QD A 179
Enrofloxacin Pigeon 5-10 IM-IV-PO- QD-BID A 866
SC
Enrofloxacin Pigeon 10-20 IM-PO-SC QD-BID A 919
Enrofloxacin Pigeon 5 Drink QD A 919

Enrofloxacin Pigeon 5 PO BID A 1473
Enrofloxacin Poultry 15 NL BID G 585
Enrofloxacin Psittacine 2.5-20 PO QD A 179

Enrofloxacin Psittacine 11-17.5 Drink NL B 750
8/22/2005
Enrofloxacin Psittacine 10-20 IM NL E 632 Neonate dosage, may cause joint defects
Enrofloxacin Raptor 15 IM-PO BID E 1240 Broad spectrum including Pseudomonas,
Klebsiella, Mycoplasma
5:28 PM
Enrofloxacin Ratite 1.5-2.5 PO-SC BID G 1308 For Gram negative infections
Epinephrine Avian 0.1 IO-IP-IT-IV NL E 1473

Page 272
Epoetin Alfa Avian 0.1 SC q2-3d E 1151 For anemia
Ergonovine Maleate Avian 0.06 IM Once E 111, 1473, 1650 With or without calcium gluconate for egg
binding
Erythromycin Avian 0.125 g/L Drink NL E 111

Erythromycin Avian 25 IM QD E 565
Erythromycin Avian 100 PO NL E 704
Erythromycin Avian 200 mg/kg Feed QD E 704 Soft food
Erythromycin Avian 10-20 g/L Nebulize TD E 704 Diluted in 15 ml 0.9% saline solution
Erythromycin Chicken 0.102 g/L Drink QD A 544 Chick dosage
Erythromycin Finch 0.2 g/kg food Feed QD E 1572
Erythromycin Finch 0.125 g/L Drink QD E 1572
Erythromycin Pigeon 100 PO NL A 1055
Erythromycin Pigeon 2.2 g/L Drink QD E 704 Erythrocin Soluble®, 5 g per teaspoon
Erythromycin Poultry 0.25 g/L Feed QD C 564
Erythromycin Poultry 10-20 Drink QD C 705
Erythromycin Poultry 50-100 NL BID G 585
Erythromycin Psittacine 44-88 PO BID E 741 For sinusitis
Erythromycin Psittacine 10-20 PO BID E 1240 For mycoplasmal sinusitis and air sacculitis
Erythromycin Psittacine 10-20 Parenteral- BID E 1473

PO
Erythromycin Ratite 5-10 PO TID G 1308
Estradiol Avian 10-15 IM QW B 677 Induce molting X 4 weeks
Ethambutol HCl Amazon, Yellow-cheeked 30 NL QD G 713 Add rifampin + isoniazid

8/22/2005
Ethambutol HCl Avian 30 PO QD D 1470

Ethambutol HCl Avian 15 PO BID E 1473
Ethambutol HCl Avian 30 PO QD E 1650 Add enrofloxacin + rifabutin for
mycobacteriosis
5:28 PM
Ethambutol HCl Avian 10 PO BID G 55 Add rifampin + streptomycin for

mycobacteriosis
Ethambutol HCl Crane, Whooping 30 PO QD G 207 Add rifampin
Ethambutol HCl Psittacine 15-20 PO BID E 1240 For mycobacteriosis
Page 273
Ethambutol HCl Raptor 20 PO BID E 1240
Etorphine Cassowary, Double-wattled 0.15 IM PRN G 447 Add acepromazine

Etorphine Ostrich 0.04-0.07 IM PRN B 447 Add acepromazine
Etorphine Ostrich 0.04 IM PRN B 447 Add acepromazine + xylazine
F10 Avian 1:250 dilution Nebulize QD-BID G 1197 Nebulize as antifungal, antichlamydophilial
and antibacterial
F10 Avian 1:200 dilution Topical QD G 1302 Daily spray onto feathers for yeast and
supplement to feather picking therapy
F10 Avian 1:125 dilution Nebulize TID B 1465
F10 Avian 1:125 Dilution Nebulize BID G 1268 Add omega interferon, prevents secondary
infection
F10 Raptor 1:250 Dilution Nebulize BID-TID G 742 Add itraconazole, 15 to 30 minutes per day
for mild aspergillosis
Fatty Acids, Omega Psittacine 0.22 ml/kg PO NL E 1756 Add aspirin, use < 6:1 ratio omega 6:omega
3, use until renal histology normalizes for
renal disease
Fatty Acids, Omega Psittacine 0.11 ml/kg PO QD G 1263 Mix 5:1 N-6:N-3 omega fatty acids for
glomerulonephritis or acute pancreatitis
Febantel Ostrich 20 NL NL C 283

Febantel Ostrich 5 PO NL G 481
Febantel Pigeon 30 PO q3w A 888 For ascarids and capillaria
Fenbendazole Anseriformes 20 PO Once D 1150 Control nematodes

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274

Fenbendazole Anseriformes 5-10 PO QD E 111, 1473
Fenbendazole Avian 25 NL QD D 1221 Repeat in 2 weeks for capillariasis
Fenbendazole Avian 100 NL q2w D 1221 For capillariasis
Fenbendazole Avian 2 PO QD D 1470 For liver parasitic disease
Fenbendazole Avian 20-50 PO q10d E 111 For ascarids

Fenbendazole Avian 20-50 PO QD E 111 For flukes and capillaria
Fenbendazole Avian 50 PO QD E 1617 For ascarids, may need 5-day treatment for
capillaria, repeat in 2 weeks,

Fenbendazole Avian 20-100 PO Once G 57 Avoid during breeding season and molting
8/22/2005
Fenbendazole Bird, Aquatic 22 NL NL E 1478

Fenbendazole Bird, Aquatic 50 PO QD E 1503 Repeat in 2 weeks for ascarids
5:28 PM
Fenbendazole Bird, Aquatic 100 PO q2w E 1503

Fenbendazole Bustard 30 PO Once E 1240
Fenbendazole Bustard, Houbara 25 PO Once G 932 Prophylaxis for round worms
Fendendazole Cockatiels N/A G May have lethal reaction
Fenbendazole Crane 100 PO QD E 629 Repeat q2w as needed
Page 274
Fenbendazole Crane 50-100 PO QD E 1361 Repeat in 2 weeks for gapeworms and

capillarids
Fenbendazole Falcon 20 PO QD E 1240 For Serratospiculum
Fenbendazole Finch 10-25 PO QD E 1572
Fenbendazole Grouse 0.5-0.7 Feed QD C 704 For Trichostrongylus
Fenbendazole Gull 50 PO QD E 1357 For capillariasis
Fenbendazole Gull 25 PO q2w E 1357 For ascaridiasis
Fenbendazole Ostrich 15 PO NL B 524 With or without resorantel
Fenbendazole Ostrich 30 PO NL B 526 Add resorantel
Fenbendazole Ostrich 15 PO NL G 481
Fenbendazole Parakeet, Australian 50 Gavage Once E 1186 For roundworms
Fenbendazole Partridge 8 Feed QD C 704 For Capillaria
Fenbendazole Partridge 12 Feed Once C 704 For Syngamus, Heterakis , ascarids
Fenbendazole Penguin 50 PO NL E 1478 For nematodes and flukes
Fenbendazole Pheasant 12 PO Once C 706
Fenbendazole Pheasant 8 PO QD C 706
Fenbendazole Pigeon 16 PO Once C 704
Fenbendazole Pigeon 20 PO QD C 706 For gastrointestinal roundworms
Fenbendazole Pigeon 20-50 PO QD E 1240 For capillariasis
Fenbendazole Pigeon 8 PO Once E 1240 At 8 weeks of age
Fenbendazole Pigeon 7.5 PO Once E 1432
Fenbendazole Pigeon 7.5-20 PO Once G 232
Fenbendazole Pigeon 10-12 PO QD G 260
Fenbendazole Pigeon 50 PO QD G 590
Fenbendazole Pigeon 15 PO q10d G 1208 For ascarids or Capillaria, not for use during
molting
Fenbendazole Psittacine 20-50 PO r2w E 763
Fenbendazole Psittacine 15 PO QD E 1240 May medicate feed for 7 days
8/22/2005
Fenbendazole Psittacine 100 PO q2w E 1613 For ascaridiasis

Fenbendazole Psittacine 50 PO QD E 1613 For capillariasis
Fenbendazole Raptor 10-50 NL q10d E 1132 For ascaridiasis
Fenbendazole Raptor 30-50 NL Once E 1132 For flukes
5:28 PM
Fenbendazole Raptor 25 PO QD E 1159 For nematodes

Fenbendazole Ratite 15 PO NL G 418 With or without resorantel
Fentanyl Citrate Avian 0.2 SC NL B 1341 Some hyperactivity for first 15 to 30 minutes
Page 275
Ferric Subsulfate Avian N/A Topical PRN E 1473 For hemorrhage
Fipronil Avian 7.5-15 NL Once G 1729 For larger birds

Fipronil Canary N/A Topical Once G 1729 Spray on gloved finger and rub under wings
and on dorsal and ventral surfaces of body
for red mites
Fipronil Dove, Duck 7.5-15 NL Once G 1729
Fipronil Raptor Light Spray Topical Once B 1568 For wild injured raptors with ectoparasites
Fipronil Raptor N/A Topical Once E 1359 For ectoparasites
Flax Seed Oil Amazon, Yellow-naped 0.022 ml/kg body wt. Feed QD G 1033 Dilute 1:4 with corn oil
Flax Seed Oil Avian 0.1-0.2 ml/kg PO NL G 1682 Mix 1:4 with corn oil prior to dosing for renal
disease
Floxacillin Hawk 125 PO BID G 1110

Floxacillin Raptor 250 PO NL E 1463 For bacterial infections
Flubendazole Anseriformes 0.24 mg/kg feed Feed QD D 1150 Control nematodes

Flubendazole Galliformes 30-60 g/ton feed Feed QD C 704, 706 For gastrointestinal roundworms, gapeworms
and tapeworms
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276

Fluconazole Amazon Parrot 20 IV-PO q2d D 1330 For ketoconazole-resistant Candida , tissue-
based yeasts, eye, cerebral spinal, long-term
Aspergillus
Fluconazole Avian 8 NL QD D 1221 For cryptococcosis
Fluconazole Avian 20 PO q2d D 1221 For candidiasis

Fluconazole Avian 5 IV-PO QD D 1330
Fluconazole Avian 20 IV-PO q2d D 1330 Adult doase
Fluconazole Avian 4-6 IV-PO BID D 1330 Juvenile dose

Fluconazole Bird, Aquatic 15 PO QD E 1478 For prevention of aspergillosis, may also
8/22/2005
nebulize
Fluconazole Bird, Aquatic 8 PO BID E 1503
Fluconazole Bird, Aquatic 15 PO BID E 1559
5:28 PM
Fluconazole Chicken 100 Gavage BID G 1348 For macrorhabdosis (formerly megabacteria
or avian gastric yeast), toxic to budgerigars
Fluconazole Penguin, African 30 PO BID G 128

Fluconazole Pigeon 5-10 PO BID G 56 Prophylaxis
Page 276
Fluconazole Psittacine 5-15 PO BID D 1446

Fluconazole Psittacine 2-5 PO QD G 697
Fluconazole Raptor 2-5 PO QD E 1240 For generalized aspergillosis
Fluconazole Raptor 5 PO QD E 1359 For candidiasis
Fluconazole Raptor 2-5 PO QD E 1400 Aspergillosis
Flucytosine Avian 250 PO BID D 1221 For candidiasis

Flucytosine Avian 50-100 PO BID D 674, 1330 For Aspergillus or Candida prophylaxis, add
amphotericin B or azoles for therapy
Flucytosine Avian 40-50 PO TID E 626 Add IV and IT amphotericin B for

aspergillosis therapy
Flucytosine Avian 50-60 PO BID E 626 Aspergillus prophylaxis
Flucytosine Avian 20-50 PO BID E 1492
Flucytosine Bird, Aquatic 50-60 NL BID E 1503 Aspergillosis prophylaxis
Flucytosine Bird, Aquatic 100 PO TID E 1503 For aspergillosis adjunct therapy
Flucytosine Hornbill, Great 250 PO BID G 1587
Flucytosine Penguin, African 250 PO BID G 1353 May give long-term
Flucytosine Psittacine 75-120 PO BID D 1330 For Aspergillus or Candida prophylaxis, add
amphotericin B or azoles for therapy
Flucytosine Psittacine 100-250 PO BID D 1330
Flucytosine Raptor 120 PO BID B 1178 Add IT and IV amphotericin B + rifampin
for aspergillosis
Flucytosine Raptor 60 PO BID D 1330 For aspergillus or Candida prophylaxis birds
> 500 g, add H1176amphotericin B or azoles
for therapy
8/22/2005
Flucytosine Ratite 80-100 PO BID G 1308

Flucytosine Swan 50-75 PO BID G 86, 697
Flumazenil Anseriformes 0.05 IV PRN D 1503, 1533 Add atipamezole to reverse ketamine +
5:28 PM
medetomidine + midazolam
Flumazenil Avian 0.1 NL PRN E 1481 Reverse benzodiazepines
Flumazenil Avian 0.05 IV PRN E 1533
Flumazenil Pigeon 0.04 IM PRN G 1644 Reverse midazolam
Page 277
Flunixin Meglumine Anseriformes 1 SC QD E 1190

Flunixin Meglumine Anseriformes 1-10 IM NL E 1150 For joint lameness
Flunixin Meglumine Avian 1-10 IM QD D 1533 May cause renal ischemia at higher dosages
Flunixin Meglumine Bird, Aquatic 1-10 IM QD E 1503 May cause renal ischemia at higher dosages
Flunixin Meglumine Bustard, Houbara 2 NL NL G 1594 Swelling in foot deformity of neonate

Flunixin Meglumine Duck, Mallard 5 NL NL A 1339 Residual physiological effect 12 hours
Flunixin Meglumine Duck, Mallard 5 IM BID A 1490 For frostbite
Flunixin Meglumine Pigeon 1-10 IM-IV QD E 1432
Flunixin Meglumine Psittacine 1-10 IM NL E 1240
Flunixin Meglumine Raptor 2-10 IM QD D 1400
Fluoxetine HCl Avian 1 NL NL E 1186 For behavioral problems such as feather

picking
Fluoxetine HCl Avian 1 NL QD E 1477 For feather picking
Fluoxetine HCl Psittacine 0.4 PO QD D 1446 For behavioral feather picking
Furaltadone Avian 0.47 mg./kcal PO QD E 1180

Furaltadone Pigeon 15-20 PO QD E 565
Furaltadone Pigeon 0.125 g/L Drink QD E 1492, 1650 For salmonellosis
Furaltadone Pigeon 0.4 g/L Drink QD E 1240 Add tetracycline for trichomoniasis and
hexamitiasis, not for adults feeding young <
10 days old
Furazolidone + Pigeon 15-20 PO QD F 1061
Furaltadone
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278

Furosemide Amazon, Yellow-naped 0.15 PO BID G 1033

Furosemide Avian 0.165 IM BID G 1309 Diuretic, lories sensitive
Furosemide Avian 0.1-0.2 IM-PO QD-BID E 1152 For diuresis, risk of toxicosis especially in
small birds
Furosemide Avian 0.15-2 IM QD-BID E 1650 For ascites and edema, not for lorikeets
Furosemide Avian 0.15-2 IM-SC QD-BID E 111, 1470
Furosemide Avian 0.1-0.2 IM BID E 1431

Furosemide Avian 1-2 NL QD-BID E 1470 For congestive heart failure with liver disease
8/22/2005
Furosemide Pigeon 0.5-3 PO BID-TID G 590

Furosemide Pigeon 2.2 IM-IV-PO BID G 590
5:28 PM
Furosemide Psittacine 0.15-2 IM-SC QD-BID E 1240

Furosemide Raptor 1.5 IM QID E 1240
Furosemide Raptor 1 IM-IV PRN E 1359
Furosemide Raptor 1.5 IM TID-QID E 1400
Furosemide Raptor 1.5 IM PRN G 234
Page 278
Furosemide Secretary Bird 2.2 IM BID G 41
Fusidate Sodium Avian 2% ointment Topical BID E 1240 For mild/early bumblefoot and other skin
lesions, may penetrate intact skin, effective
against S. aureus
Gadopentetate Avian 0.25 mmol/kg IV Once G 1754 For head magnetic resonance imaging studies
Dimeglumine
Gentamicin Sulfate Avian 10 IT QD E 704

Gentamicin Sulfate Avian 5-10 IM BID-TID E 704
Gentamicin Sulfate Avian 5 g/L Nebulize TID E 741, 924 For sinusitis or airsacculitis
Gentamicin Sulfate Avian 4 IM NL E 924 For Pseudomonas , nephrotoxic
Gentamicin Sulfate Avian 5-10 NL QD E 1170 Relatively renal toxic particularly if
dehydrated
Gentamicin Sulfate Avian 5 g/L Flush BID E 1183 Nasal or sinus
Gentamicin Sulfate Avian 2.5 IM BID E 1434
Gentamicin Sulfate Avian 3-5 IM QD-BID E 1492
Gentamicin Sulfate Avian 3-5 IM QD-BID E 1650 For resistant organisms
Gentamicin Sulfate Bustard 5 IM QD-BID E 1240 For first 3 days of life to prevent yolk sac
infections after assisted hatch
Gentamicin Sulfate Chicken 1.5 IM TID A 715
Gentamicin Sulfate Chicken 2 IM BID A 1056 For roosters
Gentamicin Sulfate Chicken 10 IM BID-QID A 1143
Gentamicin Sulfate Crane 5 IM TID A 458

Gentamicin Sulfate Duck 5 IM QID A 847
Gentamicin Sulfate Duck, Eagle, Macaw, Owl 10 IM BID-QID A 1143
Gentamicin Sulfate Emu 5 IM TID A 418
8/22/2005
Gentamicin Sulfate Emu 2.5 IM BID A 847

Gentamicin Sulfate Hawk, Red-tailed 2.5 IM TID A 714
Gentamicin Sulfate Owl, Great-horned 2.5 IM TID A 714
Gentamicin Sulfate Pheasant 5 IM TID A 458
5:28 PM
Gentamicin Sulfate Pigeon 10 IM QID A 847

Gentamicin Sulfate Pigeon 20 IM BID-QID A 1143
Gentamicin Sulfate Psittacine 10 IM BID-TID E 565
Gentamicin Sulfate Psittacine 5-10 IT QD E 741 Add carbenicillin for pneumonia
Page 279
Gentamicin Sulfate Quail 10 IM QID A 458

Gentamicin Sulfate Raptor 2.5 IM TID A 565, 714
Gentamicin Sulfate Ratite 5 IM QD G 1308 May cause visceral gout
Gentamicin Sulfate Turkey 3 IM BID A 880
Gentian Violet Macaw, Hyacinth N/A Topical NL E 1240 Excellent for crop or skin fold candidiasis in
chicks
Glipizide Cockatoo, Rose-breasted 0.05 g/L Drink QD G 1726 Crush tablet into water for diabetes mellitus
Glucosamine Sulfate Avian 10 drops/kg PO TID E 1205 For joint disease
Glyburide Cockatiel 0.00125-0.0025 g/L Drink QD G 1720 For polyuria/polydipsia
Glycerin Raptor < 5 ml/kg PO NL E 1463 For impaction, may give cloacally
Glycopyrrolate Pigeon 0.01 IM PRN G 1644 Add midazolam for anesthesia premed
Gonadotropin, Chorionic Avian 500-1000 ug/kg IM QD E 1474 Treat chronic egg laying, inject day one, on
day 3 if egg, on day 7 if second egg, use up to
3-6 w
Gonadotropin, Chorionic Goose 0.5 mg TD Parenteral q3-4d B 894 Increase spermiation and early puberty in
ganders
Griseofulvin Ostrich 30-50 Drink QD G 531, 1308

Griseofulvin Pigeon 10 PO QD E 1240 For dermatophytosis
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280

Halofuginon HBr Poultry Feed QD C 705 For coccidial prophylaxis

Halofuginon HBr Chicken 3 g/ton food Feed QD E 564 Seven day slaughter withdrawal
Haloperidol Avian 0.1 PO BID D 1475

Haloperidol Avian 0.17 Drink QD E 704 Body weight less than 1 kg, gradually increase
dosage to 0.9 mg/kg
Haloperidol Avian 0.2 Drink QD E 704

Haloperidol Avian 0.4 Drink QD E 704 Maintenance dose
8/22/2005
Haloperidol Avian 0.4 NL NL E 1186 For behavioral problems such as feather

picking
Haloperidol Avian 1-2 IM q2-3w E 1431
5:28 PM
Haloperidol Avian 0.2-0.4 PO QD E 1431

Haloperidol Avian 0.1-0.15 NL NL E 1477 For self-mutilation
Haloperidol Avian 0.2 PO BID E 1492 For birds < 1 kg for feather picking and self-
mutilation, most effective in cockatoos
Page 280
Haloperidol Parrot, Quaker 0.08 PO BID E 1492 For feather picking and self-mutilation
Haloperidol Psittacine 0.15 PO BID E 111 Control feather picking and mutilation, birds
over 1 kg
Haloperidol Psittacine 1-2 IM q2-3w E 111 Control feather picking and mutilation
Haloperidol Psittacine 0.2 PO BID E 111
Haloperidol Psittacine 0.4 PO QD E 1240 For feather picking
Halothane Avian N/A IH PRN E 1617 Induction, maintain with 1-1.5%

Halothane Pigeon N/A IH PRN E 1432 1.5-3% maintenance
Heparin Sodium Avian 40-50 U/kg IV Once E 1151 Add aminophylline, dexamethasone Na
phosphate, fluids, oxygen for
polytetraflouroethylene gas poison
Heparin Sodium Avian 0.1 ml of 1000U/ml Nebulize QD G 1705 Add to 6.5 ml saline
Heparin Sodium Avian 1.0 ml of 1000U/ml Topical QD G 1705 Add aloe vera
Heparin Sodium Swan 55 IV Once G 1707 Emaciated near death
Hepasan Avian 1 ml/kg PO QD G 1035 For liver disease

Hepasan Psittacine 1 ml/kg PO QD G 1722 Liver support
Hetastarch Avian 10-15 ml/kg IV TID E 1650 For emergency care, reduce crystalloid fluids
Hetastarch Avian 10-15 ml/kg IV TID E 1151 For hypoproteinemia

Hetastarch Hawk, Red-tailed 10 ml/kg IV NL G 1626 Supportive therapy post-trauma
Hexyl Pyropheoborbide-a Hornbill, Great 0.3 IV q2m G 1587 For squamous cell carcinoma
8/22/2005
Hyaluronidase Avian 150 U/L fluids SC NL G 1103 Mix with fluids to aid in absorption
Hyaluronidase Avian 1.5 KIU/L Flush NL G 1719 Mix into nasal and sinus flushes
Hyaluronidase Avian 1.5 KIU/L Nebulize NL G 1719 Mix into nebulization fluid
Hyaluronidase Avian 1.5 KIU/L IV NL G 1719 For egg yolk stroke
5:28 PM
Hydrocortisone Sodium Avian 10 IV NL E 1470 For lead toxicity and severe infection with
Succinate liver disease
Page 281
Hydroxychloroquine Pigeon 4 tablets/L Drink NL G 590 Change daily

Sulfate
Hydroxyzine HCl Avian 2 PO TID G 1324 For pruritis

Hydroxyzine HCl Psittacine 2 PO TID D 1446 For hypersensitivity-triggered feather picking
Hypericum Avian 10 drops/kg PO TID E 1205 For feather picking, anxiety
Imidacloprid Raptor 7 IT-IV NL E 1359 For babesiosis
Imidocarb HCl Raptor 7 NL q3w E 1359 For babesiosis
Imiquimod Amazon, Blue-fronted cream Vent q2-3d B 1281 For cloacal papillomatosis, apply to cloacal
surface
Indomethacin Avian 0.4 IM NL E 1232

Indomethacin Chicken 2 PO NL A 772 Effective for 8-10 hours
Indomethacin, Copper Avian 0.4 IM QD E 1492 For acute/chronic inflammation from
trauma, infection or organ dysfunction
Insulin, NPH Avian 0.01-0.1 U TD Parenteral NL E 1650 For diabetes mellitus in birds larger than
budgerigar
Insulin, NPH Avian 0.07 U/kg IM QD G 1325 For diabetes, monitor blood glucose
Insulin, NPH Budgerigar 0.067-3.3 U/kg IM BID E 1326 For diabetes

Insulin, NPH Budgerigar 0.002 U TD IM PRN G 58
Insulin, NPH Psittacine 0.01-0.1 U TD IM PRN G 58, 88
281
282

Insulin, Regular Avian 0.0013 mg/kcal IM QD E 1180
Insulin, Zinc Suspension Toucan, Toco 0.1-0.5 U TD IM PRN G 58
Interferon, Alpha Avian 15 KIU/m² SC q2d E 1470 Give 15, 000 Units/m² of body surface for
lymphosarcoma
Interferon, Omega Avian 1000 KIU TD IM q2d B 1465 Add F10® for circovirus prevention and
limited effectiveness therapy of 90 days
Interferon, Omega Avian 1000 KIU TD Parenteral QD-BID G 1268 Add F10® for circovirus therapy
8/22/2005
Iodine, Lugol's Avian 4 drops solution/L Drink NL E 1186 Used to keep drinking water uncontaminated
Iodine, Lugol's Raptor 4 drops/L 7% soln Drink QD E 1612

5:28 PM
Iodophor Avian N/A Topical PRN E 1151 Use 0.5-1% solution for wound debridement
and flushing
Iodophor Avian N/A Topical NL E 1240 For wounds, apply and wash off after 3
minutes, very safe
Page 282
Iodophor Raptor N/A Topical NL E 1400 For wounds, wash off within 5 minutes
Iohexol Avian 700-800 IV NL E 1182 Use 70-80% iodine concentration for

urography
Iohexol Cockatiel 240 PO NL G 1623
Iopamidol Avian 0.8-1.2 IN NL G 1270 Use 20% concentration, sinus contrast study,
flush with saline when completed
Ipronidazole Avian 0.125 g/L Drink QD E 111, 741

Ipronidazole Pigeon 0.250 g/L Drink QD G 590 Change daily
Ipronidazole Psittacine 0.232 g/L PO NL E 111
Iron Dextran Anseriformes 10 IM QW D 1150 For hemapoiesis

Iron Dextran Avian 10 IM QW G 62
Iron Dextran Psittacine 10 IM QW-q10d E 1240 Hemapoiesis
Iron Dextran Raptor 10 IM Once E 1400 For iron-deficiency anemia
Isoflurane Avian N/A IH PRN E 1483 Maintain 1.5-3%
Isoniazid Amazon, Yellow-cheeked 30 NL QD G 713 Add ethambutol + rifampin, antibacterial

Isoniazid Avian 30 PO QD D 1470 Add ethambutol + rifampin, antibacterial
Isoniazid Avian 15 PO BID E 1473 Antiparasitic
Isoxuprine HCl Raptor 5-10 PO QD E 1359, 1400 For wing tip edema
Itraconazole Amazon Parrot 10 PO QD A 16 Dissolve in 0.1N HCl, dilute with orange

juice to tube feed
8/22/2005
Itraconazole Amazon, Blue-fronted 5-10 PO BID A 1739 Continue once daily for duration of therapy
Itraconazole Anseriformes 5-10 PO BID E 1473

Itraconazole Anseriformes 10 PO QD G 708
5:28 PM
Itraconazole Avian 10 PO QD A 577

Itraconazole Avian 5-10 NL BID E 1239
Itraconazole Bird, Aquatic 20 PO QD E 1503 For aspergillosis prophylaxis
Itraconazole Bird, Aquatic 15 PO QD E 1559 For aspergillosis prophylaxis
Page 283
Itraconazole Chicken 10 PO BID A 1376 Add miconazole for epidermal Aspergillus and
Alternaria cysts after surgical removal
Itraconazole Cockatiel 5 PO QD D 1330 Dissolve 100 mg capsule 2 ml HCl + 18 ml

orange juice for candidiasis
Itraconazole Crane 10 PO BID B 1189 Add enrofloxacin + clotrimazole for
aspergillosis
Itraconazole Crane 5-10 PO BID E 1361
Itraconazole Emu 5-10 PO QD G 16
Itraconazole Falcon 10-20 PO QD G 746 For aspergillosis
Itraconazole Gull 5 PO QD E 1357
Itraconazole Penguin 10 NL BID G 1353 Aspergillosis therapy long-term
Itraconazole Pigeon 6 PO BID A 709
Itraconazole Pigeon 26 PO BID A 709 For respiratory disease, this dosage may be
toxic
Itraconazole Psittacine 10 NL QD A 1424 For aspergillosis
Itraconazole Psittacine 5-10 PO BID D 1446 For cutaneous cryptococcosis or aspergillosis
Itraconazole Raptor 5-10 NL BID E 1188 Continue QD for 4 months for

asymptomatic cases of aspergillosis
Itraconazole Raptor 10 PO BID G 742 Add amphotericin B or enilconazole + F10®
for mild aspergillosis
Itraconazole Ratite 6-10 PO QD G 1308 Reduce dosage if neurologic signs occur
Ivermectin Anseriformes 0.2 PO-SC Once D 1150, 1190, 1240 Control nematodes and nasal or duck leeches
Ivermectin Avian 0.2 IM r10d E 741, 924

283
284

Ivermectin Bird, Aquatic 0.4-0.8 NL NL E 1559 For parasites
Ivermectin Budgerigar 0.2 Topical NL E 1240 Injectable form may be toxic
Ivermectin Budgerigar 0.4 IM-PO q10d G 1309
Ivermectin Bustard, Houbara 0.3 PO Once G 932
Ivermectin Canary 0.2 PO QW G 861 For air sac mites and scaly leg mites
Ivermectin Crane 0.2 IM-PO q2w E 629 Nematodes and mites
Ivermectin Emu 0.2 SC NL G 1308 Effective against chandlerellosis
Ivermectin Falcon 2-3 IM Once B 1427 For serratospiculiasis

Ivermectin Falcon 1 SC Once B 1585 For capillariasis
8/22/2005
Ivermectin Passerine 0.2-0.4 PO-Topical QW E 1438 For mites

Ivermectin Penguin 0.4-1 PO NL E 1478 For nematodes
Ivermectin Pigeon 0.3 SC NL G 57
Ivermectin Pigeon 0.2 PO NL G 232
5:28 PM
Ivermectin Pigeon 0.5-1 Parenteral- NL G 260

PO
Ivermectin Psittacine 0.2 IM-PO-SC q2-4w D 1446
Ivermectin Raptor 0.4 SC NL G 57
Page 284
Ivermectin Raptor 0.2 SC Once G 234

Ivermectin Raptor 0.2 IM NL G 1409 For capillariasis
Ivermectin Ratite 0.2 SC NL G 1308
Ivermectin Stork, Saddle-billed 0.2 PO QD G 1645 For microfilaria
Kanamycin Sulfate Anseriformes 20-40 IM BID G 739 For large waterfowl

Kanamycin Sulfate Avian 10-20 IM BID E 565
Kanamycin Sulfate Ratite 20-40 IM BID G 739
Kaolin + Pectin Psittacine 2 ml/kg PO BID-QID G 632 Neonate dosage

Kaolin + Pectin Raptor 67 drops/kg PO TID E 1612 For diarrhea
Ketamine HCl Amazon Parrot 10-20 IM PRN E 243 Add xylazine

Ketamine HCl Anseriformes 25 NL PRN D 1403 Add diazepam, supplement at 15 mg/kg
PRN
Ketamine HCl Anseriformes 10 IV PRN D 1503 Add medetomidine + midazolam,
atipamezole + flumazenil reverses, good
anesthesia 30 minutes
Ketamine HCl Avian 5-25 NL PRN C 1392
Ketamine HCl Avian 10-30 IM PRN E 243 Add diazepam, higher dosage for smaller bird
Ketamine HCl Avian 20 IM PRN E 704 Add midazolam

Ketamine HCl Avian 5-10 IM PRN E 704 Add medetomidine
Ketamine HCl Avian 10-25 IM PRN G 53 Add midazolam
Ketamine HCl Avian 10-50 IM PRN G 53 Add diazepam
Ketamine HCl Bird, Aquatic 3-8 IM PRN E 1503 Add medetomidine

Ketamine HCl Bird, Aquatic 2.5-5 IV PRN E 1503 Add xylazine
Ketamine HCl Canary 100-200 IM PRN G 1328
Ketamine HCl Cassowary 2.2 IV PRN E 1533 Add xylazine
Ketamine HCl Chicken 20-100 IM PRN G 1328
8/22/2005
Ketamine HCl Chicken 4-5 Parenteral PRN G 1718 Add butorphanol + medetomidine,
preanesthetic for isoflurane
Ketamine HCl Cockatiel 25 IM PRN E 243 Add xylazine
5:28 PM
Ketamine HCl Cockatoo, Palm 5 IM-SC PRN E 924 Sedative

Ketamine HCl Duck, Mallard 8.8 IM PRN B 764 Add medetomidine + midazolam, 33%
mortality
Ketamine HCl Duck, Pekin 20 IV Once B 718
Ketamine HCl Emu 3 NL PRN C 1392 Tranquilization
Page 285
Ketamine HCl Emu 2.2 IV PRN E 1533 Add xylazine

Ketamine HCl Falcon, Peregrine 30 IV PRN D 1401 Add diazepam, supplement at 5 mg/kg IV
PRN
Ketamine HCl Finch 100-200 IM PRN G 1328
Ketamine HCl Galliformes 3 Parenteral PRN G 1718 Add butorphanol + medetomidine,
preanesthetic for isoflurane
Ketamine HCl Goose 5-10 IM-IV PRN B 1577 Add medetomidine
Ketamine HCl Goose 20-50 IM PRN G 1328
Ketamine HCl Guinea Fowl 25 IM PRN B 553 Add xylazine
Ketamine HCl Hawk 25-30 IM PRN E 243 Add xylazine
Ketamine HCl Hawk 4-5 Parenteral PRN G 1718 Add butorphanol + medetomidine,
preanesthetic for isoflurane, improves quality
of anesthesia
Ketamine HCl Hawk, Broad-winged 30-40 IV PRN B 1092 Combine with diazepam
Ketamine HCl Heron 20 NL PRN G 1356
Ketamine HCl Ostrich 5 IV PRN B 555 Add xylazine + alphaxalone/alphadolone
Ketamine HCl Ostrich 2 IM PRN B 1628 Add medetomidine

Ketamine HCl Owl 10 IM-SC PRN E 924 Sedative
Ketamine HCl Pelican 7 IM PRN G 595
Ketamine HCl Pigeon 20 IM PRN B 779 Follow with propofol
Ketamine HCl Pigeon 5 IM PRN B 1588 Add medetomidine, usually moderate to
heavy sedation
Ketamine HCl Poultry 50 IM PRN E 4

Ketamine HCl Poultry 30 IM-SC PRN E 924 Sedative
Ketamine HCl Psittacine 3-7 IM PRN B 1577 Add medetomidine
285
286

Ketamine HCl Psittacine 2-5 IV PRN B 1577 Add medetomidine

Ketamine HCl Psittacine 10 NL PRN D 1401 Add diazepam, supplement at 5 mg/kg PRN
Ketamine HCl Psittacine 3-7 IM PRN E 649 Add medetomidine

Ketamine HCl Psittacine 2.5-7 IV PRN E 649 Add medetomidine
Ketamine HCl Psittacine 20 IM-SC PRN E 924 Sedative
Ketamine HCl Raptor 25-35 IM PRN B 1176 For laparoscopy

Ketamine HCl Raptor 2-4 IV PRN B 1577 Add medetomidine
8/22/2005
Ketamine HCl Raptor 3-5 IM PRN B 1577 Add medetomidine

Ketamine HCl Ratite 3-7 IM PRN E 4 Add medetomidine
Ketamine HCl Ratite 2-4 IV PRN E 243 Proceed with xylazine
5:28 PM
Ketamine HCl Ratite 3-20 NL PRN E 1386 May add diazepam or xylazine if desired
Ketamine HCl Rhea 6.6 IM PRN G 1628 Add butorphanol + medetomidine
Ketamine HCl Spoonbill 20 NL PRN G 1356
Ketamine HCl Stork 20 NL PRN G 1356
Ketamine HCl Swan 4 IV PRN G 1291 Add medetomidine, gas anesthesia premed
Page 286
Ketamine HCl Swan, Mute 12.5 IV PRN E 1190 Add xylazine

Ketamine HCl Vulture 10 IM PRN B 568 Add xylazine
Ketoconazole Amazon Parrot 30 PO BID B 68

Ketoconazole Amazon, Yellow-naped 12.5 PO BID G 740
Ketoconazole Avian 10-30 PO BID D 1330 Dissolve 50 mg tablet 0.2 ml HCl + 0.8 ml
water, mix with acid juice, lactulose,
methylcellulose
Ketoconazole Avian 10-30 PO BID D 1743 For systemic yeast
Ketoconazole Bird, Aquatic 25 PO BID E 1503 For candidiasis and aspergillosis therapy not
responding to nystatin
Ketoconazole Canary 0.2 g/kg soft food Feed QD D 1330
Ketoconazole Canary 0.2 g/L Drink QD E 695
Ketoconazole Ostrich 10 PO QD G 401
Ketoconazole Passerine, Small 1 g/L Drink NL E 1187
Ketoconazole Passerine, Small 0.2 g/kg food Feed Once E 1187
Ketoconazole Pigeon 30 PO BID A 68
Ketoconazole Pigeon 3 PO QD E 704 Tables crushed and water suspension
Ketoconazole Pigeon 3 Gavage QD E 1240 For resistant candidiasis, Mucor and
Penicillium
Ketoconazole Psittacine 25 PO BID E 763 For candidiasis or adjunct for aspergillosis
therapy, disguise taste in food
Ketoconazole Psittacine 10 PO BID E 1240 For resistant candidiasis, Mucor and

Penicillium
8/22/2005
Ketoconazole Raptor 15 PO BID E 1132

Ketoconazole Raptor 25 IM BID E 1240 For resistant candidiasis, Mucor and
Penicillium
Ketoconazole Raptor 60 PO BID E 1240 "
5:28 PM
Ketoconazole Raptor 25 PO BID E 1359

Ketoconazole Ratite 5-10 PO QD G 1309
Ketoconazole Swan 12.5 PO BID D 1330 Dissolve 50 mg tablet 0.2 ml HCl + 0.8 ml
water, mix with acid juice, lactulose,
methylcellulose
Page 287
Ketoprofen Anseriformes 1 IM QD D 1150 For pain relief or arthritis

Ketoprofen Avian 2 IM NL D 1240, 1533
Ketoprofen Avian 1-4 IM NL E 1167
Ketoprofen Duck 5 IM NL B 1339 Effective 30 to 70 minutes, given during
isoflurane anesthesia
Ketoprofen Pigeon 1 mg TD IM-SC QD-BID E 1240 Pain relief, arthritis, antiinflammatory
Ketoprofen Psittacine 2 IM NL E 1240 "
Ketoprofen Quail 2 PO NL B 1674
Lactulose Amazon Parrot 0..07 g TD PO BID-TID G 1309 For hepatic encephalopathy

Lactulose Avian 0.3 ml/kg PO NL E 1492 For liver disease
Lactulose Psittacine 200 PO BID-TID G 632 Neonate dosage
Lasalocid Chicken 75 Feed QD B 958 For coccidial prophylaxis

Lasalocid Galliformes 90-120 g/ton Feed QD C 705 For coccidial prophylaxis
Leuprolide Acetate Amazon, Yellow-naped 0.75-1 Parenteral q2-3w G 1033 Depot formulation
Leuprolide Acetate Avian 0.1 IM NL D 1475 For feather picking triggering by excessive
reproductive behavior
Leuprolide Acetate Avian 0.5-1 IM q2w E 1151 After egg binding
Leuprolide Acetate Avian 0.1-0.14 Parenteral NL E 1474 Treat chronic egg laying
Leuprolide Acetate Avian 0.052-0.156 IM NL E 1570 Use 30-day depot formulation for egg
chronic egg laying

Leuprolide Acetate Avian 0.75 IM q2w G 994 For birds 300 g or less
Leuprolide Acetate Avian 0.5 IM q2w G 994 For birds more than 300 g
287
288

Leuprolide Acetate Avian 0.75 IM q2w G 1278 Induce molt
Leuprolide Acetate Psittacine 0.1 IM QD D 1446 For sexually-triggered feather picking
Leuprolide Acetate Raptor 0.25 IM q2-3w E 1359 For cystic ovaries
Levamisole HCl Anseriformes 25-50 SC Once D 1150, 1190 Control nematodes

Levamisole HCl Avian 2 PO QD D 1470 For liver parasitic disease
Levamisole HCl Avian 2 IM-SC q2w E 111
Levamisole HCl Avian 10-20 PO q2w E 704

Levamisole HCl Avian 8 IM-SC r10d E 741 Not for debilitated birds or lories, use
8/22/2005
13.65% injectable
Levamisole HCl Avian 10-20 PO-SC q2w E 1434
Levamisole HCl Avian 5 IM-SC q2w E 1473
5:28 PM
Levamisole HCl Avian 0.8 g/L Drink QD E 1479 For roundworms, cecal worms and hair
worms
Levamisole HCl Avian 40-50 PO NL E 1492 For most worms
Levamisole HCl Crane 25 PO q2w E 1361 Chick dosage for intestinal strongyles, acarids
and capillarids
Page 288
Levamisole HCl Crane 40 PO q2w E 1361 For intestinal strongyles, ascarids and
capillarids
Levamisole HCl Finch 40-50 PO NL E 1650 For most worms except tapeworm,
particularly effective on acuaria in Australian
finch
Levamisole HCl Galliformes 40 PO Once E 1503
Levamisole HCl Galliformes 40 PO Once E 1526
Levamisole HCl Magpie 30 SC NL G 1609
Levamisole HCl Ostrich 30 PO NL B 526 Add resorantel
Levamisole HCl Parakeet, Australian 15 Gavage q10d G 1309 For intestinal nematodes, use injectable
Levamisole HCl Pheasant 25 SC NL G 678 Histomoniasis therapy
Levamisole HCl Pigeon 15 IM QD E 704
Levamisole HCl Pigeon 0.18 g/L Drink QD E 704
Levamisole HCl Pigeon 40 PO Once E 1503
Levamisole HCl Pigeon 40 PO Once E 1526
Levamisole HCl Pigeon 10-20 PO Once G 232 Repeat in 2 weeks if needed
Levamisole HCl Pigeon 40 PO Once G 260
Levamisole HCl Poultry 18-36 PO Once G 1332
Levamisole HCl Poultry 1.25-2.5 PO-SC NL E 111
Levamisole HCl Psittacine 20 IM r2w E 763 Emesis common
Levamisole HCl Psittacine 20-50 PO QD E 1240 Loft treatment for capillariasis and ascariasis,
follow up with parenteral therapy
Levamisole HCl Psittacine 2-5 IM-SC q10d E 1240 Immunostimulant, low therapeutic index
Levamisole HCl Quail 25 SC NL G 678 Histomoniasis therapy

Levamisole HCl Quail 20 SC NL G 678 Anthelmintic
Levamisole HCl Raptor 10-20 PO-SC QD E 1400 Narrow therapeutic margin
Levamisole HCl Raptor 15 PO-SC NL E 1463 Anthelmintic
8/22/2005
Levamisole HCl Raptor 2 SC q4-6d D 1612 Immune stimulant

Levamisole HCl Ratite 30 IM-PO QM G 1308 Begin at 1 month of age, juvenile dose for
Libyastrongylus douglassi
Levamisole HCl Ratite 30 IM-PO q3m G 1308 Adult dose for Libyastrongylus douglassi
5:28 PM
Levothyroxine Sodium Avian 20 ug/kg PO QD-BID E 111

Levothyroxine Sodium Avian 1 IM-PO NL E 924 For severe feather disorders and lipomas
Levothyroxine Sodium Avian 20-100 ug/kg PO BID E 1431 Monitor levels to avoid thyrotoxicosis
Page 289
Levothyroxine Sodium Avian 20 ug/kg PO QD-BID E 1473

Levothyroxine Sodium Avian 0.0008-0.0025 g/L Drink QD E 1492 For goiter and hypothyroidism
Levothyroxine Sodium Avian 0.02-0.04 PO QD G 58
Levothyroxine Sodium Avian 0.02 PO QD-BID G 88
Levothyroxine Sodium Budgerigar 0.004-0.008 g/L Drink QD D 1446 For lipomatous growth and xanthomas
Levothyroxine Sodium Budgerigar 0.003 g/L Drink QD G 1309 For hypothyroidism, stir water and offer for
15 minutes, repeat daily
Levothyroxine Sodium Psittacine 0.020-0.1 PO BID E 1240 For hypothyroidism
Levothyroxine Sodium Raptor 1 PO QD E 1160 To induce molting
Lidocaine Avian 2-3 SC NL B 1346 Local infiltration

Lidocaine Raptor 2 SC NL E 1400 Dilute to 0.4%, infuse locally, use with
caution in small birds
Lidocaine Raptor 10 SC NL E 1463 Dilute to 0.2% for large bird local analgesia
Lincomycin HCl Amazon Parrot 75 PO BID E 111, 1431

Lincomycin HCl Avian 50 PO BID E 1234 For bumblefoot
Lincomycin HCl Avian 0.2 g/L Drink QD E 1431 For infected foot lesions
Lincomycin HCl Avian 100 IM BID E 1431 For infected foot lesions
Lincomycin HCl Hawk 50 PO BID G 1110 Therapy prior to tendon surgical repair
Lincomycin HCl Pigeon 25-50 IM NL G 260
Lincomycin HCl Pigeon 35-50 PO QD G 590
Lincomycin HCl Poultry 2.2 mg/kg food Feed QD C 564
Lincomycin HCl Poultry 0.017 g/L Drink QD C 564

289
290

Lincomycin HCl Psittacine 100 IM BID E 1240 For Gram positive bumblefoot, dermatitis
and mycoplasmal respiratory infection.
Lincomycin HCl Raptor 110 PO QD E 741 For skin disease

Lincomycin HCl + Avian 50 PO QD E 565

Spectinomycin HCl
Lincomycin HCl + Chicken 50 PO QD B 1065

Spectinomycin HCl
8/22/2005
Lincomycin HCl + Falcon 30 IM TID E 1027 Broad spectrum for mycoplasma and
Spectinomycin HCl salmonella
Lincomycin HCl + Pigeon 50 PO QD F 1061
5:28 PM
Spectinomycin HCl
Lithium Carbonate Avian 6-25 NL BID E 1477 For avian behavior problems, mood stabilizer
and antipsychotic, no longer used in birds
Page 290
LL-E19020 Poultry 0.01-50 Feed QD G 564 Improves feed efficiency
Maduramicin Avian 7.5 PO QD E 1650 For Plasmodium

Maduramicin Chicken 5 Feed QD B 958 For coccidial prophylaxis
Magnesium Sulfate Anseriformes 500-1000 PO QD E 1240 Increase gut motility and aid passage of lead
Magnesium Sulfate Bird, Aquatic 500-1000 PO NL E 1503 Precipitates lead and cathartic
Magnesium Sulfate Budgerigar 53 IM PRN B 1084 Add chloral hydrate + pentobarbital sodium,
reduce dose 15 to 20% in debilitated birds
Magnesium Sulfate Canary 53 IM PRN B 1084 See above

Magnesium Sulfate Chicken 53 IM PRN B 1084 See above
Magnesium Sulfate Crow, Eastern 53 IM PRN B 1084 See above
Magnesium Sulfate Eagle, Golden 40.3 IM PRN B 1086 See above
Magnesium Sulfate Gull (Herring, laughing) 53 IM PRN B 1084 See above
Magnesium Sulfate Hawk, Marsh 32.4 IM PRN B 1086 See above
Magnesium Sulfate Ostrich 1.25-30 ml TD PO NL G 401
Magnesium Sulfate Pigeon 53 IM PRN B 1084 Add chloral hydrate + pentobarbital sodium,
Magnesium Sulfate Raptor 250-1000 PO QD E 1400 For oral heavy metal poisoning
Magnesium Sulfate Raptor 500-1000 PO QD E 1240 Increase gut motility and aid passage of lead
Malathion Avian 1 g/L Topical NL E 1479 Remove birds and treat environment for flea,
lice, mange and mite treatment and aid in tick
control
8/22/2005
Malathion Avian 1 g/L Dip NL E 1479 For flea, lice, mange and mite treatment and
aid in tick control
Malathion Raptor 5% mixture Topical q10d G 1411 For chewing lice
5:29 PM
Mannitol Avian 0.5 IV QD E 111 Give slowly
Marbofloxacin Buzzard, Common 2 IV BID A 778, 1428

Page 291
Marbofloxacin Buzzard, Common 10 PO QD A 979

Marbofloxacin Chicken 2 PO QD A 765
Marbofloxacin Raptor 10 IM-PO QD E 1433
Marbofloxacin Raptor 15-20 IM-PO QD G 1068 For sinusitis
Mebendazole Anseriformes 5-15 PO QD D 1,150,111 Control Syngamus

Mebendazole Avian 25 PO QD E 1492, 1650 For all intestinal worms
Mebendazole Canary 10 PO BID G 57 Avoid during breeding season
Mebendazole Fowl, Domestic 0.06 g/kg food Feed QD E 1051
Mebendazole Pigeon 5-6 PO QD G 260
Mebendazole Psittacine 25 PO BID E 111, 1473
Mebendazole Raptor 25 PO BID E 111
Meclofenamic Acid Avian 2.2 PO QD D 1533

Meclofenamic Acid Avian 2.2 PO QD G 201, 1320
Meclofenamic Acid Avian 2.2 PO QD E 1573
Meclofenamic Acid Bird, Aquatic 2.2 PO QD E 1503
Medetomidine HCl Amazon, Yellow-crowned 2 IM PRN B 1629 Sedation produced not reliable, reverse with
atipamezole
Medetomidine HCl Anseriformes 0.05 IV PRN D 1503 Add ketamine + midazolam
Medetomidine HCl Anseriformes 0.6-0.85 IM PRN E 1231 Add ketamine
Medetomidine HCl Anseriformes 0.06 Parenteral PRN G 1718 Add butorphanol + ketamine, preanesthetic
for isoflurane
Medetomidine HCl Avian 0.1 IM NL G 704, 1320

Medetomidine HCl Bird, Aquatic 0.025-0.075 IV PRN E 1503 Add ketamine, reverse with atipamezole
Medetomidine HCl Bird, Aquatic 0.05-0.1 IM PRN E 1503 Add ketamine, reverse with atipamezole
291
292

Medetomidine HCl Cassowary, Double-wattled 0.26-0.31 IM PRN B 1229 For restraint of captive birds
Medetomidine HCl Chicken 0.1 IM PRN E 1573 Sedation
Medetomidine HCl Chicken 0.06-0.08 Parenteral PRN G 1718 Add butorphanol + ketamine, preanesthetic
for isoflurane
Medetomidine HCl Duck, Mallard 0.44 IM PRN B 764 Add ketamine + midazolam, 33% mortality
Medetomidine HCl Goose 0.1-0.2 IM-IV PRN B 1577 Add ketamine

Medetomidine HCl Hawk 0.06-0.08 Parenteral PRN G 1718 Add butorphanol + ketamine
Medetomidine HCl Ostrich 0.08 IM PRN B 1628 Add ketamine
8/22/2005
Medetomidine HCl Ostrich 0.1 IM PRN E 1573 Sedation

Medetomidine HCl Pigeon 0..08 IM PRN B 1588 Add ketamine, usually moderate to heavy
sedation
5:29 PM
Medetomidine HCl Pigeon 0.2 IM PRN B 1588 Variable light sedation

Medetomidine HCl Psittacine 0.075-0.15 IM PRN B 1577 Add ketamine
Medetomidine HCl Psittacine 0.05-0.1 IV PRN B 1577 Add ketamine
Medetomidine HCl Psittacine 0.06-0.085 IM PRN E 1240 Add ketamine
Medetomidine HCl Raptor 0.1-0.3 IM NL E 1400 Can be reversed, combined with ketamine for
Page 292
anesthesia
Medetomidine HCl Raptor 0.025-0.075 IV PRN B 1577 Add ketamine
Medetomidine HCl Raptor 0.05-0.1 IM PRN B 1577 Add ketamine
Medetomidine HCl Raptor 0.15-0.35 IM PRN E 1240 Add ketamine
Medetomidine HCl Raptor 0.2 NL PRN E 1433 Add ketamine, reverse with atipamezole
Medetomidine HCl Ratite 0.05-0.15 IM PRN E 4 Add ketamine
Medetomidine HCl Rhea 0.73 IM PRN G 1628 Add butorphanol + ketamine
Medetomidine HCl Swan 0.15 IV PRN G 1291 Add ketamine, gas anesthesia premed
Medroxyprogesterone Lower dose for larger birds. Side effects:

Acetate lethargy, inappetance, polydipsia, fatty liver
Medroxyprogesterone Avian 25 IM-SC QD E 111 For 700 g bird

Acetate
Medroxyprogesterone Avian 40 IM-SC QD E 111 For 150 to 300 g bird
Acetate
Medroxyprogesterone Avian 50 IM-SC QD E 111 For <150 g bird
Acetate
Medroxyprogesterone Avian 30 IM-SC QD E 111 For 300 to 700 g bird
Acetate
Medroxyprogesterone Avian 5-25 IM-SC QD E 111
Acetate
Medroxyprogesterone Avian 5-10 IM-SC NL E 704 For persistent egg laying
Acetate
Medroxyprogesterone Avian 2-10 PO-SC QW E 924 Repeat after 4 months for ovulation
Acetate suppression
Medroxyprogesterone Psittacine 25-50 IM-SC q4-6w E 1240 Lower dose for larger birds. Side effects:
8/22/2005
Acetate lethargy, inappetance, polydipsia, fatty liver
Mefloquine HCl Passerine 30 PO PRN E 1438 Give BID on day 1, give daily on days 2 and
5:29 PM
3 and once per week
Megestrol Acetate Avian 2.5 NL QD E 1431 Then continue q3-4d for feather picking with
hormonal etiology
Page 293
Megestrol Acetate Cockatoo, Rose-breasted 0.2 g/L Drink NL G 1609 For self-mutilation
Megestrol Acetate Cockatoo, Rose-breasted 0.2 g/kg food Feed Once G 1609 For self-mutilation
Meloxicam Avian 0.1 IM-PO QD E 1167, 1431

Meloxicam Avian 0.1-0.2 IM QD E 1431 Long course well tolerated
Meloxicam Avian 0.1 - 1.0 PO QD G 1341
Meloxicam Avian 0.1 NL QD G 1484
Meloxicam Avian 0.1 PO QD G 1671, 1675
Meloxicam Avian 0.1 PO QD E 1431 Long course well tolerated
Meloxicam Crane 0.5 PO BID G 1341
Meloxicam Raptor 0.1-0.2 IM-PO QD E 1400 For arthritis and other painful conditions
Meloxicam Raptor 0.1 IM-PO QD E 1359, 1433
Meperidine HCl Raptor 3-5 NL QID G 1481

Meperidine HCl Raptor 3-5 NL NL G 1483, 1484
Metformin (glucophage) Avian 100 mg/L water Drink QD G T. Lightfoot, 2005 Hyperglycemia
Methocarbamol Avian 50 IV NL G 201
Methohexital Sodium Chicken 5-10 IV PRN G 497

Methohexital Sodium Dove 5 g/L bait Feed Once G 1763 Corn is usual bait
Methohexital Sodium Duck 5-10 IV PRN G 498

Methohexital Sodium Goose 5-10 IV PRN G 498
Methohexital Sodium Poultry 4-8 IV PRN G 496
293
294

Methoprene Raptor 0.02 g/L Topical NL E 1068 Add permethrin + piperonyl butoxide for
ectoparasites
Methylprednisolone Avian 0.5-1 IA-IM NL D 1533

Acetate
Methylprednisolone Acetate Bird, Aquatic 0.5-1 IA-IM NL E 1503
Methylprednisolone Acetate Raptor 5 IM QW E 1463

8/22/2005
Methylprednisolone Avian 0.5-1 IM-IV NL D 1554 For shock

5:29 PM
Sodium Succinate
Metoclopramide HCl Avian 0.3 IM-IV-PO NL E 111

Metoclopramide HCl Avian 0.5 IM BID-TID E 1151 To improve motility, this dosage not for
macaws
Page 294
Metoclopramide HCl Avian 0.5 IM-IV-PO NL E 1473

Metoclopramide HCl Avian 0.5 Parenteral NL E 1650 Increase gastric motility
Metoclopramide HCl Hawk, Red-tailed 0.5 IM NL G 1626 Supportive therapy post-trauma
Metoclopramide HCl Lorikeet, Rainbow 0.5 SC BID G 1620 For vomiting
Metoclopramide HCl Macaw 0.1 IM-PO NL E 1151 To improve motility- Use low dose
Metoclopramide HCl Ostrich 0.1 IV NL G 1255 Add psyllium for proventricular obstruction
Metoclopramide HCl Psittacine 0.5 IM-IV-PO TID E 1240 Antiemetic and for gut stasis
Metoclopramide HCl Psittacine 0.5 NL BID G 1263 For ileus
Metoclopramide HCl Raptor 0.5-2 IM-SC q4-6h E 1359 For gastrointestinal stasis
Metomidate HCl Avian 10 IM PRN E 1130

Metomidate HCl Duck, Mallard 17 PO PRN B 1095
Metomidate HCl Eagle, African Hawk 15.2 IM PRN G 1611
Metomidate HCl Eagle, Tawny 9.6 IM PRN G 1611
Metomidate HCl Hawk, African Harrier 14.4-16 IM PRN G 1611
Metomidate HCl Ostrich 15-20 IM PRN G 481 With or without azaperone for captive animal
Metomidate HCl Owl, Barn 10.2 IM PRN G 1611

Metomidate HCl Raptor 10 IM PRN E 1463 Smaller dosages for vultures
Metomidate HCl Raptor 5 IM PRN E 1463 For sedation
Metomidate HCl Turkey 17 g/L whole corn Feed Once E 1386 Safer than chloralose
Metronidazole Avian 25 PO BID D 1221 For clostridiosis
Metronidazole Avian 25-50 PO QD E 704, 924

Metronidazole Avian 0.2 g/L Drink NL E 1180
Metronidazole Avian 50 PO NL E 1434
Metronidazole Avian 5 IM BID E 1434
8/22/2005
Metronidazole Avian 10-30 PO BID E 1650 For anaerobic infections

Metronidazole Avian 10 IM QD E 1650 For anaerobic infections
Metronidazole Avian 50 PO QD G 55
Metronidazole Avian 20 PO-SC QD C 705 For trichomoniasis
5:29 PM
Metronidazole Avian 10-30 PO BID D 1470 For liver parasitic disease

Metronidazole Avian 10 IM QD D 1470 For liver parasitic disease
Metronidazole Canary 0.1 g/kg food Feed Once E 1187
Metronidazole Chicken 30 PO BID A 795
Page 295
Metronidazole Falcon 50 PO QD E 1027 For trichomoniasis

Metronidazole Ostrich 1.25 g/L Drink QD E 627 Antihistomoniasis
Metronidazole Passerine 0.1 g/L Drink QD E 1437 Add drug to food at the same time
Metronidazole Passerine 0.1 g/kg soft food Feed QD E 1437 Add drug to drink at the same time
Metronidazole Pigeon 200 PO QD E 704
Metronidazole Pigeon 200-250 PO QD G 260
Metronidazole Poultry 20 Drink QD C 705
Metronidazole Poultry 110 PO BID G 585
Metronidazole Psittacine 10-30 PO BID E 111, 1473
Metronidazole Psittacine 25 PO BID E 763
Metronidazole Raptor 30-50 PO QD E 1359 For trichomoniasis, may increase dosage to
100 mg/kg
Metronidazole Raptor 50 PO QD E 1400, 1433 For trichomoniasis
Metronidazole Raptor 100 PO NL E 1463 For trichomoniasis
Metronidazole Raptor 50 PO QD G 61, 234
Metronidazole Raptor 10-40 PO QD G 94 Juvenile dosage
Metronidazole Raptor 100 PO QD G 1068
Metronidazole Raptor 30-65 PO QD G 1409 For trichomoniasis
Metronidazole Ratite 20-25 PO BID G 1308 For anaerobic infections
Metronidazole Stork, Saddle-billed 42 PO BID G 1645 Add amikacin + enrofloxacin
Miconazole Nitrate Amazon, Red Lored 2 mg Nebulize QD G 700 Add acetylcysteine

Miconazole Nitrate Avian 20 IV TID D 1330
Miconazole Nitrate Avian 10-20 IM QD E 565
Miconazole Nitrate Avian 20 IM NL E 924 For candidiasis, Aspergillus, Mucor and

Penicillium
295
296

Miconazole Nitrate Avian 40 IV NL E 924 For candidiasis, Aspergillus, Mucor and
Penicillium
Miconazole Nitrate Falcon cream Topical BID G 1589
Miconazole Nitrate Psittacine 20 IM-IV QD E 704
Miconazole Nitrate Raptor 10 IM-IV QD E 704
Midazolam HCl Anseriformes 2 IV PRN D 1503, 1533 Add ketamine + medetomidine

Midazolam HCl Anseriformes 1-2 IV PRN E 1503 "

Midazolam HCl Avian 1-2 IM-IV NL E 1573 "
8/22/2005
Midazolam HCl Avian 1 IM NL G 201

Midazolam HCl Avian 1-2 IM-IV NL G 1320 Use with an analgesic for pain control
Midazolam HCl Avian 4 IM PRN E 704 Add ketamine
5:29 PM
Midazolam HCl Avian 0.2 IM PRN E 1181, 1231 Add ketamine, smooth induction and
recovery
Midazolam HCl Duck, Mallard 4 IM Once G 1468 Pre-gas anesthesia
Midazolam HCl Emu 0.4 IV PRN G 418
Midazolam HCl Ostrich 0.15 IV PRN G 418
Page 296
Midazolam HCl Pheasant, Ring-necked 1 IM PRN G 1644 Anesthesia premed

Midazolam HCl Pigeon 0.5 IM PRN B 1588 Add medetomidine, usually moderate to
heavy sedation
Midazolam HCl Pigeon 2 IM PRN G 1644 Add glycopyrrolate for anesthesia premed,
reverse with flumazenil
Midazolam HCl Psittacine 0.2 IM-SC PRN E 1240 Use in combination with ketamine
Midazolam HCl Raptor 0.5-1 IM-IV TID E 1240, 1400 Control seizures
Midazolam HCl Swan 0.1-1 NL PRN G 1291 May add butorphanol, premed for gas
anesthesia, lower dosage if add butorphanol
Midazolam HCl Turkey 0.1-1 NL PRN G 1291 "
Milbemycin Oxime Galliformes 2 PO QM B 588

Milbemycin Oxime Galliformes 2 PO NL E 1492, 1650 For Heterakis, Capillaria and ascarids
Milk Thistle Amazon Parrot 2 drops mixture TD PO BID G 1488 Mixture is 5 drops extract per 7.5 ml
lactulose, useful for treating birds on all seed
diet
Mineral Oil Avian 5 ml/kg Gavage Once E 1309, 1554 To flush GI - laxative
Minocycline HCl Budgerigar 5.5 g/kg seed Feed QD A 731 Hulled medicated millet
Minocycline HCl Hawk, Red-shouldered 5 PO BID G 1179 Add levamisole + Staphylococcus toxoid for
bumblefoot
Miporamicin Poultry 0.1 g/kg Feed QD G 564

8/22/2005
Monensin Sodium Chicken 0.1 g/kg Feed QD B 869 Preventive for coccidiosis
Monensin Sodium Chicken 100 Feed QD B 958 For coccidial prophylaxis
Monensin Sodium Chicken 100-120 g/ton Feed QD C 705 For coccidiosis
Monensin Sodium Crane 0.099 g/kg food Feed Once E 111
5:29 PM
Monensin Sodium Galliformes 0.099 g/kg food Feed QD E 1473

Monensin Sodium Pigeon 1-1.2 g/kg feed Feed Once E 1492 For coccidiosis
Monensin Sodium Pigeon 1-1.2 g/kg food Feed QD E 1650 For coccidia
Monensin Sodium Turkey 90-100 g/ton Feed QD C 705 For coccidiosis
Page 297
Morphine Sulfate Galliformes 2.5-3 IM-SC NL E 111, 1473
Moxidectin Avian 0.2-0.8 NL Once D 1221 For capillariasis

Moxidectin Cardinal, Red-crested 0.2 PO NL G 1585 For capillariasis
Moxidectin Falcon 1 PO QW G 1068 For Serratospiculum , Capillaria , Physlaoptera and
Acanthocephalae
Moxidectin Finch 2 PO NL E 1479 For lice, mites and nematodes
Moxidectin Penguin 0.2 PO NL E 1478 For nematodes
Moxidectin Pigeon 0.25 mg TD PO NL D 1479 For lice, mites and nematodes
Moxidectin Psittacine 0.2 Gavage Once D 1479 For lice, mites and nematodes
Moxidectin Raptor 0.2 PO QD E 1359 For capillariasis
Moxidectin Sparrowhawk 0.2 SC NL G 1585 For nematodiasis
Mullein Avian 10 drops/kg PO TID E 1205 Respiratory, wound support
Mycobacterium Vaccae Crane, Whooping 0.05 ml TD ID q2m G 207

Vaccine
Nalbuphine HCl Guinea Fowl 1-2 IM q3h G 252
Naloxone HCl Avian 0.05-0.25 IM-IV PRN E 1573

Naloxone HCl Psittacine 0.05-0.25 IM-IV NL G 1320 Use slow IV
Naloxone HCl Ratite 0.05-0.067 NL PRN G 418
Naltrexone HCl Avian 1.5 Drink NL E 704 Behavior modification, feather picking
Naltrexone HCl Ostrich 300 mg TD IV PRN B 521 Reverse carfentanil
297
298

Naltrexone HCl Psittacine 1.5 PO BID E 1240 Prevent self-mutilation
Nandrolone Psittacine 0.4 IM-SC q3w E 1240 For chronic and debilitating disease, may
cause liver disease
Nandrolone Raptor 0.4 IM-SC q3w E 1240 "
Narasin Chicken 70 Feed QD B 958 For coccidial prophylaxis

Narasin Chicken 60-80 mg/kg food Feed QD E 564 Add nicarbazin, 5-day slaughter withdrawal,
prophylactic
8/22/2005
Neomycin Sulfate Avian 1.25 g/L Drink NL E 111

Neomycin Sulfate Avian 10 PO QD E 565
5:29 PM
Neomycin Sulfate Avian 20 PO NL E 924 Gram negative, poor absorption

Neomycin Sulfate Chicken 11 Drink BID C 1307 For bacterial enteritis
Neomycin Sulfate Chicken .077-.154 g/kg food Feed QD C 1307 For bacterial enteritis
Neomycin Sulfate Duck .077-.154 g/kg food Feed QD C 1307 For bacterial enteritis
Neomycin Sulfate Duck 11 Drink BID G 1307 For bacterial enteritis
Page 298
Neomycin Sulfate Passerine 0.2 g/kg soft food Feed QD E 1437 Add drug to drink at the same time
Neomycin Sulfate Passerine 0.2 g/L Drink QD E 1437 Add drug to food at the same time
Neomycin Sulfate Poultry 0.035-0.08 g/L Drink QD C 564 Prophylactic
Neomycin Sulfate Poultry 38.5-154 mg/kg food Feed QD C 564
Neomycin Sulfate Poultry 11 PO QD C 564
Neomycin Sulfate Raptor 15 PO NL E 1463 For bacterial infections
Netobimin Avian 0.035-0.08 g/L Drink QD E 1492 For tapeworms, ascarids and Heterakis
Netobimin Bird, Aquatic 0.35 g/L Drink QD E 1503
Netobimin Raptor 20 PO QD B 1568
Nicarbazin Chicken 20-50 mg/kg food Feed QD E 564 Add narasin, 5-day slaughter withdrawal,
prophylactic
Niclosamide Avian 50 PO q2w E 111

Niclosamide Avian 150-250 PO NL G 57
Niclosamide Avian 5 g/kg food Feed QD G 57
Niclosamide Crane 250 NL q2w G 596
Niclosamide Falcon 200 PO Once E 1027 For tapeworms
Niclosamide Finch 500 Feed QW E 111
Niclosamide Ostrich 100 PO q6w G 401
Niclosamide Ostrich 50 PO NL G 481
Niclosamide Pelican, Brown 103-160 PO Once B 1089
Niclosamide Pigeon 75 PO NL G 57
Niclosamide Raptor 156 PO Once D 1612 For cestodiasis

Niclosamide Raptor 125 PO NL E 1068 For cestodes
Nifursol Poultry 77 mg/kg food Feed QD C 564 Prophylactic

8/22/2005
Nifursol Turkey 75 mg/kg food Feed QD E 564 Nutritional use, 5-day slaughter withdrawal
Nifursol Turkey 50 g/ton Feed QD C 705 For histomoniasis

5:29 PM
Nithiamide Raptor 40 PO NL E 1463 For trichomoniasis
Nitrofurazone Avian 1.25 ml/L Drink QD E 741 For coccidial infections

Nitrofurazone Chicken 55 mg/kg food Feed QD E 564 5-day slaughter withdrawal, prophylactic
Page 299
Nitrofurazone Lorikeet 0.625 cc/L Drink NL E 111 Dosage based on 9.2% powder
Nitrofurazone Poultry 55 mg/kg food Feed QD C 564
Nitrofurazone Psittacine 1.25 cc/L Drink NL E 111 Dosage based on 9.2% powder
Nitromide Chicken 250 mg/kg food Feed QD E 564 Add sulfanitran + roxarsone, 5-day slaughter
withdrawal
Nitroxinil Galliformes 24 Drink QD C 706 For gapeworms
Nordihydroquaiaretic Avian 2 drops/kg PO BID E 1205 Use with caution in egg layers or w/ hepatic
disease
Norfloxacin Chicken 10 PO BID A 789

Norfloxacin Chicken 8 PO QD A 830
Norfloxacin Chicken 20-40 Drink NL A 840 For Hemophilus paragallinarum infection.
Norfloxacin Goose 10 PO BID A 789
Norfloxacin Ostrich 30 Drink QD G 562
Norfloxacin Poultry 8 PO QD G 564
Norfloxacin Turkey 10 PO QID A 789
Norfloxacin Turkey 10 SC QD A 1020
Nortriptyline HCl Psittacine 0.016 g/L Drink NL E 111 Control feather picking
Nosiheptide Chicken 5-10 mg/kg Feed QD G 564 Improves feed efficiency

Novobiocin Sodium Anseriformes 385 mg/kg food Feed Once G 597

299
300

Novobiocin Sodium Duck, Pekin 0.3 g/kg food Feed Once B 984 Prophylaxis for Pasteurella multocida in
ducklings.
Nystatin Anseriformes 300 KIU/kg PO BID D 1150 For candidiasis

Nystatin Avian 200 KIU/kg Feed QD E 704 Soft food
Nystatin Avian 0.05 g/kg food PO NL E 924 For candidiasis
Nystatin Avian 300 KIU/kg PO BID E 1221 For candidiasis

Nystatin Avian 200-300 KIU/kg PO BID G 1373 For candidiasis
8/22/2005
Nystatin Avian 100 KIU/L Drink QD G 1744 For candidiasis

Nystatin Finch 333 KIU/kg PO QD E 1572 For candidiasis
Nystatin Hummingbird 100 KIU/ml Topical q4-6h G 599 For mouth lesions
Nystatin Hummingbird 25 KIU/L Nectar Drink QD G 599
5:29 PM
Nystatin Ostrich 2500 KIU/kg food Feed Once G 283

Nystatin Ostrich 12.5 KIU/kg PO QD G 401
Nystatin Ostrich 0.24 g/kg feed Feed QD G 1254 For candidiasis
Nystatin Ostrich 20-50 KIU/kg PO QD G 1254
Page 300
Nystatin Passerine 100 KIU/L Drink QD D 1330 Add to food also, upper GI Candidiasis
Nystatin Pigeon 20-100 KIU PO QD E 704
Nystatin Pigeon 100-150 KIU/kg PO BID G 590
Nystatin Poultry 110 mg/kg food Feed QD C 564 Half dosage is prophylactic
Nystatin Psittacine 300 KIU/kg PO-Topical BID-TID D 1330 Upper GI candidiasis
Nystatin Psittacine 333 KIU/kg PO TID E 763 For candidiasis, use lesser dosage to diet for
neonates on antibiotic therapy
Nystatin Raptor 100 KIU/kg PO TID D 1612
Nystatin Raptor 1 KIU/kg PO BID E 1132
Nystatin Raptor 20 KIU/kg PO BID E 1188
Nystatin Ratite 300 KIU/kg PO NL G 418
Nystatin Ratite 100 KIU TD PO TID G 594
Nystatin Turkey 0.055-0.11 g/kg food Feed QD C 1307
Oleandomycin Phosphate Avian 1.17 mg/kcal PO QD E 1180
Oleandomycin Phosphate Avian 0.58 mg/kcal IM QD E 1180

Oleandomycin Phosphate Pigeon 25 IM QD E 565
Oleandomycin Phosphate Pigeon 50 PO QD E 565
Ormetoprim + Chicken 0.2 g/kg food Feed QD E 564 5-day slaughter withdrawal, prophylactic
Sulfadimethoxine
Ormetoprim + Crane 0.41 g/kg food Feed QD E 1361 For coccidiosis
Sulfadimethoxine
Ormetoprim + Duck 0.22 g/kg Feed Once B 825 For Pasteurella multocida in ducklings
Sulfadimethoxine
Ormetoprim + Duck 0.2-0.8 g/kg food Feed Once B 860 For riemerellosis and colibacillosis
8/22/2005
Sulfadimethoxine
Ormetoprim + Poultry 0.3-0.5 g/L Drink QD G 585
Sulfadimethoxine
Ormetoprim + Turkey 0.44 g/kg Feed Once B 846 Prophylaxis for Pasteurella multocida
5:29 PM
Sulfadimethoxine
Ormetoprim + Turkey 0.1 g/kg food Feed QD E 564 5-day slaughter withdrawal, prophylactic
Sulfadimethoxine
Page 301
Oxacillin Sodium Psittacine 100 PO TID D 1446 For staphylococcal dermatitis
Oxfendazole Avian 10 NL q2w D 1221 For capillariasis

Oxfendazole Avian 40 PO QD D 1470 For liver parasitic disease
Oxfendazole Avian 4 PO QD D 1479 For most intestinal worms including
tapeworms
Oxfendazole Avian 0.1-0.2 g/L Drink QD D 1479 For most intestinal worms including
tapeworms
Oxfendazole Avian 10 PO QD E 1650 For most intestinal worms
Oxfendazole Avian 0.1-0.2 g/L Drink QD E 1650 For most intestinal worms
Oxfendazole Ostrich 5 PO q3w G 401 Begin at age 4 months, alternate therapeutic
agent
Oxfendazole Pigeon 10-40 PO Once G 590
Oxfendazole Raptor 10 PO QW G 1068
Oxytetracycline Amazon Parrot 22-58 IM QD-BID A 266

Oxytetracycline Anseriformes 2.5 g/L Drink QD E 1240 For chlamydophilosis
Oxytetracycline Anseriformes 50 mg TD PO QD E 1240
Oxytetracycline Avian 5000 mg/kg Feed QD E 704 Add citric acid, therapeutic dosage
Oxytetracycline Avian 50-100 IM QD E 1431
Oxytetracycline Avian 50 IM QD-BID E 1492
Oxytetracycline Avian 100 PO QD-BID E 1492
Oxytetracycline Bird, Aquatic 100 SC QD E 1503 For respiratory infections
Oxytetracycline Budgerigar 2 g/L Nebulize q4-6h A 876 For respiratory disease
Oxytetracycline Chicken 2.5 g/L Drink NL A 802 Add oxytetracycline feed also
Oxytetracycline Ostrich 10 IM QD G 401 Double dosage for birds below 5 kg
Oxytetracycline Owl 16 IM QD A 55
301
302

Oxytetracycline Pheasant 43 IM QD A 55
Oxytetracycline Pigeon 50 IM-SC QD A 1067
Oxytetracycline Pigeon 0.133-0.444 g/L Drink QD E 704
Oxytetracycline Pigeon 100 IM q2d E 704
Oxytetracycline Pigeon 20 IM q2d E 1240 Add tetracycline for birds over 700 g
Oxytetracycline Pigeon 80 IM q2d E 1240 Add tetracycline for birds under 400 g
Oxytetracycline Poultry 0.0265-0.106 g/L Drink QD C 564
Oxytetracycline Poultry 6.25-200 mg TD PO QD C 564

Oxytetracycline Poultry 110-220 mg/kg food Feed QD C 564 Add neomycin
8/22/2005
Oxytetracycline Poultry 0.06-0.25 g/L Drink QD C 705

Oxytetracycline Psittacine 58 IM QD A 55
Oxytetracycline Psittacine 50 IM QD E 1240
5:33 PM
Oxytetracycline Psittacine 50-100 SC q2-3d E 1365 For chlamydophilosis

Oxytetracycline Raptor 25-50 IM-PO TD E 1240 IM injection may cause muscle necrosis
Oxytetracycline Turkey 2.5 g/L Drink NL A 802 Add oxytetracycline feed also
Oxytetracycline Turkey 2500 ppm Feed Once A 802 Add oxytetracycline drinking water also
Oxytetracycline Turkey 220 mg/kg food Feed QD E 564 3-day slaughter withdrawal, prophylactic
Page 302
Oxytetracycline Amazon Parrot 60 IM QD A 847

Amphoteric
Oxytetracycline Amphoteric Amazon, Blue-fronted 75 SC q3d E 703 For chlamydophilosis
Oxytetracycline Amphoteric Anseriformes 200 IM QD D 1150 For pasteurellosis and other bacteria
Oxytetracycline Amphoteric Avian 50 SC q3-5d E 1648 For respiratory infections, may cause muscle
necrosis
Oxytetracycline Amphoteric Bird, Aquatic 50 SC q3-5d E 1503 For respiratory infections
Oxytetracycline Amphoteric Cockatoo, Goffin 50-100 IM-SC q3d A 380
Oxytetracycline Amphoteric Macaw, Blue and Gold 50-75 SC q2-3d E 1170 Causes irritation at injection site
Oxytetracycline Amphoteric Ostrich 20 IM q3d G 401 Double dosage for birds below 5 kg
Oxytetracycline Amphoteric Psittacine 50-100 IM-SC q2-3d E 565
Oxytetracycline Amphoteric Raptor 50-200 IM q3-5d E 1240 For pasteurellosis
Oxytetracycline Amphoteric Turkey 150 SC q3d A 727 Long-lasting formulation
Oxytocin Anseriformes 3-5 IU/kg IM NL D 1150 Egg binding

Oxytocin Avian 0.5-1 IU TD IM NL E 924 Use with calcium and vitamin A for egg
expulsion
Oxytocin Avian 5 U/kg IV-SC Once E 1151 To help with egg expulsion, add calcium,
8/22/2005
fluids and heat

Oxytocin Avian 2 IU/kg NL NL E 1431 For egg binding, give calcium borogluconate
also
Oxytocin Ostrich 5 IU TD IV Once B 1257 Give 2 to 4 minutes before semen collection
5:33 PM
Paromomycin Sulfate Avian 100 PO BID E 1474 For neonate with cryptosporidiosis
Page 303
Penetran Avian Topical NL G 1486 For rashes, ulceration, local irritation, trauma,
bites, burns, etc.
Penetran Avian 2.5 ml/L spray Topical NL G 1103 For picking or itching
Penicillamine Anseriformes 55 PO BID D 1150 For heavy metal poisoning

Penicillamine Avian 55 PO BID D 1221 For lead or zinc toxicosis, may use in
conjunction with edetate calcium disodium
Penicillamine Avian 52 PO QD F 1236 For copper toxicosis

Penicillamine Avian 55 PO BID G 87 Repeat after 3 to 5 days
Penicillamine Psittacine 50-55 PO BID E 1240 Chelation agent for copper, zinc, mercury
and lead
Penicillamine Raptor 55 PO BID E 1240 For heavy metal poisoning
Penicillin Anseriformes 50 KIU/kg Parenteral NL G 597

Penicillin Poultry 44 KIU/kg PO QD C 564 Add streptomycin
Penicillin Poultry 55-110 mg/kg food Feed QD C 564 Prophylactic
Penicillin Poultry 375 KIU/L Drink QD C 564
Penicillin Poultry 110 mg/kg food Feed QD C 564
Penicillin Poultry 2.65 mg/kg food Feed QD E 564 Add streptomycin, nutritional use, no
slaughter withdrawal
Penicillin Raptor <100 KIU/kg IM-IV NL E 1463 Use crystalline formulation for bacterial
infections
Penicillin G Benzathine Rhea 100 KIU TD SC QD G 582 Add tylosin

Penicillin G Benzathine Turkey 100 IM QD A 385 Add penicillin G procaine for Pasteurella
multocida
303
304

Penicillin G Potassium Avian 66-133 KIU/kg IM NL F 1209

Penicillin G Potassium Falcon, Lanner 20 KIU/kg IM QID B 1175 Post-surgical treatment of bumblefoot
Penicillin G Procaine Galliformes 100 IM q2d E 111, 1473
Penicillin G Procaine Turkey 100 IM Once A 385 Loading dose, add penicillin G with procaine
benzathine for Pasteurella multocida
Pentobarbital + Chloral Avian 160-180 IM PRN F 1209 Dosage base on combined mg of

Hydrate + Magnesium pentobarbital/chloral hydrate/magnesium
8/22/2005
Sulfat e sulfate
5:33 PM
Pentobarbital Sodium Avian 5 IM PRN E 1130

Pentobarbital Sodium Avian 50 IM PRN F 1209
Pentobarbital Sodium Budgerigar 24 IM PRN B 1084 Add chloral hydrate + magnesium sulfate,
Page 304
Pentobarbital Sodium Canary 24 IM PRN B 1084 See above

Pentobarbital Sodium Chicken 16.2 IM PRN B 1080 Add thiopental sodium
Pentobarbital Sodium Cockatoo, Major Mitchell's 100 mg TD IV NL G 1590
Pentobarbital Sodium Cowbird 100-150 g/kg food Feed Once B 1094
Pentobarbital Sodium Crane, European 24 IM PRN B 1084 Add chloral hydrate + magnesium sulfate,
Pentobarbital Sodium Duck, Mallard 22 PO PRN B 1095

Pentobarbital Sodium Duck, Northern Pintail 390 IV Once B 1593 Precede with ketamine by 15 minutes
Pentobarbital Sodium Eagle, Golden 18.2 IM PRN B 1086 Add chloral hydrate + magnesium sulfate,
reduce dose 15 to 20% in debilitated birds,
fledgling
Pentobarbital Sodium Emu 13.3 IV PRN G 283 Premedicate with diazepam
Pentobarbital Sodium Galliformes 50-100 PO PRN E 1130 Use tablets
Pentobarbital Sodium Goose 50-100 PO PRN E 1130 Use tablets
Pentobarbital Sodium Gull, California 24 IM PRN B 1084 Add chloral hydrate + magnesium sulfate,
Pentobarbital Sodium Hawk 14.7 IM PRN B 1086 "

Pentobarbital Sodium Penguin 33 NL Once G 595
Pentobarbital Sodium Pigeon 24 IM PRN B 1084 Add chloral hydrate + magnesium sulfate,
Pentobarbital Sodium Quail, Japanese 25-50 g/kg food Feed Once B 1094
Pentobarbital Sodium Raptor < 20 PO PRN E 1463 For sedation

Pentobarbital Sodium Raptor 30 IM-IV PRN E 1463 Not usually recommended
Pentobarbital Sodium Skua, McCormick's 47 IM-IV PRN B 1075
Pentobarbital Sodium Swan, Mute 25 mg TD IV PRN G 1074 Adult
8/22/2005
Pentobarbital Sodium Turkey 16.2 IM PRN B 1080 Add thiopental sodium
Pentoxifylline Avian 15 PO BID-TID G 1489 Add aloe vera for frostbite, vasodilator
5:33 PM
Permethrin Pigeon dusting Topical NL E 1240 For fleas and lice

Permethrin Psittacine dusting Topical NL E 1240 Ectoparasite control
Phenobarbital Avian 1-5 PO BID E 111, 1473

Page 305
Phenobarbital Avian 3.5-7 NL BID D 1475 Control of seizures

Phenobarbital Avian 0.048-0.080 g/L Drink PRN G 58
Phenobarbital Psittacine 3 PO BID E 1240 For feather picking, may cause deep sedation
and inability to perch
Phenobarbital Raptor < 30 PO PRN E 1463 For sedation
Phenobarbital Raptor 20 PO NL D 1612 For neurologic signs with organochlorine
toxicity
Phenylbutazone Ostrich 2.2 PO QD G 710

Phenylbutazone Psittacine 3.5-7 PO BID-TID E 1473
Phenylbutazone Raptor 3.5-7 PO BID-TID E 111
Phytonadione Avian 2.5-5 Parenteral BID-QID E 1492 For anticoagulant rodenticide

Phytonadione Raptor 0.2-2.5 IM-PO QD E 1433 For anticoagulant poisoning
Piperacillin Sodium Amazon Parrot 75-100 IM q4-6h A 1473

Piperacillin Sodium Avian 4.31 mg/kcal IM-IV TID-QID E 1180 Synergistic with aminoglycosides
Piperacillin Sodium Avian 2.55 mg/kcal IM-IV q4-6h E 1180 Synergistic with aminoglycosides
Piperacillin Sodium Avian 10 g/L saline Flush BID-QID E 1183 Nasal or sinus
Piperacillin Sodium Avian 10 g/L saline Nebulize BID-QID E 1185 10 to 30 minutes
Piperacillin Sodium Avian 100-200 IM TID-QID E 1650 Synergistic with aminoglycosides
Piperacillin Sodium Avian 150 IM BID G 55
Piperacillin Sodium Bird, Aquatic 100-200 IM BID E 1478 Post-trauma infections
Piperacillin Sodium Budgerigar 200 IM TID A 411
Piperacillin Sodium Cockatoo, Citron-crested 90 Parenteral BID G 740 Add amikacin

Piperacillin Sodium Crane 100 IM-IV-SC BID E 629
Piperacillin Sodium Duck, Ruddy 100 IM BID G 1468 Begin pre-operatively for tendon surgery
305
306

Piperacillin Sodium Falcon 200 IM TID-QID E 1027 Broad spectrum
Piperacillin Sodium Gull 100 IM BID E 1357
Piperacillin Sodium Lorikeet, Rainbow 100 IM BID G 1620
Piperacillin Sodium Macaw 4 mg TD per egg Parenteral q4d G 820 For embryonic death, begin first dose at day
14, use 26 ga needle

Piperacillin Sodium Pigeon 100 IM BID-TID G 260
Piperacillin Sodium Pigeon 100-200 IM BID G 590
Piperacillin Sodium Psittacine 100 IM BID A 411

Piperacillin Sodium Psittacine 50-100 SC TID E 632 Neonate dosage
8/22/2005
Piperacillin Sodium Psittacine 100-200 IM-IV BID-TID E 1240, 1756

Piperacillin Sodium Raptor 100 IM-IV BID E 1433
5:33 PM
Piperacillin Sodium + Avian 150-200 IM-IV QD-BID G 1279 Substitute for piperacillin sodium, DO NOT
Tazobactam Sodium use aminoglycosides concurrently
Piperacillin Sodium + Falcon, Peregrine 200 IM BID G 1426
Tazobactam Sodium
Page 306
Piperazine Anseriformes 45-200 PO NL E 111

Piperazine Avian 100-500 PO q2w E 1650 For roundworms
Piperazine Crane 4-5.26 g/L Drink QD G 596 Repeat in 2 weeks
Piperazine Finch 0.3 g/L Drink NL E 1572
Piperazine Galliformes 100-500 PO q2w E 111
Piperazine Pigeon 1.9 g/L Drink QD C 704 For 30 birds
Piperazine Pigeon 500 mg Drink TD C 706 For capillaria
Piperazine Pigeon 250 mg Drink TD C 706 For ascaridiasis
Piperazine Pigeon 12.5 Drink QD E 1240 Repeat every 10 to 14 days
Piperazine Pigeon 35 PO QD G 260
Piperazine Poultry 1 g/L Drink QD G 57
Piperazine Poultry 100-500 PO q10d G 1309 For ascarids
Piperazine Psittacine 250 PO NL G 57
Piperazine Quail 30-50 mg TD PO NL G 678 Anthelmintic
Piperazine Raptor 100 PO NL E 57, 1463 Anthelmintic
Piperonyl Butoxide Raptor 6.25 g/L Topical NL E 1068 Add permethrin + methoprene for
ectoparasites
Piroxicam Crane 0.5 PO BID G 1671
Policosanol Amazon Parrot 1 mg TD PO BID G 1273 For hyperlipidemia or hypercholesterolemia
Policosanol Amazon, Yellow-naped 2 PO QD G 1466 Mix with lactulose for hyperlipidemia of
triglyceride and cholesterol
Polymyxin B Sulfate Avian 10-15 IM-PO NL E 924

Polymyxin B Sulfate Avian 1000 mg/kcal PO BID E 1180
8/22/2005
Polymyxin B Sulfate Avian 3000 KIU/L Drink NL E 1180

Polymyxin B Sulfate Avian 50 KIU/kg PO BID E 565
Polymyxin B Sulfate Canary 50 KIU/L Drink QD E 695
Polymyxin B Sulfate Canary 50 KIU/kg food Feed QD E 695
5:33 PM
Polymyxin B Sulfate Canary 500 KIU/L Drink NL E 1187

Polymyxin B Sulfate Canary 500 KIU/kg food Feed Once E 1187
Polymyxin B Sulfate Passerine 100 KIU/kg food Feed QD E 1437 Add drug to drink at the same time
Polymyxin B Sulfate Passerine 100 KIU/L Drink QD E 1437 Add drug to food at the same time
Page 307
Polymyxin B Sulfate Passerine, Small 500 KIU/L Drink NL E 1187

Polymyxin B Sulfate Passerine, Small 500 KIU/kg food Feed Once E 1187
Polysulfated Crane, Demoiselle 50 mg TD IA Once G 579 Musculosketal joint therapy

Glycosaminoglycan
Polysulfated Pheasant, Peacock 12.5 mg TD IM Once G 579 Musculosketal joint therapy
Glycosaminoglycan
Polysulfated Vulture, King 20 mg TD IM QW G 579 Musculosketal joint therapy
Glycosaminoglycan
Potassium Bromide Cockatoo, Umbrella 80 PO QD G 1691 For control of seizures

Potassium Bromide Parrot, Grey 80 PO QD G 1274 Seizure control
Potassium Bromide Pigeon 80 PO QD G 1274 Seizure control
Potassium Chloride Avian 0.3 IV NL E 1473

Potassium Chloride Avian 0.1-0.3 IV NL E 111
Potassium Permanganate Falcon 14 g/m³ NL Once G 1029 Add formaldehyde for fumigation TOXIC
Pralidoxime Chloride Avian 10-30 IM QD E 111

Pralidoxime Chloride Raptor 100 NL BID-QID E 1400 For organophosphate poisoning
Pralidoxime Chloride Raptor 20 IM PRN G 50 Continue only if first dose produces response
Pralidoxime Iodide Avian 10-100 Parenteral NL E 1492 Reduce dosage if used with atropine for
organophosphates
307
308

Pralidoxime Iodide Avian 10-100 Parenteral BID-TID E 1650 Use lower dosage if used with atropine for
organophosphate toxicity
Pralidoxime Iodide Raptors 100 IM Once B 1093 For monocrotophos toxicity
Pralidoxime Mesylate Anseriformes 100 IM QID D 1150 For organophosphate toxicity

Pralidoxime Mesylate Psittacine 100 IM QID E 1240
Praziquantel Anseriformes 10-20 PO-SC q10d D 1150 Control cestodes

Praziquantel Avian 10-20 PO QD D 1470 For liver parasitic disease
8/22/2005
Praziquantel Avian 9 IM QD D 1470 Continue PO for 11 days for liver parasitic

disease
Praziquantel Avian 10 PO NL E 1648 For tapeworms
5:33 PM
Praziquantel Bird, Aquatic 10 PO NL E 1503 For tapeworms

Praziquantel Bustard 10 PO-SC Once E 1240 For cestodes and trematodes
Praziquantel Finch 10-20 PO q10-14d E 1572
Praziquantel Finch 12 mg/kg Feed Once E 1617 Crush tablet and mix with enough food for 1
day, scatter throughout aviary
Page 308
Praziquantel Ostrich 7.5 PO NL C 283

Praziquantel Ostrich 5 PO NL G 481
Praziquantel Passerine, Small 10 NL NL E 1187 For trematodes
Praziquantel Penguin 10-20 PO NL E 1478 For cestodes
Praziquantel Pigeon 11.4 SC QM E 704
Praziquantel Pigeon 10-20 PO q2w E 704 Tablet crushed in water suspension
Praziquantel Pigeon 10 PO NL E 1192 For cestodes
Praziquantel Psittacine 9 IM NL E 763 For tapeworms
Praziquantel Psittacine 10-20 PO Once E 1240 For tapeworms repeat after 10 days
Praziquantel Raptor 50 PO-SC NL E 1068 For trematodes and cestodes
Praziquantel Raptor 30 NL q10d E 1132 For tapeworms and flukes
Praziquantel Raptor 5-10 PO-SC QD E 1240
Praziquantel Raptor 10-50 PO q2w E 1359 For tapeworms
Prednisolone Avian 2 PO BID E 1431 May predispose to mycotic infection

Prednisolone Avian 6.7 PO NL E 1526 Use decreasing dosage for long-term therapy
Prednisolone Psittacine 2 PO BID E 1240 Also analgesic

Prednisolone Raptor 0.5-1 IM Once E 1400
Prednisolone Raptor 2-4 IM-IV Once E 1400 For shock
Prednisolone Sodium Avian 0.5-1 IM-IV NL E 111
Phosphate
Prednisolone Sodium Avian 2-4 IM-IV NL E 111 Immunosuppressive
Phosphate
Prednisolone Sodium Raptor 10-30 IM-IV PRN G 234
8/22/2005
Phosphate
Prednisolone Sodium Avian 0.5-1 IM-IV Once E 1151 For neurologic emergencies
Succinate
5:33 PM
Prednisolone Sodium Avian 10-20 IM-IV NL D 1554 For shock

Succinate
Primaquine Phosphate Avian 0.03 PO QD D 1470 For liver parasitic disease

Page 309
Primaquine Phosphate Avian 1 PO QW E 1479

Primaquine Phosphate Avian 1 PO QW E 1492 Add chloroquine for Plasmodium
Primaquine Phosphate Avian 0.3-1 PO TID G 57 Usually in combination with chloroquine
Primaquine Phosphate Falcon 0.75 NL Once E 1177 Add chloroquine

Primaquine Phosphate Penguin 0.03 PO QW D 1470 For liver parasitic disease prophylaxis
Primaquine Phosphate Penguin 0.03 PO QD E 111, 1473
Primaquine Phosphate Penguin 1 PO QD B 262 Add chloroquine phosphate
Primaquine Phosphate Psittacine 1 PO QD E 1365 For sarcocystosis
Primaquine Phosphate Raptor 1 PO QD G 61 Add chloroquine
Primaquine Phosphate Raptor 1 PO QW G 94 Add chloroquine phosphate, juvenile dosage
Primidone Amazon Parrot 125 mg TD Drink QD G 1753 Long-term seizure control

Primidone Raptor 125 PO PRN E 1463 For sedation
Probenecid Avian 200 NL q2d E 704 For body weight > 200g, to decrease
excretion rate of penicillin/cephalosporin
during therapy
Probenecid Macaw 125 PO QID G 45 Uricosiuric
Probiotic Anseriformes 21 ml/kg food Feed Once E 1240 For hand-rearing (6 hours old) and
convalescing birds, Avipro Pediatric®
Probiotic Anseriformes 5 scoops/L Drink NL E 1240 Double dosage for stressed bird, Avipro®
Probiotic Avian 5 cc/L Feed Once E 111 Add to hand feeding formula
309
310

Probiotic Avian 1 pinch TD Feed QD E 111
Probiotic Psittacine 21 ml/kg food Feed Once E 1240 For hand-rearing (6 hours old) and
convalescing birds, Avipro Pediatric®
Probiotic Psittacine 5 scoops/L Drink NL E 1240 Double dosage for stressed bird, Avipro®
Probiotic Psittacine 5 ml/L food Feed Once E 1473 Hand feeding formula
Probiotic Psittacine pinch TD PO QD E 1473
Probiotic Ratite PO NL G 418

8/22/2005
Proflavine Avian 30 mg TD Topical QD-BID E 1240 For wounds, stimulate granulation
Propentofylline Avian 5 PO QD G 1240 Vasodilator for wing tip edema or dry

5:33 PM
gangrene
Propentofylline Raptor 5 PO BID E 1400 Improve circulation (wing tip edema)
Propofol Amazon, Hispaniolan 5 IV PRN B 1436 Maintain anesthesia by continuous infusion at

1 mg/kg per minute
Page 310
Propofol Anseriformes 8 IV PRN E 1190 Induction agent

Propofol Avian 1.33-14 IV PRN E 1181 Short duration, smooth induction, high safety
margin
Propofol Duck, Mallard 10 IV PRN B 1358 Administer over 1 minute, follow with 4
mg/kg, respiratory depression
Propofol Ostrich 3 IV PRN B 1628 Maintain with 0.2 mg/kg/min constant rate
infusion
Propofol Pigeon 4.1-8.6 IV PRN B 779 Follows ketamine
Propofol Pigeon 14 IV PRN B 779 Preliminary to inhalation anesthesia
Propofol Psittacine 1.33 IV PRN E 1240 For anesthesia induction
Propofol Swan 6 IV Once G 1695 Induction for isoflurane
Propofol Swan (Black, Mute) 10 IV PRN B 1291 Gas anesthesia premed
Propolis Chicken 30 mg TD Once B 1632 Immune and growth stimulant
Propranolol HCl Avian 0.2 IM NL E 111

Propranolol HCl Avian 0.04 IV NL E 111
Prostaglandin E (See Raptor N/A Topical PRN E 1400 For egg binding, use gel formulation
Dinoprostone)
Psyllium Hydrophilic Avian 2.5 ml/kg PO NL G 87 Mix with syringeable food, bulking agent to
Mucilloid remove GI materials
Psyllium Hydrophilic Bird, Aquatic 40 ml/L soft food Feed Once E 1478 Add sodium + magnesium sulfate + mineral
Mucilloid oil for lead poisoning, add bran
Pyrantel Pamoate Anseriformes 7 PO q2w E 1358 For nematodes

Pyrantel Pamoate Avian 4.5-25 PO q2w D 111,1221, 1473 For nematodiasis
8/22/2005
Pyrantel Pamoate Crane 4.5 PO q10d E 1361 For intestinal nematodes

Pyrantel Pamoate Finch 4.5 PO q10-14d E 1572
Pyrantel Pamoate Passerine 100 PO Once G 1335 For intestinal nematodes
Pyrantel Pamoate Pigeon 20-25 PO QW-q2w E 1364
5:33 PM
Pyrantel Pamoate Psittacine 4.5 PO q10d E 1240 For nematodes

Pyrantel Pamoate Psittacine 100 PO NL G 57, 1335
Pyrantel Pamoate Raptor 20 PO Once E 1240, 1400 For nematodes
Pyrantel Pamoate Raptor 4.5 PO q2w G 94 Juvenile dosage
Page 311
Pyrantel Pamoate Ratite 5-7 PO NL G 418
Pyrethrin Crane 0.1% powder Topical QW-q2w E 1361 For ectoparasites, apply lightly
Pyrethrin Finch Topical QD E 1572 Dust feathers
Pyrethrin Raptor 0.5-2% mixture Topical q10d G 1411 For chewing lice
Pyrimethamine Anseriformes 0.25-0.5 PO BID D 1150 For sarcocystosis and toxoplasmosis

Pyrimethamine Avian 0.5 PO BID D 1470
Pyrimethamine Avian 0.3 PO NL E 1650 For Leucocytozoon, Plasmodium
Pyrimethamine Raptor 0.25-0.5 PO BID E 1400 For sarcocystosis, toxoplasmosis and other
protozoal infections
Pyrimethamine Raptor 0.5 PO BID E 1433 For leucocytozoonosis
Pyrimethamine + Anseriformes 0.06 g/L Drink QD D 1150 2 days off, then repeat for coccidiosis
Sulfaquinoxaline
Pyrimethamine + Psittacine 0.06 g/L Drink QD E 1240 Wait 2 days then repeat for coccidiosis
Sulfaquinoxaline
Quinacrine HCl Avian 5-10 PO QD E 111

Quinacrine HCl Avian 240 NL QD E 1479 For Plasmodium
Quinacrine HCl Avian 7.5 PO QD E 1650 For Plasmodium
Quinacrine HCl Canary 240 PO BID G 57
Quinacrine HCl Pigeon 10 mg TD PO QD G 47
Quinacrine HCl Psittacine 5-10 PO QD E 1473
Red Clover Avian 10 drops/kg PO QD E 1435 Use low alcohol formulation for soft shelled
egg
311
312

Red Palm Oil Avian 10-60 drops/kg PO QD G 1727 May give over food
Rescue Remedy Finch 2 drops TD PO Once G 1723 For stress of handling or minor procedures
Reserpine Raptor 2-4 PO PRN E 1463 For prolonged sedation

Resorantel Ostrich 130 PO NL B 283,401, 524 Add fenbendazole or levamisole

8/22/2005
Rifabutin Avian 15 PO QD D 1470 Add ethambutol + enrofloxacin for

mycobacteriosis
5:34 PM
Rifabutin Avian 1.15 mg/kcal PO QD E 1180 Add ethambutol + azithromycin or

clarithromycin for mycobacteriosis
Rifampin Amazon, Yellow-cheeked 45 NL QD G 713 Add ethambutol + isoniazid

Rifampin Avian 10-20 PO BID E 111, 1473
Page 312
Rifampin Avian 15 PO QD G 1154 Add ciprofloxacin + ethambutol for

mycobacteriosis
Rifampin Bustard, Houbara 20 PO BID G 932 For bacterial diarrhea
Rifampin Crane, Whooping 45 PO QD G 207 Add ethambutol
Rifampin Psittacine 15 PO BID E 1240 For avian tuberculosis
Rifampin Raptor 30 PO TID B 1178 Add IT and IV amphotericin B + flucytosine
for aspergillosis
Rimantadine HCl Poultry 0.1 g/L Drink NL G 435
Robenidine HCl Chicken 33 mg/kg food Feed QD E 564 7-day slaughter withdrawal, prophylactic
Robenidine HCl Pheasant, Ring-necked 0.033 g/kg Feed QD B 895 For coccidiosis
Ronidazole Avian 0.323 mg/kcal PO QD E 1180 For flagellates

Ronidazole Avian 0.65 g/L Drink NL E 1180
Ronidazole Avian 1 g/L Drink QD E 1479 Treat 4 times yearly for trichomoniasis
Ronidazole Avian 6-10 PO QD G 57
Ronidazole Budgerigar 1 g/L Drink QD E 1479 Treat 4 times yearly for trichomoniasis
Ronidazole Canary 0.4 g/L Drink QD E 695
Ronidazole Canary 0.4 g/kg food Feed Once E 1187
Ronidazole Finch 0.1 g/L Drink QD E 1572
Ronidazole Finch 6-10 PO QD E 1572
Ronidazole Finch 0.05 g/kg food Feed QD G 1334 For cochlosomiasis
Ronidazole Finch 0.05 g/L Drink QD G 1334 For cochlosomiasis
Ronidazole Passerine 0.04 g/L Drink QD D 1438 For trichomoniasis, giardiasis and
cochlosomiasis
Ronidazole Pigeon 6-10 NL QD D 1221 For trichomoniasis
Ronidazole Pigeon 0.1 g/L Drink QD E 1192 For hexamitiasis, add trimethoprim or
8/22/2005
enrofloxacin in severe infections

Ronidazole Pigeon 0.1-0.2 g/L Drink NL E 1192 For treatment of trichomoniasis, give
periodically for 2 to 3 days for prophylaxis
5:34 PM
Ronidazole Pigeon 12.5 Drink QD E 1240 For trichomoniasis treatment

Ronidazole Pigeon 10 PO NL E 1432 "
Ronidazole Pigeon 0.1 g/L Drink NL E 1432 "
Page 313
Roxarsone Poultry 25-50 mg/kg food Feed QD E 564 Nutritional use, no slaughter withdrawal
Salicylic Acid Psittacine Topical q2w D 1446 Add 3 g tannic acid + 3 g salicylic acid +
ethyl alcohol for 100 ml of solution for
dermatomycosis
Salinomycin Chicken 0.06 g/kg Feed QD B 869 Preventive for coccidiosis

Salinomycin Chicken 0.075 g/kg Feed QD B 869 Preventive for coccidiosis
Salinomycin Chicken 60 Feed QD B 958 For coccidial prophylaxis
Salinomycin Chicken 44-66 mg/kg food Feed QD E 564 No slaughter withdrawal, prophylactic
Salinomycin Pheasant, Ring-necked 60 ppm Feed Once B 783 For coccidiosis
Salinomycin Poultry 60 g/ton Feed QD C 705 For coccidiosis
Sarafloxacin HCl Chicken 10 PO BID-TID A 787

Sarafloxacin HCl Chicken 8 Drink QD B 855 Continuous or 4-hour pulse dose
Sarafloxacin HCl Chicken 0.02 g/L Drink QD B 864 For Escherichia coli infections
Sarafloxacin HCl Turkey 0.05 g/L Drink NL A 805
Secobarbital Sodium Blackbird, Red-winged 0.025-0.03 PO PRN G 1769 Add chloralose

Secobarbital Sodium Dove 5 g/L bait Feed Once G 1763 Bait is usually corn
Secobarbital Sodium Duck, Mallard 25 PO PRN B 1095
Selenium Psittacine 0.06 NL q3d-q2w G 1613

Semduramycin Chicken PO QD G 564

313
314

Seromycin Avian 10 PO BID G 1154 Add lamprene + ethambutol HCl, add
ciprofloxacin or enrofloxacin or streptomycin
for advanced cases
Silver Nitrate Avian Topical q10d E 1650 For cautery of papillomas
Silver, Colloidal Avian 2 drops/kg PO QD E 1435 Broad spectrum

Silver, Colloidal Avian 40 drops/L Drink QD E 1435 Broad spectrum

8/22/2005
Sodium Bicarbonate Avian 1 mEq/kg IV-SC PRN G 1309 First dose IV, remainder SC, maximum total
dose 4 mEq/kg for metabolic acidosis
5:34 PM
Sodium Bicarbonate Avian 1-4 mEq/kg IV NL E 1473 Give slowly over 15 to 30 minutes, do not
exceed 4 mEq/kg
Sodium Bicarbonate Avian 5 mEq/kg IO-IV Once G 1311 For cardiopulmonary resuscitation
30 ml/kg
Page 314
Sodium Chloride Avian PO TID-QID E 1151 Use 0.9% solution

Sodium Chloride Bird, Aquatic 10 g/L Gavage QD D 1559 To maintain activity of salt gland of marine
birds kept on freshwater
Sodium Chloride Bird, Aquatic 100 Feed QD E 1501 For pelagic sea birds kept in fresh water
Sodium Chloride Bird, Aquatic 100 PO NL E 1503 For procelliform birds kept in fresh water
Sodium Chloride Penguin 150-1667 PO QD G 1353 Supplement fish diet

Sodium Chloride Psittacine 50 ml/kg IM-IV-SC QD E 1240 Use 0.9% solution
Sodium Chloride Raptor 1-2% solution Topical NL E 1400 1-2% solution for wounds, wash off within 5
minutes
Sodium Hypochlorite Finch 30 ml/L Topical NL E 1572 For salmonellosis environmental cleanup, use
household bleach
Sodium Iodide Avian 60 IM PRN G 54

Sodium Iodide Avian 67-200 IM NL F 1209
Sodium Iodide Budgerigar 2 mg TD IM PRN G 85
Sodium Iodide Budgerigar 134-200 IM QD G 1212 For acute thyroid hyperplasia
Sodium Iodide Budgerigar 67 IM QD G 1212 For chronic thyroid hyperplasia
Sodium Lactate Solution Avian 50 ml/kg IV NL E 111 Maintenance fluids
Sodium Lactate Solution Avian 10-30 ml/kg IV NL E 1650 Emergency care, give slowly, warm fluid
Sodium Lactate Solution Avian 25 ml/kg IO-IV-SC NL G 1311
Sodium Lactate Solution Avian 50-100 ml/kg IO-IV-SC BID G 1756 For hyperuricemia, give until level drops to
normal
Sodium Lactate Solution Hawk, Red-tailed 20 ml/kg IV NL G 1626 Supportive therapy post-trauma
Sodium Lactate Solution Lory, Red 50 ml/kg SC NL G 1621 Intra-operative fluids
8/22/2005
Sodium Lactate Solution Psittacine 50-100 ml/kg IO-IP-IV-SC NL E 1688

5:34 PM
Sodium Sulfate Avian 2000 PO QD E 111 Large birds, give slurry

Sodium Sulfate Avian 500-1000 PO NL E 1554 For botulism to flush gastrointestinal tract
Sodium Sulfate Avian 125-250 PO NL G 1746 For removal of metals from GI tract
Page 315
Somatostatin Toucan, Sulfur-breasted 0.003 SC BID G 589
Spectinomycin HCl Avian 30 PO QD E 565

Spectinomycin HCl Avian 1 g/L Drink QD E 704
Spectinomycin HCl Avian 10-45 IM NL E 704
Spectinomycin HCl Avian 0.58 mg/kcal IM-SC TID E 1180
Spectinomycin HCl Avian 1 g/L Drink NL E 1180
Spectinomycin HCl Canary 0.2-0.4 g/L Drink NL E 1187
Spectinomycin HCl Chicken 5 mg TD SC Once B 848 Day-old neonates
Spectinomycin HCl Chicken 2 g/L Drink NL C 1307 For Mycoplasma gallisepticum in broilers
Spectinomycin HCl Chicken 0.5 g/L Drink NL C 1307 For improved weight gain in broilers
Spectinomycin HCl Duck 5 SC Once B 841 For E. coli and Salmonella
Spectinomycin HCl Finch 0.2-0.4 g/L Drink QD E 1572
Spectinomycin HCl Finch 0.4 g/kg food Feed QD E 1572
Spectinomycin HCl Passerine 0.2-0.4 g/L Drink QD E 1437 Add drug to food at the same time
Spectinomycin HCl Passerine 0.4 g/kg soft food Feed QD E 1437 Add drug to drink at the same time
Spectinomycin HCl Passerine, Small 0.4 g/kg food Feed Once E 1187
Spectinomycin HCl Passerine, Small 0.2-0.4 g/L Drink NL E 1187
Spectinomycin HCl Pigeon 25 IM-SC TID E 565, 1061
Spectinomycin HCl Pigeon 30 PO QD F 1061
Spectinomycin HCl Pigeon 0.15-0.25 g/L Drink NL G 260
Spectinomycin HCl Poultry 0.264-0.53 g/L Drink QD C 564
Spectinomycin HCl Poultry 0.132 g/L Drink QD C 564 Prophylactic
Spectinomycin HCl Poultry 2.5-20 mg TD SC QD C 564 Chick dosage

Spectinomycin HCl Psittacine 10-30 IM BID-TID E 1240 Gram negative enteritis
Spectinomycin HCl Psittacine 35 IN NL E 1240 Give 1/3 each nare, remainder IM
315
316

Spectinomycin HCl Raptor 50 IM BID G 234
Spectinomycin HCl Turkey 12.5-25 mg TD SC NL C 1307 Dilute 1:4 normal saline for newly hatched
chicks
Spectinomycin HCl Turkey 10 mg TD SC NL C 1307 Inject in base of the neck of 1 to 3-day-old
poults for airsacculitis
Spiramycin Avian 250 PO QD E 565

Spiramycin Avian 100 IM-PO NL E 924

Spiramycin Avian 2 g/L Drink NL E 1180
8/22/2005
Spiramycin Avian 0.58 mg/kcal IM QD E 1180

Spiramycin Avian 1.08 mg/kcal PO QD E 1180
Spiramycin Canary 0.2-0.4 g/L Drink QD E 695
5:34 PM
Spiramycin Canary 400 mg/kg food Feed QD E 695

Spiramycin Passerine, Small 0.2-0.4 g/L Drink NL E 1187
Spiramycin Passerine, Small 0.4 g/kg food Feed Once E 1187
Spiramycin Pigeon 25 IM QD E 565, 1061
Spiramycin Pigeon 50 PO QD F 1061
Page 316
Spiramycin Poultry 0.4 g/L Drink QD C 564

Spiramycin Raptor 20 IM NL E 1463 For bacterial infections
Stanozolol Avian 25-50 IM q3d-QW E 111, 1209, 1240

Stanozolol Avian 25-50 IM q3-4d E 1473
Stanozolol Avian 25-50 IM q3d-QW G 1309 Anabolic agent
Stanozolol Psittacine 0.016 g/L Drink NL E 763 For debilitation, anorexia and anemia
Stanozolol Psittacine 0.5-1 Parenteral NL E 763 For debilitation, anorexia and anemia
Streptomycin Sulfate Avian 10-30 IM BID-TID E 111

Streptomycin Sulfate Avian 33 IM BID-TID E 741 Used in large birds and poultry
Streptomycin Sulfate Avian 15 IM-PO NL E 924 Poor spectrum
Streptomycin Sulfate Avian 0.65 mg/kcal IM BID-TID E 1180
Streptomycin Sulfate Avian 1.28-4.67 mg/kcal PO QD E 1180
Streptomycin Sulfate Avian 10-30 IM BID-TID E 1470
Streptomycin Sulfate Avian 30 IM BID G 55, 1154 Add ethambutol + rifampin for
mycobacteriosis
Streptomycin Sulfate Avian 10 IM BID G 819 Add rifampin + ethambutol for avian
tuberculosis
Streptomycin Sulfate Chicken 25-50 IM QD A 320
Streptomycin Sulfate Chicken 50-100 PO QD E 565
Streptomycin Sulfate Pheasant 220 mg/kg food Feed QD G 678
Streptomycin Sulfate Pheasant 55-110 mg/kg food Feed QD G 678
Streptomycin Sulfate Pigeon 100-200 PO QD E 565, 1061
Streptomycin Sulfate Pigeon 25-50 IM QD F 1061

Streptomycin Sulfate Poultry 55 PO QD C 564
Streptomycin Sulfate Poultry 0.068-0.1 g/L Drink QD C 564
Streptomycin Sulfate Poultry 13.2 mg/kg food Feed QD E 564 Add penicillin, nutritional use, no slaughter
withdrawal
8/22/2005
Streptomycin Sulfate Quail 55-110 mg/kg food Feed QD G 678

Streptomycin Sulfate Raptor 15 PO NL E 1463 May give with kaolin or sulfonamide for
bacterial infections
5:34 PM
Succimer Avian 25-35 PO BID D 1221, 1470 Preferred oral drug for lead toxicosis
Succimer Avian 30 PO QD E 1120 For zinc toxicoses
Succimer Avian 30 PO BID E 1151 Metal chelating agent
Page 317
Succimer Avian 25-35 PO BID E 1236 Give 5 days per week for lead toxicosis
Succimer Avian 15-35 PO BID G 1337 For lead poisoning
Succimer Bird, Aquatic 25-35 PO BID D 1478
Succimer Psittacine 30 NL NL G 1710 For zinc toxicity
Succimer Raptor 25 PO BID E 1359 After 2 days off, repeat over 3-5 weeks for
lead toxicity
Sucralfate Avian 25 PO TID E 1492 Mix with water for GI bleeding

Sucralfate Lorikeet, Rainbow 24 PO BID G 1620 For intestinal ulcers
Sucralfate Psittacine 25 PO TID E 111
Sucrose Raptor < 5 ml/kg 5% soln PO PRN E 1400 Mild purgative, may stimulate appetite
Sulfachlorpyridazine Avian 0.175 g/L Drink QD E 1240 Antibacterial,* use 5-10 days
Sulfachlorpyridazine Avian 0.125 ml powder Drink QDlllllll G 1309 Antibacterial*
*Vetisulid Oral Powder® is 560 mg/ml
volume for flock treatment for E. coli
Sulfachlorpyridazine Avian 59 g/L Drink QD E 1479 Use 5 days per week, reduces shedding of
Atoxoplasma
Sulfachlorpyridazine Avian 0.4 g/L Drink QD G 57 Repeat after 2 days, antiparasitic
Sulfachlorpyridazine Canary 0.15 g/L Drink QD-q2d E 1187 Give 5 days per week until molting complete
in juveniles with atoxopasmosis
Sulfachlorpyridazine Canary 0.3 g/L Drink QD-q2d E 1187 Give 5 days per week for coccidiosis
Sulfachlorpyridazine Canary 0.15-.0.3 g/L Drink NL E 1187

Sulfachlorpyridazine Passerine 0.15 g/L Drink QD G 1334 Give 5 days of each week, continue until after
molting
317
318

Sulfachlorpyridazine Passerine, Small 0.15-.0.3 g/L Drink NL E 1187
Sulfachlorpyridazine Pigeon 0.3 g/L Drink QD G 260
Sulfachlorpyridazine Pigeon 0.3 g/L Drink QD G 260
Sulfadiazine, Silver Psittacine 1% cream formula Topical NL D 1448 Post-surgical wound care
Sulfadiazine, Penguin, African 300-400 Feed BID D 1614 Precede with sulfamethazine injectable, give
Sulfamerazine, dose in fish for malaria

Sulfamethazine
8/22/2005
Sulfadimethoxine Avian 24 IM NL F 1209

Sulfadimethoxine Avian 25 IM-PO NL E 924
5:34 PM
Sulfadimethoxine Chicken 0.5 g/L Drink NL B 826 For Pasteurella multocida and Hemophilus
gallinarum
Sulfadimethoxine Crane 50 PO QD E 1361 For coccidiosis
Sulfadimethoxine Falcon 25 (50 loading dose) PO QD E 1027 For coccidiosis, do not deprive of water
Sulfadimethoxine Gull 25 PO BID E 1357 coccidiosis
Page 318
Sulfadimethoxine Pigeon 25 PO BID G 590

Sulfadimethoxine Pigeon 250 IM BID A 992 For coccidiosis
Sulfadimethoxine Pigeon 0.5 g/L Drink QD E 1432 For coccidiosis and atoxoplasmosis
Sulfadimethoxine Pigeon 0.19-0.25 g/L Drink QD G 260 Loading dose 375 mg/L
Sulfadimethoxine Poultry 0.25-0.5 g/L Drink QD C 564
Sulfadimethoxine Raptor 25 NL QD E 1132 Double dose for first day for coccidiosis
Sulfadimethoxine Raptor 25-50 PO QD G 94 Juvenile dosage, repeat after 2 days
Sulfadoxine + Avian 1 PO QW E 1479

Pyrimethamine
Sulfadoxine + Avian 0.3 PO NL E 1650 Dosage based on pyrimethamine for
Pyrimethamine Leucocytozoon and Plasmodium
Sulfadoxine + Psittacine 0.5 PO BID E 1365 For sarcocystosis
Pyrimethamine
Sulfamerazine Avian 2 g/L Drink QD E 924 Repeat after 2 days for coccidiosis
Sulfamethazine Avian 30 IM-SC NL E 704

Sulfamethazine Avian 0.2 g/L Drink QD E 704 Repeat after 2 days
Sulfamethazine Avian 50 PO NL E 704
Sulfamethazine Avian 1 g/L Drink NL E 741 For coccidiosis plus mild respiratory and
enteric diseases
Sulfamethazine Avian 1 g/L Drink NL E 741 For coccidiosis plus mild respiratory and
enteric diseases
Sulfamethazine Avian 0.15 g/L Drink NL E 1180
Sulfamethazine Avian 0.125 g/L Drink QD G 57 Use liquid formulation, wait 2 days then
repeat
Sulfamethazine Budgerigar 7 PO QD G 57 Wait 2 days then repeat
Sulfamethazine Canary 0.15 g/L Drink NL E 1187
8/22/2005
Sulfamethazine Canary 0.15 g/L Drink QD E 695

Sulfamethazine Chicken 1 g/L Drink QD E 564 12-day slaughter withdrawal
Sulfamethazine Passerine 0.15 g/L Drink QD E 1437
Sulfamethazine Passerine, Small 0.15 g/L Drink NL E 1187
5:34 PM
Sulfamethazine Penguin, African 83-125 IM BID D 1614 Switch to sulfadiazine + sulfamerazine +

sulfamethazine when able to give orally for
malaria
Sulfamethazine Pigeon 2 g/L Drink QD E 704 Repeat 1 to 2 times at 2-day intervals
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Sulfamethazine Pigeon 2 g/L Drink QD E 704 Repeat after 5 days

Sulfamethazine Pigeon 2 g/L Drink QD E 1240 Wait 2 days then repeat for 3 treatment cycles
for coccidiosis, perhaps toxoplasmosis
Sulfamethazine Pigeon 3.33-6.66 g/L Drink QD E 1240 For coccidiosis, perhaps Toxoplasmosis
Sulfamethazine Pigeon 3.33-6.66 g/L Drink QD E 1432
Sulfamethazine Pigeon 1.1 g/L Drink QD G 232
Sulfamethazine Pigeon 1.1 g/L Drink QD G 260 Loading dose 375 mg/L, treat with B
vitamins for 5 days then repeat
Sulfamethazine Poultry 0.19-0.25 g/L PO QD C 564
Sulfamethazine Poultry 1 g/L Drink QD C 564
Sulfamethazine Raptor 1 g/L Drink QD E 1612 Repeat after 2 days
Sulfanitran Chicken 300 mg/kg food Feed QD E 564 Add nitromide + roxarsone, 5-day slaughter
withdrawal, prophylactic
Sulfanitran Poultry 300 mg/kg food Feed QD E 564 Add nitromide + roxarsone, nutritional use,
no slaughter withdrawal
Sulfaquinoxaline Anseriformes 500 mg/kg food Feed Once G 597

Sulfaquinoxaline Chicken 0.17 g/L Drink QD E 564 10-day slaughter withdrawal
Sulfaquinoxaline Duck 0.25 g/kg Feed Once B 825 For Riemerella anatipestifer in ducklings
Sulfaquinoxaline Lory 100 PO QD G 57
Sulfaquinoxaline Pigeon 100 PO QD G 57
Sulfaquinoxaline Poultry 0.397 g/L Drink QD C 564
Sulfaquinoxaline Raptor 0.034 g/L Drink QD E 1612 Repeat after 2 days

Sulfaquinoxaline Turkey 0.17 g/L Drink QD E 564 10-day slaughter withdrawal
319
320

Sulfaquinoxaline + Avian 0.1 g/kg feed Feed QD E 1492 For coccidiosis
Diaveridine
Sulfaquinoxaline + Avian 0.1 g/L Drink QD E 1492 For coccidiosis
Diaveridine
Sulfaquinoxaline + Avian 0.1 g/kg food Feed QD E 1650 For coccidiosis

Diaveridine
Sulfaquinoxaline + Avian 0.1 g/L Drink QD E 1650 For coccidiosis
Diaveridine
Sulfaquinoxaline + Chicken 0.5 g/kg feed Feed q4d E 1479 Coccidial preventive for market broilers
8/22/2005
Diaveridine
Sulfaquinoxaline + Chicken 0.55 g/kg feed Feed QD E 1479 Coccidial preventive for replacement/breeder
Diaveridine 0 to 8-week old broilers
5:34 PM
Sulfaquinoxaline + Chicken 0.33 g/kg feed Feed QD E 1479 Coccidial preventive for replacement/breeder
Diaveridine 8 to 12-week old broilers
Sulfaquinoxaline + Poultry 0.56 g/L Drink QD E 1479 Repeat after 3 days, coccidiosis therapy
Page 320
Diaveridine
Sulfaquinoxaline + Poultry 0.56 g/L Drink q4d E 1479 Coccidial preventive
Diaveridine
Sulfathiazole Sodium Poultry 1 g/L Drink QD C 564
Sulfatroxazole Pigeon 50 PO BID A 565 Add trimethoprim
Sulfonamide Avian 0.045 g/L Drink QD E 924 Repeat after 2 days for coccidiosis
Tamoxifen Citrate Galliformes 40 NL NL B 677 Induce molting
Tannic Acid Avian 3g Topical PRN E 1240 Add aspirin + ethyl alcohol to prepare 100
ml for fungal dermatitis
Tannic Acid Psittacine Topical q2w D 1446 Add 3 g tannic acid + 3 g salicylic acid +
ethyl alcohol for 100 ml of solution for
dermatomycosis
Tea Ramphastid Dilute solution Drink QD G 1470 Prevent hemochromatosis by limiting iron
uptake, no citrus in diet
Terbinafine Avian 10-15 PO QD-BID E 1668 May combine with itraconazole for systemic
mycosis
Terbinafine Avian 10-15 PO QD-BID G 1338 For mycosis
Terbinafine Parrot, Grey Congo 1g/L aqueous Nebulize TID G 1743 For respiratory aspergillosis
Terbinafine Raptor 30 PO QD E 1359 Prophylactic
Testosterone Avian 10 IM QW E 924 For feather disorders

8/22/2005
Testosterone Avian 8 IM QW E 1473

Testosterone Canary 2.5 IM QW D 1441 For baldness
Testosterone Cypionate Psittacine 8 IM QW E 1240 Use with great care
5:34 PM
Tetanus Antitoxin Falcon, Saker 250 IU IM QD G 822 Loading dose of 125 IU each IV and IM in
lesion for localized tetanus
Tetracycline Avian 0.031-0.124 g/L Drink NL E 111

Page 321
Tetracycline Avian 200-250 PO BID E 111

Tetracycline Avian 1.25 ml/L Drink NL E 741
Tetracycline Galliformes 30-60 Drink QD E 704
Tetracycline Pheasant 0.04-0.12 g/L Feed QD G 678
Tetracycline Pheasant 55-110 mg/kg food Feed QD G 678
Tetracycline Pigeon 220 mg/kg food Drink QD E 704 50%, 2.5 g per teaspoon
Tetracycline Pigeon 0.549 g/L Drink QD E 1240 For chlamydophilosis
Tetracycline Pigeon 50 mg TD PO QD G 47 Remove grit from diet during treatment
Tetracycline Poultry 60 Drink QD C 705
Tetracycline Psittacine 50 PO TID E 565
Tetracycline Psittacine 1 g/L soft food Feed Once E 763 May add long-lasting oxytetracycline
Tetracycline Quail 220 mg/kg food Feed QD G 678
Tetracycline Quail 55-110 mg/kg food Feed QD G 678
Thiabendazole Anseriformes 550 NL NL G 1325 For thorny headed worms

Thiabendazole Avian 100 PO QD E 111 For Syngamus
Thiabendazole Avian 250-500 PO q2w E 111 For ascarids
Thiabendazole Avian 200 PO q10d E 924 For Syngamus, Amidostomum
Thiabendazole Avian 100 PO QD G 1309 For Syngamus trachei
Thiabendazole Avian 250-500 PO q10d G 1309 For ascarids
Thiabendazole Chicken 5 g/kg food Feed QD G 1325 For ascarids, Capillaria and gapeworms
Thiabendazole Chicken 44 PO Once G 1325 For Ascarids, Capillaria and gapeworms
Thiabendazole Crane 100 PO QW-q2w E 1361 For intestinal strongyles, ascarids
Thiabendazole Falcon 100 PO Once G 1325 For ascarids, Capillaria and gapeworms
Thiabendazole Pigeon 44 PO Once G 1325 For Ascarids, Capillaria and gapeworms

Thiabendazole Raptor 100-200 PO BID E 1400 Control of nematodes, may interfere with egg
laying
321
322

Thiabendazole Ratite 50 NL NL G 418
Thiabendazole Turkey 44 PO Once G 1325 For ascarids, Capillaria and gapeworms
Thiamine Anseriformes 25 mg/kg fish Feed Once E 1190

Thiamine Anseriformes 25 Feed QD G 46 Supplement for fish eaters

Thiamine Avian 1-2 IM-PO Once E 1650 For hypovitaminosis B1
Thiamine Bird, Piscivorous 0.2 g/kg fish Feed QD E 1554 For fish diet
Thiamine Bird, Piscivorous 1-2 PO QD E 1554 For fish diet

8/22/2005
Thiamine Crane 1-2 PO QD E 111

Thiamine Duck 100 μg/L Drink QD E 1358 For stargazing and weight loss in ducklings
Thiamine Eagle, Bald 1-3 NL QW E 1188 If eating frozen fish

5:36 PM
Thiamine Osprey 1-3 NL QW E 1188 If eating frozen fish

Thiamine Raptor 1-2 PO QD E 111
Thiamine Raptor 2 PO QW E 1068 While feeding frozen fish
Thiamine Raptor 0.2-0.25 g/kg fish Feed QD E 1132 For fish diets
Page 322
Thiamine Raptor 25 IM NL E 1433

Thiamine Raptor 1 IM NL E 1463
Thiopental Sodium Chicken 16.2 IM PRN B 1080 Add pentobarbital sodium

Thiopental Sodium Chicken 10-12.5 NL PRN B 1126
Thiopental Sodium Duck, Mallard 54 PO PRN B 1095
Thiopental Sodium Turkey 16.2 IM PRN B 1080 Add pentobarbital sodium
Thyroid Stimulating Amazon Parrot 1 IU TD IM Once B 88

Hormone
Thyroid Stimulating Cockatiel 0.1 U TD IM Once B 88
Hormone
Thyroid Stimulating Parrot, Grey 1 U TD IM NL B 533
Hormone
Thyroid Stimulating Pigeon 1 U TD IM Once B 88
Hormone
Thyroid Stimulating Psittacine 1-2 IU/kg IM NL E 1473
Hormone
Tiamulin Avian 25-50 PO QD E 565

Tiamulin Avian 1.08 mg/kcal PO QD E 1180
Tiamulin Avian 25 PO QD E 1492 For mycoplasmosis
Tiamulin Chicken 0.25 g/L Drink NL B 857 For Mycoplasma
Tiamulin Galliformes 25-30 Drink QD E 704 Use 1/2 strength for prophylaxis
Tiamulin Pigeon 0.225 g/L Drink QD E 704
Ticarcillin Avian 150-200 IM-IV TID-QID E 111

Ticarcillin Avian 5.1 mg/kcal IM-IV q2-4h E 1180 Synergistic with aminoglycosides
Ticarcillin Raptors 200 IM TID E 1027
8/22/2005
Ticarcillin Pigeon 200 IM-IV BID-TID G 590

Ticarcillin Psittacine 200 IM BID-QID E 565
Tiletamine + Zolazepam Albatross 2 IV PRN E 1617 Induction for gas anesthesia

5:36 PM
Tiletamine + Zolazepam Avian 5-10 IM PRN E 1181, 1231 Good immobilization

Tiletamine + Zolazepam Avian 2 IV PRN E 1617 Induction for gas anesthesia
Tiletamine + Zolazepam Budgerigar 15-20 IM PRN E 243
Page 323
Tiletamine + Zolazepam Budgerigar 20-22 IM PRN G 518

Tiletamine + Zolazepam Cassowary 2-3 IV PRN E 1533
Tiletamine + Zolazepam Chicken 30 IM Once B 1737
Tiletamine + Zolazepam Cockatoo, G Sulfur-crested 2.64-25.2 IM PRN G 518
Tiletamine + Zolazepam Dove, Ring-necked 50-75 IM PRN B 1393
Tiletamine + Zolazepam Duck 5-10 IM PRN E 243
Tiletamine + Zolazepam Eagle, Bald 15 NL PRN D 1401 Supplement with 15 mg/kg ketamine
Tiletamine + Zolazepam Egret, Cattle 2 IV PRN E 1617 Induction for gas anesthesia
Tiletamine + Zolazepam Emu 2-3 IV PRN E 1533
Tiletamine + Zolazepam Emu 5-10 IM PRN E 1617 Induction for gas anesthesia
Tiletamine + Zolazepam Flamingo 22 IM PRN G 518
Tiletamine + Zolazepam Flamingo, Chilean 6.6 IM PRN B 1393
Tiletamine + Zolazepam Gannet 2 IV PRN E 1617 Induction for gas anesthesia
Tiletamine + Zolazepam Goose, Lesser Magellan 6.6-8.8 IM PRN B 1393
Tiletamine + Zolazepam Goose, White-fronted 2.7 IM PRN B 1393
Tiletamine + Zolazepam Hawk 15 NL PRN D 1401 May cause salivation and poor
immobilization
Tiletamine + Zolazepam Hornbill, Rhinoceros 28.7 IM PRN G 518
Tiletamine + Zolazepam Ibis, Wood 11 IM PRN G 518
Tiletamine + Zolazepam Jabirus 2 IV PRN E 1617 Induction for gas anesthesia
Tiletamine + Zolazepam Macaw, Scarlet 4.4-11 IM PRN B 1393
Tiletamine + Zolazepam Osprey 9.26-17.6 IM PRN G 518
Tiletamine + Zolazepam Ostrich 5-20 IM PRN B 522 Chick dosage
Tiletamine + Zolazepam Ostrich 4-5 IM PRN B 1393
Tiletamine + Zolazepam Ostrich 5-10 IM PRN G 481 Add diazepam just prior to recovery for
captive animal
323
324

Tiletamine + Zolazepam Owl 10 NL PRN D 1401 Supplement with 10 mg/kg ketamine PRN
Tiletamine + Zolazepam Parakeet, Ring-necked 26 IM PRN B 1393

Tiletamine + Zolazepam Parrot, Patagonian 11 IM PRN G 518
Tiletamine + Zolazepam Partridge, Crested Wood 10 IM PRN B 1393

Tiletamine + Zolazepam Pea Fowl 11.3 IM PRN G 518
Tiletamine + Zolazepam Pelican 2 IV PRN E 1617 Induction for gas anesthesia
Tiletamine + Zolazepam Pheasant, Golden 16.6 IM PRN B 1393

Tiletamine + Zolazepam Pigeon 40-60 IM PRN B 1393
8/22/2005
Tiletamine + Zolazepam Pigeon 30-60 IM Once B 1737

Tiletamine + Zolazepam Plover 17.6 IM PRN G 518
Tiletamine + Zolazepam Psittacine 10 NL PRN D 1401
5:36 PM
Tiletamine + Zolazepam Psittacine 5-10 IM PRN E 1240 Provides good immobilization

Tiletamine + Zolazepam Raptor 10-20 IM NL D 1400
Tiletamine + Zolazepam Ratite 2-5 IM PRN G 418 Supplement with ketamine PRN
Tiletamine + Zolazepam Stork 2-5 IM NL E 243 Sedation
Tiletamine + Zolazepam Swan, Black 6.6 NL PRN D 1401 Supplement with 6.6 mg/kg ketamine PRN
Page 324
Tiletamine + Zolazepam Teal, Blue-winged 22-35 IM PRN B 1393

Tiletamine + Zolazepam Woodcock 44 IM PRN G 518
Tilmicosin Chicken 0.075 g/L Drink NL A 804 For Mycoplasma

Tilmicosin Chicken 0.25-0.5 g/L Drink NL B 768 For Mycoplasma
Tilmicosin Chicken 0.1-0.3 g/L Drink NL B 798
Tinidazole Avian 50 PO NL G 57
Tobramycin Avian 10 IM BID-TID E 565

Tobramycin Avian 5 IM BID-TID E 704
Tobramycin Avian 5 g/L Nebulize TID E 741 For sinusitis or airsacculitis
Tobramycin Crane 2.5-5 IM BID E 1473
Tobramycin Parrot, Grey 10 IM TID E 741 Possible polyuria
Tobramycin Pheasant 2.5-5 IM BID E 1473
Tobramycin Psittacine 2.5-5 IM BID E 111
Tobramycin Psittacine 5-10 IT QD E 741 Add carbenicillin for pneumonia
Tobramycin Raptor 2.5-5 IM BID E 1240 For resistant Pseudomonas
Tobramycin Raptor 5-10 IM-IV BID E 1400 Less nephrotoxic than other aminoglycosides
Tobramycin Raptor 10 IM BID G 234
Tolazoline HCl Avian 15 IV PRN E 1320 Reverse xylazine +detomidine +
medetomidine
Tolazoline HCl Ostrich 1 IV PRN G 481 Reverse xylazine
Tolazoline HCl Raptor 15 IV PRN G 201
8/22/2005
Toltrazuril Anseriformes 0.0125 g/L Drink QD D 1150 For coccidiosis

Toltrazuril Avian 7 PO QD D 1221 Antiprotozoal
Toltrazuril Avian 0.15 g/L Drink NL E 1180
Toltrazuril Avian 0.090 mg/kcal PO QD E 1180 Coccidiostatic
5:36 PM
Toltrazuril Avian 7-10 PO QD E 1554 For coccidiosis

Toltrazuril Chicken 6 PO QD E 1479 May repeat after 5 days for treatment and
control of Eimeria coccidiosis
Toltrazuril Chicken 25 PO QD G 564
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Toltrazuril Falcon 25 PO QW B 1134 For Caryospora infestation

Toltrazuril Kestrel, European 25 PO QD B 1131 For Caryospora infection
Toltrazuril Kiwi 25 PO Once G 1223 For coccidiosis
Toltrazuril Mynah, Bali 12.5 PO QD D 1438 For coccidiosis
Toltrazuril Turkey 0.025 g/L Drink QD B 1025
Tribromoethanol Bird, Seed-eater 2 g/kg grain Feed Once E 4 Add chloralose

Tribromoethanol Bird, Seed-eater 0.025 g/L Feed Once E 4
Tribromoethanol Booby 125 PO PRN B 1081 Add amylene hydrate
Tribromoethanol Cormorant 125 PO PRN B 1081 Add amylene hydrate
Tribromoethanol Duck, Mallard 100-158 PO PRN B 1095
Tribromoethanol Frigatebird, Magnificent 125 PO PRN B 1081 Add amylene hydrate
Tribromoethanol Turkey 40-44 g/L bait Feed Once G 1767 Corn is usual bait
Trichlorfon Raptors 1.5 g/L (0.15%) Topical NL G 1408 Spray for mites
Tricide Avian 5 g/L Topical NL G 1278 Spray on wounds and dermatitis

Tricide Avian 5 g/L Flush NL G 1278 Sinus flush, add antibiotic to solution,
potentiates antibiotics amikacin, neomycin,
enrofloxacin
Trimethoprim + Sulfa Anseriformes 0.048 g/L Drink QD E 1240 For nephritis, septicemia, hepatitis. For E.
coli, Pasteurella, Proteus, Salmonella, Listeria
Trimethoprim + Sulfa Avian 25 IM BID E 1434

Trimethoprim + Sulfa Avian 50 IM QD E 1434
Trimethoprim + Sulfa Avian 30-60 PO-SC BID E 1483 Emergency therapy
325
326

Trimethoprim + Sulfa Avian 50-100 PO BID G 1319
Trimethoprim + Sulfa Avian 0.15-0.4 g/L Drink NL E 1180 Dosage based on trimethoprim
Trimethoprim + Sulfa Avian 20-50 PO BID E 1431 For coccidiosis
Trimethoprim + Sulfa Avian 1 g/L Drink QD E 1431 For coccidiosis
Trimethoprim + Sulfa Avian 10 IM BID E 1431 For coccidiosis

Trimethoprim + Sulfa Bustard 8-30 IM BID E 1240 For nephritis, septicemia, hepatitis. For E.
Trimethoprim + Sulfa Canary 0.05-0.1 g/L Drink QD E 695 Dosage based on trimethoprim
8/22/2005
Trimethoprim + Sulfa Canary 0.1 g/kg food Feed QD E 695 Dosage based on trimethoprim
Trimethoprim + Sulfa Canary 0.2 g/kg food Feed Once E 1187 Dosage based on trimethoprim only
Trimethoprim + Sulfa Canary 0.15-0.4 g/L Drink NL E 1187 Dosage based on trimethoprim only
5:36 PM
Trimethoprim + Chicken 46-62 Drink QD A 1023

Sulfadiazine
Trimethoprim + Goose 0.3-0.7 g/kg Feed Once A 776 For Pasteurella multocida, trimethoprim to sulfa
Sulfachlorpyridazine ratio 1:5
Trimethoprim + Sulfa Ostrich 15 IM QD G 401
Page 326
Trimethoprim + Sulfa Passerine 0.2 g/L Drink QD E 1437 Dosage based on trimethoprim, add drug to
food at the same time
Trimethoprim + Sulfa Passerine 0.2 g/kg Feed QD E 1437 Dosage based on trimethoprim, add drug to
drink at the same time
Trimethoprim + Sulfa Penguin, African 110 PO BID G 128
Trimethoprim + Sulfa Pigeon 120 PO QD E 704
Trimethoprim + Sulfa Poultry 55 PO BID G 585
Trimethoprim + Sulfa Poultry 0.3-0.5 g/L Drink QD G 585
Trimethoprim + Sulfa Psittacine 20 PO BID-TID E 1240 For nephritis, septicemia, hepatitis. For E.
Trimethoprim + Sulfa Psittacine 8 IM BID E 1240 For nephritis, septicemia, hepatitis. For E.
Trimethoprim + Sulfa Psittacine 16-100 PO BID-TID E 1756 Use lower dosage for birds under 300 g for
bacterial nephritis
Trimethoprim + Sulfa Psittacine 52.8 IM QD-BID G 1309 For respiratory and enteric infections
Trimethoprim + Sulfa Raptor 30 SC BID E 1240 For nephritis, septicemia, hepatitis. For E.
Trimethoprim + Sulfa Raptor 20-50 PO BID E 1433 Do not use on dehydrated birds
Trimethoprim + Sulfa Raptor 60 PO BID E 1400 For coccidiosis, repeat after 2 days
Trimethoprim + Sulfa Raptor 17.5 PO QD G 94 Juvenile dosage
Trimethoprim + Sulfa Raptor 50 IM BID G 234
Trimethoprim + Sulfa Ratite 30-50 IM BID G 1308 For toxoplasmosis

Trimethoprim + Pigeon 60 PO QD A 968
Sulfamethoxazole
Trimethoprim + Psittacine 16-24 PO BID-TID A 1473
8/22/2005
Sulfamethoxazole
Trimethoprim + Psittacine 8 IM BID A 1473
Sulfamethoxazole
Trimethoprim + Pigeon 60 PO BID A 968
5:36 PM
Sulfatroxazole
Tubocurarine Cl Raptor 3 g/L Ophthalmic NL E 111 Every 5 minutes

Page 327
Tylosin Anseriformes 20-30 IM TID D 1150 For mycoplasmosis

Tylosin Anseriformes 20 PO TID D 1150 For mycoplasmosis
Tylosin Anseriformes 10 g/L Flush QD D 1150 For mycoplasmosis, use 10 ml per bird
Tylosin Avian 0.75 g/L Drink NL E 1180
Tylosin Avian 0.86 mg/kcal IM TID-QID E 1180
Tylosin Avian 1.08 mg/kcal PO QD E 1180
Tylosin Avian 10 g/L saline Flush BID E 1183 Nasal or sinus
Tylosin Avian 10 g/L saline Nebulize BID E 1185 10 to 60 minutes
Tylosin Avian 15 IM TID E 1240 For birds > 1 kg for upper respiratory
infection for Mycoplasma, Pasteurella,
Chlamydophila
Tylosin Avian 10 IM BID E 1617 For Mycoplasma
Tylosin Avian 10 g/L Nebulize TID-QID E 1650 Add dimethyl sulfoxide, adjunct to parenteral
therapy for air sacculitis
Tylosin Avian 10-40 IM BID E 1650 May use with lincomycin + spectinomycin
for mycoplasmosis
Tylosin Bird, Aquatic 10 IM BID E 1503 For Mycoplasma
Tylosin Bustard, Houbara 20 IM TID G 932 For Mycoplasma
Tylosin Canary 0.25-0.4 g/L Drink QD E 695
Tylosin Canary 0.4 g/kg food Feed Once E 1187
Tylosin Chicken 0.5 g/L Drink NL A 838 For Mycoplasma gallisepticum , less effective
than danofloxacin
Tylosin Chicken 0.25 g/L Drink QD B 1016 Add colistin for chronic respiratory disease
with E. coli
Tylosin Cockatiel Mix powder 1:10 Ophthalmic BID-TID E 111 Mix powder with sterile water 1 to 10
327
328

Tylosin Cockatiel 1:10 dilution water Topical QD-TID E 741 Eye spray, powder 250 g/8.8 oz,
conjunctivitis, may use with tylosin in water
Tylosin Crane 15 SC TID A 596

Tylosin Emu 15-25 IM TID-QID E 1473

Tylosin Falcon 30 IM TID E 1027 For Mycoplasma
Tylosin Finch 0.4 g/kg food Feed QD E 1572
Tylosin Finch 0.25-0.4 g/L Drink QD E 1572

Tylosin Finch, House 1 g/L Drink QD D 1439 Add ciprofloxacin for mycoplasmosis
8/22/2005
Tylosin Finch, House 0.3 g/L Drink QD D 1439 Preventive for mycoplasmosis
Tylosin Ostrich 11.4 PO TID G 467
Tylosin Passerine 0.25-0.4 g/L Drink QD E 1437 Add drug to food at the same time
5:36 PM
Tylosin Passerine, Small 0.25-0.4 g/L Drink NL E 1187

Tylosin Pigeon 25 IM QID A 847
Tylosin Pigeon 15-25 IM TID-QID E 111
Tylosin Pigeon 50 PO QD E 704
Tylosin Pigeon 0.5 g/L Drink QD E 704
Page 328
Tylosin Pigeon 15-25 IM TID-QID E 1473

Tylosin Psittacine Mix powder 1:10 Ophthalmic BID-TID E 111 Mix powder with sterile water 1 to 10
Tylosin Psittacine 40 IM NL E 763 Initial Mycoplasma therapy, used in

combination with aminoglycosides
Tylosin Psittacine 20-40 IM TID E 1240
Tylosin Quail 15-25 IM TID-QID E 1473
Tylosin Raptor 15 IM QD D 1612 For chronic air sacculitis
Tylosin Raptor 20 IM BID G 234
Tylosin Rhea 12.5 mg TD Parenteral Once G 582 Into distended sinus
Tylosin Rhea 50 mg TD SC QD G 582 Add penicillin G benzathine
Urate Oxidase Hawk, Red-tailed 100-200 KIU/kg NL NL A 1761 Uricolytic

Urate Oxidase Pigeon 20-600 KIU/kg NL NL A 1761 Uricolytic
Valnemulin Chicken 0.5 g/L Drink QD B 873 For Mycoplasma
Vasotocin, Arginine Sparrow, House 0.0004-0.0016 IV PRN B 1759 Dosage is dosage per minute, used for
antidiuresis
Vecuronium Bromide Avian 1 drop 4mg/ml soln Ophthalmic q15min E 1233
Vecuronium Bromide Cockatoo 0.8 g/L Ophthalmic NL G 218
Vincristine Sulfate Avian 0.75 mg/m2 surface IO QW E 1470 For lymphosarcoma - Check curent literature
8/22/2005
Vinegar, Apple Cider Avian 15 ml/L Drink QD D 1330 For low-grade candidiasis
Vinegar, Apple Cider Avian 60-120 ml/L Drink QD E 1205 For dysbiosis, Clostridium , GI tract bacteriosis
Vinegar, Apple Cider Avian 60-120 ml/L Drink QD E 1487 For dysbiosis, candidiasis, chronic bacterial
5:36 PM
diarrhea, Gram negative infections, foul smell

feces
Virginiamycin Poultry 22 mg/kg food Feed QD C 564

Page 329
Vitamin A Amazon, Red Lored 20 KIU/kg IM Once G 700

Vitamin A Avian < 50 KIU/kg NL Once E 1481 For clinical deficiency
Vitamin A Raptor < 20 KIU/kg IM QW E 1400 For hypovitaminosis A and epithelial
regeneration (bumblefoot)
Vitamin B Complex Amazon, Yellow-naped 1 Parenteral NL G 1697 Dosage based on thiamine

Vitamin B Complex Avian 1-3 IM QW E 1470 After hemorrhage with liver disease
Vitamin B Complex Avian 10 IM NL E 1650 Dosage based on thiamine for emergency
care
Vitamin B Complex Bird, Aquatic 10-30 IM-SC QW E 1503 For debilitation, anemia, appetite stimulant,
neurological disorders
Vitamin B Complex Hawk, Red-tailed 10 PO Once G 1644 Dosage based on thiamine for debilitation
Vitamin B Complex Psittacine 10-30 (thiamine dose) IM q2d E 1240 Dosage based on thiamine, neuromuscular
disease, hepatic disorders, thiamine-
responsive seizures
Vitamin B Complex Raptor 10-30 IM QW E 1240 Dosage based on thiamine, stimulate appetite
Vitamin D Avian 6.6 KIU/kg IM Once G 58 Add calcium gluconate + oxytocin
Vitamin E Avian 40 IM-PO NL E 924 Antioxidant, metal toxicity

Vitamin E Avian 0.05-0.1 Parenteral QW E 1650 For hypovitaminosis E
Vitamin E Bird, Aquatic 0.1 KIU/kg oil fish Feed Once E 1478
Vitamin E Ostrich 0.2-0.3 KIU/kg IM NL G 93 Juvenile dose
329
330

Vitamin E + Selenium Amazon, Red Lored 1 mg Se, 25 mg E IM Once G 700
Vitamin E + Selenium Avian 0.05-0.1 IM q2w E 111
Vitamin E + Selenium Ostrich 4-100 KIU TD IM QM G 401
Vitamin E + Selenium Raptor SC q3d E 1240 0.05 mg selenium + 3.4 IU vitamin E total
dose for muscular weakness, capture

myopathy, deficiency
Vitamin K Amazon, Yellow-naped 0.2 Parenteral NL G 1697

Vitamin K Avian 0.2-2.2 IM q4-8h G 87 Follow with daily dose for 1 to 4 weeks
8/22/2005
Vitamin K Avian 0.2-2.5 IM PRN E 1151 For hematochezia

Vitamin K Avian 0.025-2.5 NL BID F 58 Give every 2 to 3 weeks
Vitamin K Avian 0.2-2.5 Parenteral NL G 246
5:36 PM
Vitamin K Lory, Chattering 0.2 IM BID G 42

Vitamin K Psittacine 0.25-0.5 IM q2d-QW E 632 Neonate dosage
Vitamins A, D, E Avian 36.3 KIU/kg IM QW E 111 Give 33 KIU vitamin A + 3.3 KIU vitamin
D per kg
Page 330
Vitamins A, D, E Pigeon 33 KIU Vit A/kg IM QW G 590 Dosage based on Vitamin A

Vitamins A, D, E Psittacine 33-66 KIU/kg IM QW E 1240 For deficiencies, reproductive disorders and
bone healing
Xylazine HCl Amazon Parrot 1-2 IM PRN E 243 Add ketamine

Xylazine HCl Amazon Parrot 1-2 mg TD IV PRN G 1609 Add ketamine, mix together in syringe, may
start with half dose
Xylazine HCl Avian 4 IM PRN E 704 Add ketamine
Xylazine HCl Avian 2.2 IM PRN E 1181 Add ketamine, reverse with atipamezole,
prolonged recovery if not reversed
Xylazine HCl Avian 2.2 IV PRN E 1431 Add ketamine, good for short surgical
procedures, must reverse
Xylazine HCl Budgerigar 6.5 IM PRN E 243 Add ketamine
Xylazine HCl Cassowary 0.25 IV PRN E 1617 Add ketamine, use yohimbine to shorten
recovery
Xylazine HCl Cassowary 1 IM PRN E 1617 Add ketamine, use yohimbine to shorten
recovery
Xylazine HCl Cockatiel 2.5 IM PRN E 243 Add ketamine
Xylazine HCl Crane 1 NL PRN E 1189 Add ketamine for anesthesia
Xylazine HCl Emu 0.25 IV PRN E 1617 Add ketamine, use yohimbine to shorten
recovery
Xylazine HCl Falcon 2 IM PRN E 243 Add ketamine
Xylazine HCl Hawk 2.2 NL PRN G 1388 Add ketamine
Xylazine HCl Ostrich 0.66 IM PRN B 447 Add acepromazine + etorphine

Xylazine HCl Ostrich 150 mg TD IM PRN G 283 Add carfentanil
Xylazine HCl Parrot, Grey 1.5 IM PRN E 243 Add ketamine
Xylazine HCl Pigeon 10 IM PRN G 1481 Add butorphanol + ketamine for surgery
8/22/2005
Xylazine HCl Psittacine 1-2.2 IM-IV PRN E 1240 Use in combination with ketamine 1:3 or 1:5,
reverse with yohimbine
Xylazine HCl Psittacine 1-10 IM PRN E 1573 Sedation for small birds at high dosages
Xylazine HCl Psittacine 1-10 IM PRN G 201 Sedation, small psittacine
5:36 PM
Xylazine HCl Raptor 0.5 IV PRN D 1401 Add ketamine

Xylazine HCl Raptor 3 IM PRN E 4 Add ketamine
Xylazine HCl Raptor 1-2.2 IM-IV PRN E 1240 Use in combination with ketamine 1:3 or 1:5,
reverse with yohimbine
Page 331
Xylazine HCl Raptor 2 IV PRN G 1174 Add ketamine for diurnal raptors, lasts 1
hour
Xylazine HCl Raptor 0.25-0.5 IV PRN G 1174 Add ketamine, lower dosage regimen
produces less respiratory disturbance
Xylazine HCl Ratite 2.2 IM PRN E 4 Add ketamine
Xylazine HCl Ratite 1-2.2 IM PRN E 4 Immobilization
Xylazine HCl Ratite 0.5-1 IM PRN E 243 Add ketamine after 15 minutes
Xylazine HCl Ratite 1-2.2 Parenteral PRN G 418 Heavy sedation
Xylazine HCl Stork 0.2-0.4 IM PRN E 243 Sedation
Xylazine HCl Swan (Black, Mute) 2 mg TD IV PRN G 1291 Add ketamine, give 3/4 dose initially,
remainder if needed, gas anesthesia premed
Xylazine HCl Swan, Mute 0.28 IV PRN E 1190 Add ketamine
Yeast Cell Derivatives Avian N/A Topical PRN E 111 Promote skin healing, Preparation H®
Yohimbine HCl Avian 1 IO-IV PRN E 243

Yohimbine HCl Avian 0.1-0.2 IV PRN E 1181 Reverse xylazine
Yohimbine HCl Avian 0.1 NL PRN E 1231 Reversal of xylazine
Yohimbine HCl Avian 0.125-1 NL PRN E 1481 Reverse xylazine
Yohimbine HCl Budgerigar 0.11-0.27 IM Once G 83
Yohimbine HCl Cassowary 0.2 IV PRN E 1533 Shorten ketamine + xylazine anesthesia
Yohimbine HCl Emu 0.2 IV PRN E 1617 To shorten xylazine recovery
Yohimbine HCl Guinea Fowl 1 IV PRN B 553
Yohimbine HCl Guinea Fowl 0.15 NL PRN D 1401 Antagonize ketamine/xylazine anesthesia
331
332

Yohimbine HCl Hawk, Red-tailed 0.1 NL PRN D 1401 Antagonize ketamine/xylazine anesthesia
Yohimbine HCl Ostrich 0.125 NL PRN D 1401 Antagonist for xylazine

Yohimbine HCl Ostrich 12.5 mg TD IV PRN G 283
Yohimbine HCl Ostrich 0.125 IV PRN G 481 Reverse xylazine

Yohimbine HCl Psittacine 0.1-0.2 IV PRN E 1240 Reverse xylazine
Yohimbine HCl Raptor 0.1-0.2 IV PRN E 1240 Reverse xylazine
Yohimbine HCl Raptor 0.1 IV PRN G 201

Yohimbine HCl Ratite 0.125 IV PRN G 418
8/22/2005
Yunnan Paiyao Avian 1 ml/kg PO QD E 1435 Stock solution 2 capsules per 15 ml lactulose
5:36 PM
Yunnan Paiyao Avian 1.25-2.5 ml TD PO BID G 1112 Mix with 3 (cockatiel) to 10 (macaw) ml
water, use 1 day pre-operative, also use as
topical flush
Zeranol Ostrich 12 mg TD SC NL C 283 Implant growth promotion

Page 332
Zinc Methionine Raptor 25 PO QD E 1359 Antioxidant therapy, administer during lead

chelation therapy
333
Abbreviations
Abbreviation Translation Abbreviation Translation
< less than IN intranasal
> greater than indef indefinite
>= greater than or equal IO intraosseous
Bath 1 day or more in therapeutic liquid IO-IP-IT-IV intraosseous or intraperitoneal or intratracheal or
intravenous
BID two times daily
BID-q2d two times daily to every two days IO-IP-IV-SC intraosseous or intraperitoneal or intravenous or
subcutaneous
BID-QID two to four times daily
IO-IT-IV intraosseous or intratracheal or intravenous
BID-TID two to three times daily
IO-IV intraosseous or intravenous
cm² square centimeter
IO-IV-SC intraosseous or intravenous or subcutaneous
cm³ cubic centimeter
IP intraperitoneal or intracoelomic or intrapleuroperitoneal
d day
IP-IM intraperitoneal or intramuscular
d>w days to weeks
IP-IV intraperitoneal or intravenous
Dip less than 1 day in therapeutic liquid
IP-IV-PO intraperitoneal or intravenous or by mouth
doses number of doses to give
IP-IV-SC intraperitoneal or intravenous or subcutaneous
Drink drinking water
IP-PO intraperitoneal or by mouth
Epidural epidural injection
IP-SC intraperitoneal or subcutaneous
Feed include in feed
IT intratracheal
Flow constant flow
IT-IV intratracheal or intravenous
Flush flush
IT-IV-PO intratracheal, intravenous and orally
Fog fog the environment
IU International Units
g gram
IUt intrauterine
ga gauge
IV intravenous
GI gastrointestinal
IV-PO intravenous or by mouth
gr grain
IV-PO-SC intravenous or by mouth or subcutaneous
h hour
IV-SC intravenous or subcutaneous
IA intraarticular
kcal kilocalories
IA-IM intraarticular or intramuscular
kg kilogram
ICa intracardiac
KHz kilohertz
ICa-IP-IV intracardiac or intraperitoneal or intravenous
KIU thousand International Units
ICr intracranial
L liter
ID intradermal
life lifelong therapy
IH inhalation
long long therapy regimen
IM intramuscular
m month
IM-IN-IO-IV intramuscular or intranasal or intraosseous or
intravenous m² square meter
IM-IN-IV intramuscular or intranasal or intravenous m³ cubic meter
IM-IO-IT-IV intramuscular or intraosseous or intratracheal or MD maximum dose

intravenous mEq milliequivalent
IM-IO-IV intramuscular or intraosseous or intravenous mg milligram
IM-IP intramuscular or intraperitoneal min minute
IM-IP-IV intramuscular or intraperitoneal or intravenous MIU million International Units
IM-IP-IV-SC intramuscular or intravenous or intraperitoneal or ml milliliter
subcutaneous
mm² square millimeter
IM-IP-PO intramuscular or intraperitoneal or by mouth mmol millimoles
IM-IP-PO-SC intramuscular or intraperitoneal or by mouth or mol molar solution
subcutaneous
months for several months
IM-IP-SC intramuscular or intraperitoneal or subcutaneous
N normal solution
IM-IV intramuscular or intravenous
nebulize nebulization
IM-IV-PO intramuscular or intravenous or by mouth
NL not listed
IM-IV-PO-SC intramuscular or intravenous or by mouth or
subcutaneous once give single dose
IM-IV-SC intramuscular or intravenous or subcutaneous ophthalmic in the eye
IM-PO intramuscular or by mouth oz ounce
IM-PO-SC intramuscular or by mouth or subcutaneous Parenteral-PO parenteral or by mouth
IM-SC intramuscular or subcutaneous PO by mouth
IM-Topical intramuscular or topical PO-SC by mouth or subcutaneous

PO-SC-Topical by mouth or subcutaneous or topical
Abbreviation Translation Abbreviation Translation

PO-Topical by mouth or apply topically q5h every five hours
ppm parts per million q5min every five minutes
ppt parts per thousand q60h every sixty hours
PRN as needed q6d every six days
q10-14d every ten to fourteen days q6m every six months
q10d every ten days q6m-QA every six months to every year
q1-2h every one to two hours q6w every six weeks
q1-4h every one to four hours q7w every seven weeks
q15min every fifteen minutes QA every year
q2-3d every two days to three days QD every day
q2-3h every two to three hours QD-BID every day to two times daily
q2-3w every two to three weeks QD-q2d every day or every two days
q2-4d every two days to four days QD-q3d every day to every three days
q2-4h every two to four hours QD-QID every day to four times daily
q2-4w every two weeks to four weeks QD-QW every day to every week
q2-5d every two days to five days QD-TID every day to three times daily
q2-6h every two to six hours QH every hour
q2d every two days QID four times daily
q2d-QW every two days to every week QM every month
q2h every two hours QM-q2m every month to every two months
q2m every two months qow every other week
q2w every two weeks QS add sufficient quantity
q30min every thirty minutes QW every week
q33h every thirty three hours QW-q10d every week to ten days
q3-4d every three to four days QW-q2w ever week to every two weeks
q3-4h every three to four hours QW-q3w every week to every three weeks
q3-4w every three to four weeks r10d repeat in ten days
q3-5d every three to five days r2m repeat in two months
q36h every thirty six hours r2w repeat in two weeks
q3-6h every three to six hours r6m repeat in six months
q3-6w every three to six weeks r7-10d repeat in seven to ten days
q3-7d every three to seven days ra repeat annually
q3-8h every three to eight hours rm repeat in one month
q3d every three days rw repeat in one week
q3d-q2w every 3 days to two weeks SC subcutaneous
q3d-QW every three days to every week SCJ subconjunctival
q3h every three hours SC-Topical subcutaneous or topical
q3m every three months sec second
q3w every three weeks short short therapy regimen
q4-5d every four to five days slowly administer slowly
q4-5h every four to five hours soln solution
q4-6d every four to six days TD total dose
q4-6h every four to six hours TID three times daily
q4-6m every four to six months TID-q2d three times daily to every two days
q4-6w every four to six weeks TID-QID three to four times daily
q4-8h every four to eight hours topical apply topically
q4d every four days vapor vapor in enclosure
q4d-QW every four days to weekly vent anus, rectum or cloaca
q4h every four hours w week
q4m every four months weeks for several weeks
q5d every five days y year
q5d-QW every five days to every week µg microgram
335
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10_IntegrativeMed.qxd 8/22/2005 3:38 PM Page 343
CHAPTER
10
Integrative
Therapies
ROBERT D. NESS, DVM
Integrative therapies constitute a very wide range of dis-

ciplines from around the world. Many of these therapies
can be utilized to treat pet birds, although none was
specifically developed for avian species. Because birds
have not been domesticated, remaining genetically and
evolutionarily close to their wild counterparts, they tend
to be very responsive to natural therapies. Certain
modalities, such as chiropractic and acupuncture, must
be modified for differences in avian anatomy and physi-
ology. Others can easily be extrapolated to pet birds
from human or other mammals with only slight adjust-
Greg J. Harrison
ments. Some examples include homeopathy, flower

essences, nutriceuticals and many herbs. Other thera-
pies, such as diffusion aromatherapy, must be used with
caution to avoid toxic reactions. Integrative therapy in
birds has existed for centuries in poultry medicine
through acupuncture and herbal therapy in China.
Many terms have been used to describe these forms of

Ed. Note: According to the American Holistic Veterinary treatment, including integrative therapy, alternative ther-
Medicine Association, “...the word ‘holistic’ means tak- apy, holistic care and complementary medicine. Each of
ing in the whole picture of the patient – the environ- these terms has specific implications and none of them
ment, the disease pattern, the relationship of pet with is entirely accurate. Alternative therapy suggests another
owner – and developing a treatment protocol using a way to do the same thing. Complementary implies that it
wide range of therapies for healing the patient.” This augments conventional therapy. Holistic refers to treat-
includes integrating conventional protocols with possi- ment of the whole patient in a complete approach, but
ble complementary and alternative therapies – what- usually infers that it is separate from conventional ther-
apy. Integrative therapy involves the integration of a vari-
ever are the most efficacious, least invasive, least
ety of modalities into a more complete healthcare sys-
expensive and least harmful paths to cure. The chapter
tem. This term is most appropriately applied when the
presented here is a brief introduction to selected inte-
varying therapies are used in conjunction with conven-
grative therapies in order to familiarize the avian prac- tional Western therapy.
titioner with those that have been used in pet bird prac-
tice and to offer options for possible further study. Several integrative modalities are described below, with
specific indications for birds. This is not intended to be
an exhaustive list of therapies for birds or serve as a
complete description of these therapies. Rather, this is unique from those of mammals in several ways. Birds
an introduction into the wide array of holistic modalities are bipedal with modified forelimbs as wings. Many of
and their potential implications for pet birds. Further the long bones in their limbs are pneumatic, allowing
training and education is recommended prior to wide- for extension of the air sac system as well as less weight
spread implementation of these therapies in practice. for flying. The air sacs also may perfuse certain segments
Veterinary certification programs are available for some of the vertebral spine. The avian spine is divided into
of these modalities, including animal chiropractic and cervical, thoracic, synsacral, free-caudal and pygostyle
veterinary acupuncture. A list of resources and programs (fused-caudal) sections.20 The number of cervical verte-
is provided in Table 10.6. brae varies with species, with budgerigars having 11 and
Amazon parrots having 12. The last cervical vertebrae
and first 3 thoracic vertebrae are fused in Galliformes.
The number of thoracic vertebrae varies from 3 to 10,
Integrative Modalities depending on species. Ribs are present on both cervical
and thoracic vertebrae. A large portion of the avian spine
ANIMAL CHIROPRACTIC is fused into the synsacrum, including the lower tho-
racic, lumbar, sacral and caudal spine. There are 10 to
The practice of chiropractic is credited to D.D. Palmer
23 synsacral vertebrae and 5 to 9 caudal vertebrae. The
during the mid-1890s.27 D.D. Palmer’s son, B.J. Palmer,
ilium and ischium are fused together and to the syn-
further developed the practice through research and
sacrum. The pubic bones are unfused, except in ratites.
clinical practice. Although the Palmers are known as the
founders of current chiropractic care, adjustments have Chiropractic care can be used in a variety of avian cases
been used for thousands of years. B.J. Palmer estab- from trauma to reproductive conditions. Traumatic
lished the first chiropractic school in Davenport, Iowa, injury to the cervical vertebrae is a sequela to flying into
known as Palmer Chiropractic College. a wall or window. Torticollis and localized feather pick-
ing also can be potential chiropractic cases. Adjustment
Chiropractic is defined as “that science and art which
of the thoracic spine may correct certain respiratory or
utilizes the inherent recuperative powers of the body
digestive disturbances with underlying neurologic or
and deals with the relationship between the nervous sys-
neuromuscular origin. Dystocia can be the result of an
tem and the spinal column, including its immediate
abnormal egg, metabolic disturbance or abnormal pelvic
articulations, and the role of this relationship in the
anatomy. The latter etiologies may be assisted by chiro-
restoration and maintenance of health.”27 Because all
practic adjustment.22
functions of the body are innervated and controlled by
nerves, the implications of chiropractic care in health
management are enormous. Not only can chiropractic VETERINARY ACUPUNCTURE
therapy treat a stiff neck or back pain, it may be useful Acupuncture has been used for at least 5000 years in
in many systemic and metabolic disorders. China, which is considered the site of origin. Early
acupuncture needles were made from stone and fish
Chiropractic therapy is directed at the release of fixa- bones. About 500 A.D., the practice of acupuncture
tions and subluxations of the spine. The term subluxa- spread to Japan and Korea, which established their own
tion is used to describe a misaligned vertebra that is forms. By the 6th century, acupuncture had spread
unable to properly move in relation to adjacent verte- throughout Asia. By the 17th century, it was found in
brae. This can be either a structural or functional Europe, and finally arrived in North America during the
malalignment, which may not be obvious on radiograph 19th and 20th centuries. It was not until 1971 that
or conventional physical examination. These subluxa- acupuncture made its way into American culture. This
tions are corrected by a precise manipulation of the was the result of a New York Times journalist being
spine known as an adjustment. An adjustment involves treated with acupuncture while on assignment in China.
the application of a high-velocity, low-amplitude manual He had his appendix removed and was treated with
force to release fixations without damage to the motor acupuncture for postoperative pain. Over the past 30
unit.27 A motor unit is defined as two adjacent vertebrae years, acupuncture has slowly become more mainstream
and the associated structures between them, including in American culture.
ligaments, blood vessels, nerves, joints and muscles. The
adjustment must be specific in regard to the force and Veterinary acupuncture also has a long history. Evidence
angle applied to the specific vertebral joint. of elephant acupuncture dates back about 3000 years in
Sri Lanka. The Chinese Chou Dynasty dating back to
In general, any vertebrate is a potential chiropractic 1066 to 221 B.C. recorded several veterinary applica-
patient, including birds. The avian skeletal system is tions. The father of Chinese veterinary medicine is Shun
Chapter 10 | I N T E G R A T I V E T H E R A P I E S
345
Yang (Pao Lo), who was the first full-time practitioner of juvenile and some adult parrots, columbiformes, water-
Chinese veterinary medicine in 430 B.C.31 Veterinary fowl and poultry readily accept dry needles. The use of
acupuncture has developed in various parts of the 36- or 38-gauge by 15-mm needles is appropriate for
world, especially in Asia, over the past 2000 years. In parrots, poultry and other larger birds. Plastic Seirin #5
1974, the National Association of Veterinary Acupuncture needles can be made lightweight and better balanced by
(NAVA) was established as the first veterinary acupunc- cutting off the plastic handle for better retention of the
ture association in the West, but was active for only 5 needle in birds. Smaller birds may require Sooji Chim
years.10 Later in 1974, the International Veterinary hand needles (Korean gauge 8-mm length).
Acupuncture Society (IVAS) was established and has
since become a core association for veterinary acupunc- An effective alternative to traditional needling is aqua-
ture in the United States and the world. Since 1998, puncture. This technique involves the injection of
three other teaching organizations in the USA have cyanocobalamin (vitamin B12) or saline into the acupoint
offered training in veterinary acupuncture. using a 27- to 29-gauge hypodermic needle and 0.5- to
1-ml syringe. Medium to large size parrots receive up to
Acupuncture is one part of the holistic health system 0.10 ml per site, while smaller birds get as little as 0.01
known as Traditional Chinese Medicine (TCM). Other ml per site. The aquapuncture technique has the added
TCM components include proper nutrition, exercise, advantage of providing a longer lasting effect at the site.
herbal remedies and appropriate lifestyle. The main
premise of TCM is that we are all part of nature, and Another technique for potential use in birds is laser ther-
health is achieved by establishing balance with the natu- apy. Low-intensity, cold laser lights are effective in pene-
ral world. This balance of nature is characterized by the trating the thin skin of birds to stimulate the shallow
Chinese concept of Yin-Yang, which is the balance acupoints on birds. Disadvantages of laser therapy
between such things as light and dark, wet and dry and include the lack of specificity for acupoint stimulation in
hot and cold. areas where multiple points are close together and lack
of stimulation of deeper acupoints. Gold beads or wire
Acupuncture involves the placement of fine needles into implants have been used in birds for chronic cases
specific points on the body to elicit a physiologic and requiring much longer periods of stimulation. Acupunc-
energetic response along energetic pathways known as ture techniques seldom used in pet birds include elec-
meridians. Meridians are interconnected energetic path- troacupuncture and moxibustion, since birds are Yang
ways that run throughout the body. These pathways by nature and both of these are strong Yang-stimulating
carry the body’s Qi (vital life force or energy). The pres- techniques.24
ence of Qi is what defines the existence of life. The
placement of acupuncture needles into points along The clinical applications of veterinary acupuncture
these meridians enables the body to restore itself to include everything from pain management to treatment
homeostasis by affecting the Qi flow. of systemic diseases. Acupuncture is effective for many
chronic disorders such as allergies, arthritis, urinary
The physiologic effects of acupuncture are being studied incontinence and reproductive disorders. Typically,
and verified by scientific methods. The anatomic loca- acupuncture is combined with Chinese herbs and
tions of acupuncture points coincide with sites of an proper nutrition to achieve the greatest effect.
increased density of nerve endings, small capillary beds
and mast cell aggregation. As a result, a measurable Acupuncture and Traditional Chinese Veterinary
physiologic effect in beta-endorphin release, stimulation Medicine (TCVM) have been developing over the past 20
of circulation and decrease in inflammation results from years in pet bird medicine. Historically, the use of
acupuncture stimulation. In pain control, experiments acupuncture on birds in China was primarily restricted
have shown a modification in neural impulse transmis- to poultry, which was fairly limited due to the lack of
sion from the spinal cord to the brain after acupuncture. economic benefit in treatment of individual birds.
This effect is known as “gate control” theory, which pro- Rather, the administration of herbal treatments was
poses that acupuncture can block the action of pain more common for flock treatment.7 However, the use of
fibers in the spinal cord.26 acupuncture in pet birds has gained some popularity in
the USA in recent years, especially for the treatment of
A variety of acupuncture techniques exist. The use of the feather picking.1,28 Despite the lack of historical docu-
different techniques depends on the species and general mentation, acupuncture can be beneficial in the treat-
cooperation of the patient, type and severity of the con- ment of many pet bird conditions.
dition being treated, and personal preference of the
acupuncturist. Traditional dry needling is commonly The use of acupuncture in birds poses various chal-
used in mammals but is more difficult in birds. Most lenges from their anatomic differences and physiologic
characteristics. Birds have a high metabolic rate and rela- tors is just as important in TCVM as in conventional
tively high body temperature (42.4° C) with rapid heart therapy. Crop stasis is thought of as a problem with the
and respiratory rates. They have hollow bodies with air Stomach or Liver meridian. The TCVM diagnosis of egg
sacs, pneumatic bones and hollow feather shafts. As binding is a Kidney Qi condition. Kidney disease is not
compared to mammals, birds are relatively dry, possess- treated as directly with TCVM in birds as in mammals
ing minimal moisturizing glands. These characteristics because the kidney association point is not available,
make birds Yang by nature.24 As a result, birds have a yielding to the use of various kidney meridian points
tendency toward a relative or true Yang excess when based on the TCVM diagnosis. Applying the basic con-
they are sick. The stress and anxiety inherent in the cepts of TCVM to establish a diagnosis and treat accord-
restraint of birds also must be considered when using ingly is more effective than applying a standard set of
acupuncture. In addition, because birds instinctively procedures to a conventional diagnosis. As a point of
mask signs of disease, they must be thoroughly exam- reference, Table 10.1 has a list of common acupoints
ined to reveal their true status prior to selection of the used in the treatment of common conditions in pet
acupuncture points. birds. In addition, Figs 10.1-10.3 illustrate the position
of these points.16
Acupuncture points are commonly extrapolated from
one species to another, and special points are commonly HERBAL THERAPY
described for individual species. Avian acupuncture
The use of specific herbs for medicinal purposes dates
employs the same techniques to locate and describe
back thousands of years. Several herbs are mentioned in
acupuncture points. Transpositional points from mam-
the Bible, and archeologists have documented herb use
mals constitute the majority of the acupoints in birds,
back to prehistoric times. Herbs are used around the
and these may be of TCM origin or special points
world, including Western herbs from North America,
defined in other species. Special TCM points for poultry
Ayurvedic herbs from India and traditional Chinese herbs.
without a mammalian counterpart also are used in pet
birds, including Gu Duan (end of thigh), used for Approximately 25% of our conventional drugs are
drooping wings, and Bei Ji (back of the body spine), derived from plants. Conventional drugs typically con-
which is a grouping of three points used to treat respira- tain a single active constituent from the plant, whereas
tory disease. A few points that have been specifically herbs provide a broader and more balanced effect on
described for pet birds include some of the back Shu the body through the synergistic actions of the herbal
points, which do not correspond to the mammalian components. Herbs are best prescribed to treat the
counterparts because of the fused synsacrum. Detailed entire individual and not only the clinical signs. Herbal
descriptions and indications of specific avian acupoints blends and formulations combine the benefits of multi-
are defined in the listed references.24 ple herbs, which typically produce a synergistic action
while minimizing the potential toxic effects of a single
Certain disorders in TCVM are more frequently seen in herb. Herbs provide many unique qualities that are very
birds. In general, these include Liver Yin deficiency, limited in conventional medicine, such as anticancer,
Heart Yin deficiency, stagnant Liver Qi, Kidney Yin defi- antiviral and immunoregulation properties.
ciency, Blood deficiency, Lung Yin deficiency and Lung
Dryness. Kidney Essence deficiency is common in cock- Currently, herbal products are not regulated or con-
atiels and budgerigars that have been inbred for genera- trolled. Therefore, practitioners and clients must remain
tions. External pathologic factors, described as Wind- cautious in administering a product without evaluating
Damp and Damp-Heat, are common in the Western diag- the company and verifying that the active component of
nosis of microbial infections.16 the herb or plant actually is in the formulation. Product
labels can bear the name of an herb or plant substance as
Acupuncture can be effective in the treatment of many long as some portion of it is present in the formulation,
conventional Western conditions diagnosed in pet birds. but it does not always imply that the medicinally active
Bacterial infections are commonly diagnosed in birds constituent is included. Standardized extracts are avail-
and are described as Damp-Heat or other pathogenic able for certain herbs through concentrating the active
Heat conditions in TCVM. Conjunctivitis can be treated ingredients, resulting in more of a plant drug than an
with local points and specific meridian points for herbal medicine.29 Standardizing alters the physical and
Liver/Kidney Yin deficiency. Sinusitis is often the result of energetic nature of the herb. This process also eliminates
a Wind-Cold or Wind-Heat condition, based on the char- the synergistic effects of the myriad chemical compo-
acteristics of the discharge. Various other TCVM condi- nents in the plant. For some herbs such as milk thistle,
tions can present with sinusitis as a clinical sign. standardization is advantageous, since the specific active
Identification and specific treatment of underlying fac- constituent is clearly known and purified in the process.
347
Table 10.1 | Acupuncture Points in Birds

Acupoint Name Characteristics Indication / Action
LU-1 Avian Fei Tang Alarm point for Lung Acute resp. disease, fever, wing weakness
LU-2 Avian Yi Gen Cold, fever, tracheitis, ptosis of wing
LU-7 Lie Que Master point for head & neck Neck stiffness, resp. disease, weak carpus
LU-9 Tai Yuan Tonification for LU channel Regulate Lung Qi, clear Lung & Liver heat
LI-4 He Gu Master point for face & mouth Facial swelling, eye pain, egg binding, diarrhea
LI-10 Shou San Li Tonifies Qi Abdominal pain, Bi syndrome of wing
LI-11 Qu Chi He Sea point, tonification point Pain of elbow, abdominal pain & regurgitation
ST-6 Jian Che Facial paresis & swelling, neck pain & stiffness
ST-35 Avian Xi Gai Inflamed, painful & swollen knee, leg weakness
ST-36 Zu San Li Master point upper abdomen Tonifies Qi & Blood, raises Yang, body strength
ST-37 Shang Ju Xu Lower He-Sea point of LI Chronic diarrhea & loose stool, remove LI damp
ST-40 Feng Long Connecting point Resp. disease, muscle atrophy & weak, mental
ST-41 Avian Gou Qian Tonification point Bi syndrome in hock & digits, pharyngitis
SP-6 San Yin Jiao “Three Yin meeting” of leg Egg binding, cloacal prolapse, leg paralysis/pain
SP-9 Yin Ling Quan Sea & Water point Distended abdomen, edema, diarrhea, knee pain
SP-10 Xue Hai Sea of blood Blood disorders, urticaria, pain in medial thigh
SP-11 Avian Kua Nei Blood letting point Inflammation, swelling or poor mobility in legs
HT-7 Shen Men “Mind door,” source point Mental disorder, epilepsy, feather picking
SI-3 Hou Xi Tonification point, opening of GV Neck rigidity, wing contracture, back problems
BL-11 Avian Xin Shu Assn. point for Heart Mental disorders, irritability, epilepsy
BL-12 Avian Fei Shu Assn. point for Lung Respiratory disease/infection, fever
BL-13 Avian Wei Shu Assn. point for Stomach Crop disease, vomiting/regurg., indigestion
BL-14 Avian Pi Shu Assn. point for Spleen Maldigestion, indigestion, diarrhea, vomiting
BL-15 Xiao Chang Shu Assn. point for Small Intestine Lower abdominal pain, diarrhea
BL-16 Avian Gan Shu Assn. point for Liver Hepatopathy, conjunctivitis, inflamed cloaca
BL-17 Avian Xin Shu Assn. point for Large Intestine Pain in lower back, LI & cloacal disorders
BL-40 Avian Xi Wan Master point of back & legs Inflammation, pain, & swelling of feet & knee
BL-60 Kun Lun Expels Wind & clears Heat Pain in back, shoulder & wing, egg binding
BL-62 Shen Mai Eliminate interior Wind Epilepsy, mental confusion, pain in back & legs
KI-1 Avian Jiaodi Foot base, sedation point Calms mind, tonifies Yin, remove Yin-heat
KI-3 Tai Xi Greater stream, source point Infertility, sore throat, back pain, insomnia
KI-6 Zhao Hai Nourishes Yin, cools blood, Calms mind, anxiety, soft-shelled eggs, Yin def.
PC-6 Nei Guan Inner gate, master chest/lung Mental disorder, pain, epilepsy, fever
PC-7 Da Ling Source point, sedation point Gastric pain, regurgitation, panic, epilepsy
TH-4 Yang Chi Yang pond, source point Pain in wing & shoulder, kidney disease
TH-5 Wai Guan Outer gate, connecting point Motor problems in wing, behavior problems
TH-10 Tian Jing Heavenly well Mood swings, Bi syndrome of wing, damp-heat
TH-23 Avian Yan Jiao Eye correct Eye problems, expels wind, pain relief
GB-13 Benshen Point of Yang Linking Vessel Emotional problems, epilepsy, calming point
GB-29 Ju Liao Removes channel obstructions Pain & paralysis of back & legs
GB-31 Avian Kua Wai Expels Wind - relieves itching Inflammation, swelling & difficult leg movement
GB-34 Xi Yang Guan Relaxes Sinews Pain & swelling of knee (Bi syndrome)
GV-1 Avian Hou Hai Regulates GV & CV Loss of appetite, mental depression, prolapse
GV-2 Avian Wai Gen Extinguishes interior Wind Diarrhea, mental depression, cloacal prolapse
GV-12 Avian Bei Ji TCVM poultry point All respiratory diseases
GV-13 Avian Bei Ji Similar to Tao Dao, clear heat All respiratory diseases
GV-14 Avian Bei Ji GV, Bl, GB & ST meeting point All respiratory diseases
GV-20 Avian Guan Ji Meeting point of all Yang channel Mental stress, depression, cloacal prolapse
GV-24 Shenting Du Meeting point of GV & ST Severe anxiety & fear (calms mind)
Ba Feng Avian Jiao Pan TCVM poultry bleeding point Relax Sinew, pain & infection in feet
Gu Duan Avian Gu Duan TCVM poultry point Ptosis of wing (poultry), Bi syndrome of pelvis
Used with permission from Mosby ©2000 from ref 17

Fig 10.2 | Acupuncture points of birds, dorsal view.
Other factors that affect the potency and medicinally

active components of the herb include the method and
time of harvest, the parts and preparation of the plant
that are included and the handling and processing of the
Fig 10.1 | Acupuncture points of birds, lateral view.
finished product. Only well-known and respected herbal
companies should be considered when purchasing
herbal products. Whenever possible, fresh herbs or veg-
etable glycerin-based extracts should be used.
Herbs are effective in the treatment of many conditions

in birds. Herbal remedies are much more effective than
conventional therapy in treating metabolic conditions
such as liver and kidney diseases. Herbs are an excellent
alternative to antibiotics in the treatment of infectious
diseases, with wider antibacterial effects in addition to
various antifungal and antiviral actions. Many of these
herbal remedies also support the immune system to
assist in the full recovery of the patient. Some herbal for-
mulations serve as detoxification agents, antioxidants
and anticancer therapies. Table 10.2 lists several com-
mon herbal remedies with potential indications in avian

therapy.18
Liver disease is a common diagnosis in pet birds.

Hepatic lipidosis is often the result of poor nutrition,
typically sunflower seed-based diets. Other chronic con-
ditions leading to hepatic disease in birds include
repeated aflatoxin exposure, heavy metal toxicity and
Chlamydophila spp. Hepatic fibrosis and cirrhosis are
potential sequelae to these conditions. However, con-
Fig 10.3 | Acupuncture points of the avian leg and foot. ventional therapy falls short in treatment of these liver
diseases. Certain herbs have been used for centuries in
the treatment of liver disease in people, and these can
349
Table 10.2 | Herbal Remedies for Birds

Herbal Remedy Scientific Name Healing Properties Indications
Astragalus Astragalus membranaceous Immune system booster, especially on the Enteritis and diarrhea, pancreatic disorders, respiratory
digestive tract disease, uric acid excretion
Burdock Root Arctium lappa Nutritive liver tonic, blood cleansing, Chronic liver disease, environmental toxins, skin
gallbladder stimulant and diuretic disease and irritation
Chamomile Matricaria recutita Analgesic, calming, anti-inflammatory and Calming effects, eg, feather-picking birds
symptom relief of GI disorders
Chaparral Larrea tridentata Anticancer, antioxidant, analgesic, Cancer treatment with red clover
antiseptic and anti-arthritic Do not use in egg laying, hand-feeding, or
liver-diseased birds
Dandelion Taraxacum officinale Potent diuretic (leaf) and increase bile produc- Diuresis - ascites and respiratory fluid, liver disease -
tion and excretion (root) increase bile flow
Echinacea Echinacea Immune booster (especially against viruses) Early course of infection, chronic sinusitis viral or
candida infections, PBFD support
Elderberry Sambucus nigra Anti-inflammatory, alterative and antiviral Viral infection, viral skin disorders, acute rhinitis and
sinusitis
Essiac Combination of herbs - Anticancer formulation and lessens pain of Pain, cancer
Indian rhubarb, Slippery cancer
elm, Burdock root &
Sheepshead sorrel
Feverfew Tanacetum parthenium Analgesic and lowers fever Relieves non-specific pain and inflammation,
especially of GI tract
Ginseng Panax Potent immune and energy booster (use less Anemia, immune deficiencies, diarrhea, chronic
than 2 weeks) enteritis, cystic ovaries, cancer
Hawthorn Berry Crataegus Cardiac supportive, lowers blood pressure Heart disease, supports heart in several aspects
Marshmallow Althea officinalis Antitussive, soothing of membranes and Cloacaliths and uroliths, mycobacteria, GI inflamma-
emollient tion, feather picking
Milk Thistle Silybum marianum Hepatoprotective, hepatoregenerative and Hepatitis, hepatic lipidosis, cirrhosis, bile duct
potent antioxidant inflammation, hepatic toxicosis
Mullein Verbascum thapsus Emollient, antitussive, antispasmodic, expecto- Self-induced trauma, ear infections,
rant and vulnerary properties respiratory disorder, diarrhea
Olive Leaf Olea europaea Antimicrobial (bacterial, viral and fungal) and Virtually any infection (potent effect)
diuretic ascites - promote fluid excretion
Red Clover Trifolium pratense Anticancer, blood cleansing, diuretic, tonic, Cancer therapy (with other herbs)
nutritive, estrogenic supports debilitated patients
St. John’s Wort Hypericum perforatum Sedative, antidepressive effects, anti-inflamma- Pruritic or painful feather picking,
tory and astringent chronic viral infection, anxiety
Valerian Root Valeriana officinalis Tranquilizer and sedative Nervousness, convulsions/epilepsy, pain relief,
insomnia
be extrapolated for use in birds and other pets. Some of species should be an organic formulated diet, with lim-
the herbs that support and protect the liver include milk ited portions of fresh organic fruit, vegetables and rice.
thistle (Silybum marianum), dandelion (Taraxacum Seeds and nuts should be considered treat items and fed
officinale), Oregon grape (Mahonia spp.), burdock root in limited proportions because they are breeding stimu-
(Arctium lappa) and licorice root (Glycyrrhiza glabra).23 lants (see Chapter 4, Nutritional Considerations).
The recommended diet varies according to species, age,

NUTRICEUTICAL SUPPLEMENTS health status and activity level. In addition, certain nutri-
Nutriceuticals are micronutrients, macronutrients and tional supplements may be indicated in the face of dis-
other nutritional supplements that are used as therapeu- ease or metabolic challenges to further complement an
tic agents. Examples include vitamins and minerals, pro- otherwise balanced diet.
biotics, digestive enzymes and antioxidants. This is the
clinical application of nutrition in the treatment of dis- Nutriceuticals are used for various digestive disorders and
ease and metabolic disorders. It is commonly stated that other metabolic conditions in pet birds.18 Some of the
malnutrition is the underlying cause of many of the dis- commonly used supplements are aloe juice, apple cider
ease syndromes encountered in birds and exotic pets. vinegar, probioticsa and digestive enzymes. Aloe vera (Fig
Significant advances have been made in avian nutrition 10.4) provides an effective boost to the immune system, a
with the advent of formulated diets, but it is only the soothing anti-inflammatory effect on the GI tract and is an
beginning. Specific nutritional requirements have not excellent source of vitamins, minerals and amino acids.
been established for the various bird species commonly Aloe can be administered orally in the form of a gel or
kept as pets, therefore current recommendations and juice at the dose of 1 drop per 100 g body weight 3 to 6
diets are based on anecdotal experience and limited times daily or in the drinking water at the rate of 2 ml per
nutritional studies. The primary diet of most pet bird 4 ounces of drinking water. Apple cider vinegar is an
important mineral for the body to prevent degradation

of tissues at the cellular level.
HOMEOPATHY
Homeopathy as practiced today is credited to Dr. Samuel
Hahnemann, a German medical doctor from the mid-
1800s. The governing principle of homeopathic medi-
cine is “similia similibus curantur” or “like cures like.”
This concept is based on using a very diluted form of a
substance to treat a condition or group of symptoms,
which in its full strength would cause the same set of
Greg J. Harrison
symptoms in the patient. These remedies are made from
plants, minerals, drugs, viruses, bacteria or animal sub-
stances. Homeopathic remedies work on the deep ener-
Fig 10.4 | Aloe is a hardy plant grown in the full sun. It is
often the best source of bioactivity. The gel from inside the getic level of the patient to undermine the constitutional
plant’s leaves is used for wounds. For internal consumption, the cause of the disease, rather than mask its symptoms.4
pointed edges are removed and the entire leaf is chopped up
and offered, or further ground and gavaged. Homeopathy is very effective in pet birds.13 Birds are
highly energetic beings and thus are particularly respon-
sive to energetic therapies. In choosing an appropriate
acidifier of the intestinal tract and entire body. Specific
homeopathic remedy, the practitioner must be thor-
avian indications for apple cider vinegar (organic, non- oughly acquainted with the Western medical examina-
pasteurized) include chronic bacterial or yeast infections, tion, conventional diagnosis, particular behavior charac-
chronic diarrhea or foul stools and proventricular dilation teristics and situational conditions of the avian patient.
disease support. It is dosed at 1 to 2 tablespoons per 8 The mental and emotional disturbances may be difficult
ounces of drinking water, as the only water source for 2 to discern, because most bird owners do not fully
weeks. Probiotics are supplements of beneficial bacteriaa understand the normal behavior and nature of their pet.
given to reestablish the normal bacterial flora in the diges- Evaluating the bird in its own environment, either per-
tive tract. They may be administered to birds after antibi- sonally or by videotape, is invaluable in evaluating these
otic therapy or severe GI disturbances. aspects of the diagnosis.
Digestive enzymes are beneficial in birds with pancreatic Because most pet birds do not visit the veterinary clinic
disease or primary digestive disorders leading to until they are quite ill, allopathic medications (antibi-
maldigestion. The classic essential enzymes provided in otics or antifungals) may be required to get the patient
most formulations include protease, lipase and amylase. through the crisis before treating with the homeopathic
These may be combined with other specific enzymes or remedy. Due to the critical nature of clinically sick birds
herbs, depending on the condition. in practice, the practitioner may not have the opportu-
nity to try a second remedy if the first is ineffective. The
Supplements used in the treatment of inflammatory con- first indication of a remedy failure in these cases may be
ditions and arthritis include glucosamine, methyl sul- death of the patient. Initial supportive care with allo-
fonal methane (MSM) and proanthocyanidins.18 Proan- pathic and other holistic therapies to stabilize the critical
thocyanidins are a group of strong antioxidants that patient either before or in addition to the homeopathic
scavenge destructive free radicals and include grape remedy is recommended by the author.
seed extract, pine bark extract, bilberry and citrus
bioflavonoids. These substances provide excellent The practice of homeopathy involves matching the
antioxidant effects that reduce inflammation, improve patient’s symptoms with an appropriate remedy. The
cellular integrity and eliminate free radicals from the first step involves making a list of the clinical signs from
body. Glucosamine sulfate is the preferred and most an evaluation and thorough history of the patient. This
effective form of glucosamine products. It has reparative list is then used to look up rubrics, or lists of potential
effects on arthritis. Some formulations of glucosamine remedies, for each clinical sign from a homeopathic
contain chondroitin or MSM for further joint support, repertory. The rubrics are compared for overlapping
but glucosamine is shown to be effective alone. MSM is a remedies, which are selected as possible treatments.
sulfur-based supplement that is proposed to have anti- These are then compared in a homeopathic materia
inflammatory effects on joints and generally supports medica, which describes all the symptoms potentially
healthy tissue and cells. Sulfur is suspected to be an treated with that remedy. The remedy that matches the
351
symptoms or clinical signs most accurately is selected as ity of the condition and the characteristics of the patient.
the first remedy of choice. The most detailed repertories
and materia medica are based on human symptoms and Homeopathic remedies are made by serial dilutions of
responses, however, limited veterinary references exist toxic substances that, if used in full strength, would cause
and continue to be developed. An avian homeopathic symptoms similar to those being treated. Substances are
repertory (Table 10.3) has been compiled16 and a simpli- diluted serially, either in 1/10 (X potency) or 1/100 (C
fied materia medica (Table 10.4) summarized.3 The potency) stages. Therefore, a 30C potency is a tincture of
potency and frequency are selected based on the sever- the homeopathic substance diluted 1/100, 30 times.
Table 10.3 | Avian Homeopathic Repertory

Location Condition Treatment
Beak Cere, brown hypertrophy Arnica montana, graphites, lycopodium clavatum, pulsatilla pratensis
Easily cracked Antimonium crudum, natrum muriaticum, silicea
Dryness Silicea, thuja occidentalis
Exfoliation Arsenicum album, graphites
Overgrown, distorted Calcarea carbonica, graphites, silicea, sulphur, thuja occidentalis
Chronic liver disease Argentum nitricum, carbo vegetabilis, chelidonium, calcarea carbonica, graphites, kali carbonicum, lycopodium
clavatum, mercurius solubilis, natrum muriaticum, nux vomica, phosphorus, silicea, sulfur, thuja occidentalis
Extremeties Arthritis Amazons - ruta graveolens
Budgerigars - bryonia alba, kali iodatum, rhododendron chrysanthum, rhus toxicodendron, sulphur, urtica urens
General - aconitum nepellus, arnica montana, belladonna, bryonia alba, ferrum phosphoricum, kali iodatum,
ledum palustre, lithium carbonicum, lycopodium clavatum, merdurius solubilis, natrum muriaticum, rhododen-
dron chrysanthum, rhus toxicodendron, ruta graveolens, silicea, sulphur, tuberculinum avium
Cold ameliorates - kali sulphuricum, ledum palustre, pulsatilla pratensis, sulphur
Broken bones Symphytum
Bruising, associated with - arnica montana
Feet Red and ulcerated Sulphur
Paralysis Argentum nitricum, cocculus indicus, gelsemium sempervirens, hypericum perfoliatum, kali carbonicum,
plumbum metallicum
Splay-legged Calcarea carbonica, calcarea fluorica, calcarea phosphorica, fluoricum acidum, gelsemium sempervirens,
phosphorus, silicea
Feathers Beak and feather disease Hypericum, sulphur
Bronzing of Arsenicum album, nux vomica, sulphur
Growth, none Arsenicum album, nux vomica, selenium
Grooming disorders Arnica montana, arsenicum album, calcarea carbonica, folliculinum, ignatia amara, natrum muriaticum,
(plucking or chewing) nux vomica, phosphoricum acidum, sepia, silicea, sulphur, thallium, tuberculinum avium, veratrum album
African Greys - arsenicum album, natrum muriaticum
Separation anxiety, with - natrum muriaticum
Amazon parrots, in - nux voica, sepia, sulphur, veratrum album
Females - aconitum napellus, apis mellifica, calcaria carbonica, chamomilla, lycopodium clavatum,
pulsatilla pratensis, silicea, sulphur
Males - apis mellifica, camphora officinarum, cantharis, conium maculatum, nux vomica, staphisagria,
tuberculinum avium
Aggression, general Nux vomica, tuberculinum avium
Cockatoos, in - arnica montana, arsenicum album, chamomilla, ignatia, natrum muriaticum, nux vomica, sepia
Males, in - nux vomica
Females, in - pulsatilla pratensis, silicea
Folliculitis, secondary to - hepar sulphuris, hypericum perforatum, kali bichromicum, mercurius solubilis,
sarsaparilla, staphisagria, sulphur
Frantic - belladonna, stramonium, veratrum album
Macaws, in - nux vomica, tuberculinum avium
Males, in - nux vomica
Sexual - nux vomica, sepia
Female Binding, egg Calcarea carbonica, kali carbonicum, pulsatillapratensis
Blood on eggs, with - pulsatilla pratensis
Soft-shelled eggs - calcarea carbonica, kali carbonica
Egg laying Kali carbonica, lycopodium clavatum, pulsatilla pratensis, sepia
Soft-shelled eggs - kali carbonica
Stopping of - sepia
Infertility Natrum muriaticum, sepia, silicea
Ovarian cysts Arsenicum album, belladonna
Oviduct Kali carbonica, pulsatilla pratensis, sepia
Table 10.3 | Avian Homeopathic Repertory (continued)

Location Description Treatment
Generalities Abscesses, Granulomas Tuberculinum avium
Anemia Calcarea carbonicum, ferrum metallicum, plumbum metallicum, sulfur
Anesthesia, slow to recover Acetic acid, carbo vegetabilis, phosphoric acid
Ailments from - acetic acid, carbo vegetabilis, hepar sulphurous, phosphorus, phosphoric acid
Cancer Calcarea carbonica, carcinosinum, graphites, lycopodium clavatum, nitricum acidum, phosphorus, silicea,
sulphur, thuja occidentalis
Budgerigars, in - calcarea carbonica, carcinosinum, graphites, lycopodium
Familial history of - carcinosinum, lycopodium clavatum
Candida albicans infection Calcarea carbonica, calcarea phosphorica, china officinalis, helonias dioica, lycopodium clavatum, medor-
rhinum, pulsatilla pratensis, natrum phosphoricum, nitricum acidum, sepia, thuja occidentalis
Emaciation Arsenicum album, calcaria carbonica, calcaria phosphorica, iodium, natrum muriaticum, nux vomica,
lycopodium clavatum, pulsatilla pratensis, phosphorus, sepia, silicea, sulphur, tuberculinum bovinum
Appetite ravenous with - baryta carbonica, baryta iodata, calcaria carbonica, calcaria phosphorica, causticum
hahnemanni, china officinalis, cina, iodium, lycopodium clavatum, natrum muriaticum, nux vomica, silicea, sulphur
Exposure to tobacco Gelsemium sempervirens, nux vomica, tabacum
smoke, ailments
Lead poisoning Alum, aurum metallicum, causticum, lycopodium clavatum, mercurius solubilis
Pyemia Arsenicum album, calcaria carbonica, hippozaenium, lachesis, pyrogenium
Sepsis Arsenicum album, arsenicum iodatum, baptisia tinctoria, china officinalis, crotalus horidus, echinacea
angustifolia, lachesis
Trauma Aconium napellus, arnica montana, hepar sulphuris calcareum, rhus toxocodendron, ruta graveolens,
symphytum officinale
Head, with seizures - belladonna
Neurologic symptoms, with - hypericum perforatum
Vaccinations, acute Aconitum napellus, apis mellifica, belladonna, thuja occidentalis
reactions
Ailments after - aconitum napellus, apis mellifica, belladonna, mercurius solubilis, phosphorus, silicea,
sulphur, thuja occidentalis
Weakness, unable to rise Carbo vegetabilis
due to severe illness
Zinc poisoning Aurum metallicum, mercurius solubilis
Heart Cardiomyopathy Crataegus oxyacantha et monogyna, digitalis purpurea
Cyanosis Digitalis purpurea
Heart, general Crataegus oxyacantha et monogyna, digitalis purpurea, rhus toxocodendron
Liver Liver disease, general Nux vomica, lycopodium clavatum, phosphorus
Fatty liver disease Calcaria carbonica, carbo vegetabilis, chelidonium majus, kali bichromica, kali carbonica, lyssinum
(hydrophobinum), lycopodium clavatum, mercurius solubilis, nux vomica, phosphorus, picricum acidum, sulphur
Mind Agitated, overstimulated Lachesis, stramonium, veratrum album
Outlet, without - ignatia amara, lachesis, nux vomica
Aggression Nux vomica, pulsatilla pratensis
Anger Arsenicum album, chamomilla, ignatia amara, lycopodium clavatum, nitricum acidum, nux vomica
Underlying - nux vomica
Violent - aconitum napellus, lycopodium clavatum, nitricum acidum, pulsatilla pratensis
Anxiety Aconitum napellus, argentum nitricum, arsenicum album, belladonna, calcaria carbonica, calcaria phosphorica,
cannabis indica, carboneum vegetabilis, conium maculatum, euphasia officinalis, hyoscyamus niger, ignatia
amara, kali carbonicum, kali nitricum, lachesis, lycopodium clavatum, mercurius solubilis, natrum muriaticum,
nitricum acidum, phosphorus, pulsatilla pratensis, sepia, silicia, sulphur, thuja occidentalis, veratrum album
Cowardliness Gelsemium sempervirens, lycopodium clavatum
Dependent on others Baryta carbonica, pulsatilla pratensis
Fatigue, mental, from Conium maculatum, kali phosphoricum, picricum acidum
inability to adapt to new
surroundings
Fear, violently throwing Aconitum napellus, belladonna, lycopodium clavatum, nux vomica, stramonium, veratrum album
self around cage
Grief Causticum hahnemanni, natrum muriaticum
Irritability Kali sulphuricum, natrum muriaticum, nitricum acidum, nux vomica, phosphorus, sepia
Idle, while - calcarea carbonica
Jealous, bites owner when Calcarea sulphuricum, hyoscyamus niger, lachesis, lycopodium clavatum, nux vomica, pulsatilla pratensis,
others approach stramonium
Rigid, unable to adapt to Calcarea carbonicum, kali carbonicum
captivity
Sensitivity Gelsemium sempervirens, natrum muriaticum, pulsatilla pratensis, silicia
Timid Kali sulphuricum, pulsatilla pratensis
353
Table 10.3 | Avian Homeopathic Repertory (continued)

Location Description Condition
Mouth Pharynx Inflamed, chronic - graphites, sulphur
Choanae, elongated - phosphorus
Choanal papillae, eroded - phosphorus
Nerves Ataxia Arsenicum album, calcaria carbonica, nux vomica, phosphorus, plumbum metallicum, silicea, stramonium, zinc
Nerves, general Rhus toxicodendron, hypericum perforatum
Paralysis Argentum nitricum, cocculus indicus, gelsemium sempervirens, hypericum perforatum, kali carbonicum,
lachesis, phosphorus, plumbum metallicum, zinc
Renal tumors, with - hypericum perforatum, lycopodium clavatum
Seizures Aconitum napellus, belladonna, calcaria carbonica, ignatia amara, lycopodium clavatum, silicia
Status epilepticus - aconitum napellus, belladonna
Weakness Iodium, nux vomica, plumbum metallicum, silicea, zinc, zinc phosphoricum
Nose Catarrh Graphites
Colds, get easily Graphites
Coryza Graphites
Dry, obstructed - phosphorus
Pharyngitis Nux vomica, phosphorus, sulphur
Sinusitis Arsenicum album, bryonia alba, hepar sulphuris, calcareum, kali bichromicum, kali nitricum, lycopodium
clavatum, mercurius solubilis, natrum muriaticum, nux vomica, phosphorus, pulsatilla pratensis, silicea
Pediatrics Infantile behavior Baryta carbonica
Separation anxiety Nux vomica
Slow development Calcaria carbonica
Stunted growth, in chicks Baryta carbonica
Respiratory Chronic colds Graphites
Chronic upper respiratory Arsenicum album, graphites, sulphur
infection
Table 10.4 | Avian Homeopathic Materia Medica

Materia Indication Usage Comments
Acetic acid Antidote for vaporized anesthetics. It can liquefy catarrh, which causes desperate gasping for breath.
(glacial) Antidotes include aconite, ignatia and opium.
It must be neutralized before use of other medications - aconite is the anti-
dotes for it.
Not compatible with Arnica, Lachesis, Mercuris and Causticum.
Aconitum napellus For effects of shock from injury, with fear; First aid for skin injuries from cat scratches and tears, inflammation.
(monkshood) physical and mental restlessness. Diarrhea during very hot weather.
Useful where there is redness of skin and bird is very restless and frightened.
State of collapse, where heat and fear are present.
Alumen Useful in cases of diarrhea, especially when Antidote for lead poisoning and other mercurials.
(common potash alum) bird is eating well and will not cease eating
to produce a dropping.
Apis Mellifica (honey bee) Most cases of swelling, especially from Useful in cases of reddened eyes with surrounding swelling.
bee stings.
Argentum nitricum Loss of balance and coordination of mind Trembling in affected parts.
(nitrate of silver) and body. Legs are withered, bird agitated.
Ocular ulcers and abundant discharge.
Arnica First aid for any injuries from blows, with Use for concussion.
(leopard’s bane) bruising or danger of concussion. Sprains or strains respond well.
Useful before and after surgery.
For broken skin with bruising, do not apply directly to wound, but dose
internally.
Okay to use as ointment to bruises if skin is intact.
Causes of diarrhea caused by accident or shock from surgery respond well.
Useful for problems caused by old injuries.
Aconite is complementary.
Arsenicum album Bird is restless and prepared to bite. Useful in cases of food poisoning, often caused by bad meat; usually with
(arsenic trioxide) Body temperature is normal and eyes green-stained vent feathers.
bright. For red, swollen legs, but not as puffy as for Apis.
Gradual weight loss from impaired nutrition.
Ill effects from fright.
Paralysis with atrophy of legs.
Putrid odor from discharges.
Ailments during varying weather conditions.
Aurum metallum Cases where bird is quiet and ready to Knees weak, worse in cold weather; usually remedy for winter complaints.
(gold) give up and die. Sometimes is glassy eyed. Antidote for lead poisoning.
Table 10.4 | Avian Homeopathic Materia Medica (continued)

Materia Indication Usage and Comments
Belladonna Bird is restless, unnaturally glaring eyes; Useful for swollen joints; tottering gait.
(deadly nightshade) convulsive movements; aversion to water; Cold legs and feet with jerking limbs.
changeable attitudes. Wants to stand up and will not lie down.
It attacks one moment and hides the next.
Bellis perennis Use for results of accidents with nerve Lameness from strains and sprains; sore joints and muscular stiffness.
(daisy) injuries. First remedy in injuries to deeper tissues and after major surgery.
Calcarea carbonica Useful for abscesses in deep muscles. For relapses during convalescence.
ostrearum Helps blood to clot.
(carbonate of lime) Eyes sensitive to light.
Bird hides head in corner.
Swollen eyelids.
Extreme difficulty in breathing.
Calcarea Suphurica Follows Ruta well in cases of leg stiffness. Useful for inflammation with thick yellow discharge.
(plaster of paris) Diarrhea with blood.
Calendula officinalis Great healer of wounds. Stops bleeding and aids in formation of healthy tissue.
(marigold) Applied topically as tincture or cream or taken internally as tablet.
Useful for lacerations.
Carbo vegetabilis Bird is usually slow, quiet and cold. Used for food poisoning caused by fish.
(vegetable charcoal) Eyes partially closed.
Dulcamara Ailments caused by damp. Recurrent rheumatism during wet weather.
(bittersweet) Birds that look ill during cold, wet weather, but no specific cause.
Stiff legs; drooping wings; any weakness; chills - during wet weather.
Euphrasia Use for red, sore eyes; ocular discharge.
(eyebright)
Gelsemium Bird is tired; weakness or paralysis; No fear of handling, and fatigued after slightest movement.
(yellow jasmine) chilliness. Negative response to fear or fright.
Hamamelis virginica Stops bleeding. Ideal after surgery - superior to morphine for pain.
(witch hazel) Great value in open, painful wounds.
Bruised soreness of affected parts.
Hepar sulphuris calcareum Use for suppuration with pain; unhealthy Use on sensitive ulcers and abscesses that bleed easily.
(Hahnemann’s calcium sulphide) skin.
Hypercal Useful for wounds. Cleansing, healing and pain removing.
Hypericum Useful for injuries involving nerves, Injured nerves after predator attack.
(St. John’s wort) especially toes and claws. Relieves pain after surgery.
Paralysis of legs due to mechanical spinal injury (higher potency).
Ignatia For grief and loss of mate. Very nervous birds; ideal for female birds that are quick, but submissive.
(St. Ignatius’ bean) For fear. Rapid characteristic change from quiet to panic.
Fluctuating signs between appearing ill and healthy.
Useful for injuries of the spine.
Ipecacuanha For upset stomach, where bird is hot. Respiratory trouble; congestion in chest or throat; gasping for breath.
(ipecac root) General weakness of body, eyes partially closed.
Lachesis Dirty and infected wounds; sepsis; Dark appearance of wounds.
(bushmaster) risk of gangrene.
Lathyrus Paralysis without pain. Legs dangle when picked up.
(chick pea) Cold limbs.
Slow recovery of nerve function.
Cannot lift feet off ground, yet cannot lower hocks to ground.
Ledum Use for puncture wounds, especially if Useful as antitetanus.
(marsh tea) wound is cold. Bottom of feet painful, reluctant to stand on them.
Lycopodium Ailments that develop slowly. Functional powers weakening with failure of digestive function, with
(club moss) liver disturbance.
Manganum aceticum Progressive paralysis with wasting of limbs. Feeble and staggering gait; leans forward while walking, so falls onto beak.
(manganese acetate) Swelling of joints; sore feet.
Worse in cold weather.
Mercurius hydrargyrum Indicated in weight loss; feather loss; Ulceration of mouth and throat; abscesses; foul-smelling excretions;
(quick silver) tremors, great prostration; sensitivity to tendency for pus formation, usually greenish, thin and streaked with blood.
heat. Antidote for mercury poisoning.
Natrum muriatum Indicated for weakness and weariness. Ill effects of fright.
(chloride of sodium) Easily irritable.
Complements Ignatia.
Opium-papaver somniferum Drowsy stupor. Painfulness. Lack of reac- Does not respond to indicated remedies.
(dried latex of poppy) tion to stimuli. Warm to hot bodied. Birds tuck their heads under their wings and refuse to wake up,
poorly responsive.
Oxalicum acidum For short, jerky breathing, with Paralysis due to spinal injury.
(sorrel acid - oxalic acid) constriction.
Petrolrum Antidote for oil pollution, especially oiled
(crude rock oil) birds that have digested oil off feathers.
Plumbum metallicum Lead poisoning, especially paralysis Progressive muscle atrophy, excessive and rapid emaciation.
(lead) of wing. Anemia.
Do not give many doses of this remedy.
355
Table 10.4 | Avian Homeopathic Materia Medica (continued)

Materia Indication Usage and Comments
Phosphoricum acidum Loss of vital fluids, after diarrhea or Listlessness.
(phosphoric acid) blood loss. Dyspnea.
Effects of shock; gives up on life.
Psorinum Bird is cold and poor response to indicated Foul odor to secretions.
(scabies vesicle) remedy. Single dose of 30C or 200C usually sufficient, followed by indicated remedy.
Pulsatilla Usually indicated in female changeable in Signs improve when outside; little to no thirst; worse from heat.
(artificial sepsin - pyrogen) characteristics. Limbs are painful; stiffness in legs; swollen veins in wings; red, inflamed
and swollen feet.
Bird wants to sit or lie down.
Pyrogenium Food poisoning, with offensive brown-black Offensive discharge; pain and burning in affected areas.
(artificial sepsin - pyrogen) diarrhea. Patient is restless.
Great antiseptic.
Rhus Toxicodendrom Rheumatic pains are worse when limbs are Ailments from strains; getting wet while hot.
(poison ivy) kept still; bird stiff until it gets moving. Rheumatism in cold weather.
Limbs stiff, paralyzed; hot, painful swelling of joints.
Worse in cold air.
Ruta graveolens Strained limbs, usually after Arnica stops Ideal for stiff legs and/or wings.
(rue bitter wort) working.
Silicea Promotes suppuration; brings abscesses to Bird is cold and tired.
(silica pure flint) a “head.” Slow recovery after respiratory problems.
Loss of strength in legs; bottom of feet are sore.
Scirrhinum Specific for cancer. Use with care.
Sulphur Used with Aconite in cases of collapse Used with Ipecac in cases of collapse.
(sublimated sulphur) where Aconite is indicated. Complaints that relapse.
Birds are lazy, but snappy; thin and weak; good appetite.
Helps paralyzed legs after use of Rhus tox.
Symphytum Healing of broken bones, tendons and Increases strength and rate of healing.
(comfrey) sinews. Helps heal injured eyes.
Urtica urens For burns and scalds. Used in tincture, cream or tablet.
(stinging nettle)
Zincum Metallicum Lameness and weakness with twitching of Sensitive to noise; lethargic; cold feet.
(zinc) various muscles. Works well with Manganese acetate.
Succession is carried out at each stage to release the cur- and the concepts of homeopathy. Dr. Bach developed
ative energy of the substance to imprint on the memory various vaccines during his tenure in immunology, and
of the water at the energetic level as well as remove the then developed some of the first nosodes, oral homeo-
toxic and harmful effects of the substance.4 The end pathic vaccines. In his clinical experience, Dr. Bach real-
result is a homeopathic substance that contains only the ized the importance of the mental and emotional states
energetic signature of the toxic substance, but no physi- of mind in the recovery from illness. In 1930, he
cal amount of the substance itself. embarked on a quest to develop a treatment method that
did not depend on the destruction or alteration of one
living thing to benefit another, which ultimately lead to
FLOWER ESSENCE THERAPY
the discovery of his first twelve healing herbs with a natu-
Healing with flower essences proposes similar principles ral affinity to mental traits. In all, 38 healing remedies
to homeopathy. Both forms of therapy are based on cur- were identified, which he believed would remedy all the
ing the patient by restoring the body’s energy pattern negative states of mind that afflict mankind.
and vibrational characteristics. The underlying premise
is that all life forms possess an innate vibrational energy A variety of other flower essences have been described
force that is disrupted by conditions and circumstances in the past 30 years. In the 1970s, Richard Katz and
of our environment, leading to disease and illness.8 Patricia Kaminski developed the California Flower
These disruptions are further related to emotional and Essences. Ian White described the Australian bush flower
behavioral specifics, which can be characterized and essences in the 1980s, influenced by the Australian
treated with the vital energy or essence of certain flow- Aborigines’ traditional knowledge and experience with
ers. The aroma or essence of a flower naturally elicits an native plants. Other flower essence lines include the
emotional response, similar to the way music affects an Alaskan (1980s), Bailey in Britain and Celestial Remedies
individual’s mood. (1990s), to name a few.8 All of these flower essence lines
are based on the same premises described by Dr. Bach.
Dr. Edward Bach is credited for the development of the
first 100-year-old therapeutic system of flower essence Flower essences can be very effective in the treatment of
therapy.2 Dr. Bach was a distinguished British physician in clinical and behavioral issues of birds and other pets.
the early 1900s with a strong influence from Hahnemann The underlying premise in using flower essences to treat
conditions in birds is the presence of an emotional com- vibrational energy of the patient to restore the energetic
ponent to the problem. These formulations act on the imbalance causing the disease or condition. By increasing
energetic signature of different emotions that produce the vital force of the patient, aromatherapy strengthens
the outward behaviors. It is commonly accepted that the natural immune system and promotes self-healing.9
emotional and psychological stress can lead to physical
illness; therefore, the flower essences can be incorpo- Birds are extremely susceptible to any aerosolized
rated into a holistic treatment plan. agents, including essential oils used in aromatherapy.
Therefore, care must be taken not to overwhelm the
In general, birds are more emotional than most other ani- bird’s respiratory system with too strong a treatment. An
mals.2 The stress and anxiety experienced by birds during electric aromatic diffuser can be used in a well-ventilated
treatment may be more detrimental than the disease con- room for 5-minute intervals, several times daily for cer-
dition itself; therefore, the use of a flower essence prior to tain conditions. The scent of the essential oils should be
and during a veterinary exam and treatment may signifi- barely detectable, or else it is too strong for the bird’s
cantly improve the chances of survival. Birds also respond respiratory system. Some aromatic agents may inherently
quickly to the remedies, probably due to their sensitive be too strong or noxious for use around birds, there-
emotional natures. Most formulations of flower essence fore, these should be used with caution. This therapy is
are based in brandy, which can be harmful to the patient used less commonly in birds, except for cases of stress
if given directly. Therefore, these remedies should be reduction, due to the potential respiratory risks.
diluted in spring water before they are administered to
birds at the rate of 10 to 12 drops per ounce of water. Some conditions in pet birds respond well to aromather-
apy, including certain respiratory ailments and stress and
Birds present with a number of medical conditions that anxiety issues. A respiratory essential oil blend for diffu-
have an emotional or behavioral basis. Feather picking is sion consists of eucalyptus (50%), pine (25%), tea tree
by far the most common and frustrating of these condi- (10%), and niaouli or cajeput (15%).9 This blend is dif-
tions. A more progressive and intense manifestation is fused near the cage several times daily for 5-minute
self-mutilation, as exhibited in Moluccan cockatoos chew- intervals. A 15-ml essential oil blend for stress and anxi-
ing into the pectoral muscles of their chests. Biting and ety is composed of lavender (10 ml), marjoram (4 ml)
screaming are other undesirable behaviors that are merely and neroli (1 ml).9 This is diffused for 5 minutes near
displaced natural behaviors, which can be modified with the cage, repeated 4 to 5 times daily. A diffusion of
flower essence remedies. Birds that suffer from a physical lavender, bergamot or ylang ylang in the exam room
loss of a companion, physical injury or medical illness can provides a calming and relaxing effect on the patient,
be supported with these remedies as part of their therapy. client and doctor.23 The electric aromatic diffuser can be
turned on in the waiting room or exam room for 5 to 10
The choice of remedies is individualized for each patient. minutes every 3 to 4 hours during the day.
Oversimplification by using a single remedy for a particu-
lar problem is much less effective than thoroughly evalu-
ating the patient and formulating a remedy of various
ENERGY THERAPY
flower essences. Of course, there are certain remediesa Various forms of energy therapies have developed
that are commonly effective for a particular condition through the ages in many cultures. Some of the cur-
such as the stress and anxiety of a veterinary visit or treat- rently practiced energy therapies include Reiki, thera-
ment. Rescue Remedy is a classical formulation of five peutic touch and pranic healing. These healing practices
flower remedies, consisting of star-of-Bethlehem, rock- involve directing the ability to consciously modulate the
rose, impatiens, cherry plum and clematis. This remedy energies of a living being. These healing practices
can be sprayed in the exam room, sprayed directly onto involve the healer or practitioner serving as a conduit
the bird or given directly by mouth.15 A list of the classic for the universal energy to stabilize or balance the
Bach Flower Essences and their basic uses is summarized patient’s innate energy field.
in Table 10.5.2,8 Extensive repertories of other flower
Therapeutic touch is an example of this type of therapy
essences exist for man11 and animals.5
that is practiced throughout the world. Dolores Krieger
and Dora Kunz developed this practice based on the fol-
AROMATHERAPY lowing four basic scientific premises:12 1) Humans and ani-
The therapeutic application of aromatic essential oils is mals are physically open energy systems. This implies that
known as aromatherapy. The administration of the oils by the transfer of energy between living things is a natural
diffusion or aerosolization is most common, but topical and continuous process; 2) Humans and animals are bilat-
and oral applications also are effective routes for some erally symmetrical, implying a pattern to the underlying
formulations. The essential oils act on the underlying energy field; 3) Illness is an imbalance in an individual’s
357
Table 10.5 | Flower Essences Therapeutic touch and other energy therapies produce
Essence Remedies Restores certain consistent and reliable results.12 The first response
Agrimony Concealed distress Inner peace experienced within a few minutes of a treatment is relax-
Aspen Fear of unknown, Courage ation. Clinically, there is a significant reduction or elimi-
apprehension
nation of pain. Healing responses tend to be accelerated,
Beech Intolerance, bad temper Tolerance, flexibility
presumably by boosting the patient’s immune system.
Centaury Submissiveness, compliance Assertiveness,
resistance Psychosomatic illnesses are alleviated through the effects
Cerato Lack of confidence Confidence on the patient’s autonomic nervous system.
Cherry Plum Uncontrolled behavior, Control
compulsiveness The success of these therapies is based on the learned
Chestnut Bud Learning difficulty, repetitive Ability to learn skills and techniques combined with intentionality. Proper
behavior
centering and focus is critical in assessing the patient’s
Chicory Possessiveness, attention Normal caring &
seeking protectiveness energy field for subtle changes and asymmetry. With prac-
Clematis Absentmindedness Alertness tice and deliberate intent, the healing practitioner can bal-
Crab Apple Uncleanliness, infection, Cleanliness, dignity ance the patient’s energy. This technique is very useful in
poisoning
calming and soothing nervous or distressed patients; it
Elm Inadequacy, overwhelmed Competence
also helps ease the induction and recovery from anesthe-
Gentian Discouragement, setback Perseverance
sia. The pain and discomfort from trauma or illness, as
Gorse Hopelessness, despair Endurance
Heather Loneliness, inattentiveness Quiet composure
well as boosting the body’s innate healing response, can
Holly Malice, intense dislike Harmlessness be relieved through this energy modulation.
Homesick, inability to cope Adjust to present cir-
Honeysuckle
with present conditions cumstances
Hornbeam Weakness, unresponsiveness Vitality
Impatiens Impatient, irritability Patience Integrative Therapies for
Larch
Mimulus
Hesitancy, loss of confidence
Fear of known things,
Confidence
Courage
Common Avian Conditions
nervousness
Mustard Depression, gloominess Serenity FEATHER PICKING
Oak Lack of resilience in normal Resilience
strong bird Feather picking is a clinical sign of a multitude of poten-
Olive Fatigue & exhaustion Strength tial diseases and disorders and not a diagnosis in itself.
Pine Guilt & contriteness Positive attitude The underlying causes include systemic or metabolic dis-
Red Chestnut Overprotectiveness, Confidence, trust orders (see Chapter 4, Nutritional Considerations,
overconcern
Section II Nutritional Disorders), infectious diseases,
Rockrose Terror, hysteria Courage, calm
allergies, parasites and psychogenic disturbances. Most
Rock Water Rigidity, repression, Flexibility, spontane-
inflexibility ity, gentleness cases are psychogenic in nature, but they should have a
Scleranthus Imbalance, uncertainty Stability, balance complete diagnostic analysis to rule out other contribut-
Star-of-Bethlehem Mental, emotional & physical Mental, emotional & ing factors. Treatments for feather-picking disorders vary
shock physical calmness
considerably but should be based on the individual
Sweet Chestnut Extreme mental & physical Endurance
distress assessment with an attempt to address the underlying
Vervain Impulsiveness, hyperactivity Restraint factors as well as the psychogenic manifestations.
Vine Dominance, territoriality Positive leadership
abilities Many integrative therapies can be utilized to complement
Walnut Difficulty coping with change Adaptability the conventional approach to treating a feather-picking
Water Violet Indifference, aloofness, Social contact bird. Some of these address the psychogenic component
reserve
of the problem, including Bach flower essences, herbal
White Chestnut Restlessness, sleepiness, Ability to rest
preoccupation therapy and aromatherapy.21 Other modalities address the
Wild Oat Lack of direction Direction deeper energetic components, such as acupuncture and
Wild Rose Resignation, apathy Will to live homeopathy. Some treatments are directed at stabilizing
Willow Maliciousness, spitefulness Good temper the nutritional or metabolic imbalances, such as nutriceu-
ticals and antioxidant therapy.
energy field, with healing being achieved by balancing Acupuncture is reported as a viable option for the treat-
this energy field; and 4) Humans have natural abilities to ment of feather picking in pet birds.1,7,16,24,28 The conven-
transform and transcend their conditions of living. Other tional diagnosis of feather picking is often attributed to
forms of energy therapy and healing arts are based on the social/emotional well-being, psychological status or
similar assumptions and current scientific premises. stressful environmental conditions of the bird. This
determination relates to a TCVM diagnosis as a Shen dis- John’s wort has many properties that make it particularly
turbance (deficient Heart Blood), Phlegm and Heat dis- useful in the treatment of feather picking. Numerous sci-
turbance of the Heart, Heat invading the Pericardium, or entific studies have determined that Saint John’s wort is
excess Liver Yang.28 Certain acupuncture points are rou- an effective antidepressant.29 In addition, it serves as a
tinely used in birds with feather-picking issues, but the nerve tonic and speeds wound healing, which is useful
final selection of points should be based on a complete in soothing and repairing the damaged feather follicles.
assessment of the patient and TCVM diagnosis. Some of Saint John’s wort has good antibacterial and antiviral
the routine points include SP-6, ST-36, LI-4, LI-11, PC-6 properties, beneficial in cases of infectious folliculitis or
and HT-7. SP-6 is used to tonify and strengthen Yin. ST- systemic diseases. Several other herbs are sedative and
36 is the master point of the abdomen and used to treat soothing in nature, including valerian root, passion-
deficiencies, dispel Cold and tonify Qi and Blood. LI-4 flower and kava kava.29 These may be effective individu-
helps to expel Wind Heat and to release the Exterior, ally or in combination for the management of very nerv-
tonify defensive Qi and calm the spirit. LI-11 is used to ous and hyperactive patients.
clear Heat, resolve Dampness, and regulate Nutritive Qi
and Blood. PC-6 can calm the mind, regulate Heart Qi Bach Flower Essence is excellent at addressing the
and relieve irritability due to stagnation of Liver Qi. HT-7 underlying emotional and behavioral issues that often
is useful in calming the mind, quieting the spirit, serve as the root of the feather-picking condition.8,19 A
improving thinking and regulating other emotional combination of three to five different essences may be
issues. Other potential points used for feather-picking indicated for an individual case. Some essences address
cases include GV-20, LIV-3, GB-34, SP-10, SP-11, BL-12 the underlying issue of fear or anxiety, such as aspen,
and BL-15. Table 10.1 lists the common avian acupunc- agrimony, cherry plum, mimulus and rockrose. Others
ture points and general indications for use. The treat- are useful when birds are picking at certain times or sit-
ment regimen is dependent on each case but is usually uations, such as red chestnut or heather for when the
started at once to twice weekly for the first several weeks bird picks when left alone or scleranthus for when pick-
and gradually reduced, based on the patient’s response. ing occurs during breeding season. Mustard or gorse
Each session should begin with an assessment of the may be indicated if the bird is feather picking out of
patient’s condition and response, with adjustment of the depression. Walnut is helpful when feather picking
selected acupuncture points as indicated. begins after a move or other change in the environment.
Wild oat can be given if the bird is simply over-preening,
Homeopathy is useful at addressing the underlying ener- while agrimony is a better choice for self-mutilation.
getics of the feather-grooming problem but must be indi- Chicory is a good choice when the picking is used to get
vidualized for each patient.19 A homeopathic remedy is attention, whereas cherry plum is used when the picking
prescribed based on the full assessment of the patient; seems to be compulsive in nature. Most flower essence
however, certain remedies commonly surface as primary formulas also should contain a combination remedyb of
choices. Some of these include aconitum napellus, apis impatiens, clematis, rockrose, cherry plum and star-of-
mellifica, arnica montana, arsenica album, belladonna, Bethlehem for stress and anxiety. This formula also is
ignatia, natrum muriaticum, nux vomica, pulsatilla used to calm patients for veterinary examinations, aid in
pratensis, psorinum, sepia, staphisagria, stramonium, recovery after surgery and treat shock and distress dur-
tuberculinum avium and veratrum album.19 An avian ing severe illness or injury. Table 10.5 contains a sum-
homeopathic repertory has been summarized in Table mary of the flower essences and general indications.
10.3. In general, the study of homeopathic remedies for
mental problems will reveal the proper remedy. Each A variety of nutriceuticals can be added to balance the
type of bird has general personality characteristics that nutritional deficiencies and resolve underlying metabolic
can influence the choice of remedy. For instance, cocka- conditions leading to feather picking.1,19 Aloe vera has
toos are very social birds, thus requiring a remedy that anti-inflammatory and vulnerary effects, which assist heal-
addresses social issues when separated from the flock. ing of damaged and irritated skin and feather follicles in
Alternately, Amazon parrots and macaws are more likely feather-picking cases. Aloe also provides a multitude of
to be suffering from internal systemic diseases, requiring nutrients for healthy feather condition, including natural
a remedy to address those problems as well. The home- vitamins, minerals and amino acids. Antioxidants are often
opathic remedy, potency or frequency may have to be beneficial in treating chronic feather-picking cases by scav-
adjusted based on the patient’s response and discontin- enging free radicals and supporting the healing process of
ued upon resolution of the problem. damaged skin and feathers. Potent antioxidants, also
called oligomeric proanthocyanidins, include grape seed
Western herbs are helpful in treating the psychological extract, pycnogenol, bilberry and citrus bioflavonoids.
issues and calming the feather-picking patient.19 Saint These are available in various forms, either individually or
359
in combination, and can be added to the food or water as tive, cholagogue, anti-inflammatory, vulnerary and
a general supplement. A potent amino acid supplement, anthelmintic effects on the GI tract.14 Aloe vera juice can
5-hydroxy L-tryptophan, has been suggested for feather- be dosed orally at 1 to 2 drops per 100 g body weight or
grooming problems.19 Being very potent, only a few grains added to the drinking water at the rate of 2 ml per 4
should be added to the food daily. Omega-3 fatty acids ounces of drinking water. Apple cider vinegar is an
have been suggested for a variety of veterinary conditions excellent acidifier to the intestinal tract and general
including feather disorders. The benefits of omega-3 fatty nutritive.19 Indications for use include chronic diarrhea,
acids pertinent to feather-picking disorders include treat- dysbiosis, candidiasis and chronic bacterial enteritis.
ment of seborrhea and pruritus as well as mood stabiliza- Apple cider vinegar can be added to the drinking water
tion.1 These fatty acid supplements also help reduce at the rate of 1 to 2 tablespoons per 8 ounces of water
inflammation by modifying the arachidonic acid cascade. for up to 2 weeks. A line of rice-based intestinal support
productsc is commercially available. Rice is highly
DIGESTIVE DISORDERS digestible and gluten free, thereby being a good hypoal-
The digestive tract of birds is often disrupted by infec- lergenic whole-grain product. Certain protein fractions
tious and metabolic conditions. This can include any- of rice support gastrointestinal secretory function and
thing from sour crop caused by Candida albicans to repair of mucosal cells.14 Therefore, these rice-based
cloacal papillomas. Whenever possible, the underlying products are well suited for management of gastroin-
cause of the gastrointestinal (GI) disorder also must be testinal inflammatory and allergy disorders, including
identified and rectified. Many of these disturbances, chronic vomiting, chronic diarrhea, dysbiosis, food
however, can be stabilized with the use of nutriceuticals allergy and gram-negative enteritis. One rice-based prod-
and herbal formulations. Several aspects of the digestive uct, Ultraclearc, is dosed at 1 g per kg body weight, given
process can be addressed with these supplements, 3 times daily.
including soothing and protecting the GI mucosa, bal-
ancing the microbial population and providing nutritive The digestive system of birds has evolved with plant
support. enzymes for proper digestion.19 As more cooked and
processed foods are fed to pet birds, fewer digestive
The GI mucosa is easily inflamed and irritated by invad- enzymes are found in the diet because cooking inactivates
ing pathogens or foreign agents. As a result, the inflamed the plant enzymes. Animal source digestive enzymes, such
mucosa will be less effective in the absorption of nutri-
as pancreatic enzymes, are less effective in birds, because
ents and proper digestion. Several Western herbs are
they are inactive in acidic environments such as the bird’s
highly effective in soothing the inflamed GI mucosa.29
crop and proventriculus. Therefore, pet birds should be
Slippery elm bark has a soothing, protecting and lubricat-
provided plant sources of digestive enzymesd, which are
ing effect on the GI tract. In addition, it serves as an
stable and active over a wide pH range. A source of natu-
astringent and nutritive. The tannin constituents tighten
ral enzymes produced by Saccharomyces cerevisiae in fer-
the digestive mucosa to relieve inflammation and prevent
mentation vats has empirically shown to have beneficial
further fluid loss in the intestines. The mucilage con-
effects in birds (G.J. Harrison, personal communication,
stituents help lubricate the digestive tract and facilitate
2003).
the removal of waste material. Slippery elm is effective in
many digestive conditions on several levels. Marshmallow
A wide variety of digestive disorders in birds, including
root provides a soothing, lubricating and protective bar-
bulky stools, intestinal gas, undigested food in feces,
rier to mucosal surfaces through its mucilage compo-
slow crop emptying, chronic bacterial enteritis, weight
nent. This makes marshmallow beneficial in cases of GI
loss and chronic immunosuppression, benefit from the
ulceration or irritation. Marshmallow is best taken inter-
addition of digestive enzymes.
nally as a tea or low-alcohol tincture. Licorice root is an
excellent anti-inflammatory and demulcent herb. It is
Probiotics are microbial supplements given to reestablish
good at healing GI ulcerations and reducing the gastric
a balanced gastrointestinal microflora. These products
acid secretions while producing anti-inflammatory effects
generally contain various species of Lactobacillus and
similar to corticosteroids.
Bifidobacterium, which are intended to repopulate the
Several nutriceutical products have beneficial nutritive patient’s intestinal tract with beneficial bacteria. Probiotics
and supportive effects on the digestive tract. Aloe vera is are indicated after chronic digestive disease or extended
an excellent nutritive and anti-inflammatory agent. Aloe or excessive use of antibiotics, where the normal bacterial
vera is effective in treating inflammatory bowel disor- flora would be disrupted. Avian-specific productsa are rec-
ders and constipation. The active constituents of Aloe ommended; however, limited benefit may result from
vera include barbaloin and isobarbaloin. Aloe has purga- mammalian products or active yogurt culture.
LIVER DISEASE duct occlusion. Because of its strong stimulatory effects,

Liver disease is a common diagnosis in birds. Severe it should be used with caution in animals with preexist-
liver damage in birds is commonly seen in a variety of ing liver damage.
chronic conditions ranging from nutritional disorders to
Burdock root (Arctium lappa) has been used for thou-
psittacosis. The usual presentation is elongation and
sands of years for a variety of ailments such as eczema,
bruising of the beak and toenails. Hepatic lipidosis is
allergies, constipation and toxicity. Burdock root is very
common in pet birds that become obese due to their
cleansing to the blood and stimulating to the liver. It
sedentary life and malnutritive seed diets. Therefore,
possesses strong antioxidant and nutritive properties.
nutritional management is crucial in managing liver dis-
The fresh root has broad antibacterial effects and anti-
orders in birds. Certain hepatic tumors are common in
tumor action.
budgerigars, and bile duct carcinomas are found in
Amazon parrots. Iron storage disease is seen in mynahs
Licorice (Glycyrrhiza glabra) neutralizes liver toxins.
and toucans (see Chapter 15, Evaluating and Treating
Scientific articles credit a specific licorice derivative
the Liver).
known as glycyrrhizin for successfully treating chronic
Several Western herbs have liver-protective and liver- hepatitis.29 Licorice also has been shown to increase the
supportive properties. Some of them actually stimulate production of interferon, which is commonly used to
the regeneration of the liver cells. Herbs often perform treat hepatitis B. Licorice also is used in combination
more effectively as a synergistic formula rather than as with other herbs as a potentiator, to strengthen the
the individual herbs. Some of the more common hepato- effects of the herbal formula.
tonic herbs are listed below with their associated bene-
In addition, some Chinese herbal formulations have very
fits and indications.23
beneficial effects on the liver. The herbal treatment
Milk thistle seed (Silybum marianum) has been used for should be based on a TCVM diagnosis. However, herbal
2000 years to treat a wide variety of liver diseases. It is formulations containing bupleurum and gardenia are
used for treatment of cirrhosis, hepatitis and various particularly useful in treating most liver conditions in
forms of hepatotoxicity. Milk thistle is indicated whenever birds.14 Coptis and Scute Combination (Huang Lian Jie
the liver has been damaged or is at risk for damage. Du Tang) is indicated in cases of viral or bacterial hepati-
Studies have shown that the chemical component, sily- tis with elevated white blood cell counts.15 Another use-
marin, has hepatoprotective properties. It has been ful TCVM approach is acupuncture, with acupoints
found to serve as an antioxidant, decrease free radicals being selected by the TCVM diagnosis.
and increase hepatocyte synthesis. Other studies have
Liver detoxification is crucial in the management of
shown that silymarin inhibits cytochrome P-450 enzymes
many primary and secondary hepatic diseases. Certain
in liver microsomes. As a result, milk thistle should not
treatments that are very effective in this detoxification
be used with drugs metabolized by the P-450 enzyme.
process include herbal formulations and antioxidant
There are no other known drug or herbal interactions.
therapy and/or rice-based intestinal products such as
Elevations in liver enzymes and bile acids are possible
Ultraclear Pluse. These products are very useful in the
during the first few days of using milk thistle (G.J.
management of gastrointestinal inflammation and
Harrison, personal communication, 2003).
allergy, as well as detoxification of the liver.14 Oligomeric
Dandelion root (Taraxacum officinale) acts by gently proanthocyanidins (OPC) are powerful antioxidants that
and safely stimulating the liver into an increased state of scavenge free radicals, thus preventing further cellular
efficiency. The improved liver function resultantly degeneration. These products are very useful in chronic
improves digestion, increases the elimination of waste and degenerative diseases that involve cellular decay and
from the blood and body and reduces the burden on the degeneration. Examples of OPC antioxidants include
kidneys and immune system. The root has been used for pycnogenol, grape seed extract, bilberry and citrus
centuries to treat jaundice. This herb makes an excellent bioflavonoids. Herbal formulations for liver detoxifica-
adjunctive therapy with gentle liver support and general tion include those described above as well as other
nutritive properties. herbs that address the individual patient needs.
Oregon grape (Mahonia spp.) is a stronger and faster Liver regeneration is often overlooked in the treatment
acting hepatic stimulant than dandelion root. It is indi- of liver disease by conventional means. However, several
cated in cases suggestive of a deficient liver, such as holistic products are available to facilitate liver regenera-
poor protein digestion, constipation, or poor skin and tion. Milk thistle is effective in regenerating hepatocytes
feather condition. Since this herb stimulates bile produc- in addition to the other benefits discussed previously.
tion, its use should be avoided in suspected cases of bile Specific products with liver-regenerative potential are
361
commercially available.14 Livaplexf is a liver glandular patient, based on the TCVM diagnosis.
combined with other liver-supportive nutrients. Lipogeng
is indicated in cases of hepatic lipidosis. Specific nutriceutical products that are marketed for
mammals may be useful in birds with similar conditions.
These products often include kidney glandulars, vita-
RENAL DISEASE mins, herbs and enzymes. Arginase is the enzyme neces-
Kidney disease is frequently diagnosed in pet birds but sary for the detoxification of arginine from the kidney.14
seldom specifically treated. Conventional treatments Kidney-supportive products are commercially available.h,i,j
often attempt to correct only the clinical signs, such as
lowering the elevated uric acid level in gout cases or Recommended dietary changes include lower protein
reducing urine output in cases of polyuria. Specific diag- diets, but debate continues regarding the degree of pro-
nosis of the renal disorder is important in developing an tein restriction that is beneficial and safe.6 Cases impli-
effective treatment plan. Certain natural supplements cating protein as a contributing factor in renal diseases
and holistic remedies can be generalized to support such as gout consistently have very high protein levels.
renal function and healing of the kidney (see Chapter Most importantly is a proper balancing of the diet with
16, Evaluating and Treating the Kidneys). normal protein levels and natural, organic foods (see
Omega-3 fatty acids (n-3 FA) have several renal benefits.6
The supplementation of n-3 FA can increase renal blood
flow and nephron glomerular filtration rate, lower sys-
EGG BINDING
temic arterial blood pressure and reduce hyperlipidemia. Egg binding is failure of the oviduct to pass an egg into
Specifically, the n-3 FA supplements reduce total triglyc- the cloaca. In a TCVM perspective, this would be failure
erides and very low-density lipoprotein concentrations; n- of the Kidney Qi to warm the lower burner, thus weak-
3 FA reduce inflammation by modulating the arachidonic ening the oviduct.16 If the egg is stuck due to lack of
acid cascade. In addition, n-3 FA decrease plasma viscosity. lubrication in the oviduct, the TCVM assessment would
Sources of omega-3 and omega-6 fatty acids include fish be failure of the Spleen to transport and move fluids
oils, flax seed, borage and pumpkin oils. The specific dos- where needed, and failure in production of Qi for egg
ing for n-3 FA has not been established, but it is suggested laying. Egg binding is diagnosed as interior Cold defi-
that the ratio of n-6 to n-3 FA may be of greater impor- ciency with a build up of phlegm. Potential acupuncture
tance in the overall analysis. One recommendation for points include SP-6, ST-36, GV-20 and PC-6. SP-6 is cho-
dosing suggests mixing flax seed oil with 4 parts corn oil sen to strengthen the Spleen, tonify the Kidneys and
and dosing at 0.10 to 0.20 ml per kg body weight.1 calm the mind. ST-36 is the Master point of the
abdomen. In addition, ST-36 tonifies the Spleen,
Various Western herbal remedies have positive effects on strengthens the body and tonifies Qi. GV-20 is used to
the kidneys.29 Dandelion leaf is a potent natural diuretic lift the spirit, clear the mind and tonify Yang. PC-6 calms
and excellent nutritive herb. The leaves provide a wide the mind and tonifies the uterus. Other acupoints are
range of vitamins and minerals including potassium, selected on an individual basis, depending on the over-
which is commonly lost with mainstream diuresis. all condition of the patient.
Couch grass serves as an excellent tonic and disinfectant
of the urinary tract. It is a soothing, anti-inflammatory Chiropractic adjustment of the pelvis and synsacrum of
demulcent and saponin-based diuretic with mild antimi- the hen may be necessary for the proper passage of an
crobial effects. Couch grass is a specific remedy for egg. Improper nerve innervation of the oviduct can result
chronic or acute cases of cystitis and urethritis in mam- in poor oviduct contractions with slowing or blockage of
mals. Herbs with good antimicrobial effects and an affin- the egg-laying process. In addition, the pelvis may not
ity for the kidneys include echinacea, Oregon grape and widen properly due to erratic nerve innervation or hor-
thyme. Marshmallow root is a very safe and gentle monal imbalances. Relief of the fixations and subluxa-
mucilage, providing a soothing and protective barrier to tions will aid in proper nerve innervation of the repro-
mucosal surfaces, including the urinary tract. ductive tract and ease the egg-laying process.
Chinese herbal products formulated as Kidney Proper vitamin and calcium levels are critical in the lay-
Yin/Yang/Qi tonics are beneficial for certain renal dis- ing of eggs. Low blood calcium can affect various aspects
eases. Classic formulations include Six Flavor Tea, Eight of egg laying. Calcium is necessary for the production of
Flavor Tea, Rehmannia 6 and Rehmannia 8. Other the eggshell, resulting in soft-shelled eggs when defi-
Chinese herbal formulations may be indicated, depend- cient. Calcium also is required for the normal contrac-
ing on the TCVM diagnosis and concurrent problems. tion of muscles, including the smooth muscle in the wall
Acupuncture also may be beneficial in managing the of the oviduct. In addition, calcium must be balanced
with phosphorus and vitamin D3 for optimal utilization NEOPLASIA

and absorption. An excellent source of calcium is cal-
Tumors and various cancers are prevalent in certain
cium lactate, which can be powdered onto soft foods.19
species of pet birds. Budgerigars have the highest inci-
Commercial broad-spectrum vitamin and mineral sup-
dence of neoplasia in pet psittacines. Various types of
plements formulated for birds may also be appropriate tumors and cancers have been reported in many avian
sources of calcium and related minerals (see Chapter 4, species. Therapeutic options are often very limited when
Nutritional Considerations: Section I, Nutrition and approached conventionally. However, many of these can-
Dietary Supplementation, Chapter 5, Calcium cers can be managed with nutriceuticals, herbal reme-
Metabolism and Chapter 19, Endocrine Considerations). dies and other integrative therapies.
IMMUNE DEFICIENCY AND The general life-style and environment play a vital role in
CHRONIC INFECTIONS the risk of developing cancer in pets as well as people.25
A well-balanced and positive emotional environment
Many diseases in birds, as in any other species, begin with
helps set the tone for health. Toxic conditions, such as
a suppressed immune system. The weakened immune
smoke, chemical products, strong aerosolized sprays and
system can be the result of physical or psychological con-
odors, should be avoided. Exposure to cooking in coated
ditions. The physical causes include poor genetic consti-
cookware or plastics should be minimized. Provide fresh,
tution, malnutrition, toxic agents or infectious debilita-
clean air in a well-ventilated room and natural unfiltered
tion. Psychological sources may be environmental stress, sunlight. Encourage the bird to fly and/or otherwise exer-
lack of socialization, sexual frustration and abuse or neg- cise.
lect. The course of disease when exposed to an infectious
agent is dependent on the stability of the immune system. Good nutrition with a wide variety of healthy foods and
a basis of an organic formulated diet should be pro-
Nutriceutical supplements can boost the immune system vided. A variety of organic foods should be offered,
by providing proper nutritional support and immune- including whole grains, raw fruits and vegetables. Foods
strengthening components. Apple cider vinegar and Aloe high in essential vitamins and minerals are often the
vera are two examples of nutritional supplements. same as those with good antioxidant and anticancer
Antioxidants boost the immune system by clearing free properties. These include certain vegetables such as
radicals that otherwise would cause tissue degradation asparagus, tomatoes, bell pepper, turnips, kale, cauli-
and immune suppression. These products can simply be flower and broccoli. Certain fruits also provide excellent
added to the drinking water or food on a daily basis. nutrients, including apples, cranberries, pomegranate,
Aloe vera and most antioxidants can be given as contin- cherry, fig, grapes and mango. Foods rich in fiber and
uous daily supplements, whereas apple cider vinegar is antioxidants are recommended to fight off cancer and
best administered for up to 2 weeks or as needed. support the body’s immune system.29 Excellent foods to
include in a diet for cancer patients include Spirulina
Several Western herbs are effective immune boosters.
spp, kelp, garlic, onions, tumeric and parsley.25 Foods to
Certain herbs specifically boost the patient’s immune avoid include white flour, sugar, meats, fats and dairy
system, such as Spirulina sp. and pau d arco. Other products. The diet also should minimize salt intake and
herbs support the immune system through their antimi- excessive vitamin and mineral supplementation.
crobial properties. Herbs with antimicrobial effects
include echinacea spp, goldenseal, Oregon grape and Herbs assist the body in fighting cancer by providing
olive leaf.29 These are often used in combination with tonic support of organs and systems. Herbal formula-
other herbs as formulations. Certain Chinese herbs pos- tions that support the liver, kidneys and lymphatics help
sess immune-stimulating properties and antimicrobial strengthen the immune system by cleansing the body of
effects, including Huang Lian Jie Du Tang (Coptis and toxins and metabolic waste products.29 The classic Essiac
Scute) and Yin Qiao San (Lonicera and Forsythia and Hoxsey formulas were designed for this purpose.
Formula).15 These formulations likely have changed over the years,
but still contain an array of alterative and cholagogue
The energetic modalities such as acupuncture and herbs primed to cleanse the body, improve digestion
homeopathy have strong immune-modulating effects. and eliminate waste products.
These therapies treat at the deep energetic level of the
patient to boost its innate immune response. As a result, Some notable individual herbs with strong anticancer
the immune-stabilizing effects are stronger and longer effects include red clover, burdock root and dandelion
lasting (see Table 10.1 for specific acupuncture points root. Red clover is an effective anticancer herb; it inhibits
and Table 10.4 for homeopathic remedies in birds). the activity of carcinogenic compounds, improves blood
363
structure and strengthens lymphatic functions.29 Liver-sup- Anticancer herbal formulations should be individualized
portive herbs useful in fighting cancers include yellow for each cancer patient, based on their specific cancer
dock and milk thistle. Yellow dock serves as a strong liver and the debilitating effects on the body. A typical herbal
stimulant, while milk thistle protects the liver from harm- formulation usually contains three to five herbs. An
ful by-products of the cancer or cancer therapy. Diuretic example of a general tonic anticancer support formula-
herbs like dandelion leaf and nettle aid in removal of sys- tion consists of 2 parts red clover, 1 part astragalus, 1
part dandelion root and 1 part garlic.29 This formula,
temic waste through the kidneys and urinary tract. Herbs
which can easily be adjusted for the particular patient or
that assist toxic waste removal by soothing and protecting
condition, provides good systemic support, immunos-
the mucus membranes of the urinary and digestive tracts
timulation and cleansing properties.
include slippery elm, marshmallow, flaxseed, psyllium and
plantain. Finally, immunostimulant herbs that strengthen Nutriceuticals are common among the anticancer reme-
the cancer patient’s immune response include astragalus dies on the market for pets and people. Inositol with IP-
and garlic. 6k is a classic example of a nutriceutical product shown
Table 10.6 | Holistic Resources and Organizations

Chi-Institute
Professional Holistic Organizations 9708 West Hwy 318
Academy of Veterinary Homeopathy (AVH) Reddick, FL 32686
751 NE 168th Street Phone: 1-352-591-5385
North Miami, FL 33162-2427 Fax: 1-352-591-2854
Phone: 1-305-652-5372 E-mail: [email protected]
Fax: 1-305-653-7244
E-mail: [email protected]
Colorado State University
The American Academy of Veterinary Acupuncture (AAVA) College of Veterinary Medicine & Biomedical Sciences
PO Box 419 1601 Campus Delivery
Hygiene, CO 80533-0419 Fort Collins, CO 80523-1601
Phone: 1-303-772-6726 Phone: 1-970-491-7051
E-mail: [email protected] Fax: 1-970-491-2250
American Holistic Veterinary Medical Association (AHVMA) Web site: www.cvmbs.colostate.edu
2218 Old Emmorton Road
Bel Air, MD 21014 Animal Chiropractic
Phone: 1-410-569-0795 Options for Animals
Fax: 1-410-569-2346 Animal Chiropractic Center
E-mail: [email protected] 623 Main St.
Hillsdale, Illinois 61257
American Veterinary Chiropractic Association (AVCA) Phone: 1-309-658-2920
623 Main Street Fax: 1-309-658-2622
Hillsdale, IL 61257 Web site: www.animalchiro.com
Phone: 1-309-658-2920
Fax: 1-309-658-2622 Healing Oasis Wellness Center
E-mail: [email protected] 2555 Wisconsin St.
Sturtevant, WI 53177
International Veterinary Acupuncture Society (IVAS) Phone: 1-262-878-9549
PO Box 271395 Fax: 1-262-886-6460
Fort Collins, CO 80527 Web site: www.thehealingoasis.com
Phone: 1-970-266-0666
Fax: 1-970-266-0777 Internet Resources
E-mail: [email protected] Complementary and Alternative Veterinary Medicine
www.AltVetMed.com
Certification Programs
Veterinary Acupuncture Veterinary Medicine Internet Resources
IVAS www.holisticmed.com/www/veterinary.html
PO Box 271395
Fort Collins, CO 80527 Bach Flower Remedies Internet Resources
Phone: 1-970-266-0666 www.holisticmed.com/www/bach.html
Fax: 1-970-266-0777
E-mail: [email protected] Botanical/Herbal Medicine Resources
www.rosenthal.hs.columbia.edu/Botanicals.html
Herbal Database
www.herbmed.org
to fight cancer by stimulation of the body’s natural killer Products Mentioned in the Text
cell activity.30 Antioxidants are popular additions to holis- a. Parrot-specific Lactobacillus (Munich), www.janezek.de
b. Rescue Remedy, Bach Flower Remedies Ltd, Nelson Bach USA Ltd,
tic cancer therapies because of the stabilizing effects on Wilmington, MA 01887, USA
c. Ultraclear, Metagenics, 1152 Ensell Rd, Lake Zurich, IL 60047, USA,
the patient’s tissues produced through the scavenging of www.metagenics.com
free radicals. Antioxidants can be in the gentle form of d. Avian Enzyme, HBD International Inc, Brentwood, TN, USA,
vitamin C or the very potent form of proanthocyanidins e. Ultraclear Plus, Metagenics, 1152 Ensell Rd, Lake Zurich, IL 60047, USA,
such as grape seed extract or pycnogenol. Certain mush- www.metagenics.com
f. Livaplex, Standard Process, PO Box 904, Palmyra, WI 53156, USA,
rooms also have shown potential in the treatment of www.standardprocess.com
g. Lipogen, Metagenics, 1152 Ensell Rd, Lake Zurich, IL 60047, USA,
cancer, including Reishi, Maitake and Shiitake.25 www.metagenics.com
Coenzyme Q10 and N,N Dimethylglycine (DMG) are h. Arginex, Standard Process, PO Box 904, Palmyra, WI 53156, USA,
www.standardprocess.com
examples of immune-stimulating nutriceuticals with i. Renatrophin, Standard Process, PO Box 904, Palmyra, WI 53156, USA,
www.standardprocess.com
potential use in cancer therapy.14 These products also are j. Renagen, Metagenics, 1152 Ensell Rd, Lake Zurich, IL 60047, USA,
effective in the treatment of chronic diseases, which www.metagenics.com
k. Cellular Forte, Phytopharmica, Integrative Therapeutics, 9775 SW
debilitate the body’s innate healing process. Commerce Circle, Suite A-6, Wilsonville, OR 97070, USA, www.phy-
topharmica.com
References and England, The CW Daniel Co Ltd, St. Louis, MO, Mosby, 1998, pp Modern Medicine. St. Louis, MO,
1994. 649-663. Mosby, 1994, pp 291-314.
Suggested Reading 10. Jaggar DH, Robinson NG: History 17. McCluggage DM: Acupuncture for 25. Pitchford P: Healing with Whole
1. Baillie JW: Alternative therapy ideas of veterinary acupuncture. In the avian patient. In Schoen AM Foods: Oriental Traditions and
for feather picking. Proc Assoc Schoen AM (ed): Veterinary (ed): Veterinary Acupuncture: Modern Nutrition. Berkeley, CA,
Avian Vet, 2001, pp 191-196. Acupuncture: Ancient Art to Ancient Art to Modern Medicine North Atlantic Books, 1993.
2. Ball S, Howard J: Bach Flower Modern Medicine 2nd ed. St. 2nd ed. St. Louis, MO, Mosby, 26. Steiss JE: The neurophysiologic
Remedies for Animals. Saffron Louis, MO, Mosby, 2001, pp 3-17. 2001, pp 307-332. basis of acupuncture. In Schoen
Walden Essex, England, The CW 11. Kaminski P, Katz R: Flower 18. McCluggage DM: Overview of AM (ed): Veterinary Acupuncture:
Daniel Co Ltd, 1999. Essence Repertory. Nevada City, nutriceutical and herbal therapies Ancient Art to Modern Medicine
3. Chapman BM: Homeopathic CA, Flower Essence Society, 1998. in birds. Exotic DVM 3(6):8-11, 2nd ed. St. Louis, MO, Mosby,
Treatment for Birds. Saffron 12. Kreiger D: Accepting Your Power 2002. 2001, pp 27-46.
Walden Essex, England, The CW to Heal, The Personal Practice of 19. McCluggage DM, Higdon PL: 27. Willoughby S: Chiropractic Care.
Daniel Co Ltd, 1991. Therapeutic Touch. Santa Fe, NM, Holistic Care for Birds. New York, In Schoen AM, Wynn SG (eds):
4. Day C: The Homeopathic Bear & Co Publishing, 1993. Howell Book House, 1999. Complementary and Alternative
Treatment of Small Animals, 13. McCluggage DM: Avian holistic 20. McMillan MC: Imaging tech- Medicine, Principles and Practice.
Principles and Practice. Saffron veterinary medical care. Proc niques. In Ritchie BW, Harrison St. Louis, MO, Mosby, 1998, pp
Walden Essex, England, The CW Amer Holistic Vet Med Assoc, GJ, Harrison LR (eds): Avian 185-200.
Daniel Co Ltd, 1998. 1995. Medicine: Principles and 28. Worell AB, Farber WL: The use of
5. Devi L: Flower Essences for 14. McCluggage DM: Avian holistic Application. Brentwood, TN, acupuncture in the treatment of
Animals. Hillsboro, OR, Beyond medicine: Acupuncture, nutriceu- HBD Int’l Inc, 1999, pp 249-250. feather picking in psittacines. Proc
Words Publishing, 2000. ticals, and botanical medicine. 21. Ness RD: Alternatives for the anx- Assoc Avian Vet, 1993, pp 1-6.
6. Echols S: Management of specific Proc Assoc Avian Vet, 1997, pp ious pet. Exotic DVM 3(6):12, 29. Wulff-Tilford ML, Tilford GL:
avian renal diseases. Proc Assoc 519-533. 2002. Herbs for Pets. Irving, CA, BowTie
Avian Vet, 1999, pp 101-108. 15. McCluggage DM: Traditional 22. Ness RD: Chiropractic care for Press, 1999.
7. Ferguson B: Basic avian acupunc- Chinese medicine in birds. Proc exotic pets. Exotic DVM 2(1):15- 30. Wynn SG: Emerging Therapies,
ture. Exotic DVM 4(3): 31-34, Assoc Avian Vet, 1997, pp 535- 18, 2000. Using Herbs and Nutraceutical
2002. 541. 23. Ness RD: Herbal treatment for Supplements for Small Animals.
8. Graham H, Vlamis G: Bach Flower 16. McCluggage DM: Holistic medi- liver disease. Exotic DVM 3(6):15- Lakewood, CO, AAHA Press, 1999.
Remedies for Animals. Tallahassee, cine in exotic species practice. In 16, 2002. 31. Xie H: Traditional Chinese
FL, Findhorn Press, 1999. Schoen AM, Wynn SG (eds): 24. Partington M: Avian acupuncture. Veterinary Medicine. Beijing,
9. Grosjean N: Veterinary Aroma- Complementary and Alternative In Schoen AM (ed): Veterinary China, Beijing Agricultural
therapy. Saffron Walden Essex, Medicine, Principles and Practice. Acupuncture: Ancient Art to University Press, 1994.
11_Low Risk Pest Management.qxd 8/22/2005 3:53 PM Page 365
CHAPTER
11
Low-risk Pest
Management
DIANA POST, VMD
Information in this chapter is provided to help ensure

that wherever birds are being maintained, pest problems
can be dealt with effectively and potentially hazardous
conditions can be avoided.
The Environmental Protection Agency’s (EPA) classifica-

tion of pesticides as “low risk” refers to the potential
effects in humans, not companion animals or wildlife.
This should be kept in mind when a chemical pesticide
is being promoted as a “low-risk” alternative. Check with
Rachel Carson Council (RCC),8,16 Biointegral Resource
Center (BIRC)13 or other organizations for non-chemical
Greg J. Harrison
alternatives that can represent low risks to pets, wildlife

and the ecosystem, as well as to people.
Most veterinarians have traditionally used pesticides to

control the parasite problems of their patients. However,
many of them have adopted a hands-off approach
toward routine environmental pest control for ants,
cockroaches, rodents, etc, leaving this to the specialized
domain of certified exterminators and trusting them to
use the products properly. A recent incident serves as a
warning to animal health care professionals to reevalu-
ate this practice. The incident happened in January 2003
following use of the intensely toxic rodenticide zinc
phosphide. The fatal poisoning of two valuable red pan-
das at the National Zoo resulted in part from failure of
veterinary medical personnel to give sufficiently critical
oversight to rodent control procedures.
A promising outcome of the zinc phosphide incident has

been the National Zoo’s adoption of Integrated Pest Man-
agement (IPM) procedures for its animal facilities. IPM in
principle involves greater reliance on a variety of low-risk
pest management practices and the use of toxic chemi-
cals only as a last resort. Pest problems where compan-
ion birds reside can be controlled with similar strategies.
Those in charge of keeping animals healthy cannot pest control methods used truly afforded the lowest pos-
afford to delegate pest control measures without first sible risk to birds. In an ironic twist, the owner was able
making certain that the intended procedures provide the to collect financial compensation for theoretical damage
lowest possible risk to non-target individuals. In the to his own health that the birds’ deaths had indicated.12
future, with this greater awareness, we are confident
that veterinarians will be able to promote low-risk pest
management methods for use on premises where ani-
COULD CHEMICAL PESTICIDES IN
USE TODAY RESULT IN BIRD
mals are under their care. This can happen only if veteri-
INJURIES?
narians understand certain concepts and how they work.
Although chlorpyrifos and diazinon are no longer avail-
Justifications for avoiding use of chemical pesticides able for indoor use in the USA, neurotoxic chemicals
near companion birds can be similar to those given by (including cholinesterase inhibitors, pyrethroids as well
the United States Environmental Protection Agency as newer entities such as fipronil) are registered for
(USEPA) for avoiding them around another vulnerable indoor use and can contact a pet bird through diffusing
population — children: “Chemical pesticides…may from application sites such as rugs, furniture, the skin of
cause a range of harm, such as cancer, (as well as) acute a dog or cat, and bait stations, even if the bird is removed
or chronic injury to…(respiratory), nervous, reproduc- during the actual application process. Two newer insecti-
tive, endocrine and immune systems…”22 There are addi- cides, fipronil and imidacloprid, have been associated
tional reasons for bird owners to avoid chemical pesti-
with adverse reactions in people and pets when used in
cides. Tests for acute toxicity of pesticide products are
flea control programs (J.H. Gainer, personal communica-
performed on rodents. Since birds are generally more
tion, 2003). Both insecticides are registered for addi-
sensitive to chemical pesticides than most mammals
tional uses in and around the home.
including rodents, the required tests may not be predic-
tive for toxicity in birds. By persisting indoors for months or years on rugs or fur-
niture, certain chemical pesticides may present the
Sensitivities to chemicals can vary widely among avian
species and it is not possible to designate a single repre- potential for adverse effects. When applied outdoors,
sentative bird species to serve as the surrogate for all these same chemicals, plus others registered for outdoor
others in testing pesticide hazards.9 Due to birds’ use only, can drift indoors through open windows, con-
increased vulnerability, they have been used to provide tacting a caged bird kept nearby, or they can gain access
early warnings of toxic environmental conditions poten- from air intake ducts or be carried indoors on shoes.
tially harmful to those less sensitive, for example, the Birds and/or their environments may be treated with
canaries were used to protect coal miners from asphyxia- cholinesterase inhibitors such as the insecticide carbaryl
tion due to methane gases that replace oxygen and tend (recommended for mite control) or outdated remedies
to collect in coal mines. such as the toxic substance paradichlorobenzene (found
in moth crystals) used around cages. Further, the effects
Sentinel birds can suffer serious adverse consequences of multiple chemical exposures can be additive or even
in the process of protecting people.12,19 If environments synergistic, with greater likelihood of adverse reactions
are safe for birds, however, then people sharing homes occurring as a result.
with them will likely benefit as well.
Due to concern over West Nile virus, chemical pesticides
A CASE HISTORY may be broadcast from an aircraft or from a land-based
vehicle in an effort to reduce mosquitoes. Pet birds (and
Before it was banned in 2000 for indoor application, the
organophosphate insecticide chlorpyrifos was widely other sensitive individuals) can be protected from con-
used. Chlorpyrifos treatments for cockroaches in a home- tact with these sprays by closing windows and air intake
based aviary resulted in the eventual loss of the entire ducts when the application occurs. If possible, a pet
breeding bird population of 15 pairs and their offspring. owner should obtain information from local govern-
The toxic nature of the chemical as well as actions by the ments, professional pest control companies, landscapers
parties involved contributed to this unfortunate out- or neighbors who apply pesticides as to time, place and
come. The applicator called the pesticide “safe” and did nature of the pesticide product being sprayed close to
not appear to know its potential danger to birds, although the home. Greater surveillance of marketed products is
the owner specifically questioned him about it. The aviary needed to collect adverse reaction information. This is
owner accepted the exterminator’s assurances of safety especially important for products used in the home and
and failed to get a second opinion from those knowl- applied to pet animals, such as those products with
edgeable in pesticide toxicity to make certain that the fipronil and imidacloprid as active ingredients.
Chapter 11 | L O W - R I S K P E S T M A N A G E M E N T
367
INDOOR AIR QUALITY AND pest, a non-threatening, neutral insect visitor or even a
PESTICIDES beneficial insect (distinguishing the latter can be espe-
We have much to learn about the persistence of chemical cially important for outdoor pest control); see The
pesticides indoors. However, what we do know raises Importance of Identifying the Pest and Lessons from a
troubling concerns even for those chemical agents consid- Lacewing below.
ered to be less acutely hazardous to birds and people —
the pyrethroids. Since the recent banning of chlorpyrifos INDOOR PEST MANAGEMENT
and diazinon for indoor use, chemicals of the pyrethroid STRATEGIES
class have become more popular. The indoor half-life of
Indoor — Primary Strategy
long-lasting pyrethroids such as permethrin, deltamethrin,
cypermethrin and cyfluthrin may be up to 10 years.17 After determining that a pest is present and there is a
Pyrethroids are synthetic versions of the naturally occur- problem, the primary strategy involves preventing the
ring pyrethrins. The latter are much less persistent and pest from having access to a life-support system consist-
less acutely toxic, but they can still evoke allergic reac- ing of water, food and indoor habitat. Frequently, these
tions.6 A study reported that a percentage of the human measures are the only ones required to significantly
population in contact with pyrethroid-treated carpets had reduce or eliminate problem pest populations. They also
vague signs of discomfort (headaches, respiratory disor- are prerequisites to further management actions;5 see
ders, burning eyes, dizziness, tiredness, pain of muscles, each pest for particulars.
bones and joints). In a significant number of subjects,
these adverse effects regressed when the carpeting was Indoor — Secondary Strategy
removed. A scientist working on the study has ques- Once the primary strategy has been implemented, fur-
tioned, “…whether the indoor use of pyrethroids is safe ther action may be needed. Secondary control methods
enough to avoid adverse health effects.”17 Could birds be change the pests’ habitat while presenting low risks to
harmed due to presence of pyrethroids indoors? Perhaps people, pets and the environment;5 see each pest for
yes, but we do not know with certainty. However, we do particulars.
know that a number of alternative methods are available
in place of synthetic chemical pesticides for management
OUTDOOR PEST MANAGEMENT
of pests, both indoors and out.
STRATEGIES
Outdoor — Primary Strategy
General Principles and Many lawn and garden pests can be avoided by taking
into account the local growing conditions, choosing nat-
Examples urally disease-resistant plants that are also non-invasive
native varieties, as well as by using organic fertilizer and
Approaches to management of indoor and outdoor pests compost. Awareness of soil conditions and knowledge of
can be very different. Indoors, it is frequently possible to native plant species can help guide landscaping deci-
exclude the pest and employ low-risk products when sions.21 Exclusion is used less frequently than for indoor
necessary. Biological controls are rarely used indoors. pests, but if needed it can be accomplished with row
Outdoors, exclusion is less common and biological con- covers, netting or fences to keep insects, birds and even
trols are routinely used, especially by organic farmers deer away from plants.
and landscapers using biosustainable methods. Soils not
designed to grow plants or crops need more pesticides.
Outdoor — Secondary Strategy
When pests are found at unacceptable levels and inter-
BEFORE ANY CONTROL ACTION vention is needed, the secondary strategy makes use of
IS TAKEN mechanical and biological controls. There are astonishing
Accurate identification of the “pest” in question is the biological controls (most suitable for outdoors only) for
first step to successful management, especially when use against pest insects. For example, beneficial insects
dealing with an insect. Entomologists at institutions, such as lady beetles (ladybugs) obligingly prey upon
local extension service employees or professional pest aphids and other pests. Females of the non-stinging
control personnel can be useful here. Ants, cockroaches, Brachonid wasps deposit eggs in the body of pests,
moths, etc, may vary by species in their preferred habi- resulting in the growth of wasp larvae at the expense of
tats, food choices and life cycles. Accurate identification the pest. Such insects can be invited to a garden through
should help with selecting effective management meth- selective plantings and/or they can be purchased from
ods, deciding whether the organism in question is a true suppliers (see Suggested Reading for “If You Plant It,
Table 11.1 | Biological Control Resources

Refer to these resources for more information on biological control
products and low-risk pest control methods:
1. Rachel Carson Council, Inc (RCC) 3. Gardens Alive!
www.RachelCarsonCouncil.com www.GardensAlive.com
E-mail: [email protected] E-mail:
Phone: 301-593-7507 [email protected]
2. Biointegral Resource Center (BIRC) Phone: 812-537-8650
www.birc.org
Phone: 510-524-2567
They Will Come” and Table 11.1). Bacteria, fungi, viruses

and nematodes also are available for selective pest con-
trol. Birds can act as biological controls for insects; so
Greg J. Harrison
can turtles, amphibians and even fish. For some large
herbivores such as deer, contraception can be an effec-
tive control method. For mosquito management out-
Fig 11.1 | Ants following a crack in the cement to a food
doors, see the discussion below on Mosquitoes.
source. Ants leave a chemical trail that soap and water can
erase.
EXAMPLES OF INSECT
IDENTIFICATION
colonies. Carpenter ants can cause considerable damage
The Importance of Identifying the Pest in moist areas by excavating galleries and establishing
A family with two small children moved into a country residences in wall voids. Ants living outdoors, however,
house where they encountered a large number of tiny like spiders, can be considered as non-threatening or
red insects that the mother believed to be fleas. Instead beneficial through helping to control insects including
of spraying the house, as advised by a local extermina- fleas, termites and fly larvae. Denying access to ants
tor, the mother contacted RCC for advice. RCC loaned seeking shelter indoors, as well as eliminating access to
her a yellow/green intermittent light flea trap that she water and food, can significantly reduce ant populations
used to obtain specimens of the insects. Her local USDA along with those of other insects.
extension agent identified the insects as red clover
mites, non-biting insects. Using her vacuum cleaner, as Preventing Indoor Access
recommended by RCC, she was able to rid the house of
Prevent access by having a sweep on the door where it
the mites without resorting to the chemical spray.8
touches the floor that is in continuous contact with the
floor (vertical strips of plastic are not effective at keeping
Lessons from a Lacewing
ants out); caulking cracks in the walls and around pipes
Environmentalist Anna Edey described how she became can prevent ants from coming indoors. In an emergency,
an expert in recognizing beneficial insects: “One time I duct tape can be used to seal up an ant access area until
saw a little cluster of 10 to 15 very fine hairs about one- it can be caulked.13 It is important to be sure that the
half inch long protruding straight up from a hibiscus caulk does not contain volatile components that may be
leaf. Each hair had a tiny pinhead-sized egg…at the end irritating to chemically sensitive people and pets.
of it…I decided it looked like a virulent fungus…I
nipped off the leaf and discarded it. Later I found out
Preventing Water Access
that I had destroyed the eggs of one of the most valu-
able beneficial insects, the green lacewing.”16 Ants are attracted to moisture, so any leaks in ceilings or
walls and conditions that predispose to moisture should
be promptly repaired. These can come from water pipes,
downspouts, damaged roofing tiles as well as structures
that do not allow for proper ventilation.
Indoor Low-Risk Pest Preventing Food Access

Management Ants are attracted to and consume both sugar and pro-
tein, so spilled food should be removed quickly and the
ANTS area wiped with a soapy water solution. Pet food dishes
Ants (Fig 11.1) are one of the most abundant social can be placed in a moat/dish (for example a shallow pie
insect species on earth. They can become pests in build- pan) of soapy water to prevent ant access. The soap is
ings as they search for water, food or places to establish important to reduce surface tension so the ants drown.13
369
Food should be stored in ant-proof containers. These members. It is important to avoid using bait stations in
consist of a glass jar with a rubber seal or a plastic con- the same vicinity as pesticides with pyrethrins acting as
tainer with a tight-fitting lid. Ants sometimes get into the repellents (see Suggested Reading “What’s Wrong with
refrigerator if the seal around the door is faulty. My Bait?”).
Kitchen areas should be kept clean and dry with fre- Baits may take longer to establish control, especially if the
quent sweeping, vacuuming and washing up of spills. If active ingredient is an insect growth regulator. Low-risk
water accumulates in a pan under the refrigerator, the baits should be placed where they will not come in con-
pan should be regularly emptied and cleaned. tact with people or pets, or where a curious bird cannot
find one and chew on it. Ants respond to either sugar or
Dishes can be soaked in soapy water if immediate wash-
protein baits and they may alternate their preferences.
ing is not possible. Food containers should be rinsed of
all food residues before discarding. If possible, trash Ideally, the pesticide chemicals in baits should not be
should be stored outside until collected. volatile, as that would present a hazard to sensitive peo-
ple or pets. Since new formulations may not follow this
Water, food and droppings in birdcages can attract ants.
rule, monitoring for adverse signs associated with place-
Birds can be protected by placing a circle of sticky mate-
ment of baits is recommended. The chemical fipronil is
rial such as double-sided tape completely around the
believed to adversely affect chemically sensitive people
birdcage stand, since ants do not like to cross sticky
when present in bait stations (W. Currie, personal com-
material.5 The same type of sticky material also can be
munication, 2002).
placed around the chain or rope from which the birdcage
is suspended. Since birds can become immobilized on
An innovative device, the ant guard, has successfully pre-
sticky tape, it should be placed where birds will not rou-
vented, among other things, fire ants from gaining
tinely encounter it. Sticky barriers also can be used out-
access to nursing home patients in their beds. In appear-
doors to discourage ants, although wild birds can be at
ance it resembles the metal collar-like rat guard used to
greater risk from this placement, especially if they feed
block rats from crawling up ships mooring ropes. These
on insects caught on the sticky tape. Alternatively, the
initial ant guards have had a chemical deterrent in the
birdcage stand can be placed in a moat of soapy water.
form of the pyrethroid insecticide, permethrin, painted
Ants seem to find extruded polystyrene foam insulation on the inside of the collar. If the chemical component
(also known as “blue board”) to be ideal for locating could consist of a very low-risk repellent or toxicant
colonies. This could be important to those considering instead of permethrin, then it is very likely that ant
remodeling where ants could be a potential problem. guards could enjoy a host of additional uses.7
Changing Habitat — Indoor Carpenter Ants

If ants continue to be present indoors, a non-volatile pes- A pest control professional probably should be consulted
ticide can be applied in such a way that children and pets for carpenter ants, the large ants that take up residence
will not be able to come in contact with it. For example, in wall voids and woodwork but regularly travel to the
diatomaceous earth or silica aerogel, either alone or in outside. Frequently, individuals can be seen traveling
conjunction with boric acid powder, can be placed in along the outside wall from the ground, or up a shrub
floor cracks and crevices and behind cabinets — sites that is touching the outside wall, and entering the wall
usually accessible only to ants. Dust products should not through cracks. These ants often remove wood and other
be inhaled. Contracting with a professional for any appli- substances that pile up in small mounds near the entry
cations or employing safety equipment if the homeowner sites. These access points should be closed when the
uses them can minimize problems. Diatomaceous earth colony is treated. Indoors, the colony can be located by
should not be the kind used in swimming pool filters; it listening with a stethoscope for the characteristic noise
has been polished and therefore is not effective and pres- made by the ants. The most easily heard sounds made by
ents a serious respiratory hazard. Alternatively, bait sta- carpenter ants are intermittent clicks. The chewing
tions or gel with a pesticide and an ant attractant can be sounds that they produce are softer and harder to detect.
applied in areas not accessible to pets or people, but These sounds can be generated during day or nighttime
where ants will pick it up and carry it to the colony. hours (J. Ward, personal communication, 2004). Once its
Pesticide bait stations for ants can be placed around the parameters are identified, the colony can be treated with
floor if they are not accessible to children and pets. boric acid powder and/or diatomaceous earth, blown
Pesticide concentrations in most bait stations are low into the wall void through a series of strategically placed
enough not to kill the individual ants until they have holes drilled on the inside wall of the area they occupy.
returned to the colony and shared the bait with other Afterward, a professional should fill in the holes.
370
Greg J. Harrison
Greg J. Harrison
Fig 11.2 | Palmetto bugs (roaches) are common in the tropics Fig 11.3 | The small (German) roach is much harder to elimi-
around dense foliage. Food sources can encourage them nate than its larger cousin. After eliminating food sources, a
indoors in any setting. thorough (steam) cleaning and sealing of cracks is a must.
Following the wall treatment, baits can be used until all ing all exterior and interior cracks and holes in founda-
signs of the carpenter ants are gone. tions, walls, sills, sinks, gas, water and electrical lines;
covering prong holes in electrical outlets at all times;
screening air and ventilation vents, open sewer lines and
COCKROACHES
drains. Stainless steel baskets can be used in sink and
Cockroaches (Fig 11.2, 11.3) like buildings because they floor drains to prevent entry of cockroaches from
provide all the essential elements needed for survival sewers.13 Even the tiniest crevices must be attended to
including shelter (sometimes called harborage), moisture since an adult roach can hide in cracks as small as one-
and food. Cockroaches are strongly attracted to water. sixteenth inch and young nymphs can get through a
Although they can survive without food, they must have void even smaller.
frequent access to water.4 They prefer shelter where they
can touch the area above them with their antennae, such Preventing Water Access
as areas under cabinets.4 Cockroach problems almost
always indicate the presence of excessive moisture and Leaking faucets and pipes should be repaired. If possi-
poor sanitation, as well as access to harborage or shelter. ble, standing water should be eliminated or covered.
Reducing access to indoors, to moisture and food can Screens should be placed on fish tanks.13
prevent infestations. Otherwise, cockroach populations
are very difficult to manage because small residual popu- Preventing Food Access
lations can survive in even the most sanitary of environ- Foods should be stored in insect-proof jars with rubber
ments. Further, residual populations can explode into gaskets or tight-fitting lids and/or be kept in the refriger-
major problems. The use of chemical pesticide applica- ator. Food and grease should be removed each day from
tions can never be regarded as a substitute for either pre- stoves and counters. (A fingerprint left on a countertop
vention or good sanitation practices. Pesticidal suppres- by someone who has eaten fried chicken can feed a
sion of cockroach populations without a change in the roach for several days.5) Thorough cleanup of food parti-
environmental conditions that support them only gives a cles on and under tables and counters should be done
false and temporary sense of security and may result in as soon as possible after meals. Dishes not promptly
chemical resistance in pest populations.5 Cockroach food washed should be immersed in soapy water. Pet food,
can consist of that eaten by people and pets, as well as caches of crackers, nuts or even cough drops should be
soiled paper and glue.13 stored in the refrigerator between meals and dry food
should be stored in plastic containers with snap-on
Preventing Indoor Access lids.13 Garbage should be placed in a plastic container
with a tight snap-on lid.13 Refrigerators can pose weak
In a home or apartment, good barrier maintenance is
links in cockroach management programs because they
mandatory if cockroaches are to be denied access. This
provide heat, harborage around coils, a constant water
requires elimination of the holes and cracks that cock-
supply and hiding places that are difficult to treat.4
roaches use to gain entry. Before sealing see Boric Acid
below. Access can be denied to cockroaches and other
insects through the following measures: installing tight- School for Shaft Squatters
fitting windows, doors, screens and door sweeps; caulk- A school cafeteria was being switched to low-risk pest
371
management and all the appropriate steps had been socks and looking for small, black, moving forms. Flea
taken to restrict access, remove sources of water and problems in cats can be avoided by keeping them
food, and treat known harborage, but cockroaches were indoors or allowing access to a deck, screened or other-
still present. Finally, the pest management manager wise not in contact with the ground, to prevent the cats’
checked the hollow steel tube legs of the cafeteria tables picking up fleas from infested ground sites.
and found a previously overlooked cockroach harbor-
age. When this site was treated the cockroach problem Changing Habitat — Indoors
resolved (W. Currie, personal communication, 2003).
Washing pet bedding in hot water and drying in a dryer
where possible along with vacuuming and disposing of
Advantages of Cleaning
the vacuum contents so that the eggs do not continue to
Regular vacuuming reduces cockroaches’ food sources. develop inside the vacuum bag can remove fleas.
Cleaning out clutter reduces nesting and breeding sites, Frequent cleaning of non-carpeted floor areas and any-
as well as possible food sources such as glue and soiled where the pet sleeps will help reduce numbers of devel-
paper. oping fleas. Furniture and rugs can be shampooed in
cases of heavy flea infestation.
Changing Habitat
A light trap for fleas can be used to locate high popula-
At the first sign of a cockroach problem, sticky traps can
tion levels and measure control methods. Light traps are
be placed to detect the pests’ preferred shelter sites and
cardboard box-like stationary devices consisting of a
later for monitoring to determine whether control
light source to attract the adult fleas, as well as a sticky
efforts have succeeded. The traps should be non-toxic
surface, which fleas encounter and on which they
and placed along the edges of walls or counters where
become caught when they jump toward the light.
roaches normally travel.13 Cracks or crevices in floors or
walls can be treated with boric acid before being closed
Use of a fine-toothed comb (32 teeth per inch) is
by caulking or other means. See Boric Acid below.
recommended when combing a pet for fleas. It is best to
comb pets on a white sheet to catch any eggs or larvae
FLEAS removed by the flea comb. Fleas should be dropped in
The flea usually infesting USA homes is the cat flea, soapy water after removing them. When combing is
Ctenocephalides felis. Adult fleas most commonly obtain completed, the sheet should be picked up by the cor-
blood meals from mammalian hosts including dogs and ners and taken to be washed. Cats and dogs can be
people as well as cats. These organisms are parasites bathed using flea shampoo and, before they are com-
requiring a blood meal to reproduce. Fleas spend part pletely dry, combed to remove fleas while the fleas are
of their life cycle on the host animal, but can develop off still immobilized from the bathing procedure. Washing
the host so long as they have access to droppings from flea-infested clothing or other material in hot water and
the adult flea, since the droppings contain partially drying in a dryer will destroy all stages in the flea life
digested blood and serve as a food source for immature cycle. Dogs and cats can be treated with an oral flea con-
fleas. Fleas can reproduce indoors where the pet sleeps trol medication, Program,d that prevents fleas from
or rests, as well as outdoors during the warmer months developing.
in shaded areas such as crawl spaces under houses.
Since fleas are parasites, they do not depend on non- Changing Habitat — Outdoors
living sources of food to survive. If a pet goes outdoors, grass and vegetation should be
kept short in places where the pet sleeps or rests.
Preventing Indoor Access Sunlight can inhibit flea development. If possible, pets
Animals coming into the house for the first time or after and wildlife should be prohibited from having access to
being away at a kennel or in transit should be inspected areas such as porch crawl spaces, which are permanently
and, if necessary, bathed or vacuumed for fleas before shaded and ideal for flea development. A strain of the
being given access to indoors. This helps prevent seed- nematode Steinernema feltiae can attack larval stages of
ing of the premises. If people have visited a known flea- fleas20 (A. Pye, personal communication, 2003). The
infested area, they should change clothes or vacuum nematodes are sprayed outdoors on the soil where they
their clothes upon entering the house. The car and pet can take up residence and help reduce numbers of
carrier should be vacuumed and washed if necessary. viable fleas. Products containing this nematode species
Once the vacuum has been used it needs to be cleaned are commercially availablea (see Table 11.1 for Gardens
and treated for fleas or they will escape. Residents can Alive!, another resource for this organism). Nematodes
check for fleas indoors by walking around with white are not intended for use as indoor flea controls.
INSECT INFESTATION OF FOOD

Larvae of beetles and moths and grain mites can infest
stored grain or birdseed. Some insects lay their eggs in
the grains in the field and therefore are present as eggs
in seeds and even flour. The heat associated with pro-
cessing the grains usually eliminates the eggs from pelli-
tized and extruded products. Many of these insects can
crawl down the threads of an ordinary screw-cap jar, or
penetrate a single paper or cloth bag, so it is necessary
Greg J. Harrison
to use a glass jar with a rubber gasket or containers with
tight-fitting lids to exclude them. For storage, bulk seed
should be divided into 5- and 10-lb. containers so only
small amounts will be lost if some of it becomes contam- Fig 11.4 | Spiders are often misunderstood and killed. Moving
them, removing their webs and reducing the insect attractions
inated. One solution is to use 5-gallon buckets of the that cause spiders to be attracted contributes to insect control in
type used by bakeries. These buckets usually have tight- the long run.
fitting plastic or metal lids.13 Food should be stored in a
cool and dry environment. Most pests will not infest CLOTHES MOTHS
products if the humidity is below 6%.13 An inexpensive
The larvae of clothes moths attack various types of
instrument can measure the humidity in the storage
household material including blankets, upholstery and
area. Alternatively, grain and seeds can be stored in the
carpets. Clothes moth larvae avoid light and require
freezer. Food spills should be promptly cleaned up.
material stained with food or sweat to provide the
proper nutrients to grow. These moths do not attack
Preventing Indoor Access
clean clothes or fabrics stored in sealed containers.
At the time of purchase and/or when they are first Carcasses of dead mice in wall voids can attract moths.
brought into the home, foodstuffs should be inspected Unoccupied bird or bat nests in attics can be a source of
for possible mite infestation in the form of web-like clothes moths and other insects.
structures on or around the material.13
Infestation by clothes moths can be managed chiefly
Changing Habitat by prevention. Clothes should be thoroughly cleaned
before storing in tight containers. Vacuuming around the
Bacillus thuringiensis (B.t.) is a commercially available home and furniture is a way of controlling moths.
bacterial species that causes disease in certain insects by Exposure to heat is a direct way to kill clothes moths. If
acting as a stomach poison. B.t. can be applied to stored the temperature can be maintained at or above 100° F
grains for protection against the larval form of the (37° C) for several hours to days, all stages of the insect
Indianmeal moth. These insects seldom feed below a can be killed. Attics can often reach such temperatures in
surface layer more than 4 inches deep in a grain bin, the summer. Extremely cold temperatures (sealed bags in
so B.t. can be effective if applied to the surface.13 See a freezer) for several days also can control clothes moths.
Low-Risk Agents below. Traps to monitor for the presence of clothes moths can
be hung in the closet as an early warning device.13
Parasitoids such as the tiny Trichogramma can kill the
egg stages of the moth. This approach could be very
helpful for controlling long-standing infestations in the YELLOW JACKETS
home or aviary that have proved resistant to the normal Yellow jackets are a form of wasp that usually nest in the
physical or sanitary methods already described.13 ground, but they can at times nest in walls of homes.
Indoors they can actually excavate through plaster and
All stages of the Indianmeal moth are killed by freezing at in rare cases penetrate into adjacent rooms. Professional
0° F (-17° C) for 4 days. A pheromone trap for monitor- control using low-risk methods and performed at night
ing is commercially available. Once infestation is found, to minimize disturbing the insects can be effective.
the material can either be placed in a freezer or heated to When proper precautions are taken so as to not endan-
kill pests. The material should then be discarded. ger residents, injecting a spray of pyrethrins and
Seriously infested products with webs are often second- diatomaceous earth and then closing the access to the
arily contaminated with toxic levels of molds. Therefore, outdoors can be effective in eliminating the colony from
they should not be fed after freezing or heating. a wall void. See also Traps to follow.
373
SPIDERS stored in mouse-proof containers or rooms. Stored materi-

The presence of spiders can indicate that there are flies als should be kept away from walls and off the floor.
in the house. Spiders are useful and should be removed If corn gluten herbicide is being used, it should be
to outdoors whenever possible (Fig 11.4). Spiders can be stored over the winter in a container that mice cannot
removed to the outside mechanically with a glass and a penetrate. Any birdseed should be stored in tight con-
piece of stiff cardboard or by using a vacuum that will tainers or kept under refrigeration.
usually kill most spiders. Once the flies have been con-
trolled and the spiders removed mechanically or by vac-
Changing Habitat — Indoors
uum, they can be kept out by the same exclusion meth-
Types of Traps
ods as those used for cockroaches and ants, and by
When used correctly, snap traps are very effective for
caulking and using screens and door sweeps. There is
controlling mice. Traps must be set in the right places,
usually no need to use a chemical spray.
in high numbers and in the right position (see below) or
mice will avoid them.4 If used properly, snap traps inflict
MICE less suffering than do glue traps and possibly the so-
Adult house mice can weigh from 0.5 to 1.0 oz (15 to called humane box traps, since if animals are released in
30 g). House mice breed year-round under optimum a distant territory they will likely be attacked as aliens by
indoor conditions. Outdoors, these mice are seasonal resident mice.
breeders in the spring and fall. They are active primarily
at night but also can be seen moving about during the Setting Traps
day. Mice thoroughly investigate any change in their ter- The territory of mice rarely extends farther than 30 feet
ritory.4 They can squeeze through openings slightly more from the nest, and more often is about 10 feet. If mice
than one-quarter inch in diameter. They prefer cereals to are sighted throughout a building it usually means there
other food items. Management and prevention of infes- are numerous locations where traps should be set. Traps
tations by house mice is a three-part process: mouse- should be placed wherever there are obvious signs of
proofing, sanitation and population reduction indoors mice. Probably the biggest mistake made when trapping
with traps. When a mouse population already exists, mice is not using enough traps.4 Traps should be set
some kind of lethal control is necessary. Otherwise, the every 3 to 6 feet in prime mouse habitat. They should be
reproductive capability of the mice and their remarkable set in a three-dimensional sphere about 10 feet in diam-
ability to find food in almost any habitat will keep their eter around the signs.
populations steady or increasing.4 The practice of using
poisons on mice may lead to dead mice in wall voids, Baits
resulting in a moth infestation that can spread to cloth- Choosing good baits for mice and rats increases the
ing. Clothes moths are often attracted to the carcasses of effectiveness of mousetraps. Peanut butter (the chunky
dead animals. Other insects and bacteria can result from kind) is considered one of the best baits; food baits
poisoned, decomposing mice; and pets, including pet should be fresh to be effective. A cotton ball, which
birds, can be at risk from feeding on the dead mice or females like to use for nest material, also can be used.
the rodenticide used for rodent control. The cotton should be tied securely to the trigger.
Preventing Indoor Access

Mice are found around human housing, especially in
rural habitats. During the autumn and winter, they read-
Outdoor Low-Risk Pest
ily move into buildings that are not made rodent-proof. Management
All holes must be sealed to limit the movement of mice
into and through a building. Holes in foundation walls WEED MANAGEMENT
for pipes, utility lines and vents should be plugged with
Synthetic chemical pesticides do not need to be routinely
quarter-inch hardware cloth, copper mesh or steel
used against most types of weeds.11 For poison ivy, dig-
wool.4 Doors and windows should fit tightly and be
ging out the root and/or applying a 9% solution of vine-
caulked if necessary.
gar (used for pickling) are effective. For other broadleaf
weeds, corn gluten meal (Fig 11.5) is an effective pre-
Preventing Food Access emergent herbicide and can be used in spring and fall.
Practicing good sanitation is a way to reduce the food sup- Herbicidal soap is available for spot-treating weeds. On
ply. It enhances the effectiveness of traps and makes detec- paved surfaces, boiling water, steam, a flamer or other
tion of a mouse infestation easier. Bulk foods should be heat source can be used to remove unwanted vegetation.
Greg J. Harrison
Fig 11.6 | The beneficial dragonfly acts as flying insect control
by consuming large numbers of pest insects.
Greg J. Harrison
Fig 11.5 | Corn gluten meal serves as a pre-

emergence herbicide and then deteriorates into
a soil nutrient supply source.
INSECT PESTS OF THE LAWN AND

GARDEN
Greg J. Harrison
In many instances, the need for chemical insecticides
can be replaced with management strategies and natural
enemies of pests. Biological controls are commercially Fig 11.7 | Swarms of dragonflies are seen seasonally during
available. Beneficial insects also can be encouraged by the height of the pest insect season.
providing certain plants in the garden needed by the
insects for stages of their life cycles when they are not
11.7) that act as biological controls by consuming adult
preying on pests (see Table 11.1 for RCC Web site for
further details and information on grubs in the lawn; see mosquitoes. For special outdoor occasions, there are
also reference 16 and Suggested Reading “If You Plant It mosquito-trapping devicesb, some quite successful, that
They Will Come”). generate carbon dioxide, heat and synthetic attractants.
Effective natural mosquito repellents include garlic oil,

MOSQUITOES catnip and botanicals such as mint, citronella, geraniol,
Mosquito Management linalool, elemol (from the Osage orange tree), etc, used
singly or in combination. There also is the synthetic
In most naturally occurring streams or even backyard
chemical repellent DEET (best used at 30% concentra-
ponds, living organisms such as fish, amphibians and
tion or less, applied to clothing, not to skin).
insects feed on mosquito larvae and prevent the emer-
gence of adults. Biological control of adults includes
Mosquito repellent products can be sorted into three cat-
birds and bats.3 In artificially occurring standing water,
egories according to where they are applied: those placed
the mechanical emptying of containers every 4 to 5 days
on the clothing or skin; those dispersed into the air near
is the best prevention for adult mosquito emergence.
people by a battery-powered device; and those applied to
When water cannot be changed due to high volume
the ground area-wide, as granules or liquid or as liquid
and/or there is not a system with naturally occurring bio-
sprayed at ground level. More research is needed on the
logical controls, B.t. preparations (see below) can be
effectiveness of repellents in various delivery systems,
used to kill off the developing mosquito larvae in stand-
even for active ingredients of the natural, non-synthetic
ing water, as will dish soap or a thin coating of olive oil.
type. The area repellent products require more research
It is most important to clean out rain gutters so that they into their potential environmental hazards. Could they,
empty freely after a storm. Habitat should be provided for example, adversely affect beneficial insects and other
for wildlife such as birds, bats and dragonflies (Figs 11.6, life forms? See Garlic Juice Products below.
375
Low-Risk Agents CORN GLUTEN MEAL

The pre-emergent weed suppression qualities of corn
gluten meal (CGM) were discovered in 1987. CGM, a
BACILLUS THURINGIENSIS (B. t.) waste product of corn milling that has been used in ani-
B.t is a spore-forming bacteria named for a town in mal feed, is 60% protein and 10% nitrogen by weight.
Germany. Its insecticidal properties were first found in Protein is the active ingredient in CGM. It inhibits the
1911 in diseased flour moths. B.t. contains a protein growth of roots at the time of a plant’s germination.
(endotoxin) that is toxic for many caterpillars and other
Timing of the application of this pre-emergent herbicide
insect larvae. Varieties have been discovered that affect a
is very important. The precise moment in the year most
relatively narrow range of hosts, specifically mosquitoes,
advantageous for CGM weed control varies with growing
as well as certain moths and beetles. B.t. products in gen-
conditions. The local cooperative extension service can
eral lack toxicity for non-target species and the natural
be very helpful with advice on when best to apply CGM.
insect enemies of pests. B.t has been granted an exemp-
For example, in the Northeast, to manage crabgrass in a
tion from establishing a tolerance for use on food crops
lawn situation in the spring, CGM should be applied at
due to its low toxicity for humans when taken by mouth.13
the time of the crocus bloom and before the forsythia
bloom takes place. If applied later, after the weeds have
However, spray preparations of B.t. products have
already germinated, the nitrogen in CGM could help the
apparently been associated with adverse reactions when
emerging weeds thrive (M. Talbot, personal communica-
inhaled by certain sensitive individuals. Although in
tion, 2004). See Table 11.1 for Gardens Alive!, a resource
most cases B.t.would not be recommended for home
for CGM. The use of CGM as an herbicide is patented by
use indoors against moth infestation, it is available com-
Iowa State University.
mercially for that situation as well as for outdoor use
against mosquito larvae, gypsy moth larvae and other
garden pests.13 B.t. preparations used for mosquito con- DIATOMACEOUS EARTH
trol include dunks and granules intended for use in Diatomaceous earth is obtained from the fossilized silica
standing water. shell remains of diatoms, marine plankton. It has abra-
sive, sorptive and desiccant properties. It can be used
alone or in conjunction with boric acid and/or pyrethrins
BORIC ACID (naturally occurring pesticides from chrysanthemums —
Boric acid is a crystalline material derived from borax, see below). As with any dust preparation, a mask, gog-
(a combination of sodium, boron and oxygen mined gles and gloves should be worn by the applicator to pro-
from the earth). It acts as a stomach poison when tect the eyes, respiratory system and skin.13
ingested by the cockroach or ant causing the insect to
starve, which can take 5 to 10 days. It can be toxic to NEMATODES
mammals when ingested in high doses. Boric acid does
Nematodes are tiny worms. Most species live in the soil
not represent a volatile danger in its powder form. It is
and a few species are internal parasites of higher organ-
considered “virtually vaporless.”13 It must be kept away
isms including man. When fleas are replicating out-
from food, children and pets including pet birds to pre-
doors, certain species of nematodes may be effective in
vent oral consumption. Those applying boric acid pow- inhibiting their developmenta.
der should wear a dust mask, gloves, long sleeves and
eye protection. It is considered a low-risk alternative
when used indoors and placed in areas not accessible to
PARASITOIDS
pets or people, provided that precautions are taken See Clothes Moths.
and/or the formulation does not include another active
ingredient or inert component that may volatilize and PYRETHRINS
induce adverse effects through inhalation or dermal con- Pyrethrins are short-lived biological pesticides isolated
tact. If boric acid is applied to cracks, crevices and wall from chrysanthemums. They act as neurotoxic agents
voids, the areas should subsequently be sealed by caulk- and have the ability to paralyze insects. They can be
ing or closed off by another means so that it will not used in conjunction with diatomaceous earth or silica
present a problem to non-target individuals.13 Boric acid aerogel (see below). They are usually formulated with
remains active for months and cockroaches appear not the agent piperonyl butoxide to prevent metabolism of
to have developed any resistance after 50 years of use. the pyrethrin. Untoward allergic-type reactions in people
Boric acid can be toxic under conditions of high expo- or pets may take place when pyrethrins are used.
sure, so it is important to limit access. Pyrethrins have very low acute toxicity for most
GARLIC JUICE PRODUCTS

Neither the author nor the editors have any experience
with garlic products. A veterinarian in the Netherlands
states that one productc is very effective in controlling
mosquitoes in the yard (J. Hooimeijer, personal commu-
nication, 2003). The smell is a potential problem for
people who are sensitive to garlic. Originally garlic was
developed for control of pest insects on organic veg-
etable crops. The farmers using the product found mos-
quitoes were no longer a problem in the fields for rather
Greg J. Harrison
long periods of time after its use on vegetables.
Fig 11.8 | Leaf mold on this sea grape plant is a result of mites TRAPS
and the soil in the pot is not supporting healthy plant growth. A variety of traps are commercially available including
Repotting and an application of liquid dish soap are considered
the following:
an effective control.
• A yellow jacket outdoor trap for use away from the
area where people are gathering, consisting of one-
mammals and birds, but they are highly toxic to fish.2 way ports and baited with cat food, sugar-containing
cola drinks or meat. After yellow jackets enter the trap,
SILICA AEROGEL placing the trap in the sun will kill them. This should
be used only during the late summer when yellow
Silica aerogel is an amorphous, non-abrasive, chemically
jackets are aggressive toward people and their food.
inert, dust-like material. It results from the reaction of
Traps can be purchased from local hardware stores.
sodium silicate and sulfuric acid. Silica aerogels can
• Ant and cockroach indoor traps have attractants and
absorb water and oil. When used as insecticide, it is
insecticides at sufficiently low concentrations for ants
believed to absorb the waxy protective coating on an
and cockroaches to carry the poison back to members
insect’s cuticle — an action that can result in dehydration
of the colony without endangering other life forms.
and death of the insect. Silica aerogel particles are capa-
• A mosquito outdoor trapb uses propane to generate
ble of irritating human lungs and eyes, so a dust mask,
carbon dioxide and heat. In addition, certain models
goggles and gloves should be worn during application.13
may contain specific attractants such as octanol. These
traps are designed to lure and kill only insects that
SOAPY WATER seek a blood meal. They spare the non-biting forms.
A soap solution reduces the surface tension of water; • Moth traps use pheromones.
as a result, insects are unable to float and they drown.
Some plant pests are deterred by the use of soapy water Products Mentioned in the Text
applications (Fig 11.8). (See Ants - Preventing Access to a. Scan Mask, Biologic Co, www.biologicco.com
b. Mosquito Magnet, www.mosquitomagnet.com
Food). c. Garlic Spray, www.garlicbarrier.com/mosquitobarrier.html
d. Program - Lufenaron - Novartis
377
References 7. Grossman, Joel ESA 2002 Annual 15. Post D: The Other Road to Flea Talbot & Assoc, Inc, 2003.
Meeting Highlights-Part Two. In Control. Rachel Carson Council, 22. United States Environmental
1. Bichsel P, Lyman R: Pyrethroid toxi- The IPM Practitioner, V. XXV, Inc, 1994. Protection Agency: Region 8
city in felines: Prognosis good to #5/6, May/June 2003. 16. Post D, Collins M: EcoHeal IPM Pesticides/Toxic Chemicals &
guarded. DVM Magazine, June 8. Health-Based Integrated Pest for Outdoors. Rachel Carson Children, 2001.
2003. Management (IPM) for Indoors. Council, Inc, 2000.
2. Briggs, SAB and the staff of Rachel Rachel Carson Council, Inc, 2000. 17. Prohl A, et al: Activities of an Suggested Reading
Carson Council: Basic Guide to 9. Hoffman DJ: Wildlife Toxicity Environmental Analysis Van in the
Pesticides Their Characteristics and Testing. In Handbook of Ecotox German Federal State Schleswig- 1. If You Plant It They Will Come
Hazards. Hemisphere Press, 1992. 2nd ed. CRC Press, 2003. Holstein. Environ Health This brochure available from RCC
3. Christensen B: In defense of bats. 10. Katz H: Li’l Hummer, Non-toxic Perspectives, V. 105, #8, Aug lists vegetation designed to attract
Letter, JAVMA, v.222, #10, May 15, Pest Control. IPM Practitioner, 1997. and nurture beneficial insects.
2003. XVI, #4, April 1994. 18. Quarles W: New Flea Control 2. Questionnaire for Interviewing
4. Currie W: How Integrated Pest 11. Lerner J: Garden upkeep is good Products—Blessing or Curse? Potential Pest Control
Management Can Reduce Your for the mind, body and soil. The Common Sense Pest Quarterly, Specialists
Risk From Exposure to Pests and to Washington Post, April 19, 2003. VXIII, #2, Spring 1997. This handout available from RCC
Highly Toxic Pesticides. Proc 12. Mohan R: Dursban Toxicosis in a 19. Ramelmeier J, Post D: A Silent was designed to help individuals
Seminar Three—Ants, Pet Bird Breeding Operation. Killer of Birds in Our Care: Heat- find pest control specialists that
Cockroaches, Rodents and Turf. Proc Assoc Avian Vet, 1990, pp Generated PTFE Fumes. Rachel favor low risk methods of pest
University of the District of 112-114. Carson Council, Inc, 2002. control.
Columbia, Washington, D.C.,1992. 13. Olkowski W, Daar S, Olkowski H: 20. Silverman J, et al: Infection of the 3. What’s Wrong with My Bait?
5. Currie W: Integrated Pest Common Sense Pest Control: cat flea Ctenocephalides felis This article from the BIRC publica-
Management Procedures Manual. Least-toxic solutions for your (Bouche) by Neoplectana car- tion Common Sense Pest Control
International Pest Management home, garden, pets and commu- pocapsae Weiser. J Nematology provides hints on how to use baits
Institute, August 2002. nity. The Taunton Press, 1991. 14:394-397, 1982. safely and successfully. It is available
6. Gainer JH, et al: Adverse effects in 14. Payne P, Dryden M: Feline flea 21. Talbot M: Principles of Ecological from BIRC or RCC. See Table 11.1
human beings, dogs and cats asso- control. In Clinical Edge, Landscaping; A Primer on for contact information.
ciated with the use of flea and tick Thomson Veterinary Healthcare Environmentally Sensitive Design,
products. Pesticides, People and Communications (under a grant Installation and Care of Our
Nature 1(2):135-142, 1999. from Pfizer Animal Health), 2003. Lawns and Landscapes. Michael
12_Cardiology.qxd 8/22/2005 4:04 PM Page 379
CHAPTER
12
Evaluating and Treating the
Cardiovascular
System
MICHAEL PEES, D r med vet, German vet spec for birds/reptiles ;
MARIA-ELISABETH KRAUTWALD-JUNGHANNS, P rof Dr med vet ,
Dr habil, Dipl ECAMS , German vet spec for birds/reptiles ;
JENS STRAUB, D r med vet, German vet spec for birds/reptiles
Anatomical Considerations
The avian heart is located within the cranial part of the
thoracoabdominal cavity parallel to the spine in close
proximity to the sternum. No diaphragm is present and
the apex of the heart is surrounded by the liver lobes.
The pericardium covers the heart and normally encloses
a small quantity of fluid within the pericardial space.
The anatomy of the avian heart is similar to the mam-

malian heart, although some morphological peculiarities
exist. As in mammals, it is four chambered and function-
ally divided into the right and the left sides each consist-
ing of an atrium and a ventricle. The right ventricle is
sickle-moon shaped and surrounds the left ventricle.
The wall thickness of the ventricles changes from the
base to the apex of the heart (for measurements see
Table 12.6). The triangular right atrioventricular (AV)
valve is muscular and unlike the right atrioventricular
valve in the mammalian heart, does not contain chordae
tendinae. Contraction assists emptying of the right ven-
tricle during systole. In some species, the right cranial
and the caudal V. cava form a Sinus venosus that is sepa-
rate from the right atrium. In contrast, the ascending
aorta curves to the right in birds rather than the left side
of the body in mammals.2,25,26,41,44,45,53
Diagnostics sity of the large vessels should be assessed.
Diagnosis of cardiovascular diseases in cage and aviary Alterations of cardiac shape and size are often seen as an
birds is complicated by several factors. Only a few sys- enlargement of the heart silhouette. This can be caused
tematic investigations on post mortem diagnosis of car- by different etiologies (eg, hypertrophy, dilatation, peri-
diac diseases have been conducted.4,24 All descriptions of cardial effusion, aneurysm, inflammation or neoplasia).
ante mortem diagnostics are case reports, based on indi- Radiographic differentiation between these etiologies is
vidual experience. Documented normal reference values difficult. In cases of an existing pericardial effusion, the
are rare. Clinical signs of cardiac disease in birds are conventional radiograph may reveal cardiomegaly with
often nonspecific and may be accompanied by other an irregular cardiac silhouette.
concurrent disease conditions disguising the clinical pic-
ture. Diagnostic techniques in living birds are limited by An increased radiodensity of the large heart vessels can
the size of the patients and high heart rates. Fortunately, be seen on the ventrodorsal projection as roundish
within recent years, modern imaging techniques (like shadows superimposed on the base of the heart and in
echocardiography) have been evaluated in birds and ini- the lateral projections as an enlarged and radiodense
tial reference values for the assessment of cardiac func- aortic shadow. These findings may indicate atherosclero-
tion are now available. Since these techniques require sis, whereas their lack does not prove the absence of
special equipment and experience, they are not com- pathological alterations.
monly performed in practice. Nevertheless, the practi-
tioner should be aware of the diagnostic potential of Furthermore, radiographs may reveal secondary changes
ultrasound and other imaging techniques in avian car- in other organs, such as increased radiodensity of the
diac disease. lungs, enlargement of the hepatic silhouette, or ascites
in the case of congestive heart failure (see Fig 12.10).
Birds with acute circulatory problems have to be han- Ascites can also mask the radiographic detail of the tho-
dled as emergency cases. Handling should be kept to a racocoelomic cavity and the air sac shadows may be
minimum and diagnostic procedures be carefully decreased and/or displaced.
selected. The bird should be maintained in an upright
position to prevent circulatory failure. Echocardiography In birds, measurements of the length and width of the
may therefore be less stressful in these patients than cardiac silhouette on radiographs are limited. Initial
radiographic examination. examinations have been performed in Canada geese and
psittacines.12,46 Measuring the length of the cardiac sil-
CLINICAL EXAMINATION houette is often complicated by superimposition of the
The clinical diagnosis of cardiovascular disease in living apex of the heart on the liver on both the lateral and
birds can be difficult. There is no palpable pulse in ventrodorsal projections or the ventral aspect of the
birds. In addition, auscultation, an important standard heart on the sternum on the lateral projection.
technique in mammals, is difficult to interpret in birds. Measurements of the width of the cardiac silhouette (see
“h” in Fig 12.1) should be performed on the ventrodor-
Birds suffering from cardiac disease are often presented sal radiograph with exact superimposition of the keel
to the veterinarian with a history of weakness and and the spine. To assess the width of the cardiac silhou-
lethargy. In some cases, cardiovascular failure can be sus- ette, the measured value should be taken at the level of
pected on the basis of bluish discoloration of the perior- the maximum width of the cardiac silhouette, and com-
bital skin (especially in African grey parrots) and abdom- pared to the maximum width of the thorax (see “t” in
inal distension. Nonspecific symptoms like dyspnea and Fig 12.1). The sternal length should be taken on the
exercise intolerance may also lead to a tentative diagno- radiograph or on the patient using a standard sliding
sis of a cardiac problem and provide an indication for calliper. In medium sized psittacines (approximately 200
further diagnostic procedures. to 500 g) the width of the cardiac silhouette should be
approximately 36 to 41% of the length of the sternum or
STANDARD RADIOLOGY 51 to 61% of the width of the thorax respectively. There
Radiology is a commonly performed and well estab- is a strong correlation between the width of the cardiac
lished imaging technique in avian medicine. It may silhouette and the width of the thorax.46 In Canadian
(often by chance) disclose signs of cardiovascular dis- geese the width of the cardiac silhouette is 47 to 57% of
ease and indicate the need for further diagnostics, espe- the width of the thorax.12 This study also showed that
cially echocardiography. Position, size and shape of the the movements of the thorax due to respiration are not
heart and other internal organs as well as the radioden- as important as might be expected.
Chapter 12 | E V A L U A T I N G A N D T R E A T I N G T H E C A R D I O V A S C U L A R S Y S T E M
381
Fig 12.2 | Angiocardiography: filling of the heart in a common

buzzard (Buteo buteo).
Fig 12.1 | Schematic illustration of the distances to be meas-

ured for the evaluation of the avian heart on ventrodorsal radi- echocardiography has been considered inaccurate and
ographs (h = maximum width of the heart size, t = width of the difficult in birds. Bone and air block the passage of ultra-
thorax at the level of the maximum width of the cardiac silhou- sound waves. Standardized views and protocols for
ette (microchip can be seen in the left pectoral muscle). mammals recommended by the American College of
Veterinary Internal Medicine50 cannot be used in birds
ANGIOCARDIOGRAPHY and comparison of the measurements with those in
Although few reports about the use of angiocardiogra- mammal or human medicine are not valid.15 However, in
phy in birds exist, the authors’ initial experiences show a recent years, case reports regarding the use of echo-
high potential value for its use in diagnosing cardiac cardiography for diagnosis of cardiac disease in birds
problems. Angiocardiography cannot replace echocar- have demonstrated the potential of this diagnostic pro-
diography but it might give additional information, espe- cedure.29,30,47,52 Initial studies have been conducted and
cially in birds with insufficient detail demonstrated on standardized protocols for echocardiographic examina-
echocardiographic examination. Examination of the tion in avian patients have been established.15,34,46,47
heart vessels is another indication for angiocardiography.
Improved technology has produced ultrasound equip-
In one report, an aneurysm of the right coronary artery
ment that is effective and affordable for avian echocar-
was demonstrated in a white cockatoo (Cacatua alba)
diography. Parameters of these machines should include
using angiocardiography.52
1) minimum 100 frames/second
Angiocardiography should be performed under anaesthe- 2) Doppler function
sia. A venous catheter is placed within the jugular or 3) microcurved or phased array probes
basilic vein. Iodinated contrast media (eg, Iopamidol, 510 4) minimum 7.5 MHz frequency
mg/ml adequate 250 mg iodine per ml) is used according
to mammalian angiocardiography, but the dosage in birds On avian patients that are tolerant of restraint, echocar-
(2-4 ml/kg of pamidol ie, 1,020-2,040 mg body mass) is diography can be performed awake; stress-sensitive birds
twice as high as commonly used in mammals. Administra- should be anesthetized.
tion rate in medium sized birds should be approximately
Because the food-filled gastrointestinal tract might be
1 to 2 ml of contrast medium per second.
interposed between the scanner and the heart ideally
Due to the rapid heart rate in birds, assessment of con- the GI-tract should be empty. Therefore it is recom-
tractility may be difficult to evaluate, but hypertrophy mended to fast the bird before ultrasound examination.
(ventricles), dilatation (ventricles, atria), stenosis (ves- Granivorous birds should be fasted for about 2 (small
sels, valves) and aneurysm (vessels) can be detected (see psittacines) to 12 (pigeons) hours. Raptors should gen-
Fig 12.2). erally be fasted for a longer period.
Echocardiographic measurements should be done in

ECHOCARDIOGRAPHY relation to the patient’s size. Two parameters should be
In veterinary medicine, echocardiographic examination determined: first, the bird’s weight (although this might
has become a very important diagnostic tool, and is indi- be misleading in seriously ill birds that are emaciated),
cated for assessment of cardiac function and the struc- and second, the length of the sternum, taken on the
ture of the heart. For a long time, due to anatomical radiograph or on the patient using a standard sliding
peculiarities (especially the position of the airsacs), calliper. Simultaneous ECG recording and triggering is
shows the heart lying on the inner surface of the ster-

num. The horizontal view (“four-chamber view”) is pro-
duced by a counter-clockwise 90 degree rotation of the
scanner.
B-mode-echocardiography (2-D-echocardiography)
Due to the fact that only long axis views are possible
with the ventromedian approach, M-Mode echo can not
be used in birds to evaluate contractility and wall thick-
ness. Therefore, measurements have to be taken on the
2-D-echocardiograph.
Longitudinal Vertical View (“Two Chamber View”)

The vertical view shows the left ventricle and the left
atrium (which is often not completely distinguishable
from the surrounding tissue) as well as the left atrioven-
tricular valve. Sometimes border areas of the right ven-
tricle may also be seen next to the total reflexion of the
sternum (Fig 12.4) but cannot be used for assessment. In
this view, artifacts caused by reflexions of the sternal
bone may produce a second “heart” lying outside the
thoracoabdominal cavity (mirror picture artifact).
Fig 12.3 | Two-dimensional echocardiography, schematic
views: ventromedian approach, horizontal (a) and vertical (b)
view. Important measurement points, values see Tables 12.1
Longitudinal Horizontal View
and 12.2. (1 = left ventricle, 2 = right ventricle, 3 = left atrium, (“Four Chamber View”)
4 = right atrium, 5 = aortic root, 6 = interventricular septum, In the four-chamber view, both ventricles, the interven-
* = no assessment possible in B view)
tricular septum, both atria, the atrioventricular valves
and the aortic root with the aortic valves can be visual-
recommended to allow measurements at defined stages ized (see Fig 12.4). In this view it is difficult to outline
of the heart cycle. For the examination, birds should be the borders of the atria.
held in an upright position in order to minimize stress
and its influence on the cardiovascular system. Measurements in 2-D-echocardiography
Measurements have to be taken from 2-D images, since
Because of the avian anatomy, suitable echocardio- there is no possibility for a suitable cross section for M-
graphic windows to the heart are limited. There are two Mode technique. Additionally, the images are of very
possibilities: the ventromedian and the parasternal small structures. Therefore the interpretation of meas-
approach.15 In psittacines and raptors, the ventromedian urements is limited and small changes in size may not
approach is routinely used. With this approach the be detected with the current techniques.
homogenous liver tissue serves as an acoustic window.
The scanner is placed on the midline directly behind the To measure specific cardiac parameters, the position of
sternum and the beam plane is directed craniodorsally. the transducer must be adjusted until the maximum
In birds with sufficient space between the last ribs and expansion of the chamber is visible. Measuring points
the pelvis (eg, pigeons), the parasternal approach can be are demonstrated in Fig 12.3. All parameters should be
used. The transducer is placed on the right side of the measured in systole and diastole at the point of the
body, since in the left part of the thoracoabdominal cav- widest distance using the inner edge method.56 Measure-
ity, the grit-filled ventriculus is present and often makes ments of the left ventricle are possible in both views, but
visualization of the heart impossible. The probe is are easier to obtain in the vertical view. In psittacines,
placed behind the last ribs and the plane is directed there is a strong correlation between the sternal
craniomedially. length/the body mass and the length of the left ventricle
(LVL); the expected length can be estimated with the for-
With the ventromedian approach, two longitudinal mula LVL = 0.5 + 0.33 x sternal length.32 Measuring the
(comparable to “long axis” in mammal echocardiogra- length of the right ventricle is more difficult because it is
phy) views of the heart are obtained (Fig 12.3). The verti- visible as an acute-angled triangle. Additionally, the mus-
cal view (corresponding to the “two-chamber view”) cular right atrioventricular valve is — due to its motility
383
a width of the transverse left ven-

tricular diameter during systole in
relation to the diastolic diameter
(%FS = (diastole - systole)
100/diastole). The values are dif-
ferent than those in mammals,
which might be due to anatomi-
cal peculiarities (see above).
Contractility of the right ventricle
is significantly higher than the
value found for the left one.
b
The relationship of the width of
the ventricle to the length can
give information about dilatation.
For psittacines, a relatively con-
stant value (systolic 0.33, dias-
tolic 0.40) (see Table 12.3) has
been noted.32,33,34
Volume calculations, based on

simplified models of the chamber
volume of the left ventricle, have
c
not yet been documented as
diagnostic.34
Preliminary reference values for

morphometry and assessment of
cardiac function have been estab-
lished for psittacines,32,33,34 birds
of prey3 and pigeons15 (Tables
12.1-12.3).
Fig 12.4 | Two dimensional echocardiography, normal hearts. a: vertical view, blue fronted
Amazon (Amazona aestiva), b: horizontal view, systole, carrion crow (Corvus corone), c: hori-
zontal view, diastole, carrion crow (Corvus corone). (1 = left ventricle, 2 = left atrium, 2a =
left atrioventricular valves, 3 = right ventricle, 4 = aortic root, 4a = aortic valves, 5 = liver Doppler-echocardiography
tissue, 6 = sternal reflexion).
To date, there only a few reports
of Doppler echocardiography in
birds. The principles are the
— an imprecise margin for right ventricular measure- same as in mammalian echocardiography, but specific
ment. The outer walls of the heart are often difficult to problems exist. The frame rate when color Doppler
distinguish from the surrounding tissue. The thickness mode is used is significantly lower in most ultrasound
of the interventricular septum may give information devices. This makes it difficult to assess blood flow. Also,
about ventricular hypertrophy. Measurements of the pulsed-wave Doppler has limitations due to the high
atria are imprecise and therefore of limited use. The velocity of flow in the avian heart.
importance of atrial contraction for blood flow into the
Color-Doppler can be used for the detection of valvular
ventricles is limited, therefore assessment may not be
insufficiencies (reported in an Indian Hill Mynah Bird).39
important.42
It is also helpful for the positioning of the gate for spec-
tral Doppler-analysis to determine the degree of valvular
Calculations for Functional Assessment insufficiency. In one case, the use of color Doppler for
(Tables 12.1-12.3)
diagnosis of an aneurysm in a coronary artery has been
On the basis of the measurements obtained, the fractional reported.52 With the standard ventromedian approach,
shortening (FS) can be calculated. This is one functional the diastolic inflow into the ventricles is displayed red
parameter for evaluating the capability of ventricular con- (flowing towards the transducer) and the systolic outflow
traction. It is calculated as the relative reduction of the blue (flowing away from the scanner) (see Fig 12.5).
384
Table 12.1 | Longitudinal and Transverse Diameter of the Left Ventricle in Systole and Diastole (mm)*
LVLSV LVLDV LVTSV LVTDV LVLSH LVLDH LVTSH LVTDH
Psittacus erithacus erithacus 22.2 ± 1.9 23.9 ± 1.9 7.0 ± 1.1 9.1 ± 1.5 22.5 ± 1.9 24.0 ± 1.9 6.8 ± 1.0 8.6 ± 1.0
Psittacus erithacus timneh 18.4 ± 1.9 19.5 ± 1.9 6.9 ± 0.8 8.9 ± 1.4 17.9 ± 2.4 18.6 ± 3.0 5.9 ± 0.2 7.6 ± 1.3
Amazona spp. 20.7 ± 1.5 21.8 ± 1.9 6.7 ± 1.1 8.7 ± 1.2 21.1 ± 2.3 22.1 ± 2.2 6.7 ± 1.2 8.4 ± 1.0
Cacatua spp. 18.9 ± 1.7 19.4 ± 1.8 6.6 ± 1.7 8.8 ± 1.8 19.0 ± 1.3 19.9 ± 1.6 6.4 ± 1.7 8.3 ± 1.5
Poicephalus s. senegalus 14.5 ± 1.1 15.1 ± 1.0 5.2 ± 0.9 6.9 ± 1.0 14.4 ± 1.2 15.1 ± 2.0 4.6 ± 0.3 5.9 ± 0.5
Diurnal raptors (male) 17.7 ± 1.2 19.3 ± 1.6 6.6 ± 0.9 7.5 ± 1.0 14.7 ± 2.0 16.5 ± 1.8 6.1 ± 0.8 7.4 ± 1.0
Diurnal raptors (female) 18.2 ± 4.7 20.1 ± 5.2 7.7 ± 1.8 8.9 ± 2.1 14.7 ± 4.5 16.3 ± 4.5 6.8 ± 1.7 8.3 ± 1.8
Pigeons (parasternal approach) — — — — 17.9 ± 1.0 20.1 ± 1.4 5.2 ± 0.4 7.4 ± 0.6
*Psittaciformes according to Pees,32,33,34 birds of prey according to Boskovic,3 pigeons according to Krautwald-Junghanns15
V = vertical view; H = horizontal view
LVLS = left ventricle, longitudinal diameter systole; LVLD = left ventricle, longitudinal diameter diastole;
LVTS = left ventricle, transverse diameter systole; LVTD = left ventricle, transverse diameter diastole
Table 12.2 | Longitudinal and Transverse Diameters of the Right Ventricle in Systole and Diastole (mm)*
RVLSH RVLDH RVTSH RVTDH IVSSH IVSDH AOSH AODH
Psittacus erithacus erithacus 9.2 ± 1.4 11.5 ± 1.9 2.8 ± 0.9 4.8 ± 1.1 2.9 ± 0.5 2.5 ± 0.3 3.6 ± 0.4 4.0 ± 0.6
Amazona spp. 9.4 ± 1.8 10.3 ± 1.3 3.1 ± 0.7 5.2 ± 1.3 2.2 ± 0.1 2.1 ± 0.4 3.0 ± 0.5 3.4 ± 0.6
Cacatua spp. 10.3 ± 1.2 11.3 ± 2.3 2.3 ± 0.0 3.5 ± 0.5 1.9 ± 0.3 1.7 ± 0.4 — —
Poicephalus s. senegalus 7.5 ± 1.1 7.6 ± 0.2 2.5 ± 0.4 3.3 ± 0.3 1.9 ± 0.3 1.7 ± 0.2 2.5 ± 0.3 2.4 ± 0.0
Diurnal raptors (male) 12.6 ± 1.9 13.8 ± 1.8 2.1 ± 0.5 2.5 ± 0.7 1.8 ± 0.4 1.9 ± 0.4 — 2.7 ± 0.4
Diurnal raptors (female) 13.0 ± 4,6 14.2 ± 4.2 2.2 ± 0.8 2.5 ± 1.1 2.0 ± 0.8 2.0 ± 0.7 — 2.9 ± 0.4
Pigeons (parasternal approach) — 9.9 ± 0.8 — 4.0 ± 0.5 3.8 ± 0.1 3.3 ± 0.2 — 3.0 ± 0.1
*Mean value ± standard deviation (Psittaciformes according to Pees,32,33,34 birds of prey according to Boskovic3, pigeons according to Krautwald-
Junghanns15)
H = horizontal view
RVLS = right ventricle, longitudinal diameter systole; RVLD = right ventricle, longitudinal diameter diastole; RVTS = right ventricle, transverse
diameter systole; RVTD = right ventricle, transverse diameter diastole; IVSS = interventricular septum, thickness systole; IVSD = interventric-
ular septum, thickness diastole; AOS = aorta, diameter systole; AOD = aorta, diameter diastole
Table 12.3 | Calculated Parameters in Psittacines*
Relation Width to Length of the Ventricles Fraction Shortening %
LVSV LVDV RVSH RVDH LVTH RVT H
Psittacus erithacus erithacus 0.32 ± 0.05 0.39 ± 0.07 0.31 ± 0.08 0.43 ± 0.1 22.6 ± 4.4 40.8 ± 11.9
Amazona spp. 0.32 ± 0.04 0.40 ± 0.05 0.35 ± 0.11 0.51 ± 0.13 22.8 ± 4.2 34.1 ± 3.7
Cacatua spp. 0.35 ± 0.08 0.45 ± 0.09 0.23 ± 0.03 0.32 ± 0.07 25.6 ± 7.0 33.3 ± 10.3
Poicephalus s. senegalus 0.36 ±0.06 0.46 ± 0.07 0.30 ± 0.07 0.44 ± 0.04 24.9 ± 3.1 37.1
All examined psittacines 0.33 ± 0.05 0.4 ± 0.07 0.31 ± 0.08 0.43 ± 0.1 23.1 ± 4.6 39.6 ± 11.4
*Mean value ± standard deviation (Pees32,33,34)
V = vertical view; H = horizontal view
LVS = left ventricle systole; LVD = left ventricle diastole; RVS = right ventricle systole;
RVD = right ventricle diastole; LVT = left ventricle, transverse diameter; RVT = right ventricle, transverse diameter
Spectral Doppler-echocardiography is the standard could only be differentiated in a few cases.5

method for noninvasive blood flow velocity measure- Measurements are given in Table 12.4.
ments in mammalian medicine. Signals are displayed as
two-dimensional time versus velocity graphs. Two differ- CW Dopplers are useful for the detection of very high
ent types of spectral Doppler are of interest: pulsed- blood flow velocities but do not allow the measurement
wave (PW) and continuous-wave (CW). PW Doppler is of the flow velocity at a certain point. No studies regard-
limited to velocities lower than 2 m/second but allows ing the use of CW Dopplers in birds have been pub-
lished so far.
measurements within an operator-specified sample vol-
ume or “gate”. Diastolic inflow into the left and the right
Birds under stress significantly increase their intracardial
ventricle, as well as systolic aortic outflow, have been
blood flow velocity. It is recommended that Doppler-
measured in psittacines and raptors using PW Doppler
echocardiography be performed under anesthesia in
(Fig 12.6).5,43,47,49 For the mitral inflow, two peaks could
these patients.
be recorded (E-wave corresponding to ventricular filling,
A-wave to atrial contraction); E:A was positive for
macaws and African grey parrots, whereas in cockatoos it ELECTROCARDIOGRAPHY (ECG)
was negative.5 Blood flow within the pulmonary artery Although electrocardiography was the first
385
Fig 12.5 | Color-Doppler echocardiography, carrion crow

(Corvus corone): a) Filling of the left ventricle (red inflow). b)
Systolic outflow into the aorta (blue). Red colored areas are
caused by fluid moving towards the transducer, blue areas show
movement away from the transducer.
described technique for ante mortem diagnosis of car-

diac diseases, it is used less frequently in birds com-
pared to mammals. Difficulties may occur with the con-
I. Kiefer
nection of the leads to the skin and stress may cause
alterations of the recorded ECG. Additionally, no refer- Fig 12.6 | Pulsed wave Doppler echocardiography: a) Diastolic
inflow into the left ventricle, channel-billed toucan (Ramphastos
ence values have been published for many of the bird
vitellinus). b) Systolic aortic blood flow, carrion crow (Corvus
species. corone).
The main indication for ECG is diagnosis and control of

arrhythmias and conduction disorders. It may also be Table 12.4 | Doppler Derived Intracardial Blood Flow
Velocities in Birds*
valuable for detecting enlargement of the ventricles and
Species Diastolic Diastolic Systolic
metabolic disorders.38 ECG can be used for monitoring Inflow Left Inflow Right Outflow
cardiac function during anesthesia and for recording car- Ventricle Ventricle Aortic Root
(m/s) (m/s) (m/s)
diac stages (systole, diastole) while performing other
Amazona spp.A,43,48,49 0.18 ± 0.03 0.22 ± 0.05 0.83 ± 0.08
imaging techniques (eg, echocardiography). Another
Cacatua galeritaA,5 0.32 ± 0.15 — 0.78 ± 0.19
indication for performing ECG is monitoring cardiac Psittacus erithacusA,5 0.39 ± 0.06 — 0.89 ± 0.13
disease therapy. Ara sp.A,5 0.54 ± 0.07 — 0.81 ± 0.16
Buteo buteoA,43,48,49 0.14 ± 0.01 0.14 ± 0.02 1.18 ± 0.05
There are many reports on how to perform ECGs in Buteo buteoC,43,48,49 0.22 ± 0.03 0.19 ± 0.03 1.36 ± 0.16
birds. Some authors recommend examination under Parabuteo unicinctusC,43,48,49 0.19 ± 0.03 0.21 ± 0.03 1.09 ± 0.17
anesthesia, others prefer recording the ECG in the Tyto albaC,43,48,49 0.2 ± 0.03 0.22 ± 0.06 1.08 ± 0.12
awake bird. Anesthesia may induce alterations in the Falco spp.C,43,48,49 0.21 ± 0.03 0.21 ± 0.04 0.95 ± 0.07
ECG. With isoflurane anesthesia, arrhythmias have been Falco spp.C,43,48,49 0.28 ± 0.05 0.27 ± 0.05 1.25 ± 0.09
described, such as second- and third degree AV-block, *Straub;43,48,49 Carrani5

A = anesthetized
sinus arrest, T-wave depression and atrial premature C = accustomed to handling, conscious
contraction.1
For the clinical application of an ECG in avian patients,

six leads, as commonly performed in mammals, can be
used. Due to the high cardiac heart rate, electrocardio-
graphs in avian medicine must be able to run at a paper
speed of at least 100 mm/second. Leads are attached on
the right wing (RA), left wing (LA) and left leg (LL), and
the right leg is connected to the ground (Lumeij and
Ritchie, 1994). If the ECG is used to monitor anesthesia
or to trigger echocardiographic images, bipolar leads (fol-
lowing the electrical heart axis; with one attached cra-
nially to the sternum and slightly paramedian on the right
side of the body, and the other one attached caudally to
the sternum, slightly on the left side) may be sufficient.
Several techniques for attachment of the leads to the Fig 12.7 | Schematic view of a normal ECG-complex, lead II, in
a healthy macaw. Measurement points following Lumeij.22
skin have been described (subcutaneous needles, alliga-
tor clips, specially constructed feather clips). In the
authors’ experience, alligator clips can be effectively
used in birds, when clipped on the proximal part of the and the right ventricular free wall as well as the interven-
rachis of the feathers. By using alligator clips without tricular septum should be made using precision cal-
sharp teeth there is no damage to the feathers. To get lipers. Additionally, measurements of the length of the
electrical contact with the skin, water soluble ECG gel or left ventricle should be ascertained (Fig 12.8).
small amounts of alcohol are applied between the skin
and clip. To date, the amount of scientific data concerning the
morphometry of the avian heart is limited. Scientific
The avian ECG is quite different from the mammalian studies have been performed in two psittacine species
ECG. A schematic lead II-ECG-complex typical for a (Melopsittacus undulatus, Alisterus scapularis) and the
healthy bird is shown in Fig 12.7. Reference values exist common buzzard (Buteo buteo).44,45 Interestingly, by
for racing pigeons,21 Amazons and African grey parrots23 comparing the relative values (thickness of the myocar-
and some macaw species.6 A complete overview of the dium in relation to the length of the sternum and the
electrophysiologic evaluation of the avian heart and the length of the left side of the interventricular septum,
clinical use of the ECG in birds is given by Lumeij and respectively) of these different species, it is speculated
Ritchie.22 that the hearts of most avian species follow a set mor-
phological pattern. The myocardium of the ventricles as
POST MORTEM MORPHOMETRY well as the interventricular septum shows changes of the
thickness from the base to the apex of the heart. Whilst
Whilst reproducible measurements of the thickness of
the thickness of the left ventricular free wall decreases in
the atrial myocardium are nearly impossible, the thick-
the direction of the apex the interventricular septum
ness of the ventricular myocardium is readily detectable.
and the right ventricular free wall become thicker from
Due to the huge number of different species that are
the base to the middle region and then decrease in
seen in avian practice, the establishment of reference
thickness towards the apex (Fig 12.8 and Table 12.6).
values for each species is impossible. Fortunately, cur-
rent investigations could prove that relative values (as a
%) rather than absolute values (in mm) are of signifi-
cance in the assessment of the avian myocardium. Therapy of Cardiovascular
Dissection of the heart under standardized conditions is
Diseases
a basic requirement for performing measurements of the The therapy of avian cardiac disease is still in its infancy.
ventricular myocardium thickness at necropsy. The heart Only a few scientific studies exist, and many drugs rou-
should be placed on its left side on a cutting board. A tinely used in mammals have not as yet been tested in
longitudinal cut running through the apex of the heart, caged and aviary birds. Overdosing may cause severe
the uppermost region of the right ventricular wall and side effects; and the pharmacodynamics of drugs in
the center of the interventricular septum has to be per- birds is often different due to physiological differences.
formed. All blood clots must be removed and the mass
of the heart should be determined. Measurements of the Nevertheless, the principles of cardiac therapy are the
thickness of the myocardium at three regions of the left same as in mammal medicine. Stabilization of the
387
Table 12.5 | Reference Values for Electrocardiograms in Selected Avian Species*

Parameter Columbia Psittacus Amazon Macaw sp.23
sp.21 erithacus22 sp.22 Small sp. Large sp.
Inner limits for P2.5 and P97.5 Mean value ±
with a probability of 90%t standard deviation
Heart rate (1/min) 160-300 340-600 340-600 389 ± 85 275 ± 72
Heart axis (°) (-83) - (-99) (-79) - (-103) (-90) - (-107) -97 ± 5 -98 ± 8
P-wave duration (s)M 0.015-0.02 0.012-0.018 0.008-0.017 0.016 ± 0.002 0.019 ± 0.002
P-wave 0.4-0.6 0.25-0.55 0.25-0.60 0.34 ± 0.11 0.24 ± 0.05
amplitude (mV)M
PR interval 0.045-0.07 0.04-0.055 0.042-0.055 0.050 ± 0.010 0.053 ± 0.009
duration (s)M
QRS complex 0.013-0.016 0.01-0.016 0.01-0.015 0.017 ± 0.002 0.018 ± 0.002
duration (s)M
R amplitude (mV)M 0-0.5 0-0.2 0-0.65 0.04 ± 0 0.08 ± 0.04
S amplitude (mV)M 1.5-2.8 0.9-2.2 0.7-2.3 0.624 ± 0.234 0.624 ± 0.234
(QRS-ampl.) (QRS-ampl.)
T amplitude (mV)M 0.3-0.8 0.18-0.6 0.3-0.8 0.4 ± 0.09 0.25 ± 0.1
QT Interval Duration
Anaesthetized (s)M — 0.039-0.07 0.038-0.055 0.081 ± 0.006 0.104 ± 0.018
Unanaesthetized (s)M 0.06-0.075 0.048-0.08 0.05-0.095 — — Fig 12.8 | Heart of a common buzzard
*Lumeij and Stokhof;21 Nap;23 Casares6
(Buteo buteo). Illustration of the measuring
M = measurements taken in lead II points for the post-mortem evaluation of the
myocardial thickness: a to c = left ventricular
free wall, a = basal, b = middle, c = apical;
Table 12.6 | Approximate Thickness of the Ventricular Myocardium in d to f = interventricular septum, d = basal, e
Relation to the Length of the Sternum and the Length of the Left Ventricle in = middle, f = apical; g to i = right ventricu-
Melopsittacus undulatus, Alisterus s. scapularis and Buteo buteo lar free wall, g = basal, h = middle, i = api-
Myocardium % of Sternal Length % of the Length of cal; distance d to c = length of the left ven-
Interventricular Septum* tricle close to the interventricular septum.
Basal Middle Apical Basal Middle Apical
(Point a) (Point b) (Point c) (Point a) (Point b) (Point c)
Left ventricle 7-10% 7-10% 2-4% 20-30% 20-30% 5-10%
Interventricular septum 5.5-7.5% 6.5-9.0% 5-7% 12-22% 16-30% 12-21%
Right ventricle 1.5-2.7% 1.8-3.0% 1.3-2.5% 4.5-8.0% 5.0-8.5% 3.5-6.5%
Straub44,45
*Measured on the left side of the interventricular septum points a, b, c, etc. are ref. in Fig 12.8.
patient is essential, and besides symptomatic therapy, sac volume can lead to dyspnea and hypoxemia damag-
the underlying disease has to be diagnosed and treated. ing the heart.
Because cardiac disease in birds is often not diagnosed Cardiac therapy’s goals are to reduce congestion
until the heart decompensates, the veterinarian com- (diuretics, ACE inhibitors) and improve cardiac output
monly has to deal with advanced changes. Due to weak- (ACE inhibitors) which can improve renal/hepatic func-
ness, emaciation and high-grade circulatory problems, tion. The following supportive measures should also be
these birds are often presented as emergencies. Stress taken:
during handling, examination and treatment may be • Incubation in a warm environment (80° F (25° C) or
fatal. above), with sufficient air humidity (60% relative
humidity or above) in order to improve circulation
and to reduce energy loss.
ACCOMPANYING THERAPY • Reduction of stress: handling should be reduced to a
Accompanying therapy is essential to maintain circula- minimum. Positioning of the patient in ventrodorsal
tory stability and organ function. Liver and kidney func- recumbency (eg, for radiology) is a risk and should be
tion may be affected by circulatory problems. The liver considered carefully. Diagnostic procedures in an
may be congested, renal blood flow may be reduced, upright position should be performed (eg, echocardio-
and the resulting increase of toxic metabolites and uri- graphy). The environment should be calm and tem-
nary excreted substances may affect the general condi- porarily darkened.
tion of the bird. The function of the lung can be • Fluid administration is essential to prevent circula-
reduced as a direct result from left heart failure causing tory collapse and shock and to prevent dehydration
pulmonary congestion. Fibrotic lungs will increase the due to increased diuresis due to therapy with ACE-
work load of the right ventricle. In addition, reduced air inhibitors, and furosemide. Therapy should be
started intravenously or via intraosseus canula. leads to diuresis (and indirectly to an improvement of
Maintenance administration may be subcutaneous or renal function), and a decrease of blood pressure. The
(preferably) orally. Careful monitoring must be done effect on the heart is a decreased pre- and afterload so
so the patient is not volume overloaded which would that cardiac workload is eased and the cardiac muscle
increase congestion. cells may be able to recover.
• Addition of electrolytes, vitamins, amino acids and
buffer solution may also be indicated. Although scientific studies regarding the pharmacokinet-
• Fluid aspiration from the thoracoabdominal cavity is ics of enalapril in birds are lacking, clinical experiences
easily performed in avian patients (if possible, do it with this drug exist. The results indicate that its use in
ultrasound-guided) and helps to reduce dyspnea due to birds with cardiovascular disease may be beneficial.
ascites. For pericardiocentesis, see pericardial effusion. Empirical dosage used for treatment of birds is 5
mg/kg/day, with reduction to 1 mg/kg/day following
improvement of cardiac function. Tolerance is much bet-
DRUGS FOR CARDIAC THERAPY ter when compared to cardiac glycosides and long term
(see Table 12.7) administration is possible. Observed side effects after
high-dose therapy (5 mg/kg/day) were an increase of
Heart Glycosides (Digoxin)
PCV and signs of dehydration. These effects were not
Heart glycosides have a positive inotropic effect on the
present when the dose was reduced to 1 mg/kg BID
contraction of cardiac muscle. Also relaxation of cardiac
orally.29,47
muscle will be improved and the heart rate will
decrease. These effects lead to a reduction of oxygen
Diuretics (Furosemide)
demand and an improvement in circulation of the car-
diac vessels. Therefore digoxin works best for cardiac Indications for furosemide are pulmonary edema,
diseases that involve volume overloads (insufficient ascites, and pericardial effusion as well as an increased
valves), decreased contractility (dilatative cardiomyopa- pre- and afterload. The recommended dosage used in
thy), or supraventricular tachycardia. The increased car- birds is 0.15 to 2.0 mg/kg/day PO/IM.36 Long term admin-
diac function decreases ascites and edema. To date, istration may lead to a potassium deficiency and there-
there are only two scientific studies on the use of glyco- fore cause heart arrhythmias. Since there is a risk of
sides in pet birds. Pharmacokinetics of digoxin has been dehydration, especially in small birds, additional careful
examined in sparrows (Passer domesticus), budgerigars fluid administration is essential.
(Melopsittacus undulatus), and quaker (Myiopsitta
monachus).11,54 In the authors’ experience, the main use for diuretics is
in the initial therapy of cardiac failure with fluid accumu-
The therapeutic margin of cardiac glycosides is small, lation (ascites, pericardial effusion) in combination with
and half-life varies greatly between species. Overdosing ACE-inhibitors or glycosides.
may lead to accumulation of cardiac glycosides, and side
effects include arrythmias. Contraindications are ventric- Antiarrhythmics (ß-blockers)
ular tachycardia, second and third degree atrioventricu-
A protective effect against the development of athero-
lar heart block, hypercalcemia, potassium deficiency and
sclerotic plaques has been demonstrated using
stenotic valves. Cardiac side effects are documented with
oxprenolol in poultry (2 mg/kg/day).27 Other uses, such
the combination of glycosides and ketoconazole (ther-
as for supraventricular or ventricular arrhythmias, have
apy of aspergillosis) in humans.
not been described.
In the authors’ experience, cardiac glycosides are useful
Before using antiarrhythmics, it is important to exclude
for emergencies. Chronic administration may be prob-
metabolic causes for the arrhythmia (eg, potassium defi-
lematic due to difficulties in controlling the side effects
ciency, see diuretics). The safety margin of these drugs is
and plasma levels. An initial recommended dose of
small, and the half-life is normally very short, but the
digoxin is 0.02 to 0.05 mg/kg (20 to 50 µg/kg) q 12 h.
clinical effects can last longer, especially if cardiac failure
Maintenance should be dosed carefully at 0.01 mg/kg (10
is present.
µg/kg) q 12 h.11,54
Angiotensin Converting Enzymes (ACE-) Calcium Sensitizers (Pimobendan)

Inhibitors (Enalapril) Calcium sensitizers are substances with a positive
Angiotensin II is responsible for the constriction of arte- inotropic effect. The pharmacokinetic mechanism is
rial and venous vessels and the retention of sodium and unknown and there are no scientific reports of the use
water by the kidneys. The inhibition of this hormone of calcium sensitizers in birds.
389
Table 12.7| Cardiac Medications in Birds*

Drug Indication Application / Dose Remarks / Side effects
Digoxin Systolic myocardial failure PO 0.02-0.05 mg/kg BM BID • Low therapeutic index
initially, following 0.01 mg/kg BM BID • Overdosing: bradycardia, arrhythmia, diarrhea,
vomitus
Enalapril Myocardial failure, increased pre-/ PO 2.5 mg/kg BM BID initially, after • High therapeutic index
afterload one week 1 mg/kg BM BID • Side effect: dehydration
Furosemide Pericardial effusion, edema, PO, IM 0.15-2.0 mg/kg BM SID/BID • Risk of dehydration esp. in smaller birds (lorikeets)
increased pre-/afterload • Side effect: arrhythmia caused by potassium
deficiency
Oxprenolol Cardioprotection, prevention from PO 2 mg/kg BM SID • Possible side effects: hypotonia, arrhythmia,
arteriosclerotic plaques (poultry) tachycardia, AV-block
g-Strophantin Circulatory system stimulant PO drop-wise, to effect • In case of long-time overdosage, heart hypertrophy
(only available in EU) IV, IM 1 ml/kg BM especially in smaller birds possible
Atropine Conduction disturbances, IM 0.01-0.1 mg/kg BM SID • Only short-time
bradycardia • Overdosing: arrhythmia,
gastrointestinal stasis
Etilefrine Hypotonia PO drop-wise, to effect • Possible side effects: tachycardia, arrhythmia,
(only available in EU) hypertonia
*Hamlin and Stalnaker;11 Wilson;54 Lumeij and Ritchie;22 Ritchie and Harrison;36 Pees;29 Krautwald-Junghanns and Kummerfeld.19
SID = 1x/day, BID = 2x/day, PO = orally, IM = intramuscular, BM = body mass
Pathology of Table 12.8 | Incidence of Selected Cardiac and Vascular

Diseases in 107 Psittacine Birds. Macroscopic Findings
Cardiovascular Diseases (Findings in 39 Birds (36.4 %)*
Findings Cases
Caged birds, in comparison with free living birds, are Pericardium Pericarditis 16 (14.9%)
frequently compromised by restricted exercise, nutri- Pericardial effusion 6 (5.6%)
tional deficiencies and abnormal climactic conditions. Myocardium Hypertrophy/dilatation 16 (14.9%)

Petechial bleeding 6 (5.6%)
Combined with the bird’s natural physiologically high
Endocardium Endocarditis valvularis 1 (0.9%)
blood pressure, the risk factor for cardiovascular disease
Aorta/A. pulmonalis Yellow discoloration/hardening 11 (10.3%)
in pet birds is significant.
*Braun;4 Krautwald-Junghanns20
Recent post mortem studies show the frequency of car-

diac pathology in pet birds. According to these studies, The syndrome “congestive heart failure (CHF)” results
heart disease occurs commonly in avian species. from inadequate cardiac output and an increased pre-
Oglesbee and Oglesbee24 found gross and histological load. Fluid retention is caused by elevated venous and
evidence for cardiac disease in 26 of 269 psittacine birds. capillary pressures. In left heart failure, an increase of
A study of 107 psittacines submitted for routine necropsy the pressure in the left atrium and the pulmonary veins
found macroscopic lesions of the heart and/or the large leads to pulmonary edema. In birds with right heart fail-
vessels in more than one third of the birds4,20,42 (Table ure, ascites, liver congestion and hydropericardium are
12.8). In 99% of these 107 birds, at least low-grade histo- commonly seen.
logic changes were present (predominantly inflammatory
mixed-cellular infiltration, bacterial infiltration, and/or fat
cell accumulation within the myocardium).
CONGENITAL DISEASES
Due to the high physiological load of the avian heart, con-
Diseases of the heart may occur as the result of congeni- genital cardiovascular disorders often lead to early embry-
tal, infectious, toxic or idiopathic etiologies. No data cur- onic or fledgling death. They are rarely presented as clini-
rently exist on age-related cardiovascular diseases in pet cal diseases in birds, ante mortem diagnosis is rare and
birds. A variety of cardiac abnormalities occur secondar- the cause is normally found only at necropsy. In one case,
ily as acquired disease and/or compensation/decompen- evidence for a congenital defect of the muscular right atri-
sation due to other organ failure (ie, lung and liver), oventricular valve could be found in a 35-year-old Amazon
neoplasia or systemic infections.16,17,20 diagnosed with dilatation of the right ventricle.30
CAUSES OF (CONGESTIVE) PERICARDIAL DISEASES (PERICAR-

HEART FAILURE DITIS, PERICARDIAL EFFUSION)
Heart failure is the clinical syndrome resulting from Pericardial changes frequently found in birds include
abnormalities of cardiac function (eg, myocardial failure, inflammation (pericarditis) and effusion (hydroperi-
valvular regurgitation). cardium, hemopericardium).
Fig 12.9 | Necropsy, blue fronted Amazon Fig 12.10 | Radiograph, ventrodorsal view,
(Amazona aestiva aestiva), pericarditis urica. Uric African grey parrot (Psittacus erithacus), tentative
acid deposits can be seen on pericardium (1) diagnosis of cardiac disease (corresponding to
that covers the heart and the serosa of the liver Fig 12.11). The heart (1) and the liver (2)
(2). The yellowish discoloration of the large ves- shadow are enlarged. Detail recognition in the
sels (3) is an indication for arteriosclerosis. thoracoabdominal cavity is reduced; the air sacs
(3) are compressed.
Inflammation of the pericardium may develop in the findings are enlargement of the heart and liver shadow
process of infectious diseases of surrounding tissue. as well as loss of detail (Fig 12.10). ECG may show low
Common causes are generalized trichomonas infections voltage,22 but allows only a tentative diagnosis (adipose
in pigeons, mycotic infections originating from the respi- tissue and space-requiring processes like tumors can
ratory tract, and bacterial infections including mycobac- cause low voltage on the ECG as well).29 The only reli-
teriosis. Deposits of uric acid in the pericardium may be able ante mortem diagnostic test for pericardial effusion
seen with visceral gout (Fig 12.9). is echocardiography. Hydropericardium can be visual-
ized as an anechoic area between the myocardium and
Hydropericardium is the cardiac change most frequently the pericardium (Fig 12.11). For further examinations
diagnosed ante mortem. It may develop with infectious (cytology, microbiology) an ultrasound guided aspirate
exudative pericarditis, but can also occur due to conges- from the pericardial space may be taken. In most cases,
tion in cardiac failure, metabolic disorders (protein defi- pericardial effusion is non-infectious and clear.
ciency) or as an idiopathic syndrome. Hemopericardium Nevertheless, inflammatory cells may indicate infection,
is generally found following trauma or sclerosis with and culture may help to identify bacterial or fungal
subsequent rupture of vessels, and is almost always fatal. causes.
Clinical symptoms in birds with pericarditis are often Treatment of exudative pericarditis, in addition to treat-
nonspecific. Diagnosis is usually confirmed at necropsy. ing the underlying condition, may include administra-
Radiography may reveal cardiomegaly with an irregular tion of furosemide or another diuretic. Treatment for
cardiac silhouette. Echocardiography is of limited use for visceral gout is generally unrewarding (see Chapter 16,
diagnosis if there is no pericardial effusion. Endoscopy is Evaluating and Treating the Kidneys). For treatment of
the most reliable ante mortem diagnostic aid, although hydropericardium due to congestive heart failure,
there is an increased risk during anaesthesia (see diuretics in combination with ACE inhibitors are indi-
Chapter 24, Diagnostic Value of Endoscopy and Biopsy). cated.29,47 Pericardial effusion may result in diastolic
In cases of acute visceral gout, plasma uric acid levels heart failure, ie, in an insufficient filling of the ventricles
may be increased. in diastole due to compression of the atria by the fluid
in the pericardial cavity. This is a contraindication for the
Common symptoms in birds with pericardial effusion use of glycosides. An ultrasound guided pericardiocente-
are abdominal distension, dyspnea and exercise intoler- sis may be performed to remove fluid from the pericar-
ance. Hydropericardium is often combined with conges- dial space. Repeated echocardiography can be used to
tion of the liver and ascites. The typical radiographic evaluate success of the therapy.
391
ent as generalized weakness and as respiratory impair-

ment. Hepatic congestion and ascites often cause
abdominal distension.
Radiographs may demonstrate a consolidated, enlarged

and sharply delineated shadow of the entire heart and
liver. The appearance of the lung fields may demonstrate
homogenous or non-homogenous increased opacity of
the honeycomb pattern of the lungs which indicates pul-
monary edema.
In birds with dilatative cardiomyopathy, the ECG may

show an increased R-wave and a negative P-wave. The
heart axis can change to between 0° and -170°.
Arrhythmias are often seen with cardiomyopathy and
Fig 12.11 | 2-D-Echocardiography, African grey parrot (Psittacus myocarditis.22
erithacus), pericardial effusion and ascites (4) (corresponding to
Fig 12.10). The pericardial effusion (1) can be seen as an ane-
In 2-D echocardiography, altered wall thicknesses and
choic area between the heart (2) and the pericardium (3).
diameters of the ventricles as well as decreased contrac-
tility can be seen (measurements see Tables 12.1-12.3).
MYOCARDIAL DISEASES In birds with right heart failure, the right ventricle is
(MYOCARDIAL FAILURE) often as large as the left (Fig 12.12). Accompanying com-
mon findings are hydropericardium, ascites and con-
A decreased myocardial contractility (myocardial failure)
gested liver parenchyma (see dilated vessels, Fig 12.13).
may be primary, idiopathic (dilatative cardiomyopathy),
or secondary, as a result of systemic diseases of infec- In case of suspected cardiomyopathy, blood-chemistry
tious (myocarditis), toxic, metabolic (lipomatosis cordis, evaluation should include AST, CK, uric acid, LDH and
arteriosclerosis) and neoplastic origin. Frequently, an electrolytes.
increased workload (eg, due to arteriosclerosis and pul-
monary hypertension) leads to hypertrophy of the ven- In addition to treatment of the underlying cardiac dis-
tricles and can eventually result in decompensation and ease, supportive care including cage rest and diet
dilatation. Valvular insufficiencies can also lead to ven- change is important. Diuretics are indicated when
tricular dilatation and eventually failure.30 In psittacines, edema (eg, pulmonary edema) or ascites are present. In
myocarditis is described as a complication in neuro- the authors’ experience, a combination of glycosides,
pathic proventricular dilatation disease.40,51 Iron deposi- ACE-inhibitors and diuretics seems to be the most effec-
tion in the myocardium combined with dilatation of the tive initial therapy for cases of acute heart failure. For
ventricles occurs in mynah birds with iron storage dis- long-term therapy, ACE-inhibitors are preferable.29,47
ease.9 After prolonged transport of wild birds, myocar-
dial necrosis may be seen as neurogenic arrhythmias as a
ENDOCARDIAL DISEASES (ENDO-
consequence of metabolic disturbances. CARDITIS, VALVULAR INSUFFI-
CIENCY, VALVULAR STENOSIS)
Mostly myocardial failure is right-sided. Systemic lung
diseases (ie, chronic mycosis) frequently result in dilata- Alterations of the endocardium, in particular the valves,
tion of the right ventricle (including the right, muscular may be idiopathic.30 However, these changes are found
AV valve) and the right atrium and therefore the venous more frequently secondary to infections with strepto-
part of the circulatory system. Isolated left-sided myocar- cocci, staphylococci, Pasteurella multocida or E.
dial failure is rare, since the resulting pulmonary conges- coli.20,22,35
tion also affects the right ventricle and leads to a second-
Independent of the etiology, functional damage of the
arily increased afterload and eventually right-sided CHF.
AV valves leads to regurgitation and to left heart failure
Although one case report suggests that myocardial com- with pulmonary edema (small circulatory cycle) and/or
pensation of valvular insufficiencies may occur for right heart disease with liver congestion (large circula-
years, decompensation and development of clinical tory cycle) and can cause general cardiac failure.
signs seem to develop more quickly in birds than they Thickening of the right AV valve is normally caused by
do in mammals.30 muscular hypertrophy. It may be a consequence of valvu-
lar insufficiency or due to hypertrophy of the whole
Clinical signs of myocardial failure of any cause can pres- right ventricle (see Fig 12.12). This alteration occurs
Fig 12.12 | 2-D-Echocardiography, yellow-crowned Amazon Fig 12.13 | 2-D-Echocardiography, African grey parrot
(Amazona ochrocephala), right heart failure. The right ventricle (Psittacus erithacus). Liver (1) congestion and ascites (3). Dilated
(1) is as large as the left one, the muscular right atrioventricular vessels (2) can be demonstrated in the liver tissue.
valve (2) is clearly thickened (3 = ascites).
more often than alterations of the left AV valve. Chronic etiological factors are discussed; the most frequent
inflammation of the semilunar valves can also result in causes are hyperlipidemia, endothelial inflammation, tox-
stenosis.20 ins, immune complexes, hypertonia and/or stress factors.
Age and nutritional deficiencies over many years, as well
Clinically, nonspecific symptoms (weakness, dyspnea, as lack of exercise seem to play a role in the develop-
distended abdomen) may be noticed. ment of arteriosclerosis.13 Psittacines commonly affected
by arteriosclerosis are amazons (especially blue fronted
Radiographic investigation gives information about car-
Amazons), African grey parrots and cockatoos.4,13,20
diac size and congestion of organs (see Myocardial
Diseases section) but radiographic diagnosis of endocar- Macroscopic changes include arterial wall thickening,
dial alterations is not possible. intimal roughening, induration and yellowish discol-
2-D-Echocardiography can show accompanying myocar- oration.10 Calcification can cause plaque-like or diffuse
dial thickening and changes of the valves, especially hardening of the larger arteries like the aorta and bra-
thickening of the right atrioventricular valve (see Fig chiocephalic trunk (Fig 12.14). Arteriosclerosis cannot be
12.12).30,35 Doppler echocardiography is the imaging tool diagnosed by gross findings alone, but requires histolog-
of choice for demonstration of valvular regurgitation in ical examination, especially in earlier stages.10,20
mammals. Although initial examinations have been per-
A diagnosis of arteriosclerosis is often made at necropsy.
formed in birds (see Echocardiography), little has been
Clinical findings are usually absent or may only lead to a
published about the use of Doppler echocardiography in
tentative diagnosis. Possible symptoms include lethargy,
case of suspected valvular damage. In an Indian hill
neurological signs (tremor, paralysis of the legs),
mynah, color flow and spectral Doppler have been used
decreased exercise tolerance and dyspnea.8,13,14 Acute
for demonstration of mitral regurgitation.37,39
death may occur.
A good prognosis may be given in cases of acute endo-
Radiologically, an increased radiodensity and widening
carditis with aggressive treatment of the causal agent
of the aorta may be seen in advanced cases, sometimes
(Myocardial Diseases section).
in connection with left atrial or left ventricular enlarge-
In patients with valvular regurgitation, glycosides can be ment. Echocardiography may be useful for diagnosis of
used, whereas in case of stenosis, these drugs are con- the arteriosclerotic processes of the large vessels close to
traindicated. A decrease in the heart rate to a normal the heart, but no systematic studies have been done to
range and decreased congestion may be interpreted as date. In a white cockatoo, an aneurysm of a coronary
therapeutic success. artery associated with arteriosclerosis has been diag-
nosed by echocardiography.52
ARTERIOSCLEROSIS Effective therapy for arteriosclerosis is not known for

Arteriosclerosis is the most frequently described patho- birds. In poultry, ß-blockers (eg, oxprenolol) proved to
logic change of the vessels in psittacine birds.4,10 Different have a protective effect against the development of
393
arteriosclerotic plaques. Unfortunately it is not possible

to remove plaques which are already present.27,28
Diuretics may be indicated as well as ACE-inhibitors if
heart failure occurs.7 Balanced food supply and suffi-
cient opportunities to exercise are important preventive
factors. Proper flight exercise and diet will prevent obe-
sity, a major contributor to this cardiac disease.
CIRCULATORY DISTURBANCES
(CIRCULATORY COLLAPSE, SHOCK)
Physiologically, the avian circulatory system has a large
load capacity. Unexpected deaths, after catching small
birds, can sometimes be attributed to asphyxia (strong
pressure on the sternum). Long restraint of fractious
S. Braun
birds may lead to circulatory collapse, especially in birds
with dyspnea, ascites (resulting in displacement of the Fig 12.14 | Necropsy, African grey parrot (Psittacus
air sacs) or cardiac failure. Hypovolemic, septic (toxic- erithacus), with arteriosclerosis. Thickening and discol-
oration of the wall of the large vessels (arrows).
infectious) and neurogenic shock as well as anaesthetic
complications may also be a cause. Overcrowding of car-
riers or transporting in temperatures near or above 100° Ringer’s solution (LRS) or half-strength LRS + 2.5% dex-
F (38° C) may lead to circulatory collapse. trose (IV, intraosseus cannula, for maintenance also SC) is
indicated. Infusions with sodium bicarbonate solution
Clinical symptoms of circulatory collapse start as respira- should be given in case of metabolic acidosis, recom-
tory signs with spread wings/ legs and tachypnea/ dysp- mended dosage is 1 mEq/kg (=1 ml/kg), in intervals of
nea. This is followed rapidly by respiratory arrest, con- 15 to 30 minutes up to a maximum of 4 mEq/kg.55
vulsions with opisthotonus, and a loss of consciousness. Additionally, oxygen supply is indicated. If faced with res-
piratory arrest administration of doxapram (respiratory
Further diagnostics should only be done after stabiliza-
stimulant, orally dropwise to effect) may be useful. Oral
tion of the patient. If possible, the bird should be kept
upright for examination (eg, circulatory risk during posi- /IV/IM administration of g-strophantin (see Table 12.7)
tioning for radiology). The treatment for shock is always may successfully stabilize patients presenting in circula-
handled as an emergency situation. The bird must imme- tory failure. Sympathomimetics (etilifrine) may be admin-
diately be brought to a calm and darkened area. A vol- istered orally to increase the stroke volume in case of
ume substitution with warmed (100-103° F) lactated heart failure (in particular, in case of cardiogenic shock).
Parts of this chapter are copied or paraphrased from Proc Assoc Avian Vet, 2001, pp 225-330.
Permission granted by AAV 2003.
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23. Nap AMP, Lumeij JT, Stokhof Herzfunktion. Tierärztl Praxis Gompf RE, Baade H, Krautwald-
AA(1992). Electrocardiogram of 31(K), 180-187, 2003. Junghanns ME (2001). Doppler- 52. Vink-Nooteboom M, Schoemaker
the African Grey (Psittacus eritha- 33. Pees M, Straub J, Krautwald- echocardiography in birds. NJ, Kik MJL, Lumeij JT,
cus) and Amazon (Amazona sp.) Junghanns ME (2003c). Echo- Proceedings of the 6th European Wolvekamp WTC (1998). Clinical
parrot. Avian Pathol 21, 45-53. cardiographical examinations of AAV Main Conference, Munich, diagnosis of aneurysm of the right
24. Oglesbee BL, Oglesbee MJ healthy psittacine birds under 92-94. coronary artery in a white cocka-
(1998). Results of post-mortem special consideration of the 44. Straub J, Valerius KP, Pees M, too (Cacatua alba). J Small Anim
examination of psittacine birds African Grey parrot (Psittacus Krautwald-Junghanns ME Pract 39: 533-537.
with cardiac disease: 26 cases erithacus erithacus). Proc 7th (2002a). Morphometry of the 53. West NH, Langille BL, Jones DR
(1991-1995). JAVMA 212, 1737- Europ AAV Conf, Puerto de la heart of budgerigars (Melo- (1981). Cardiovascular system. In:
1742. Cruz, 161-167. psittacus), Alisterus parrots King, AS, McLelland J (eds): Form
25. Orosz S (1997). Anatomy of the 34. Pees M, Straub J, Krautwald- (Alisterus s. scapularis) and com- and Function in Birds (Vol. 2).
cardiovascular system. In: Altman Junghanns ME (2004). Echo- mon buzzards (Buteo buteo). Academic Press, London, New
RB, Clubb SL, Dorrestein GM, cardiographical examinations of Research in Veterinary Science 72, York, 235-251.
Quesenberry K (eds): Avian medi- psittacine birds with special refer- 147-151. 54. Wilson RC, Zenoble RD, Horton
cine and surgery. WB Saunders ence to the African grey parrot. 45. Straub J, Valerius KP, Pees M, CR, and Ramsey DT (1989).
Co, Philadelphia, 489-490. Vet Rec, 155,73-76. Krautwald-Junghanns ME Single dose digoxin pharmacoki-
26. Owen R (1866). Anatomy of ver- 35. Randolph J, Moise S, Graham D, (2002b). Untersuchungen zur netics in quaker conure. J Zoo
tebrates. Vol II. Birds and mam- Murphy C (1984). Bacterial endo- Myokarddicke bei Wellensittichen Wildl Med 20, 432-434.
mals. Longmans, Green, and Co., carditis and thromboembolism of (Melopsittacus undulatus) und
London. a pelvic limb in an emu. J Am Vet Königssittichen (Alisterus s. 55. Wilson H (2003). Avian
27. Pauletto P, Pessina AC. Pagnan A, Med Assoc 11, 1409-1410. scapularis). Berliner und Emergency and Critical Care.
Thiene G, Semplicini A, Vescovo 36. Ritchie BW, Harrison GJ (1994). Münchener Tierärztliche Proceedings of the Assoc Avian
G, Mazzucato A, Scannapieco G, Formulary. In: Ritchie BW, Wochenschrift 115, 440-444. Vet, Pittsburgh, 261-268.
Angelini A, Dal Palu C (1985). Harrison GJ, Harrison LR (eds): 46. Straub J, Pees M, Krautwald- 56. Wyatt HL, Heng MK, Meerbaum S
Evidence of reduced atheroscle- Avian Medicine, Principles and Junghanns ME (2002c). (1979). Cross-sectional echocar-
rotic lesions in broad breasted Application, Brentwood, TN, Measurement of the cardiac sil- diography I. Analysis of mathe-
white turkeys treated with HBD Int’l Inc, 457-478. houette in psittacines. Journal of matic models for quantifying
oxprenolol. Artery 12, 220-233. 37. Rosenthal K and Stamoulis M the American Veterinary Medical mass of the left ventricles in dogs.
28. Pauletto P, Vescovo G, Scanna- (1992). Congestive heart failure Association 221, 76-79. Circulation 60, 1104-1113.
13_Integument.qxd 8/22/2005 4:17 PM Page 395
CHAPTER
13
Integument
ROBERT E. SCHMIDT, DVM, P hD, D ipl ACVP;
TERESA L. LIGHTFOOT, DVM, D ipl ABVP-A vian
Skin and feather problems are common disorders in pet

avian species (Fig 13.1a). The skin has limited responses
to insults. A variety of causes will lead to similar clinical
signs and possibly similar gross and histologic changes.
The clinician’s challenge is to use available diagnostic
methods to determine an etiology and rational therapeu-
tic approach.
Birds often present with feather loss or picking. The

appearance of the skin may vary from grossly normal to
severely inflamed and/or necrotic (Fig 13.1b). In assess-
ing gross morphologic changes, the effect of self-trauma
must be considered. Although the lesions may be due to
a primary problem within the skin and/or feathers, a
variety of internal disorders, as well as behavioral prob-
Bob Doneley
lems, can also result in external lesions.
Fig 13.1a | Mustached parakeet with facial

dermatitis resulting in feather loss and
replacement. Pin feathers predominate in the
History
affected area.
Arriving at a meaningful diagnosis requires a logical
process that considers the differential diagnostic possi-
bilities. History is essential. A complete history should
include information on the bird’s environment, changes
in routine and diet. (See Chapter 4, Nutritional Consid-
erations and Chapter 6, Maximizing Information from
the Physical Examination for more specific information).
A description of the physical surroundings of the bird is

needed, including such things as temperature and
humidity, which can influence normal molting and
Greg J. Harrison
which may play a part in clinical disease syndromes. The

conditions of other birds in the household/aviary should
also be determined. References are available for feather
Fig 13.1b | A burn from administrating scalding hot food. anatomy review.6
Microwaved food is often the source.
Physical Examination Table 13.1 | Diagnostics for Avian Skin Lesions

• Skin scraping • Biopsy of affected
Refer to Chapter 6, Maximizing Information from the • Gram’s stain of superficial skin/feather follicles
Physical Examination for the description of a complete skin scrape • Serum biochemistries,
physical examination. During the physical examination, • Culture of skin scrape including bile acids
specific dermatologic lesions should be examined and • Gram’s stain of follicle • Consider radiographs
classified. Examination includes the distribution of • Culture of follicle • Viral DNA test
• CBC
lesions, presence or absence of pruritus, relative condi-
tions of the skin and feathers and presence of plaques,
Table 13.2 | Therapy Pending Diagnostic Results
ulcers and exudates. The association of individual lesions
Clinical Therapy
with specific conditions is not as well documented in Presentations
birds as it is in domestic pets. Notation of these dermato- Feather loss or • Dietary assessment and correction
logic abnormalities will aid in both the clinical descrip- skin abnormality • Environmental assessment and correction
with no self-trauma • Preliminary therapy based on Gram’s stain
tion to accompany biopsy submissions and in tracking by results, if applicable
• Viral profiling with supportive care
the practitioner of the course of the disease. A simple
Pruritus • Topical therapy (see Chapter 9, Therapeutic
anatomic illustration, such as is used in dog and cat med-
Agents)
icine can be valuable in recording these lesions. See • Systemic antipruritic/tricyclic antidepressant
(eg, diphenhydramine, amitriptyline, see
Chapter 6, Maximizing Information from the Physical Chapter 9, Therapeutic Agents)
Examination for an example of this stamp. • Dietary assessment and correction
• Environmental assessment and correction
• Preliminary therapy based on Gram’s stain
results, if applicable
DIAGNOSTICS • Behavior consultation
Evaluation of systemic illness and organ function via a Self-mutilation • Barrier to mutilation (Elizabethan collar or
modified extension collar)
complete blood count (see Chapter 22, Diagnostic Value • Antibiotics for systemic infection
of Hematology) and serum biochemistries (see Chapter • Topical antibiotic/antifungal (eg, 1% silver
a
sulfadiazine cream )
23, Diagnostic Value of Biochemistry) should be per- • Preliminary therapy based on Gram’s stain
formed. Specific tests for syndromes such as PBFD circo- results, if applicable
• Consider psychotropic medications
virus may be indicated (see Chapter 32, Implications of (see Chapter 3, Concepts in Behavior and
Viruses in Clinical Disorders). An evaluation for nutri- Chapter 9, Therapeutic Agents)
• Behavior consultation
tional deficiency or toxicities should be made from the
dietary history (see Chapters 4, Nutritional Considera-
tions and Chapter 6, Maximizing Information from the of an overwhelming microbial population can be diag-
Physical Examination). nostic, although the sensitivity of the organism to vari-
ous antimicrobials cannot be determined from
Several diagnostic procedures are available in order to histopathology. In the absence of a definitive etiologic
gain information about skin lesions (Tables 13.1, 13.2). agent, allergy, self-trauma or endocrinopathy may be
Scrapings may reveal the presence of mites, but in some suggested from the biopsy.
lesions the mites are deep within the subcutis and will
be missed by superficial scraping. Impression smears can Pulling of feathers and submission for histopathology
give an indication of inflammation vs. neoplasia. Bacteria may lead to a diagnosis in some cases, but if the feathers
and fungi are also seen in impression smears, but their are normal the possibility of primary skin disease cannot
significance may be difficult to determine. Feather pulp be ruled out.
smears potentially provide information concerning
inflammatory processes within the pulp. Care must be Because skin disease can reflect internal disease, appro-
taken not to confuse melanin granules with bacteria. priate laboratory tests or radiographic examination may
Melanin granules will be uniform with tapered ends and be indicated in cases where a thorough examination has
will not be stained, having a natural brown-black color. ruled out primary disease of the skin or feathers. (See
Chapter 15, Evaluating and Treating the Liver and
Culture is important but must be done correctly or the Chapter 4, Nutritional Considerations).
significance of the isolate is questionable. If folliculitis is
suspected, aspiration of the follicle by sterile needle and
syringe is necessary.
Congenital and Acquired
Skin and feather biopsy is an important tool, but its
effectiveness is compromised by the lack of clinical his-
Malformations
tory and description in many submissions. The presence Occasional feather cysts are seen in all species. In some
Chapter 13 | I N T E G U M E N T
397
Infectious Diseases
PARASITIC
The primary parasitic skin disease is mite infestation.
Several different types of mites are found affecting both
feathered and unfeathered skin. Most of these parasites
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are present in the superficial portion of the skin, which
is usually hyperkeratotic and acanthotic, leading to gross
thickening, irregularity and flaking. Severe and/or
chronic infestation of the cere can result in malforma-
Fig 13.2 | Feather cyst containing concentrically laminated tion of the beak (Fig 13.3a).
keratin that must be differentiated from caseous exudate.
Mites are usually superficial and can be demonstrated by
skin scraping. Some species of mite and some individual
canaries there is an apparent inherited predisposition cases will require deep scrapings or biopsy to identify.
that is associated with color. Neoplasia has recently been
found in the formation of feather follicle cysts in canaries. Knemidocoptes spp. is most prevalent in budgerigars
and passerines. The presentation in budgerigars is usu-
Grossly, feather cysts present as an oval or elongated ally a pronounced hyperkeratosis of the cere and adja-
swelling of the feather follicle with accumulation of yel- cent tissue. Occasionally the vent and legs of budgeri-
low-white material (keratin) (Fig 13.2). The gross lesions gars will be affected (Fig 13.3b). A fine pinhole appear-
must be differentiated from follicular infections. The ance of affected tissue on the cere is typical with this
causes of acquired feather cyst formation are usually not mite infestation. Clinical disease seems to require some
determined but can include infection, trauma or any degree of immune compromise.
condition that interferes with normal growth of the
implicated feather. Passerines with Knemidocoptes spp. generally present
with “tassel foot.” This hyperkeratosis of the legs is often
Resection of a feather follicle cyst is indicated in the accompanied in chronic cases with a curling and over-
presence of self-trauma or recurrent infection. (See growth of the nails.
Chapter 35, Surgical Resolution of Soft Tissue Disorders
for this procedure). Ivermectin has been utilized topically, orally and via
injection for the treatment of mites, including Knemido-
Congenital or developmental beak abnormalities are coptes spp. (See Chapter 9, Therapeutic Agents). In
encountered with some frequency. Improper incubation budgerigars that are otherwise clinically healthy, the
or feeding techniques have been implicated but have not infestation commonly clears, although recurrence is pos-
been documented as causative. The two most common sible. Passerines with Knemidocoptes spp. infestation
presentations are mandibular prognathism and scissors often improve but may not clear with ivermectin therapy.
beak. (See Chapter 14, Evaluating and Treating the Gastro- This may be due to secondary staphylococcal or mycotic
intestinal System for correction of beak deformities). infections.
Abnormalities of the beak or claws can be a reflection of Lice are uncommon in well cared for pet birds. See
abnormalities of the underlying bone. They can also Chapter 6, Maximizing Information from the Physical
result from trauma, infection or neoplasia interfering Examination for photos. Unless the infestation is severe,
with growth of the germinal epithelium of the beak or gross lesions are not seen. Treatment with ivermectin is
claw keratin. The result can be asynchronous growth or generally effective, although pyrethrin and carbaryl pow-
incomplete keratinization. Vitamin deficiencies that cause ders are also used successfully.
problems in domestic poultry are not well documented
in pet avian species. Hepatopathy has been linked to
MYCOTIC
beak and nail deformities in psittacines, but whether this
is a direct result of the hepatic insufficiency or a sequela Folliculitis due to dermatophytes appears to be less
to nutritional disease is not well documented. common in birds than its counterpart in mammals,
based on biopsy material. When present, there may be
See Chapter 6, Maximizing Information from the Physical gross swelling of follicles with variable hyperkeratosis
Examination and Chapter 15, Evaluating and Treating the and crust formation (Fig 13.4). A variable amount of
Liver for photos of feather, beak and nail deformities. necrotic debris may be seen.
Courtesy Exotic DVM
Greg J. Harrison
Fig 13.3a | Roughened, inflamed cere and face due to Fig 13.3b | A close up view of a Knemidocoptes spp. mite
Knemidocoptes spp. mite infestation. infestation showing the characteristic pin-point tunnels in the
skin that can be used to make the diagnosis.
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Teresa Lightfoot
Fig 13.4 | Swelling of follicles in a bird with Fig 13.5 | Amazon with Malassezia spp. facial dermatitis.
dermatomycosis.
Recent research indicates that Malassezia spp., BACTERIAL

Aspergillus spp. and other fungi may play a role in some
Two primary forms of bacterial skin disease are com-
cases of dermatitis or feather picking. Clinical reports of
monly seen. Folliculitis is often associated with Staphy-
improvement in feather plucking following nebulization lococcus spp. Grossly there is swelling of the perifollicu-
with antifungal agents for respiratory disease lend cre- lar skin with a variable amount of reddening. The lesion
dence to this possibility. (M. Stanford, personal communi- must be differentiated from mycotic folliculitis.
cation, August, 2001). Further research is needed to deter-
mine whether fungal infection or sensitivity to Aspergillus Generalized bacterial dermatitis (pyoderma) is usually
spp. may play a role in dermatitis and feather picking. intensely pruritic leading to self trauma that results in a
more severe superficial lesion. Reddening, exudation
Malassezia spp. is occasionally found as an etiologic and crust formation are associated with necrosis (Fig
agent, generally documented on cytology or histopathol- 13.6). The necrosis may extend through the epidermis
ogy, for feather loss and dermatitis. Treatment is largely into the dermis in severe cases. Bacteria, usually gram-
anecdotal and follows the sensitivities of this organism positive cocci, may or may not be present in samples
noted in other species. Oral fluconazole and topical taken for microscopic examination.
clotrimazole or chlorhexidine spray have been used with
good results. This may be an under-reported syndrome Long-term antibiotic therapy is often needed in these
related to feather destructive behavior (Fig 13.5). cases. A positive culture and sensitivity will allow the
selection of the appropriate antibiotic. A Gram’s stain
Saprophytic fungi have been noted to cause black discol- performed at the time of culture may improve interpre-
oration of feathers in birds. The prevalence of this type tation of the culture results. In the absence of a positive
of fungal growth is unknown but it seems most likely to culture, treatment may be selected based on the com-
occur in birds with marginal hygiene and/or health. mon sensitivities of the class of organisms identified in
399
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Fig 13.6 | Generalized bacterial dermatitis leading to necrosis, Fig 13.7 | Localized periocular inflammation and minimal
reddening and crust formation. feather loss in a lovebird with circovirus infection.
the Gram’s stain. Treatment failures are often the result One study was conducted on 32 peach-faced (rose-
of either continued self-trauma or insufficient length of faced) lovebirds (Apapornis roseicollis) with skin and
antibiotic therapy. feather problems.6 Birds with chronic ulcerative dermati-
tis (CUD), the feather-less syndrome (FLS) or polyfolli-
A specialized form of bacterial dermatitis is severe culitis (PF) were screened for avian polyomavirus (APV)
chronic-active pododermatitis. (See Bumblefoot/ and psittacine beak and feather disease (PBFD). Of the
Pododermatitis under Non-Infectious Diseases). birds with CUD, greater than fifty percent were positive
for APV, and approximately 20% were positive for PBFDV.
Focal granulomatous dermatitis due to mycobacterial Of the birds with FLS, 16% were positive for APV and
infection is also seen. Clinically, the lesion presents as a 65% were PBFD positive. All birds with PF were negative
lump or multiple lumps that histologically are com- for APV and PBFD. The history of all of these birds also
prised of large macrophages and a variable number of indicated malnutrition (Harrison/Gerlach, personal com-
heterophils and plasma cells. Acid-fast bacteria are found munication).
in the macrophages.
A generalized feather disease is seen in African grey par-
rots infected with circovirus, but often the disease is
VIRAL
confined to the tail feathers, or there may be no feather
Circovirus involvement at all. African grey parrots may show
ectopic red feathers; however, this abnormal coloration
Psittacine beak and feather disease virus (PBFDV) is one
may also be caused by nutritional factors.
of several avian circoviruses. This virus is enzootic in
many species of free-ranging Australian parrots and has Eclectus parrots do not show typical feather lesions of
also been found in free-ranging African parrots. PBFDV, but affected birds may have a delayed molt and
old, poor quality feathering. An older age of onset of clini-
PBFDV in nestlings is acute in onset and generalized so
cal signs of circovirus has been noted in Eclectus spp.
that it affects all growing feathers. Acutely affected birds
may die within 2 months of the onset of disease. The Infection in cockatoos leads to deformed feathers,
chronic form of disease is generally seen in older birds feather loss and variable skin lesions. Beak lesions are
when these birds go through their first molt. Dystrophic less common than feather changes but are a prominent
feathers replace normal ones during the molt. Powder- feature of this disease in some species of Cacatua.
down feathers may be the first affected in cockatoos Variable necrosis and loss of keratin can be seen.
(Cacatua spp.). Secondary candidiasis of the beak is common in affected
cockatoos (Fig 13.8).
Currently, PBFDV in the United States is most commonly
seen in lovebirds (Agapornis spp.), budgerigars, lories, Necrosis and annular constriction of the base of the
lorikeets, Eclectus spp. and African grey parrots feather shaft and hemorrhage in the feather pulp are
(Psittacus erythacus). Feather lesions in lovebirds are noted. There may be severe shedding of affected feath-
usually not as severe as in cockatoos and may be local- ers. Affected feathers are stunted and may have thick-
ized (Fig 13.7). Some lovebirds show no signs of disease. ened, hyperkeratotic sheaths, pulp hemorrhage, annular
400
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Courtesy Exotic DVM
Fig 13.8 | Severe feather loss and dystrophy as well as beak Fig 13.9 | Detail of feathers from Fig 13.8.
necrosis in a cockatoo with circovirus infection.
Judith St. Leger
Judith St. Leger

Fig 13.10 | Columbiforme circovirus. Fig 13.11 | Columbiforme circovirus.
Judith St. Leger
Judith St. Leger
Fig 13.12 | Columbiforme circovirus. Fig 13.13 | Columbiforme circovirus.
constrictions of the calamus, curling or stress lines on Polyoma/Papilloma Virus

the vanes (Fig 13.9). Discoloration of feathers may be the Papilloma virus can cause proliferative skin lesions that
initial sign in some birds. As mentioned above, African are multiple and may superficially resemble mite infesta-
grey parrots may develop red feathers, and yellow feath- tion (Fig 13.14). This has been confirmed in African grey
ers have been seen to replace green feathers in other parrots. The lesions are fronds of hyperplastic epithelial
species of parrots. cells supported by a vascular stroma. Radiosurgery, elec-
trocautery and cryosurgery have all been utilized to
Gross lesions of circovirus infection are usually not seen
resect the papillomas and to attempt to stimulate an
in non-psittacine birds; however, feather dystrophy simi-
immune response.
lar to that seen in psittacines has been reported in
pigeons, doves and finches (Figs 13.10-13.13).
401
other psittacine species and grossly there may be der-

mal/follicular hemorrhage. See Chapter 32, Implications
of Viruses in Clinical Disorders.
Poxvirus
This is an ubiquitous viral infection seen in all avian
species. Fortunately the pox virus is relatively species-
specific. Lesions are common on the head face and feet,
but can also be present in other locations (Fig 13.15).
The lesions are proliferative and may have rough or
smooth surfaces depending on chronicity, self-trauma
and the degree of secondary bacterial infection. In some
cases much of the superficial portion of the lesion can
be comprised of necrotic debris and crusts associated
Teresa Lightfoot
with bacterial or yeast infection, and care must be taken
to ensure that any material removed for biopsy or cytol-
ogy contains epidermal tissue (Fig 13.16). If no epider-
Fig 13.14 | Viral-induced papillomas on the
mis is present the correct diagnosis will probably not be
face of an African grey parrot.
made. Impression smears will contain epithelial cells
with ballooning degeneration and cytoplasmic inclusion
bodies (Fig 13.17).
Polyomavirus was originally reported as a disease of
budgerigars with feather loss. Primary feathers may The severity and location of lesions will dictate whether
appear abnormal. Polyomavirus infection is also seen in euthanasia is indicated or if treatment should be
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Fig 13.15 | Facial lesions due to poxvirus infection in a canary. Fig 13.16 | Typical poxvirus-induced lesions of the leg and
toes in the canary from Fig 13.15.
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Fig 13.17 | Impression smear of proliferative epidermis in Fig 13.18 | Depigmented, proliferative lesion (arrow) associ-
poxvirus infection. Note ballooning degeneration and cytoplas- ated with cytomegalic herpesvirus infection of the skin of a blue
mic inclusion bodies. and gold macaw.
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Courtesy Exotic DVM

Fig 13.19 | Color change in feathers secondary to nutritional Fig 13.20 | Stress bars in growing feathers. This is a nonspe-
problems, possibly a carotene deficiency. cific change that can be associated with a variety of insults dur-
ing feather formation.
attempted. Despite supportive care, permanent deformity proper nutrient metabolism even though nutrition is
of eyelid margins and other facial tissue is common. adequate. Gastro-intestinal, hepatic and pancreatic dis-
eases are potential underlying causes. The diagnostic
Herpesvirus approach to chronic non-inflammatory skin disease
In cases of systemic herpes infection there is occasion- should include examination and laboratory testing to
ally involvement of the epidermis of the skin or feather rule out disease processes in internal organs.
leading to necrosis and inclusion body formation. Since
the generalized disease is usually catastrophic, little PHYSICAL/ENVIRONMENTAL
attention is paid to what may be grossly minimal skin AGENTS
lesions. In some psittacines, particularly macaws and Trauma, burns, excessive cold and other physical factors
cockatoos, proliferative lesions of the lower legs and feet often cause skin lesions, and although the cause may be
have been described due to a herpes virus infection. obvious, histories are occasionally not obtained (Tables
Solitary or multiple proliferative nodules or plaques are 13.3-13.5). Gross changes include loss of feathers, vary-
more common in Cacatua spp., while depigmentation is ing degrees of hemorrhage, necrosis, and superficial
more often encountered in macaws (Fig 13.18). The crust formation. Severe necrosis and sloughing of epi-
presence of these lesions in susceptible species should dermis and possibly portions of dermis can be seen in
lead to herpes virus infection being included in the dif- injuries due to both heat and cold. Discoloration of the
ferential diagnosis. lesions is variable. Traumatic injuries are characterized
by variable amounts of hemorrhage, edema and inflam-
mation, depending on severity of the insult and time
Non-Infectious Disease elapsed prior to examination (Figs 13.21, 13.22).
Beak trauma is a common presentation in psittacines.

NUTRITIONAL/METABOLIC Injury from a bite from another bird is the most fre-
A number of specific and non-specific nutritional prob- quent cause. Damage from cage wires or cage equip-
lems can result in poor feather quality and skin disease. ment is also common.
This may be the most common cause of primary feather
abnormalities. See Chapter 6, Maximizing Information Treatment and prognosis depend entirely on the severity
from the Physical Examination. of the injury. If proper beak occlusion is maintained,
then treatment can be limited to prevention of infection.
Depigmentation or altered pigmentation, improper Topical and systemic antibiotics are warranted if the
molting and poor quality feathers can be seen (Figs injury sustained is extensive or deep.
13.19, 13.20) (see Chapter 4, Nutritional Considera-
tions). Gross changes are rarely specific. These lesions A hemostatic matrix such as Surgicell®d can be used to
are not inflammatory, but poor nutrition can predispose both stop bleeding and to provide a slow release of
the bird to skin infections and subsequent inflammation. antibiotic. Antibiotics that are used in polymethyl
methacrylate applications should provide a selection
Metabolic disease could also result from failure of that is not tissue toxic and has good bioavailability (see
403
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Fig 13.21 | Subcutaneous hemorrhage secondary to trauma. Fig 13.22 | Severe edema of the subcutis following trauma.
Chapter 9, Therapeutic Agents).

Table 13.3 | Thermal Burn Treatment Protocol
• Stabilization of patient first: More extensive trauma that either involves the occlusal
1. Fluids, electrolytes surfaces or the growth plates of the beak warrants a
2. Treat for potential septicemia/endotoxemia guarded prognosis (see Chapter 14, Evaluating and
• Topical treatment if weight bearing surfaces affected
Treating the Gastrointestinal System). Attention must be
(ie, plantar surfaces of feet)
• Bandaging if potential exists for self-mutilation of affected paid to adequate supportive care including analgesia,
area and maintenance of fluid and caloric intake.
Table 13.4 | Treatment of Band Injuries

BUMBLEFOOT/PODODERMATITIS:
(Figs 13.23-13.25)
DECUBITAL SORES
• Removal of band with minimal additional tissue damage Plantar decubital ulceration is common in older, obese
(ie, Veterinary Specialty Products band cutters)b and nutritionally deficient psittacines. See photos and
• Assessment of distal foot for viability. classification of fat deposition in Chapter 6, Maximizing
• Hydroscopic dressing to preserve tissue, vascularity and
Information from the Physical Examination. Amazons,
innervation (ie, Biodres®)c
budgerigars and cockatiels are over-represented in the
• Antibiotics as indicated for prevention of infection; both
topical and systemic current population. Vitamin A deficiency weakens the
• Prevention of self trauma and frequent reassessment for epithelium of affected birds (see Chapter 4, Nutritional
continued viability and absence of infection. Considerations). Obesity and inactivity produce exces-
sive pressure on plantar surfaces. Subsequent erosions
and then ulcers occur. Localized staphylococcal infection
Table 13.5 | Broken Blood Feather Treatment
is a common sequela (Fig 13.26).
• Keep quiet and confined to allow blood pressure to lower
and bleeding to stop. Presentation may be subclinical and encountered on a
• Apply a styptic powder to the broken feather area or twist
routine annual examination. Correction of the underly-
off and apply to the tip.
• If occurs in the hospital, observing the bird for a few ing predisposing factors will often reverse this disease
hours after powdering is often indicated to prevent exci- process. Perches must be altered in diameter and tex-
tation and subsequent bleeding in transport. ture. The application of Vetrap®e or a similar product to
• When danger of hemorrhage is no longer present, assess the perch provides both padding and change in diame-
feather damage.
ter when the material is wrapped at varying intervals and
• May trim end of feather to decrease movement or pain.
thicknesses. Diet should be corrected to decrease caloric
• Pulling of affected feather may result in follicular damage
and abnormal growth of subsequent feather. intake and increase general nutritional balance, with
• Imping may be indicated for cases of chronic/repeat emphasis on replacement of Vitamin A precursors (see
trauma. Chapter 4, Nutritional Considerations).
• Long-term treatment for recurrent blood feather trauma,
1. Wing trim should be redesigned (see Chapter 1, More advanced cases of decubital ulceration require
Clinical Practice).
additional therapy. Systemic infection may be involved,
2. Nutrition should be assessed (see Chapter 4,
and a complete blood count should be performed.
Nutritional Considerations).
Bandaging of the feet with the application of topical
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Teresa Lightfoot
Fig 13.23 | Leg band injury. Aluminum breeder band is Fig 13.24 | Leg band injury. Removal with the appropriate
embedded in skin and underlying tissue. equipment is necessary to prevent fracturing the leg. In this
case, band cutters by Veterinary Specialty Products, Boca Raton,
FL, USA, were used.
Courtesy Exotic DVM

Teresa Lightfoot
Fig 13.25 | Leg band injury. Although minimal viable tissue Fig 13.26 | Bacterial pododermatitis. This lesion usually devel-
remains beneath the removed band, the innervation and circu- ops following pressure necrosis with a subsequent bacterial
lation to the foot are still intact. Frequent bandage changes infection.
allowed this area to granulate and amputation was avoided.
However, many band injuries of this severity will require ampu-
tation and the owners should be so forewarned.
antibiotic and sufficient padding to reduce and better teroidal antiinflamatory drugs) or synthetic opioids may
distribute pressure on the plantar surfaces is required in be needed (Table 13.6) (see Chapter 9, Therapeutic
many cases. Pain relief in the form of NSAIDs (nons- Agents). Debridement should be approached cautiously,
since significant bleeding can occur from the decubitus.
Table 13.6 | Treatment of Decubital Sores When osteomyelitis is involved, the prognosis for recov-
(Bumblefoot) ery decreases dramatically. If systemic infection and pain
• Topical antimicrobials can be controlled, therapy can be approached as above.
• Hydrophilic dressings The owner must be forewarned that the therapy will be
• Padded foot bandages of long duration and the prognosis is guarded. Ethical
• Anti-inflammatory/analgesics (ie, butorphanol/meloxicam)
considerations arise when the degree of affectation is
• Systemic antibiotics when indicated
• Consider use of antibiotic impregnated matrix such that the bird can not stand without severe pain.
• Debridement and suturing of more extensive lesions
• Long-term treatment requires owner compliance
1. Alter/pad perches
2. Exercise
3. Assess and alter diet with particular attention to correct-
Endocrinopathies
ing obesity and providing adequate Vitamin A precursors Endocrine disorders can lead to generalized feather loss
(See Chapter 34, Surgical Resolution of Orthopedic
Disorders and Chapter 4, Nutritional Considerations). and abnormal feathering. There is usually no specific
pattern or features that grossly indicate endocrine disor-
405
avian patients may be of great benefit in separating this

category of disease from other conditions.
According to Patricia MacWhirter, DVM (personal com-

munication, December 2003) an early researcher into
avian intradermal testing: “Intradermal skin testing can
be carried out in birds using the apteria on either side of
the sternum. A statistically significant difference has
been found in the occurrence of positive intradermal
Courtesy Exotic DVM

skin test reactions to Aspergillus, sunflower, house dust
mites (D. pteronyssinus and D. farinae) and/or maize
(corn) in a variety of psittacine species showing evidence
of feather plucking, feather chewing or self injurious
Fig 13.27 | Excessive fat deposits in the skin of a bird with behavior compared with normal birds. This suggests that
hypothyroidism. allergy may play a role in the occurrence of these syn-
dromes. However, response to treatment by attempted
avoidance of the suspected allergen(s) or the use of vac-
ders. To confirm a diagnosis of endocrine related skin cines has to date often not been successful. Skin testing
disease, appropriate clinical laboratory testing is neces- can be problematic to carry out because of the need for
sary. Confirmation can also result from finding appropri- fresh allergens and accurate injection, the small area of
ate endocrine gland lesions at necropsy (Fig 13.27). bare skin available and difficulties in getting consistent
Although currently Thyroid Stimulating Hormone (TSH) results with positive controls. While promising, the tech-
for avian thyroid stimulation assays is not commercially nique is probably best suited to specialist dermatology
available, research has shown that a 2 to 4 fold increase practices and more research is needed before it can be
in circulating T4 is a normal response in birds to admin- routinely recommended.” See Chapter 4, Nutritional
istration of TSH. Interpretation of a baseline T4 level has Considerations.
limitations as it does in domestic pet medicine, but may
be useful diagnostically (see Chapter 19, Endocrine
Considerations).
Chronic Internal Disease
HYPERSENSITIVITY In many cases of chronic internal disease, including
Allergic skin disease in birds is occasionally reported, infectious, degenerative and neoplastic conditions, there
but is not well documented, and confirmation can be is poor feather quality and loss of feathers.
difficult. Gross changes include feather loss (often self-
induced), reddening and occasionally, surface exudates.
Some of the gross lesions may be secondary to self
NEOPLASIA
trauma. (See Chapter 20, Overview of Tumors).
Periocular and occasionally periaural pruritic, hyperkera-

Epithelial
totic lesions are observed seasonally in outdoor birds in
the southeastern US. When a biopsy is performed and Epithelial tumors originate in the surface epithelium, fol-
these birds are housed indoors pending receipt of licular epithelium or the uropygial glands. The uropygial
histopathology results, the lesion generally clears. Both gland may become abscessed as a result of occlusion of
pollen and insect sensitivity have been theorized. the papilla. This condition is treated much like an anal
sac abscess in a dog, with debridement, reestablishment
Definitive diagnosis of allergic skin disease is difficult. of patency of the duct and antibiotics as indicated. In
Food elimination has lead to improvement in some cases some cases, neoplasia of the gland may underlie the
(see Chapter 4, Nutritional Considerations: Section II, infected state. Uropygial gland tumors can be either ade-
Nutritional Disorders) and successful treatment with anti- nomas or carcinomas, and gross differentiation is diffi-
inflammatory drugs is presumptive evidence of allergy. cult. Both will present as swellings that may be second-
The greatly diminished response of the avian patient to arily inflamed in some cases. Adenomas are usually well
histamine administration has hindered the development circumscribed and encapsulated with carcinomas being
of avian skin testing methods. Recent research has estab- less differentiated and more infiltrative into surrounding
lished positive and negative controls and preliminary tissue. See Chapter 35, Surgical Resolution of Soft Tissue
standards for this testing.8 Diagnostic skin testing for Disorders for surgical considerations.
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Fig 13.28 | Aggressive squamous cell carcinoma with loss of Fig 13.29 | Large mass typical of subcutaneous lipoma.
normal skin and severe secondary inflammation.
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Fig 13.30 | Circumscribed red mass consistent with heman- Fig 13.31 | Deeply located fibrosarcoma replacing soft tissue
gioma. and bone.
Papillomas of the skin are not common and may be virally from melanomas (Fig 13.30).
induced in African grey parrots (see previous discussion).
Fibromas and fibrosarcomas may both be seen but the
Squamous cell carcinomas are often ulcerated and hem- later are more common. They present as nodular masses
orrhagic as well as infiltrative (Fig 13.28). They may that may be ulcerative and infiltrative into deep tissues
involve any portion of the skin and no particular site (Fig 13.31).
predilection has been identified. In some cases there is
no obvious ulceration or inflammation in the early Dermal lymphosarcoma may present as a diffuse thick-
stages. Metastasis is not common, but occurs, particu- ening of the skin with loss of feathers. This condition
larly in chronic cases. This neoplasia often appears can be misdiagnosed as chronic resistant inflammation
grossly as a delayed or non-healing cutaneous infection, unless biopsied.
and diagnosis is therefore often delayed.
Melanocytic Tumors
Basal cell tumors often originate in feather cysts, and Melanoma has been diagnosed in several psittacine
although expansile, are usually benign. birds. The tumor is not common and is usually malig-
nant. These tumors often occur on the face and may
Mesenchymal tumors include those of vascular, fibrous,
involve the beak. They are brown-black, raised masses
adipose and connective tissue origin. These tumors orig-
with poorly defined margins (Fig 13.32).
inate in the dermis or subcutis but may expand to
involve the epidermis with secondary ulceration. Gross Mast cell tumors have only been reported in chickens
differentiation can be difficult with malignant tumors. and owls.
Lipomas are common and have the gross appearance of
a mass of normal fat (Fig 13.29). Hemangiomas are often Granular cell tumors are infrequent in birds, and are
dark red and hemorrhagic. They must be differentiated seen primarily in psittacine birds, particularly Amazon
407
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Fig 13.32 | Eclectus spp. female with malignant melanoma of Fig 13.33 | Xanthoma that has replaced much of the wing.
the face and cere. This is a common location for the condition.
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Fig 13.35 | Same Eclectus after 9 months of dietary

correction, with no additional therapy.
Fig 13.34 | Seven year old male Eclectus with xanthoma. This
bird had been feather picking for 5 years. Hormonal manipula-
tion and psychotropic drugs had temporarily decreased his
plucking, but were not curative. When the xanthoma developed,
dietary change to an organic formula resulted in resolution of
the xanthoma and decreased feather destructive behavior.
parrots. They are small smooth nodules. (See Chapter

20, Overview of Tumors).
Feather Destructive
Behavior
Various degrees of feather destructive behavior, from
Non-neoplastic over-preening to feather plucking and self-mutilation,
Proliferative Lesions are commonly encountered in avian practice. Based on
skin biopsies, many of these cases have an underlying
Xanthomatosis is a condition of uncertain etiology. lesion that would account for pruritus and self-trauma.
Xanthomas are seen most commonly in cockatiels and In some birds there is no evidence of skin or systemic
budgerigars and usually are present on the wing as a
disease or condition and these cases are considered
variable-sized, yellow mass (Fig 13.33). Alternate com-
behavioral problems after other causes have been ruled
mon presentation sites include the sterno-pubic area
out. Since self-trauma can lead to lesions, histologic
and the keel. Surgical resection may be necessary in
changes must be carefully assessed before a diagnosis of
advanced cases and in those where the affected area is
traumatized. In some species and some cases, nutri- behavioral feather picking is made. In addition to com-
tional therapy has been reported as successful. Feeding plete physical and laboratory examination, history is very
a balanced diet with increased Vitamin A precursors is important for a proper diagnosis of this condition. (See
the predominant dietary change initiated in the therapy Chapter 3, Concepts in Behavior and Chapter 4,
of affected birds (Figs 13.34, 13.35). Nutritional Considerations).
Skin Conditions
Several syndromes with no identified etiologies are
commonly recognized by practitioners. These include
chronic ulcerative dermatitis, Quaker (Monk) parakeet
(Myiopsitta monachus) mutilation, and Amazon foot
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necrosis.
CHRONIC ULCERATIVE Fig 13.36 | Bandaging for Amazon foot necrosis. Topical
DERMATITIS antimicrobial agents and hydrophilic bandage material may aid
Chronic ulcerative dermatitis (CUD) is commonly in healing. Bandaging both feet, even if only one is affected,
tends to divert the patient’s attention and prevent removal of
reported in lovebirds and presents as self-trauma. The
the bandaging.
affected area is usually the patagium or neck and back. A
linear lesion is generally encountered, and the bird
often presents with either a chronic scarified area or Table 13.7 | Treatment Protocol for Quaker
with an acutely lacerated and hemorrhagic wound. As Mutilation Syndrome
discussed under viruses, recent research on a small pop- • E. collar often necessary to prevent severe/fatal self-muti-
ulation indicates that polyoma virus, circovirus or both lation.
• Be aware that self-mutilation may be displaced to an
may be involved in this syndrome.6 The finding of a viral
accessible body part.
etiology in some cases of chronic ulcerative dermatitis in
• Diazepam or other anti-anxiety/anti-psychotic drug
lovebirds would be consistent with reports of flock out- • Antibiotic for secondary infection.
breaks of this condition. Other cases seem to occur in • Wound dressing as needed.
isolated individuals. Antibiotics are often clinically useful • Owners should be informed of guarded prognosis.
in controlling what is likely a secondary bacterial infec-
tion. Elizabethan collaring may be necessary to prevent
self-mutilation and blood loss. Even when the primary
The potential for a contact dermatitis would suggest that
lesion is healed, scar tissue often restricts movement
prior to handling these birds the owners wash their
and recurrence of self-mutilation is the rule. Some prac-
hands to rid them of residual nicotine, hand lotions, etc.
titioners have associated Omega-3 fatty acid supplemen-
Inhalant hypersensitivity has been theorized. Nutritional
tation with clinical improvement. Use of psychotropic
deficiencies or toxicities and hormonal influences have
drugs and/or antihistamines has been reported with
also been suggested. A recurrence and seasonality is
equivocal results.
commonly reported (Fig 13.36).
QUAKER MUTILATION SYNDROME POLYFOLLICULITIS

A syndrome in Quaker (Monk) parakeets has been noted
Follicular malformations and dystrophy are occasionally
for many years in which sudden and aggressive self-muti-
seen. The most recognized has been called “polyfolliculi-
lation is encountered (Table 13.7). Feather destructive
tis.” This is a misnomer as in many cases there is no
behavior does not seem to be a precursor to this syn-
inflammation. The condition is seen in budgerigars,
drome. The mutilation is often directed at the neck and
cockatiels and lovebirds and presents as multiple feather
chest area. Self trauma can include fatal damage to the
shafts from a single follicle. Feathers are thick and short
crop and the jugular vein. With no etiology yet deter-
and may have retained sheaths. Grossly they present as
mined, treatment is limited to providing a mechanical
fluctuant subcutaneous swellings that contain slightly
barrier to the self-trauma and supportive care. Due to
viscid fluid.
the severity and chronicity of this syndrome, euthanasia
is often elected. Increased submissions for pathology Calcinosis circumscripta is an unusual condition in
may identify an etiology. Theories of potential etiologies birds. It presents as nodular lesions that may have a
and/or associated conditions include: viral, obesity, white, chalky appearance grossly.
hepatic lipidosis, pancreatic insufficiency and lipemia
(M. Rae, personal communication, 2002).
OTHER SKIN CONDITIONS
Occasionally severe inflammation is seen associated with
AMAZON FOOT NECROSIS collagen necrosis. A severe granulocytic response is pres-
Amazon foot necrosis has historically been more preva- ent, and many of these cells may be eosinophils, how-
lent on the west coast of the USA than in other areas. ever they are difficult to distinguish from heterophils
409
histologically. The lesion is similar to idiopathic col- the pattern and type of inflammation a tentative diagno-
lagenolytic inflammation seen in several mammalian sis may be made, but until many more cases with com-
species. plete histories and follow-up information become avail-
able, many lesions will have obscure origins.
Autoimmune skin disease has not been documented in
birds, but several cases with intraepidermal pustule for- Products Mentioned in Text
mation and acantholysis have been seen. Unfortunately a. Silvadene, Marion Labs, Inc., Kansas City MO
b. Veterinary Specialty Products Bandcutter, PO Box 812005, Boca Raton,
these few cases were lost to follow-up. FL, USA, 33481, 1-800-362-8138, www.vet-products.com
c. BioDres, DVM Pharmaceuticals, Miami, FL, USA,
www.dvmpharmaceuticals.com/about_dvm.html
In many skin diagnoses there are inflammatory lesions
d. Surgicell®, Johnson & Johnson’s, www.jnjgateway.com
whose exact etiology cannot be determined. Based on e. Vetrap - 3M Animal Care Products, St. Paul, MN, USA, www.3m.com
References and pp 33-52. Avian Med. Surg. 13: 192-200. Wilkins. pp 387-396.
11. Hadley NF, 1991. Integumental 21. Quist CF, Latimer KS, Goldade SL, 30b. Schmidt RE: Pictorial guide to
Suggested Reading lipids of plants and animals-com- Rivera A, Dein FJ. 1999. Granular selected avian skin desseases.
1. Andre JP, Delverdier M, Cabanie parative function and biochem- cell tumor in an endangered
Exotic DVM 4(1): 27-32, 2002.
D, Bartel G. 1993. Malignant istry. Advances in Lipid Res. 24: Puerto Rican Amazon parrot
melanoma in an African grey par- 303-320. (Amazona vittata). Avian Path. 31. Schmidt RE. 1992. Morphologic
rot. JAAV 7: 83-85. 12. Jacobson ER, Mladinich CR, 28: 345-348. diagnosis of avian neoplasms. Sem.
2. Brush, AH 1993. The origin of Clubb S, Sundberg FP, Lancaster 22. Raidal SR. 1995. Viral skin dis- Avian Exot. Pet Med. 1: 73-79.
feathers: A novel approach. Avian WD. 1983. A papilloma-like virus eases of birds. Sem. Avian Exot. 32. Spearman RFC, Hardy J. 1989.
Biology, Farner, DS, et. al. Eds. infection in an African Grey par- Pet. Med. 4: 77-82. Integument. Chapt. 1 In: Form
Vol. IX. New York, Academic rot. JAVMA 183: 1307-1308. 23. Raidal SR, Riddoch PA. 1997. A and function in birds. King, AS,
Press, pp 121-11162. 13. Latimer KS. 1994. Oncology. In: feather disese in Senegal doves McLelland, J (Eds). Vol. 3. New
3. Chitty J, A novel disinfectant in Ritchie BW, Harrison GJ, Harrison (Streptopelia senegalensis) mor-
York, Academic Press. pp1-52.
psittacine respiratory disease, AAV LR, eds. Avian Medicine: phologically similar to psittacine
Proceedings 2002, p 25-27. Principles and Application. beak and feather disease. Avian 33. St. Leger J: Feather Dystrophy
4. Clubb SL, Herron A, Feather dis- Brentwood, TN: HBD Int’l, Inc, Path. 26: 829-836. Associated with circovirus infec-
coloration due to saprophytic pp 640-672. 24. Ramis, A, Latimer, KS, Niagro FD, tion in columbiformes. In Proc of
fungal growth, Proc Annual AAV, 14. Latimer KS, Niagro FD, Rakich Campagnoli, RP, et al. 1994. the 47th Western Poultry Disease
1998, p 71-76. PM, Campagnoli, RP, et al, 1992. Diagnosis of psittacine beak and Conference. March 8-10, 1998.
5. Cooper JE, Harrison GJ: Comparison of DNA dot-blot feather disease (PBFD) viral infec- 34. Tell LA, Woods LW, Mathews KG.
Dermatology. In: Ritchie BW, hybridization immunoperoxidase tion, avian polyomavirus infection,
1997. Basal-cell carcinoma in a
Harrison GJ, Harrison LR, (eds): staining and routine histopathol- adenovirus infection and herpes-
blue-fronted Amazon parrot
Avian Medicine: Principles and ogy in the diagnosis of psittacine virus infection in psittacine tissues
beak and feather disease in paraf- using DNA in-situ hybridization. (Amazona aestiva). Avian Dis. 41:
Application. Brentwood, TN:
HBD Int’l, Inc, p 613-621. fin-embedded cutaneous tissues. Avian Path. 23: 643-657. 755-759.
6. Cornelissen JMM, Gerlach H, JAAV 6:165-168. 25. Ramis A, Latimer KS, Gilbert X, 35. Trinkaus K, Wenisch S, Leiser R,
Miller H, et al: An investigation 15. McDonald, SE, Lowenstine, LJ, Campagnoli R. 1998. A concur- Gravendyck M, Kaleta EF. 1998.
into the possible role of circo and Ardans, AA. 1981 Avian pox in rent outbreak of psittacine beak Psittacine beak and feather dis-
avian polyoma virus infections in blue-fronted Amazon parrots. and feather disease virus and ease infected cells show a pattern
the etiology of three distinct skin JAVMA 179: 1218-1222. avian polyomavirus infection in of apoptosis in psittacine skin.
and feather problems (CUD, FLS, 16. Macwhirter P, Mueller R, Gill J, budgerigars (Melopsittacus undu- Avian Path: 27 551-561.
PF) in the rose-faced lovebird Ongoing research report: latus). Avian Path. 27: 43-50.
(Agapornis roseicollis). Proc Euro Allergen testing as a part of 26. Rece RL. 1992. Observations on 36. Tsai SS, Chang SF, Chi YC, Cher
Col Avian Med and Surg, 2001, p diagnostic protocol in self-muti- naturally occurring neoplasms in RS, et al. 1997. Unusual lesions
3-5, Munich, Germany. lating psittaciformes. Proc AAV birds in the state of Victoria, associated with avian poxvirus
7. Ferrer, L, Ramis, A, Fernandex, J, Annual Conf 1999, p. 125-129. Australia. Avian Path. 21: 3-32. infection in rosy-faced Lovebirds
Majo, N 1997. Granulomatous 17. Pass, DA. 1989. Pathology of the 27. Ritchie BW, Harrison GJ, Harrison (Agapornis roseicollis). Avian
dermatitis caused by a avian integument: A review. Avian LR, (eds) Avian Medicine: Path. 26: 75-82.
Mycobacterium genavense in 2 Path. 18: 1-72. Principles and Application. 37. Van Sant F, Impression cytology:
psittacine birds. Vet. Dermatol. 8: 18. Patnaik, AK. 1993. Histologic and Brentwood, TN: HBD Int’l, Inc, New insights into avian skin flora.
213-219. immunohistochemical studies of 1997.
Proc Annual Conf AAV, 1999, p.
8. Foil C, Daigle J, Heatley J, Daigle granular cell tumors in 7 dogs, 3 28. Ritchie BW, Niagro FD, Lukert PD,
139-141.
J, Tully TN: Intradermal skin cats, one horse and one bird. Vet Latimer KS. et al. 1989. A review
testing in Amazon parrots: Pathol 30: 176-185. of psittacine beak and feather dis- 38. Welle K, Application of Imping
establishing a protocol, Proc 19. Pizarro M, Villegas P, Rodriques A, ease. JAAV 3: 143-150. feathers in psittacine birds. AAV
Annual Conf AAV, 2001, p 103- Rowland GN. 1994. Filariasis 29. Samour J, Naldo J, Therapeutic Proc 1998.
105. (Pelecitus spp) in the cervical Management of Pox Lesions on 39. Wheeldon DB, Culbertson MR Jr.
9. Garcia A, Latimer KS, Niagro, FD, subcutaneous tissue of a pigeon the Cere of Captive Falcons, 1982. Feather folliculoma in the
Norton, TM, et al. 1993. Avian with trichomoniasis. Avian Dis. Proceedings of the AAV Annual canary (Serinus canarius). Vet
polyomavirus infection in three 38: 385-389. Conf, p. 233-235, 2002.
Pathol 19: 204-206.
black-bellied seed crackers 20. Pye GW, Carpenter JW, Goggin, 30a. Schmidt RE. Pathologic aspects of
(Pyrenestes ostrinus). JAAV 7: 79- JM, Bacmeister, C. 1999. the skin and feathers. Chap. 26A in: 40. Woods LW, Latimer KS. 2000.
82. Metastatic squamous cell carci- Diseases of cage and aviary birds. Circovirus infection of
10. Grahm DL, 1985. The avian noma in a salmon-crested cocka- Rosskopf WJ Jr, Woerpel, RW (Eds) nonpsittacine birds. J. Avian Med
integument. Proc. AAV, Boulder, too (Cacatua moluccensis). J 3rd Ed. Baltimore, Williams & Surg 14: 154-163.
14_Gastrointestinal.qxd 8/22/2005 6:14 PM Page 411
CHAPTER
14
Gastrointestinal
System
S T A C E Y G E L I S , B S c, BVS c ( H ons), MACVS c ( A vian H ealth)
The avian gastrointestinal tract (GIT) has undergone a

multitude of changes during evolution to become a
unique anatomical and physiological structure when
compared to other animal orders. On the one hand it
has evolved to take advantage of the physical and chemi-
cal characteristics of a wide variety of food types.1 On
the other hand, it has had to do so within the limitations
of the requirements for flight.2 To this end, birds have
evolved a lightweight beak and muscular ventriculus,
which replaces the heavy bone, muscular and dental
structure characteristic of reptiles and mammals. The
Greg J. Harrison
ventriculus and small intestine are the heaviest struc-

tures within the gastrointestinal tract and are located
near the bird’s centre of gravity within the abdomen.
The overall length of the GIT is also less than that of a
comparable mammal, another weight-saving flight adap-
tation. Interestingly, these characteristics are still shared
with the flightless species such as ratites and penguins.
In addition, the actual digestive process needs to be
rapid to support the high metabolic rate typical of
flighted birds.3
Gastrointestinal adaptations to the wide range of ecolog-

ical niches that birds occupy mean that birds can take
advantage of a huge variety of foodstuffs. The GIT hence
shows the greatest degree of diversity of all the organ
systems between different avian taxa. However, the pres-
sures of convergent evolution have also meant that
many distantly related species have developed a similar
gastrointestinal anatomy to take advantage of particular
food niches.3,4 Examples of these will be presented in the
discussion of each section of the GIT.
The avian GIT also has the capacity to accommodate chisel-shaped rostrum that pushes against a prominent
changes which occur during the life cycle of a bird and ridge found on the undersurface of the rhinotheca.
also which occur due to seasonal environmental condi- Psittacines also have developed a prokinetic maxilla that
tions and hence differing available foodstuffs over the allows them to move their mandible and maxilla inde-
course of a year or years. pendently. This allows an increased gape of the beak, an
improved ability to position food items in the beak, as
well as providing flexion and shock absorption associ-
ated with seed and nut cracking and also with some
Anatomy and Physiology behaviors such as pecking.5 The strength generated by
of the Digestive Tract these structures is exemplified by the Hyacinth macaw’s
ability to crack palm nuts in order to extract the kernel.
The avian gastrointestinal tract is a double-ended open Pigeons, on the other hand, have a typical seedeater’s
tube (as is also seen in mammals) that begins at the bill being mildly conical.6 It is also not as keratinized as
beak and finishes at the vent. In sequential order it is in psittacines. Raptors tend to also have curved, hook-
composed of a mouth, esophagus, crop, proventriculus, like bills but lack the prokinetic maxilla.6 Their bill is
ventriculus (gizzard), intestine, ceca, rectum and cloaca. adapted to tearing and shredding meat. “Darwin’s
Some of these structures may be vestigial or even lost Finches” on the Galapagos Islands best exemplify the
during the evolution of some species. The progress of variability in beak shape brought about by the need to
food through the tract follows a specific digestive adapt to changing environments. Here, the species are
sequence including premoistening and softening, acidi- all similarly colored, but are separated on the basis of
fying, grinding, hydrolyzing, emulsifying and propulsion bill shape and feeding habits. Each has evolved to its
of the end products.1 This propulsion is not always in a own ecological niche, avoiding interspecific compe-
unidirectional pattern as will be outlined later. tition.7 The avian bill is often endowed with sensitive
nerve endings, particularly in species that use the bill to
probe for food. Examples include waders, diving ducks
BEAK, MOUTH, TONGUE AND
PHARYNX and woodpeckers.3
The beak or bill is the avian substitute for teeth and lips Unlike mammals, birds do not have a soft palate or a
and forms the entrance to the oral cavity. It is used for pharyngeal isthmus, nor do they have a sharp demarca-
grasping and processing foods, as well as for climbing tion between the mouth and pharynx.2 Instead, they
and various behavioral functions such as biting, preen- have a combined oropharynx (Figs 14.1a,b). A longitudi-
ing and displaying. It consists of the mandibular bones, nal fissure, the choana, which connects the oral and
the premaxilla and maxilla and their horny covering, the nasal cavities, splits the palate. The choana is variably
rhamphotheca. The upper bill covering is known as the developed. In pigeons it is narrow and lacks papillae. In
rhinotheca, which covers the premaxillary bones and falcons it forms a narrow “V”- shape with few papillae.
partly covers the maxillary bones. It is usually composed In psittacines, it forms a wide “V” and is bordered by
of hard keratin, although in waterfowl only the tip is caudally-pointed sensory papillae.6 The choanal slit
hard, and in shorebirds the entire bill is relatively soft.2 closes during swallowing. The infundibular cleft is
The keratin layer covering the lower bill or mandible is located at the caudal edge of the choana and is the cau-
known as the gnathotheca. Both keratin layers are con- dal opening of the left and right pharyngotympanic
tinually lost by wear and replaced by new growth. Beak (Eustachian) tubes (Rami infundibuli Fig 14.1a) from
shape is influenced by the location and rate of wear and the middle ear.6 The palate forms a roof over the ante-
hence regrowth, which is in large part determined by rior part of the oral cavity. In finches, canaries, budgeri-
diet. This may subtly change over time as food types gars and cockatiels it contains two ridges that assist in
change. For example, the anterior of the outer edges of the removal of husks from seeds before ingestion.1
the beak, the tomia, may be sharp in some species to
assist in cutting seed coats.1 Other anatomical character- The tongue (Fig 14.1b) originates from the floor of the
istics further facilitate the feeding process. The lower oropharynx and is mobilized by the hyoid apparatus and
beak is loosely attached to the skull, allowing for a large its multiple articulating bones and musculature. It func-
gape. The size of the gape determines the maximum size tions to collect, manipulate and swallow food. Again,
of food particles that can be swallowed. This is particu- great species diversity exists in tongue development.
larly important in fruit-eating species such as toucans. The tongues of passerines and pigeons tend to be
Psittacines typically have a very powerful beak. The smooth, short and simple. Psittacines are unique
rhinotheca is broad with a curved rostral tip, giving the amongst birds in having additional striated muscles in
typical hooked appearance. The gnathotheca has a blunt the anterior regions of their tongues that are independ-
Chapter 14 | E V A L U A T I N G A N D T R E A T I N G T H E G A S T R O I N T E S T I N A L S Y S T E M
413
Rhinal cavity C
Choana
Rami infundibuli
Choanal
papillae
T
Espen Odberg
Madeline Rae
M
Fig 14.1a | Ventral dorsal view of the palate area of the Fig 14.1b | Frontal view of orapharnyx of an Amazon parrot.
orapharnyx. T=tongue, M=mandible, C=choanal slit. Note the reduction of
papillae.
ent of the hyoid apparatus and permit added flexibility they ingest. These glands are located in the roof, cheeks
and manipulative capabilities.1 The typical psittacine and floor of the oropharynx. Raptors have less developed
tongue is thick and muscular and its maneuverability salivary glands and piscivorous (fish-eating) species have
allows for the extraction of seeds and nuts from their poorly developed glands, or lack them all together. This
husks, cones or pods. Lories and lorikeets have relatively is presumed to be related to the lubricated nature of the
long tongues that end in fine papillae that aid in the har- food they ingest. The content of the saliva produced also
vesting of pollens and the collection of nectar from flow- varies between species. The salivary glands of house spar-
ers by capillary action.8,9 In birds of prey the tongue is rows secrete significant amounts of amylase whereas
rasp-like, with a roughened tip and many small caudally those of chickens and turkeys secrete little amylase.13
pointed papillae near the base.6,10 In ducks and other
waterfowl which strain food particles, the rostral part of Esophagus and Crop
the tongue is scoop-like and has a double row of over-
The esophagus is a thin-walled distensible tube that
lapping bristles on its lateral borders. These bristles
delivers food from the oropharynx to the proventriculus.
work with the beak lamellae to filter particles.2 It is inter-
It allows birds to swallow their food items whole. In
esting to note that birds have poor taste sensitivity com-
birds the esophagus is divided into a cervical and a tho-
pared to humans. For example, parrots have approxi-
racic region. In the budgerigar, it lies dorsal to the tra-
mately 350 taste receptors compared with 9000 in
chea in the anterior regions of the neck and then runs
humans11, and chickens have up to 300 taste buds.12
along the right side.14 The esophagus’ distensibility is
These are mostly located on the palate near salivary
facilitated by a number of longitudinal folds. These folds
glands and on the posterior tongue. However, the beak,
are large and extensive in owls (Strigiformes) and
tongue and oral cavity have many touch receptors that
species that swallow whole prey items, or those that
make the mouth an important sensory area.1
store large amounts of food material such as gulls
The laryngeal mound lies immediately behind the (Larus spp.). By contrast, parrots exhibit minimal
tongue in most species and contains the glottis, the esophageal fold development and possess a relatively
opening to the trachea. In most species the glottis lies narrow esophagus.6 Mucus-secreting glands are present
directly under the caudal portion of the choana or just in the esophageal mucosa of most birds, particularly in
caudal to the choana in raptors. The laryngeal mound the thoracic esophagus. These glands are actually absent
contains rows of caudally directed papillae that assist in from the cervical esophagus of budgerigars.
the propulsion of food towards the esophagus during
The avian esophageal wall consists of a mucosa, submu-
swallowing.2 Birds lack an epiglottis.
cosa, a muscular tunic and a serosal layer. It generally
contains only smooth muscle cells with a circular muscle
Salivary Glands
layer predominating.10 Peristaltic contractions of inner
There is great species variability in the number and distri- circular and outer longitudinal muscles propel food pos-
bution of salivary glands.2 Granivorous species such as teriorly through the esophagus.1
some parrots, pigeons, chickens and finches have a large
number of glands to assist in swallowing the dry feeds The crop or ingluvies is an expansion of the cervical
esophagus that functions as a food storage organ.1,2,6 It first part being the proventriculus or glandular stomach
mostly lies on the right side of the neck and when dis- and the second structure is called the ventriculus (giz-
tended may also lie on the left side and will rest on the zard) or muscular stomach.
furcula. The crop has varying degrees of development in
different species. In its simplest form, it is merely a spin- The relative size and shape of these structures is based
dle-shaped enlargement of the cervical esophagus. This on diet and is hence quite variable. In carnivorous and
arrangement is seen in ducks (Anas spp.) and owls.6 piscivorous species both structures are very distensible
Parrots have well-developed crops that lie at the caudal and may be difficult to differentiate grossly. This is due
cervical esophagus. A prominent right pouch and a small to the soft nature of their diet. In birds that eat hard
left pouch typifies parrots. Pigeon crops have a more food items, the proventriculus is relatively thin-walled
complicated structure. Both right and left lateral and glandular. The ventriculus is muscular, thick-walled
pouches or diverticulae are well-developed. The lateral and powerful. The intermediate zone connects the
pouches produce a holocrine secretion from the crop two.2,6 This gastric arrangement is typical of granivores,
epithelium — “crop milk” — which is fed to the squabs omnivores, insectivores and herbivores and hence most
during the breeding season.15 It is produced in response of the commonly found species in captivity.
to prolactin. It contains 12.4% protein, 8.6% lipids,
The proventriculus is confluent with the esophagus cra-
1.37% ash and 74% water.2 Therefore it is mainly a pro-
nially but has its own distinctly different structure. It
tein and fatty acid source for these chicks, and is devoid
lacks ridges, except in carnivorous and piscivorous
of carbohydrate and calcium. Both males and females
species, and is lined with a mucous membrane. Its
produce crop milk. Sheets of striated muscle that attach
epithelium contains two principal types of glands that
to the crop adventitia support the large crop. Parrot and
make up most of the thickness of the proventricular
pigeon crops possess a functional sphincter at the junc-
wall.2 The first of these, the tubular glands, secrete
tion of the crop and the thoracic esophagus. This helps
mucus. The second type, the gastric glands, secrete
to form and regulate the boluses of food being propelled
hydrochloric acid and pepsin. This provides an acidic
to the proventriculus.6 It should be noted that birds lack
environment for digestion. Typically, the fasted chicken
the true upper and lower esophageal sphincters found
has a pH of 2.6, whilst that of a pigeon is 2.1.6 Nectarivo-
in mammals.1 Some granivorous species such as the
rous parrots have gland-free spaces between the longitu-
European goldfinch (Carduelis carduelis) lack a true
dinal rows of glands. This allows for distension of the
crop but have a very expandable esophageal pouch that
glandular stomach that may be an adaptation to pollen
can store food items.1 Gulls, penguins and ostriches lack
digestion.16,18
a crop but have a very distensible esophagus.2
The proventriculus contains two muscular layers, the
The crop’s storage function allows birds to ingest and
innermost circular layer and the outer longitudinal layer.
store feed in the evening before roosting, thus providing
The outer longitudinal layer is poorly developed or
for overnight energy needs. It also allows birds to rap-
absent in parrots, waterfowl and some passerines. In
idly ingest food items in a short period of time, and then
these birds the myenteric plexus is located immediately
take refuge in safe cover where the meal can be digested
under the serosal layer rather than between the two
at a more leisurely rate. The crop also acts to soften
muscle layers.2
ingested food by holding swallowed water and by con-
tributing mucus to the saliva. Enzymes within the food
The intermediate zone between the proventriculus and
or microbes present in the crop may further contribute
ventriculus is aglandular and lacks folds. In parrots and
to digestion.16,17 Any glucose released in the crop can be
pigeons, it closes tightly during ventricular contractions
absorbed by the crop mucosa, but this is of minimal
to segregate the ventriculus from the proventriculus.6
importance.2
The ventriculus or gizzard has evolved to mechanically
The crop is particularly well-developed in chicks to store
break food down. Hence it is best developed in species
food fed by the parents. The parents of altricial chicks
that ingest hard foods such as granivores,1,2,6 and also in
premoisten and soften food in their crops and esopha-
insectivores that need to break down the hard exoskele-
gus before regurgitating it to their chicks. The crop also
tons of their prey.18 It is also the location where
provides an important immunological function in
hydrochloric acid and pepsin can further chemically
pigeons feeding squabs.15
break food particles down. It consists of two pairs of
opposing muscles. The caudoventral and craniodorsal
THE AVIAN STOMACH: PROVEN- thin muscles line the caudal and cranial sac of the giz-
TRICULUS AND VENTRICULUS zard respectively. The cranioventral and caudodorsal
The avian stomach consists of 2 distinct structures, the thick muscles are responsible for the powerful grinding
415
contractions seen in the gizzard.16 The asymmetrical tion around the ventriculus.6,20 The paired thin muscles
arrangement of these four muscles provides mixing and contract first and the isthmus closes, segregating the
grinding actions during contractions.1 The ventriculus is ventriculus from the proventriculus. As these muscles
lined by the koilin, a cuticle layer, which acts as a grind- reach maximum contraction, the pylorus opens allowing
ing surface and protects the underlying mucosa from the digesta to pass into the duodenum. The thin muscles
acid and pepsin produced by the proventriculus. The then relax as the thick muscles contract. This coincides
koilin is made up of a combination of proteinaceous with the closing of the pylorus and the beginning of
rod-like projections produced by the deep tubular peristaltic contractions along the duodenum. The isth-
glands lining the gizzard, together with desquamated mus may also open to allow the passage of ingesta back
epithelial cells that form a matrix.1,2,6 The hardened com- into the proventriculus for the addition of fresh acid and
posite frequently has raised areas and distinct longitudi- pepsin, allowing additional time for the breakup of large
nal and transverse grooves that aid in mechanical break- lipid globules and the breakdown of proteins. In partic-
down of foods. It is thickest in species with well-devel- ular, lipid is retained in the anterior region of the tract
oped, muscular stomachs. It is continuously worn and and digested more slowly than are protein or carbohy-
replaced in many species, but in falcons it may occasion- drates.21,22 This cycle of contraction occurs as a seamless
ally be sloughed and shed. The koilin lining may be movement that gives the appearance that the gizzard is
green, brown or yellow in color due to bile staining flipping.6 This coordinated complex of contractions is
caused by ventricular reflux from the small intestine. controlled intrinsically by the myenteric plexus.
This is a normal finding.6
Raptors have a more simple stomach arrangement that
The gizzard is separated from the small intestine by a has to produce the pellets, indigestible contents of fur,
small pyloric fold that regulates the passage of food into bone, teeth, feathers, claws, as well as perform the nor-
the small intestine by slowing the movement of large mal digestive function. Neck extension and head pump-
particles.19 In lorikeets and honeyeaters (both nectarivo- ing assist the peristaltic propulsion of food into the
rous species), the proventricular and pyloric openings of proventriculus. The stomach fills with digestive juices
the gizzard lie in a median plane, which is thought to over the next hour and vigorous, high frequency waves
allow rapid passage of ingesta.8 of contractions occur in a clockwise direction from the
isthmus to the pylorus. This is followed by a 7- to 9-hour
It is interesting to note that the size of the gizzard can
period of chemical digestion where forceful proventricu-
change with diet within the same species, being thicker
lar contractions occur at low frequency. By the end of
and larger when dry seeds are eaten and softer and
this period, digestion is complete. Next, a short phase of
lighter in summer when fruits are eaten.1
paired contractions removes any further liquid from the
The role of grit in avian digestion is an interesting one. indigestible pellet. This is followed by a further 5- to 6-
Insoluble grit may lodge in the gizzard and add to the hour phase of pellet compaction after which it is
maceration of the food, particularly in species that do expelled by retroperistalsis. The timing of pellet ejection
not dehusk the seed before swallowing it, eg, pigeons, varies with the species.
and galliforms like quail. It is controversial whether
birds deliberately seek insoluble grit to aid in digestion INTESTINES AND PANCREAS
or whether its ingestion is incidental to eating digestible
The small intestine is the main site for enzymatic diges-
foods or soils containing minerals and trace elements.6
tion and nutrient absorption in the avian gut. It is less
Grit is absent from the stomachs of nectarivorous birds,
differentiated between species than are the more proxi-
which also have poorly developed gizzards.18
mal regions of the gastrointestinal tract. The duodenum
arises from the pylorus and forms a loop that encircles
GASTRIC MOTILITY the bulk of the pancreas. The pancreas is trilobed in
Food passes through the proventriculus very quickly most species with the third lobe or splenic pancreas
where it is coated with hydrochloric acid and pepsin, sometimes not being directly attached to the other two
with little enzymatic digestion. Digestion is controlled by lobes. In budgerigars, the three pancreatic lobes are each
the vagus nerve and by the hormones gastrin, secretin, drained by a separate duct. Two of these ducts empty
cholecystokinin and pancreatic polypeptides. The food is into the distal duodenal loop adjacent to the bile duct
propelled into the ventriculus where most of the whilst the other duct empties into the opposite side of
mechanical digestion occurs by a combination of coordi- the duodenum.14 In pigeons, all three pancreatic ducts
nated muscle contractions and the action of grit. The empty into the distal duodenum.6 The exocrine pancreas
exact process varies with species. In turkeys and parrots, contains enzymes similar to those found in mammals
for example, the muscles contract in a clockwise direc- such as amylase, lipases, trypsin and chymotrypsin,
416
carboxypeptidases A, B and C, deoxyribonucleases, The ceca are important in fermentation of vegetable mat-
ribonucleases and elastases.1 It also produces bicarbon- ter and in water balance and are hence most developed
ate that buffers the intestinal pH. It is also important to in chickens, ratites and ducks.27 They are absent or ves-
remember that the intestinal wall mucosa also produces tigial in parrots and small insectivorous passerines,
amylase, maltase, sucrase, enterokinase, lipases and pep- appearing histologically as a nodule of lymphatic tissue
tidases and so contributes to enzymatic digestion.6 These at the small intestinal-rectal junction. In the domestic
enzymes are produced in response to duodenal disten- pigeon they are entirely lymphatic in structure and are
sion, hydrochloric acid, vagal stimulation, cholecys- called the cecal tonsils. They are, however, well devel-
tokinin, secretin and vasoactive intestinal peptide.2,23 oped in herbivorous or omnivorous passerines.16
Birds have not been shown to possess any intestinal lac-
tases so they should not be fed significant quantities of The avian rectum or colon is found between the ileoce-
lactose-containing foods.24 Amylase levels are actually cal junction and the cloacal coprodeum. Except in the
highest in the jejunum, but the jejunum and ileum can- ostrich, it is very short and has a smaller relative diame-
not be readily differentiated from the duodenum in ter than the mammalian large intestine and is struc-
birds. In general, the jejunum is thought to begin just turally dissimilar, being similar to the small intestine
after the ascending duodenal loop begins to turn back except for having shorter villi that are richer in lymphoid
on itself, where the jejunal branches of the cranial follicles. The avian rectum exhibits marked retroperistal-
mesenteric artery begin. The ileum is thought to begin sis, carrying urine from the urodeum and coprodeum
at the vitelline (Meckel’s) diverticulum and end at the into the colon up to the ceca.6 This allows for further
recto-cecal junction.6 There is great variation in jejunal water resorption in the colon and hence aids in water
and ileal anatomy in different species. conservation. In the pigeon the rectum enters the
coprodeum from the right side, whereas in the parrot it
Nectarivorous and insectivorous birds have shorter intes- enters from the left side at a 60 to 90° angle.6
tines than do similar sized granivorous or herbivorous
species.25 This is believed to be due to the highly CLOACA
digestible nature of their diet.
The avian cloaca is a three-chambered structure that is
The intestinal epithelium contains villi, microvilli and responsible for the terminal deposition of digestive, uri-
crypts. The villi’s increased surface area allows efficient nary and reproductive products. It is much wider than
absorption of nutrients and their rich capillary system the rectum. The first, most proximal chamber, is the
enables transport of these nutrients to the portal blood coprodeum into which the rectum empties. It is the
system. A thick layer of mucus produced by goblet cells largest chamber of the psittacine cloaca and has a flat,
in the epithelium protects the intestinal epithelium from vascular, avillous mucosa, covered by columnar epithe-
the digestive juices and from physical abrasion, particu- lium and an extensive branching vascular pattern.6,28 It is
larly anteriorly near the gizzard. Two muscle layers sur- separated from the second chamber, the urodeum by an
round the intestine, the inner circular and outer longitu- encircling sphincter-like ridge, the coprodeal fold. This
dinal layers that allow mixing and propulsion of the fold can completely close off the coprodeum from the
digesta through the intestinal tract. other chambers of the cloaca, preventing contamination
of eggs or semen during egg laying or ejaculation.
The avian duodenum is unique in its ability to exhibit
both normograde and retroperistalsis.6 These retrograde The urodeum is the smallest cloacal chamber in
peristaltic waves bring the digesta back towards and into psittacines, columbiforms and falconiforms. It receives
the ventriculus, as is evidenced by the presence of bile the ureters and also the oviduct in females and the duc-
staining in the ventricular koilin. These waves are power- tus deferens in males. The ureters enter the urodeum on
ful and visibly distinct from the normal peristaltic waves. either side of the dorsal midline, and in pigeons and par-
They occur every 15 to 20 minutes in the turkey20 and up rots these openings are simple. In females, the oviduct
to once a minute in parrots on a moderate fat diet.6 has a rosette-like opening on the left dorso-lateral wall. It
is smaller and less prominent in juveniles and hence dif-
The liver also empties into the distal duodenum via the ficult to visualize in these birds.28 A membranous tissue
bile ducts. Its primary digestive function is the production may occlude this opening in females that have not yet
of bile acids and salts that assist in the emulsification of laid in species such as the ostrich.29 In males, the ductus
fats, allowing their digestion by lipases. These acids and deferens enters the urodeum on symmetrical, raised
salts, together with cholesterol and phospholipids, are papillae located on the left and right dorsolateral walls. It
secreted into the bile canaliculi that drain into the bile is separated distally from the proctodeum by the uro-
duct. Gall bladders are present in raptors and waterfowl, proctodeal fold. The urodeal mucosa is smoother and
but are absent in many psittacines and pigeons.6,26 less vascular than that of the coprodeum.
417
The urodeum exhibits retroperistalsis, pushing urates

and urine cranially into the coprodeum and rectum
Gastrointestinal Diseases
where water and solutes are further resorbed, thus maxi-
DISORDERS OF THE BEAK
mizing water conservation.6,21,30 This retroperistalsis
explains why urates and feces are sometimes intertwined Deformities
when passed from the cloaca. Deformities of the bill of young birds, both congenital
and acquired, have been described. Congenital deformi-
The proctodeum is the final cloacal chamber and is ties have been mostly described in poultry and water-
slightly larger than the urodeum in most species. The fowl. Some of these are part of a more generalized prob-
uroproctodeal fold is more developed dorsally and grad- lem, such as Micromelic Syndrome of white Pekin duck-
ually loses prominence ventrally. This chamber is the lings, an autosomal recessive mutation which causes a
most frequent site of papillomas in psittacines. It also short maxilla, reduced overall size, shortened limbs, cer-
gives rise to the Bursa of Fabricius on the dorsal midline vical subcutaneous edema and abnormal feathering.32
just caudal to the uroproctodeal fold. The bursa is most Others are specific to the beak such as variations in the
prominent in the juvenile bird where its lymphoid tissue shape and curvature causing malocclusion, often leading
is responsible for the production of B-lymphocytes. In to the maxilla being caught inside the lower mandible
(prognathism) (Fig 14.2).33 “Scissor-beak” is a condition
mature birds the lymphoid tissue involutes but the
where the upper beak rhinotheca is bent to one side,
bursa’s opening and chamber frequently persist and can
resulting in the overgrowth of the gnathotheca in
be viewed during cloacoscopy. The timing of bursal invo-
psittacine chicks (Fig 14.4a). The condition becomes
lution is usually between 2 and 6 months of age, but progressively worse due to the continued forces applied
varies between species.6 during the bird’s normal beak usage and as the chick
grows.34,35 It has also been noted in other avian species
The cloacal blood supply is via the pudendal artery and
such as ostriches,36 softbills and passerines32 where either
vein. Innervation is via the pudendal nerve that follows the mandible or maxilla may deviate. Multiple potential
the ureters to the dorsal cloacal wall where the cloacal etiologies have been described including heredity, incu-
ganglia are found.28 These are important surgical land- bation problems, malnutrition, infectious sinusitis, viral
marks. diseases and trauma.36,37,38*
The final structure of the gastrointestinal tract is the In young psittacines, incorrect hand feeding techniques
vent, a transverse opening in the ventrocaudal body wall may result in bruising of the rictus on one side of the
through which body wastes and reproductive products beak, leading to uneven growth and scissor beak.38,39
*
Eds. Note: In most psittacine rearing facilities establish-
are expelled. It is demarcated by lips dorsally and ven-
ing a formulated diet program for adults and young-
trally and is surrounded by voluntary muscles that form
sters has eliminated these problems completely. Facial
a sphincter. This provides birds with some control over
bones are not as malleable in properly fed parents or
defecation. For example hens that are incubating may
their offspring. Treatment involves altering the forces
pass a large urofeces in the morning when nest that direct the rostral growth of the affected part of the
changeover occurs. Some psittacines can also be toilet beak. Surgical techniques to achieve this have been
trained to defecate on command. The act of defecation described.38,40 In addition, revision of incubation and
involves the partial eversion of the vent lips, resulting in chick feeding practices and nutrition may be warranted.
the formation of a circular orifice through which feces,
Mandibular compression has also been described in young
urates and urine can be expelled.1
macaws.35 Prognathism, where the upper beak tucks into
Cloacal “sucking” has been noted in psittacines in juve- the lower beak, is another congenital beak deformity
sometimes seen in chicks, particularly cockatoos.35,41 The
niles and breeding females, where material is brought in
etiology of this condition is unknown. If attended to early,
from the outside via the vent lips under negative pres-
it can be corrected with physiotherapy by applying trac-
sure.28,31 In chicks, this is thought to have an immune
tion rostrally to the maxillary beak several times daily. If
stimulation function by exposing the B cells in the bursa
the maxillia is calcified, physiotherapy and beak trimming
to external antigens. In breeding females it is thought to may help.42 In more severe cases, dental acrylic prostheses
facilitate sperm transport and hence fertilization in (Fig 14.3) can be applied to the tip of the maxillary beak
species where the male lacks a phallus.31 See Chapter 18, to force it to stretch out over the mandible41 or KE wires
Evaluating and Treating the Reproductive System for fur- and rubber bands or cable ties can be used in a modified
ther discussion of the vent. Doyle technique (Figs 14.4a-f, 14.5a-f).40
Greg J. Harrison
Greg J. Harrison
Fig 14.2 | Baby umbrella cockatoo with mandibular Fig 14.3 | Acrylic applied to beak tip
prognathism. to allow new growth pressure to over-
come the prognathic condition. A metal
transverse pin made from a hypodermic
needle is often implanted to help the
acrylic maintain adhesion to the beak.
Crusty scab-like lesions at the commisures of the beak owner is prepared to accept the care and cost involved
have been associated with biotin and pantothenic acid with long-term management. Loss of the distal third of
deficiencies in gallinaceous birds and ostriches.36,43 the bill has potential for regeneration, at least in
Vitamin D and calcium deficiencies have resulted in soft psittacines,48 but not in other species such as ostriches
beaks due to insufficient mineralization in many (Struthio camelus) in which beak growth stops in adult-
species.33,44 Malnutrition and hypovitaminosis A were hood.37 Trimming and reshaping using a mild grinding
associated with significant beak deformities in hand- tool, such as an electric motor drill, can treat minor dis-
reared African grey parrot (Psittacus erithacus) chicks tal fractures. Rhamphothecal fractures can be stabilized
(see Chapter 5, Calcium Metabolism).44 These were seen with tissue glues such as cyanoacrylate (Figs 14.6a-i).49,50
as significant grooved ridges and indentations of the More serious fractures may require surgery with pins,
rhinotheca and gnathotheca. Birds with rhinothecal wires, sutures, plating or acrylic remodeling techniques,
overgrowth characterized by intralaminal hemorrhages depending on species, patient size, nature and location
have often been diagnosed with previous or current liver of the injury or fracture (Fig 14.7).37,47,51,52 It should be
disease and malnutrition.44 Assessing liver function, cor- noted that fractures and avulsions of the upper rham-
recting the diet and trimming the beak as required are photheca are the most challenging due to the kinetic
all useful management tools. nature of the maxilla (in psittacines), the forces exerted
and the presence of small bones.47 Damage to the germi-
native layer of the rhamphotheca or gnathotheca or of
Traumatic Lesions
the underlying bone means that the affected area will
Traumatic lesions to beaks are amongst the most com- not regenerate keratin (Fig 14.8).50,52 If the associated
monly seen problems. These frequently occur as a result beak structure has been avulsed and if the damage is
of intra- or interspecific aggression, parent birds that great enough, the entire mandible or maxilla may be lost
mutilate chicks, accidents or predator attack. Iatrogenic and not regenerate. Acrylic prosthetics have been used
causes have also been described from incorrect han- as a temporary means of restoring beak function and
dling, use of mouth specula or incorrect beak trim- appearance until new keratin growth occurs.52 In perma-
ming.39 It should be remembered that the avian beak nent injuries, these prosthetic beaks need to be remod-
lacks a subcutis, and hence the thin dermal fibrovascular eled, replaced or reapplied on a regular basis, as they
stroma is directly apposed to the periosteum. Therefore invariably work loose. In cranes, this is every 3 to 6
pressure necrosis of parts of the rhamphotheca and months.53 Natural prosthetic devices have been success-
gnathotheca can lead to permanent beak defects.46 fully used in toucans utilizing the beaks from dead birds
Immediate treatment for trauma cases involves stopping of the same or similar species. The surgeon should
hemorrhage, counteracting shock via fluid therapy, pro- instruct the owner that these prostheses are also, like
viding analgesia and preventing infection. Nutritional the acrylic or metal repairs, only temporary.47
support then needs to be provided.39,47 The decision as
to how to best manage the injuries needs to be made Palatine bone luxation has been described in blue-and-
early, to decide if indeed the bird is salvageable or if the gold macaws (Ara ararauna) following trauma in which
419
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 14.4c | The final shape of the transverse
sinal pin for a beak traction technique.
Fig 14.4a | Scissor beak in an Fig 14.4b | Bands used for beak ortho-
umbrella cockatoo. donture. A electrician’s black cable tie and
an orthodonture rubber band are shown.
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 14.4d | Band applied to beak with Fig 14.4e| Bandage material is placed over the Fig 14.4f | Several weeks after
enough pressure on the transverse rubber bands to avoid removal or becoming correction and removal of appliance.
sinal pins to correct the deviation. snagged. Traction was applied for 2 weeks.
the palatine bones became hooked onto the interorbital PCR or HA (hemagglutination assay)55,56 for presence of
septum.40,54 The luxation was reduced under general the virus or HI (hemagglutination-inhibition) for anti-
anesthesia by using digital pressure on the maxilla both body levels.56 Histopathology of affected tissues is also
directly and via an intramedullary pin placed through useful. Severely affected birds are usually euthanized, as
the infraorbital sinuses.54 there is no specific treatment for this disease except for
supportive care which includes maximizing hygiene,
Infectious Causes of Beak Malformation providing soft foods, treatment of any secondary infec-
tions and immunostimulation.
Various infectious disease processes can involve the
beak. Psittacine circovirus disease (Psittacine Beak and Poxvirus infections are seen on the unfeathered regions
Feather Disease) infects numerous psittacine species, of many avian species, but less commonly in psittacines.57
both wild and captive, where it can cause beak lesions as This Avipoxvirus classically causes raised lesions which
part of the chronic presentation of the disease, particu- may or may not become necrotic and then secondarily
larly in young cockatoos.55 Affected beaks typically infected. These may be found on the beak or at the
become abnormally elongated and may develop trans- beak/skin margin and also in the oropharynx. The beak
verse or longitudinal fractures.56,57 In some cases only the and mouth may become painful and disfigured, and the
tips may be fractured. There may be necrosis of the bird may show reluctance to eat. Transmission requires
palate and ulcers of the mouth. As the disease pro- direct contact with open wounds or inoculation via an
gresses, the beak may fracture and avulse, exposing the insect vector. In one case, the basal layers of the beak
underlying bone, which can be very painful. Secondary epidermis were infected causing sloughing of the kera-
bacterial and fungal infections may complicate the infec- tinized layers.57 Although species-specific strains are trans-
tion and cause life-threatening disease. Diagnosis is by mitted by mosquitoes, cross-species infections may occur,
Greg J. Harrison
Greg J. Harrison
Fig 14.5a | Young cockatiel that was having its beak ground as Fig 14.5b | A hypodermic needle is used to pre-drill a hole in
a first step in the therapy for prognathism. the frontal bones. Then a stainless steel pin is placed trans-
versely through the frontal sinus.
Greg J. Harrison
Greg J. Harrison
Fig 14.5c | The first hook is bent into one end. Fig 14.5d | A second bend is made in the transverse pin and a
second S-shaped pin is formed and inserted in the distal
rhinotheca.
Greg J. Harrison
Greg J. Harrison
Fig 14.5e | An orthodonture rubber band is placed around the Fig 14.5f | The finished traction device is in place. The extra
left dorsal transverse sinus pin’s hook and the ventral S-pin. A length of the rubber bands have been cut off just above the
hemostat is placed around the tensed rubber band and stainless stainless steel suture retention knot on the rubber bands. A
steel suture is placed to keep the traction on the rubber band plastic protective collar has been placed on the bird.
once the hemostat is removed. The unused portion of the band
is cut off.
421
Greg J. Harrison
Greg J. Harrison
Fig 14.6a | A sun conure has been bitten by a larger bird. The Fig 14.6b | An electric motor drill has a small shank shim replac-
walls of the rhinotheca are fractured and compressed into the ing the larger variety. This allows the use of a small dental burr to
maxillary sinus diverticulum of the infraorbital sinus. hone out the damaged rhinotheca and bone seen in 14.6a.
Greg J. Harrison
Greg J. Harrison
Fig 14.6c | A dental burr is used to hone out the damaged tis- Fig 14.6d | Microsurgical forceps grasp the slab and bone and
sue around the edges of the depressed slab of rhinotheca and remove it from the site to avoid a sequestration.
bone.
Greg J. Harrison
Greg J. Harrison
Fig 14.6e | The rhinal cavity mucosa was not penetrated so an Fig 14.6f | A thin layer of cyanoacrylic solventb is layered over
absorbable layer of calcium hydroxidea is applied as a bed for the calcium layer.
the regrowth of the bone, periosteum and rhinotheca. This layer
is dried. The warm air from the electric motor can hasten this
step.
Greg J. Harrison
Greg J. Harrison
Fig 14.6g | Powdered dental acrylic resinc is sprinkled over the Fig 14.6h | The process has been repeated on both sides of
solvent layer, and the powder liquifies. the conure’s damaged maxilla. In a couple of weeks the acrylic
will dehisce and the underlying tissue continue to heal with no
further attention. No antibiotics or antifungals were used pre- or
Greg J. Harrison post-operatively.
Greg J. Harrison
Fig 14.6i | The kit used to perform the procedure, 14.6 a-h.
Fig 14.7 | A fractured mandibular symphysis has been

repaired using a pair of S-shaped hooks like those used in Fig.
14.5d,e. One is placed on each side of the fracture site and the
impaction bands applied. A layer of acrylic helps hold the pins
and protects the fracture site.
Greg J. Harrison
Fig 14.8 | This gray-cheeked conure had a proximal traumatic

maxillary amputation, involving the germinal area, and will likely
not regrow. The conure is shown several months post-injury.
usually with less pathogenic consequences.58 Diagnosis is Disinfection with lipid solvents (eg, quaternary ammo-
by viral culture or histopathological demonstration of nium compounds, sodium hypochlorite) and exclusion
proliferated epithelial cells with intracytoplasmic inclu- of potential insect vectors will help to stop further spread
sions or Bollinger bodies. No specific antiviral treatment of the infection. In outbreak situations, euthanasia of
exists but lesions can be topically debrided and treated severely affected birds may be carried out. Vaccines are
with antimicrobials for secondary infections as deemed also available for some strains.59
necessary. Systemic antibiotics and fluid therapy along
with supplemental vitamin A may aid recovery. Avian polyomavirus (APV) has been seen to cause tubu-
423
lar elongation of the lower mandible in Gouldian finch

(Erythrura gouldiae) juveniles that have survived out-
breaks of the disease.60 These birds also exhibited
delayed fledging and did not grow well. Other passerine
infections with this virus have been associated with out-
breaks of sudden death.61 It has been postulated but not
proven that recovered passerines may in fact become
persistently infected and may shed the virus intermit-
tently. Vertical transmission of the virus through the egg
has also been postulated.61
Parvovirus infection in ducklings reportedly caused
Bob Doneley
stunted beaks with protruding tongues in survivors.62
Primary bacterial and fungal infections of the beak are

Fig 14.9 | Knemidocoptes mites and gross over-growth of the
usually associated with trauma. They may cause necrosis,
beak.
inflammation, hemorrhage, hyperkeratosis and the accu-
mulation of necrotic debris with or without malodor.
Cytology, culture and sensitivity are required to diagnose hyphae were detected in the beak matrix but no species
these infections. identification was presented.
Cryptococcosis has been associated with proliferative Knemidocoptes spp. mites can cause proliferation and
masses causing disruption of the nares, rhamphotheca inflammation of the psittacine beak (Fig 14.9) and are
and deeper beak and sinus structures in several psittacine commonly seen in budgerigars, particularly young or
species.63,65 In some cases these lesions may be mistaken immunosuppressed birds. Close inspection reveals the
for neoplasms. They are characterized by gelatinous exu- characteristic honeycomb patterning resulting from the
dates which, when stained, contain large oval budding mites tunneling into the skin. In chronic lesions, the ger-
yeasts (4 to 7 µm) surrounded by a capsule 2 to 4 times minal layer of the rhinothecal and gnathothecal epithe-
the diameter of the cell.64,65 Gram’s stain, India ink, and lium can be so disrupted that permanent beak deformi-
Wright’s stain have all been used to diagnose this infec- ties result. Diagnosis is by way of skin scrapings. Treat-
tion cytologically. It can also be easily cultured on ment is simple with ivermectin/moxidectin, topical
Sabouraud- dextrose agar. There is usually little surround- ectoparaciticides or even paraffin oil over the lesion that
ing inflammation, restricted to mild numbers of epithe- suffocates the mites being successful. Spiruroid
lioid macrophages, multinucleated giant cells and het- (Oxyspirura spp.) infections in cranes have also been
erophils. Cryptococcus neoformans var. neoformans has a linked to beak deformities, as has trichomoniasis in
worldwide distribution, grows poorly at temperatures cockatiels.44
over 40° C and hence rarely causes problems in birds. It is
Mycotoxins from Fusarium spp. in moldy food have
commonly found in pigeon droppings. C. neoformans
resulted in beak deformities in poultry.32
var. gattii is restricted to river red gums (Eucalyptus
camaldulensis) and forest red gums (E. tereticornis) and
grows poorly above 37° C and is most commonly identi- Neoplasia
fied in avian infections.63 Treatments such as fluconazole A number of neoplasms involving the beak have been
orally at 8 mg/kg/day for at least two months, ketocona- described. Fibrosarcomas are considered the most com-
zole at 2 mg/kg BID per os gradually increased to 25 mon neoplasms of the beak, whilst squamous cell carci-
mg/kg bid per os and surgery to debulk the proliferative nomas and malignant melanomas are also seen. They
masses have all been suggested.63-65 However, recurrence cause distortion of the beak and surrounding tissue.
of lesions weeks to months after treatment is common, Cytology of fine needle aspirates or histopathology on
with early detection and aggressive therapy most likely to biopsy specimens provide a diagnosis, give information
yield favorable results. Cryptococcosis is a potential as to the likelihood of success with surgical debulking or
zoonotic infection so public health issues need to be con- chemotherapy and provide a prognosis for the patient.57,66
sidered before treatment is instituted.
Fungal infections causing beak necrosis in Gouldian DISEASES OF THE OROPHARYNX

finches (Erythrura gouldiae) have also been described.60 AND ITS STRUCTURES
Affected birds had rhamphothecas that were character- Diseases of the oropharynx are characterized by
ized by a flaky white or yellow appearance. Fungal anorexia, dysphagia, halitosis, gaping, rubbing of the
beak or more generalized signs of ill thrift such as monocytosis. Mycobacterium genavense has recently
lethargy and disheveled plumage. Direct visual examina- been recognized as the causative agent in many avian
tion of the oral cavity under illumination will reveal infections that were previously attributed to M. avium
most lesions, especially if magnification is used. This can subsp avium.70,71 M. tuberculosis has only infrequently
be done with the patient awake or under general anes- been responsible for disease in birds, even though it is
thesia. Further magnification in difficult to examine the primary cause of tuberculosis in people.72
places can be achieved via endoscopy. Offending lesions Mycobacteriosis is a chronic debilitating disease with
can be swabbed or biopsied and the material obtained the potential for zoonotic spread, particularly in the
can be stained on slides, cultured or sent for cytological immunosuppressed person.72 Therefore the decision to
or histological examination. treat or to euthanize is an important consideration.
Multiple drug therapy is essential if treatment is to be
Infectious Causes attempted due to the high level of resistance to any sin-
gle antimicrobial. Several treatment modalities based on
Various viral infections have been found to infect the
human trials have been suggested.73,74 Currently the com-
avian oropharynx. As mentioned previously, poxvirus can
bination of clarithromycin, ethambutol and rifabutin is
cause proliferative caseous lesions in the mouth and
esophagus. Pigeon herpesvirus (PHV-1) can cause the treatment of choice in humans and has been used
mucosal ulceration and diphtheritic membrane formation with enrofloxacin in psittacines with success (see Chapter
in the oropharynx, cere or beak commissure as part of 28, Implication of Mycobacteria in Clinical Disorders).74
the overall infection.44,67 It affects young birds and the
Candidiasis is a very common cause of stomatitis in
immunosuppressed most severely and should be sus-
birds, particularly in young, immunosuppressed birds,
pected in flocks that suffer repeated bouts of trichomoni-
those on antibiotics and in lorikeets because of the high
asis that are difficult to control. Spread is via fecal and
sugar content of some nectar mixes. The causative agent
pharyngeal secretions, and latent carriers are important
is usually Candida albicans, although other species may
reservoirs of infection.67 Diagnosis is presumptively based
be involved. It is opportunistic and can be a primary or
on the presence of basophilic and eosinophilic intranu-
secondary pathogen. It causes white oral plaques with a
clear inclusion bodies seen on histology or cytology of
caseous exudate. It is easily cultured and, when smears
affected tissue, particularly epithelial cells. Virus isolation
of lesions are made, the characteristic budding spores
and neutralizing antibody techniques are also available.
may be seen. Gram’s stain, Diff-Quik and new methylene
Abscesses and micro abscesses, plaques and granulomas blue stains may help visualization. Histopathology is
are consistent with a number of diseases including viral, required to confirm that the yeast is causing the infec-
bacterial, yeast and parasitic infections, hypovitaminosis tion, however the presence of large numbers of budding
A and even chemical burns. Bacterial infections in the yeasts or the presence of hyphal forms is suggestive.
mouth can be caused by a variety of bacteria. Some of the Treatment may be topical and/or systemic. Mild infec-
more frequently isolated pathogens include Staphylo- tions may respond to oral nystatin at 300,000 IU/Kg
coccus spp., E. coli, Klebsiella spp., Pseudomonas aerug- orally twice daily and/or topical chlorhexidine or oral
inosa and other gram-negative bacteria.37,44,68 The lesions miconazole formulations. More severe infections may
may be localized or cause a generalized stomatitis and require systemic antifungal therapy such as ketoconazole
are usually secondary to oropharyngeal trauma, other (10 to 30 mg/kg orally twice daily), fluconazole (20
infectious diseases or other causes of immunosuppres- mg/kg orally every 48 hours),75 flucytosine at 250 mg/kg
sion. Treatment should include systemic antibiotics based orally twice daily for 14 to 17 days or itraconazole (10
on culture and sensitivity results, local debridement, sup- mg/kg orally twice daily for 21 days).76
portive care, identification and, where possible, correc-
tion of underlying immunosuppressive factors. Parasites are another cause of oropharyngeal pathology.
Capillaria spp. are the most common nematode in the
Mycobacterial granulomas may sometimes be seen in the upper gastrointestinal tract. They may cause oral inflam-
mouth, though they are more commonly associated with matory masses, diphtheritic oral lesions or hemorrhagic
lesions in the intestinal tract and liver and other intra- inflammation of the commisure of the beak.75 They are
coelomic organs.69 Fine needle aspirates of lesions and more commonly found in the small intestine.77 They
acid-fast staining may reveal the presence of the myco- parasitize most species of birds including psittacines,
bacterial organisms within macrophages. Where possible, passerines, columbiforms, gallinaceous birds and rap-
cultures to speciate the type of mycobacteria should be tors.77,78 Affected birds exhibit head flicking, dysphagia,
carried out, although recently PCR testing that gives weight loss and diarrhea. The adult parasites are very
more rapid results has become available.70 Hematology is thin and can be difficult to see, but may be found in
characterized by a very high leukocytosis, often with a smears of lesions, as may their characteristic bi-opercu-
425
lated ova. Ova may also be detected upon fecal floata- thought to acquire infection through ingestion of
tion, but they are intermittent shedders of ova and pro- infected pigeons. However, freezing carcasses has
duce less than most ascarids. Their life cycle can be proven not to work (S. Hudelson, personal communica-
direct or indirect using earthworms as intermediate tion, 2004). Carrier states exist and are thought to be
hosts.77 They can be quite resistant to anthelmintics so responsible for reinfecting flock mates. Such birds
high doses may need to be instituted. Examples include should be culled. Treatments suggested include ronida-
benzimidazoles (fenbendazole 100 mg/kg once or 25 zole (6 to 10 mg/kg once daily for 7 to 14 days),
mg/kg daily for 5 days, oxfendazole 10 mg/kg,) lev- dimetridazole (100 to 400 mg/L drinking water),
amisole (40 mg/kg, beware of narrow safety margin); metronidazole (20 to 50 mg/kg twice daily) and carnida-
moxidectin 200 µg/kg (used up to 800 µg/kg by this zole (20 to 30 mg/kg once).75,77,78,81 A dose of 50 mg of
author).77,78 Ivermectin at standard doses (200 µg/kg) carnidazole has been reported to be most effective (S.
has been ineffective.78 Benzimidazole or levamisole Hudelson, personal communication, 2004). Note that
treatments should be repeated in 14 days. dimetridazole has a low safety margin and should be
Environmental hygiene to prevent reinfection and avoided in hot weather, during breeding or when racing
removing potential intermediate hosts are all important pigeons. Diphtheritic plaques may need to be removed
control measures. by debridement. Antibiotics for secondary infections
may also be required.68 Regular monitoring of flocks for
Spiruroids have been diagnosed in raptors, corvids and infection is recommended in pigeons and budgerigars.
other species, and may cause raised granulomatous reac-
tions in the mouth and crop. The worms, or their thick- Nutritional Causes
walled embryonated eggs, may be found in oral, crop or
Hypovitaminosis A can lead to squamous metaplasia of
fecal samples. Treatments include oral dosing with mox-
the oropharyngeal epithelium, particularly glandular
idectin77 and/or manual removal of adults. Contracaecum
epithelium, leading to plaque and granuloma forma-
spp. have been associated with severe oral infections in
tion.44,75,82 In psittacines, this typically involves the sub-
young piscivorous birds, particularly pelicans.44 In birds
mandibular or lingual salivary glands. Sometimes affected
of prey, Synhimanthus falconis has been reported in the
birds exhibit a subcutaneous swelling caudal to the
oropharynx44 and Serratospiculum amaculatum, a para-
mandible. The choanal papillae are often shortened and
site of the air sacs, can cause diphtheritic lesions of the
stunted. If severely damaged, the choanal papillae fail to
oropharynx, which need to be differentiated from those
regenerate, so caution is warranted when using this sign
caused by trichomoniasis.77,79,80 Their eggs can be found in
for diagnosis. Affected birds typically have a history of
oral mucus or in feces.
being fed a predominately seed-based diet. Dietary cor-
Trichomoniasis is commonly found in pigeons, budgeri- rection via parenteral vitamin A supplementation or use
gars and raptors and is occasionally seen in other of reputable formulated diets is needed. Some granulo-
species such as cockatiels, Amazon parrots, conures, mas may be excised surgically. Secondary bacterial infec-
tions may be found and should be treated as required. In
canaries and zebra finches.44,79 The causative organism,
gallinaceous birds, lesions are confined to the mucous
usually Trichomonas gallinae, can exist as different
glands of the pharynx and their ducts. Keratinization of
strains with different pathogenicities. In pigeons and
the glandular epithelium causes blockage of duct open-
raptors, white or yellow caseated plaques may be seen
ings, hence secretions and necrotic debris accumulate.
in the oral cavity. These usually extend to the crop and
These appear as small white hyperkeratotic lesions (see
esophagus and may go as far as the proventriculus.
These plaques may need to be differentiated from other
diseases such as candidiasis and poxvirus infection.
Budgies usually show no oral lesions. Affected birds Traumatic Causes
usually exhibit regurgitation, dysphagia, weight loss, Traumatic injuries can occur in the oropharynx due to
listlessness, palpable mucous in the oropharynx and fighting or accidental trauma. Injuries of the psittacine
crop and, in severe cases, vomiting blood and death. In tongue are common due to its frequent use as a probing
pigeons the disease may be generalized, infecting the and sensing organ. Tongues are very vascular, and in
liver, umbilicus and cloaca, especially in squabs. psittacines well muscled, so control of bleeding is a first
Diagnosis is via wet mount examination of oral lesions priority. This may involve the use of electrocautery or
or crop fluid, revealing the motile flagellated organism suturing. The birds may easily remove sutures. Some
under high power magnification. Warming samples authors have found the need to wire the beak closed to
increases protozoan activity. The life cycle is by direct prevent suture removal.75 In this case a pharyngostomy
oral contact between birds, and spread through com- tube may need to be placed until the wound heals.
mon drinking water is also important. Raptors are Caustic injuries can be caused by the ingestion of certain
chemicals, for example silver nitrate cautery sticks,

access to excessively hot foods or ingestion of tri-
chotecenes, especially T2 toxin.44 These often cause
anorexia and dysphagia due to the pain experienced.
Analgesia may be of added benefit in these cases, as well
as supportive care (pharyngostomy feeding, fluids,
antibiotics) until healing is complete. Foreign bodies
including wire, wood and plastic have also been known
to cause penetrating wounds.
Greg J. Harrison
Neoplastic Causes
Neoplastic diseases of the oral cavity have been docu-
mented and include epithelial and mesenchymal Fig 14.10a | Tubefeeding a sick bird is a frequent event
tumors.57 The most common problem seen in new world in an avian veterinary facility. The round ball tipped nee-
dles can make the job easier for one person.
psittacines is oral papillomatosis. Lesions range from
mild mucosal roughening to overt verrucous masses.
They can also be found in the crop, esophagus, proven-
triculus, and cloaca and have been associated with bile
duct carcinomas. Severe lesions can ulcerate, hemor-
rhage or cause gastrointestinal or distal reproductive
tract obstruction. Their exact cause is unknown.
Although histologically the lesions appear similar to
those of mammalian papillomaviruses, there is no
immunohistochemical or DNA evidence to support the
presence of an avian papilloma virus. Instead, her-
Greg J. Harrison
pesvirus is consistently being detected in these papillo-
matous lesions.83 True parrot papillomavirus has been
reported in only one African grey parrot.84 Squamous
cell carcinomas, fibrosarcomas and lymphosarcomas Fig 14.10b | The clear delicate esophagus can be pal-
pated for the tube presence or visualized by wetting the
have also been reported.85 They can be quite painful and right ventral-lateral cervical area. The ball is easily seen
cause inappetence. Diagnosis is based on biopsy and his- through the transparent esophagus and skin of the neck
tological examination. in small thin birds.
DISEASES OF THE ESOPHAGUS

AND CROP
Many of the diseases found in the oropharynx are, not
surprisingly, also found in the esophagus and crop. The
esophagus can be injured as a result of tube-feeding hematoma
(Figs 14.10a-c).
Infections
Viral infections such as poxvirus and herpesvirus have
Greg J. Harrison
been reported. Proventricular dilatation disease (PDD),

of suspected viral origin, may also affect the crop but
will be more fully discussed later. Bacterial infections,
Fig 14.10c | A similar feeding tube in a lovebird with a
both primary and secondary, are commonly seen with hemotoma in the crop area from trauma resulting from
crop diseases. In mild infections, there may be bacterial bruising that can occur from improper restraint and flail-
growth and mucosal colonization with little inflamma- ing when a bird is being tubed. Although this is very
uncommon, it is even less likely to occur if a speculum
tory response. Severe infections, however, are character-
and a soft catheter are used.
ized by hemorrhage, necrosis and sometimes fibrinopu-
rulent exudates of the mucosal surface.57
Typically, crop motility is impaired with delayed crop

emptying and regurgitation. Birds can quickly become
427
Greg J. Harrison
Greg J. Harrison
Fig 14.11a | A crop burn, usually in a handfeeding baby
that is fed scalding food heated by a microwave oven. The
area is soft and friable and is best allowed to form a scab Fig 14.11b | Several days after becoming a dark, hard scab
prior to any surgery. the burnt area will open allowing food to fall from the crop.
Topical acrylic glues can expand the time the scab is retained
and often can be kept in place long enough for the damage to
completely heal, avoiding surgery completely.
listless, toxemic, dehydrated and, if untreated, die. Yeast days. The dehisced wound, which is externally visible,
infections may also be involved, and the organisms are allows food to fall out of the crop as the chick is fed.
typical of Candida spp. infections. Candida spp. has Treatment involves addressing any dehydration and
also been described as a primary crop pathogen in some infection problems. It may be best to manage this
species, namely lovebirds (Agapornis spp.) and cock- condition medically for the first 3 to 5 days to allow the
atiels.86 As well as the clinical signs listed above, a palpa- burn to scab over and fully fistulate before surgery is
bly thickened crop wall may be found. Causative organ- attempted. Premature surgical closure usually results in
isms can be diagnosed via examination of wet and wound dehiscence due to continued necrosis of the sur-
stained smears obtained via crop washes and culture rounding skin that may not have been noticeable at the
and sensitivity. Treatment involves the use of oral topical time of initial surgery. Surgery involves anesthesia and
and/or systemic antifungals, crop washes, antiemetics debridement of the affected area, removing all dead and
and fluid therapy. Predisposing management factors discolored tissue, and closure of the deficit in at least
need to be addressed, particularly in hand-reared birds. two layers, ensuring that the crop and skin are closed
separately. Beware of reduced crop capacity immediately
A large number of endoparasites are known to infect the
post-surgery, until healing and crop expansion can occur
crop. The most familiar parasitic disease of the crop is
(see Chapter 35, Surgical Resolution of Soft Tissue
trichomoniasis, which was discussed previously. A host
Disorders).87 Other causes of crop trauma such as force-
of nematodes and trematodes can also be found in the
ful use of feeding/medicating tubes, bite wounds or for-
crop and esophagus. As well as Capillaria spp. already
eign bodies can be similarly treated. Caution — food
mentioned, Echinura uncinata, Gongylonema ingluvi-
traumatically placed subcutaneously or within the neck
cola (quail and gallinaceous birds) and Dispharynx
structures must be flushed and debrided immediately in
nasuata have all been found to invade the crop
the event feeding has caused a rent — let heal by sec-
esophageal mucosa.44,77
ondary intention healing (Figs 14.12a-f).
Noninfectious Diseases Ingluvial foreign bodies include food items, grasses,

Primary non-infectious diseases of this region include wood, metal and plastic items usually accidentally
crop burns, foreign body penetration, lacerations and ingested by birds. In hand-reared chicks, plastic feeding
impactions, hypovitaminosis A and ingluvioliths. tubes can come loose and be accidentally swallowed dur-
Excessively hot feeding formulas may lead to full thick- ing the vigorous head pumping which birds may do dur-
ness burns of the crop and skin in hand-reared chicks ing feeding. Diagnosing these problems is via history,
and occasionally in adults.44,85 The burns usually occur in crop/esophageal palpation, radiography (both plain and
the anteroventral region of the crop. Initially the area contrast) or endoscopy. The offending items can be
may appear just dry, but subsequently reddening and removed manually, endoscopically or surgically via an
edema may occur, followed by blistering and often ingluviotomy. Impactions of the crop frequently occur as
necrosis (Figs 14.11a,b). This process may take several a result of a sudden change of food. In ducks and poultry
a b
3
3
2
1 1
Greg J. Harrison
Greg J. Harrison
Fig 14.12a,b | A baby macaw an hour after having hand-feeding formula traumatically intro-
duced into the cervical neck tissues. This injury occurs from using a syringe for feeding. Macaws
“pump” hard and if the head is not controlled the syringe tip can penetrate the pharyngeal tis-
sues resulting in food being deposited into the cervical tissue. Edema and some hemorrhage also
adds to the swelling. The food must be flushed out within hours, or septicemia may be rapid and
overwhelming. 1. A normal crop with some food present. 2. Vertical swelling from food deposited
into tissues. 3. Horizontal swelling of tissues.
Greg J. Harrison
Greg J. Harrison
Fig 14.12c | An incision over the food swelling — avoiding the Fig 14.12d | The incision has reached the pocketed food and it
esophagus, crop and vascular structures of the cervical region. spills out.
Greg J. Harrison
Greg J. Harrison
Fig 14.12e | A cotton-tipped wood applicator enters the oral pene- Fig 14.12f | Rubber band seton tied in place. Flushing of the
tration wound and exits the neck incision. The cotton tip is grasped wound QID with Normosol®, and a tissue disinfectant is per-
with a forcep and the forcep is pulled up and out through the mouth. formed. Antibiotics and antifungals are administered in a hand
A cut rubber band is grasped by the forcep and pulled out of the inci- feeding formula that is fed via a silicone tube to assure the food
sion and tied in place to act as a seton to allow flushing for 2 days. gets into the crop.
429
it has been associated with sudden access to lush grasses

and sprouted grains.44 In caged birds, ad libitum supply
of grit has been associated with crop impactions and, on
occasions, this has resulted from the overzealous feeding
of grit to chicks.88 In raptors it is associated with the sud-
den availability of roughage in a previously low-roughage
diet. Diagnosis and treatment are as described for foreign
bodies.
Ingluvioliths are various mineral concretions that occa-

sionally develop in the crops of some birds, particularly
Greg J. Harrison
budgerigars. Calculi consisting of urates surrounding
seed husks, potassium phosphate, oxalate and cystine
have been described. The exact cause of these is not
known, but it is speculated that birds that have experi-
Fig 14.13 | The passing of whole seeds is characteristic of gas-
enced periods of starvation may have been forced to eat trointestinal disease. Many causes such as lead, parasites, PDD
seed husks and urates.44 In some instances these calculi and pancreatitis are possible.
become large enough that they need to be removed.
This can be achieved via endoscopy or ingluviotomy.
DISEASES OF THE PROVENTRICULUS
As well as the neoplasms mentioned in the oropharynx, AND VENTRICULUS
the crop and esophagus could suffer from tumors of Diseases of the proventriculus and ventriculus can have
smooth muscle origin such as leiomyomas and varying clinical signs ranging from regurgitation, weight
leiomyosarcomas. Although asymptomatic when small, loss, appetite changes (either anorexia or polyphagia),
they can become very large, necrotic and hemorrhagic. undigested seed in the feces (Fig 14.13) and lethargy.
They are characterized microscopically by interlacing Most diseases of these organs produce similar clinical
bundles of fusiform cells with moderate amounts of signs that make their identification more challenging.
cytoplasm.57 Carcinomas of the submucosal glands also
occur. They are often large, sometimes necrotic and
Infectious
hemorrhagic, and involve much of the esophageal or
crop wall with invasion into surrounding tissue.57 Perhaps the most common gastrointestinal disease is
proventricular dilatation disease (PDD). The suspected
cause is a virus. It has been diagnosed in over 50
Crop Stasis
species of psittacines, but also in several other avian
Crop stasis or “sour crop” is a clinical sign of disease, species including Canada geese, canaries, weavers, tou-
and not a disease in itself. Clinical signs include regurgi- cans, spoonbills and honeycreepers.89 It is characterized
tation, delayed crop emptying, a sour odor, inappetence, by a lymphoplasmacytic infiltration of peripheral and
dehydration, anorexia and listlessness.87 “Sour crop” is central nerve tissue. It commonly affects the myenteric
usually complicated by bacterial and or fungal infection plexuses supplying the gastrointestinal tract, resulting
that may be primary, but is more often secondary. Crop in atrophy of the smooth muscles of the crop, proven-
stasis is most often seen in hand-reared chicks and triculus, ventriculus or small intestine. This causes
results from poor management. Food fed at the wrong delayed gastrointestinal motility and organ dilatation. It
temperature or consistency, not allowing the crop to can also affect the Purkinje cells of the heart, the adre-
empty between feedings, poor hygiene, incorrect incu- nal medulla, the brain and the spinal cord. The lesions
bation temperatures and humidity and concurrent dis- can be very segmental which may explain the variation
ease are all examples of possible causes of crop stasis in in clinical signs seen.90
chicks. In adults, the condition can result from various
crop infections, systemic or metabolic disease, heavy Gastrointestinal clinical signs include progressive weight
metal toxicity, foreign body ingestion or even PDD. loss, regurgitation, crop impaction, passage of undi-
Normal psittacine crop floras include few gram-positive gested food and eventually death, usually within 12
bacteria and scant non-budding yeasts. Treatment of this months. An 80 to 120 nm enveloped virus has occasion-
condition involves identifying and treating the underly- ally been isolated from infected birds and has been used
ing disease, as well as crop flushes with mild antiseptic experimentally to induce infection in some birds.89 A
solutions, antimicrobial therapy as appropriate and sup- virus is certainly suspected but not proven. The virus
portive fluid therapy. See Chapter 7 Emergency and itself may not be the cause of the disease; however the
Critical Care. inflammatory response may be. However, its exact identity
is unknown at the time of writing. Diagnosis is based on is based on culture, with fecal cultures often taken.
finding lymphoplasmacytic infiltrates in ganglia and asso- Fecal Gram’s stain may also show gram-negative over-
ciated nerves of the myenteric plexus of the gastrointesti- growth. Candida spp. infiltrating the proventricular and
nal tract.90,91 However, given the segmental nature of the ventricular wall have also been documented, particu-
disease, it is difficult to know which area of myenteric larly in finches.60,76 Treatments as outlined earlier, opti-
plexus to biopsy. Thus, a positive biopsy is diagnostic but mal nutrition, hygiene and correcting predisposing
a negative biopsy does not rule out the disease.90 The stressors are all important management tools.
crop is considered the safest area from which biopsies
can be taken. Biopsy sections should contain blood ves- A number of nematodes have been diagnosed in the
sels, as these are most likely to contain nerve tissue. The avian proventriculus. Echinura uncinata, Gongylonema
proventriculus has a thin wall and acid secreting glands spp., Cyrnea spp., Tetrameres spp. and Dyspharynx
which make it a risky choice for biopsy. Similarly, ventric- nasuata have all been found. Ventricular parasites
include Amidostomum spp., Cheilospirura spp.,
ular biopsies are not recommended, as there is real risk
Epomidiostomum spp. and Acuaria spp.44,77 Of these,
of damaging the myenteric plexus.
Acuaria spp. appear to be the most commonly encoun-
Large amounts of the suspect virus are shed by infected tered. They are commonly found to infect finches, but
birds and transmission is proposed to occur via the galliforms are also susceptible. These “gizzard worms”
fecal-oral route.91 The virus is fragile in the environment are fine and hair-like and burrow just under the koilin
and, hence, hygiene and management are vital in pre- lining of the ventriculus, impairing gizzard function and
venting spread of infection. The virus’s environmental digestion of food. Affected birds usually exhibit ill thrift,
fragility may explain why epornitics occur more com- may have undigested seed in the droppings and die.
monly in indoor aviaries rather than outdoor collec- Secondary bacterial infections further complicate the
tions. Although many birds eventually die from this disinfection. The life cycle is indirect, so removal of insects
ease, some chronically infected parrots have been from the environment is important. Anthelmintics such
detected which have lived for years, intermittently shed- as ivermectin, moxidectin, benzimidazoles and
ding the virus. These may be reservoirs for reinfection levamisole have all been used with varying degrees of
in aviary situations. Although there is no cure for the success.77
disease, celecoxib, a Cox-2 NSAID, has been used to
Cryptosporidiosis is a protozoal disease usually seen to
improve clinical signs by decreasing the inflammatory
infect the intestine of immunosuppressed animals,
reaction around affected nerves.92 The dose given was
including birds. In finches, however, it has a predilection
10 mg/kg orally every 24 hours for 6 to 24 weeks.
for the proventriculus, where it causes necrosis and
Improvement in clinical signs occurred in 7 to 14 days.
hyperplasia of glandular epithelial cells.113 Finch isolates
Treatment was ceased once birds resumed normal body
are different genetically from other species and may rep-
weight, condition and diet. The longest survivor
resent a unique species of Cryptosporidium.114 Affected
reported was a blue and gold macaw (Ara ararauna)
birds show decreasing body weight and yellowish drop-
that finished therapy two years previously and remained
pings which may contain undigested seed. Azithromycin,
in normal physical condition, eating a normal diet and
roxithromycin, toltrazuril and paromomycin have met
had no radiographic signs of PDD and was negative on
with some success as treatments.113 Underlying immuno-
biopsy. However, no comment was made as to whether suppressive diseases or environmental stressors need to
virus particles continued to be shed in its stools. be identified and corrected.
Macrorhabdus, previously known as avian gastric yeast

(AGY) or megabacteria, have been reported to infect a Non-infectious
large range of pet and wild birds (see Chapter 30, Proventricular or ventricular foreign bodies are more
Implications of Macrorhabdus in Clinical Disorders). commonly encountered in ratites, galliforms and water-
fowl, but are also seen in psittacines and other species.
Bacterial infections in the proventriculus and ventricu- Psittacine chicks which ingest indigestible fabric fibers or
lus can be primary but are usually secondary to other bedding material such as ground corncob, kitty litter,
immunosuppressive or disease states. The organisms crushed nut shells, shredded paper, styrofoam, grit, plas-
most often associated with disease are gram negative tic, rubber or wood shavings may develop proventricu-
and include E. coli, Klebsiella spp., Salmonella spp. lar/ventricular impactions.44,75 In older parrots, these
and Enterobacter spp.85 These often affect the intestine, same items plus other cage or household items may be
thus giving clinical signs including diarrhea, maldiges- ingested. In flightless birds, and in particular ostriches,
tion/malabsorption, anorexia and weight loss. Diagnosis exposure of birds to a new substrate may predispose
431
them to proventricular/ventricular impaction. Other ill- triculus and macerated by the ventriculus leading to
nesses may lead to a depressed appetite or pica.115 rapid absorption. The mucosal linings become very irri-
Affected birds classically have poor appetites, pass scant tated, and in severe cases, the ventricular koilin may be
feces, exhibit regurgitation especially if force-fed, and damaged. Pancreatic damage may also be a result of zinc
are depressed and lethargic. Diagnosis is via radiogra- toxicosis. Affected birds may show variable clinical signs
phy, endoscopy, palpation (in larger species) or which include inappetence, decreased fecal volume,
exploratory laparotomy. Where nails or other ferric com- regurgitation and vomiting, ileus, green diarrhea,
pounds are suspected, this author has also seen metal polyuria, polydypsia, CNS signs (particularly with lead
detectors successfully used. Fiber will only show up on poisoning) and feather picking.118,120 Lead poisoning in
gastroscopy (Fig 14.15). waterfowl causes weight loss, limb and neck weakness,
and bright green feces.119 A tentative diagnosis is based
Treatment depends on the severity of the impaction, or on a suggestive history, clinical signs and the presence of
the nature of the foreign body ingested. If the bird is radiodense particles within the gastrointestinal tract on
bright, the impaction is not complete and the offending survey radiographs. However, the client is often unaware
item is capable of being passed by the bird, then medical of exposure to heavy metals, the clinical signs are non-
treatment may be adequate. This may include supportive specific and the heavy metal is not visible on radi-
fluid therapy and antibiotics, the administration of psyl- ographs. Definitive diagnosis is based on the presence of
lium (beware in cockatiels) or paraffin liquid and force- elevated blood lead or zinc levels.90,118, 121,122 Elevated lev-
feeding with easily assimilated high-energy soft foods. els of amylase, CPK and uric acid may be found with
Metoclopramide may help stimulate small intestinal zinc intoxication.120 The acute cases respond well to
motility and thus assist in ventricular/proventricular chelation therapy with edetate calcium disodium (EDTA)
emptying. Prevention of access to the offending items is at 30 to 50 mg/kg once to four times daily by intramus-
also necessary. Attempts should be made to identify cular or intravenous injection, depending on the severity
underlying disease states that have a bearing on the final of signs and amount of heavy metal ingested.90,120-122
outcome. Other chelating agents such as penicillamine given orally
at 55 mg/kg twice daily can be used in conjunction with
Some items may be able to be removed endoscopically. CaEDTA.118 Succimer is the preferred oral lead chelator
This can be done through the mouth or via an inglu- at 25 to 35 mg/kg orally twice daily.81,118 Concurrent par-
viotomy. In the ostrich, a technique of proventricular enteral fluid therapy is essential for rehydration and
flushing is described.116 With the bird held firmly above assisting excretion of the metals. Where gastrointestinal
the tarsus, it is turned upside down, its glottis closed function permits, gavaging of high energy/electrolyte flu-
and a hose connected to a steady stream of water is ids and lubricants such as mineral oil, peanut butter,
passed from the mouth to the proventriculus. Massaging psyllium, magnesium sulphate or sodium sulphate have
the proventriculus helps to loosen the impaction. The all been suggested. These products have been found to
loosened material often passes out the mouth with the be ineffective in waterfowl.118 Antibiotics for secondary
hose in situ. This is repeated until clean water passes bacterial infections can be given and antiemetics and
out the mouth. Needless to say, this procedure requires intestinal prokinetic agents (eg, metoclopramide) may
considerable manpower but is useful where general also be helpful. If possible, the offending particles
anesthesia is not an option and medical therapy has should be removed via endoscopy or ingluviotomy/gas-
failed. In many cases, however, surgery is indicated to troscopy. Particles that have a ferrous or iron base can
relieve the impaction or remove the foreign body. These also be removed by inserting a feeding catheter
techniques have been described elsewhere.115,117 equipped with powerful neodymium-ferro-borium alloy
magnets (Fig 14.14).44 Pure lead, zinc, or many of their
Heavy metal toxicities can also lead to gastrointestinal, alloys cannot be removed with a magnet. It should be
renal and CNS signs as part of their pathophysiology. remembered that lead is not normally found in animals,
Psittacines in particular fall victim to inadvertent acute as it is not involved in any normal biochemical path-
lead and zinc intoxication due to their curious nature way.118,122 It also accumulates in the body over time. Zinc
and penchant for chewing any object they may find. on the other hand is an essential trace metal and so
Items varying from galvanized cage wire to paint, curtain needed in low levels. It is not stored in the body over
weights, stained glass windows, jewelry, coins, wine bot- time but is excreted.118,121 Chronic zinc toxicities are thus
tle foil, toys and mirror backing are possible sources for due to continued or repeated exposure.
these heavy metals.118 Waterfowl ingest lead shot whilst
feeding, mistaking it for gravel.119 Falcons ingest lead by Ulceration of the proventriculus occurs occasionally in pet
eating prey that has been shot. The ingested heavy metal birds but more commonly in flightless birds secondary
pieces are acted on by the acidic content of the proven- to foreign body ingestion or disease states. No common
Greg J. Harrison
Greg J. Harrison
Fig 14.14 | A set of magnets installed in the end of a rubber Fig 14.15 | Nylon fiber retrieved from the proventriculus of a
catheter that have attached to copper coated ferrous shot. This cockatiel on a seed diet that was allowed to pull apart a nylon
device can be used to remove ferrous metals, some of which can carpet.
be galvanized and thus contain zinc and/or lead in toxic amounts.
etiologic agent has been identified, but a link has been Surgery of the gastrointestinal tract is discussed in
suggested between chronically stressful environments Chapter 35, Surgical Resolution of Soft Tissue Disorders.
and the occurrence of proventricular ulcers.90 Ulceration
may also be secondary to zinc toxicity.85,121 Clinical signs DISEASES OF THE INTESTINES
are non- specific but may include anorexia, regurgita- AND PANCREAS
tion, gastrointestinal pain, lethargy and melena. Once an
Intestinal tract disorders usually manifest themselves
ulcer perforates, most birds will die from sepsis and
clinically as changes in the color, bulk and nature of the
shock within 6 to twelve hours.90 Thus, early detection of
feces produced. Thus, diarrhea, maldigestion, volumi-
an ulcer is imperative but can be difficult. Gastroscopy
nous droppings and/or melena may be evident in
should be considered in any patient with persistent
affected birds. Anorexia, depression and weight loss
signs of gastrointestinal pain or melena. Some of the
often accompany these enteric signs.
human rapid tests for melena are useful for detecting
the presence of digested blood in the feces of seed eat-
Infectious
ing birds.*
The majority of intestinal pathology is at least in part
*
Eds. Note: some debate continues on the specificity of attributable to infectious agents. By far the most common
such tests. cause of diarrhea in pet birds is due to bacterial infec-
tions, although these are seen less commonly in adult
There is a report of proventricular obstruction in an raptors.57,78,90 Gram-negative bacteria are most commonly
adult male eclectus parrot caused by a tubular diverticu- implicated. Enterobacteriacae are most frequently iso-
lum of the ventriculus.123 This diverticulum consisted of lated including E. coli, Salmonella spp., Klebsiella sp.,
dysplastic koilin and smooth muscle and caused com- Yersinia sp., Pseudomonas aeruginosa and Proteus sp.90
plete obstruction of proventricular outflow. No inflam- They can be both primary and secondary pathogens. The
mation, organisms or neoplastic changes were associ- gross lesions induced in the affected intestine include
ated with the lesion. The cause was undetermined. redness, exudation and occasionally ulceration. Histo-
logically, necrosis, fibrin deposition and predominately
Neoplasms of the proventriculus and ventriculus are heterophilic infiltrates are noted,57 although the bacteria
seen in a number of species, particularly in budgerigars may not always be present in all lesions.
and grey-cheeked (Brotogeris pyrrhopterus) and Amazon
parrots. Proventricular carcinomas are most commonly Gram-positive bacteria have also been responsible for
found at the isthmus and are usually flat rather than intestinal disease. Enterococcus hirae has caused enteri-
nodular.124 They are invasive, often extending through tis and septicemia in 10 psittacine species.126 Campylo-
the muscular layers and may reach the ventricular wall bacter spp. especially C. jejuni has been associated with
and serosa.57,125 However, they rarely metastasize.125 yellowish diarrhea and enteritis in many avian species
Clinical signs may include anorexia, regurgitation, including psittacines,85 passerines, waterfowl, galli-
weight loss, maldigestion and melena. Papillomas may formes107 and ostriches.127 Affected birds, which are often
occur as discussed previously and smooth muscle young, exhibit lethargy, anorexia, diarrhea and emacia-
tumors are uncommon.57 tion. Erythromycin and tetracyclines are the frontline
433
treatments for this bacterium.107 Clostridial infections intestinal capillaries is evident, and the enterocytes con-
have also been diagnosed in many avian species and are tain large basophilic intranuclear inclusions.57
known for their ability to produce potent toxins.107
Clostridium perfringens can cause necrotic enteritis and The intestine is the primary site of infection by various
foul-smelling feces in psittacines, ostriches,127 and other protozoal agents. Coccidia are some of the most wide-
species. C. tertium has been reported in a cockatoo with spread and well-known agents, consisting of several gen-
megacolon and chronic, foul-smelling diarrhea. This era affecting a wide range of birds. Coccidia’s patho-
resulted in severe dilation of the colon characterized by genicity may range from inapparent infections to severe
a lymphoplasmacytic inflammatory reaction. The sporu- hemorrhagic diarrhea and death. Eimeria is most com-
lated form of this bacterium has a “safety-pin” appear- mon in pigeons and galliformes, whereas Isospora is pri-
ance that is quite visible under Gram’s stain (see marily found in psittacines and passerines.129 Both
Chapter 4, Nutritional Considerations, Section II, species have direct life cycles, with transmission occur-
Nutritional Disorders). Anaerobic culture yields a defini- ring via ingestion of sporulated oocysts in fecal-contami-
tive diagnosis. Treatment involves the use of metronida- nated food or water.129 Disease is often precipitated by
zole (25 mg/kg orally twice daily)75 or clindamycin (100 stress. Diagnosis is via detection of large numbers of
mg/kg orally once daily).81,107 oocysts in the fecal wet smears or floatation. Antiproto-
zoal treatments include toltrazuril (7 mg/kg orally every
Mycobacteriosis is typically a chronic wasting infection 24 hours), sulfa-based drugs or amprolium.77,81 Crypto-
in birds, primarily affecting the gastrointestinal tract sporidiosis has been diagnosed in over 30 avian species
rather than the respiratory tract, as is the case with mam- and is considered an uncommon disease of the young
mals. Most avian species are susceptible. Waterfowl, and immunosuppressed (Figs 14.16a-c).130 The only con-
flightless birds, grey-cheeked parakeets, older Amazon firmed speciation in a non-galliformes was the detection
and Pionus parrots, budgerigars, siskins, Gouldian of Cryptosporidium meleagridis in an Indian ring-neck
finches, toucans and pigeons are particularly suscepti- parrot chick presented with diarrhea and delayed crop
ble.69,75 It is particularly a problem where birds are con- emptying.131 Treatment has been covered previously.
gregated. The intestine appears to be the primary site Microsporidia, primarily Encephalitozoon hellem, has
affected. The submucosa becomes infiltrated with large been diagnosed in lovebirds, budgerigars, Amazon and
numbers of histiocytes that contain many acid-fast organ- eclectus parrots132 and Gouldian finches.133 Infection has
isms. This affects the bowel’s ability to digest and absorb been linked to concurrent disease, especially circovirus
ingesta. Other granulomatous lesions may be found in infections,132 and other causes of immunosuppression.
the liver and spleen, the bone marrow and the respira-
tory tract. In other cases, only skin lesions are noted. Flagellated protozoa are also recognized as causes of
The course of this disease may take years. enteritis. Giardiasis has been diagnosed in a variety of
psittacines, poultry, waterfowl, finches and toucans.77
Primary mycotic intestinal infections are rare, but sec- Clinical signs vary from inapparent infections to weight
ondary invasion by Candida spp. or Zygomycetes spp. loss, failure to thrive, diarrhea75 or even feather picking in
are sometimes seen.57 cockatiels in the USA.134 Diagnosis is via direct fresh fecal
examination for the presence of the pear-shaped tropho-
Viral diseases can cause severe disease to the intestine.
zoites, trichrome fecal staining or ELISA testing. Treat-
PDD can cause segmental damage to the intestinal
ments used successfully include ronidazole, metronida-
smooth muscle, nerves and ganglia.
zole, dimetridazole and fenbendazole.75,77,134 Hexamita/
The clinical picture of paramyxoviruses (PMV) can Spironucleus spp. occasionally cause enteric signs of vari-
include diarrhea and melena. The pathogenicity, types of able pathogenicity in galliforms, pigeons and parrots.77, 134
lesions and clinical signs seen depend on the serotype They can be recognized by their cigar shape and rapid
and strain of the virus and the host’s susceptibility. PMV- motility and are more difficult to clear than are giardia.134
1, which causes Newcastle Disease, has caused gross Cochlosoma spp. cause lethargy and moist bulky drop-
hemorrhage (due to vasculitis of the intestinal wall) and pings, as well as dehydration and death in young
necrosis of submucosal lymphoid tissue in the intestines Gouldian finches being fostered under Bengalese finches.
of some birds.57 Adult birds are unaffected, although they may have
bulkier stools. The Bengalese finches act as an asympto-
Adenoviruses also cause hemorrhagic enteritis in matic carrier, as do a range of other finches, but not
psittacines, American kestrels and turkeys, and a green- adult Gouldian finches.135 The organism is characterized
ish diarrhea in pigeons and galliforms.57,128 In affected by its six anterior flagella and a helicoidal anterior ventral
psittacines, gross necrosis and hemorrhage are noted. sucker; it is diagnosed on wet mounts of fresh fecal sam-
Histologically, inflammation is variable, thrombosis of ples. Transmission is via the fecal-oral oral route, and the
Marc Kramer
Marc Kramer
Marc Kramer
Fig 14.16a | Acid fast stain of a fresh stool Fig 14.16b | Another form of cryp- Fig 14.16c | A necropsy specimen had a
specimen showing a form of cryptosporidium. tosporidium from the stool. Acid fast proventricular scraping acid fast stained. The
stain. tissue forms of cryptosporidia are shown.
organism appears to be very sensitive to antiprotozoal

drugs such as ronidazole and metronidazole.135
Nematode parasites are commonly diagnosed in

Australian psittacines, although other psittacines have
also been infected.129,136 Pigeons, galliforms, waterfowl
and toucans are just some of the other species suscepti-
ble. Nematodes are particularly a problem in wild-caught
birds or those housed in planted aviaries that favor the
parasite’s life cycle. Ascarids and Capillaria spp. are
most commonly diagnosed (Fig 14.17). They cause ill
Gwen Flinchum
thrift, weight loss, diarrhea and death. Transmission is
either direct by ingestion of embryonated eggs or indi-
rect via ingestion of an intermediate host, depending on
the parasite species. Diagnosis is via fecal floatation and Fig 14.17 | A lethal intestinal nematode obstruction in this
identification of the offending eggs. Treatments include Quaker parakeet is an unusual finding in captive raised pet
benzimidazoles, levamisole, ivermectin, moxidectin and birds in the USA. To compound the issue, a fecal exam for para-
sites was negative.
pyrantel (4.5 to 25 mg/kg per os repeated in 14
days).81,136 Capillaria spp. can be particularly difficult to
eradicate, and high doses of anthelmintics may need to larly cockatoos, African greys and eclectus parrots.129
be given. Beware of toxicities associated with high Infections may cause diarrhea, ill thrift and death, partic-
doses. For example, Columbiformes appear susceptible ularly in finches.138 Diagnosis is via the presence of
to toxicosis after treatment with fenbendazole or alben- proglottids in the feces. These may rupture, releasing
dazole at 50 to 100 mg/kg.137 Secondary bacterial infec- the eggs. Microscopically, the eggs contain the hexacanth
tions may also need to be addressed, and supportive larvae with six hooks on the oncosphere. In some birds,
care such as warmth, fluid therapy, nutritional support the cestode can be visible, protruding from the cloaca
and intestinal lubricants and laxatives may all be helpful. after defecation. However, proglottids may not always be
Environmental control is paramount. Avoiding contact shed or may not rupture, so infections can be missed.
with contaminated feces and providing a dry environ- Praziquantel (10 to 30 mg/kg orally, repeated in 14
ment to stop embryonation of eggs are all important. days)77,81,138 appears to be the most effective cestocide.
Decreasing environmental load and reinfection of an Avoidance of exposure to intermediate hosts is impor-
aviary by suitable housing and quarantining of new birds tant in control.
are all recommended.
Intussusception
Cestode infections can cause problems in the avian
intestinal tract. Since their life cycles are largely indirect Intussusception of the distal small intestine is less com-
and involve an intermediate host such as an insect, mol- mon in birds than in mammals and mostly occurs in gal-
lusk or arthropod, cestodes are more a problem of birds linaceous birds secondary to enteritis.44 As the proximal
with access to the ground.77,129 They are most common in segment telescopes into the distal segment, blood flow
insectivorous finches and parrots of wild stock, particu- is impaired and intestinal necrosis follows. Rectal intus-
435
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 14.18a | A malnourished female Fig 14.18b | Same budgerigar in (a) Fig 14.18c | The swelling was caused by
budgerigar with rhinal discharge over a showing swollen abdomen. massive fecal retention. A celomic mass, usu-
hyperkeratotic cere. ally a tumor, is involved in such an obstruc-
tion. Changing the angle of the vent allowed
Fig 14.18d | An intestinal 5-10 cc of feces to be removed, temporarily
obstruction resulting from auto- giving the bird and the owner time to decide
obstruction in a parrot due to a on the final fate.
necrotic intestinal lining slough.
The cause was never determined.
The necrotic section passed on
day 3 of tube feeding and fluids,
Greg J. Harrison
and the bird recovered.
susception may result in the rectum telescoping onto and contrast radiography may reveal dilated gas-filled
itself or into the coprodeum, where it may protrude bowel loops and identify the location of any obstruc-
from the vent lips. Both of these are medical and surgi- tions. Supportive therapy with fluids, antibiotics, particu-
cal emergencies, which may involve resection of the larly for anaerobes, and analgesia are all recommended.
offending piece of bowel using magnification, and very Corrective surgery may then be performed to either
fine sutures. (6-0 to 8-0).90 remove or relieve any obstructions or to resect any
debilitated sections of bowel.
Ileus
Neoplasia
Ileus or intestinal hypomotility/amotility can be caused
by both physical obstructions (in the intestinal lumen, Primary intestinal neoplasms include carcinomas, papil-
wall or as a result of external extra-intestinal compres- lomas, smooth muscle tumors and lymphosacoma.57,85
sion) and by poor motor function. Examples of the for- Lymphosarcoma presents as diffuse or nodular thicken-
mer include foreign bodies, neoplasia, heavy parasite ing that may be mistaken for other conditions such as
burdens, granulomas, strictures and various torsions and mycobacteriosis. Leiomyomas and leiomyosarcomas
adhesions. Paralytic ileus can be caused by enteritides, present as firm, red-brown masses within the intestinal
PDD, peritonitis, lead toxicity and thrombosis of wall and can only be distinguished from one another
splanchnic vessels.44 The impaired section of bowel histologically (Figs 14.18a-d).57
dilates with intestinal fluid and gas. The bird becomes
dehydrated. Ischemic necrosis of the intestinal wall leads DISEASES OF THE CLOACA
to further fluid and protein loss. Gram-negative bacteria
proliferate and produce endotoxins that can result in Infectious
shock. Death can occur within 24 to 48 hours. Depend- Speculums allow complete observation of the cloaca (Fig
ing on how acutely the bird is affected, clinical signs can 14.19). Internal Papillomatous Disease (IPD) can be
vary from vomiting, diarrhea, depression, listlessness, responsible for the irregular, cobblestone mucosal
anorexia, decreased fecal output and emaciation.44,90 In lesions seen in the psittacine proctodeum (Figs 14.20).
affected birds, abdominal palpation is resented.37,115 Plain IPD is one of the most common cloacal masses seen in
Greg J. Harrison
Espen Odberg
Fig 14.19 | A cloacal speculum can make observation of this Fig 14.20 | Gastrointestinal disorders often involve papillo-
complex structure much more understandable. The probe on the matosis. Any case of loose or smelly stool in a susceptible
left side is in the vagina of a female cockatoo with PBFD. The species should be investigated.
fold containing the vaginal orifice separates the urodeum from
the proctodeum. The bird is in dorsal-ventral position.
birds, particularly South American species. Moderate to involve impaired defecation with retention of urates that
severe lesions may lead to partial proctodeal obstruc- may cause dehydration. This may solidify and chemically
tion.31 Affected birds typically present with tenesmus, alter the urate mass, causing it to form a solid structure.
bloody droppings, malodorous feces, flatulence and Gentle removal, application of topical cleaning, antibi-
staining of the vent and tail feathers with urofeces. otic and anti-inflammatory agents, systemic antibiotics
Definitive diagnosis is via biopsy, but affected lesions will and regular monitoring of the affected area may be
usually blanch when dilute acetic acid is applied to required. In chronic cases, recovery can be slow and
them. Various treatments have been suggested. These characterized by repeated recurrences.
include sharp surgical excision, electrosurgery, silver
nitrate cautery, cryosurgery, laser surgery and mucosal Cloacal Prolapses
stripping.139 All procedures carry the risk of causing iatro-
genic traumatic cloacitis. Recurrences of the papillomas Cloacal prolapses are not uncommon in birds and can
are common. Some lesions spontaneously regress but take one of several forms. Oviductal prolapse occurs in
may recur. An empirical report of a commercial pepper egg-laying females that strain excessively to lay due to
diet allowing regression, as long as birds were fed the uterine or egg-related factors. These often need to be
diet, has been reported (G. Harrison, personal commu- surgically repaired, which may involve a hysterectomy if
nication, 2000) (see Chapter 32, Implications of Viruses the oviduct damage is severe. Endoscopy may need to
in Clinical Disorders). be performed to differentiate oviductal from rectal pro-
lapses. Idiopathic coprodeal prolapse is seen in male
Bacterial cloacitis is rare in most birds but can create sig- cockatoos in particular and less commonly in other
nificant pathology when it occurs. It can occur as a result psittacines. The exact cause is unknown, but it is sus-
of localized trauma (such as cloacoliths, chronic cloacal pected that affected birds have never been fully weaned,
prolapse), coexisting disease (such as internal papilloma- are bonded to their human companions and interpret
tous disease) or nutritional deficiencies. Candida spp. their owner’s behavior such as petting as sexually stimu-
have most commonly been isolated from the proctodeum lating. This is distinct from the overt masturbation exhib-
and vent lips but Trichosporon begielli has been found in ited by some cock birds in the presence of the owner.
one immunocompromised macaw.31 These infections Various surgical techniques have been described, includ-
should be treated with appropriate antimicrobials both ing cloacopexy of the ventral cloaca to the abdominal
topically and systemically, and any underlying causes need wall and ventplasty. Hormonal investigations and chemi-
to be corrected. cal and surgical neutering are all being evaluated.31
Behavioral modification may be appropriate. A true
Cloacoliths are firm aggregations of urates that collect in intestinal prolapse can occur if a rent from the cloaca or
the cloaca. They will at times also contain fecal material. rectum is opened into the abdomen (Fig 14.21).
They are often the result of iatrogenic intervention for
other cloacal disease (eg, surgery or during forceful cloa-
cal examination or sampling). The exact pathogenesis of Phallic Prolapses
cloacolith formation is unknown but is believed to Phallic prolapses have been described in waterfowl and
437
high fat meals, zinc toxicosis and secondary damage from

egg yolk peritonitis.141 Birds on all seed diets seem partic-
ularly prone to pancreatitis. Psittacines, particularly
quaker parakeets, may die suddenly from acute pancreatic
necrosis.57 The pancreas from affected birds appears pale
and firm and may exhibit variable degrees of hemorrhage.
There is often necrosis of adjacent fat. Histologically, the
lesions include coagulation necrosis of pancreatic acini,
Greg J. Harrison
intralobular hemorrhage and necrotic foci in mesenteric
adipose tissue.57 Zinc toxicity targets the pancreas, causing
vacuolation and degeneration of acinar cells. Grossly, the
Fig 14.21 | A massive intestinal prolapse contains the
pancreas may appear normal or exhibit mild parenchymal
congested pancreas. This can only occur from a fistula mottling.57
from the cloaca or rectum into the peritoneal cavity.
Diagnosis of pancreatitis can be difficult. Clinical signs
are non-specific but may reflect gastrointestinal dysfunc-
ostriches and result from excessive sexual stimulation, par- tion and pain. Vomiting, diarrhea, anorexia, lethargy,
ticularly in younger males, as well as other causes of phal- ileus, weight loss, polyuria and polydypsia and abdomi-
lic trauma and underlying systemic disease.139 Cleaning nal distension are some of the signs noted.140,141 Signs of
and replacement of the phallus in the ostrich so that the abdominal pain include kicking, feather plucking (espe-
tip is resting in the dorsal cloacal sulcus and sexual rest cially around the abdomen), falling off the perch, wide-
are the treatments of choice. Occasionally stay sutures based stance, sudden flight attempts, aggression and
across the vent may be required to keep the phallus in obsessive chewing. Measurement of blood amylase levels
place. Treatment with antibiotics and anti-inflammatories has been described, but absolute normal values are yet
may be necessary if the phallus has been traumatized.139 undetermined for most species. However, amylase levels
above 1,100 IU/dl are considered elevated.140,141 Increases
Neoplasia of only 2 to 3 fold may be attributed to extra-pancreatic
Cloacal carcinomas are infiltrative tumors leading to causes such as gastrointestinal disease (eg, small intes-
thickening of the cloacal wall. Smooth muscle cloacal tinal obstruction), renal disease or glucocorticoid admin-
tumors are infrequently reported.57 istration. Thus, interpretation of blood levels needs to be
done with care. Pancreatic biopsy is the method of
choice for diagnosing pancreatic disease. This can be
Diseases of the Exocrine Pancreas achieved via laparotomy or endoscopically through the
Although diseases affecting the pancreas will often right thoracic air sac. A histological examination may also
impair both endocrine and exocrine function, only the shed light on likely effective treatments and prognosis.
exocrine effects will be discussed here.
Treatments for pancreatitis are based on mammalian
Pancreatitis occurs when the digestive enzymes such as strategies.140,141 Fluid therapy to improve pancreatic perfu-
trypsin, protease and phospholipase are prematurely acti- sion is important. Converting birds onto low-fat pelleted
vated within the gland and begin to digest it. The result- diets is preferred to withholding food due to the high
ant damage to the cell wall leads to the release and activa- metabolic caloric requirements of most birds. Analgesia
tion of these enzymes into the ducts and extracellularly. (eg, butorphanol, carprofen) to counteract abdominal
Free radicals are produced causing further damage. The pain, intestinal motility stimulants such as metoclo-
initiating cause of this autodigestion can be difficult to pramide or cisapride to counteract intestinal ileus and
pinpoint, but several factors have been recognized.140 Viral parenteral antibiotic therapy are all of value in dealing
infections such as Paramyxovirus type 3, herpesvirus, with this disease. Any underlying causes should also be
polyomavirus, adenovirus and avian influenza A can cause treated (eg, zinc toxicosis). Some workers have used
necrosis and variable inflammation. PMV-3 can also cause omega-3 fatty acids for their lipid stabilizing and anti-
chronic pancreatitis leading to a firm and irregular pan- inflammatory properties.140,141 In life-threatening cases,
creas. Histologically, a variably lymphoplasmocytic inflam- plasma transfusions may help by replacing protease in-
mation can be seen, with the formation of lymphoid folli- hibitors and thus stopping further pancreatic damage.141
cles evident. Neophema spp. seem particularly susceptible
to this form of the disease.75 A number of bacterial agents Pancreatic enzyme therapy may help stop pain by
have also been associated with pancreatitis. Non-infec- inhibiting the endogenous production of pancreatic
tious causes include obesity associated with fatty diets or enzymes; it is useful in treating pancreatic insufficiency,
which may follow a bout of acute pancreatitis.141 Exocrine masses that have caused adhesions between viscera and
pancreatic insufficiency manifests in the production of peritonitis.57
pale voluminous feces. It can result from any chronic
inflammatory process that may affect the pancreas, Products mentioned in text
including those listed as causing acute pancreatitis. a. Hypo-Cal.® Calcium hydroxide. Ellman International, Inc., Hewlett, NY
www.ellman.com.
Pancreatic neoplasms can be either benign or malignant. b. Temp-Plus® Liquid. Ellman International, Inc., Hewlett, NY
www.ellman.com.
Birds suffering from IPD seem to have a high incidence
c. Temp-Plus Resin.® Ellman International, Inc., Hewlett, NY
of pancreatic adenocarcinomas142 that may present as www.ellman.com.
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129: Greiner EC, Ritchie BW: Avian Vet Aust Comm, Canberra, macaw. AAV Newsletter and 140. Speer B: A clinical look at the
Parasites. In Ritchie BW, ACT, 1998, pp 31-33. Clinical Forum. June-August avian pancreas in health and dis-
Harrison GJ, Harrison LR (eds): 133. Carlisle MS, Snowden K, Gill J, 2002, pp 7-10. ease. Proc Assoc Avian Vet, St
Avian Medicine: Principles and et al. Microsporidiosis in a 137. Howard LL, Papendick R, Stalis Paul, 1998, pp 57-64.
Application. Lake Worth, FL, Gouldian finch (Erythrura IH, et al: Fenbendazole and 141. Doneley B. Acute pancreatitis in
Wingers, pp 1007-1029, 1994. [Chloebia] gouldiae. Aust Vet J albendazole toxicity in pigeons psittacine birds. Proc Assoc
130. O’Donoghue PJ: 80:41-44, 2002. and doves. J Avian Med Surg Avian Vet Aust Comm.Echuca
Cryptosporidium and cryp- 134. Fudge A: Cockatiel disorders 16(3):203-210, 2002. VIC 2000, pp 261-267.
tosporidiosis in man and animals, seen in the USA. Proc Assoc 138. Filippich LJ: The effectiveness of 142. Kennedy FA, Sattler-Augustin S,
Int J Parasitol, 25:139-195, 1995. Avian Vet Aust Comm, Hobart, anthelmintics in finches. Proc Mahler JR, et al: Oropharyngeal
131. Morgan UM, Xiao L, Limor, J et TAS, 2001, pp 83-92. Assoc Avian Vet Aust and cloacal papillomas in two
al: Cryptosporidium meleagridis 135. Filippich LJ, O’Donoghue PJ: Comm.Currumbin QLD 1994, macaws with neoplasia with
in an Indian ring-necked parrot Cochlosoma infection in finches. pp 141-143. hepatic metastasis. J Avian Med
(Psittacula krameri). Aust Vet Proc Assoc Avian Vet Aust 139. Black D: Troubleshooting repro- Surg 10:89-95, 1996.
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CHAPTER
15
Liver
MANFRED HOCHLEITHNER, Dr med vet, Dipl ECAMS;
CLAUDIA HOCHLEITHNER, Dr med vet; LORI DANIELLE HARRISON, DVM
Hepatic dysfunction is among the most common med-

ical problems seen in companion birds.7,16 In many cases,
the involvement of the liver in the overall disease
process is not obvious. This chapter reviews the basic
pathophysiology, diagnosis, clinical signs and the current
therapies for liver disease.
The Role and Function

of the Liver
The liver is the largest organ in the body, but its relative
size varies among species. The liver performs many criti-
cal functions that maintain homeostasis. Liver functions
include synthesis of cholesterol and bile acids and the
generation and utilization of glycogen. It also is the site
for metabolism of various substances in preparation for
their excretion from the body via the bile or urine. It is
the site of production of plasma proteins, albumin, fib-
rinogen, lipoproteins and a variety of alpha and beta
globulins. The liver produces all clotting factors. The
liver filters from the blood infectious agents and foreign
materials that have been absorbed by the intestines. This
helps prevent these materials from gaining access to the
systemic circulation. Energy is produced by oxidative
phosphorylation and beta-oxidation of fatty acids in
hepatic mitochondria. This energy is used to sustain the
activity of the liver and to provide a reservoir of glyco-
gen for the body.
HEPATIC DYSFUNCTION
Hepatic dysfunction occurs after severe injury or
repeated significant insults. The liver has considerable
functional reserve and regenerative capacity. Only lesions
that affect the majority of hepatic parenchyma are likely
to produce the signs of hepatic failure. Focal lesions
rarely destroy sufficient parenchyma to deplete the liver’s
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by loss of normal hepatic architecture due to nodular

regeneration of parenchyma, fibrosis and, often, biliary
duct hyperplasia (Fig 15.1). Often, clinical manifestations
of hepatic failure do not occur until the end stage. The
cause of the hepatic damage that leads to end stage liver
failure frequently cannot be determined by the time
signs of hepatic failure are observed.
Diagnosis and Clinical

Signs of Liver Disease
Clinical signs of hepatic failure in birds are variable and
Fig 15.1 | The marked change in color and liver texture are can range from mild inappetence and inactivity to acute
characteristic of cirrhosis. hemorrhage and death. A large percent of liver tissue
must be affected before any obvious clinical signs are
observed because of the liver’s large functional reserve
reserve. The term hepatic failure implies loss of adequate
(Table 15.1).
function from either acute or chronic damage, however,
usually not all functions are lost at the same time.
All birds on a poor diet (seeds, poor-quality formulated
diets) should be presumed to have decreased functional
METABOLIC DISTURBANCES AS A hepatic mass (see The Improper Diet Cascade in
RESULT OF HEPATOPATHY Chapter 4, Nutritional Considerations: Section II,
Decreased hepatic function can be manifested by a vari- Nutritional Disorders). The liver’s ability to regenerate
ety of metabolic disturbances. The type and duration of may mask underlying liver disease in its early stages.
the disorder may influence the nature of the metabolic
perturbation. Coagulopathies, hypoalbuminemia, cuta- There are some clinical signs that are highly suggestive
neous manifestations and increased resistance in the of hepatic failure, however, none are pathognomonic.
blood flow through the liver due to fibrosis are common. Hepatic failure is associated with yellow or green discol-
orations of the urates and/or the feces, which may result
from biliverdinuria or bilirubinuria (Fig 15.2). Feathers
RESPONSE OF THE LIVER develop a glossy black color due to the exposure of
The destruction of hepatic parenchyma results in regen- melanin from total loss of normal green or blue pigment.
eration, fibrosis and/or biliary hyperplasia. The liver can Hepatomegaly and/or ascites may cause dyspnea. Weight
rapidly and efficiently regenerate lost hepatic mass. loss, poor feathering, diarrhea, overgrowth and bruising
Extensive hepatic necrosis is usually followed by paren- of the beak and nails, bruising or bleeding of the skin
chymal regeneration without scarring, as long as the
normal extra-cellular matrix remains intact. Chronic Table 15.1 | Clinical Signs of Liver Disease
hepatic injury most commonly manifests as fibrosis. Clinical Sign Non-specific More Specific
Early fibrosis may respond to treatment or removal of Anorexia ✓
the source of injury, but more advanced fibrosis is gener- Lethargy ✓
ally irreversible with the therapies currently available. Weight loss ✓
Hepatic fibrosis can be produced by a variety of hepatic Weakness ✓
injuries. The hepatic stellate cells change from the typi- Diarrhea ✓
Polyuria ✓
cal lipid-storing cells to cells with a myofibroblastic
Polydipsia ✓
appearance that subsequently develop the ability to syn-
Poor feathers ✓
thesize collagen, leading to hepatic fibrosis. Stellate cells
Dyspnea ✓
can be activated by various cytokines produced either by ✓
Green or yellow urates
inflammatory cells that infiltrate damaged hepatic Abdominal swelling ✓
parenchyma or by constituent cells of the liver (Kupffer Ascites ✓
cells, endothelial cells, hepatocytes). Damage to the Coagulopathies ✓
extracellular matrix also stimulates activation of hepatic Melena ✓
stellate cells, as do various toxins. End-stage liver disease Abnormal beak/nails ✓
or cirrhosis as a result of chronic fibrosis is characterized Malcolored feathers ✓
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Chapter 15 | E V A L U A T I N G A N D T R E A T I N G T H E L I V E R
443
Table 15.2 | Diagnostic Approach to Assess Liver

Disease in Birds
History
Baseline testing Complete blood count/chemistries/urinalysis
Non-invasive imaging Radiology and ultrasound
Screening for See Chapter 21, Preventive Medicine and
infectious diseases Screening
Liver function testing Bile acids
Abdominocentesis Culture, cytology, chemistries
Coagulation testing See Chapter 23, Diagnostic Value of Biochemistry
Liver biopsy Culture, cytology, histopathology
Table 15.3 | Radiographic Findings

Common
Radiographic
Findings Interpretation Comments
Hepatomegaly Hepatic lipidosis, The liver shadow of neonates
Fig 15.2 | Yellow urates. See Chapter 23, Diagnostic Value of cardiac-portal hyper- can appear bigger because
tension, infection (viral, the proventriculus in neonates
Biochemistry, for a discussion of biliverdin (green) versus biliru- bacterial, fungal) is relatively larger.
bin (yellow).
Normal Early stage of Normal size may indicate
hepatic size hepatopathies normal liver.
Microhepatia End stage cirrhosis, Species predilection exists:
and prolonged clotting time may be associated with congenital small liver, umbrella, Moluccan and palm
hepatic failure. Clinical disorders of any type that fre- emaciation, chronic cockatoos, macaws.
malnutrition
quently recur or are resistant to diagnosis and therapy
often involve liver malfunction. Diagnostic testing is used Table 15.4 | Hepatomegaly
to support the diagnosis of liver disease (Table 15.2). Common Causes in Neonates Common Causes in Adults
Normal neonate Obesity
Hepatic lipidosis Hepatic lipidosis
CLINICAL PATHOLOGY Hepatic hematoma Bacterial hepatitis: Chlamydophila
spp., Mycobacterium spp.
Analytes such as alanine aminotransferase (ALT), lactate
Viral hepatitis Lymphoma
dehydrogenase (LDH) and serum alkaline phosphatase
Lymphoma Hepatic adenocarcinoma
(SAP) are not sensitive or specific for liver disorders in
Fungal hepatitis
birds7,11 (see Chapter 23, Diagnostic Value of Biochem- Viral hepatitis: herpes
istry). Aspartate amino transaminase (AST) is sensitive Iron storage disease
but not specific for hepatocyte necrosis in birds because Ovarian disorders
AST also is released from damaged muscle tissue. AST
levels should be examined in conjunction with creatine
failure. Carotene pigments from the diet may be respon-
phosphokinase (CPK). If only AST is elevated, liver dam-
sible for yellow skin and plasma color.14 A study in broil-
age is more likely.
ers with gross hepatic bile duct lesions traced the yellow
Elevations of bile acids are often consistent with hepatic color of the pericardium and carcass to bilirubin.19 In
insufficiency and decreased liver function.16 Therefore, some cases, bacterial reduction may be responsible for
bile acid assays are useful in determining chronic, long- the degradation of avian biliverdin to bilirubin. One
standing and non-inflammatory states of decreased practitioner has found elevated bilirubin levels in cock-
hepatic function that may not be reflected in hepatic atiels with yellow urine, urates and feathers that were
enzyme elevation. Since food (protein) does not affect normally white, but turning yellow to gold (G. Harrison,
bile acids in psittacines, pre- and postprandial sampling personal communication). Other liver function tests are
is unnecessary. Species differences may exist. See available, but currently their use in the practical setting
Chapter 23, Diagnostic Value of Biochemistry. is limited. These tests include clearance of indocyanine
green and bromsulphalein.
An elevated white blood cell count (WBC) is common in
bacterial and fungal infections, while a depressed WBC
RADIOLOGY
is more common in toxic and viral disorders. Lowered
serum total solids, hypoalbuminemia, hyperglobulinemia, Hepatomegaly and microhepatia are common findings in
and hypokalemia also are indicative of hepatic compro- birds. Great variations appear among psittacine species
mise. but also between individuals. Baseline radiographs of
each individual bird should be taken as a part of the
Biliverdin is the most important bile pigment in birds; routine examination and may be used for comparison in
therefore, icterus is not a typical clinical sign of hepatic subsequent years (Tables 15.3, 15.4).
15_Liver.qxd 8/23/2005 5:16 PM Page 444
suspected of harboring mycobacteria.17 The information

was useful, but the 4.2% death rate would not be accept-
able in pet bird practice (see Chapter 24, Diagnostic
Value of Endoscopy and Biopsy).
Non-infectious Diseases
of the Liver
The liver’s function as a primary organ of filtration
makes it susceptible to a myriad of environmental toxins
and irritants (Table 15.5).
Fig 15.3 | The normal liver with a sharp border

and dark brown mahogany color as seen HEMATOMA
through the membranes of the air sacs.
Hepatic hematoma may present similarly to or in con-
junction with pediatric hepatic lipidosis. Hepatic hema-
ULTRASOUND toma often occurs in young birds because they have a
prominent abdomen, which provides very little keel pro-
This test provides information concerning the size and
tection for the underlying organs. In obese birds, the
structure of the liver. In most cases, it is not stressful. To
liver is more friable and extends farther into the unpro-
prevent hypothermia and ensure good contact of the
tected region of the caudal abdomen. The hematoma
probe with the bird, warmed lubricating jelly should be
may be visible through the abdominal skin. The extent
used.
of anemia and the bird’s physical condition will dictate
treatment decisions. Parenteral fluids must be given with
ENDOSCOPIC EXAMINATION care. Homologous blood or plasma transfusions can be
AND BIOPSY beneficial using guidelines as in mammals. The ultimate
Liver biopsies are frequently utilized to establish a defini- treatment is husbandry and the appropriate amounts of
tive diagnosis of the pathophysiology of liver disease (Fig a proper diet.
15.3). The risk to the patient in order to gain this infor-
mation must be considered. Coagulopathies associated
with hepatopathies increase the risk of severe bleeding.
HEPATIC LIPIDOSIS
These authors find very few situations in which liver Lipids are normally transported to the liver from the gas-
biopsies are advantageous to the individual avian patient. trointestinal tract and adipose tissue in the form of chylo-
Many infectious agents responsible for hepatopathy can microns and free fatty acids, respectively. Within hepato-
be diagnosed via serology. Viral infections that are not cytes, free fatty acids are esterified to triglycerides that
readily diagnosed via serology are often of short dura- are complexed with apoproteins to form low-density
tion. When a diagnosis has been made, treatment for lipoproteins, which are released into plasma as a readily
many pathological conditions is purely supportive. Liver available energy source. Hepatic lipidosis, or fatty liver,
biopsy will not change the prognosis in most cases of occurs when the rate of triglyceride accumulation within
hepatic dysfunction in parrots. Exceptions would include hepatocytes exceeds either their rate of metabolic degra-
infection with Mycobacterium spp., various neoplasias dation or their release as lipoproteins. Hepatic lipidosis
and conditions unresponsive to therapy. In an aviary situ- is not a specific disease entity but can occur as a sequel
ation, hepatic biopsy or submission of necropsy speci- to a variety of perturbations of normal lipid metabolism.
mens can be a significant means of identifying and elimi- Excessive dietary intake of fat or increased mobilization
nating disease. The risk of loss of an individual may ben- of triglycerides from adipose tissue subsequent to
efit the entire flock and to justify the procedure. increased demand, such as in starvation or endocrine
abnormalities, may be responsible (see Chapter 4, Nutri-
A retrospective study of liver biopsies of 71 birds was tional Considerations: Section II, Nutritional Disorders).
performed in a zoological collection. Important diagnos- Abnormal hepatocyte function can lead to an accumula-
tic findings included the identification of iron storage tion of triglycerides due to decreased energy for oxida-
disease in mynahs and toucans; presumptive Atoxo- tion of fatty acids. Excessive dietary intake of carbohy-
plasma hepatitis in mynahs; chronic active hepatitis drates can result in the increased synthesis of fatty acids
associated with intestinal coccidial infections; and acid- and excessive triglyceride formation. Hepatotoxins or
fast organisms or severe amyloidosis in ducks and geese drugs can impair secretion of lipoprotein from the liver.
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445
Table 15.5 | Causes of Non-infectious Liver Disease Table 15.6 | Treatment for Pediatric Hepatic Lipidosis
• Congenital • Cool oxygenation: place the bird in an oxygen
• Traumatic: hematoma chamber at 21º C
• Hepatic lipidosis: pediatric versus adult • Non-lactated fluids when stable
• Amyloidosis • Antibiotics that do not require hepatic transformation
• Iron storage disease or elimination if bacterial infection warrants
• Toxins • Hand-feed small amounts with increased frequency
• Malnutrition • Metabolic aids: lactulosea, milk thistleb, policosanolc
Table 15.7 | Treatment of Adult Hepatic Lipidosis

Decreased apoprotein synthesis can occur subsequent to
decreased production and export of lipoprotein from • Fluid therapy guideline: 60-90 ml/kg of non-lactated
fluids every 24 hours
hepatocytes. Deficiencies of the amino acids biotin,
• Nutritional support
choline and methionine have been shown to cause • Metabolic aids: lactulosea, milk thistleb, policosanolc,
hepatic lipidosis in mammals and some species of birds. psylliumg, Ayurvedic herbs,h SAMe
More than one defect can occur in any given hepatic dis- • Treatment of secondary infections
order. Hepatic lipidosis is most commonly seen in the
neonate and the obese, malnourished adult bird. See
Chapter 19, Endocrine Considerations. may be present. Complete blood count and serum bio-
chemistries help confirm the diagnosis and direct treat-
Hepatic Lipidosis (Pediatric): The liver in neonates is ment. The serum is often very lipemic in spite of fasting.
typically larger relative to the total body weight than in An elevated WBC is often observed. Serum chemistries
adult birds. Baby birds affected with hepatic lipidosis may be normal or may demonstrate an increase in levels
present with a common history of being handfed with a of bile acids, AST, LDH, cholesterol and triglycerides.
commercial formula to which the owners have added a
high-fat supplement. The higher fat content of macaw Sick birds’ caloric needs are 2 to 3 times normal. Diets
hand-feeding formulas is also implicated in this syn- too low in fat cannot provide sufficient calories. Start the
drome when these formulas are inappropriately used on patient on a 100% carbohydrate dietd, add metabolic
other species (especially cockatoos). Affected babies are detoxifiere then slowly convert to a sick bird support for-
often grossly overweight for their age and exhibit severe mula or a hand-feeding mixturef with adequate caloric
respiratory distress. These birds must be handled gently content. Further supportive care includes fluid therapy,
and minimally to avoid exacerbation of the condition. metabolic aids (lactulosea, milk thistleb, psylliumg, poli-
Cool oxygenation is the best first step. The enlarged liver cosanolc) and antibiotics if needed (Table 15.7). Improve-
reduces lung and air sac capacity. These neonates usually ment of nutritional status is critical for complete recov-
present when the stress of feeding and breathing at the ery and prevention of recurrence (see Chapter 7,
same time has exceeded their oxygen reserves. General Emergency and Critical Care).
nutritional changes that are required include reducing
the quantity of food per feeding, adjusting the fat type
AMYLOIDOSIS
and content and adding lactulose to the formula. Oral or
parenteral fluid supplementation, when tolerated, should Amyloidosis is a term used for various diseases that lead
be added to keep the initially hyperthermic bird hydrated to the deposition of proteins in internal organs. The pro-
and to detoxify the body. When possible, further diagnos- teins are composed of beta-pleated sheets of non-branch-
tic testing should be pursued to check for concurrent ing fibrils. The physical properties of amyloid are respon-
infection or other diseases (Table 15.6). sible for its birefringence and apple green appearance in
Congo red-stained sections viewed under polarized light.
Hepatic Lipidosis (Adult Bird): A second group that is In primary amyloidosis, amyloid light chain protein is
predisposed to hepatic lipidosis is the obese adult bird derived from immunoglobulin light chains synthesized by
being fed a high-fat diet, which is common in birds with plasma cells in affected tissues. Primary amyloidosis may
ovarian disorders and hypercholesterolemia. This syn- be localized or systemic.18 In secondary amyloidosis, the
drome can occur in many species, but seems most com- most common type seen in veterinary medicine, the liver
mon in Amazona spp. Long-standing malnutrition in an synthesizes serum amyloid-associated protein, which is
obese bird contributes to the cause of this syndrome. the precursor to amyloid-associated fibrils. Secondary
Septicemia can occur secondarily. The most common amyloidosis occurs as a consequence of prolonged
clinical presentation is an anorectic bird with a quiet inflammation resulting from chronic infection, tissue
demeanor, although other signs of hepatic dysfunction destruction, stress or chronic antigenic stimulation.18 The
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446
third type, inherited or familial amyloidosis, has been Table 15.8 | Treatment for Iron Storage Disease
described only in some mammalian species. Initial Ongoing
Oxygenation Phlebotomy
Regardless of the cause, amyloid accumulates in the inter- Diuretics Low-iron dietk
cellular spaces and impairs the normal access of plasma to Defroxamine2,i
hepatocytes. Amyloid deposits can produce varying
degrees of hepatomegaly, and extensive accumulations Table 15.9 | Infectious Diseases of the Liver
cause the liver to appear pale. In severe cases, affected Type Disease
Bacterial E. coli, Salmonella spp., Klebsiella spp., Chlamydophila
birds may have clinical signs of either hepatic dysfunction spp., Mycobacterium spp., Mycoplasma spp.
or failure. While hepatic amyloidosis is usually fatal, a case Viral Herpesvirus, polyomavirus, adenovirus, reovirus
was described in a falcon with hepatomegaly, ascites, leu- Fungal Aspergillus spp., Candida spp.
cocytosis, elevated AST, bile acids and iron levels. Protozoan Atoxoplasma spp., Histomonas spp., Trichomonas spp.,
Leucocytozoan spp.
Abdominocentesis was performed and a milk thistle deriv-
Nematodes
ative was administered for a month. The bird survived for
Trematodes
over 3 years.18 Resolution of the primary cause is the goal
in preventing the progression of this condition.
ported to the liver. The liver possesses enzymes capable
IRON STORAGE DISEASE of metabolizing a variety of endogenous and exogenous
substances for elimination from the body. This metabolic
Pathological storage of iron in the liver (iron storage dis-
process may alter some substances such that they
ease) has to be differentiated from hemosiderosis.
become more toxic. Toxin production may result in
Hemosiderosis is defined as the excessive accumulation
necrosis of hepatocytes, which may be replaced by
of iron in hepatocytes without the alteration of normal
fibrotic cells or infiltrated with lipids. This process can
tissue morphology.13 High-risk species for iron storage
be self-perpetuating, even if the inciting agent is no
disease include ramphastids (toucans), mynah birds,
longer present.9
starlings and birds of paradise. High amounts of dietary
iron seem to be the main cause, although complete
pathogenesis is unknown. Most of the susceptible
species live in a naturally iron-poor nutritional environ- Infectious Diseases
ment.4,21 The mynah was found to have high intestinal
absorption and transfer capacity of iron leading to high
of the Liver
retention levels4 (see Chapter 4, Nutritional Considera- The pathogenesis, diagnosis and treatment of the indi-
tions). Dyspnea, hepatomegaly, ascites and sudden death vidual infectious diseases are beyond the scope of this
are the most common clinical presentations. chapter. See Chapter 28, Implications of Mycobacteria in
Clinical Disorders; Chapter 29, Implications of Mycoses
Symptomatic therapy to stabilize the bird’s respiratory
in Clinical Disorders; and Chapter 32, Implications of
problems should be followed by long-term therapy
Viruses in Clinical Disorders. The reader is referred to
based on weekly phlebotomy of 1 to 2% of body weight.
other references for more details on infectious diseases
Dietary sources of iron such as grapes and raisins should
that affect the liver (Table 15.9).
be eliminated, and birds should be maintained on a low-
iron (20-50 ppm) formulated diet.k Therapy with a
chelating agenti, has been described as useful (Table
15.8).2 Items that enhance iron uptake, such as vitamin Therapy for Liver Disease
C, should be avoided. Iron uptake interference by
dietary chemicals such as tannin may provide natural This section reviews anecdotal and research-based ther-
protection from excessive iron absorption.25b apy for hepatobiliary disease in birds; the mechanism of
action, potential indications, efficacy as reported in
humans and side effects. The liver can regenerate lost
TOXINS hepatic mass rapidly and efficiently. The therapy for
The liver is the most common site for toxic injuries. The hepatic dysfunction is directed at regeneration.
liver receives the major amount of its blood supply from Potentially hepatotoxic drugs should be avoided. High-
the portal vein, which drains blood from the gastroin- quality nutrients are the best source of support for the
testinal tract. Therefore, ingested toxic substances regeneration of liver cells. The specific etiologic agent of
including plants, aflatoxins and bacterial products, as liver disease is often undetermined. Clinical objectives
well as metals, minerals, pharmaceuticals and other for treatment of liver disease can be divided into support-
chemicals absorbed into the portal blood are trans- ive care and pharmacologic therapy.
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447
SUPPORTIVE CARE associated with respiratory embarrassment or anorexia.

Diuretics may be useful in controlling fluid retention.
Supportive care for birds with hepatic damage includes
Dietary sodium restriction also is recommended, but the
reducing stress, fluid therapy, nutritional support and
efficacy is unknown.
treatment of encephalopathy, ascites, coagulopathies and
gastrointestinal ulceration. Proper caging options range
from a cool, oxygenated incubator in a low-stress area to Coagulopathies
the bird’s normal cage in its household environment. Cholestasis can cause impaired production of coagula-
Lowering perches and padding can protect birds with tion factors and antithrombin III as well as vitamin K
coagulopathies. If infectious disease is suspected, then malabsorption. Normal avian values are not available.
quarantine would be warranted. Coagulopathies may be observed as petechia, hemor-
rhage or melena. Blood component therapy may be indi-
Fluid therapy will flush toxins and toxic by-products cated. Vitamin K1 can be administered for hemorrhage
through the metabolic pathways and from cells, organs associated with vitamin K deficiency.
and blood (see Chapter 7, Emergency and Critical Care).
The selection of fluids for replacement therapy may be Gastrointestinal Ulceration
based on serum biochemistry results and physical exam The empiric indications for the use of H2 blockers
findings and should be devoid of lactate. The volume to include nausea, inappetence and melena. Famotidine or
be administered will vary, depending on existing fluid ranitidine are recommended, since cimetidine and
deficits and continuing loss. Administration of colloidsj omeprazole are involved in cytochrome P450 inhibition
may be effective in severe non-responsive hypoalbu- and potential drug interactions in mammals.23 Sucralfate
minemia, however, clotting times should be monitored. may enhance healing of ulcers in patients with impaired
Conspecific plasma or whole blood may be a better mucosal blood flow, but this agent may bind and pre-
option. vent absorption of other drugs.
Nutritional support with gavage-feeding should be pro-

vided three to four times daily for the anorectic patient. PHARMACOLOGIC THERAPY
Calculate the metabolized energy requirements to deter- The proper choice of therapy depends on a definitive
mine the volume of food to use (see Chapter 4, Nutri- diagnosis. Technical or financial restrictions often pre-
tional Considerations). A high-quality balanced formula clude obtaining a definitive diagnosis in avian veterinary
with appropriate levels of vitamins and minerals and medicine. Therapeutic agents used are chosen for their
devoid of potential hepatotoxic agents, such as pesti- anti-inflammatory, antifibrotic, hepatoprotectant, antimi-
cides and preservatives, should be provided. crobial, diuretic, procoagulant, antacid or bivalent
chelating actions. The pharmacologic therapies the
Hepatic Encephalopathy authors recommend for hepatic failure in birds have not
been validated by controlled studies. The personal expe-
The goal of therapy for hepatic encephalopathy is to
riences of the authors as well as anecdotal reports from
restore normal neurologic function. In mammalian medi-
colleagues support their use in therapy.
cine, this is accomplished by dietary protein restriction,
lactulosea therapy and antimicrobials. Lactulosea is a syn-
thetic non-absorbable disaccharide commonly used in IMMUNOSUPPRESSANTS
mammalian medicine for the treatment of elevated The use of glucocorticoids in avian medicine is contro-
blood ammonia levels seen in hepatic encephalopathy. It versial. They cause immunosuppression by a variety of
is fermented in the gut by bacteria into acetic acid and pathways. Glucocorticoids may exacerbate an underlying
lactic acid, which reduces the pH. The acidification infection, increase hepatic lipid deposition, derange
causes ammonia (NH3) to migrate from the blood into adrenal function and may be contraindicated unless a
the colon where it is trapped as an ammonium ion definitive diagnosis is determined (see Stress in Chapter
(NH4+) and expelled with the feces. These acids also 19, Endocrine Considerations). They are the treatment
increase osmotic pressure drawing water into the bowel, of choice in humans with autoimmune hepatitis.
causing a laxative effect. Lactulosea has minimal side
effects and is therefore considered safe to administer to Azathioprine is a thiopurine analogue metabolized in the
all birds during gavage-feeding. liver to 6-mercaptopurine. Its metabolites inhibit the pro-
liferation of rapidly dividing cells and modify T-lympho-
cyte function. Azathioprine is indicated when glucocorti-
Ascites
coids are not controlling the immune response or are not
Removal of a large volume of coelomic fluid can cause tolerated by the patient. No data exist on the efficiency of
severe protein loss. Removal is indicated if the ascites is conversion of azathioprine to its active metabolites in
15_Liver.qxd 8/23/2005 5:16 PM Page 448
hepatic insufficiency in birds. Serious side effects include the antioxidant glutathione20 (see Chapter 4, Nutritional
dose-dependent bone marrow suppression, pancreatitis Considerations: Section II, Nutritional Disorders). There
and idiosyncratic hepatotoxicity in mammals. are no side effects reported in veterinary medicine.
Neurological side effects were reported in humans taking
tricyclic antidepressants.12 Early empirical results of SAMe
ANTIFIBROTICS
use in birds with elevated cholesterol and fatty disorders
Colchicine is indicated when there is evidence of fibro- are encouraging.
plasia or bridging fibrosis. Colchicine helps prevent fibro-
sis by a variety of inhibitory actions. It also may protect Milk thistleb (Silybum marianum: silymarin) is an
the liver via stabilization of hepatocytes’ plasma mem- extract from the seeds of milk thistle. It is thought to
branes. Most common side effects are associated with have antioxidant effects via scavenging of reactive oxy-
gastrointestinal upset, but in humans a peripheral neu- gen radicals, and to have anti-inflammatory effects via
ropathy and bone marrow suppression have been inhibition of 5-lipoxygenase.3 Side effects of GI upset
reported. Formulations of colchicine containing pro- and allergic rashes are rare in humans. It is a nutritional
benecid can inhibit biliary and renal excretion of many supplement, not a pharmaceutical. See Chapter 10,
drugs. Elemental zinc and glucocorticoids also have Integrative Therapies for more information.
antifibrotic properties, but should be used with caution.
Policosanolc is a blend of compounds isolated from
natural plant waxes. It decreases blood triglyceride and
CHELATING AGENTS reduces low-density lipoprotein cholesterol, inhibits
Chelating agents are used to chelate bivalent metals abnormal platelet aggregation, protects against low-
such as zinc, lead, copper and sometimes iron. Copper density lipoprotein oxidation, suppresses arterial inflam-
induced liver disease is not a common problem in avian matory factors and increases beneficial high-density
medicine. lipoprotein cholesterol.
HEPATOPROTECTANTS
Hepatoprotectants comprise a varied group of com- Monitoring Parameters
pounds that may protect hepatocytes from injury caused
by free radicals, bile salts, drugs, environmental toxins The best test for monitoring the treatment of liver dis-
and other insults. ease is the test(s) that was used to confirm the diagnosis
in the first place. If hepatic lipidosis was diagnosed in an
Ursodiol, ursodeoxycholic acid, is a hydrophilic bile acid obese Amazon by history and clinical signs, hepatomegaly
that competes with other bile acids for absorption in the noted on radiographs and an elevated serum bile acid
ileum, and shifts the bile acid profile in favor of less assay, then repeat radiographs and serum bile acid assay
toxic hydrophilic forms. It is suspected to reduce hepato- would be indicated. Repeat biopsies would give the
cellular injury and fibrosis, modulate immune response most definitive answer, but are not always best for the
and act indirectly as an antioxidant by preventing bile individual patient.
acid-induced peroxidation. Ursodiol is indicated in
mammals for chronic active hepatitis, cholangiohepatitis, Products Mentioned in the Text
and disorders involving cholestasis or elevated bile a. Lactulose, Cephulac, Marion Merrell Doug, Kansas City, MO, USA
b. Milk Thistle, Silybum marianum, Nature’s Answer, Hauppauge, NY, USA
acids. No efficacy studies have been performed with c. Policosanol, Mountain States Health Products, Inc, Lyons Co, USA, 1-800-
birds. GI upset has been reported rarely in humans. 647-0074
d. Ultrafuel, Malt dextran and fructose, Twin Laboratories, Inc,
Ursodiol is contraindicated in bile duct obstruction Ronkonkoma, NY 11779, USA
because it is choleretic. e. Ultra Clear Plus, Ultra Balance Medical Foods, 5800 Soundview Dr, Gig
Harbor, WA, 98335, USA, www.ultrabalance.com
f. Juvenile Hand-Feeding Formula, HBD International, Inc, 7108 Crossroads
Vitamin E is a potent antioxidant. Studies indicate that it Blvd., Suite 325, Brentwood, TN 37127, USA, 1-800-346-0269,
protects against bile salt-induced oxidant injury in-vitro.29 www.harrisonsbirdfoods.com
g. Metamucil, Proctor and Gamble Pharmaceuticals, Cincinnati, OH, USA
It is indicated as an empirical therapy for inflammatory h. Ayurvedic herbs, Hepasan, Indian Herbs Research and Supply Co Ltd,
hepatopathies. The side effects are minimal unless there Institut fur Veterinarpharanakologic und — toxikologie, Winterhurstrasse
260, 80547 Zurich, Schueiz, http:/www.vetpharm.unezh.ch
is a massive overdose or if it used with selenium (see i. Desferal, Novartis Pharmaceuticals Corp, East Hanover, NJ, USA
Chapter 4, Nutritional Considerations). j. Hetastarch, DuPont Pharmaceuticals, Wilmington, DE, USA
k. Harrison’s Bird Foods, HBD International, Inc, 7108 Crossroads Blvd.,
Suite 325, Brentwood, TN 37127, USA, 1-800-346-0269 www.harrisons-
S-adenosylmethionine (SAMe) is an indirect precursor of birdfoods.com
15_Liver.qxd 8/23/2005 5:16 PM Page 449
449
References and 8. Garner MM, et al: Three psittacine phia, WB Saunders Co, 1986, p 24. Ritchie BW: Diagnosis and man-
fatalities due to an unidentified 526. agement of common problems in
Suggested Reading sporozoan parasite infection in a 16. Lumeij S: Hepatology. In Ritchie companion birds. Proc Assoc
1. Conn HO, Leevy CM: Comparison closed psittacine aviary. Proc BW, Harrison GJ, Harrison LR, Avian Vet, 2001, pp 99-119.
of lactulose and neomycin in the Assoc Avian Vet, 2001, p 56. (eds): Avian Medicine: Principles 25a. Ritchie BW, Harrison GJ:
treatment of chronic portal-sys- 9. Hardy RM: Diseases of the liver and Application. Brentwood, TN, Formulary. In Ritchie BW,
temic encephalopathy. Gastro- and their treatment. In Ettinger HBD International, Inc., 1999, pp Harrison GJ, Harrison LR (eds):
enterology 72:573-583, 1977. SJ (ed): Textbook of Veterinary 522-536. Avian Medicine: Principles and
2. Cornelissen H, Ducatella R, Roels Internal Medicine Vol. II, 17. McGavin MD, Carton WW, Application. Brentwood, TN,
R: Successful treatment of a chan- Philadelphia, WB Saunders Co, Zachary JF (eds): Thomson’s HBD International, Inc., 1999, p
nel-billed toucan with iron storage 1989, pp 1479-1527. Special Veterinary Pathology 3rd 465.
disease by chelation therapy: 10. Hess L: Possible complications ed. St. Louis, Mosby, 2001, pp 81-
associated with topical corticos- 124. 25b. Seibels B, et al: Effective use of
Sequential monitoring of the iron
teroid use in birds. Proc Assoc tea to limit dietary iron available
content of the liver during treat- 18. McKinney PA: Amyloidosis in
Avian Vet, 2001, pp 29-32. Falconiformes. Proc Assoc Avian to starlings (Sturnus vulgaris). J
ment period by quantitative chemi-
Vet Australian Com, 2002, pp 257- Zoo Wildl Med 2003; 34:314-316.
cal and image analysis. J Avian Med 11. Hochleithner M: Biochemistries.
Surg 9:131-137, 1995. In Ritchie BW, Harrison GJ, 264. 26. Spalding MG, et al: Hepatic
3. Dehmlow C, Murawski N, de Groot Harrison LR (eds): Avian 19. Mizobe M, et al: High perform- encephalopathy associated with
H: Scavenging of reactive oxygen Medicine: Principles and ance liquid chromatographic hemochromatosis in a toco tou-
species and inhibition of arachi- Application. Brentwood, TN, analysis of bilirubin and biliverdin can. J Am Vet Assoc 189(9):1122-
donic acid metabolism by silibinin HBD International, Inc., 1999, pp from jaundiced broilers. J Vet 23, 1986.
in human cells. Life Sci 58:1591- 223-245. Med Sci, 59(8):677-680, 1997. 27. Stanford M: Effect of dietary
1600, 1996. 12. Irulea LM, et al: Toxic interaction 20. Osman E, Owen JS, Burroughs change on fecal Gram’s stains in
4. Dorrenstein GM, et al: of S-adenosylmethionine and AK: Review article: S-Adenosyl-L- the African grey parrot. Exotic
Hemochromatosis/iron storage: clomipramine. Amer J Psychiatr Methionine — A new therapeutic DVM, 4(6):12, 2003.
New developments. Proc Assoc 150:522, 1993. agent in liver disease? Aliment 28. Stone EG, Redig PT: Preliminary
Avian Vet, 2000, pp 233-237. 13. Jacobs A.: Iron metabolism, defi- Pharmacol Ther 7:21-28, 1993.
evaluation of hetastarch for the
5. Flinchum GB: Potential use of poli- ciency and overload. In Scott BR 21. Otten BA, et al: Mineral content management of hypoproteinemia
cosanol in the treatment of hyper- (ed): Price’s Textbook of the of food items commonly ingested and hypovolemia. Proc Assoc
lipidemia in pet birds. Exotic DVM Practice of Medicine. Oxford, by keel-billed toucans Avian Vet, 1994, pp 197-199.
5(3): 19-23. Oxford University Press, 1978, pp (Ramphastos sulfuratus). J Avian
6. Flora K, et al: Milk thistle (Silybum 1118-1129. Med Surg 15(3):194-196, 2001. 29. Twedt D, et al: Vitamin E protects
marianum) for the therapy of liver 14. Lin GL, Cornelius CE: Bilirubin 22. Pepping J: Milk thistle: Silybum against oxidative damage of bile
disease. Amer J Gastroenterology and biliverdin excretion by the marianum. Amer J Health Syst acids in isolated hepatocytes
93(2):139-142, 1998. chicken. Amer J Phys 226:881- Pharm, 56:1195-97, 1999. (abstract). Proc 16th ACVIM
7. Fudge A: Avian liver and gastroin- 885, 1974. 23. Reynolds JC: The clinical impor- Forum, 1998, p 705.
testinal testing. In Fudge A (ed): 15. Lothrop C, et al: Miscellaneous tance of drug interactions with 30. Weber MA, et al: Benefits and
Laboratory Medicine: Avian and Diseases. In Harrison GJ, antiulcer therapy. J Clin complications of liver biopsy in
Exotic Pets. Philadelphia, WB Harrison LR (eds): Clinical Avian Gastroenterol Suppl 2:S54-S63, birds. Proc Assoc Avian Vet, 2001,
Saunders Co, 2000, pp 47-55. Medicine and Surgery. Philadel- 1990. pp 211-213.
15_Liver.qxd 8/23/2005 5:16 PM Page 450
PrepagesV2.qxd 8/24/2005 9:09 AM Page I
Clinical
Avian
Medicine
VOLUME II
GREG J. HARRISON, DVM
Diplomate Emeritus American Board of Veterinary Practitioners (Avian)
Palm Beach, Florida
TERESA L. LIGHTFOOT, BS, DVM

Diplomate American Board of Veterinary Practitioners (Avian)
Florida Veterinary Specialists
Tampa, Florida
PrepagesV2.qxd 8/24/2005 9:09 AM Page II
II
Spix Publishing, Inc.,

Palm Beach, Florida
Library of Congress Control Number: 2005922214
Clinical Avian Medicine (2-volume set) ISBN: 00-9754994-0-8
Production: Zoological Education Network
Cover Design: Jean Coffinberry
Cover photos: Peter Coutteel (canaries), Jan Hooimeijer (racing pigeons), Lorenzo Crosta (little blue penguins), Gwen
Flinchum (black swans), Jaime Samour (saker falcon), E. Albertini (great grey owl), Auckland Zoo (North
Island brown kiwi), Greg Harrison (Lady Gouldian finches)
Proofreading: K. Stormy Hudelson, DVM, Dipl ABVP-Avian, Paul Hudelson
Indexing: Ann Truesdale, DVM
Administrative Assistants: Lesley Flahie, Patty Wolf
Technical Assistance: Chris Lane
Printing and Binding: Four Colour Imports
Advertising and Sales: HBD Intl Inc. www.harrisonsbirdfoods.com
©2006 Spix Publishing, Inc., Palm Beach, Florida

All rights reserved. No part of this book may be reproduced or used in any form or by any means, electronic or mechan-
ical, including photocopying, or by any information storage or retrieval system, without permission in writing from the
publisher. Address any inquiries to Spix Publishing Inc, 3610 South Ocean Blvd #601, Palm Beach, FL 33480-5877.
Last digit is the print number: 9 8 7 6 5 4 3 2 1

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III
Clinical Avian Medicine

C O N T E N T S V O L U M E I I (Chapters 1-15 - Volume I)
16 Evaluating and Treating the Kidneys . . . . . . . .451

M. SCOTT ECHOLS
17 Evaluating and Treating

the Nervous System . . . . . . . . . . . . . . . . . . . . . . . .493
SIMON R. PLATT

Reproductive System . . . . . . . . . . . . . . . . . . . . . . . .519
HEATHER L. BOWLES
19 Endocrine Considerations . . . . . . . . . . . . . . . . . . .541

K. STORMY HUDELSON, PAUL M. HUDELSON
20 Overview of Tumors . . . . . . . . . . . . . . . . . . . . . . . .559

Section I: Clinical Avian Neoplasia and Oncology . . . .560
TERESA L. LIGHTFOOT
Section II: A Retrospective Study of Case
Submissions to a Specialty Diagnostic Service . . . . . .566
MICHAEL M. GARNER
21 Preventive Medicine and Screening . . . . . . . . .573

DAVID N. PHALEN
22 Diagnostic Value of Hematology . . . . . . . . . . . . .587

JAIME SAMOUR
23 Diagnostic Value of Biochemistry . . . . . . . . . . . .611

KENDAL E. HARR
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IV
24 Diagnostic Value of Endoscopy

and Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .631
MICHAEL LIERZ
25 Advances in Diagnostic Imaging . . . . . . . . . . . .653

PETER HELMER
26 Diagnostic Value of Necropsy . . . . . . . . . . . . . . . .661

MADELINE A. RAE
27 Update on Chlamydophila psittaci:

A Short Comment . . . . . . . . . . . . . . . . . . . . . . . . . . .679
THOMAS N. TULLY, JR.
28 Implications of Mycobacteria in
Clinical Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . .681
CHRISTAL G. POLLOCK
29 Implications of Mycoses in
Clinical Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .691
ROBERT D. DAHLHAUSEN
30 Implications of Macrorhabdus in
Clinical Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . .705
DAVID N. PHALEN
31 Implications of Toxic Substances

in Clinical Disorders . . . . . . . . . . . . . . . . . . . . . . . .711
JILL A. RICHARDSON
32 Implications of Viruses in Clinical

Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .721
DAVID N. PHALEN
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33 Updates in Anesthesia and Monitoring . . . . . .747

THOMAS M. EDLING
34 Surgical Resolution of Orthopedic

Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .761
PETER HELMER, PATRICK T. REDIG
35 Surgical Resolution of
Soft Tissue Disorders . . . . . . . . . . . . . . . . . . . . . . .775
HEATHER L. BOWLES, ESPEN ODBERG, GREG J. HARRISON,
JACK J. KOTTWITZ
36 Management of Waterfowl . . . . . . . . . . . . . . . . . .831

GWEN B. FLINCHUM
37 Management of Racing Pigeons . . . . . . . . . . . . .849

JAN HOOIMEIJER
38 Management of Galliformes . . . . . . . . . . . . . . . . .861

GARY D. BUTCHER
39 Management of Canaries,
Finches and Mynahs . . . . . . . . . . . . . . . . . . . . . . . .879
PETER SANDMEIER, PETER COUTTEEL
40 Management of Raptors . . . . . . . . . . . . . . . . . . . . .915

JAIME SAMOUR
41 Management of Captive Ratites . . . . . . . . . . . . .957

BOB DONELEY
42 Management of Zoo and Park Birds . . . . . . . . .991

LORENZO CROSTA, LINDA TIMOSSI, MARCELLUS BÜRKLE
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VI
Appendices
I Avian Hematologic Reference Ranges . .1005
II Avian Hematologic Reference Ranges

for Clinically Normal Psittacines . . . . . .1006
III Avian Biochemical References

Ranges . . . . . . . . . . . . . . . . . . . . . . . . . . . .1007
Index
Note to the Reader

The National Research Council (NRC) has not established standards for nutritional products fed to birds; therefore, claims of
nutritional completeness can not legally or ethically be made. Human medical textbooks and those of domestic animals have
established normal laboratory values, recommended treatment regimes and nutritional disease states — all based on individu-
als meeting minimum standards of nutrition. These are not available in avian medicine.
Disclaimer
The publisher, editors, authors, reviewers and distributors involved assume no legal responsibility for use and make no claims
or warranties regarding results that may be obtained from information in this text, nor necessarily endorse the procedures,
medications, medication dosages or their uses as offered in this work. The above parties shall not be liable to any party for
any damages, nor considered negligent for any misstatement or error obtained in this text.
16_Nephrology.qxd 8/23/2005 10:41 AM Page 451
CHAPTER
16
Kidneys
M. SCOTT ECHOLS, DVM, D ipl ABVP-A vian
Renal diseases and their various classifications are well

documented in the avian literature. The precise patho-
genesis of avian renal disease, however, is not nearly as
well described as it is in mammals. Renal disease has
been shown to be fairly common in avian species. In
studied poultry, as much as 29.6% of all disease condi-
tions had abnormal pathology associated with or attrib-
utable to renal disorders.20,214,251 Amyloidosis, urate
nephrosis and gout were the most common diseases
associated with mortality in a 4-year retrospective study
conducted at a waterfowl park in Ontario, Canada.210
Thirty-seven percent of all avian cases presenting with
renal tissue for histopathological examination, included
over a 15-month period at the Schubot Exotic Bird
Health Center, had one or more histologically identified
kidney lesions.187 Nine of 75 pheasants (Phasianus
colchicus) died with nephritis, one or both ureters
impacted, and visceral gout in another comprehensive
study on avian mortality.186 These case reports and retro-
spective studies support the conclusion that renal dis-
eases are relatively common and are clinically significant
in multiple avian species.
When compared to mammalian counterparts, the

avian urogenital system has many structural and
functional differences, which have been described
previously.77,90,118,181,187,227 Differences including gross
anatomy, renal portal blood flow and protein waste
elimination should be considered when reviewing this
chapter, as findings obtained from mammalian studies
may not necessarily be applicable to birds. By better
understanding the pathophysiology of renal disease,
practitioners will be able to better diagnose, clinically
evaluate and treat kidney disorders in birds.
452 C l i n i c a l Av i a n M e d i c i n e - Vo l u m e I I
Part one of this two-part chapter will combine mam- Within each division are numerous renal lobules, each
malian and avian literature to help describe the patho- containing a cortex and a cone-shaped medulla (medullary
genesis and progression of renal disease. Various forms cone). Avian medullary cones have no inner and outer
of specific kidney disorders that have been reported in regions as described in most mammalian kidneys.40
birds are described. Discussions of treatments will be
deferred to the second half of this chapter. One of the most unique features of avian kidneys is the
presence of two types of nephrons, with and without a
Part two will focus on methods of diagnosis and man- loop of Henle.38 The loop of Henle allows for urine con-
agement of specific avian renal diseases. Many of the centration and is the primary reason that birds and
diagnostics and treatments discussed are rationalized mammals are the only classes of vertebrates that can
and based on avian renal anatomy, physiology and an consistently produce hyperosmotic urine.38,39 In birds,
understanding of the pathophysiology behind kidney only about 10 to 30% of the nephrons are of the mam-
disease, all of which are covered in the first half of the malian type.40,77,141,248 Most avian nephrons are loopless
chapter. (“reptilian” type) and stay within the cortex.141 The
looped nephrons (“mammalian” type) extend from the
cortex into the discrete medullary areas known as
medullary cones. Since birds have primarily “reptilian”
PART 1: type nephrons, which produce isoosmotic urine, urine
Pathophysiology, concentration is limited.
Pathogenesis and Neurovascular System

Classification of (Including the Renal Portal System)
Avian Renal Disease The vascular system surrounding avian kidneys is quite
complex and is one of the main reasons that renal sur-
gery is difficult in birds. Another unique feature of avian
ANATOMY
kidneys is the presence of an arterial and venous, or
Kidneys dual, afferent blood supply.141 (See Figs 16.1a-e for
anatomy of the gross renal neurovascular system). The
The avian renal system is quite unique among vertebrate arterial afferent blood supply to the kidneys is as fol-
kidneys. In-depth discussions of gross and microscopic lows. The cranial renal division is supplied by the cranial
avian kidney anatomy have been covered elsewhere as renal arteries, which branch off the aorta. The glomeruli
referenced, but pertinent features will be discussed and postglomerular tubular network of the middle and
here.27,38,39,90,113,141 In general, avian kidneys comprise 1 to caudal renal divisions are supplied by the middle and
2.6% of body weight compared to an average of 0.5% of caudal renal arteries, which branch off the ischiadic or
body weight in mammals.77 Kidney mass also is relatively external iliac arteries.77,141
larger in those birds with active salt glands.77,110 At least
in Pekin ducks (Anas platyrhynchos), females have more The renal portal system forms the second afferent blood
and larger nephrons and bigger kidneys relative to body supply, which is venous, to the kidneys.141 The external
mass.15 Finally, the left kidney in laying hens tends to be iliac, ischiadic and caudal mesenteric veins supply blood
heavier and have a higher rate of renal portal blood flow to the renal portal system.248 A ring is formed on the ven-
than the right.248 tral side of the kidneys by the cranial and caudal portal
veins, which branch off the external iliac and common
Birds have paired kidneys located within a cavity formed iliac veins.141
by the ventral surface of the synsacrum. The kidneys
extend from the caudal edge of the lungs to the caudal The renal portal system works by either directing blood
synsacrum.36 An abdominal air sac diverticulum extends to or shunting it past the kidneys as directed by the
between the synsacrum and kidney. Normal bird kidneys renal portal valve. For example, venous blood from the
are surrounded by air.36 In most birds, the kidney is limbs is shunted straight to the caudal vena cava when
composed of three divisions: cranial, middle and caudal. the renal portal valve, within the common iliac vein, is
Figs 16.1a,b demonstrate basic gross renal anatomy. The open.141 The opposite is true when the renal portal valve
middle and caudal renal divisions of most passerines are is closed, as venous flow from the legs is directed to the
fused, while the caudal renal divisions are connected afferent venous system of the kidneys.129 This, of course,
across the midline in herons, puffins and penguins.36 means that blood may pass through the kidneys prior to
Additional variations in gross renal anatomy can be any other organ. Additional shunting either to the cau-
found in other avian species. dal mesenteric vein (caudally) or internal vertebral sinus
Chapter 16 | E V A L U A T I N G A N D T R E A T I N G T H E K I D N E Y S
453
Fig 16.1a | Gross renal anatomy of a Fig 16.1b | The excess ventral perirenal Fig 16.1c | The left kidney, ductus deferens
normal immature male red-tailed hawk fat has been removed. The middle (M) and and ureter have been removed, leaving the
(Buteo jamaicensis) that died from head caudal (Cd) renal divisions are now visible. large vascular structures intact. The external
trauma. Note the testes (T), adrenal glands The immature ductus deferens runs along- iliac (EIV), caudal renal portal (CRPV), cau-
(A) and cranial renal divisions (C). This side the ureter (U) and caudal renal vein dal renal (CRV) and common iliac (CIV)
hawk has a moderate amount of fat cover- (CRV), but is not distinguishable in this veins and the approximate location of the
ing the middle and caudal renal divisions. young bird. renal portal valve (*) are identified.
Fig 16.1d | The venous system has been Fig 16.1e | The left renal, vascular, repro-
removed to demonstrate the aorta (A), ductive and endocrine systems have been
external iliac (EIA) and ischiadic (ischiatic) removed, revealing the overlying renal
(IA) arteries. fossa of the synsacrum and lumbar (LP) and
sacral plexi (SP).
(cranially), again bypassing the kidneys, also may occur This unique system accounts for some clinical con-
once blood has entered the renal portal ring. cerns.141 First is the fact that blood can be directed from
the lower limbs straight into the renal parenchyma. This
By route of the afferent caudal and cranial renal portal may increase the effect of nephrotoxic drugs and/or
vein branches, blood is delivered to the peritubular cap- enhance elimination by taking the compound directly to
illary network.141 While virtually all renal arterioles termi- the kidneys. Some drugs eliminated by tubular secretion
nate in the glomerular capillary beds, renal portal blood and given into the leg may enter the renal portal system
flow does not.248 This system allows only arterial blood and be eliminated without ever entering systemic circu-
into the glomeruli and both postglomerular arterial and lation.223 As a general rule, parenteral drugs probably
renal portal vein venous blood to the renal tubules. should be given in the cranial half of the body. Because
Blood is ultimately drained out of the kidneys via the some of the venous afferent blood comes from the cau-
centrolobular to the cranial and caudal to the renal and dal mesenteric vein (v. coccygeomesentericae), which
finally common iliac veins just proximal to the renal drains the lower intestines, alimentary tract disease may
portal valve.141 ascend into and have an effect upon the kidneys. As
addressed under Part 1: General Mechanisms and Conse- allow birds to adapt to brackish and saline environments
quences of Renal Injury, Gastrointestinal Complications, and maintain normal electrolyte balance. There is likely
the effect of lower intestinal disease upon the kidneys an intimate association between renal function and
should be considered and treatment such as antibiotics extrarenal NaCl excretion.110
for colitis instituted.
In chickens, the gland appears vestigial, but its anatomi-
Hemodynamics cal features have been studied. The (supraorbital) salt
Studied birds have an impressive ability to maintain gland is approximately 2 cm long and 2.5 mm in diame-
renal blood flow, even with severe hemodynamic alter- ter. The caudal portion is located above the orbit, adja-
ations. Chickens seem to be able to “autoregulate” (keep cent to the frontal bone, while the rostral extent is in
constant) glomerular filtration rate when the arterial the lateral wall of the nasal cavity, next to the dorsal and
blood pressure range is within 60 to 110 mmHg.73 medial turbinates.200 The salt gland’s draining duct
Arterial pressures below this “autoregulatory” range crosses under the nasal cavity and opens from the nasal
result in decreased glomerular filtration rate until urine septum, adjacent to the rostral part of the ventral
flow ceases at pressures below 50 mmHg.73 Also of inter- turbinate, into the nasal cavity.200 Fluid is then removed
est is that renal perfusion does not decrease in chickens by shaking movements of the head or by passively drip-
(Gallus domesticus) until nearly 50% of the blood vol- ping from the tip of the beak.213 Similar features also
ume has been removed.23 Despite severe hemorrhage, have been noted in the turkey nasal salt gland.200
birds are able to maintain their blood pressure, suggest-
ing other compensatory mechanisms such as extravascu- The salt glands function by providing an extrarenal path-
lar fluid mobilization are utilized to ensure normal renal way for the excretion of sodium chloride when the bird
blood flow.23 must consume salt quantities greater than its relative
ability of renal clearance.34,110 In some birds, the secreted
Local Renal Neurologic System sodium chloride can reach 10 times plasma concentra-
The lumbar and sacral nerve plexi are closely associated tions.213 The salt glands may remove more than 20% of
with the kidneys. The lumbosacral plexus is formed by the sodium chloride delivered by blood and have been
the ventral rami of about eight spinal nerves.180 From considered one of the most efficient ion-transporting
these rami, the first three form the lumbar plexus, which organs in the animal kingdom.213 One reference notes
produces the femoral and obturator nerves. In turn, that active salt glands can remove 60 to 88% of sodium
these nerves provide innervation to the stifle extensors and chloride eliminated by the bird’s body.77 Salt encrus-
and leg adductors.180 The lumbar nerve plexus forms tation may be noted around the nares of dehydrated,
dorsal to the cranial renal division and exits the pelvis heat-stressed birds and represents a gross manifestation
cranial to the hip joint.59 of the gland’s function.141
The sacral plexus is formed by the caudal five to six The gland size depends on the bird’s salt consumption,
spinal nerve ventral rami.180 These nerves go on to sup- and a hyperplastic response is considered normal in
ply innervation to the lower leg and some of the proxi- some species.213 By adding high levels of sodium to the
mal leg muscles. The sacral plexus runs through the drinking water, salt gland hyperplasia can be induced
middle renal division parenchyma and exits the pelvis in aquatic birds, but not in chickens.200 In general, birds
via the ischiadic foramen.59,180 exposed to little salt have small salt glands. Once a
bird is exposed to high salt loads, there is a rapid and
Pressure on the nerve plexi can result in non-weight-
profound hyperplasia and hypertrophy response that
bearing lameness.180 This is the reason why some birds
results in a greatly enhanced salt-secretory capacity
with renal diseases, especially those that cause renomeg-
within 1 to 7 days.213
aly such as cancer, result in one-leg lameness in clini-
cally affected birds. Other causes of one-leg lameness in Diseases of the salt glands are rarely described. This may
birds include egg-laying disorders, bumblefoot, testicular imply that salt glands either are infrequently evaluated
cancer and trauma, and should be considered before or are truly uncommonly affected by disease conditions.
making a diagnosis of renal disease. One study found that domestic ducks induced with
plumbism had high concentrations of lead in the salt
Salt Glands glands.34 The authors hypothesized that in ducks, salt
Salt glands are present in almost all birds, but have glands are involved in the elimination of lead. Also, lead
important functional significance in waterfowl, marine toxicity results in obvious renal impairment and possibly
birds, and some raptors and desert avian species.15,34,200,213 damages the salt glands, making it difficult for wild
Birds have limited ability to produce hypertonic urine. waterfowl to adapt to different saline environments.34
As a compensatory mechanism, the extrarenal salt glands High cadmium intake significantly increased salt gland
455
mass in Pekin ducks (Anas platyrhynchos) and, com- tioned previously, birds have the ability to produce con-
bined with the toxic renal effects, was believed to centrated urine, but because avian nephrons are primarily
adversely affect osmoregulation.15 Salt gland enlargement loopless, urine concentration within the kidney is limited.
from hyperplasia and inflammation are noted inciden- In birds, the process for concentrating urine is believed
tally in range-reared tom turkeys.200 Reported clinical to be similar to that in mammals, but in avian species,
signs are mild and consist of localized or unilateral sodium chloride acts as the major solute, not urea or
swelling above the eye.200 potassium. The end effect is that sodium chloride does
not have as much osmotic force as does urea, further
PHYSIOLOGY limiting the concentration of avian urine.223 Although
birds inhabiting arid environments generally produce
Roles of the Avian Kidney more concentrated urine than those from the tropics,
Undoubtedly, the kidneys play numerous vital roles in many exceptions exist.38,39 This leads to other water con-
birds. One primary role of the kidney is elimination of servation methods that are variable between species.
metabolic wastes. The kidneys also aid the liver in detoxi-
In response to dehydration in birds, glomerular filtra-
fication.248 Because the kidneys are responsible for elimi-
tion and urine flow rate are consistently decreased while
nating numerous metabolites, tissue concentrations of
solute concentration increases. In studied birds, arginine
antibiotics (apramycin and ciprofloxacin) and toxins
vasotocin is the natural avian antidiuretic hormone and
(lead and cadmium) are often highest in renal tissue.3,7,10,178
is believed to be the primary mediator in response to
As a result, various compounds are best identified and
dehydration.88,89,204 Increased plasma osmolarity is likely
quantified in the kidney tissue.
the major stimulus for release of arginine vasotocin.131
Renal regulation of water via electrolyte (Na+, K+, Cl-) Arginine vasotocin acts by controlling tubular water per-
balance is essential to maintaining intra- and extra- meability, and thus the concentrating capacity of the
cellular fluid volumes and osmolalities.248 By regulating avian kidney.33
fluid volume, the kidneys also regulate blood pressure.
As a component of water and possibly protein conserva-
Arginine vasotocin is likely the primary mediator in
tion, birds have the ability to absorb significant amounts
response to dehydration, but norepinephrine, aldos-
of excreted (renal) water in the colon and ceca.28 This
terone, rennin, angiotensin II and prolactin also may
system also allows some birds to regulate electrolyte loss
each have an effect on avian kidneys and osmo-
through the urine.248 The ureters empty into the
regulation.27,88,89,96,131,204,205
urodeum where reverse peristaltic waves of the cloaca
The avian kidney has other endocrine functions and it is cause a reflux of urine into the cloaca and ceca, which
likely that future studies will elucidate more roles of this are sites of water reabsorption.28,220,236
complex organ. One function of the kidney is the pro-
The amount of water reabsorbed is highly variable
duction of the active form of vitamin D (1,25- [OH]2D3)
among different avian species. Rock ptarmigan (Lagopus
via the renal enzyme (25[OH]D3)-1-hydroxylase.66,244
mutus) ceca play a minimal role in digestion, but
Parathyroid hormone also has been shown to have a
account for 98% of water absorbed in the hindgut.252 In
profound effect on renal excretion patterns of calcium
domestic turkeys (Meleagris gallopavo), 20 to 40% of
and phosphate in birds.61,70 As a result, the kidney is
the urine is refluxed into the ceca, from which 80% of all
partly responsible for mineral metabolism.248 The avian
fluids that enter are absorbed. It has been shown that
kidney also is the target organ for numerous growth
77% of the water, 72% of sodium and 82% of potassium
factors, the functions of which are not yet known.57
from ureteral urine in Gambel’s quail (Callipepla gam-
In addition to production in the liver, chick kidneys
belii) is subsequently reabsorbed in the ceca, lower
secrete apolipoproteins and are believed to contribute
intestine, cloaca and rectum.28,252 In domestic fowl, it has
to the plasma lipoprotein pool.232 This may be a func-
been estimated that 13 to 28 ml/kg body weight per day
tional response to the lipids coming from the terminal
of fluid is absorbed in the cloaca.248
ileum, via the renal portal system, that contributes to
production of lipoproteins.232 Cecectomized birds often have changes in fluid regula-
tion. Cecectomized Gambel’s quail and great horned
Fluid Regulation owls (Bubo virginianus) temporarily drank more water
Fluid regulation in birds is complex, as is true in many than controls. Water intake gradually returned to preop-
other animals. Birds have the ability to absorb and secrete erative levels, suggesting a compensatory response
various electrolytes and nutrients, which have some effect either in the intestines or kidneys.252 Cecectomized great
on fluid regulation. These osmoregulatory mechanisms horned owls and chickens also have shown a transient
are covered in depth in other references.38,39,90,223,248 As men- increase in water excretion (in the droppings).220,252
C l i n i c a l Av i a n M e d i c i n e - Vo l u m e I I
456
While the lower intestines appear to play a significant In studied species, the renal medulla and papilla are a
role in water and possibly electrolyte reabsorption, the rich source of the group of enzymes collectively called
ceca apparently do not have an obligatory role in prostaglandin synthetases.62 The action of the prosta-
osmoregulation in some species.252 Additionally, many glandin synthetase cyclo-oxygenase upon arachidonic
birds have no functional or anatomic ceca. acid results in the formation of numerous prostaglandins
(PE2, PGF2a and PGD2) and thromboxanes (thromboxane
No studies were found that demonstrate the effect of A2 [TXA] and thromboxane B2), all of which have varying
lower intestinal disease on osmoregulation. Regardless, actions on cells. In response to renal ischemia and vaso-
diseases such as typhlitis and colitis may adversely affect constriction, prostaglandin and thromboxane production
water and electrolyte balance beyond simple intestinal is altered (primarily increased). These “alterations” subse-
fluid loss, and should be a consideration when treating quently result in varying effects on the body and kidney
affected birds. Aside from nephrotoxic drugs such as including changes in renal vascular resistance, blood
aminoglycosides, no studies were found that show a flow, recruitment of inflammatory cells and other physio-
clear correlation between antibiotic use for treatment of logic effects. Non-steroidal anti-inflammatories act to
colitis/typhlitis and altered osmoregulation. inhibit prostaglandin synthetase and represent another
method by which to “alter” these arachidonic acid by-
Uricotelism products and their subsequent actions.62
Uricotelism is simply the excretion of uric acid as the Specifically, TXA production, secondary to toxic or
end product of nitrogen metabolism. Birds lack car- ischemic injury, is considered the main cause of renal
bamyl phosphate synthetase, an enzyme needed to syn- vasoconstriction associated with acute renal failure and
thesize urea from amino acid nitrogen.99 While birds pro- is believed to play a pathogenic role in many forms of
duce very little urea, the avian urea cycle is important, kidney disease.92,93,95 Thromboxane A2, again an eicosanoid
but is primarily related to renal detoxification processes derived from the action of cyclooxygenase on arachi-
and not nitrogenous waste excretion.248 In birds, xan- donic acid, is produced by many mammalian cells
thine dehydrogenase is the terminal enzyme of purine including glomerular epithelial and mesangial cells,
metabolism and ultimately produces uric acid as the end renal medulla tubular cells and especially platelets.91-95
product of nitrogen metabolism.106,132 This is an adapta-
tion that allows birds to minimize urinary water loss. In mammals, TXA causes mesangial cell contraction
Because uric acid is osmotically inactive, little water is and is a potent vasoconstrictor. Both of these actions
required to excrete this nitrogenous waste.248 The true can result in decreased glomerular filtration rate
advantage of water conservation in adult birds is debat- (GFR).31,91,94,95 Renal vasoconstriction decreases GFR and
able, though. The real advantage of uricotelism may sim- delivery of oxygen and nutrients to tubular cells, result-
ply be the storage of nitrogenous waste in eggs where a ing in renal damage.95 Thromboxane A2 also promotes
water-soluble product such as urea may prove toxic to platelet aggregation and may be partially responsible for
the developing embryo.248 hemostatic abnormalities noted with renal disease.91,190
As histologic progression of renal disease continues
when TXA is inhibited, it is possible that TXA only helps
GENERAL MECHANISMS AND
CONSEQUENCES OF RENAL INJURY initiate kidney pathology.93
Initiation of Renal Disease The above-described outcomes of increased TXA pro-

duction serve only to show some of the possible nega-
Proposed mechanisms of the process of initiation of tive effects of one by-product created as a result of renal
renal injury and perpetuation of disease are complex, injury. Management of these negative effects may be
but have been described in mammals. These “mam- needed, especially when a clearly identified cause such
malian” mechanisms may or may not apply directly to as bacteria in the kidney parenchyma is not found. This
birds, but help form the basis on which some treatments then brings up the reasoning behind using products
are considered (see Part 2: Treatment, Nutritional such as omega-3 fatty acids and low-dose NSAIDs (non-
Supplementation and Non-steroidal Anti-inflammato- steroidal anti-inflammatory drugs) when managing some
ries). For this reason, some of the inflammatory cascade forms of renal disease.
that occurs with renal disease is described.
The products resulting from the arachidonic acid cas- Brief Review of Selected Potential
cade have effects throughout the body. For the purposes Consequences of Renal Disease
of this discussion, the cyclo-oxygenase pathway of the Kidneys are dynamic organs and are directly or indi-
arachidonic acid cascade will be briefly covered. rectly associated with multiple body systems. As a result,
457
renal disorders can lead to or be caused from multiple Abnormal Lipid Metabolism
other disease processes. Some processes, such as hyper- Aberrant lipid metabolism as evidenced by increased
tension, hypercoagulability and the nephrotic syndrome, serum total cholesterol, low-density lipoproteins and
are well described in mammalian renal disease, but are triglycerides has been noted in humans, cats and dogs
never or rarely discussed in the avian literature. with renal disease.31,179 In rats, lipid accumulation is
known to stimulate glomerular mesangial cell and
Hemostatic Abnormalities excess matrix production known as glomerulosclerosis.31
Abnormalities of hemostasis are noted with some forms Hyperlipidemia has been associated with glomeruloscle-
of renal disease and may lead to additional kidney or rosis and/or loss of renal function in rats, guinea pigs,
systemic disease. Platelet aggregation and activation rabbits and dogs.190 Glomerulosclerosis is histologically
occur secondary to complement activated antigen- similar to atherosclerosis and may share a common
antibody interactions and renal endothelial dam- pathogenesis.190 Although scarcely noted in the avian lit-
age.23,86,91,94 Activated platelets may then release vasoactive erature, abnormal lipid intake, production and/or
and inflammatory products (including TXA), growth metabolism may be associated with renal disease in
stimulation factors and facilitate the coagulation birds, as described below.
cascade.91,94 These reactions can result in glomerular
High-cholesterol diets actually may induce renal disease
damage via glomerular basement membrane thickening
in birds. Pigeons supplemented with dietary cholesterol
and, potentially, hyalinization and sclerosis.94
(0.2%, 0.4% and 0.5% of the diet) had a high incidence of
end-stage renal disease, atherosclerosis and increased
Fibrinous renal vessel thrombi have been noted in red-
mortality rate compared with controls.121 Although spe-
faced lovebirds (Agapornis pullarius) with membranous
cific data was not presented, pigeon mortality was influ-
glomerulopathy and in chickens with Erysipelothrix rhu-
enced largely by the degree and duration of hypercholes-
siopathiae sepsis. However, thrombus formation has
terolemia.121 The implication herein is that diets high in
been suggested to be rare in birds compared with mam-
cholesterol may lead to renal disease, at least in pigeons.
mals.86,212 Using multiple staining methods, it could not
be confirmed that fibrin-like thrombi noted histologically
Gout
in various psittacine birds with polyomavirus-associated
glomerulopathy were truly composed of fibrin.189 Renal disease may lead to numerous other conditions
including gout, which can further damage the kidneys or
Gastrointestinal Complications additional body systems.214 Gout reportedly may be
Gastrointestinal ulcerations are reported in some ani- caused by reduced excretion of urates or by increased
mals with uremia and advanced renal disease, but are dietary protein (although this has been disputed as dis-
rarely mentioned concurrently in clinical reports of birds cussed under Part 2: Treatment, Dietary Modification).236
Dehydration and many forms of renal disease including
with kidney disorders.26 In chickens, gizzard erosions
obstructed ureters and general kidney damage can result
have been associated with naturally occurring urolithia-
in decreased uric acid elimination. As blood levels of
sis.148 Due to the overall lack of reports in the reviewed
uric acid rise and exceed the solubility of sodium urate
literature, it is unlikely that birds with renal disease
in plasma (hyperuricemia), monosodium urate crystal
develop gastrointestinal ulcers.
precipitation is initiated.236 It has been concluded that
Intestinal inflammation may lead to renal disease. In gout may not prove to be a nutritional disease in birds
except under unusual circumstances such as deficiency
humans, inflammatory bowel disease (IBD) can be
of vitamin A.207
related to renal disorders.183 In humans, those with IBD
have a 10 to 100 times greater risk of developing nephro- Visceral gout results secondarily from elevated plasma
lithiasis compared with other hospitalized patients.183 uric acid levels and its resultant deposition on visceral
Human IBD patients also may have an increased risk of organs9 (Fig 16.2). During visceral gout, urate deposi-
glomerulonephritis and tubulointerstitial nephritis.183 The tions are commonly found on the pericardium, liver and
avian coccygeomesenteric vein drains the mesentery of spleen.134 Additionally, uric acid deposits are noted histo-
the hindgut into the hepatic portal and/or the renal por- logically within the lamina propria of the proventriculus,
tal vein.226 Colitis may serve as a source of infectious ventriculus and sometimes intestine and within the kid-
agents, toxins and inflammatory products to the avian ney, but can be found on or in any tissue. Visceral gout
kidney if blood flow draining the colon is diverted into may appear as a white coating when on the capsular sur-
the renal vasculature. As a result, antibiotic therapy face of affected tissue. Visceral gout has been associated
should be considered in all cases of colitis, especially with multiple forms of renal pathology.9,214 Experimentally,
when renal disease is suspected or confirmed. visceral gout has been induced in chickens fed excessive
Drury Reavill
Fig 16.2 | An adult cockatiel (Nymphicus Fig 16.3 | An adult budgerigar Fig 16.4 | An adult female black lory
hollandicus) with visceral gout. Note the (Melopsittacus undulatus) with articular gout (Chalcopsitta atra) with severe renomegaly
whitish deposits encasing the heart. The secondary to renal carcinoma. The post- and visceral and articular gout. This female
bird died with renal failure due to chronic mortem picture shows subcutaneous recently laid two eggs, but the ovary
renal fibrosis and interstitial nephritis. “gouty” deposits over the dorsal tar- (arrow) was quiescent at the time of death.
sometatarsus and ventral phalanges. The Histologically, renal tubular necrosis with
skin has been teased open with a needle. urate stasis and multiple acute “gout tophi”
were noted. The etiology was not defined.
dietary calcium and a diet deficient in vitamin A, admin- even if the patient is clinically normal or improved.64
istered various nephrotoxic agents, and following When repeating kidney biopsies, the author has noticed
ureteral ligation and urolithiasis.9,214 no increase in scarring (gross or histologic lesions) or
other abnormalities at the prior surgery sites, suggesting
Articular gout results from the accumulation of urates in some treated birds have good regenerative and/or heal-
the synovial capsules and tendon sheaths of the joints9 ing properties. Although these repeat biopsies are
(Fig 16.3). Diffuse urate deposits on visceral surfaces do encouraging, the long-term health of these patients’
not occur in articular gout.214 However, visceral and artic- kidneys is still unknown.
ular gout can be present in the same bird (Fig 16.4).
Gross lesions typically consist of soft swellings on the feet
GENERAL RENAL DISEASE
at the metatarsophalangeal and interphalangeal joints.214
CATEGORIES
These swellings appear to be painful, as noted in clinical
cases. Spontaneous articular gout in birds without under- Nephritis
lying renal pathology is relatively uncommon and Nephritis is simply inflammation of the kidney and may
appears to have a hereditary basis, at least in chickens.214 involve the interstitium, tubules and/or the glomerulus
(although “glomerulonephritis” is typically reserved for
Continuing Damage glomerular lesions). While “pyelonephritis” has been
Once renal damage occurs, persistent and progressive described in birds, this term is technically incorrect, as
kidney damage is likely to occur, even if the initial insult avian species lack a renal pelvis.116,214 Nephritis is a non-
is treated and “cured.”114 In humans, 50 to 60% of chil- specific description, but some histological patterns and
dren with pyelonephritis develop irreversible lesions of (especially) identification of infectious organisms help
define the etiology.
the renal parenchyma.13 Although no refereed literature
describes the post-treatment progression of renal lesions
in living avian patients, the author reported repeated Glomerulopathies
kidney biopsies in numerous birds in an effort to help In the literature reviewed for this chapter, glomerular
evaluate their clinical progression.64 Repeat biopsies have disease has been loosely termed “glomerulonephritis,”
shown that in birds with histologic confirmation of vari- but unless inflammation is specifically present, the term
ous kidney diseases, some mild renal lesions persist, “glomerulopathy” would be more appropriate. Glomeru-
459
lonephritis describes inflammation of the glomerulus, cient) chickens develop glomerulonephritis. Although
usually considered mediated by the deposition of gross histologic lesions are similar, bursectomized chick-
immune complexes or antiglomerular basement mem- ens develop no IgG glomerular basement membrane
brane antibodies.22,94,239 A more accurate description of deposits compared to controls when glomerulonephritis
glomerular lesions, based on light and electron micro- is induced in both groups.22 These and other findings
scopy and immunohistochemistry, helps define the support the conclusion that cell-mediated immunity or
actual type of glomerulopathy present. some other non-humoral immune response is responsi-
ble for inducing glomerulonephritis in chickens.22,237
Glomerular disease is the most important cause of end- Interestingly, in the above described study, even birds
stage renal disease in humans worldwide and of chronic with massive mesangial enlargement maintained normal
renal insufficiency/failure in dogs.109,237,239 Proteinuria is glomerular filtration.22 Due to the small centrally oriented
the hallmark sign of glomerulonephritis in mammals avian glomerular mesangium, the capillary loops were
prior to the onset of clinical renal insufficiency..94 How- only slightly displaced to the periphery without compro-
ever, chicken leukocytes lack proteolytic enzymes that mising function.22 Given our current knowledge regard-
would potentially damage the glomerular basement ing the differences between avian and mammalian
membrane (and allow protein leakage) and birds may, in species, renal biopsy is the best way to definitively diag-
fact, not develop pathologic proteinuria with glomeru- nose glomerular (and other) kidney diseases in birds (see
lopathies.22 In one study, no pathologic proteinuria was Part 2: Diagnostic Tests, Biopsy).
found in chickens with experimental autoimmune
glomerulonephritis.21 As noted below, glomerulopathies Infectious Diseases
are well documented in avian species, but numerous
Bacterial
differences exist when comparing this disease in birds
Certain patterns may be expected with bacterial nephri-
and mammals.
tis. Chickens experimentally infected with E. coli (E. coli
01K67[B12]), Staphylococcus aureus and Actinomyces
The cause of glomerulopathies is generally assumed to
pyogenes developed a fairly consistent pattern and pro-
be immune-mediated, but the inciting etiology is often
gression of renal disease.219
unknown. Membranous nephropathy, the most common
cause of nephrotic syndrome in humans, is usually idio- Birds inoculated subcutaneously developed more severe
pathic and specific etiologies are identified in only 20% renal lesions and these lesions were noted earlier than
of cases.196 With few exceptions, the causes of glomeru- those exposed to bacteria per os. Additionally, lesions
lopathies in birds are poorly studied. Polyomavirus infec- were more severe in birds infected with E. coli and
tion is associated with membranous glomerulopathy in S. aureus compared to the slight reaction induced from
psittacines.86,189 Glomerular pathology has been noted in A. pyogenes. Gross renal changes included congestion,
chickens with various septic conditions and naturally enlargement and hemorrhagic foci. Although specific
occurring multicentric histiocytosis.102,219 Glomerulo- timelines were not given in regard to lesion develop-
pathies also can be induced experimentally in chickens ment, bird kidneys were histologically examined at 4, 7,
by intravenous fungal injections, Plasmodium galli- 10, 14 and 21 days postinoculation. The early-stage
naceum infections and by feeding aflatoxin.158,214 Grossly lesions consisted of acute interstitial nephritis (mainly
normal 6- to 7-week-old broiler chickens at slaughter lymphocytes, plasma cells and macrophages), prominent
have been diagnosed with proliferative glomerulonephri- congestion and hemorrhage. The lesions progressed to
tis of unknown etiology.193 Proliferative glomerulopathy nephrotoxic nephritis and included tubular epithelial
can be induced in pigeons fed diets high in choles- cell degeneration and necrosis with the formation of
terol.121 It has been suggested that because of the exten- hyaline casts and eosinophilic material. Later histology
sive (dual) renal blood supply, severe chronic glomeru- showed decreased congestion, persistence of mononu-
lonephritis may persist without any clinical manifesta- clear cells, introduction of connective tissue running
tion in birds.214 It has been further suggested that avian around hyperplastic tubules and glomerular lesions.219
glomerulonephritis may be present in far more birds
than it is currently diagnosed.214 Certain renal histologic characteristics, with or without
organisms present, may suggest an ascending or hema-
Although humorally mediated immunity is frequently dis- togenous bacterial infection in the avian kidney. The typ-
cussed as the etiology of glomerulopathies, research has ical lesions suggestive of bacterial nephritis include
strongly suggested that cell-mediated immunity plays an tubular dilatation and impaction with inflammatory
important role in producing glomerular disease in chick- cells.214 As nephritis becomes chronic, tubular necrosis,
ens and other animals.22,109,237 Under experimental condi- cyst formation, distortion and interstitial fibrosis with
tions, cyclophosphamide bursectomized (humorally defi- mononuclear cell infiltration become evident.214
Using sterile collection and culture methods, bacterial neys. Numerous viruses may infect and affect avian kid-
nephritis is definitively diagnosed by recovering bacterial neys (Table 16.1). Histologic patterns are highly variable,
organisms from affected kidneys. Light microscopic iden- as some viruses, such as pheasant coronavirus-associated
tification of bacteria within renal tissue may be difficult, nephritis, directly affect the kidneys while others, like
as has been noted in dogs and swine with renal dis- psittacine herpesvirus and polyomavirus, damage renal
ease.26,54 In a Coturnix quail processing plant outbreak, tissue as part of a more systemic process.126,186,202
Erysipelothrix rhusiopathiae was cultured from multiple
organs.169 While the kidneys were swollen and congested, Other viruses may cause minimal to no renal disease,
no organisms were specifically noted histologically, which but can be identified in the avian kidney because of
emphasizes the importance of tissue culture.169 Specifi- viremia and/or viral replication and transmission
cally, Escherichia coli has been identified in chickens as a through the urinary tract. For example, the reovirus that
cause of bacterial nephritis (pyelonephritis).116 As a com- causes viral arthritis of chickens infects the kidneys
ponent of systemic paratyphus, Salmonella typhimurium within a few days of inoculation, but causes minimal, if
var. Copenhagen was identified in kidney tissue and most any, renal lesions.174 Some viral infections such as the
frequently caused interstitial nephritis in a study of 78 West Nile virus are best identified in the kidney, and pro-
experimentally infected pigeons.87 The same organism vide an additional reason to save extra renal tissue
also was recovered from kidney tissue, as a component (frozen and/or formalinized) for later testing124 (Fig 16.6).
of systemic salmonellosis, in pigeons from a large pro-
Parasitic
duction colony.121 As is likely true of most viral and fungal
renal diseases, bacterial nephritis is often a component of Renal Coccidia
systemic infection and multiple organs may be involved.187 Primary and secondary renal parasites have been noted
In summary, any septicemia can potentially result in kid- throughout the avian literature and some contribute to
ney infection and inflammation (Fig 16.5). significant morbidity and mortality18,19,43,69,76,82,83,133,160,175,177,194,
217,218,236,253
(Table 16.2). Renal coccidiosis, found predomi-
Viral nately in some waterfowl and marine species, is the
Viruses perhaps have the most varied effect on avian kid- most frequently reported avian renal parasite in those
Table 16.1 | Viruses Known to Infect or Affect Avian Kidneys

Virus Common Name Renal Lesions Reference(s)
Adenovirus New gosling virus enteritis virus Renal hemorrhage 44
Hydropericardium syndrome in broiler chickens Renal hemorrhage, tubular nephrosis 2
Astrovirus Duck astrovirus (aka duck hepatitis II) Swollen congested kidneys 202
Coronavirus Infectious bronchitis virus Interstitial nephritis, urolithiasis, visceral gout 202, 231, 243
and renomegaly
Enterovirus Avian nephritis virus Renal disease of young chickens and turkeys 202
Herpesvirus Marek’s disease Renal lymphoma, renal masses 202
Psittacine herpesvirus Renomegaly 202
Pigeon herpesvirus-1 Renal necrosis 202
Orthovirus Influenza A of ratites Renomegaly and green urate-filled ureters 202
Paramyxovirus Pigeon paramyxovirus-1 Renomegaly, lymphoplasmacytic nephritis 202
Polyomavirus Hemorrhagic nephritis enteritis of geese Nephritis 101
Avian polyomavirus Basophilic and amphophilic mesangial cell 126
intranuclear inclusion bodies, minimal lesions
Psittacine polyomavirus Membranous glomerulopathy 202
Passeriforme polyomavirus Renomegaly and perirenal hemorrhage 202
Reovirus Viral arthritis or tenosynovitis of chickens None to minimal inflammation 174
Retrovirus Avian Leukosis/lymphoid leukosis Cancer-nephroblastomas, renal lymphoma/ 202
adenoma/carcinoma, leukemia
Reticuloendotheliosis virus Renal tumors 202
Togavirus West Nile virus Neptritis (Fig 16.6) 124
Avian viral serositis (EEE) Pale kidneys 202
Chukar alphavirus (EEE and WEE) Urate-distended kidneys 202
Turkey alphavirus (EEE) Renal necrosis 202
Guinea fowl alphavirus (EEE) Renomegaly 202
Crane alphavirus (EEE) Necrotic nephritis and visceral gout 202
Emu WEE Renomegaly, necrotic nephritis 202
This table should serve only as an example of the large variety of viruses known to be associated with the avian kidney.
EEE = eastern equine encephalitis WEE = western equine encephalitis
461
Fig 16.5 | A cloacal carcinoma, right ureteral obstruction Fig 16.6 | West Nile virus-associated nephritis in an immature
(arrow) and Streptococcus sp. nephritis in an adult female female Swainson’s hawk (Buteo swainsoni). Note the moderate
Amazona sp. parrot. The Streptococcus sp. isolated from the kid- deposition of fat indicating the bird was in good overall body
ney and heart blood was resistant to enrofloxacin, with which condition prior to acute death. The kidneys are pale. Two
this bird was being treated chronically for cloacal straining. ovaries also are present as indicated by the lines.
Table 16.2 | Reported Incidence of Renal Coccidia in Various Avian Species

Associated with
Affected Avian Species Eimeria Species Reference(s)
Morbidity/Mortality
Bufflehead (Bucephala albeola) Unidentified N/A 84
Canvasback (Aythya valisineria) Unidentified N/A 84
Duck, long-tailed (Clangula hymenalis) E. somateriae N/A 253
Duck, mallard (Anas platyrhynchos) E. boschadis N/A 253
Eider, common (Somateria mollissima) E. truncata, Mortality in ducklings 217, 253
E. somateriae (E. somateriae)
Gadwall (Anas strepera) Unidentified N/A 84
Goldeneye, common (Bucephala clangula) Unidentified N/A 84
Goose, bar-headed (Anser indicus) E. truncata N/A 253
Goose, Canada (Branta canadensis) E. truncata N/A 253
Goose, domestic (Anser domestica) E. truncata Mortality in goslings 83, 84, 177
Goose, greater snow (Chen caerulescens) E. truncata N/A 253
Goose, graylag (Anser anser anser) E. truncata Mortality in goslings 177, 253
Goose, lesser snow Unidentified Mild morbidity 83
(Chen caerulescens caerulescens)
Goose, Ross’s (Chen rossii) E. truncata N/A 253
Gull, black-headed (Larus ridibundus) E. renicola N/A 82
Gull, herring (Larus argentatus) E. wobeseri, E. goelandi Incidental finding, nestlings 82
Loon, common (Gavia immer) E. gaviae Inconclusive 82, 160
Oldsquaw (Clangula hyemalis) E. somateriae Unlikely 76
Owl, great-horned (Bubo virginianus) Unidentified N/A 253
Penguin, little (Eudyptula minor) Unidentified Mortality 176
Pintail, northern (Anas acuta) Unidentified N/A 84
Puffin, Atlantic (Fratercula arctica) E. fraterculae Incidental findings, nestlings 133
Redhead (Aythya americana) Unidentified N/A 84
Scaup, lesser (Aythya affinis) Unidentified N/A 84
Shearwater, Cory’s (Calonectris diomedea) Unidentified N/A 253
Shearwater, short-tailed (Puffinus tenuirostris) Unidentified N/A 253
Shoveler, northern (Anas clypeata) Unidentified N/A 84
Swan, mute (Cygnus olor) E. christianseni N/A 253
Swan, whistling (Cygnus columbianus) Unidentified N/A 84
Teal, blue-winged (Anas discors) Unidentified N/A 84
Teal, green-winged (Anas crecca) Unidentified N/A 84
Widgeon, American (Anas americana) Unidentified N/A 84
Woodcock (Scolopax minor) Unidentified N/A 253
N/A = not available
Robert E. Schmidt
Robert E. Schmidt
Fig 16.7a | Renal coccidiosis in a screamer (Chauna sp.). Note Fig 16.7b | Close up of a renal tubule with numerous oocysts
the numerous oocysts and various developing stages of the par- being released into the lumen (arrows).
asite throughout the renal tubules.
species and has been clearly associated with disease in contain different endogenous stages of coccidian
some cases.76,82-84,133,160,176,177,217,253 Reports of various other oocysts.160,177,217 The renal tubules are parasitized and
parasitic diseases affecting the kidneys are noted, but histologic lesions vary from mild dilatation to severe
their significance is not well established. tubular destruction with associated degrees of inflamma-
tory cell infiltrate (unusually mononuclear).76,83,160,177,217
Several renal coccidia species have been identified and The tubules are often distended with endogenous
primarily include Eimeria truncata, E. somateriae,
developmental stages (micro- and macrogamonts,
E. christianseni, E. boschadis, E. gaviae, E. fraterculae,
macrogametes) and maturing Eimeria spp. oocysts217
E. goelandi and E. wobeseri.82,83,133,160 Disease has ranged
(Figs 16.7a,b). In severe cases tubular nephrosis, necro-
from mild histologic changes found incidentally (most
sis and interstitial nephritis, potentially causing signifi-
species) to acute renal failure and death, such as in juve-
cant renal dysfunction, may be noted.217
nile eiders (Somateria mollissima) and domestic geese
(Anser domestica).76,83,217 Flock mortality in domestic
Sarcocystis
geese due to E. truncata has been reported to be as
high as 87%.76 Numerous other parasites have been noted in the kid-
neys of birds, but oftentimes association with disease is
Renal Eimeria spp. oocysts are passed in feces via the not clear. Canaries (Serinus canaria) experimentally
ureter and sporulate rapidly in the environment.217 infected with Sarcocystis falcatula developed mild mul-
Affected birds typically breed in large colonies or are tifocal interstitial renal infiltrates and glomerular hyper-
otherwise under crowded conditions, which likely favors trophy with mesangial hyperplasia that modestly pro-
transmission of this parasite.177,217 The prepatent period gressed with duration of infection.218 While precystic
appears to range between species and has included 5 to merogony was primarily noted in the pulmonary tissue,
21 days.83 Although transmission between different avian infected canaries had low levels of merogony in the
species is not clear, one study suggested that renal coc- kidney and other tissues. Similarly infected pigeons
cidia of geese do not infect ducks.83 developed no renal lesions.218 Sarcocystis organisms also
have been noted histologically in the renal parenchyma
The clinical gross and histologic abnormalities noted
of cockatiels, but again the significance is unclear
with renal coccidiosis seem to be fairly consistent across
(T. Lightfoot, personal communication, 2003).
affected species. Most clinically affected species are
young birds.177,217 Clinically affected birds are typically
Microsporidia
emaciated and may have diarrhea with or without
Microsporidia (Encephalitozoon spp.) have been
blood.83,160,177,217 It should be kept in mind that many
reported birds are wild and also have had intestinal par- reported in numerous avian species with variable effects
asites that may contribute to the described clinical signs. on the kidney. A psittacine beak and feather virus-posi-
Grossly, the kidneys are often enlarged with white to yel- tive eclectus parrot (Eclectus roratus) had heavily para-
lowish nodules containing urates and/or oocysts.76,83,160,217 sitized (Encephalitozoon hellem) kidney cells with asso-
ciated renal tubular distension. As has been noted in
Cytologic smears of renal tissue and ureters often other reported cases, renal cellular reaction was minimal
463
in the eclectus. Similar histological lesions and parasite diffuse lymphoplasmacytic infiltration in the wall of the
morphology and locations (liver, kidney, intestines) ureter and (parasitized) epithelial wall hyperplasia.236
also have been reported in three species of lovebirds, Regarding the experimentally infected chicks, the authors
budgerigars (Melopsittacus undulatus) and a double- concluded that Cryptosporidium baileyi can be highly
yellow headed Amazon parrot (Amazona ochroceph- pathogenic, and induce mortality and urinary tract infec-
ala).175,192,194 The author also has seen renal microspori- tions in chickens infected with Marek’s disease virus
diosis in a canary (Serinus canaria) that presented for (an immunosuppressive effect).1 Several authors have
acute illness and died shortly thereafter. Histology con- hypothesized that urinary tract Cryptosporidium infec-
firmed that numerous microsporidial organisms (not fur- tion originates in the cloaca and retrogrades into the kid-
ther defined) were present in the renal tubules and neys via the ureters.170,236 Although relatively uncommon,
were associated with tubular necrosis. Other histologic urinary tract cryptosporidiosis and associated disease
lesions were minimal to mild, placing renal failure as the seem to be primarily a concern in chickens, especially
likely cause of death. Although it is not clear what role those with concurrent immunosuppressive illness.
the kidney plays in disease, some believe that E. hellem
is an avian and human pathogen, and may be primarily Flukes
found in immunocompromised individuals.194 Scattered reports of renal flukes are noted in the litera-
ture. Spindle-shaped eggs, belonging to the blood fluke
Cryptosporidia Dendritobilharzia anatinarum, were identified in
Urinary tract cryptosporidiosis also has been noted in kidney tissue pressed between glass slides in mallards
multiple bird species with varying associated disease. (Anas platyrhynchos). The birds died from severe enteri-
Although renal cryptosporidiosis is infrequently tis associated with blood fluke eggs, but no renal histol-
reported, it has been directly associated with kidney ogy was described.43 Eggs of other schistosomes may
lesions in a 4-month-old black-throated finch (Poephila occasionally cause granulomatous ureteritis in water-
cincta), an 8-week-old Sonnerat’s junglefowl (Gallus fowl.188 Parasites of the genus Renicola also may para-
sonneratii), 4-month-old pullets and adult laying sitize the renal tubules of several waterfowl species.188,225
hens.19,85,170,199,236 Four-day-old chickens co-infected with The renicolid flukes appear to have an indirect life cycle,
Marek’s disease virus also have been studied.1 Clinical and likely first infect mollusks and then mature in the
signs ranged from acute death (finch and junglefowl) to renal tubules of susceptible species.225 Eucotylid renal
thinning, depression, leg weakness and respiratory dis- flukes may reside in the dilated ducts of the renal
tress (4-month-old pullets and 4-day-old chicks ) to medulla of pigeon and passerine kidneys. They seldom
slightly increased morbidity and mortality (adult chick- cause problems and their eggs may be found in the feces
ens).1,19,85,170,199,236 Pulmonary cryptosporidiosis also was a and confused with other fluke eggs.98 Clinical descrip-
common feature of the pullets.170 tions of affected animals are poorly described.
Similarities were noted among gross and microscopic Miscellaneous Parasites

findings. The affected black-throated finch and Sonnerat’s Other parasitic diseases also may be found incidentally
junglefowl had pale and swollen kidneys, and all birds in the kidneys of birds. Visceral larval migrans lesions
had some degree of tubular epithelial tissue change with consisting of a granulomatous reaction surrounding
organism colonization.1,19,85,170,199,236 The finch, adult layers, intact or degenerate Baylisascaris procyonis larvae in
pullets and chicks also had interstitial nephritis, while the renal (and other tissue) parenchyma of the house
the junglefowl had no inflammatory response.1,19,85,170,199,236 sparrow (Passer domesticus) were noted in one study.
Although no organisms were specifically found in the As most of the mixed species of birds had neural larval
kidneys, a diamond firetail finch (Stagnopleura bella) migrans only, the renal lesions seemed comparatively
with proventricular cryptosporidiosis also had similar uncommon.69 Chickens and pigeons have been experi-
tubular lesions in addition to multifocal amyloidosis mentally infected with Toxoplasma gondii oocysts and
(kidney included), severe chronic urate nephrosis, and evaluated for disease. While infected chickens developed
protein and cellular tubular casts.19 no clinical signs and minimal evidence of infectivity,
pigeons showed rapidly progressive disease (diarrhea,
Increased incidence of visceral gout, 1 to 2% higher trembling, incoordination, death) and toxoplasma
than expected mortality, and numerous stages of Crypto- organisms in the kidney and other tissues. The authors
sporidium sp. organisms within the epithelial cells lining stressed the importance of the pigeon crop in shedding
the renal collecting tubules and ureters (of histologically the organisms with no emphasis on the kidneys.18 It is
evaluated kidneys) were found in egg-laying chickens probable that other parasites can affect the avian kidney
from a production facility. Visceral gout was likely caused and should be kept as an unlikely or rare differential
by the partial ureteral obstruction resulting from heavy diagnosis for renal disease.
Fungal Sections I and II.

Fungal nephritis is uncommonly reported in birds. One
chicken with renal and pulmonary cryptosporidiosis had Vitamin D Intoxication
Aspergillus sp. lesions in the lungs, air sacs, thoracic Vitamin D intoxication has been discussed in birds.181,187
walls and kidneys.170 In a separate study of 4-day-old Vitamin D is converted in the liver to 25-hydroxychole-
chicks co-infected with Cryptosporidium baileyi and calciferol and then further hydroxylated to 1,25-dihy-
Marek’s disease virus, one bird had necrotic renal droxycholecalciferol in the kidney. Avian macrophages
aspergillosis.1 Fungal nephritis, caused by Aspergillus have the capacity to convert vitamin D to its active form
flavus-oryzae group, was the only lesion seen in a mori- 1,25-dihydroxycholecalciferol.119 It is 1,25-dihydroxyc-
bund grey-headed albatross.235 While focal coagulative holecalciferol that enhances the intestinal absorption of
necrosis, fibrous tissue and pronounced cellular reaction calcium and phosphate.208,211
consisting of macrophages and multinucleated giant
cells surrounding occasional fungal hyphae were noted, As a result of excessive calcium uptake, visceral calci-
the lesions spared most of the renal tissue and did not nosis, nephrocalcinosis, visceral gout and urate nephro-
account for the bird’s poor condition.235 Given the close sis are considered frequent complications of vitamin D
association between the air sacs and kidneys, direct intoxication in birds.187 Symptoms of hypervitaminosis D
extension from the respiratory system (rather than pri- include hypercalcemia, anorexia, nausea, polyuria, poly-
mary renal invasion) is the likely cause of the necrotic dipsia, demineralization of bones, disorientation, painful
fungal lesions in the kidneys. joints and muscle weakness.211 In normal animals experi-
mentally subjected to hypervitaminosis D, 25-hydroxyc-
holecalciferol, and not 1,25-dihydroxycholcalciferol,
Nephrosis
increase in the serum.208 Chicks fed Cestrum diurnum
Nephrosis is a non-specific histopathologic change charac- leaves, which contain an analog of 1,25-dihydroxychole-
terized as any degenerative, non-inflammatory lesion of calciferol, develop nephrocalcinosis and hypercalcemia,
the kidney, from cloudy swelling to necrosis, whatever the
but the ultrastructural lesions are different than is noted
cause.214 (Figs 16.8, 16.9) This is a microscopic diagnosis
with vitamin D toxicity.208
that cannot be made with gross observation. Due to its
role in elimination, the avian kidney is vulnerable to the Hypervitaminosis D & A may occur when feeding devel-
effects of many chemical toxins.214 Inflammatory changes oping birds vitamin D containing supplements (Fig
may develop, especially if the condition persists, and may 16.10). A 3.5-month-old blue and gold macaw (Ara ara-
confuse the diagnosis.214 It was noted that tubular lesions rauna) and 5.5-month-old salmon-crested cockatoo
may be reversible if the noxious substance is removed, (Cacatua moluccensis) from the same household devel-
provided the pathologic changes are not too advanced.214 oped polyuria, polydipsia and anorexia after being fed a
Causes of avian nephrosis have included avian malaria diet (including supplements) with excessive vitamins A
and hemoglobinuria, adenovirus infections, Clostridium and D3 and of calcium.211 The cockatoo was hypercal-
welchii enterotoxemia, and lead, zinc, cadmium, calcium, cemic and had radiographic evidence of renomegaly.
aminoglycosides, phenoxyacid, sodium, ochratoxin A, Hypercalcemia, hyperphosphatemia, hyperuricemia and
ethylene glycol, 2,4-D, cadmium and 3-chloro-p-toluidine elevated plasma creatine kinase were noted in the
(avicide) toxicities.2,14,15,16,30,55,72,125,154,161,178,214,224,242 This list is macaw. The calculated levels of vitamins A (119,000 IU/kg
incomplete and serves only to emphasize the diversity of feed) and D3 (26,790 IU/kg feed) were over 20 times the
potential avian nephrosis-inducing agents. Although many recommended levels (5000 IU/kg feed and 1000 IU/kg
toxins have been shown to induce nephrosis and other feed, respectively). Vitamin D3 is considered toxic at 4 to
kidney diseases, renal lesions caused by specific toxicities 10 times the recommended amount. The cockatoo died 6
are difficult to prove outside of a controlled study. days after presentation and had chronic interstitial
nephritis and calcifications in the kidney, proventriculus
Hypertonic solutions also may cause a specific osmotic
and lung. The macaw improved gradually and became
nephrosis in birds.214 Hypertonic sucrose solutions (con-
disease free after discontinuing the supplemental vita-
centration not recorded) given intravenously have
mins and minerals. Hypercalcemia was attributed to over-
caused extensive vacuolation of the proximal convoluted
supplementation with calcium and the vitamin mixture.
tubules in birds.214 Similar renal findings have been
noted in other animals and man when injected with
It has been suggested that African grey parrots (Psittacus
hypertonic sugar solutions and dextran intravenously.214
erithacus) may be susceptible to hypervitaminosis D,211
although no reviewed papers support this statement.
Selected Toxic and Nutritional Diseases Any bird species can potentially be susceptible to hyper-
Also see Chapter 4, Nutritional Considerations: vitaminosis D.
465
Drury Reavill
Fig 16.8 | A young adult male canary Fig 16.9 | An adult male cockatiel Fig 16.10 | A young blue and gold
(Serinus canaria) with tubulonecrosis, min- (Nymphicus hollandicus) with severe renal macaw (Ara ararauna) with suspected vita-
eralization and urate stasis of unknown eti- tubular mineralization and necrosis. All min D3 toxicity from excess supplementation
ology. Note the pale swollen kidneys with renal divisions are pale. The etiology is in the diet. All renal divisions are severely
almost indistinct renal divisions. Urates are undefined. swollen and indistinguishable from each
seen in both ureters (arrow points to left other. The primary histologic lesion was
ureter). nephrosis.
Hypercalcinosis clear correlation with mild and severe metastatic (renal)

High calcium intake also has been directly correlated with mineralization in birds fed 0.7% and 1.5% calcium,
renal disease in birds. Broiler chicks fed 3.27% calcium in respectively. The young birds fed 0.7% and 1.5% calcium
the diet for 15 weeks, starting at 18 days old, developed died by 24 to 32 days old and never fledged (32 to 35
numerous renal lesions throughout the study.41 Nephrosis days). Growth rate and hatchability were poor only in
was noted by 7 weeks and progressed to nephritis (10 the groups fed 1.5% calcium. While only a few adults
weeks), visceral gout (11 weeks) and replacement of the died by 5 months on diets containing 1.5% calcium,
kidney parenchyma with urate granulomas (12 weeks).41 most had metastatic renal mineralization when fed 0.7%
In two separate studies, some growing chickens fed 3% calcium. Birds fed 0.3% calcium had no evidence of
calcium and 0.38% and 0.4% phosphorous, respectively, metastatic mineralization, and had good hatchability and
developed renal lesions such as nephritis, and ureteral growth rates (D. Phalen, personal communication,
and collecting duct occlusion due to probable calcium 2003). This study suggests that some species, such as
urate salts.162 Limestone sand substrate (13.48% calcium budgerigars, may be very sensitive to dietary calcium lev-
and 0.02% phosphorous) was associated with rickets and els and that supplementation should be used cautiously.
nephrocalcinosis in young ostriches. Clinically affected
birds returned to normal and no new cases developed
Hypovitaminosis A
once the substrate was changed to acid-washed sand Hypovitaminosis A also may lead to renal disease in
(0.03% calcium and 0.02% phosphorous).162 avian patients. In birds with hypovitaminosis A, the
ureters and renal collecting ducts may undergo metapla-
In a study involving young and adult budgerigars (Melo- sia, changing the normal double-layered epithelium to
psittacus undulatus), increasing dietary calcium levels keratinized stratified squamous tissue.214 These epithe-
were shown to be more renal toxic than was excess vita- lial changes can result in decreased mucin production
min D3 (D. Phalen, personal communication, 2003). and excessive keratin leading to plug formation and
Parent birds were fed diets containing 0.3%, 0.7% and ureteral obstruction.214 The consequential (secondary)
1.5% dietary calcium with a range of 500, 1000, 1500 lesions include renal tubular dilatation and necrosis,
and 3000 IU of vitamin D3 per kg/feed. The adults subse- tophus formation and interstitial fibrosis.214 Nephrosis,
quently fed the young the same diet. When fed a diet nephritis, visceral gout and severe replacement of the
containing 3000 IU of vitamin D3 per kg/feed, there was kidney parenchyma by urate granulomas were noted in
a questionably increased mortality rate only in the birds broiler chicks fed vitamin A-deficient diets for 15 weeks
receiving 1.5% dietary calcium. However, there was a starting at 18 days old.41 See Chapter 4, Nutritional
Considerations: Section II, Nutritional Disorders, for “Diet-Induced Renal Disease of Color Variety
Hypervitaminosis A. Psittacine Birds”
Although not formally entered into the veterinary litera-
High-Cholesterol Diets ture, there appears to be a form of renal disease induced
Cholesterol supplemented in the feed can induce signifi- by feeding predominately pelletized diets to various color
cant renal disease in pigeons.121 Crystalline cholesterol variety psittacine birds (M.S. Echols, unpublished data).
and 10% lard were added to the diets of these pigeons All affected birds observed by the author have been color
under experimental conditions. The kidneys of some variety cockatiels (Nymphicus hollandicus), lovebirds
affected birds are firm, diffusely off-white, have an irregu- (Agapornis spp.), budgerigars and parrotlets (Forpus
lar capsular surface and may be enlarged up to 3 times spp.) and have eaten a predominately commercial pel-
their normal size. All renal components are susceptible letized diet. As most of the major brands of commercial
and lesions may include tubular degeneration and dilata- pelletized diets have been involved, there appears to be
tion, glomerular hypercellularity and hypertrophy (prolif- no predilection toward any one manufacturer’s product.
erative glomerulopathy), periglomerular fibrosis, lipid- With the exception of a history of predominately com-
laden cells within the glomeruli and multifocal, acute mercial pelletized diet, affected birds do not display any
intersitial nephritis.121 Since only mortality and necropsy characteristics pathognomonic for “diet-induced renal
results were reported, clinical information such as diag- disease.” Of the birds with suspected “diet-induced renal
nosis and management/treatment were not provided. disease,” in which the kidneys have been histopathologi-
However, this does bring up the potential complication cally examined (pre- and postmortem), lesions have been
of feeding some birds high-cholesterol foods. limited to non-specific tubular nephrosis and were
reversible after feeding a non-pelletized diet for 1 to 3
High-Protein Diets months. The diet should be converted to one appropri-
High-protein diets have been associated with renal ate for the species being treated.
disease in birds, but only under specific conditions.
Mycotoxic Nephropathy
Compared to a low-protein diet group, pigeons fed a
Mycotoxic nephropathy, due primarily to ochratoxin A,
high-protein diet had an observed increase in drinking
has been reported in chickens and ducks.63,149,224 Ochra-
rates and urine production.153 Unfortunately, too little
toxin A is produced by several species of Aspergillus and
information was present to draw any conclusions relat-
Penicillium.149 Ochratoxicosis occurs primarily because
ing dietary protein to renal disease. It has been shown
of ochratoxin A buildup in chick feed stored under con-
that feeding 18-day-old broiler chicks a 42.28% protein
ditions of excessive moisture, and has been identified
diet for 15 weeks did induce multiple renal abnormali-
from moldy feed, rice, groundnuts and foods prepared
ties (primarily nephrosis and visceral gout).41 Extra-
from these materials.149,157,224 Ochratoxicosis causes liver
ordinarily high protein levels in the diet of genetically
and kidney damage, and specifically induces degenera-
predisposed chickens have been shown to cause gout,
tion and vacuolation of hepatic cells and distension,
but a direct relationship with renal disease has not been
enlargement and hypertrophy of renal proximal convo-
established. A more detailed discussion of the effects of
luted tubules, respectively.63 Because of the multiple
dietary protein and hyperuricemia are discussed under
potential sources of the toxin, it is reasonable to assume
Part 2: Serum or Plasma-based Biochemistries, Uric Acid, that multiple avian species, other than chickens and
and Part 2: Dietary Modification, Protein. ducks, can be exposed to and damaged from ochratoxin.
Diets high in urea also have been linked to nephritis Other mycotoxins also have been closely correlated with
outbreaks in poultry.42 Fish meal adulterated with urea renal disease in birds. Oosporein, a toxic pigment pro-
was linked to high (6-8%) mortality in two separate duced by Chaetomium trilaterale, C. aureum and sev-
farms. Clinically affected birds had gross lesions that eral other species of filamentous fungi, is considered to
ranged from pale nephromegaly and hepatosplenomegaly be primarily a renal toxin.184,185 The importance of
to urolithiasis and visceral gout. Histologic lesions oosporein is that the toxic isolates have been found in
ranged from interstitial, perivascular and pericapsular various agricultural commodities such as animal feeds,
nephritis to proliferative glomerulopathy, and severe cereal grains and food products. Moldy corn in particu-
tubular and glomerular atrophy and fibrosis in severe lar, growing C. trilaterale, may yield high concentrations
cases. The disease was termed “nephritis-nephrosis syn- of oosporein toxin. In studied young broiler chickens
drome in poultry” and was eliminated when the urea- and turkey poults, oosporein toxicosis is dose-depend-
adulterated feed was replaced with a different balanced ent and can cause dehydration, stunted growth, pale
diet.42 See Chapter 4, Nutritional Considerations for nephromegaly and death, and appears to severely affect
more on protein levels in birds. uric acid secretion leading to hyperuricemia and visceral
467
Drury Reavill
Fig 16.11a | A young male hyacinth macaw Drury Reavill Fig 16.11b | The cyst (arrow) is opened,
(Anodorhynchus hyacinthinus) has a large renal revealing a white, pasty interior.
cyst (arrow) deforming the right
middle renal division.
and articular gout.184 Although still severely affected, ered to be congenital in nature.238 Reported renal abnor-
turkey poults seemed to tolerate higher doses of malities include complete or partial kidney agenesis,
oosporein before toxicosis was apparent than did broil- ureteral dilatation, structural glomerular changes and
ers, bringing up the issue of physiological differences predilection toward hyperuricemia (due to presumed
between these two species.185 Sterigmatocystin (STG) is proximal tubule defects).9,214,238 Renal cysts are occasion-
produced by multiple fungal species and has caused ally seen and may be congenital or acquired188 (Figs
acute liver and renal disease and death in 10- to 12-day- 16.11a,b). Polycystic renal disease has been noted in
old leghorn chicks.222 Chicks given intraperitoneal STG chickens, pigeons and a bald eagle (Haliaeetus leuco-
developed tubular nephrosis and hepatic necrosis and cephalus).228 Renal agenesis is the most frequently
died within 21 hours of injection.222 described inherited defect and has been attributed to a
simple recessive gene with variable penetrance in brown
Lead Nephropathy leghorn chickens.214 With partial renal agenesis, the cra-
Lead toxicity is the most common cause of metal poison- nial renal division is most likely affected.214 Although
ing in waterfowl and affects a wide variety of other bird birds usually die with neurological signs or massive
species.151 Although neurological and gastrointestinal interrenal hemorrhage, emus (Dromiceius novaehollan-
clinical signs are usually seen, lead can have severe diae) with inherited neuronal storage disease (gangliosi-
effects on avian kidneys. Renal lesions may include prox- dosis) develop unusual large vacuoles in the renal tubu-
imal tubular necrosis and degeneration (nephrosis), vis- lar epithelial cells of the proximal convoluted tubules.17
ceral gout and, in some birds, acid-fast intranuclear Congenital renal diseases have been reported in chick-
inclusion bodies.55 Kidney, liver and brain tissue concen- ens, pigeons, quail, a canary and a mandarin duck but
trations of 3 to 6 ppm wet weight are suggestive and likely exist in numerous other species.187,214,238
greater than 6 ppm is diagnostic for lead poisoning.125
Also see Chapter 31, Implications of Toxic Substances in
Fatty Associated Diseases
Clinical Disorders and Chapter 17, Evaluating and
Treating the Nervous System. Lipids are not histologically evident in normal avian
renal tissue, but may be noted under certain pathologic
circumstances.214 Fasting (water and food) may result in
Congenital and Hereditary Defects
reversible lipid deposition within the renal tubular
Multiple congenital renal defects are reported in epithelium.214 Defects in lipid metabolism or storage also
birds.214,238 Heritable renal diseases such as X-linked may account for renal tubule cell lipidosis.187
hereditary nephritis in Samoyed dogs and Alport’s syn-
drome in humans are discussed in many mammals, but The now rare fatty liver and kidney syndrome of broiler
are poorly described in the current avian literature.100 flocks and turkeys (due to biotin deficiency) can cause
In some large poultry flocks, up to 20% of the necrop- heavy lipid accumulation within the proximal convo-
sied birds have had evidence of “faulty kidneys” consid- luted tubules.214,247 At necropsy, the liver, kidneys and
sometimes other organs are often pale and swollen with Other clinical signs may vary, but often include diarrhea,
deposition of sudanophilic lipid droplets.247 dyspnea, abdominal distension and weight loss.130,241
A fatty liver-kidney syndrome also has been reported in The lumbar plexus lies dorsal to the cranial renal divi-
merlins (Falco columbarius).48,72 Only captive birds have sion, while the sacral plexus runs through the middle
been affected.48 Most affected merlins have been approxi- division parenchyma.180 Because of this close association,
mately 5% above normal body weight and fed a diet pre- any parenchymal inflammation or pressure on or from
dominately of day-old chicks for several months prior to within the kidney can potentially result in nerve dysfunc-
death. Most affected merlins died suddenly either while tion and resultant lameness. Additional neoplastic exten-
eating or with the keeper. A few became lethargic a few sion to the overlying spinal column also may result in
hours before death.48 As is seen in broiler chicks, merlins nerve dysfunction. Peripheral neural compression
with fatty liver-kidney syndrome develop excess fat in the should result in peripheral neuropathy with eventual
liver, kidneys and spleen. One-day-old (feeder) chicks loss of the withdrawal reflex, not seen with most spinal
contain appreciable avidin, which may bind dietary cord lesions.79 In addition to lameness and muscle atro-
biotin, in turn leading to (a theoretical) biotin deficiency. phy, ipsilateral osteopenia was noted in a cockatiel
Biotin and other deficiencies, high-fat diet, hepatic (Nymphicus hollandicus) with a renal adenocarcinoma.79
anoxia and various toxic agents, have been proposed as
causes of fatty liver-kidney syndrome of merlins, but a Unfortunately, avian renal tumors carry a poor prognosis.
definitive etiology has not been confirmed.72 In reported cases of renal cancer, most birds lived less
than 3 months following diagnosis.79 It has been stated
in reference to budgerigar renal tumors that the course
Neoplasia
of the disease may take weeks to several months.241
The avian kidney, just as with other animal tissue, is
susceptible to neoplastic conditions. Nephroblastomas
Urolithiasis and Ureteral Obstructive Disease
are the most commonly reported avian renal tumor.214
Nephroblastomas and renal adenocarcinomas comprise In birds, urolithiasis refers to the formation of large
the majority of kidney tumors in budgerigars (Melopsit- urate “stones” in the ureters, is primarily seen in pullets
tacus undulatus).173,187 Renal carcinomas are the most and caged laying hens, and can result in increased mor-
frequently reported tumor of the urinary system in non- tality and decreased egg production.50 Urolithiasis has
domestic free-ranging and captive birds.130 Malignant been reported primarily in the poultry literature on
renal tumors are more commonly seen in males than numerous occasions, but is rarely described in other
females and are more commonly observed in psittacine avian species.20,42,214,251
than passerine species.79 In one study of 74 budgerigars
suspected of having coelomic tumors, one-legged lame- Common findings include atrophic ipsilateral renal tis-
ness and abdominal enlargement were the primary clini- sue, a normal to hypertrophic (compensatory) contralat-
cal signs. In the same study, 47 birds (63.5%) had renal eral kidney and a dilated ureter obstructed with one or
tumors and were diagnosed most commonly within 5 more urate stones.20,214,251 Histologic lesions noted with
years of age.173 urolithiasis have included glomerular nephritis, tubular
nephrosis, ureteritis and pyelonephritis with interstitial
Lymphoid, myeloid and erythroleukemias, lymphoma, mononuclear infiltrates.50 One study noted that virtually
ovarian, liver and oviductal adenocarcinomas, heman- every cull hen or out-of-production hen examined at
gioma, lipoma, histiocytic cell sarcoma, neurofibroma, affected layer complexes (sites with high incidences of
granulosa cell tumor, cystadenoma with bone, squamous urolithiasis) had gross kidney lesions and kidney stones.50
cell carcinoma, unclassified carcinoma and osteogenic In birds, ureteral obstruction (as may occur with uretero-
sarcoma have all been reported either as primary or sec- liths, cloacal masses, urodeal fold thickening, etc) may
ondary renal neoplasms in birds.121,193,214,241 cause a postobstructive form of renal disease. Simple lig-
ation of a bird’s ureter results in ipsilateral renal atrophy
Like other cancers, there are likely many causes of renal and this result is similarly expected with urolithiasis.214
tumors in birds, but there is little information regarding Naturally occurring ureteroliths in chickens are known to
definitive etiologies. Avian leukosis virus (ALV) can contain uric acid, urates, calcium and ammonia.148 These
induce renal tumors in chickens. While ALV has been statements suggest that the kidney should be closely eval-
found in budgerigars with renal tumors, a definitive uated (eg, via biopsy) when urolithiasis is present.
association has not been made.173
The cause of urolithiasis in poultry flocks has not been
A common presentation with renal cancer is unilateral definitely identified.214 However, it is known that coron-
to bilateral leg weakness or paralysis and slight ataxia.241 avirus-associated nephritis in pheasants can induce inter-
469
stitial nephritis, tubular dilatation, ureteral impaction sis had amyloid deposits in the renal tubules and no to
and subsequent visceral gout.186 In addition to infectious minimal deposition in the glomeruli.171 While some of
bronchitis virus infection (IBV — a coronavirus), other the birds had concurrent inflammatory diseases such as
proposed causes of urolithiasis in poultry include water egg yolk peritonitis, the etiology of the amyloidosis was
deprivation, excess dietary calcium and nutritional elec- not determined.171 Four days after acute onset illness, a
trolyte imbalances.50 One group reported that by chang- roseate flamingo (Phoenicopterus ruber) died with
ing the form of calcium from small particle size to flakes, necrogranulomatous and septic air sacculitis, perihepatic
adding additional phosphorous and by modifying the serositis and hepatic capsulitis, hemosiderosis, athero-
IBV vaccination protocol, the investigators were able to sclerosis and systemic amyloidosis.29 The renal amyloid
significantly reduce the incidence of urolithiasis in a pre- involvement was severe, resulting in a marked glomeru-
viously affected layer flock. However, they could not lopathy and was likely the cause of death.29 Amyloid was
determine which management change resulted in the found within the connective tissue of mycobacterial
beneficial effect.50 tubercles found on the kidney surface of a hooded mer-
ganser (Lophodytes cucullatus). No details were given
Urolithiasis in psittacine species is rare, but has been
regarding the premortem disposition of the bird.209 The
reported. A 21-year-old male double-yellow headed
author has noted renal amyloidosis in pet geese. These
Amazon parrot (Amazona ochrocephala) with a lifelong
birds presented in end-stage renal failure and necropsy
history of straining to void and chronic intermittent vom-
showed severe renal amyloidosis. The underlying cause
iting for a “few years” was diagnosed with septic ureteral
was never elucidated.
fluid and ureterolithiasis.56 Dorsocaudal coelomic radio-
dense opacities were noted on screening radiographs, but
the diagnosis was ultimately made via exploratory celio- Renal Hemorrhage
tomy. Multiple surgeries were required to remove the Renal hemorrhage is sporadically reported in the litera-
stones. A kidney biopsy was not collected and a relation- ture and may exist predominantly as a secondary finding.
ship to renal disease could not be made. The ureteroliths Sudden death syndrome (SDS), also known as “perirenal
were composed of monosodium uric acid crystals and hemorrhage syndrome,” is the main cause of death in
proteinaceous material mixed randomly or forming irreg- heavy turkey flocks from 8 to 14 weeks of age.24 Primarily
ular laminae. Although the bird had dry, flaky skin, a male turkeys in good body condition die acutely with
urate-pasted vent, dull feathers and heterophilic (28,840 SDS and typically have characteristic postmortem lesions
cells/µl) leukocytosis (32,000 cells/µl), the authors con- including perirenal hemorrhage and organ congestion
cluded that the clinical signs associated with ureterolithia- including the lungs, spleen and liver.24,75,129 One group
sis in this bird were non-specific and may result in noted that most affected birds had hypertrophic car-
delayed diagnosis.56 The cause was not determined. diomyopathy and proposed that acute congestive heart
failure was the cause of death and severe passive conges-
Amyloidosis tion accounted for the perirenal hemorrhage.129 The
Amyloidosis is occasionally noted in association with cause is still unknown, but other theories include severe
avian renal disease. Amyloid deposits are often related to lactic acidosis and limited cardiac capacity, noted in pre-
chronic inflammatory disease and usually found systemi- disposed turkeys, as contributing factors.24
cally, but can affect specific tissues.29 Typically, amyloid
presents histologically as amorphous, eosinophilic, An adenovirus, new gosling viral enteritis virus (NGVEV),
homogenous material that stains red-orange with Congo has been shown to cause renal hemorrhage and hyper-
red and bright green when examined under polarized emia 4 days postinfection in newly hatched goslings.44
light. Amyloidosis is most frequently noted in captive Renal tubular and ureteral epithelial cell degeneration
Anseriformes (geese, ducks, swans), Gruiformes (cranes) and intestinal glandular epithelial cell necrosis and
and Phoenicopteridae (flamingos), but also has been sloughing also were consistently seen in the goslings
reported in numerous other species.127,201 See Chapter infected with the rapidly progressive NGVEV.44
15, Evaluating and Treating the Liver for a discussion of
amyloidosis. Hydropericardium syndrome of broiler chickens is a
contagious disease caused by an adenovirus and can
There are a few reports of amyloidosis involving the kid- result in grossly swollen kidneys with extensive renal
neys of birds. Multifocal amyloidosis was noted in a dia- hemorrhage and hydropericardium.2 Three- to six-week-
mond firetail finch (Stagnopleura bella) with proventric- old broilers are typically affected and mortality ranges
ular cryptosporidiosis, and was found specifically in the from 10 to 60%. Renal tubular nephrosis and necrosis
glomeruli and interstitial tissue around the tubules.19 within the liver, spleen and bursa of Fabricius may be
Numerous laying Japanese quail with systemic amyloido- seen microscopically.2
Other causes of renal hemorrhage also may be seen. preted with caution.163 In effort to decrease postmortem
Simple trauma, such as from an animal bite or endo- changes, perform a necropsy and fix tissues as soon after
scopic biopsy, may result in renal hemorrhage. If the death as possible.
renal capsule is left intact, a subcapsular hematoma may
form, increasing the renal size and possibly placing
pressure on the neighboring nerve plexi.134 Renal
petechial hemorrhage resulting from Clostridium
PART 2:
perfringens toxemia was reported in a rock partridge A Review of Diagnosis and
(Alectoris graeca).134
Management
Metabolic Renal Disease
HISTORY AND PHYSICAL
Metabolic renal disease includes dehydration, diabetes
EXAMINATION
mellitus, amyloidosis, gout and lipidosis, the latter three
of which have already been discussed. Diabetes mellitus A historical review of a bird’s environment, diet, source,
has been noted in a variety of birds and is seen with exposure to infectious agents and toxins, genetics and
polyuric, polydipsic glucosuria and hyperglycemia.228 behavior becomes important for both diagnosis and man-
Descriptions of the gross and microscopic effects of dia- agement of avian renal disease. Environmental factors
betes mellitus on avian kidney tissue were not found. can include exposure to known aerosolized, ingested or
topical toxins. Adverse conditions that might lead to
One of the more common metabolic derangements asso- dehydration or other stresses also may be identified. The
ciated with renal disease is dehydration. In chickens, diet should reflect what is appropriate for that species,
dehydration has been associated with nephrosis charac- and the history should include any additional dietary
terized by tubular dilatation, with or without proteina- supplementation or changes. Understanding the bird’s
ceous casts, epithelial necrosis and rare urate granulo- origin, whether from a specific aviary, store, quarantine
mas or casts.198 Food restriction during dehydration may station, the wild, etc, may suggest the possibility of prob-
lessen the nephrosis lesions.198 lems seen in other avian species from the same source.
Known exposure to infectious agents (and again, toxins)
Gross Renal Changes is especially important, as definitive diagnosis of bacter-
ial, viral, parasitic, fungal and toxic agents is not always
Gross renal changes including masses, discolorations,
possible without cultures, special stains, electron micro-
and size and shape alteration are non-specific and
scopy, in situ DNA hybridization, PCR probes or other
should be cautiously interpreted.
diagnostics. Genetic problems are poorly described in
Differential diagnoses for renomegaly include neoplasia, birds, but with intense inbreeding, development of muta-
inflammation (including infectious and non-infectious tions or conservation breeding efforts from an extremely
diseases), cystic formation, ureteral obstruction, toxic limited gene pool, it is reasonable to assume that heredi-
changes, metabolic disorders (including dehydration, tary defects will become more common. Behavioral
gout, lipidosis) and congenital abnormalities.79 Also, changes including depression, anorexia, anuria, oliguria,
non-pathological increase in kidney size has been noted polyuria, polydipsia, feather picking over the synsacrum,
in chickens fed certain dietary precursors such as ino- self-mutilation, seizures and others may be associated
sine that increase plasma uric acid levels.215 In these with renal disease and should be noted in the history.181
chickens, the renal enlargement was likely due to the
Most physical examination abnormalities associated with
increase in processing of uric acid in the kidney.215
avian renal disease are non-specific, but there are some
Renal and ureteral calculi also may be noted.
key findings that tend to warrant further investigation.
It is highly likely that a bird with articular gout has had
Postmortem Renal Change or currently has some form of renal disease. For this
Renal postmortem changes are noted in chickens as reason, consider renal biopsy in some birds with articu-
soon as 22 minutes following death at 37° C (98.6° F).163 lar gout to help rule out or specifically identify kidney
Early renal postmortem changes occur in the proximal disease. Not all birds afflicted with articular gout, how-
tubular epithelium, followed by collecting tubule epithe- ever, have renal disease. Unilateral leg lameness or pare-
lium and glomerular nuclei.163 Even with cooling to 4° C sis may accompany renal disease. This is particularly true
(39.2° F), proximal tubular changes can be observed if kidney disease causes inflammation or compression
within 45 minutes of death. The early postmortem proxi- on the lumbar and/or sacral nerve plexus that is so inti-
mal tubular changes can be confused with antemortem mately associated with the dorsal renal parenchyma.
proximal tubular degeneration and should be inter- Birds with renal disease also may exhibit dehydration,
471
generalized weakness, regurgitation and decreased mus- Table 16.3 | Selected Plasma-based Diagnostics in Birds
cle mass with or without historical anorexia, all of which Diagnostic Test Species Normal Range Reference(s)
are non-specific signs.166 Uric Acid Pigeon 94-518 µmol/L, 87, 138, 141
225-574 µmol/L
Peregrine falcon 253-996 µmol/L,
4.3-16.7 mg/dl
DIAGNOSTIC TESTS
Urea Pigeon 0.36-0.64 mmol/L, 87, 138, 141
Multiple diagnostic tests are available to help clinicians 0.27-0.94 mmol/L
identify and define multiple disease processes in birds. Peregrine falcon 0.8-2.9 mmol/L,
2.2-7.0 mg/dl
As diagnostic technology improves, so will our ability to
Creatinine Pigeon 23.7-32.3 µmol/L, 87, 141
accurately diagnose diseases in birds. The tests listed 20-56 µmol/L
below are ones that are most frequently discussed or Peregrine falcon 24-64 µmol/L,
0.27-0.72 mg/dl
used in diagnosing renal disease in birds. See Table 16.3
Urea/Uric Acid Pigeons 1-3 138, 141
for reported selected plasma-based diagnostics sometimes
Peregrine falcon 1.7-6.4
used in diagnosing renal disease in birds. Many diagnos-
Osmolality Pigeon 299.4-312.6 138, 141
tics such as fecal floatation, which help diagnose renal (mOsm/kg H2O)
Peregrine Falcon 322-356
coccidiosis, are not discussed, but should be included in Reference values for the pigeon (Columba livia domestica) and peregrine
a minimum database when evaluating sick birds. Some falcon (Falco peregrinus) are included. These reported values are high-
lighted because of their potential use in identifying renal disease and
new or unfamiliar diagnostics also are introduced. dehydration.
Considering all the diagnostic tests available, the author

has noticed a pattern of laboratory abnormalities that is
in birds with renal disease, only specific diagnostics are
often strongly correlated with many forms of renal dis-
covered.
ease in birds. This includes persistently elevated uric
acid (at least two consecutive tests on a well-hydrated Uric Acid
and fasted bird), elevated creatinine phosphokinase Plasma uric acid can be useful as a screening tool for
(CPK), mild anemia and a relative heterophilia with or advanced renal disease. With the exception of gastroin-
without a total heterophilia. Elevated CPK is a very non- testinal uricolysis, uric acid and its salts (urate) are the
specific indicator of multiple types of tissue damage and end product of nitrogen metabolism in birds.9,60,132,214,246
is not mentioned further. Using the currently available Elevated uric acid has been correlated with histologically
diagnostics, the actual type and degree of renal disease confirmed severe renal disease in chickens (tubular
can be confirmed only with a kidney biopsy. nephrosis and interstitial nephritis).224 In a separate
study involving dehydrated chickens, increased serum
Complete Blood Count (CBC) uric acid was associated with histologic renal lesions.198
Some non-specific CBC changes may be associated with Broilers given oosporein (renal toxin), developed vis-
avian renal disease. A marked (relative) heterophilia was ceral and/or articular gout, swollen, pale kidneys and
noted in two chickens with urolithiasis, but no total had a 48% increase of uric acid over control birds.184 In a
white blood cell count was given.20 Heterophilia, mono- similar study with oosporein in turkey poults, intoxi-
cytosis, lymphopenia and normocytic-normochromic cated birds had dose-dependent increases in uric acid
anemia were noted in broiler chicks with various forms (over controls) ranging from 76 to 140%.185 It was noted
of histologically confirmed renal disease, but specific that fasting hyperuricemia (>16.7 mg/dl [>1000
details were not given.41 In a different study in chickens, µmol/L]) in peregrine falcons (Falco peregrinus) indi-
clinically affected birds with histologically identified cates renal failure.141
nephritis had significant heterophilic leukocytosis when Uric acid is produced and secreted in the avian liver,
compared to “normal” birds.42 The author has reported kidney and pancreas.46,106 Although produced predomi-
that many pet birds (geese, doves, various psittacine nately in the liver, at least 17% of the uric acid found
birds) with different forms of renal disease have demon- in chicken urine may be synthesized in the kidney.46
strated a mild to marked relative heterophilia with a nor- Specifically, nephrogenic uric acid synthesis may increase
mal total white blood count.47,64,65 These changes are when plasma purine precursors are elevated.46 These
non-specific, however, and can be seen in healthy birds findings suggest the avian kidney has an important role
under stress alone.221 in the synthesis, in addition to elimination, of uric acid,
especially when increased precursors are available.46
Serum or Plasma-based Biochemistries Precursors, including body proteins degraded because of
Selected plasma biochemistries may provide several use- poor nutritional status, have been suggested as a cause
ful clues toward renal disease in avian patients. Although of elevated uric acid and should be considered in birds
many serum and plasma-based tests may be “abnormal” with hyperuricemia.155
An interesting secondary role of uric acid in birds is its In birds of prey, uric acid production is directly related
antioxidant capability. In chickens, it has been clearly to the amount of protein consumed and transient rises
shown that plasma uric acid concentrations are inversely are noted following high-protein meals.140,143 Peregrine
correlated with oxidative activity.215 It has been stated falcons (Falco peregrinus) and red-tailed hawks (Buteo
that uric acid constitutes one of the most important anti- jamaicensis) are reported to have a “significant” post-
oxidants in birds and is directly linked to their longevity.215 prandial increase in plasma uric acid concentration
(hyperuricemia) for up to 12 hours after ingesting a nat-
Uric acid is cleared mainly via tubular secretion and is ural meal.140,143 The significant postprandial uric acid
largely independent of glomerular filtration, water increase noted in peregrine falcons was up to 32 mg/dl
resorption and urine flow rate.9,140,141,187,195 Blood uric acid (reported as 1881 µmol/L) between 3 and 8 hours after
levels are mildly affected by a bird’s hydration status, but being fed.143 It has been stated that significant postpran-
rather reflect the functional capacity of the renal proxi- dial increases in both urea and uric acid persist for up to
mal tubules.187 However, in a study with dehydrated 15 hours in peregrine falcons.143 It was not clear why
chickens, uric acid levels increased after 24 to 48 hours these birds of prey did not develop gout lesions, but the
of water restriction, but only in those birds allowed free authors recommended a 24-hour fast prior to evaluating
access to food.198 Serum uric acid levels actually dropped serum uric acid in peregrine falcons.143 The authors fur-
within 24 hours in birds denied food and water.198 It has
ther recommend that a 24-hour fast should be consid-
been estimated that renal function must be below 30%
ered for all carnivorous avian species prior to blood uric
of its original capacity before hyperuricemia develops.166
acid testing. Almost identical findings of postprandial
Suggested normal avian uric acid levels range from less
hyperuricemia were noted in blackfooted penguins
than 1 to 10 mg/dl (59.48-594.8 µmol/L).214
(Spheniscus demersus) and represent another species
Hyperuricemia is defined as “any plasma uric acid con- that should be fasted before measuring uric acid levels.122
centration higher than the calculated limit of solubility
Uric acid production following a high-protein meal has
of sodium urate in plasma.” In bird plasma, this theoreti-
been studied in various psittacine birds. In one study
cal limit of solubility of sodium urate is estimated to be
with African grey parrots (Psittacus erithacus sp.),
600 µmol/L (10.8 mg/dl).143
plasma uric acid concentrations showed a positive corre-
In chickens, the uric acid renal tubule transport system lation with dietary protein consumption.105 However,
does not appear to become saturated until plasma uric even though the fed protein level was as high as 30%,
acid levels exceed 60 mg/dl (3569 µmol/L)9 which plasma uric acid levels remained within normal ranges.105
demonstrates the lack of clarity in the literature and In cockatiels fed 11, 20, 35 and 70% protein for 11
experimental dosages.9 Chickens genetically predisposed months, serum uric acid increased linearly with dietary
to hyperuricemia and fed high-protein (60%) diets protein levels.123 However, the serum uric acid level was
develop an elevated steady state of plasma uric acid significantly greater only in birds fed 70% protein diets.
(10-60 mg/dl {59.48-3569 µmol/L}) in order to excrete Because no histologic or gross renal lesions were found
their daily loads of this by-product.9 The increased basal at necropsy, the authors concluded that the rise of uric
plasma uric acid made the affected chickens susceptible acid was related to dietary protein concentration and not
to articular gout formation.9 One group suggested that kidney damage.123 It was found that feeding diets contain-
these chickens genetically predisposed to gout had a ing 13.5, 18.2 and 24.6% protein for up to 24 weeks had
defective uric acid transport mechanism at the peritubu- no effect on serum uric acid levels in parakeets.8
lar membrane.184
In consideration of the above-described causes of eleva-
Uric acid represents 80% or more of the nitrogen tions in uric acid, this single biochemistry value can help
excreted by birds.9,214 Therefore, a significant increase in identify significant renal disease. The author prefers to
the proportion of nitrogen excreted as uric acid is not repeat (fasting) uric acid levels on well-hydrated birds
likely, even with increased dietary protein consumption. before a suggestion of renal disease is made. In birds
At least in chickens, hyperuricemia is likely due to with suspect renal disease that have a single laboratory
reduced renal tubular secretion of uric acid and not value of hyperuricemia, the author will often give a total
excessive production as can occur in humans.9,214 These of 100 ml/kg SQ, SID to BID of isotonic fluids for 2 days
findings imply that renal tubular diseases are likely and then recheck the uric acid level. In the author’s
responsible for hyperuricemia, and uric acid abnormali- experience, birds with persistent hyperuricemia after fluid
ties may not be evident until very high-protein diets are therapy and/or fasting have some form of renal disease.
fed. Specifically in chickens, dysfunctional proximal con-
voluted tubules result in reduced urate secretion and Urea
can lead to hyperuricemia if severe.214 Unlike mammals, urea in birds is produced only in small
473
amounts (by renal mitochondrial breakdown of arginine) affected birds developed articular and/or visceral gout,
and does not serve as the end product of protein metab- gross renal changes and death, broilers intoxicated with
olism.187 Plasma urea in birds is excreted by glomerular oosporein (fungal nephrotoxin) had, with the exception
filtration and, unlike uric acid, blood urea concentra- of one group, no significant changes in plasma protein
tions are more significantly affected by the bird’s hydra- (biuret method) over the normal (control) birds.184
tion status.138,140,187 During normal hydration, filtered urea A single group of broilers receiving a midrange amount
is 100% excreted but is 99% reabsorbed in the tubules of oosporein had a statistically significant rise in plasma
during dehydration.138,141 Plasma urea also has been protein over controls. The cause for this single discrep-
shown to significantly increase in peregrine falcons for ancy was not determined.184 In a similar study using
up to 15 hours postmeal.143 In studied cockatiels, serum oosporein-intoxicated turkey poults, statistically signifi-
urea levels increased linearly with dietary protein levels cant decreased albumin:total protein was noted at all
(11, 20, 35 and 70%).123 Separate studies involving the levels of intoxication over controls, but total protein
domestic fowl and pigeons demonstrated decreased remained unchanged and albumin was not significantly
urea elimination and/or increased blood urea levels decreased until the highest levels of the toxin were
(6.5- to 15.3-fold increase in pigeons) in dehydrated given.185 These few studies show a couple of important
birds.138,187 It has been shown that plasma urea nitrogen facts: there is limited information properly associating
increased in a dose-dependent fashion (in turkeys) at plasma proteins with renal disease, and differing species
every level of dietary oosporein (nephrotoxin).185 These may have dissimilar plasma protein levels under similar
intoxicated turkey poults also were showing signs of disease conditions. As discussed under Part 2: Electro-
dehydration.185 It has been proposed that plasma urea is phoresis, Plasma Protein Electrophoresis, protein levels
the single most useful indicator of prerenal (dehydra- should be evaluated electrophoretically (in addition to
tion) causes of kidney failure in birds.140 the more common biochemical methods).
The urea:creatinine and urea:uric acid ratios can be

used to better define pre- and postrenal azotemia.
PLASMA ELECTROLYTES
Because reabsorption of urea is disproportionally higher The effect of renal disease on plasma electrolytes is
than both creatinine and uric acid, these ratios should poorly studied in birds. Hyperkalemia and hyperphos-
be high during dehydration and ureteral obstruction.138 phatemia have been loosely associated with renal failure,
The formulas for these ratios are listed below: but studies are limited in birds.141 No significant associa-
tions between renal disease and plasma sodium, potas-
Urea:creatinine = urea (mmol/L) x 1000 sium, calcium, magnesium, chloride and phosphate lev-
creatinine (µmol/L)
els were noted in birds from two chicken flocks with
Urea:uric acid = urea (mmol/L) x 1000 spontaneously occurring urolithiasis.20,251 Specific sample
uric acid (µmol/L) collection/storage was not discussed and the authors
conceded that their handling of the samples might have
Creatinine affected the results.20,251 Dehydrated chickens allowed
Birds produce little creatinine from its precursor, crea- free access to food developed significantly elevated
tine.166 Creatinine is eliminated by tubular secretion but serum sodium and phosphorous by 24 hours and after
clearance is variable.81 Clinically, creatinine may be 24 hours, respectively, but maintained normal potassium
elevated in pet birds by feeding high-protein diets.81 levels.198 Histologically, these chickens had mild renal
It was shown that plasma creatinine also will increase tubular dilatation.198 Turkey poults intoxicated with
significantly in dehydrated pigeons.138 The relationship oosporein (nephrotoxin) developed significantly
between creatine and creatinine in birds with renal dis- decreased plasma potassium and phosphorous, and had
ease is poorly understood, and differentiation does not no changes in sodium compared to controls.185 As the
appear to be useful clinically.81,166,181 avian kidney is responsible for electrolyte regulation, it
is reasonable to assume that electrolyte disorders can
Proteins
be present in birds with renal disease.
Although hypoproteinemia has been noted as being
associated with renal failure, few studies have evaluated
serum protein levels in birds with renal disease.141 MICROBIOLOGIC ANALYSIS
Biochemically determined low serum protein has been Microbiologic assays may be useful in identifying infec-
noted in chickens with advanced tubular nephrosis and tious causes of avian renal disease. Bacteria may enter
interstitial nephritis.224 In two chicken flocks with spon- the renal system either hematogenously, ascending from
taneously occurring urolithiasis, plasma protein level the ureters and cloaca, or as an extension of surround-
changes (method of determination not disclosed) were ing organ infection.187 The avian coccygeomesenteric
not significantly associated with renal disease.20,251 While vein drains the mesentery of the hindgut into the
hepatic portal and/or the renal portal vein.226 It is con- into the lower intestines to the ceca, where water and
ceivable that colitis may serve as a hematogenous source sometimes electrolyte reabsorption takes place.252
of infectious agents, toxins and inflammatory products Additionally, diseases of the lower intestine may alter
to the kidney if blood flow draining the colon is diverted urine production and composition. Gastrointestinal
into the renal vasculature. For this reason, collection of bleeding, inflammation, normal and abnormal organ-
a cloacal or fecal microbial culture is a rational portion isms, etc, may end up in a “urinalysis” harvested from a
of the supportive laboratory database in birds with sus- dropping, giving the false impression that red and white
pected renal disease. Severe ulcerative colitis caused by blood cells and/or infectious agents, respectively, came
Salmonella infection resulted in ascending bacterial from the urinary tract. In short, the “urine” present in a
nephritis in four African grey parrots.187 dropping is not the same urine produced from the kid-
neys. Urinalysis results should be carefully interpreted.
Bacterial nephritis in birds is often a component of sys-
temic infection and multiple organs may be involved.187
Collection
In one study, 50% of birds with systemic bacterial infec-
tions had kidney involvement, suggesting that any bacte- True urine can be collected in birds only with some diffi-
rial septicemia can potentially result in nephritis.187 culty. Once emptied of feces, specially designed cannulas
Identification of bacteria within renal tissue may be diffi- can be inserted into the cloaca for collection of ureteral
cult, as has been noted in dogs and swine with renal dis- urine. One group used a Foley catheter to occlude the
ease putatively associated with a bacterial etiology.26 rectum but not the ureters and successfully collected
Blood cultures are an appropriate consideration if sep- ureteral urine in chickens.21 Small closed-end cannulas
ticemia is suspected. Prior to blood collection, the skin constructed from micropipette tips were used to collect
over the venipuncture site is aseptically prepared by ureteral urine from house (Passer domesticus) and
thorough cleaning with alcohol and organic iodine (as song sparrows (Melospiza melodia).38 The opening of
with surgical preparation).58,107 The jugular and basilic the closed-end cannula was placed over the ureteral ori-
veins are described as appropriate blood collection sites fices.38 A similar design was used in house sparrows
in septicemic birds.25,58 Using aseptic techniques, renal to make cloacal cannulas from PE-240 tubing with a hole
biopsy specimens also can be sampled for microbial cut near the sealed end.89 The sealed end prevented
cultures. The cause of infectious nephritis in birds is not intestinal fluids from contaminating the urine once the
limited to bacteria, and various culture methods and cannula was in place.89 Under local anesthesia, 1.5-ml
other diagnostic procedures also may be useful for iden- microcentrifuge tubes were sutured into the cloacas of
tifying fungal, viral and parasitic organisms. chickens to allow collection of ureteral urine.205 Cyano-
acrylate was used to glue cannulas over the ureteral ori-
fices of chickens.73 Several obvious drawbacks include
URINALYSIS restraint or sedation of the patient while urine is slowly
Biochemical and cytological sediment analysis of avian produced, and the cannulation itself may induce diure-
urine has been advocated as potentially useful in diag- sis.249,252 Clearly, there are numerous methods, with vary-
nosing avian renal disease.128,166,181,188,228 In birds, hematuria ing degrees of difficulty, used to collect ureteral urine.
may be noted with renal disease, but should be carefully
differentiated from bleeding originating from the gas-
Casts
trointestinal and reproductive tracts.181 Hemoglobinuria,
as noted in Amazona spp. parrots with lead intoxication Urinary casts represent cellular and/or acellular material
and in other species with differing disorders, may or sloughed from the inner lining of various renal tubules.
may not be related to renal disease. Toxic, neoplastic, This material is generally in the shape (or a “cast”) of the
bacterial and viral nephropathies may be more fre- tubule from which it originated. Casts are sometimes
quently seen associated with hematuria in birds.181 White noted on histologic sections. Protein and cellular casts
blood cells were seen in 45% of urine sediment from were histologically noted in an Australian diamond fire-
pigeons with paratyphus, many of which had intersitial tail finch (Stagnopleura bella) with Cryptosporidium sp.
nephritis.87 Sediment analysis should be a part of an and multifocal amyloidosis.19 Albuminous casts in renal
avian urinalysis and specific cellular urinary components tubules of pigeons infected with virulent Trichomonas
have been discussed.128,188,228 gallinae were noted.172 Hyaline casts were identified in
kidney sections of birds experimentally infected with
Several significant factors complicate interpreting avian infectious bursal disease (Gumboro disease).214 Eosino-
urinalysis. First, urine is mixed with feces in the cloaca. philic granular casts have been found within the renal
The one possible exception is the ostrich, which appears tubules of turkeys afflicted with salt toxicosis.242 Eosino-
to eliminate urinary waste separate from the feces.168 philic tubular casts, possibly containing myoglobin, in an
Second, in many species ureteral urine is refluxed orad ostrich with acute muscle necrosis and anuric renal fail-
475
ure have been reported.187 A rhea with hemoglobinuric excrement of the bird, especially carnivorous species
nephrosis developed eosinophilic casts in the renal col- with short digestion times, and give a positive result.134
lecting tubules.16 Both hyaline and granular tubular casts Myoglobinuria also may cause positive reactions and
were present in racing pigeons infected with avian para- can be distinguished from hemoglobinuria only by spec-
myxovirus type 1.11 Granular, hyaline and albuminous trophotometry.134 Finally, porphyrinuria, as seen with
casts were seen in the renal tubules of chickens experi- lead-poisoned Amazon parrots (Amazona spp.), may
mentally infected with several pathogenic bacteria.219 result in red-colored urine visually mimicking hemo-
globinuria.134 Because of the inconsistent results and lim-
Identifying casts in urine is reported as highly signifi-
ited critical studies noted in the literature, difficulty in
cant, a sign of renal disease and/or can be a non-specific
obtaining ureteral urine and clinical experience, it is the
indicator of tubular renal disease in birds.128,134 With that
author’s opinion that the currently available chemistry
stated, the papers cited above describe histological sec-
strips have limited value in an avian urinalysis.
tions with no discussion of casts in the urine. The
author disagrees that urinary casts are highly significant Urine electrolytes and chemistries can be collected, but
or a definite sign of renal disease, as there is little infor- there is limited information on their interpretation. It
mation correlating casts found in a urinalysis with any has been suggested that because renal intracellular
type of renal disease in birds. However, casts should be enzymes are likely voided in the urine, urinary chem-
noted and may have correlation with some forms of istries might be useful in detecting kidney damage.141
avian renal disease. Epithelial casts were found in 2 Urine sodium and potassium were measured, and
out of 35 ostrich urine samples, but no correlation insignificantly changed, in house sparrows undergoing
was made with any renal parameters.168 Epithelial casts trials with the antidiuretic arginine vasotocin.89 One
were noted in 20% of urine samples from Salmonella study noted that in normal and dehydrated starlings
typhimurium-infected pigeons.87 Although many birds (Sturnus vulgaris), cloacal urine contained significantly
did have histologically confirmed renal disease, no cor-
higher concentrations of magnesium, phosphate,
relation was made between those pigeons with kidney
potassium and total osmolality than found in ureteral
lesions and those with urinary casts. The large variety of
samples.204 This study supports the recommendation that
“types” of casts reported also suggests that an inconsis-
ureteral samples must be collected to obtain a “true”
tent naming system exists within the current literature.
evaluation of avian urine, again making urinary chem-
istry evaluation impractical in a clinical setting.
Urine Chemistries and Electrolytes
Standard mammalian dipsticks may be used, but not all One renal enzyme, N-acetyl-ß-D-glucosaminidase (NAG),
components are applicable to avian urine.166 Chicken has been successfully evaluated in the urine of chickens as
urine reportedly contains non-uric acid chromogen.9 a marker for kidney damage.74 In mammals and chickens,
Non-protein chromogens are known to interfere with NAG is a renal tubular enzyme. In humans, urinary NAG
refractometric and chemical measurement of plasma has been suggested for use as an early predictor of renal
proteins and also may apply to avian urine sampling.81 tubular damage and may be a good non-invasive indicator
of disease progression.49 Elevated urinary (ureteral urine),
Few studies even mention test strips used in avian uri- but not plasma, NAG was noted at 40 days of excessive
nalyses. One study evaluated commercial urine dipsticksa vitamin D3 supplementation in chickens.74 Although the
on normal urine of 35 ostriches.168 Because ostriches can information is limited, further studies may show that
eliminate urinary waste separate from feces, these values NAG, and possibly other urinary enzymes, may become
may not apply to most other birds. In the study, 31/35 useful as early markers of renal disease in birds.
(89%) and 35/35 (100%) of the urine samples were posi-
tive for nitrite and protein, respectively. The urine chem-
Osmolality and Specific Gravity
istry strips were negative for glucose, urobilinogen,
bilirubin and ketones in all ostriches.168 No association Avian urine is typically isosmotic because the predomi-
with renal disease was made. Using the dipsticks, nitrite nant reptilian-type nephrons cannot concentrate urine
and protein also were positive in 90% (18/20) and 50% beyond plasma osmolality.141 In normal birds, urine
(10/20), respectively, of the ureteral urine samples from osmolality can maximally be increased to 2.0 to 2.5
pigeons with paratyphus.87 The same strips identified times that of plasma osmolality.27,28,40,141 Even this number
blood in all samples, which correlated to red blood cells is high for some species, as emus (Dromiceius novaehol-
seen in only 45% of urine sediments.87 If the cells in the landiae) are reported to have maximal urine to plasma
urine had been lysed, the strips would be positive and osmotic ratio of only 1.4 to 1.5.216 This is minimal in
the cytology was negative in this study. Urine strips also comparison to some mammals that can concentrate
may detect undigested hemoglobin found in the urine osmolality 25 to 30 times that of plasma.27,28,40
There is limited information on urine specific gravity or oratory using electrophoresis served as the “gold stan-
osmolality in avian health or disease. The reported aver- dard” for total protein and albumin determination.115
age (refractometrically determined) urine specific gravity
of ostriches (Struthio camelus) is 1.02 with a range of These very limited studies suggest inconsistencies in the
1.01 to 1.05.168 Consistent polyuria and hyposthenuria “gold standard” method of serum/plasma total protein
(60% had specific gravity below 1.007) was noted in and albumin determination, and question the true value
Salmonella typhimurium-infected pigeons, many of of these diagnostics in birds with renal disease. Regard-
which had interstitial nephritis.87 In a separate evalua- less, it is the author’s opinion that monitoring serum
tion, urine osmolality significantly increased up to and/or plasma protein levels has diagnostic value in
3 times control levels in postflight and dehydrated birds, even if not necessarily used in renal disease cases.
pigeons.88 The author has used urine specific gravity The author recommends consistently using one of the
diagnostically as discussed below under Water common biochemical methods of protein determination
Deprivation Testing. and comparing those results to electrophoresis, the goal
being to become familiar with test results from one or
two diagnostic methods and correlating those results to
Urine pH
(histologically) confirmed disease.
Urine pH is highly variable in birds. The urine pH may
be acid (down to 4.7) in egg-laying female birds during
calcium deposition.77 Once the egg is laid or calcium is Urinary Protein Electrophoresis
no longer being deposited, urinary pH may climb to 8.0. In mammals, proteinuria is broken down into pre-
Male birds have an approximate urine pH of 6.4. Hypoxia, glomerular, glomerular and postglomerular urinary pro-
as noted in diving ducks, may drop urine pH to 4.7.77 tein loss. Preglomerular proteinuria occurs when large
Normal ostriches have a urine pH range of 6.1 to 9.1, amounts of small molecular weight proteins (immuno-
with a mean of 7.6.168 globulin fragments, hemoglobin and myoglobin) that
readily pass through normal glomerular walls are lost
ELECTROPHORESIS in the urine.137 Glomerular proteinuria occurs when
diseased glomerular membranes allow large proteins
Plasma Protein Electrophoresis (albumin, immunoglobulins, some coagulation proteins/
Properly determined hypoalbuminemia (via plasma elec- antithrombin III) to pass.137,245 Postglomerular proteinuria
trophoresis) is not reported in confirmed active cases of results from normal genital secretions as well as urogen-
avian renal disease. However, it is possible that birds ital infections, trauma and neoplasia.137 Although uncom-
may develop low albumin/protein with some kidney dis- mon in mammals, defects resulting in proximal renal
orders. Biochemically determined hypoalbuminemia has tubular protein resorption result in (postglomerular)
been noted in some active avian renal disease cases.64,65,185 tubular proteinuria.137,245
The literature states that as the currently available bio- Avian urine normally contains a large amount of protein
chemical tests likely do not accurately report avian albu- (average of 5 mg/ml up to 15 mg/ml), especially when
min levels, serum/plasma protein electrophoresis is nec- compared to that of mammals (<0.09 mg/ml in dogs
essary to properly quantitate blood proteins and should and humans).27,111 Amino acids are freely filtered at the
be performed if hypoalbuminemia is suspected.81,139,142 glomerulus, but normally are almost completely reab-
Decreased albumin and elevated betaglobulins and sorbed by the renal tubules in birds.60 Because uric acid
alpha2 macroglobulin, as recorded with serum elec- is poorly water soluble, very little avian ureteral urine is
trophoresis, have been reported with avian nephritis.47,51 required to eliminate this protein waste. Instead, pro-
However, there are no controlled studies to support the teinuria is likely necessary to maintain the excreted uric
above statements that correlate protein electrophoresis acid-containing spheres in a colloidal suspension, pre-
abnormalities with any renal pathology in birds. venting aggregation and renal tubular blockage.28,111
Within the proximal tubule, uric acid is bound to a pro-
With the above stated, one study showed that an analyzer tein to solubilize the waste product and prevent crystal
using the biuret and bromocresol green dye-binding formation.215 The reflux of urine into the cloaca may be
methodologies for total protein and albumin determina- a mechanism to recover some of the urinary protein,
tion, respectively, had good agreement between whole as cloacally voided fluid contains very little protein
blood and plasma samples.115 On the contrary, there was compared to ureteral samples.28
poor correlation between the results from the studied
analyzer and samples evaluated via electrophoresis used Serum albumin, among other proteins, is found in both
at two major reference laboratories. Due to the discrep- the liquid urine and uric acid spheres in chickens.111 In
ancies, the authors concluded that neither reference lab- the normal junglefowl (Gallus gallus), the urinary pro-
477
teins (averaged 2.01 mg/ml urine) identified closely

matched the plasma proteins. This led to the conclusion
that protein is passed through a glomerular filtration bar-
rier differently than occurs with most mammals.111 There
are, however, differences in concentrations of plasma and
urinary proteins suggesting differential filtration and/or
absorption of some proteins by renal tubules.111
Pathologic proteinuria is poorly described in birds. In

one study, control chickens and those with experimen-
tally induced autoimmune glomerulonephritis produced
urinary protein (measured via 3% sulfosalicylic acid with
a bovine serum albumin standard) at 5 mg/24 h.21 Test
birds developed no abnormal proteinuria, but were con-
sidered moderately proteinuric after given IV colloidal Fig 16.12 | Lateral radiograph of an adult domestic goose
carbon (3 to 8 times increase in proteinuria). Colloidal with renal fibrosis and mineralization. Note the mineralized kid-
carbon induces proteinuria in other species, but the ney tissue (arrow).
mechanism is not clear.21 As discussed under Part 1:
General Renal Disease Categories, Glomerulopathies,
birds may not be capable of developing pathologic pro- ment.166,187 Improper positioning can artifactually change
teinuria with glomerular disease as is recognized in the appearance of this air-filled diverticulum.166 Because
mammals. However, it is possible that pathologic pro- the renal silhouettes are superimposed on a lateral view
teinuria develops more slowly in birds compared with of the abdomen, an oblique view also may be used to
mammals, and as a result has not been frequently dis- distinguish each kidney.79 Renal density and gross size
cussed or evaluated in clinical cases.86 If pathologic pro- changes may indicate renal disease.166,181 Radiographically
teinuria is suspected, urine protein electrophoresis visible renomegaly was noted in a salmon-crested cocka-
should be used to differentiate protein type and size.94,245 too with chronic interstitial nephritis and calcification as
If performed, it would be beneficial to compare urinary the result of hypervitaminosis D3.211 Nephrocalcinosis
protein levels from a sick patient with samples from a was detected radiographically in ostriches and appeared
healthy member of the same species. Finally, ureteral as multiple radio-opacities throughout the renal
urine should be collected to rule out any effects from parenchyma.162
protein absorption or from other proteins present in the
lower intestine. In a normal clinical setting, these collec- Ultrasound
tion requirements and limited studies make meaningful
Due to the presence of surrounding air sacs (ventrally)
urinary protein interpretation in birds impractical.
and bone (dorsally and laterally), ultrasonographic imag-
ing of normal avian kidneys is difficult.108 In one study of
IMAGING 386 mixed bird species that underwent ultrasonographic
evaluation of the urogenital tract, abnormalities such as
Radiography renal cysts (6), cancer (12) and inflammatory nephro-
Plain and contrast radiography, nuclear scintigraphy, megaly (11) were identified in only 29 patients. The
ultrasound, magnetic resonance imaging and computed authors concluded that sonographic imaging of the nor-
tomography can be used to “image” the avian kid- mal kidney was not possible.108 Some disease conditions
neys.108,134,151,166,181,206 The avian kidney lies in a fossae cre- that either obliterate the air sacs or result in fluid accu-
ated by the ventral surface of the synsacrum.79,152 With mulation in the coelomic cavity may actually improve
bone dorsal and air sacs surrounding ventrally, imaging renal ultrasonographic imaging.152 In these abnormal
of the avian renal system is difficult with some tech- situations, ultrasonography can serve as a non-invasive
niques. Indirect methods such as positive contrast radi- and safe means to evaluate coelomic structures such as
ography of the alimentary tract may be helpful in outlin- the kidneys.
ing renal masses.141
A lateral view is the best method to radiographically Intravenous Excretory Urography

view the kidneys141 (Fig 16.12). As viewed with a lateral Intravenous excretory urography has been described in
radiograph, the absence of the normal dorsal diverticu- birds as a method to gain information on kidney size,
lum of the abdominal air sac (dorsal to the kidney and shape and function.141 Use of organic iodine compounds
ventral to the synsacrum) may indicate renal enlarge- given IV in the basilic vein has been reported. The
organic iodine can be visualized radiographically in the using a complete historical, physical and laboratory eval-
heart and pulmonary artery within 10 seconds, and out- uation. Some of the many causes of PU/PD in birds
lining the kidneys and ureters 20 to 50 seconds later. include organic (liver, kidney, intestine and cardiac),
After 2 to 5 minutes, the cloaca will be outlined. This endocrine (diabetes mellitus) and metabolic (hyper-
technique should not be used in birds with severe renal calcemia) diseases.
compromise.141
A water deprivation test is carefully performed using a
It is the author’s opinion that intravenous excretory simple cage. The bird is weighed and blood and urine
urography may have some limited uses in a clinical set- are collected. Evaluate the packed cell volume (PCV),
ting as demonstrated in the case report below. A water- total solids and osmolality of blood, and specific gravity
soluble iodinated contrast agentb was successfully used and osmolality of urine. In one report of an African grey
to evaluate the ureters post-ureterotomy in a double-yel- parrot (Psittacus erithacus erithacus) undergoing a
low headed Amazon parrot (Amazona ochrocephala).56 water deprivation test, the authors evaluated plasma
The agent was dosed at 400 mg/kg and given in the right sodium, potassium and osmolality in addition to the
medial metatarsal vein. Radiographic images were taken above listed urine parameters.144
at 1, 2, 7 and 10 minutes postinjection. Ureter peristaltic
movement and size were successfully evaluated using Place the avian patient in a cage with no food or water
this technique.56 for the duration of the test. Evaluate both blood and
urine parameters every 3 to 24 hours for 12 to 48 hours,
depending on the species and physical condition of the
Renal Scintigraphy
bird. The reported African grey parrot was evaluated
Avian renal scintigraphy has been described.150 The every 24 hours.144 As a normal response some birds such
radioisotopes 99mTc-dimercaptosuccinic acid (99mTc-DMSA) as European starlings may become distressed within 24
and 99mTc-diethylenetriamine pentaacetic acid (99mTc- hours of water deprivation, which should be considered
DTPA) were used in domestic pigeons. The tested birds when interpreting the results.204 On the other hand,
were given nephrotoxic doses of gentamicin at 15 mg/kg pigeons deprived of water for 36 hours had little change
IM q 12 h for 6 days. The birds were divided into two in plasma osmolality, demonstrating the variable responses
groups and renal scintigraphy using a mean of 41.8 MBq to dehydration in differing species.88 As a general rule,
of intraosseous 99mTc-DMSA or 42.8 MBq of intraosseous smaller birds should be evaluated more frequently.
99m
Tc-DTPA was performed on the last day of gentamicin
toxicosis and again 2 days later. Pre and post-gentamicin- The bird’s behavior and laboratory results give a pre-
treated kidneys were biopsied and confirmed normal sumptive diagnosis. Birds with psychogenic polydipsia
histology pre-treatment and significant renal damage should tolerate this test well and develop more concen-
post-treatment. Uric acid was measured and interestingly trated urine (increased osmolality and specific gravity)
did not significantly correlate with renal histology or and an increase in PCV, total solids and plasma osmolal-
scintigraphy findings. The authors reported ‘decreased ity, all consistent with dehydration. This was the pattern
renal radiopharmaceutical uptake for 99mTc-DMSA and seen in the African grey parrot and subsequent treatment
99m
Tc-DTPA indicated nephrotoxicosis’. More specifically, with water restriction proved curative.144 These individual
scintigraphy using 99mTc-DTPA correlated well with renal values should all be carefully interpreted as noted in a
histologic grades. While scintigraphy using 99mTc-DMSA study of dehydrated starlings where the hematocrit
did not correlate well with renal histologic grades it may remained unchanged (compared with hydrated birds)
be used to demarcate neoplasms, cysts and other physi- and was not a reliable indicator of hydration.204
cal alterations to the renal parenchyma. While renal
scintigraphy can be performed at facilities that routinely Birds with central (lack of production of arginine vaso-
provide nuclear medicine procedures, obvious draw- tocin [AVT]) or nephrogenic (inadequate response to
backs include cost and the need to confine birds for 12 AVT) diabetes insipidus should have different results than
to 24 hours until the radiopharmaceutical used has those with psychogenic causes. Birds with diabetes insi-
degraded.150 pidus become dehydrated (as supported by plasma vari-
ables) but maintain dilute urine (low specific gravity and
osmolality). Normal house sparrows given arginine vaso-
WATER DEPRIVATION TESTING tocin (0.4 ng/kg per minute to 1.6 ng/kg per minute) had
Water deprivation testing is considered when attempting a significant drop in urine flow rate (50.2 to 28.9% of
to rule out unknown causes of polyuria/polydipsia normal, respectively) and increased urine osmolality
(PU/PD) including central and nephrogenic diabetes (150.1 to 196% of normal, respectively).89 A similar
insipidus and psychogenic polydipsia. There are numer- response would be expected in other normal birds of
ous causes of PU/PD in birds that first must be ruled out different species.
479
A strain of chickens with hereditary diabetes insipidus volume (of ureteral urine) collected per kilogram of
has been described.33 These polyuric chickens produced body weight per minute. The urine to plasma concentra-
low osmolality urine and maintained high circulating lev- tion ratio of a (usually parenterally administered)
els of AVT. The vital functions of these chickens became marker substance such as inulin is multiplied by the
impaired after 48 hours of water deprivation. When given urine flow rate. Glomerular filtration rate (milliliters per
AVT, additional to their high circulating levels, these birds kilogram body weight per minute) can then be calcu-
had minimal response. Either the birds had improperly lated by measuring the clearance of the marker sub-
responding kidneys or the AVT was defective.33 stance.73 The basic formula is as follows:
In the author’s experience with one male canary-winged Glomerular filtration rate =
UFR x urine marker substance concentration (inulin)
parakeet (Brotogeris versicolorus) with suspected dia- plasma marker substance concentration (inulin)
betes insipidus, the bird became panicked within 4 hours
as he became rapidly dehydrated, but maintained exces- The single injection, double isotope method, utilizing
sive production of dilute urine. The canary-winged para- 3
H-inulin ([methoxy-3H]-inulin) and 14C-PAH (para-[gly-
keet had normal plasma biochemistries, complete blood cyl-1-14C]-aminohippuric acid), has been shown to be a
count, screening radiographs and renal biopsy (light simple, reliable and rapid method for evaluating renal
microscopy), and had a history of severe PU/PD since function in chickens.197 If needed, the specific proce-
weaning. A diagnosis beyond presumptive diabetes insi- dures of evaluating glomerular filtration in birds can be
pidus was not made, since AVT levels were not evaluated. reviewed in the literature.73,88,90,131,197,204,249,250
IDENTIFYING URIC ACID CRYSTALS BIOPSY

Gout results when uric acid precipitates out as a solid, When history, physical examination and/or laboratory
chalky substance in joints (articular) or on tissue sur- abnormalities support the presence of renal disease, con-
faces (visceral). Articular gout material may be recovered sider biopsy. Currently, the only way to definitively diag-
using fine needle aspiration. Uric acid crystals are easily nose avian renal disease and specific pathologic patterns
confirmed using microscopy or the murexide test. Cyto- is with a kidney biopsy and histopathologic evaluation.141
logically, “gouty” material typically presents as uric acid A renal biopsy is most frequently performed during endo-
crystals surrounded by a pyogranulomatous infiltrate, scopic examination of the coelomic cavity and, specifi-
usually without organisms. The needle-shaped crystals cally, the kidneys. Before a renal biopsy is performed, the
are easy to identify on direct and stained smears. To per- cost:benefit of the surgical procedure versus conservative
form the murexide test, place a small amount of the sus- therapy must be considered, as many birds have compro-
pect material on a slide and mix with nitric acid.141 Use a mised health, especially if they have kidney disease.
flame to evaporate and/or dry the mixture. Once cool,
add one drop of concentrated ammonia. If urates are Several methods of renal biopsy, primarily via endoscopy,
present, a mauve color will appear.141 Due to their water- and detailed accounts of avian kidney anatomy and physi-
soluble nature, urates will dissolve in formalin and, ology have been previously discussed78,134,165,167,181,227,229,233,234
therefore, the crystalline form will not be seen on con- (Figs 16.13-16.18). For the most part, renal tissues can be
ventionally fixed tissue. However, urates can be seen in stored in 10% formalin for light microscopy. If available,
alcohol-fixed tissue using Gomori’s methenamine silver additional tissue may be stored in glutaraldehyde (elec-
impregnation technique.141 tron microscopy), culture media (organism recovery) and
alcohol (visualizing uric acid crystals), or frozen (PCR
studies).
EVALUATING GLOMERULAR
FILTRATION RATE Renal histologic lesions are rarely pathognomonic for a
Glomerular filtration rate has been studied in chickens specific disease process. Many different diseases cause
as a method to evaluate renal function. Glomerular fil- similar renal lesions. Additionally, different pathologists
tration rate is considered the most reliable quantitative may make differing morphologic diagnoses on the same
index of renal function, and is an important tool for the renal tissue.239 The author encourages veterinarians to
diagnosis and management of kidney disease of mam- work with a pathologist familiar with normal and abnor-
mals.156 Most methods of measuring glomerular filtration mal avian histology. Oftentimes, it is the pathologist’s
rate and effective renal plasma flow are difficult and time interpretation of a renal biopsy combined with the
consuming.197 As a result, determining glomerular filtra- attending veterinarian’s case familiarity that enables both
tion rate in birds is often limited to research situations. parties to make a definitive diagnosis or build a reason-
able differential diagnoses list compatible with the kid-
In general, urine flow rate (UFR) is first calculated as the ney lesions noted. This approach has a key role in the
Fig 16.13 | An adult domestic goose with undifferentiated Fig 16.14 | Histologically normal renal tissue from an adult
renal sarcoma. The renal architecture is destroyed and has been hyacinth macaw (Anodorhynchus hyacinthinus). Note the well-
replaced by neoplastic spindle cells. organized renal tubules, normal tubular lumen size (*) and lack
of inflammatory cells. One tubular epithelial cell is undergoing
degeneration (arrow), but the cells appear healthy otherwise.
Fig 16.15 | A mitred conure (Aratinga mitrata) with mild Fig 16.16 | An adult hyacinth macaw (Anodorhynchus
nephrosis. Note the cellular disorganization and loss of tubular hyacinthinus) with mild tubular dilatation 6 weeks post-treatment
epithelial cell structure or degeneration (arrows). for histologically suspected bacterial nephritis. Note the multiple
dilated renal tubules (*). Although there is no evidence of
inflammation, tubular dilatation can be seen with bacterial
infections and other diseases, and suggests that complete reso-
lution has not been obtained.
Fig 16.17 | A citron crested cockatoo (Cacatua sulphurea sp.)

with membranous glomerulopathy of unknown etiology. Due to
the significant mesangial enlargement, the mesangium has Fig 16.18 | An umbrella cockatoo (Cacatua alba) with granulo-
been pushed to the periphery of the glomerulus. The round matous nephritis. Note the multinucleate giant cells within the
glomerulus is outlined (*). renal interstitium (arrows).
481
formation of a viable therapeutic plan for the patient. Another poorly explored area is renal cancer therapy.
Clearly, as treatment options advance and are tested in
avian species, renal cancer therapy will likely become
more prevalent. For example, carboplatin at 5 mg/kg IV
Treatment q 1 month was used to manage a renal adenocarcinoma
(diagnosed at necropsy) in a budgerigar. The bird died
THERAPEUTIC CONSIDERATIONS approximately 3 months after initiating treatment, but
temporarily did show improvement of clinical signs
Treatment options for renal disorders in birds depend
(decreased grip in one foot and lameness changed
upon the cause and type of kidney disease and second-
to almost normal perching, 1 month after starting ther-
ary complications present. Most renal disease patients
apy).147 It was concluded that while carboplatin may be
are medically managed, as kidney surgery is difficult and
nephrotoxic in birds, this drug could possibly be useful
often not needed. Tables 16.4 and 16.5 list medications,
in treating early renal tumors that have not progressed
and their possible indications, commonly used in renal
to renal failure.147
disease patients.
As a general note in any bird with organ dysfunction,
Because of the location within the renal fossae, avian
patients should be monitored with routine physical and
kidneys are difficult to surgically remove. The close asso-
laboratory evaluation, especially when taking any med-
ciations with the lumbar and sacral plexuses and exten-
ication(s) chronically. The intervals between recheck
sive vascular network surrounding the kidneys lead to
examinations will vary on the patient’s condition and
the high probability of significant hemorrhage expected
clinician’s experience in handling the given case.
during surgery, and possible neurologic damage.79 With
that stated, focal therapeutic surgery (including endo-
scopic biopsy) for superficial renal lesions and the DIURESIS AND FLUID THERAPY
ureters may be useful in some cases. Given the concern As in other animals with renal disease, maintaining
of serious hemorrhage, most surgical renal disease cases hydration is important in birds with most kidney disor-
are managed medically. ders. Acid-base and electrolyte disorders may likely be
present in birds with renal disease. At this time, only
A few accounts of therapeutic renal surgery exist. Post- general statements concerning diuresis and fluid therapy
renal failure due to urolithiasis or some other obstruc- can be made.
tion of the ureters or cloaca may be noted. Cloacaliths
and other masses within the cloaca may be easily removed, Anuric and oliguric patients should be diuresed. Although
relieving a potential ureteral obstruction. Wideman and mannitol and furosemide have been recommended to
Laverty describe the effects of renal vein and ureter liga- induce diuresis in birds, these drugs are poorly studied
tion on kidney function in domestic fowl.250 Except for a in avian species.141,181 Mannitol (added to a solution con-
small island of tissue adjacent to the testes and cranial taining inulin and para-amino hippuric acid) was used to
renal artery, the cranial, and portions of the middle, renal induce diuresis in chickens at a dose of 2.5% given at a
divisions atrophied significantly without compromising rate of 0.2 ml/kg per minute.251 Furosemide given IV (1
overall kidney function.250 Such a study is worth review- mg/kg BID) along with SQ saline for 72 hours was used
ing if considering renal division ablation or other similar to successfully treat a red-tailed hawk (Buteo jamaicen-
radical procedures. Renal stones were successfully sis) with acute obstructive uric acid nephropathy.141
removed via extracorporeal shock wave lithotripsy in a Some birds, especially lories, may be sensitive to the
Magellanic penguin (Spheniscus magellanicus).146 effects of furosemide and its use should be judicious.203
Although multiple anesthetic procedures were required, Furosemide also may cause increased urinary excretion
ureteral stones were successfully removed from a 21-year- of Na+, K+ and Cl-.248 If furosemide is used, electrolyte
old male double-yellow headed Amazon parrot (Amazona replacement may be needed. Clinically, providing par-
ochrocephala).56 enteral fluids often induces diuresis in birds, even with
most forms of renal disease.
The author also has used minor surgery in articular gout
cases. In effort to speed the removal of (stabilized) artic- Until acid-base and electrolyte disorders are better evalu-
ular gout, make small incisions over the gouty lesions, ated in birds with renal disease, balanced electrolyte
which are often on the feet. Express the thick material solutions should be used to maintain hydration, replace
out. Anesthesia is ideal as this can be quite painful. Also, fluid losses and/or induce diuresis as needed. The esti-
this procedure tends to be bloody, and the feet often mated daily fluid requirement for most birds is 40 to 60
require minor bandaging to help prevent continued ml/kg per day.52,223 It has been recommended that 10% of
bleeding and secondary infection. the bird’s body weight should be given in fluids when
Table 16.4 | Treatment Guide for Stable Avian Patients with Renal Disease
Fluid Dietary Omega-3 Parenteral Low-dose
Surgery Antibiotics Allopurinol Colchicine
Therapy Modification Fatty Acids Vitamin A NSAIDs
Nondescript nephritis + + + + +
Glomerulopathy +++ ++
Bacterial nephritis +++ +
Parasitic nephritis +
Nephrosis ++ ++ +
Fatty nephropathy +++
Neoplasia + ++
Urolithiasis ++ + ++ +
Amyloidosis + +
Renal fibrosis +++ +
Renal (visceral) gout +++ +++ +++ + ++ +
Articular gout + ++ +++ +++ + ++ +
Note: Most birds with visceral gout are likely in renal failure and usually require immediate medical attention. Fluid therapy, nutritional support and other
appropriate supportive care may be required for any bird in poor condition, and treatment choices are based on the bird's health and attending clinician's
experience.
NSAIDs = non-steroidal anti-inflammatory drugs
+ = occasionally indicated
++ = occasionally to often indicated
+++ = often indicated
Table 16.5 | Doses and Durations of Drugs Commonly Used in Psittacine Renal Disease Patients
(M.S. Echols, unpublished data)37,78
Dose Route Duration Potential Side Effects
Ceftazidime* 75-200 mg/kg BID-QID IM, IV 4-6 weeks + for bacterial nephritis —
Ceftiofur* 100 mg/kg TID IM 4-6 weeks + for bacterial nephritis —
Ciprofloxacin* 20-40 mg/kg BID PO 4-6 weeks + for bacterial nephritis —
Enrofloxacin* 10-30 mg/kg SID-BID PO, IM 4-6 weeks + for bacterial nephritis Muscle/tissue necrosis/irritation upon injection.
Piperacillin* 100-200 mg/kg BID-TID IM, IV 6 weeks + for bacterial nephritis —
TMP Sulfa* 16-100 mg/kg BID-TID PO 6 weeks + for bacterial nephritis. May cause regurgitation. Use cautiously with
Use lower dose for birds over 300 g. dehydrated birds.
Allopurinol 10-30 mg/kg BID PO Use until hyperuricemia and/or physical signs of gout Renal toxicity noted in red-tailed hawks, but not
normalize. Use higher dose short-term (<4 weeks). psittacines.
Colchicine 0.04 mg/kg SID-BID PO Use until signs of hyperuricemia and/or histologic
fibrosis normalize. Can be used with allopurinol and —
for 6-12 months.
Omega(Ω)-3 0.22 ml/kg of a supple- PO Use at least until laboratory and/or renal histologic
fatty acids ment containing <6:1 abnormalities normalize. Can be given 6-12+ —
(Ω-6:Ω-3 fatty acids) months.
Vitamin A 2000-5000 IU/kg once IM Use single dose in conjunction with diet modification. May lead to vitamin A toxicity if used
Repeat dose in 3 weeks if needed. chronically.
Aspirin 0.5-1.0 mg/kg SID-BID PO Use until evidence of glomerulopathy is gone or lab May lead to renal disease if overdosed.
abnormalities have normalized. Can be given 6-12 Do not use in dehydrated or moderate to
months. severely compromised patients.
*Antibiotic choice should be based on culture and sensitivity (C&S) from histologically confirmed or suspected bacterial nephritis.
Otherwise, base antibiotic choice on C&S results from a separate infected lesion, septicemic blood or cloacal cultures.
BID = twice daily SID = once daily
IM = intramuscular TID = three time daily
IV = intravenously TMP = trimethoprim-sulfamethoxazole
PO = orally
For more complete dosing schedules in other species, see Chapter 9, Therapeutic Agents.
the patient is in renal failure.141 Once a dose has been Fluid therapy for critically ill birds should ideally be tai-
determined, warmed fluids are given with food lored to the bird’s electrolyte status and/or overall con-
(tube/syringe-fed), SQ, IV or IO. The IV and IO routes dition and is ultimately decided by the attending clini-
are most appropriate for critically ill patients.223 While cian. The author typically diureses ill and severely hyper-
appropriate in many cases, subcutaneous fluids are not uricemic renal disease patients. While the definition is
adequate to rehydrate patients with severe dehydration, debatable, the author generally considers severe hyper-
shock or hypothermia.223 Oral fluids are reserved for sta- uricemia to be present when one or more of the follow-
ble patients with mild dehydration that have normal ing conditions are met in clinically ill non-carnivorous
gastrointestinal function, and are contraindicated in crit- and appropriately fasted carnivorous birds:
ically ill birds.112 1. Uric acid levels exceed 30 mg/dl.
483
2. Uric acid levels are elevated (>10 mg/dl for most mum of 6 weeks of antibiotic therapy is administered.
species) and rising over a period of several days (even These suggested guidelines are based on renal histo-
if below 30 mg/dl). pathologic evaluation supporting the presence of infec-
3. There is evidence of rapidly progressive articular or tious nephritis, post-treatment resolution of clinical
visceral gout. pathology abnormalities and improved follow-up kidney
biopsy and histopathology in a small number of avian
Depending on the patient’s condition, the author will renal disease cases.64,65 There are no controlled studies
typically give 50 to 100 ml/kg of fluid BID via SQ, IV, IO evaluating antibiotic therapy in active bacterial nephritis
or combination routes. Fluid therapy (combined with cases in birds.64 Additionally, the author will generally
other medications if needed) is generally continued treat concurrent colitis (based on culture and sensitivity
until the blood uric acid level drops to either normal or results of fecal and/or cloacal cultures) for 5 to 7 days,
mildly elevated levels (10-20 mg/dl) and the bird is or until signs abate, in renal disease patients.
showing signs of improvement (eg, eating, more active).
Lower amounts of parenteral fluids are given if overhy-
dration is either suspected or a concern.
MANAGING HYPERURICEMIA,
RENAL FIBROSIS AND AMYLOIDOSIS
ANTIBIOTICS Allopurinol
Antibiotics are indicated in patients with known or sus- Allopurinol’s main action is to decrease uric acid pro-
pected bacterial nephritis. Bacterial renal infections in duction. Specifically, allopurinol inhibits xanthine oxi-
birds may result from an ascending ureteritis, extension dase, which is required to convert hypoxanthine to xan-
from local tissues (eg, peritonitis, oophoritis, salpingitis) thine and subsequently to uric acid.35,53,132,195 In chickens,
and hematogenously.187 Because of the renal portal sys- xanthine dehydrogenase, closely related to xanthine oxi-
tem and possible shunting of blood from the intestines dase, is the actual enzyme used in this pathway.35,46,195
directly to the kidneys, alimentary tract organisms may Allopurinol has been specifically shown to prevent renal
contribute to kidney disease and should be considered synthesis of urates and allow the excretion of unchanged
when using antimicrobial therapy. Drug choices are xanthine.195 Regardless, both clinical and experimental
based on an isolated renal organism (ie, identified dur- data show decreased plasma/serum and/or urinary uric
ing kidney biopsy sampling) or a suspected infectious acid levels in birds treated with allopurinol.46,53,68,132,215
agent (blood, ovarian, salpinx, or cloacal/fecal cultures Interestingly, allopurinol does not appear to affect pan-
and/or supportive histopathology). Clinical considera- creatic xanthine dehydrogenase activity, suggesting dif-
tion regarding potential antimicrobial-induced toxicities fering mechanisms of uric acid metabolism in the pan-
is important. creas and kidney.132
The distribution, elimination and toxicities of many anti- Specifically in red-tailed hawks (Buteo jamaicensis), allo-
microbials are poorly defined in most bird species, purinol has been shown to be toxic at 50 mg/kg PO SID
although an excellent review of antimicrobial use in birds with clinical signs of vomiting and laboratory-supported
with specific consideration toward the renal system is significant hyperuricemia and a renal function disorder.145
available.78 Although mammalian literature warns of The renal toxicity was even worse and included visceral
potential nephrotoxicity with amphotericin B, cephalo- gout when red-tailed hawks were given 100 mg/kg fol-
sporin, fluoroquinolone, trimethoprim/sulfonamide and lowed by 50 mg/kg of allopurinol. The toxic signs were
tetracycline use, only aminoglycosides have been consis- attributed to oxypurinol, the active metabolite of allop-
tently and definitively associated with renal disease in urinol.145 Allopurinol given at 25 mg/kg SID PO to red-
birds.71,78,117,166 Those drugs with known potential nephro- tailed hawks was shown to be safe, but had no significant
toxicity should be cautiously used in birds with renal effect on plasma uric acid concentrations.191c The authors
impairment. Until additional studies are completed in concluded that allopurinol has a very low therapeutic
birds, antimicrobials that reach high concentrations in the ratio, at best, in red-tailed hawks and that other means of
renal tissue and urine without inducing toxicity should be controlling hyperuricemia, such as urate oxidase, in this
chosen and cautiously used in kidney disease patients. species should be considered.191c With the exception of
red-tailed hawks, allopurinol use is reported to be non-
The ideal duration recommendable for treating renal toxic in birds (in studied chickens), including chicks.132,181,246
infections has not been established in birds. In cats and Although the long-term effects are not clear, allopurinol
dogs, greater than 4 to 6 weeks of antimicrobial use is given to chickens increases oxidative activity by lowering
generally recommended for treating bacterial kidney plasma uric acid, an important avian antioxidant.215
infections.136 The author’s clinical experience with bacte-
rial nephritis suggests that response is best when a mini- The author uses allopurinol as a first-line drug to lower
uric acid when fluid therapy and diet modification alone promising drug needs further evaluation to better
are not sufficient or when hyperuricemia is severe. understand its use and potential long-term effects.191b
Clinical experiences suggest that allopurinol is safe to
use at published doses in Psittaciformes and Colum-
DIETARY MODIFICATION
biformes, even when used chronically (3-6+ months).
Because of the noted toxicities in red-tailed hawks and As a general note, birds should be fed diets appropriate
until further studies are conducted, it is reasonable to for their species. Supportive dietary therapy should
assume that allopurinol should be used judiciously, if at always be considered in any anorectic patient. As is true
all, in birds of prey. with all sick birds, renal disease patients should be
weighed routinely at regular intervals and monitored for
weight loss.
Colchicine
Theoretically, colchicine can reduce serum uric acid lev- Protein
els in birds and be used to control hyperuricemia. In The question of dietary protein restriction in the face of
chicken livers, colchicine reversibly inhibits xanthine renal disease remains controversial. The current human
dehydrogenase (compared to a “pseudo-reversal” with and veterinary literature cites arguments for and against
allopurinol).67,68 Colchicine prevents the progression of both restriction and supplementation of protein with
renal disease in humans with familial Mediterranean renal disease patients.94,95,137,239 The current human
fever, a disease of recurring fever often complicated by literature cites malnutrition (potentially from protein-
amyloidosis.179 In humans, colchicine is best known for restricted diets) as the most potent predictor of death in
its antigout activity.191 In small animals, colchicine blocks end-stage renal failure.179 The resultant recommendation
the synthesis and secretion of serum amyloid A, and is that patients on protein-restricted diets should be well
decreases the formation and increases the breakdown of supervised and provided adequate calories.179
collagen. For these reasons, colchicine has been used to
treat amyloidosis and hepatic fibrosis, respectively.191 Although feeding 20% protein to chicks, including
young cockatiels, has been recommended as a general
Clinical use of colchicine suggests possible benefit in level for normal development, excessive protein intake
reducing hyperuricemia in birds with renal disease.64,65 for birds with renal disease has not been determined.207
The author also has used colchicine to reduce renal Feeding diets consisting of 60 and 80% protein (2 sepa-
(and hepatic) fibrosis in birds, and has had good success rate studies) were required to induce articular gout in
based on pre- and post-treatment tissue biopsies (M.S. genetically predisposed chickens.9 In a study using adult
Echols, unpublished data). As such, the author uses cockatiels, birds fed up to 70% protein for 11 months
colchicine as a second-line drug to reduce hyper- had no evidence of visceral or articular gout or signifi-
uricemia and a primary medication for histologically cant renal lesions. This led the authors to the conclusion
confirmed tissue fibrosis. Allopurinol and colchicine are that, in cockatiels, high dietary protein levels are not
well tolerated when given together in most birds. If diag- associated with kidney dysfunction.123 These experimen-
nosed antemortem, colchicine may be used in birds with tal diets represent unnaturally high protein levels and
amyloidosis. No controlled studies were found using do not serve as a realistic evaluation of the effect of diet
colchicine in birds with renal disease. on renal disease and/or gout in birds.
The management of hypoproteinemia also may be

Urate Oxidase
important in birds with renal disease. As mentioned
Urate oxidase also has been recently discussed as an under Part 2: Electrophoresis, Plasma Protein Electro-
alternative method to manage hyperuricemia in birds.191b phoresis, the identification of hypoproteinemia and
At least in humans, urate oxidase is reported to degrade association with renal disease in birds is unclear.
the excess of uric acid to allantoin, which the kidneys
can clear more easily than uric acid. Urate oxidase also is Until further research better defines the role of dietary
very specific for urates and uric acid and does not inter- protein needs in relation to renal disease, avian kidney
fere with the metabolism of purines as does allopurinol. disease patients should be fed a well-balanced diet
In one study, urate oxidase was given (200 and 600 U/kg appropriate for their respective species. If instituted,
and 100 and 200 U/kg IM) to pigeons and red-tailed birds fed protein-restricted diets should be carefully
hawks, respectively. When compared to controls, all dos- monitored. No current studies evaluate the effect of low
ing regimens caused a significant decrease in plasma or high-protein diets in birds with naturally occurring
uric acid concentrations within 2 days of the first dose. renal disease were available at the time of writing. A safe
The authors concluded that “urate oxidase is much recommendation is that birds with hyperuricemia and/or
more effective compared with allopurinol,” but this gout should not consume diets with protein levels greater
485
than what is considered normal for the given species. demonstrated increased renal production and excretion
of PGE2 and PGE3, which was believed to have stabilized
renal tubular lysosomal membranes.95 These n-3 FA-sup-
NUTRITIONAL SUPPLEMENTATION
plemented dogs had decreased gentamicin-induced prox-
Treatment: Omega-3 Fatty Acids imal tubular necrosis when compared to controls.95
Omega-3 fatty acids (n-3 FA) have gained popularity for Specific toxicities associated with n-3 FA supplementa-
their anti-inflammatory, lipid-stabilizing and antineoplas- tion are poorly described, but some potential adverse
tic effects, renal protective properties and other poten- effects may occur. Chickens fed diets high in n-3 FA had
tial qualities.12,190 The n-3 FA are polyunsaturated and are reduced plasma and tissue vitamin E (the body’s primary
designated by their first carbon-carbon double bond antioxidant) and plasma carotenoid levels due to lipid
occurring at the third carbon from the methyl group.190 peroxidation.4,5,230 Therefore, supplementing the diet
The n-3 FA are those rich in eicosapentaenoic (EPA), with n-3 FA increases the requirements for dietary vita-
docosahexaenoic (DHA) and/or linolenic acid.4,31 Flax min E.4,45 As supported by clinical investigations, vitamin
seed and menhaden (cold-water plankton-feeding fish) E supplementation should be considered with use of n-3
oils contain predominately linolenic acid, and EPA and FA or any other polyunsaturated fatty acids.182,230
DHA, respectively, and therefore have different n-3 FA Specifically, 160 mg/kg of vitamin E (dl-α-tocopherol
compositions.4 DHA and EPA are more readily incorpo- acetate) was shown to prevent loss of α-tocopherol in
rated into biological tissues, but also carry greater poten- tissues, and normalize or increase resistance to lipid
tial to create metabolic oxidative stress than linolenic peroxidation in chickens fed a commercial diet supple-
acid.4 The clinical impact of the differences of the vari- mented with 3% tuna oil (n-3 FA).230
ous n-3 FA has not been clearly defined.
Other potential side effects may be noted with n-3 FA
Studies evaluating n-3 FA in mammals serve as the basis supplementation in birds. Menhaden oil supplementa-
for potential treatment value in birds with selected renal tion in laying chickens has been shown to contribute to
disease. At this time, only anecdotal information exists hepatic lipidosis, likely via enhancing the lipogenic activ-
regarding use of n-3 FA in birds with renal disease. ity (along with estradiol) of the liver.240 This study cau-
tions the use of n-3 FA in reproductively active hens. In
In mammals, n-3 FA can significantly reduce thrombox- another study, chickens fed diets high in n-3 FA had no
ane A2 (TXA) synthesis in platelets and glomerular cells, alteration in primary or secondary humoral response,
and increase production of vasodilatory prostaglandins.95 but experienced a 50% reduction in antibody-dependent
n-3 FA partially substitute EPA and DHA for arachidonic cell cytotoxicity (ADCC).80 The concern presented therein
acid in membrane phospholipid.31,104,159 This pathway was that reduction in ADCC-related immune functions
decreases the release of arachidonic acid and, subse- might increase a patient’s susceptibility to certain dis-
quently, the cyclooxygenase-mediated synthesis of ease (Marek’s).80 The n-3 FA supplementation also may
TXA.31,95,190 In contrast, most animals readily convert affect the ability of antigen-presenting cells to present
omega-6 fatty acids (n-6 FA) to arachidonic acid and, antigen, again suggesting the potential for immune sys-
subsequently, eicosanoids (prostaglandins, TXA).31 As tem alteration.103 An increased incidence of infectious
with arachidonic acid, EPA also serves as a substrate for disease in birds has not definitively been associated with
the formation of vasodilatory prostaglandin/cyclins n-3 FA supplementation.
(PGI/PGE) and their respective products (PGI2 /PGE2 and
PGI3 /PGE3), all of which have similar biologic potency.95,190 Although specific doses have not been established, some
These vasodilatory prostaglandin/cyclins increase renal believe that the appropriate n-6 to n-3 FA ratio is more
blood flow and single nephron GFR.31,190 important to inhibiting eicosanoid synthesis from arachi-
donic acid than is the absolute amount of n-3 FA.95 A
In humans and rats supplemented with n-3 FA for at least dietary n-6 FA:n-3 FA ranging from 5:1 to 15:1 has been
4 to 6 weeks, single nephron GFR, plasma flow and renal proposed as desirable for dogs and cats with renal dis-
blood flow increased and/or decreased renal vascular ease.31 Using the above dietary guideline, 2 to 4 weeks
resistance occurred.95 In a separate evaluation, dogs on a are required to see any initial effects of the dietary change
low-fat diet supplemented with n-3 FA had preserved in dogs and cats.31 One study in chickens showed that
renal function and structure when induced with renal maximal n-3 FA tissue (egg yolk) levels were obtained
disease.31 Another study found that n-3 FA supplementa- after 3 to 4 weeks of supplementation.240 Long-term sup-
tion reduced glomerular capillary pressure and pre- plementation (3 to 6 months or more) is likely appropri-
vented deterioration of GFR in dogs with renal disease.32 ate if n-3 FA are to be used.
Compared with controls and thromboxane synthetase
inhibitor-treated dogs, beagles supplemented with n-3 FA The author has successfully used supplements containing
n-6 FA:n-3 FA of 4-5:1 to 1:3 combined with low-dose renal dysfunction/damage as noted by one or more of
aspirin (0.5-1.0 mg/kg PO q 12 h) to manage histologi- the following: decreased proteinuria, enzymuria and
cally confirmed glomerulopathies in avian patients (M.S. tubular necrosis, and preserved renal blood flow
Echols, unpublished data). Success was gauged on nor- and GFR in various animals with a variety of renal dis-
malized hyperuricemia (4/4), improved clinical appear- eases.92,94,95,135 Unfortunately, the beneficial effects of low-
ance (3/4) and repeat renal biopsy showing normal dose or specific NSAID therapy have not been studied in
glomerular light microscopic histology (1/1) in an African birds with renal disease.
grey parrot (Psittacus erithacus erithacus), citron-crested
cockatoo (Cacatua sulphurea citrinocristata), red-lored Although there are limited avian studies, most NSAIDs
Amazon parrot (Amazona autumnalis) and a ring-neck are eliminated by renal clearance and should be used
dove (Streptopelia risoria) (M.S. Echols, unpublished with caution, as they have been associated with a variety
data). The author also has used a supplementc containing of renal lesions in birds and mammals.6,120,137,179,196 Flunixin
n-6 FA:n-3 FA of 1:3 (0.22 ml/kg body weight, PO, SID) meglumined-induced glomerular lesions in bobwhite
alone to manage various forms of renal disease in mixed quail (Colinus virginianus) that increased in severity
avian species with no recognized adverse side effects. proportionally with the dose. In this short study, no bio-
Unfortunately, no clinical trials using fatty acids in avian chemical or electrolyte parameters were altered, but uric
renal disease were found, only anecdotal reports such as acid was not measured.120 Aspirin has been associated
noted here. with significant inhibition of prostaglandin synthesis
(specifically prostaglandin F2α) in Japanese quail.164 In
this same experiment, aspirin was shown to induce liver
Vitamin A
enlargement resulting from hepatic lipid accumulation
Parenteral vitamin A has been recommended in birds in n-6 FA-deficient Japanese quail.164 Acetylsalicylic acid
with renal disease.141 Hypovitaminosis A is a reported (aspirin) injected IV into Pekin ducks induced temporary
cause of renal failure and results from metaplasia of the diuresis lasting 30 minutes, which is in contrast to the
ureters leading to hyperkeratinization, decreased mucin antidiuretic effect seen in mammals, and had no effect
production and impaction.116,214 Vitamin A deficiency is on GFR or peripheral blood pressure.97 Several Gyps
discussed in more detail in Chapter 4, Nutritional spp. of vultures have died with renal failure and gout
Considerations. In birds with suspected hypovitaminosis as a direct result of consuming diclofenac-treated live-
A and renal disease, appropriate diet modification and stock.175b The veterinary use of diclofenac has been
short-term parenteral vitamin A are logical components specifically implicated in the decline of the critically
of therapy. In such situations, the author gives a single endangered Oriental white-backed vulture (Gyps ben-
IM vitamin A injection at the beginning of the therapy galensis) in Pakistan.175b These scattered studies serve
and recommends correcting the patient’s diet to only to point out potential varied effects of NSAIDs in
improve long-term nutritional status. The diet must be birds.
evaluated and the potential of hypervitaminosis A must
be ruled out prior to parenteral vitamin A administra- Even with the noted toxicities and lack of therapeutic
tion. See Chapter 4, Nutritional Considerations: Section studies in birds, the author feels that low-dose aspirin,
II, Nutritional Disorders for more about hypervita- and possibly other NSAIDs, use can be beneficial in
minosis A. avian kidney disease patients. In the author’s experi-
ence, low-dose aspirin (0.5-1.0 mg/kg PO q 12 h) com-
NON-STEROIDAL bined with n-3 FA supplementation is safe and may be
ANTI-INFLAMMATORY DRUGS effective at reducing the severity of some forms of avian
renal disease, especially glomerular disorders (M.S.
Non-steroidal anti-inflammatory drugs (NSAIDs) are
Echols, unpublished data). Aspirin (and n-3 FA) therapy
frequently discussed for use in human and animal renal
can be used chronically, and the author discontinues use
disease patients.92,94,95,135,179 In general, NSAIDs such as
once evidence of renal disease is gone or the disorder is
aspirin and ibuprofen are non-specific cyclooxygenase
satisfactorily managed.
inhibitors. Low doses of aspirin may actually inhibit
platelet cyclooxygenase production, but allow beneficial
(vasodilatory) prostacyclin formation and may be safe.94 TREATMENT SUMMARY
Consequently, low-dose aspirin therapy has been sug- Treatments of avian renal disease should be individual-
gested to reduce platelet aggregation and subsequent ized according to the patient’s needs, accurate renal his-
thromboembolism, and to minimize glomerular inflam- tologic diagnosis (if available), concurrent disorders and
mation for mammalian patients with some glomeru- client considerations. Identified parasites are treated
lopathies.94,137 More specific NSAIDs such as thrombox- appropriately. If ova are identified in the urine, consider
ane synthetase inhibitors have been shown to attenuate whether or not the eggs were actually released in the
487
intestines. Treatment of bacterial nephritis with appropri- Articular gout, although not a renal disease, also is
ate antibiotics should be based, in part, on culture and included. With the possible exception of “diet-induced
sensitivity results when available. Otherwise, suspected renal disease of color variety psittacine birds,” the
bacterial-induced nephritis should be treated with broad- patient’s diet should be modified as is appropriate for
spectrum bacteriocidal antibiotics that reach high kidney that avian species. Secondary infections, dehydration,
concentrations and which are non-nephrotoxic. Anti- unacceptable weight loss, etc, should be managed as
bacterials also should be considered when concurrent needed. Combination therapy should be considered
colitis is present. Removing known nephrotoxins and
when two or more histologic renal lesions are present.
addressing secondary complications may best manage
nephrosis. Such secondary complication of any renal dis-
ease may include dehydration, hyperuricemia, fibrosis,
infectious diseases and anorexia. Dietary-induced renal Prognosis
diseases can be managed with diet change or supplemen-
tation, depending on the etiology. Antineoplastic treat- The World Health Organization classification of renal
ment of certain avian renal tumors may be indicated and disease is based on distinct glomerular pathological find-
should be considered. Specifically identifying and manag- ings and is used for prognosis, treatment and out-
ing underlying diseases that may be concurrently present come.109 Presently, no such classification system exists in
may best control glomerulopathies. Confirmed glomeru- avian medicine. In fact, there are limited studies that
lar disorders in birds without an obvious underlying dis- estimate the outcome of selected avian renal disorders.
ease may be managed in some cases with low-dose One such review noted that most birds live less than 3
aspirin and N-3 FA supplementation. Nutritional manage- months following a diagnosis of a renal neoplasm.79 This
ment such as weight loss, providing a balanced diet and
may seem to offer a poor prognosis, but represents only
vitamin A supplementation also may be indicated.
one form of renal disease that is usually diagnosed late
Table 16.6 represents a quick treatment summary of and with which there are few treatment options. Based
some of the more common renal disease classifications. on the author’s experience, several forms of renal dis-
ease can be successfully managed and some resolved,
giving a good prognosis for long-term health to the indi-
Table 16.6 | Avian Renal Disease Treatment Summary vidual patient.
• Nephrosis: Parenteral vitamin A. Remove exposure to tox-
ins if known. Consider n-3 FA supplementation. Clinicians are encouraged to thoroughly evaluate each
• Glomerulopathy: If identifiable, remove/control any source
avian renal disease patient individually from diagnosis
of infection/inflammation. Give n-3 FA and low-dose
aspirin until all signs of renal disease (hyperuricemia, histo- through to management or completion of treatment.
logic changes, etc) are gone. n-3 FA can be given chroni- Consider renal biopsy as a viable tool for diagnosing and
cally if needed. managing disease. Dr. Robert Schmidt states, “The prob-
• Bacterial Nephritis: Antibiotics for a minimum of 4 to 6
lem is that clinical lab tests may indicate renal disease in
weeks.
• “Diet-induced Renal Disease of Color Variety birds, but several kidney disorders cause similar (lab)
Psittacine Birds”: Discontinue pellets and change diet over abnormalities. If you want a definitive diagnosis, biopsy
to whole grains, seeds, fruits and vegetables as is appropri-
the kidney” (R. Schmidt, personal communication,
ate for the species. If after 3 to 6 months all signs of renal
disease are gone, pellets (<50% of total diet) can be cau- 2003). Treatment completion may have to be defined, in
tiously added to the diet. some cases, as return to normal renal histology by fol-
• Renal Fibrosis: Use colchicine until histologic fibrosis low-up biopsy. Until renal diseases of birds are better
resolves. Otherwise, use colchicine for 6 to 12 months or
understood, classified and treated, the short- and long-
until laboratory abnormalities normalize. The n-3 FA also
may be beneficial. term prognoses can be estimated based only on the
• Articular Gout: Use colchicine and allopurinol together severity of kidney lesions at that time and secondary dis-
until all signs of gout and hyperuricemia have resolved. orders of the patient.
Consider diagnosing the cause of probable underlying
renal disease and manage appropriately. Give vitamin A if
hypovitaminosis A is suspected. Articular gout lesions also Products Mentioned in the Text
may be surgically opened and expressed to speed removal a. Combur-9 Stix, Boehringer Mannheim
of uric acid crystal accumulation. n-3 FA may be beneficial. www.burnsvet.com/home/default.asp
Use aggressive fluid therapy if articular or visceral gout is b. Renografin-76, Squib Diagnostics, Princeton, NJ
accumulating rapidly. See Chapter 4, Nutritional c. Optomega, USANA Health Sciences, Salt Lake City, UT,
Considerations: Section 2, Nutritional Disorders. www.unitoday.net/USPSupplements
d. Banamine, Schering-Plough Animal Health, www.spah.com
References and pigeon. Comp Immun Microbiol

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220:86-90, 1982. Borrelia burgdorferi infection: 49
cases (1987-1992). Vet Pathol
36. Canny C: Gross anatomy and
Suggested Reading 19. Blagburn BL, et al: Crypto- imaging of the avian and reptilian 34:85-96, 1997.
sporidium sp. infection in the urinary system. Sem Avian Exot 55. Degernes LA: Toxicities in water-
1. Abbassi H, et al: Renal cryp-
proventriculus of an Australian Pet Med 7(2):72-80, 1998. fowl. Sem Avian Exotic Pet Med
tosporidiosis (Cryptosporidium
diamond firetail finch (Stagno- 37. Carpenter JW, Mashima TY, 4(1):15-22, 1995.
baileyi) in specific-pathogen-free
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17_Neurology Rich.qxd 8/23/2005 11:22 AM Page 493
CHAPTER
17
Nervous System
SIMON R. PLATT, BVM&S, MRCVS, Dipl ACVIM (Neurology) ,
Dipl ECVN, RCVS Specialist in Veterinary Neurology
The nervous system plays a role in nearly all body

processes. Disease syndromes may affect the central
nervous system (CNS), which includes the brain and
spinal cord, and the peripheral nervous system, which
includes cranial nerves, spinal cord nerve roots, spinal
nerves, peripheral nerve branches and the neuromuscu-
lar junction. Evaluation of the nervous system of birds
parallels that of mammals, with modifications specific to
avian anatomy, behavior and physiology. An understand-
ing of basic avian neuroanatomy is necessary to evaluate
abnormal function of the nervous system.15,16,62,87
Suspicion of neurologic dysfunction arises from the his-

tory and physical examination. The signalment, present-
ing chief complaint, time course of clinical signs, and his-
tory may suggest the type of disease process or species-
specific disorder. A complete neurologic examination is
necessary to localize the anatomic distribution, to deter-
mine the severity of the disease process, and to assess
the prognosis for patient recovery. A minimum database
consisting of a complete blood count (CBC), serum or
plasma biochemical analysis, and cytologic evaluation of
choanal and cloacal swab samples is used to evaluate the
contribution of other body systems to the observed clini-
cal signs and physical abnormalities. If neuromuscular
disease is suspected, electrophysiological tests are indi-
cated, including electromyography and nerve conduction
velocities, and these are becoming more commonly per-
formed in birds. In recent years with the advancement of
imaging technology and the improved availability for vet-
erinary patients, scintigraphy, computed tomography and
magnetic resonance imaging have been valuable diagnos-
tic commodities in furthering our understanding of avian
CNS disease. Only when a disease location and a patho-
logic process have been identified can appropriate treat-
ment and prognosis be provided.
Anatomy and Physiology premotor neurons of the motor systems of the spinal
cord, thus controlling flying and walking. The final affec-
Complete reviews of avian neuroanatomy are docu- tors of wing and leg movement are the lower motor
mented in other texts.15,62,85,87 For a detailed description of neurons of the brachial and lumbar plexuses, respec-
the functional organization of the avian spinal cord, the tively. In-depth review of this area is covered in an avian
reader is referred to an avian physiology text.83 The gen- physiology text.15,33
eral organization of the avian spinal cord resembles that
of all other vertebrates. There are however, some special- Control of Vocalization and Respiration
izations, which birds largely share with the phylogeneti- Birds use their syrinx, an organ at the transition of the
cally related class of reptiles. Compared to the mam- trachea and bronchi, to produce sounds. Vocalization
malian cord, the most outstanding deviations are the lack depends upon the control of a few small syringeal mus-
of a cauda equina and a filum terminale and the occur- cles and the precise regulation of the stream of (expira-
rence of a sinus rhomboidalis or lumbosacralis.83 At the tory) air passing through the trachea. This requires a
microscopic level there are some significant differences close coordination of the motor centers of the syringeal
in the organization of cell groups and pathways. Birds and respiratory muscles. The caudal part of the dorsal
differ from most other vertebrates in their locomotion hypoglossal motor nucleus innervates the syringeal mus-
due to bipedal walk and flight. It has to be kept in mind cles, whereas the motor cells of the respiratory muscles
that specializations in the spinal cord may result from are part of the motor system of the spinal cord. However,
adaptations from this peculiar kind of locomotion. several cell groups in the cranial and caudal brainstem
have a role in the control of respiration. In songbirds,
Control of Eye and Head Movements these centers are all under direct telencephalic (cerebral)
A sitting bird is able to survey a large part of its surround- control.120 See Chapter 19, Endocrine Considerations.
ings using both head and eye movements. Several types
of eye movements can be distinguished such as saccades Control of Coordination
(fast flicks elicited by a sudden stimulus) and smooth Birds possess a well-developed cerebellum but, as in
pursuit (following a moving target).33 Six muscles are mammals, its precise role in the control of motor activity
responsible for all movements of the eye. Branches of the is not well understood. However, there is little doubt
oculomotor, trochlear and abducens nerves innervate that the ease and precision of motor performance
these extrinsic eye muscles. The two muscles that rotate depend upon an intact cerebellum. The axons of the
the eye dorsally are innervated by contralateral centers, Purkinje cells form the output of the cerebellar cortex;
with the other muscles innervated by ipsilateral cell the central cerebellar nuclei and some vestibular nuclei
groups. These are stimulated by the vestibular centers.37 are the targets of these fibers.33 The Purkinje cells have
an inhibitory effect on the activity of the central nuclei.
Control of Jaw and Tongue Movements
The jaw muscles have a visceral origin; therefore, the
nerves innervating these muscles and the corresponding
motor nuclei are considered visceromotor elements.33 A
Neurological Examination
complication in parrots is that they possess a so-called and Lesion Localization
kinetic skull. This means that not only the lower jaw but
A neurological examination is easily integrated into a
also the upper jaw moves to open the beak.33 Movement
routine physical examination. The objectives of the neu-
of the beak is achieved by four groups of muscles: two
rological examination are to confirm if there is a neuro-
groups of beak openers and two groups of beak closers.
logical abnormality and to specifically localize the abnor-
Movements of the tongue are caused by two groups of mality within the nervous system. In conjunction with
muscles. The extrinsic muscles are part of the visceral the history, signalment, presenting complaint and the
musculature, similar to the jaw muscles, and the intrin- physical examination, the neurological lesion localiza-
sic muscles have a somatic origin innervated by the hypo- tion is a piece of a jigsaw, essential to creating a list of
glossal nerve. Because the jaws and tongue move in differential diagnoses for the disease. However, caution
close harmony during feeding and drinking, a premotor must be used, as some manipulations necessary for the
system is needed to coordinate the activity of the tongue neurological examination could exacerbate problems
and jaw motor centers.33 such as spinal cord disease.80
Control of Locomotion OBSERVATION

The reticular formation in the brain stem also contains Observation of the bird is essential, as it allows evalua-
Chapter 17 | E V A L U A T I N G A N D T R E A T I N G T H E N E R V O U S S Y S T E M 495
tion of the bird’s mentation (level and content of con- Table 17.1 | Cranial Nerves: Function and Applicable Tests
sciousness), posture, attitude and gait. Changes in men- Cranial Nerve Nerve Function Applicable Tests
tation are revealed by a history of personality change, I. Olfactory Smell None applicable
change in awareness of surroundings and inappropriate II. Optic Vision i. Menace response
ii. Pupillary light reflex
behavioral responses.26 Consciousness is a function of
III. Oculomotor Extrinsic and intrin- i. Eyeball position
the brainstem (responsible for arousal) and the cerebral sic ocular muscles/ ii. Menace response
upper eyelid muscle iii. Pupillary light reflex
cortex (responsible for content and regulation).26,40,101,117,119
IV. Trochlear Extrinsic ocular i. Eyeball position
muscles
PALPATION V. Trigeminal Facial and beak i. Palpebral reflex
sensation/beak ii. Jaw palpation
The bird’s musculoskeletal system should be palpated movement
for asymmetry, masses, tenderness, contour and tone. A VI. Abducens Extrinsic ocular i. Eyeball position
muscles and third
mass effect, tenderness or contour change requires fur- eyelid muscle
ther investigation. The vertebral column should be pal- VII. Facial Muscles of facial None applicable
pated for deviations and pain, being cautious not to expression
apply too much pressure if there is suspicion of an insta- VIII. Vestibulocochlear Hearing and i. Startle
balance ii. Oculocephalic reflexes
bility. Unilateral muscle mass loss or atrophy may indi-
IX. Glossopharyngeal Muscles of pharynx, i. Gag reflex
cate disuse if it is chronic, or a neurogenic loss if it is larynx, crop and
syrinx
acute (within 7 to 10 days).26
X. Vagus Muscles of larynx, i. Gag reflex
pharynx, esophagus
and crop
CRANIAL NERVES (CNs)
XI. Accessory Superficial neck None applicable
Several differences exist between the neuroanatomy of muscles
avian and mammalian species.15,26 Cranial nerves have VII. Hypoglossal Muscles of tongue, i. Tongue grab/
trachea and syrinx inspection
specific functions and evaluation of these functions can
help to precisely locate a neurological lesion due to
their well-documented anatomy. The general functions
and specific tests are summarized in Table 17.1.
Simplistically, cranial nerve dysfunction may indicate a

CNS lesion (brainstem disease) or a peripheral lesion
(affecting the cranial nerves after they have exited the
brainstem and course through the skull). Evaluation of
the cranial nerves should follow observation and palpa-
tion, with particular attention paid to normal functions
of eye movement, head movement, blinking, jaw and
tongue movement, and general symmetry of the head.
Initially an ophthalmic exam should be performed, which

will assist with the evaluation of the optic (CN II), oculo-
motor (CN III), trochlear (CN IV), abducens (CN VI), and
trigeminal (CN V) nerves.15,16,62 The following tests are Fig 17.1 | The menace reaction is performed by making a
threatening gesture with fingers or hand toward one eye and
essential to the evaluation of cranial nerve function. watching for a blinking action.
The Menace Response

How to Perform intact. Normal function is demonstrated by a blink. To
Obscure the vision in one eye and make a slow, threat- localize the lesion, other cranial nerve tests would be
ening hand gesture toward the other eye (Fig 17.1). required.
How to Interpret The Pupillary Light Reflex

This is a learned response, not a reflex, to a perceived How to Perform
threat, which evaluates CNs II and V (responsible for Shine a bright light in each eye to evaluate the response
innervation of the orbicularis oculi muscle, which closes of the pupil (Fig 17.2).
the eyelids), as well as the central visual pathways and the
cerebellum.62,87 Birds that are stoic or excited may not How to Interpret
show a menace response even though nerve function is This is a reflex. Light is sensed by CN II; parasympathetic
Fig 17.2 | The pupillary light response is performed by shining Fig 17.3 | The palpebral reflex is performed by touching the
a light source into one eye at a time and monitoring the medial canthus of the palpebral fissures and watching for a
response of the pupil. blink in response.
fibers of CN III cause contraction of the iris muscle in

normal birds with direct stimulation. There is no con-
sensual response in birds due to the 100% decussation
of the optic nerves at the optic chiasm.26 However, some
raptors have an incomplete bony septum between the
globes and may respond to light reaching the contralat-
eral retina, mimicking a consensual response.82 The
response may not be as marked as that seen in mam-
mals, as birds have striated muscle in the iris, giving
Greg J. Harrison
them some voluntary control over pupil size independ-
ent of light intensity. This reflex is best evaluated as soon
as possible during the examination, as sympathetic tone
Fig 17.4 | A cockatiel (Nymphicus hollandicus) with eyelid
in restrained birds may override constriction. paresis from infraorbital sinus infection demonstrates a cranial
nerve V lesion.
Evaluation of Strabismus
How to Perform How to Interpret
Observe the bird’s head in a normal position for a devia- The normal eyelid should close. Cranial nerve V (trigem-
tion of one or both globes in the orbit(s). inal nerve) is responsible for facial sensation, whereas
the motor response to facial sensory stimulation is gen-
How to Interpret erally provided by the facial nerve (CN VII). The eyelids
Cranial nerves III, IV and VI aid vision by maintaining the are innervated by CN V in birds.39,62,87 Eyelid sensation is
globe in a central position. Deviation of the globe from provided by the ophthalmic branch (upper lid) and the
its central axis indicates dysfunction in one or more of maxillary branch (both lids) of CN V. Eyelid closure is
these nerves: ventrolateral — CN III, dorsolateral — CN provided by the mandibular branch (orbicularis oculi
IV, and medial — CN VI. In contrast to mammals, the muscle) of CN V that, when damaged, may present as
third eyelid in birds has striated muscle fibers, innervated eyelid paresis (Fig 17.4).
by CN VI, that initiate movement of the nictitans across
the cornea.20,59,62,82,87 Prolapse of the third eyelid in birds Evaluation of Jaw/Beak Tone
does not directly indicate loss of sympathetic innervation, How to Perform
as found in Horner’s syndrome in mammals. Observe the bird for a dropped lower beak and/or an
inability to eat with the beak. Assess the strength of the
The Palpebral Reflex beak safely by manually opening the beak and evaluating
the resistance to opening (Figs 17.5a,b).
How to Perform
Touch the medial canthus of the normal eyelid and How to Interpret
watch the response (Fig 17.3). The mandibular branch of CN V provides motor func-
Fig 17.5a | The beak is assessed for strength and movement. Fig 17.5b | The movement and symmetry of the tongue can be
assessed by forcing open the beak or using a speculum.
tion to the jaw.39,87 A dropped lower beak or the inability How to Perform
to chew indicates damage to CN V. Cranial nerve VII con- A wing or leg is placed in an abnormal position and a
tributes to prehension by partial innervation of the mus- correcting response by the bird is observed. Not all stan-
cles that open the jaw. dard mammalian postural reactions can be done due to
the modifications of the forelimbs in birds. However,
The Oculocephalic Reflex/Interpretation knuckling the toes over while supporting the bird can be
of Nystagmus done to evaluate how long it takes for the bird to correct.
How to Perform Placing the bird’s foot on its dorsal surface against a
Move the head from side to side in a horizontal plane and perch may be a more practical way to test proprioception
observe the resulting movement of the eyes (Fig 17.6). in the limbs. Alternatively, a piece of paper may be placed
under each foot and slowly moved sideways to see if the
How to Interpret
bird returns its foot to the standing position. Placing
In normal birds, a physiological nystagmus will be
reactions of the wings are not evaluated routinely in
induced, with the fast phase in the direction of head
birds. Placing reactions in the rear limbs may be helpful.
movement. This reflex tests the integrity of CN VIII
Visual placing may be evaluated crudely by offering a
(vestibulocochlear nerve), which is the sensory arm of
perch for the patient to step onto (Fig 17.7). Tactile plac-
this reflex, and CNs III, IV and VI, which are responsible
ing may be evaluated in birds such as ratites and raptors
for the motor movement of the eyes. Clinical signs of
that allow hooding. A perch may be touched to the dor-
peripheral vestibular disease are manifest after damage
sum of the foot to initiate a step-up.
to the inner ear or vestibular branch of CN VIII, which
effectively gives unbalanced input to the intact central How to Interpret
vestibular system.26 In the absence of head motion, spon-
Conscious proprioception is the patient’s awareness of
taneous horizontal nystagmus is consistent with CN VIII
limb position and movement without visual information.
damage, with the fast component away from the side of
The sensory branch of proprioception is carried from
the lesion. Unilateral peripheral disease may cause a
the skin, muscle and joints of the leg, through the spinal
head tilt with circling toward the side of the lesion.
cord and brainstem to the sensory motor cortex where
the brain responds by sending messages back to the
POSTURAL REACTIONS lower motor neuron for motor function, resulting in a
The postural reactions are complex, requiring intact sen- rapid correcting foot placement.26 Ascending sensory
sory and motor pathways throughout the nervous sys- pathways are located in the outermost regions of the
tem, as well as unimpaired processing and integration in spinal cord and are very sensitive to compression.40,87
the brain.26 The complexity of the postural reactions With minor spinal cord injury, proprioceptive deficits
allows detection of minor deficits in any key component may be present because of disrupted sensory pathways,
of the pathway. Postural deficits are seen caudal to or at while motor function persists because the deeper motor
the level of the lesion.40 Additional testing must be per- tracts are unaffected. Both visual and tactile placing reac-
formed to use the postural deficit to help localize the tions require an intact motor cortex and intact motor
lesion within the pathway of the deficit. pathways to the involved limb. A cortical lesion may
Fig 17.6 | By moving the head from side to side, the move- Fig 17.7 | Bringing the bird to a perch will assess the ability to
ments of the eyes can be evaluated for physiological nystagmus. place the limbs properly; this is one method of assessing propri-
oception. The bird also can be visually restricted using hooding.
Table 17.2 | Clinical Signs Associated with Upper Motor

Neuron (UMN) and Lower Motor Neuron (LMN) Diseases
Clinical Function UMN Disease LMN Disease
Motor function Paresis or paralysis Paresis or paralysis
Muscle tone Normal to increased Often reduced
Spinal reflexes Normal to decreased Decreased to absent
Muscle mass Normal to decreased Dramatically decreased after
(disuse atrophy) 5-7 days (neurogenic atrophy)
Conscious Often reduced to Often reduced to absent
proprioception absent
produce deficits in the contralateral limb, whereas a

lower lesion produces deficits in the ipsilateral limb.
Fig 17.8 | The pedal withdrawal can be evaluated by applying
a pinching stimulus to the digits and watching for flexion and
SPINAL REFLEXES withdrawal of the joints and limb, respectively.
Completion of a reflex requires an intact sensory nerve

that provides transmission to the spinal cord and an How to Interpret
intact motor nerve that elicits function from the inner- This reflex reveals information regarding the pudendal
vated muscle. The reflex arc itself does not involve the plexus and caudal segments of the spinal cord. A flaccid,
brain or the remainder of the spinal cord. Lesions in the unresponsive vent and overdistended cloaca that is eas-
motor arm of the reflex arc, termed lower motor neuron ily expressed indicate LMN damage to the pudendal
(LMN), may cause a decreased or absent reflex (hypore- nerve or its spinal roots. A hypertonic, hyperresponsive
flexia or areflexia). An exaggerated response (hyper- vent indicates UMN damage at any point cranial to the
reflexia) results from an interruption in proximal motor pudendal plexus.
pathways that modulate the reflex, termed upper motor
neuron (UMN). Lower motor neuron signs indicate dam- The Pedal Flexor Reflex
age to one or more components of the reflex arc. Upper How to Perform
motor neuron signs indicate damage anywhere between Apply a pinch stimulus to the skin of each foot and eval-
the reflex arc and the brain (Table 17.2).39,62,87 uate the response of the ipsilateral and contralateral
limb (Fig 17.8).
The Vent Sphincter Reflex
How to Interpret
How to Perform This is a withdrawal reflex in which stimulation of sen-
Pinch or prick the vent and watch for a wink-like con- sory receptors in the feet elicits contraction of flexor
traction of the external sphincter muscles and a tail bob. muscle groups in the leg. Presence of a withdrawal
Fig 17.9 | With the limb allowed free movement, the patella Fig 17.10 | The wing withdrawal can be assessed by stretching
reflex can be performed by applying a stretch stimulus to the each wing out and applying gentle pinching stimulus, watching
patellar tendon. a complete flexion and withdrawal.
reflex requires an intact ischiatic nerve (sensory and How to Interpret

motor) and an intact spinal segment at the sacral plexus, This reflex tests the integrity of the reflex arc to the
but does not require transmission along the spinal cord brachial plexus spinal segment. Absence of the wing
to the brain. Absence of the withdrawal reflex in the leg withdrawal reflex in a wing indicates damage to the
denotes extensive lower motor neuron damage involv- brachial plexus or its nerves. A positive crossed extensor
ing the sacral plexus or the ischiatic nerve. A space- reflex of a wing denotes damage cranial to the brachial
occupying mass within the kidney or pelvic canal, such plexus within the cervical spinal cord or the brain stem.
as a renal tumor or an egg, may impinge upon the lum-
bosacral plexus and its nerve, causing a hyporeflexic or CUTANEOUS SENSATION AND PAIN
areflexic withdrawal in the legs.15
Cutaneous sensation testing provides information
regarding the location and severity of a spinal cord or
The Patellar Reflex
plexus lesion.26 Birds do not have a cutaneous trunci
How to Perform muscle, so a panniculus response cannot be used to
A tap stimulus should be applied to the straight patellar help localize a spinal cord lesion; however, the feather
tendon and the response of the limb should be evalu- follicles contain sensory nerve fibers.31
ated (Fig 17.9). Certain birds, such as ostriches,26 do not
have a patella; in these species, the homologous straight Evaluation of nociception (deep pain perception) is
quadriceps tendon is stimulated. Plexor size must be reserved for those animals showing evidence of spinal
adapted to patient size for improved accuracy. Because cord disease based on abnormalities in gait, propriocep-
of interference from the inguinal web, this reflex may be tion and spinal reflexes. Nociception requires cerebral
difficult to elicit in birds.26 perception of painful or injurious stimuli. It is important
to remember that a withdrawal reflex is not an indicator
How to Interpret of pain perception and may be elicited in an animal
This is a myotatic (stretch) reflex that effectively stretches whose spinal cord has been transected cranial to the seg-
the femorotibialis muscle.87 This stretch stimulates the ment responsible for that reflex arc.26,40 See Chapter 8,
femoral nerve (lumbosacral plexus), which generates Pain Management.
muscular contraction to extend the stifle. Upper motor
neuron lesions cause hyperreflexia and should be accom-
panied by weakness.26 Disease in the lumbosacral plexus
or peripheral muscle or nerve (LMN) causes hyporeflexia.
Ancillary
Neurological Tests
The Wing Withdrawal Reflex
How to Perform SURVEY RADIOGRAPHY AND
A pinch stimulus to the major digit at the leading edge MYELOGRAPHY
of the primary flight feathers generates flexion of the After a thorough clinical examination, selective or survey
wing in the normal bird (Fig 17.10). radiography may be indicated to evaluate body systems for
their contribution to clinical signs. As it is inexpensive and administration. Seizures, the predominant side effect
non-invasive, survey radiography may be one of the best noted in mammalian myelography, have not been
screening tools to uncover a cause for neurologic disease. observed in birds, even at higher doses than those rec-
ommended above. However, this does not rule out the
Sedation or general anesthesia facilitates exact position- possibility of this occurring with iohexol myelography in
ing to yield the best image of the desired area. Both lat- birds.51 There are some avian species in which myelogra-
eral and ventrodorsal projections should be obtained, phy may not be possible. In duck, goose and swan skele-
with the beam centered over the area of interest. The tons, the thoracic and lumbar vertebrae have overlap-
axial skeleton of the bird should be extended, and the ping plates of bone that would prevent positioning a
spine should be made parallel to the cassette, support- needle in the subarachnoid space. Potential thoracolum-
ing the bird’s body with foam wedges if required. The bar puncture sites do exist in psittacines and raptors,
most helpful spinal views include the following: cervical which are the most commonly seen patients in private
(lateral and ventrodorsal), thoracic (lateral), thoracolum- practice and rehabilitation centers.
bar (lateral and ventrodorsal), and lumbar (lateral and
ventrodorsal). A fine screen and high-detail filmsa should
be used for spinal studies in birds. CEREBROSPINAL ANALYSIS
Cerebrospinal fluid (CSF) may confirm pathologic
Myelography can be performed in birds with normal
changes, determine the general nature of the pathologic
patient recovery and adds another diagnostic procedure
process or reveal a specific cause of disease.25,64 CSF is
to the armamentarium of avian veterinarians. Myelogra-
most useful in characterizing infectious, neoplastic or
phy is used to identify, characterize and localize spinal
inflammatory disorders of the spinal cord or brain. Ideally,
cord lesions to the extramedullary or intramedullary
this procedure should be performed prior to myelogra-
compartments. Myelography is indicated if precise local-
phy, as contrast will affect the analysis of the fluid.
ization of a spinal cord lesion is required, such as when
surgical intervention is contemplated. A contrast medium In birds, the cerebellomedullary cistern is very small,
is injected into the subarachnoid space and lack of opaci- and a large venous plexus exists just ventral to it.62 There
fication around the spinal cord indicates displacement of is less than a 1 mm space dorsal to the cervical spinal
that cord segment, preventing contrast material flow and cord in which the tip of the needle could be placed. This
suggesting diffuse cord swelling or a space-occupying can result in blood-contaminated samples, lack of sam-
mass compressing the cord. ples and damage to the nervous tissue.51 The damage,
which can be focal and cause acute severe hemorrhage
The synsacrum of birds is composed of the fused lumbar
in the subarachnoid space, can result in postanesthetic
and sacral vertebrae and pelvis, and necessitates thora-
recovery problems including cardiac arrest and death.51
columbar rather than lumbar puncture of the subarach-
Presently, it is recommended to use a 27-gauge needle
noid space. Another structure unique to birds is the
glycogen body, which bisects the spinal cord in the lum- for this procedure.30
bosacral region ventral to the synsacrum and causes a
How to Perform
narrowing of the subarachnoid space in this region.51 It
The patient is placed in lateral recumbency with the mid-
appears that injection of contrast medium into the sub-
line of the neck parallel to the tabletop. The caudodorsal
arachnoid space in the cerebellomedullary cistern can-
skull region is aseptically prepared. The atlanto-occipital
not be consistently repeated and trauma to the spinal
joint is flexed at a 30° angle, and a 27-gauge hypodermic
cord near the brainstem can result in death.51
needle is placed at dorsal midline, slightly caudal to the
A technique for administering a myelographic contrast occipital protuberance, and is directed rostrally at a 45°
agent, iohexolb, in the thoracolumbar region has been angle to the horizontal axis of the head. The needle is
described.51 The region for injection is found by placing advanced through the skin slowly at 1-mm intervals until
the thumb and middle finger on the bony prominences a slight change in resistance is felt. Practically, this is not
of the ileal crests, with the index finger used to palpate always easily recognized. However, the advantage of
to the first indentation cranial to the synsacrum. The using a hypodermic needle with a translucent hub, rather
quantity of the contrast medium needed to produce a than a spinal needle with a stilette, is that an immediate
diagnostic myelogram is 0.88 ml/kg, 4 times the 0.22 “flash” of fluid will appear in the hub of the needle once
ml/kg used in mammals in most institutions.51 The use of the dura has been penetrated. This limits the risk of
a 27-gauge needle for this procedure is currently recom- advancing the needle into parenchyma. In general, 0.1 to
mended,51 and the administration of approximately 0.5 0.5 ml of fluid may be collected. In small mammals,
ml/minute has been described as safe.51 Radiographs 1 ml of CSF per 5 kg body weight may be removed safely,
should be made within 10 minutes of the contrast although this has not been confirmed in birds.25
Fig 17.11 | A barred owl (Strix varia) under general anesthesia Fig 17.12 | A concentric needle is inserted into each muscle for
for an electromyographic examination. evaluation of the presence of a spontaneous electrical activity.
How to Interpret tion of the neuromuscular system is used as an aid in

The small sample volume usually obtained precludes the diagnosis of disease, to assess the progress or regres-
extensive biochemical analysis, bacterial or fungal culture, sion of the disease, and to assess the degree of recov-
and antibody titer evaluation. Color and clarity of the CSF ery.65,110 Skeletal and smooth muscle as well as the
should be evaluated immediately. Gross visual examina- myoneural junction can be examined. Concentric needle
tion of normal CSF reveals a clear and colorless fluid. electrodes are used to determine the spontaneous or
Blood contamination may be iatrogenic or due to a patho- evoked responses. They are usually 27-gauge, subcuta-
logic process.26 Turbidity indicates leukocytosis, high pro- neous or longer, insulated needles with bare tips, which
tein content or both. If the sample volume is sufficient, can be inserted into the muscle. A ground electrode
protein content may be evaluated in addition to cytologi- must always be used. The patient usually has to be anes-
cal examination. High protein concentration indicates thetized for these procedures (Fig 17.11).
breakdown of the blood-brain barrier or intrathecal pro-
tein synthesis. Preparation of the CSF sample by cytospin Electromyography
centrifugation is recommended because of the small vol-
Electromyography (EMG) is the study of the electrical
ume and low cellularity of fluid generally recovered.26 If a
activity of muscle by insertion of a recording electrode
cytocentrifuge is unavailable, the cells may be concen-
into the muscle (Fig 17.12). It examines the integrity of
trated onto a slide by sedimentation.25 The cell concentra-
the motor unit, which consists of the lower motor neu-
tion, population and morphology are evaluated. Relative
ron and the muscle fibers that it innervates. Normal rest-
erythrocyte and leukocyte numbers and protein concen-
ing muscle does not show observable electrical activity
tration should be compared with those found in the
once the electrode placement is stabilized and no audi-
peripheral blood. Reference values for leukocyte numbers
ble signal is created.110 Contraindications for electromyo-
and protein concentration in CSF have not been estab-
graphy include bleeding tendencies and unusual suscep-
lished in birds. Subjective comparison of CSF values with
tibility to recurrent systemic infections.61 Electrical activ-
those of peripheral blood and consideration of parame-
ity demonstrated can be separated into three categories:
ters used in domestic animals may aid interpretation.
insertional (associated with electrode movement), spon-
Meningitis caused by infectious agents generally induces taneous (associated with resting muscle) and evoked
a moderate increase in cell numbers and an increase in (associated with electrical stimulation of nerves).61
protein concentration compared with peripheral blood.3,26
Insertional
Non-inflammatory conditions caused by degenerative
disease or trauma cause a high protein concentration A brief burst of electrical activity accompanies needle
and a minimally increased cell count.25,26 insertion into a normally innervated muscle. This collec-
tion of monophasic and polyphasic potentials of variable
amplitude and duration ends after the needle has
ELECTRODIAGNOSTICS stopped its movement. A prolonged discharge of these
The use of electrophysiological diagnostic techniques potentials is sometimes subjectively considered as
has become a cornerstone in the investigation of neuro- abnormal, as it represents cellular hyperirritability.
muscular disease in animals. Electrodiagnostic evalua- Insertional potentials become more noticeable on the
birds. Fibrillation potentials and occasional complex

repetitive discharges were seen in the wing muscles of
two red-tailed hawks with traumatic brachial plexus
injury. Motor unit action potentials observed in these
same birds suggested that intact nerve fibers were pres-
ent.108 Fibrillation potentials and positive sharp waves
were detected diffusely in limb musculature of a turkey
vulture with a peripheral neuropathy associated with
lead toxicosis.92 Spontaneous EMG also has been used to
determine prognosis and to direct treatment in seven
wild birds with traumatic injuries involving peripheral
nerves and musculoskeletal disease.27 Widespread fibril-
lation potentials and lack of typical interference patterns
Fig 17.13 | Fibrillation potentials and positive sharp waves suggested denervation in three of these seven birds that
from a denervated muscle 5 days after brachial trauma.
had muscle atrophy and wing paralysis or paresis.
fourth or fifth day after denervation and peak in inten- Evoked

sity 8 to 10 days after denervation.26 These may be The M wave is an evoked potential resulting from the
decreased or absent in atrophied muscle.110 summation of motor unit potentials. The latency of
response represents the time taken for impulse conduc-
Spontaneous tion from the point of stimulus to the nerve terminal,
Normally, muscles are said to be “electrically silent.” Five including a neuromuscular delay of about 0.5 msec, and
to seven days after denervation in the dog, needle elec- the time taken for conduction from the end-plate region
tromyography can demonstrate spontaneous, randomly to the exploring electrode. The latency can be consid-
occurring potentials.26 These are the action potentials of ered an adequate substitute for the nerve conduction
several muscle fibers due to instability in the membrane velocity.26 The amplitude of the evoked potential is deter-
potential and are termed fibrillation potentials. The time mined by the number of muscle fibers activated by nerve
of onset of these potentials in birds has been poorly stimulation. In a severed motor nerve, conduction stops
documented, but may be earlier than seen in the dog. abruptly after about 5 to 8 days.26
Fibrillation potentials can be monophasic, biphasic and,
rarely, triphasic in wave form with a usual amplitude of Nerve Conduction Studies
20 to 300 µV and a duration of 0.5 to 5 msec (Fig 17.13), Nerve conduction studies have become a simple and reli-
both of which decrease with cicatrization.110 The pres- able test of peripheral nerve function.61 The conduction
ence of reproducible discharges in at least two different velocity is measured between the two stimulus points
areas of muscle usually suggests lower motor neuron on the nerve, thereby eliminating the time for neuro-
disease. These include diseases of the ventral horn cells, muscular transmission and generation of muscle action
radiculopathies, plexopathies, myositis, and axonal potential. It is derived as the ratio between the distance
mono- or polyneuropathies.61 Positive sharp waves with between two stimulation cathodes and the correspon-
a sawtooth appearance also are abnormal spontaneous ding latency difference.61 The proximal stimulation site is
potentials that are detected in motor unit disorders, and a point just caudal to the greater trochanter of the femur,
it has been suggested that they may precede fibrillation and the distal site is just caudal to the distal portion of
potentials by one or more days.110 Complex repetitive the tibia (Fig 17.14). At each site, the cathode is placed
discharges range from 50 µV to 1 mV in amplitude and distal to the anode. The indifferent electrode is placed
up to 50 to 100 msec in duration, representing a group subcutaneously over the midtarsometatarsus region. The
of muscle fibers firing in near synchrony.61 These dis- active electrode is placed subcutaneously on the caudal
charges typically begin suddenly and maintain a constant portion of the hypotarsus just distal to the tarsometa-
firing rate, ceasing abruptly and sounding like a machine tarsal joint overlying the digital abductor muscles.10
gun.61 These complex repetitive discharges appear as a Similar electrode configurations are needed for evalua-
“train” of identical discharges. These discharges may tion of the wing nerves (Fig 17.15). The ground electrode
occur in a variety of myopathic conditions. Needle elec- is placed subcutaneously between the distal stimulation
tromyography has been used in the cat, a species sus- site and the recording site. This technique has been
ceptible to organophosphorus-induced delayed neuro- described in detail for two avian orders.27
pathy like the bird, to monitor progression and improve-
ment.1 This could not be repeated, though, in chickens.107 Axonal damage or dysfunction will usually result in loss
Denervation is detectable on needle electromyography in of amplitude, whereas demyelination leads to prolonga-
Fig 17.14 | Needle setup for evaluation of a tibial nerve con- Fig 17.15 | Needle setup for evaluation of an ulnar nerve con-
duction velocity in a barred owl. duction velocity in a rhea.
Fig 17.16 | A reduced nerve conduction velocity is demon- Fig 17.17 | An F wave (arrow) is demonstrated
strated after stimulation of the proximal portions (top trace) of after the M wave and the stimulation artifact.
the tibial nerve and the distal portions (lower trace). The wave-
forms (M wave) demonstrated here are typical.
tion of conduction time (Fig 17.16).61 Reference ranges cially in polyneuropathies where delay of the F wave can
for the motor nerve conduction velocities of the ulnar markedly exceed the normal range. It occurs after the M
nerve and the tibial nerve in neurologically normal barred response, its initiating electrical stimulation having trav-
owls and rheas have been established.27 Based upon eled toward the spinal cord before it returns to activate
these ranges, a turkey vulture with lead toxicosis was distal muscles (Fig 17.17). Studies of the F wave can help
shown to have decreased sciatic-tibial nerve conduction in the characterization of polyneuropathies and, more
velocity compatible with a demyelinating neuropathy.92 specifically, with those that are prominently proximal,
Peripheral nerve histopathology confirmed this finding. such as radiculopathies.61 Such studies have been
attempted in normal birds, but as yet a reference range
Effect of Temperature
has not been established for clinical application.27
A linear relation normally exists between motor nerve
conduction velocity and temperature of the peripheral
Repetitive Stimulation
nerve segment within physiological limits.67
Repeated supramaximal stimulation should create repeat-
Effects of Age able, identical action potentials in the normal patient.
Immature animals have slower motor nerve conduction Any evident incremental or decremental response may
velocity than do adults.26 have physiological significance. Any defect in the neuro-
muscular transmission will usually produce a maximal
The F Wave drop in amplitude between the first and second
Measurement of the F wave can help in the assessing of responses of a train, followed by further decline up to
motor conduction along the most proximal segment of the fourth or fifth potential.61 Examples of these disor-
the nerve. This is because it results from the backfiring of ders would be myasthenia gravis in humans and com-
antidromically activated ventral horn cells. It can supple- panion animals and botulism in all species. Repetitive
ment the conventional nerve conduction studies, espe- stimulation has been performed in normal birds to
establish reference ranges for clinical application.27 The several lesions not identified on survey radiographs,
techniques were easily performed and demonstrated including fractures and early osteomyelitis, were identi-
22% alteration in potential amplitude.27 fied by bone scanning. These pathologic lesions were
confirmed by the results of necropsy. Basilic vein admin-
MUSCLE BIOPSY istration of the radionuclide was found to be superior to
medial metatarsal vein administration. This is possibly
Muscle biopsy is indicated to confirm, define and possi-
because the renal portal system provided high uptake of
bly provide a cause for motor unit disease.19,88 Biopsy
radionuclide by the liver and kidney and obscured visu-
techniques are well established in several mammalian
alization of the spine after medial metatarsal vein
species, but are not known for avian patients. The mus-
administration.75
cle selected for biopsy should be one that is clinically
affected with the disease process. In acute disease, a
severely affected muscle is selected. With chronic dis- COMPUTED TOMOGRAPHY
ease, a muscle demonstrating only moderate changes is Computed tomography imaging requires general anes-
the best choice. The muscle should be easily accessible thesia, uses ionizing radiation and is somewhat costly to
and identifiable so that minimal postoperative discom- perform. The CT scan uses x-rays and computer technol-
fort is created. Ideally, the muscle chosen for biopsy ogy to create cross-sectional images of the patient.54,68
would be one for which normal fiber type, distribution Regions of the vertebral column and the skull are evalu-
and size are known. This is not available for most avian ated for abnormalities in CNS soft tissue or its protective
patients. Studies of muscle fiber types have been done skeleton. Computed tomography provides superior soft
in chickens.16 tissue imaging with no superimposition of structures
compared with conventional radiography.77,86 With con-
SCINTIGRAPHY trast administration, soft tissue structures are better visu-
alized, especially where there is increased blood flow.86,99
Nuclear imaging or scintigraphy is a non-invasive method
for evaluation of soft tissue and osseous structures asso- The greatest value of CT lies in its ability to reveal
ciated with the nervous system.112 The technique involves changes in bony tissues and to provide greater detail of
intravenous administration of a small amount of a osseous structures than conventional radiography. Slices
gamma-emitting radionuclide alone or tagged to some are most commonly created every 2 to 3 mm in birds.86
other compound that will allow it to accumulate in cer- Although these slices may seem very close together, focal
tain tissues and exclude it from other tissues. A gamma lesions may still be missed. Decreasing slice thickness to
camera is used to record the amount of radiation emit- 2 mm decreases image quality, but may increase sensitiv-
ted from the body and to create images of the distribu- ity for small lesions. Images also can be reformatted by
tion of the radionuclide throughout the patient’s body. the computer to provide images in configurations other
Technetium-99m (99mTC) is used most often, as it has a than a transverse plane.
short half-life (approximately 6 hours) and emits pure
gamma radiation. Because the level of radiation is Computed tomography has been used to document topo-
extremely low, its use carries minimal risk for the patient graphic anatomy of the golden eagle and African grey par-
and personnel involved with the procedure. Nuclear rot,77,86 and it also has been used to specifically demon-
scans do not provide detailed anatomic imaging, but do strate brain and skull anatomy of the crested breed of the
have the potential to provide functional information domestic duck (Anas platyrhynchos).12 Computed tomog-
when used with a digital image processor. raphy has been used with some success to locate intracra-
nial lesions in birds, although it was only 80%
Scintigraphic imaging of the brain has been done in sensitive.58,99 A postmortem CT scan was used to identify
human medicine since 1960.26 In recent years, cranial spinal cord compression in a juvenile penguin (Apteno-
scintigraphic imaging has been replaced by computed dytes patagonicus) that was euthanized because of an
tomography (CT) and magnetic resonance imaging inability to stand despite 6 weeks of medical therapy;38
(MRI), but is still useful where these modalities are con- radiographs at presentation had failed to identify any
sidered too expensive or are not available. Bone scan- spinal abnormalities. Results of necropsy confirmed inter-
ning is particularly useful in identifying spinal abnormal- vertebral disc rupture and vertebral body displacement.
ities in birds.26 Superimposition of osseous structures
(ribs, synsacrum) in survey radiographs makes identifica-
tion of spinal fractures and early vertebral osteomyelitis MAGNETIC RESONANCE IMAGING
difficult. In a study of 12 birds with thoracic or pelvic Magnetic resonance imaging (MRI) uses a pulsating
limb paresis, bone scanning identified 100% of the external magnetic field and produces radiofrequency sig-
lesions identified on survey radiographs.75 In addition, nals that are used to generate images.26,112 Soft tissue con-
trast of the CNS is excellent with MRI, which also pro- (myelencephalon) and the cerebellum. The midbrain,
vides the spatial orientation of anatomic structures.26,112 pons and medulla make up the brainstem and are asso-
This modality also will help to differentiate central nerv- ciated with the majority of the cranial nerves. Disease
ous system gray and white matter. affecting the intracranial CNS may be focal or diffuse. If
it is focal, specific deficits may be identified relating to
The advantages of MRI compared with CT include the abil- dysfunction of the area affected. The various syndromes
ity to image the cranial brainstem, without artifact, in the and specific signs are described in Table 17.3.
caudal fossa of the skull, the increase in soft tissue detail,
the creation of images in various planes and the lack of
Seizures
ionizing radiation.98 However, MRI does not allow a satis-
factory depiction of aerated bones in some avian skulls.12 Definitions and Classifications
One main disadvantage of MRI besides the expense, as A seizure is a sudden, uncontrolled, transient alteration
with CT, is the requirement for general anesthesia, as in behavior characterized by a change in motor activity,
chemical sedation is not adequate to obtain satisfactory consciousness, sensation or autonomic function.28 It is
images. It also is necessary to obtain screening radiographs due to a synchronizing abnormal paroxysmal electrical
of birds before performing MRI evaluations to rule out the discharge from the brain. A generalized seizure is mani-
presence of metallic foreign bodies.98 Avian patients will fested by symmetrical and synchronous clinical signs,
frequently chew on their cages, etc, and small metal frag- which are classically tonic-clonic motions often accom-
ments may contaminate commercial feed. Ferrous metal panied by complete loss of consciousness.28 A focal
demonstrates susceptibility to the magnetic field and can
move within the body.98 Table 17.3 | Intracranial Lesion Localization and
Clinical Signs93
In a study of normal MRI brain anatomy of pigeons, Clinical Characteristics of Specific Clinical Signs
imaging required approximately 20 minutes, and trans- Syndrome/ the Location
Lesion
verse images were created every 3 mm.98 A 1.5 Tesla mag- Localization
net and a human knee surface coil were used. Lesions Cerebrum Damage to cere- i. Altered mental state
brum affects intellec- ii. Seizures
may be missed because of this distance between slices. tual, learned and iii. Behavioral change
This imaging technique also was used in a clinical case in sensory activities iv. Pleurothotonus and adversion
(vision, hearing, v. Head pressing
an attempt to identify the cause of seizure activity in a touch, pain) vi. Central blindness
mealy Amazon parrot (Amazona farinosa).98 Without Diencephalon Damage affects i. Altered mental state
contrast enhancement the lesions were not visualized; autonomic visceral ii. Seizures
functions and iii. Behavioral change
however, after the use of contrast material (gadopentate endocrine regulation iv. Endocrine disturbances
v. Abnormalities of temperature
dimegluminec 0.25 mmol/kg IV) perivascular infiltrates
Midbrain Damage affects con- i. Altered mental state
were identified, showing disruption of the blood-brain trol of alert status, as ii. Opisthotonus
barrier. Because the contrast is eliminated through the well as CN III and iii. Contralateral paresis
CN IV function iv. Ipsilateral CN III dysfunction
kidneys, postcontrast uric acid levels have been com- (mydriasis/ventrolateral
strabismus)
pared to precontrast levels to monitor for potential renal v. Contralateral CN IV dysfunc-
toxicity in birds; however, no significant changes have tion (dorsomedial strabismus)
been found.98 Further, after contrast medium-enhanced Pons and Damage affects mul- i. Altered mental state
Medulla tiple cranial nerves ii. Ipsilateral paresis
MRI studies in birds, recovery has been uneventful and (V-XII) as well as iii. Irregular respiration
cardiorespiratory iv. Ipsilateral CN V dysfunction
the birds have had normal excreta, appetites and atti- centers (decreased beak strength,
tudes.98 Magnetic resonance imaging also has been used decreased palpebral reflex,
decreased facial sensation)
to evaluate the cranium of domestic ducks.13 MRI images v. Ipsilateral CN VI dysfunction
(third eyelid protrusion and
were recorded using a relatively large slice thickness of 5 medial strabismus)
mm, which can lead to difficulty in interpreting scans of vi. Ipsilateral CN VII dysfunction
(decreased tone in facial
small volumes. musculature, decreased taste,
decreased lacrimation)
vii. Ipsilateral CN VIII damage
(ipsilateral deafness, vestibu-
lar dysfunction)
Intracranial Disease viii. Ipsilateral CN IX-XII damage
(dysphagia, regurgitation,
tongue deviation, inspiratory
dyspnea)
CLINICAL SIGNS Cerebellum Damage affects i. Normal mental status and
coordinating and behavior
Intracranial CNS structures include the forebrain (telen- reinforcing actions ii. Normal strength
iii. Opisthotonus
cephalon), thalamus (diencephalon), midbrain (mesen- iv. Dysmetric ataxia
cephalon), pons (metencephalon), medulla oblongata v. Head (intention) tremors
seizure is manifested initially by focal signs that may sec-

ondarily become generalized.
Treatment
1. Address the underlying cause.
2. Control seizure activity with diazepam (0.5-1.0 mg/kg
IV or IO).28 This can be repeated two to three times
if necessary.
3. If diazepam does not stop the activity, administer
phenobarbital (1-2 mg/kg IV/IO or IM q 6-12 h
to effect).28
Greg J. Harrison
4. Gaseous anesthesia may be warranted in seizuring
birds to allow diagnostic sampling and investigation.
5. Convert to oral phenobarbital maintenance therapy
within 48 hours (1-10 mg/kg PO q 12 h is standard
Fig 17.18 | A lovebird (Agapornis roseicol-
therapy).28 lis) demonstrates a right-sided head tilt
6. Primidone may be an alternative anticonvulsant, caused by an ipsilateral loss of muscle tone
although its active compound is phenobarbital. due to peripheral vestibular disease.
Primidone use (125 mg/day in water source) has
been reported in an Amazon parrot.52 appear worse with movement such as eating or drinking.
7. Adjust to lowest dosage required to control These are called intention tremors and are the cardinal
seizure activity. sign of cerebellar disease of any underlying etiology.
Generalized body tremors that occur mainly at rest
Head Tilt and Nystagmus could result from a multifocal or diffuse lesion localiza-
Definitions and Classifications tion. This may be a disease affecting the meninges, nerve
A head tilt is due to asymmetrical disease of the vestibu- roots, peripheral nerves or muscles. Systemic diseases
lar system (Fig 17.18). The vestibular system comprises including electrolyte imbalances, liver and renal disease,
the peripheral component, which is the vestibular por- and hypoglycemia can cause generalized tremors as can
tion of CN VIII arising in the inner ear from the semicir- primary neurologic diseases.
cular canals and the central component, which is the
nuclei of CN VIII in the medulla.28 A further central com- Treatment
ponent of this system is the flocculonodular lobe of the 1. Address the underlying cause.
cerebellum. Head tilts are usually toward the side of the 2. Attempt treatment with oral anticonvulsant therapy
disease with peripheral vestibular dysfunction, but as above.
toward any side with central dysfunction. Nystagmus that 3. Attempt treatment with anti-inflammatory doses of
is pathological is described as jerky eye movements with glucocorticoids.
two obvious phases; slow and fast. The predominant 4. Provide supportive care to maintain nutritional and
direction of the eye movements, seen at rest, can be hori- fluid demands.
zontal, rotational or vertical. Nystagmus also can be posi-
tional, which means that it is induced by a change in Depression/Stupor/Coma
position of the head. With horizontal nystagmus, the fast Definitions and Classifications
phase is usually away from the side of the lesion. Vertical Depression represents a reduced mental state, although
and positional nystagmus can indicate that the lesion is one which responds to external stimuli. Depression does
central rather than peripheral. All other directions can not necessarily indicate primary neurologic disease.
occur with both peripheral or central lesion localizations. Stupor is a state of unconsciousness from which the bird
can be roused by stimulation with a noxious stimulus
Treatment
(Fig 17.19). Coma is a state of unconsciousness from
1. Address the underlying cause and tailor therapy to the
which the bird cannot be roused by noxious stimuli.
specific etiology.
2. Provide supportive care to maintain nutritional and Treatment
fluid demands. 1. Address the underlying cause.
2. Provide supportive care to maintain nutritional and
Tremors and Involuntary Movements fluid demands.
Definitions and Classifications 3. Address ventilatory needs.
Head and or body tremors may occur with activity and 4. Address excretion needs and keep clean.
Greg J. Harrison
Greg J. Harrison
Fig 17.20 | A gross pathological specimen
from an African grey parrot (Psittacus erithacus)
with cerebral disease due to hydrocephalus.
Fig 17.19 | A painted bunting (Passerina ciris) with profound
stupor due to pesticide toxicosis.
DIFFERENTIAL DIAGNOSIS OF Table 17.4 | Differential Diagnosis of Intracranial Disease

I N T R A C R A N I A L D I S E A S E (Table 17.4) Mechanism Specific Diseases
of Disease
Degenerative Degenerative i. Lysosomal storage disease -
Gangliosidosis/Neurolipofuscinosis
Lysosomal Storage Disease ii. Avian vacuolar myelinopathy
Gangliosidosis18,60 Anomalous i. Hydrocephalus
Metabolic i. Hepatic encephalopathy
Neurolipofuscinosis53 ii. Hypoglycemia
iii. Hypocalcemia
Avian Vacuolar Myelinopathy71 Neoplastic i. Glial tumors/Ependymoma/Choroid plexus
papillomas/Adenomas/Adenocarcinomas/
This disease more commonly causes spinal and neuro- Lymphosarcoma/Lipomas
muscular signs, but intracranial signs have been reported. Nutritional i. Pyridoxine deficiency
ii. Vitamin E deficiency
Anomalous Inflammatory i. Viral encephalitis - Proventricular dilatation
disease/Avian paramyxovirus type 1 (Newcastle
Hydrocephalus 100
disease)/Polyomavirus/WEE and EEE/West Nile
virus/Avian influenza virus/Herpes (duck viral
enteritis)
Dilated ventricles can be a congenital lesion as well as a ii. Bacterial encephalitis - Salmonella/Pasteurella/
postinflammatory consequence (Fig 17.20). Streptococcus/Enterococcus/Chlamydophila/Listeria
iii. Verminous encephalitis - Chandlerella/
Baylisascaris/(fluke/Schistosomiasis)
iv. Trichomonas/Protozoal encephalitis -
Metabolic Toxoplasmosis/Leucocytozoonosis/Sarcocystis
v. Fungal encephalitis - Mucormycosis
Hepatic Encephalopathy15,29 vi. Prion - Spongiform encephalopathy
Clinical signs included depression, ataxia and blindness. Idiopathic i. Idiopathic epilepsy
Toxicity i. Lead
Hypoglycemia15 ii. Zinc
Seizure activity may occur when the glucose levels drop iii. Organophosphates and carbamates
Trauma i. Head trauma
below 100 mg/dl.
Vascular i. Atherosclerosis
Hypocalcemia
Serum calcium levels below 6.0 mg/dl with concentra-
indicating a possible sex predisposition, as there were
tions as low as 2.4 mg/dl have been reported to cause
equal numbers of males and females in the study.
opisthotonus (Fig 17.21), tonic extension of the limbs
Typically, neoplasia is a necropsy diagnosis, but it may
and convulsions.15
be found antemortem with a CT or MRI scan. Glial cell
tumors, choroid plexus papillomas, adenomas, adeno-
Neoplasia100,113
carcinomas and lymphosarcomas have all been reported
In a retrospective study of 996 budgerigars (Melopsit- as individual primary brain tumors.15
tacus undulatus), 14 (1%) intracranial tumors were
detected.113 Tumors of the ependyma (6), choroid plexus Intracranial Lipomas
(1), adenohypophysis (6) and one unclassified tumor Four birds in a flock of 125 purebred crested ducks
were found. In this study 87% of the birds were male, (Anas platyrhynchos) had cerebellar signs of unknown
Greg J. Harrison
Jan Hooimeijer
Fig 17.21 | A young cockatiel Fig 17.22 | A pigeon (Columba livia)
(Nymphicus hollandicus) demonstrates with paramyxovirus infection of the
the marked dorsiflexion of the neck central nervous system demonstrates
seen with opisthotonus. profound torticollis of the neck.
etiology.14 Gross necropsy of the euthanized ducks psittacine species.72 Viral inclusions have been found in
revealed yellow intracranial masses in the brain of each. brain tissue, however, reports of virus-induced neuro-
Histologically, these masses were intracranial lipomas logic disease are rare.72 Tremors of the head, neck and
consisting of fatty tissue separated into lobules by con- limbs, incoordination and ataxia have been described in
nective tissue. These lipomas were similar to those nestling budgerigars with APV infection. Approximately
recorded in other animals and humans.14 10% of susceptible neonates exhibited neurologic signs.72
In addition, an adult Moluccan cockatoo (Cacatua
Nutritional moluccensis) with APV infection exhibited inability to
Pyridoxine (Vitamin B6) Deficiency15 perch properly and had a slight torticollis that pro-
gressed to a semicomatose state.72 Neurologic deteriora-
Vitamin E Deficiency tion was observed over a 2-day period following a 1-week
(Nutritional Encephalomalacia)6 history of illness. Body tremors and unsteadiness on the
The recommended dietary level of vitamin E for domes- perch were signs documented in a Ducorps’s cockatoo
tic poultry is 10 to 25 IU/kg feed dry matter (DM), but (Cacatua ducorps) with concurrent APV and psittacine
this is not known for many other birds. Clinical signs are beak and feather disease virus (PBFDV).72 PBFDV (circo-
commonly seen in young chicks (2-6 weeks old) and virus) infection is often associated with clinical evidence
include ataxia, head retraction and “cycling” with legs.6 of acquired immunodeficiency, leading to a variety of sec-
This has become known as crazy chick disease.66 Gross ondary or opportunistic infections.72
and histological lesions of encephalomalacia are prima-
rily found in the cerebellum, with evidence of ischemic Proventricular Dilation Disease (PDD) is a progres-
necrosis of the cerebellar cortex and white matter, capil- sive, variably contagious and often fatal disease of
lary thrombi, hemorrhages and malacia. psittacine birds, which is presumed to be caused by an
unidentified neurotropic virus.17 The disease was first
Inflammatory recognized in macaws in the late 1970s in the USA and
Viral Encephalitis is now known to have a worldwide distribution affecting
Avian Paramyxovirus Type 1 (Newcastle Disease) more than 50 species of psittacine birds.17 Neurologic
causes a non-suppurative encephalomyelitis and has clinical signs include ataxia, tremors and seizures.
been reported to cause head shaking, head tremors, Definitive diagnosis in live and dead birds is based on
head tilt, circling and torticollis (Fig 17.22).8,69 Infection demonstration of characteristic lymphoplasmacytic
is usually reported in juvenile wild birds, racing pigeons infiltrates within autonomic nerves and ganglia at vari-
and domestic poultry.57,69 The virus will commonly cause ous levels of the digestive tract.17,48
motor dysfunction and so is discussed below.
Equine Encephalitis - Viral infections have been
Avian Polyomavirus (APV), also known as budgerigar reported in commercial, domestic, and free-living flocks
fledgling disease, is a member of the family Papovaviri- of passerines and Columbiformes for several decades.96
dae.72 Polyomavirus infection in psittacine birds may be Most infections are attributed to eastern equine
subclinical or may present as a fatal, acute, multisystemic encephalitis (EEE), but several outbreaks of western
disease.72 Although observed more frequently in budgeri- equine encephalitis (WEE) have been documented.96
gars (Melopsittacus undulatus), APV infection may result Many types of birds are natural hosts of EEE and WEE
in death of both juvenile and adult non-budgerigar viruses.96 The diseases are caused by an alpha virus in
the arbovirus group/family, and are transmitted through mission of the virus from mosquitoes.
the bites of mosquitoes.
Bacterial Encephalitis
Specific signs of WEE and EEE have been vague. In 1991, Listeria monocytogenes causes intracranial infections
the first confirmed outbreak of EEE was reported in of birds resulting in opisthotonus, ataxia, and torticollis.15
ratites, specifically emus (Dromiceius novaehollandiae)
in southeastern Louisiana.96 This outbreak coincided Chlamydophila psittaci will occasionally cause neuro-
with unseasonably heavy rainfall, an abundance of logic signs in birds following acute respiratory or gas-
arthropod vectors and close proximity to reservoir host trointestinal disease.15
species.96 Affected emus exhibit variable signs, becoming
Abscesses, granulomas, encephalitis and meningitis has
very drowsy and depressed, reluctant to stand up, trem-
been reported to be due to Salmonella typhimurium,53
bling, often remaining sitting, and developing an S-
Pasteurella multocida (fowl cholera),50 Lancefield group
shaped cervical curvature. Aroused sick birds are ataxic
D Streptococcus sp.,24,47 and Enterococcus sp. (neonatal
with leg weakness.96 Both infections can progress to
multifocal encephalomalacia with sepsis).24,44
cause paralysis and death.114
Verminous Encephalitis
Diagnosis is confirmed by isolation of the virus from the Chandlerella quiscali is a filariid nematode of grackles
brains of birds that die. Serum antibody titers for EEE, that has been reported to cause cerebrospinal nematodi-
WEE and Venezuelan equine encephalitis exposure can asis in emus.15 Clinical signs in the young include torti-
be evaluated by hemagglutination inhibition.96 Recently, collis, ataxia, recumbency and death.
an immunohistochemistry technique for confirmatory
diagnosis of EEE infection in birds has been developed.121 Baylisascaris procyonis - The common raccoon
Treatment has been supportive, consisting of oral elec- ascarid is known to cause life-threatening visceral,
trolytes and broad-spectrum antibiotics.96 Protection of cerebral and ocular larva migrans in birds in North
commercial emu flocks may be attempted by a routine America.23,32 Infected asymptomatic raccoons can harbor
vaccination schedule for both EEE and WEE. Vaccine effi- a large number of worms and shed large numbers of
cacy recently has been proven in emus, and it currently infective eggs into the environment.23 Affected birds can
is the only protective action that exists, other than mos- develop ataxia and dysmetria that progresses to inability
quito control.96,114 to stand, with severe torticollis and a head tilt.23
West Nile Virus (WNV) emerged in the northeastern Trichomonas gallinae causes disease in the domestic
USA in the summer of 1999 causing death to thousands pigeon and birds that feed on pigeons such as eagles,
of wild and zoo birds.41,106 Previously this infection has falcons and hawks; it has been responsible for avian
been reported around the Mediterranean basin.81 It is a enteric trichomoniasis.89 Caseous masses in the roof of
mosquito-borne flavivirus that is endemic in Africa and the mouth may extend to involve the brain.
Asia, occurring sporadically in temperate regions of
Europe.106 It has been shown to cause a diffuse Schistosomiasis causing granulomatous encephalitis
encephalitis and has been recovered from the brains of has been reported in swans.15
birds in winter, long after the mosquito vectors ceased
Protozoal Encephalitis
to be active, suggesting a prey-to-predator mode of
Toxoplasma gondii, a cyst-forming coccidium, is not
transmission.41 Live and inactivated vaccines for protec-
frequently identified as pathogenic in captive birds.
tion against WNV recently have been evaluated in young
Asymptomatic infection with this parasite is reportedly
domestic geese with initial promising results.78
common.74 Outbreaks of toxoplasmosis have been
reported worldwide in chickens, and in passerine and
Avian Influenza Virus has been reported to cause 75 to
psittacine birds and birds exhibited in zoos.74,122 Naturally
100% mortality in birds within 10 days of infection.91
occurring infections have been diagnosed in chickens,
Depression and neurologic dysfunction were common
ducks and many wild birds.122 Because toxoplasmosis is a
clinical manifestations of the disease.91 These signs
zoonotic disease, the source of the infection should be
include attenuated motor functions, such as paresis to
determined, if possible, to prevent infection of humans.
paralysis, vestibular dysfunction as indicated by torticol-
Household cats should be tested. Common clinical signs
lis and nystagmus, and general behavior aberrations.91
of T. gondii infection in avian species include anorexia,
Herpes (Duck Viral Enteritis) causes photophobia, blindness, head tilt, circling and ataxia.74,122 Canaries
ataxia, seizures and penile prolapse.15 (Serinus canaria) may be susceptible to a form of toxo-
plasmosis of the central nervous system and eyes that
Bunyavirus109 rarely causes clinical disease after trans- differs from the acute form seen in other species.74
Partridges (Perdix perdix) have been reported to be tory of seizures.100 In chickens, epilepsy has been found
more susceptible to toxoplasmosis than other gallina- to have genetic basis.100 Idiopathic epilepsy also may be
ceous birds.104 acquired as a result of a cerebral insult and residual
brain damage.100
Serological antibody titers have been reported (latex
agglutination test) for infected birds, but have not been
Toxicity
helpful. A single titer can rarely specifically diagnose the
disease when the birds have been previously exposed.42 Lead100/Zinc73
Treatment of suspected cases and all in-contact birds Caged birds that eat their cage wire can become intoxi-
with trimethoprim 0.08 g/ml H2O and sulfadiazine 0.04 cated if the wire is high in zinc content. A new wire
g/ml in water for 3 weeks has been advised, but eradica- fence syndrome has been reported in emus.11 The birds
tion from a captive flock may be difficult.122 gnaw away at their cage made of zinc material and even-
tually ingest so much that toxicity occurs. Some galva-
Trichomonas gallinae89
nized coatings contain as much as 99.9% zinc, but galva-
Leucocytozoonosis95 nized wire also may contain lead. The white rust associ-
ated with galvanized wire also is toxic.11 Waterfowl may
Sarcocystis spp. have been reported to cause toxo- be exposed to elevated zinc concentrations through
plasma-like infections of birds with a non-suppurative ingestion of contaminated vegetation and sediments due
meningoencephalitis.49 Infection has been reported in to the recently approved zinc-coated iron shot used for
over 60 species of birds, with Old World psittacines waterfowl hunting in the USA.73
apparently more susceptible (see Fig 17.25).15
Seizures can be a common clinical sign of zinc toxicity,
This disease has been reported in 53 capercaillies (Tetrao in conjunction with paresis, polyuria/polydipsia, weight
urogallus) examined at necropsy in Sweden and one loss, anemia and gastrointestinal abnormalities. Sudden
capercaillie from Finland.34,49 Protozoa were mainly con- death has been reported in orange-bellied parrots
fined to the brain, but systemic disease is common.34 Little (Neophema chrysogaster) due to zinc toxicoses, how-
is known about sarcocystosis of birds in general. In North ever, it was thought to be a result of the birds colliding
America, Sarcocystis falcatula is the most pathogenic and with walls or structures in the aviary, causing head
well-defined species among birds, with schizonts persist- trauma.55 Serum concentrations of zinc can be used to
ing in the tissues for up to 5.5 months.15,49 The predomi- confirm the diagnosis and should be compared to nor-
nant lesion in fatal S. falcatula infection is pneumonia, mal birds as controls. Syringes with rubber stoppers
however, Sarcocystis-associated encephalitis has been
should be avoided as this may be a source of zinc con-
described in a golden eagle (Aquila chrysaetos) and in a
tamination.11 In general, zinc levels greater than 2 ppm
straw-necked ibis (Carphibis spinicollis) in the USA.35,49
in emu are considered diagnostic for toxicity. Tissue lev-
Fungal Encephalitis els can be evaluated postmortem in suspicious cases.55
Mucormycosis is a rare infection in birds.84 The order Published reference values of zinc levels in tissues of
Mucorales includes a number of saprophytic fungi that normal birds are as follows: macaws, 75 µg/g (tissue
have been mentioned as possible etiologic agents of unspecified);55 cockatiels (Nymphicus hollandicus), 59
meningoencephalitis in birds.84 µg/g in the kidneys, 72 µg/g in the liver and 94 µg/g in
the pancreas;55 goldeneye ducks (Bucephala islandica),
Spongiform Encephalopathy 35.9 µg/g in the liver;55 and peach-faced lovebirds
Three cases of a spongiform encephalopathy of unknown (Agapornis roseicollis), 21 and 33 µg/g in the liver.55
etiology have been reported in ostriches (Struthio Treatment is discussed in Chapter 31, Implications of
camelus) from two zoos in northwestern Germany.63 Toxins in Clinical Disorders.
The birds were euthanized after showing progressive
ataxia and uncoordinated feeding behavior. The lesions Organophosphates, Carbamates and Pesticides
identified by light microscopy were similar to those of There are over 80 different registered organophosphates
prion-induced transmissible encephalopathies in mam- and carbamates in the USA, with both classes being acetyl-
mals and had gray matter vacuolation. However, a toxic cholinesterase inhibitors that bind to and subsequently
or nutritional etiology could not be ruled out.63 inactivate acetylcholinesterase, causing an accumulation
of acetylcholine at the postsynaptic receptors.15 Birds are
Idiopathic 10 to 20 times more susceptible to these inhibitors than
Epilepsy mammals. Acute intoxications can cause seizure activity.
Intermittent seizures with no other abnormality can indi- Exposure to carbamate insecticides can be detected using
cate idiopathic disease, especially if there is a long his- brain cholinesterase reactivation techniques.5,56,105
Tetraparesis/Paraparesis/Paralysis
Definitions and Classifications
The prefix tetra- indicates the involvement of all four
limbs. Tetraplegia is very rare due to the negative effect
such a lesion would have on the respiratory capabilities
of the patient. The prefix para- indicates the involvement
of just the pelvic limbs, and paralysis or the equivalent
paraplegia indicates complete loss of motor movement
in the pelvic limbs (Fig 17.26).
Johnathon Cracknell
Treatment
1. Specific treatment of the underlying etiology.
2. Skin care for recumbent birds or those that are
Fig 17.23 | A rose-crowned fruit dove (Ptilinopus regina) is exam- dragging their limbs.
ined after head trauma, demonstrating superficial skin lesions. 3. Physiotherapy.
4. Supportive care if unable to eat and drink.
Trauma Ataxia
Head Trauma (Fig 17.23)15,53 Definitions and Classifications
Vascular Ataxia indicates an uncoordinated gait and does not
necessitate an impairment of motor function, but there
Atherosclerosis
may be a concurrent paresis. Ataxia is often due to
Atherosclerosis occurs with some degree of frequency in
spinal disease, but may be due to either vestibular or
birds.15 Often this can cause acute death, but can cause
cerebellar disease. There will be no motor dysfunction
sudden onset blindness, ataxia, paresis and seizures.15
in the case of pure cerebellar ataxia.
Clinical signs may be from the cerebrovascular accidents,
and MRI or CT may be useful in their diagnosis.15 See
Chapter 12, Evaluating and Treating the Cardiovascular
System.
Table 17.5 | Spinal Lesion Localization and Clinical Signs93
Clinical Characteristics Specific Clinical Signs
Syndrome/ of the Location
Lesion
Spinal and Localization
Neuromuscular Disease Cranial

cervical spine
Damage to cranial cervi-
cal spinal cord reflects
damage to peripheral
i. No cranial nerve deficits
ii. UMNa wing, leg and
vent signs
white matter pathways iii. Possible neck pain
iv. Very rare loss of pain
CLINICAL SIGNS (Table 17.5) perception
Cervico- Damage to the cervical i. No head signs
Monoparesis/Monoplegia/Hemiparesis/ thoracic spine intumescence produces ii. LMNc wing signs
Hemiplegia clinical signs that reflect iii. UMN leg and vent signs
damage to the grey mat- unless brachial plexus
Definitions and Classifications ter and brachial plexusb lesion, only (ii)
Thoraco- Damage to spine caudal i. No head or wing signs
Paresis indicates the presence of reduced motor function lumbar spine to cervical intumescencee ii. UMN leg and vent signs
in the limbs. The suffix “-plegia” indicates the complete and cranial to lumbar iii. Possible kyphosis, spinal
intumescences reflects ± abdominal paind
loss of motor function. The prefix mono- indicates the white matter lesions iv. Variable loss of pain
perception in limbs
involvement of just one limb (Fig 17.24) and the prefix
Lumbosacral A lesion in the lumbar i. No head or wing signs
hemi- indicates the involvement of both limbs on one side syndrome intumescencee reflects ii. LMN leg signs
of the body with normality on the contralateral side. damage to central gray iii. LMN vent signs unless
matter and lumbosacral peripheral limb nerves
Monoparesis sometimes may be expressed as a “clenched” plexif only affected
iv. Variable loss of sensa-
claw (Fig 17.25). tion in legs and vent
Treatment a UMN = upper motor neuron. See Table 17.2.

b Brachial plexus includes the pectoral, medianoulnar, bicipital, ventral
1. Specific treatment of the underlying etiology. propatagial, axillary and radial peripheral nerves.
c LMN = lower motor neuron. See Table 17.2.
2. Skin care for recumbent birds or those that are d A space-occupying mass within the kidney or pelvic canal may place
pressure on lumbosacral plexus and its ischiatic nerve, mimicking lum-
dragging their limbs. bosacral syndrome.
3. Physiotherapy. e Lumbar intumescence encompasses lumbar, sacral and pudendal plexi.
f Lumbosacral plexi includes the femoral, obturator, ischiatic, pudendal,
4. Supportive care if unable to eat and drink. pelvic and coccygeal peripheral nerves.
Greg J. Harrison
Greg J. Harrison
Fig 17.24 | A palm warbler (Dendroica palmarum) with pesti- Fig 17.25 | An African grey parrot (Psittacus erithacus) with
cide toxicosis demonstrating incoordination. suspected Sarcocystis infection of the central nervous system
exhibits torticollis and bilateral clenched claws.
Table 17.6 | Differential Diagnosis of Spinal and

Neuromuscular Disease
Mechanism Specific Diseases
of Disease
Degenerative i. Psittacine focal symmetrical Poliomyelomalacia
ii. Lysosomal storage disease - Gangliosidosis
iii. Avian vacuolar myelinopathy
iv. Lafora
Neoplastic i. Abdominal neoplasia - ovarian pathology/renal
masses
Nutritional i. Vitamin E deficiency
Greg J. Harrison
ii. Thiamine (vitamin B1) deficiency

iii. Riboflavin (vitamin B2) deficiency
iv. Pyridoxine (vitamin B6) deficiency
Inflammatory i. Viral - Proventricular dilatation disease/Marek’s
disease /Avian paramyxovirus type 1 (Newcastle
Fig 17.26 | A cockatiel (Nymphicus hollandicus) with a spinal disease)/Polioencephalomyelitis of rainbow
lesion of unknown etiology demonstrates a posture often seen lorikeets/Borna/Eastern and western equine
with paraparesis. encephalitis/West Nile virus/Picornavirus
(duck viral hepatitis)
ii. Fungal - Aspergillus spp.
Toxicity i. Lead
ii. Zinc
Treatment iii. Tick Paralysis
1. Specific treatment of the underlying etiology. iv. Organophosphates, carbamates and insecticides
v. Plant toxins
2. Skin care for recumbent birds or those that are vi. Botulism
dragging their limbs. Trauma i. Peripheral nerve trauma
ii. Spinal trauma
3. Physiotherapy.
Vascular i. Fibrocartilaginous embolic myelopathy
4. Supportive care if unable to eat and drink.
DIFFERENTIAL DIAGNOSIS OF Lysosomal Storage Disease

SPINAL AND NEUROMUSCULAR Gangliosidoses are most commonly caused by deficient
D I S E A S E (Table 17.6) activity in one of the two enzymes necessary for ganglio-
Degenerative side catabolism.18 Specifically, an inherited defect in ß-
Psittacine Focal Symmetrical Poliomyelomalacia galactosidase is associated with GM1 gangliosidosis and a
This lesion has been documented in 15 adult birds in similar defect affecting the activity of ß-hexosaminidases
Australia, including five superb parrots, two budgerigars is associated with GM2 gangliosidosis.18 The enzymatic
and one lovebird (Agapornis sp), all of which were from defects lead to an accumulation of GM1 or GM2 respec-
aviaries.53 In caged birds, there was a history of one or tively, within the neurons of the central and peripheral
more birds suddenly becoming uncoordinated, having nervous system. Two related juvenile emus have been
difficulty perching, followed by posterior paralysis. Some reported with severe, progressive, eventually fatal intra-
birds could still fly. Others became tetraplegic within 2 neuronal gangliosidosis.18 Analysis of affected brain tis-
or 3 days.53 sue demonstrated significant elevations in total ganglio-
sides with low levels of lymphocyte ß-galactosidase.18 Thiamine (Vitamin B1) Deficiency
Clinical signs of thiamine deficiency include ataxia,
Avian Vacuolar Myelinopathy (AVM) ascending paralysis and opisthotonus.15 A response to
AVM has been diagnosed in wild birds in the southeastern treatment provides a presumptive diagnosis, as affected
USA. It was first documented in bald eagles (Haliaeetus birds generally respond within hours of oral or par-
leucocephalus) in 1994 and also has been found in enteral administration of vitamin B1.15
American coots (Fulica americana).115 Bald eagles are fre-
quently found dead, but have been noted to have diffi- Riboflavin (Vitamin B2) Deficiency
culty flying and can crash into or overfly perches. Birds with this deficiency have weakness, atrophy of the
Affected coots appear to fly or are wobbly in flight; they leg muscles and are seen to walk on their hocks with
are uncoordinated on land and may swim in circles or on their toes curled inward, although this does not always
their backs.71 On neurologic examination, the majority of happen because death may occur first.15,118 The condition
coots have been documented with ataxia, decreased with- has occasionally occurred in chickens, but since
drawal reflexes, proprioceptive deficits and decreased riboflavin has been added to poultry feed it has become
vent responses.71 Other signs seen in less than half of quite rare.118 Leg and wing paralysis has been reported in
examined coots include beak and tongue weakness, head racing pigeons with this disorder.118 The deficiency
tremors, absent pupillary light responses, anisocoria, causes a demyelinating peripheral neuritis. Treatment
apparent blindness and nystagmus.71 involves administration of oral or parenteral riboflavin
and diet correction.
Birds that die have no gross lesions of the nervous sys-
tem, and some coots have been documented to recover Pyridoxine (Vitamin B6) Deficiency
from this disorder with supportive care.71 Histologically, Deficiency of this vitamin causes characteristic jerky,
the disease is characterized by diffuse, spongy degenera- nervous walking, progressing to running and flapping
tion throughout the white matter of the CNS with the the wings.15
optic tectum most severely affected.71 The etiology
remains unknown.115 Inflammatory
Viral Disease
Lafora’s Disease Proventricular Dilation Disease (PDD) has been
Lafora’s disease is a presumed inherited defect of carbo- reported to cause peripheral (sciatic, brachial and vagal)
hydrate metabolism first documented in humans.103 This neuritis in psittacine birds.17
disturbance of the carbohydrate metabolism causes the
formation of typical Lafora-bodies, which consist of poly- Marek’s Disease Virus (MDV) in chickens is caused by
saccharide complexes. Similar changes have recently been an oncogenic herpesvirus and is characterized by lym-
described in two cockatiels (Nymphicus hollandicus).15 phomas and paralysis.43 Paralysis associated with MDV
infection has usually been attributed to peripheral nerve
Neoplasia lesions because gross enlargement of nerves with lym-
Primary spinal neoplasia is rare in birds. Compressive phoid infiltrates is a common feature of MD, and CNS
peripheral nerve trauma generally occurs secondary to damage has not been found consistently in paralyzed
an expanding mass that applies pressure to the nerve, birds.43 The onset of both lymphomas and paralysis usu-
because the pelvic nerves pass through the renal ally occurs 4 to 12 weeks after infection with MDV.43 A
parenchyma.15 paralytic syndrome involving the brain also is induced by
MDV and is now designated transient paralysis (TP).43
Clinically, TP is characterized by the development of a
Nutritional
flaccid paralysis 8 to 12 days after infection with an
Vitamin E/Selenium Deficiency oncogenic MDV. This initially affects neck muscles and
Clinical signs associated with vitamin E and selenium defi- later tends to become generalized.43 Most birds with TP
ciencies include tremors, ataxia, incoordination, reluc- recover completely within 24 to 48 hours, although a
tance to walk and recumbency.15 This deficiency has been few birds that become severely affected may die within
incriminated as the etiology of cockatiel paralysis syn- the same period of time.43 A more acute and fatal form of
drome. This condition appears to occur most frequently TP has recently been described in young chickens.123
in lutino cockatiels, but similar syndromes have been
reported in a variety of other species including blue and Once known as fowl paralysis and range paralysis, it was
gold macaws, eclectus parrots and African grey parrots.15 considered that gross enlargements of the peripheral
Supplementation with injectable and oral vitamin E is the nerves were a pathognomic lesion.123 However, gross
recommended treatment, however, the patient may or enlargement of peripheral nerves also can be induced
may not respond, depending on the severity of damage. by reticuloendotheliosis virus (REV).7 Both REV and
subgroup J avian leucosis virus can induce lymphoid Fungal Disease21,22,46,102

infiltrations in peripheral nerves, indicating that addi-
tional criteria may be needed for confirmation of Toxicity
etiology.7 Lead
Lead toxicity, one of the most commonly recognized poi-
Avian Paramyxovirus Type 1 (Newcastle Disease) is a
sonings of companion and free-ranging birds, is a com-
variable disease with different susceptibilities between
mon cause of neurologic abnormalities and can be
avian orders.8 The disease is produced following infec-
fatal.92 Peripheral neuropathies caused by lead intoxica-
tion and varies with virus pathotype; other factors
tion have been reported, but it is more common to see
include the species, age, immune status, general health
central nervous system abnormalities.92 Various sources
of the bird and environmental conditions.8 Clinical neu-
of lead have been documented, but the source of lead in
rologic findings in affected birds include ataxia, torticol-
any specific poisoning often remains difficult to deter-
lis, opisthotonus, head shaking and tremors, head tilt, leg
mine. A classic source of lead exposure for birds is
paralysis progressing to lateral recumbency and blind-
ingesting lead shot from the bottom of lakes in heavily
ness.8 Some birds may survive for up to 18 months after
hunted areas.92 The combination of the grinding action of
developing CNS signs, but the CNS signs do not regress
the ventriculus and its low pH (2.0-3.5) acts to solubilize
before death or euthanasia.8 Definitive diagnosis requires
ingested shot.92 Raptors may eat carcasses containing lead
virus isolation, demonstration of the viral antigen, or ris-
shot and become intoxicated.92 Inhalation of fumes from
ing specific antibody titers.8 A titer of 1:8 is usually con-
leaded gasoline is another possible route of exposure.92
sidered evidence of exposure to this virus, and in unvac-
Lead poisoning as a result of lead shot embedded in soft
cinated birds when coupled with clinical signs is consid-
tissues is rare because of the avascular fibrous tissue that
ered strong diagnostic evidence of infection.8
develops around these foreign bodies.92
Suspected Viral Polioencephalomyelitis of Rainbow Clinically, lead toxicosis may be an acute or chronic
Lorikeets (Trichoglossus haematodus) has been doc- problem, with clinical signs dependent on the amount
umented in 35 rainbow lorikeets in Australia.53 It affects and surface area of lead ingested.92 Clinical signs in birds
adults at any time of the year and usually causes an include behavioral changes, lethargy, anorexia, vomiting,
inability to fly or perch. The birds are commonly alert diarrhea, ataxia, limb paresis or paralysis, seizures, ane-
and will eat, but are characteristically affected with mia and emaciation.92 Death may occur within 48 hours
clenched claws.53 The cerebellum was affected in about after the first appearance of clinical signs.92
half of the birds, and the lesions were largely restricted
to the central cerebellar white matter and involved the Whole, unclotted blood is the sample of choice for
roof nuclei. determining lead concentrations because 90% of circu-
lating lead is contained within RBCs.92 Concentrations
Borna Disease Virus has been documented to cause a of >20 µg/dl lead in whole blood are suggestive of lead
paretic condition in young ostriches in Israel.4 Birds intoxication in psittacine birds, and concentrations >40
between 14 and 42 days old were affected. In a small to 60 µg/dl are diagnostic of lead toxicosis.92
number of cases, clinical signs of incoordination were
seen 1 to 3 days before paresis supervened. At this stage Zinc73
of the disease, the birds could stand and move with diffi- See Intracranial Disease above.
culty if given external support.4 Mortality can be remark-
Tick Paralysis
ably high. About 1% of the ostriches seemed to recover if
Tick paralysis is a disease caused by neurotoxins associ-
they were given intensive supportive care, however, they
ated with 60 species of hard and soft ticks in 10 genera.76
relapsed several months later.4
Generally, the disease is considered a motor polyneuro-
pathy characterized by a progressive, ascending, flaccid
Eastern and Western Equine Encephalitis infections
motor paralysis. Clinical signs include ataxia, paresis,
can cause weakness and paralysis of the legs.96
paralysis, areflexia, hypotonus and respiratory failure.76
Picornavirus (Duck Viral Hepatitis) has been associ- Death is common if the tick is not removed.76 The toxin
ated with neurologic signs in Galliformes, Anseriformes is associated with the female tick’s salivary glands and is
and Columbiformes of less than 28 days of age.15 Clinical probably secreted during feeding.76 Ixodes brunneus has
signs documented include depression, ataxia, paresis or been associated with tick paralysis in birds.76 All three
paralysis, and severe but fine head and neck tremors. stages of the tick feed exclusively on birds, particularly
passerines and group-feeding species; at least 64 species
West Nile Virus has been documented to cause paresis of birds are known to be hosts for this tick.76 Adult
and paralysis in many avian species.78 females are found on adult birds primarily in the colder
months of the year, with larvae and nymphs occasionally from paralysis of the cervical muscles.15 Most birds
present at the same time, causing clinical signs during exhibit hindlimb paresis first, which progresses to paral-
winter months.76 ysis of the wings, followed by loss of control of the neck
and head in the terminal stages.15 Species’ susceptibility
A definitive diagnosis of tick paralysis can be based only and clinical manifestations vary, as has been evidenced
on dramatic clinical improvement and recovery of the in rehabilitation facility outbreaks.
host, usually within 24 to 72 hours following removal of
the tick.
Trauma
Organophosphates and Carbamates Spine Trauma/Peripheral Nerve Trauma
Organophosphorus-induced delayed neurotoxicity Trauma is fairly common in free-ranging as well as com-
(OPIDN) is a neurologic condition characterized clini- panion and aviary birds. The consequences, diagnosis
cally by the delayed onset of a progressively developing and management of these traumas have been well dis-
hindlimb ataxia and paralysis.90,116 Two categories of cussed in other texts.15
OPIDN — Type I and Type II — have been identified,116
and differ from each other in the length of the delay Vascular
period prior to onset of symptoms, the type of resultant Fibrocartilaginous Embolization
clinical signs and the extent of central nervous system Emboli may involve vessels of the spinal cord, lepto-
involvement. Type I OPIDN has a longer delay period meninges or both. Fibrocartilaginous embolism (FCE)
(typically 10-21 days) and affects only the spinal cord and ischemic myelopathy have been reported in several
and brainstem, whereas type II OPIDN has a shorter 15-week-old tom turkeys with peracute onsets of paresis
delay period (4-7 days) and results in additional degen- and ataxia.111 Recovery was noted in some affected birds
eration in the midbrain and forebrain. Widespread neu- suspected to have this disease, but cartilaginous emboli
ropathology follows both oral and injectable forms of were found in the spinal cord vasculature accompanying
the compounds.116 myelomalacia in three turkeys that did not recover.111
The articular cartilage of the vertebral body endplates
Plant Toxins
are suggested to be the source of the emboli, as there
Nerium oleander2 (See Chapter 31, Implications of Toxic
were articular cartilage defects found in the affected
Substances in Clinical Disorders.
birds. There is no known treatment in any species and
Botulism (Limberneck) diagnosis is by exclusion. Recovery is possible in some
Botulism in birds is usually the result of ingestion of the cases, but supportive care would be necessary.
exotoxin of Clostridium botulinum type C. Occasionally
C. botulinum type A and type E are involved.15 This is an Products Mentioned in the Text
uncommon problem in companion birds but frequent in a. Lanex fine screens/TML film, Kodak, Rochester, NY
b. Omnipaque 240, Winthrop Pharmaceuticals, New York, NY
waterfowl.15,45,70 The classic sign is limberneck resulting c. Magnevist, Berlix Laboratories, Wayne, NJ
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9(3):241-258, 1987. 96. Randolph KD, Vanhooser SL, 29(1):177-179, 1993. Brain Res 606:119-124, 1993.
83. Necker R: Functional organization Hoffman M: Western equine 109. Shivaprasad HL, et al: Turlock- 121. Williams SM, et al: Diagnosis of
of the spinal cord. In Sturkie PD encephalitis virus in emus in like bunyavirus associated with eastern equine encephalitis by
(ed): Avian Physiology 5th ed. Oklahoma. J Vet Diagn Invest encephalomyelitis and myocardi- immunohistochemistry in two
New York, Springer-Verlag, 2000, 6:492-493, 1994. tis in an ostrich chick. J Vet Diag flocks of Michigan ring-necked
pp 71-81. 97. Redig PT, Post GC, Concannon TM: Invest 14:363-370, 2002. pheasants. Avian Dis 44:1012-
84. Orcutt CJ, Bartrick TE: Mucormy- Development of an ELISA assay for 110. Sims MH: Clinical electrodiagnos- 1016, 2000.
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18_Reproductive.qxd 8/23/2005 11:44 AM Page 519
CHAPTER
18
Reproductive
System
HEATHER L. BOWLES, DVM, D ipl ABVP-A vian ,
C e r t i f i e d i n V e t e r i n a r y A c u p u n c t u r e (C hi I n s t i t u t e )
Reproductive Embryology,
Anatomy and Physiology
FORMATION OF THE AVIAN
GONADS AND REPRODUCTIVE
ANATOMY
The avian gonads arise from more than one embryonic
source. The medulla or core arises from the meso-
nephric ducts. The outer cortex arises from a thickening
of peritoneum along the root of the dorsal mesentery
within the primitive gonadal ridge. Mesodermal germ
cells that arise from yolk-sac endoderm migrate into this
gonadal ridge, forming the ovary. The cells are initially
distributed equally to both sides. In the hen, these germ
cells are then preferentially distributed to the left side,
and migrate from the right to the left side as well.58
Some avian species do in fact have 2 ovaries, including
the brown kiwi and several raptor species. Sexual differ-
entiation begins by day 5 in passerines and domestic
fowl and by day 11 in raptor species. Differentiation of
the ovary is characterized by development of the cortex,
while the medulla develops into the testis.30,58
As the embryo develops, the germ cells undergo three

phases of oogenesis. During the first phase, the oogonia
actively divide for a defined time period and then stop at
the first prophase of the first maturation division.
During the second phase, the germ cells grow in size to
become primary oocytes. This occurs approximately at
the time of hatch in domestic fowl. During the third
phase, oocytes complete the first maturation division to
become secondary oocytes. Completion of the second AVIAN REPRODUCTIVE

maturation period results in an ovum.30,34,53,58 PHYSIOLOGY
Avian reproduction is guided by seasonal physiologic
The ovarian medulla consists of blood vessels arranged in
controls such as favorable climate, low predation risk,
irregular vascular zones, interstitial cells, autonomic
social interaction, and food and nest site availability.
nerve fibers and smooth muscle. The ova are located
Internal physiologic processes work in combination
peripherally in the cortex of the ovary. The ovarian sur-
with external factors to promote gonadal development.
face is covered by parietal peritoneum with an underly-
This annual cycle involves integration between environ-
ing layer of dense connective tissue, the tunica albuginea.
mental, physiologic and behavioral conditions. Biologic
The ovary is located just caudal to the adrenal gland,
clocks control the release of hormones and other
near the tip of the cranial division of the kidney. It lies
chemicals that regulate metabolism, reproduction and
deep to the abdominal air sac, which forms an ovulation
behavior. Photoperiod plays a key role in this system
pocket near the time of lay. This pocket is thought to
using environmental light, which stimulates neural
help receive the ovulated ovum with its yolk into the
receptors, and clock information from an internal circa-
oviductal opening. The pocket is suspended by a dorsal
dian cycle. This allows the bird to measure day length.
mesentery, the mesovarium. Vascular supply to the ovary
is through the cranial renal artery, which has several In most of our Neotropical psittacine species, birds
short branches. There are often two ovarian veins that normally start to nest when the rains begin, when
drain blood directly into the caudal vena cava. The ovary food is the most available. In temperate zone species,
has a roughened, granular appearance due to follicular reproduction is stimulated by photoperiod. The length-
development. As the hen becomes sexually active, the fol- ening day in early spring stimulates gonadal develop-
licles begin to grow in a hierarchal pattern. 30,34,53,58 ment. Warmer temperature, rainfall and behavioral dis-
plays fine-tune the physiologic events of breeding and
The oviduct enlarges to occupy the dorsal aspect of the the resulting increased secretion of sex hor-
left intestinal peritoneal portion of the coelomic cavity. mones.23,47,55,58
Seasonal growth and differentiation of the reproductive
tract is under hormonal control. In a mature hen that is There is strong evidence that the pineal gland (hypoph-
not reproductively active, the ovary and oviduct appear ysis cerebri) is largely responsible for photoperiodic
similar to that of a juvenile bird: small with no active control. However, unlike reptiles, the avian pineal gland
follicles. The oviduct develops from a thickening in does not have primary light receptors, but they do have
the peritoneal epithelium between the degenerating photoreceptors like cells in the brain and retinae. Birds
pronephric ducts and the first mesonephric tubules. do not monitor day length visually, but rather by means
These thickenings invaginate to form a tubular structure. of special receptors in the hypothalamus. After direct
This process occurs bilaterally and symmetrically in both stimulation of the photoreceptors, neurosecretory cells
sexes, but regression and disappearance of the ducts in the hypothalamus induce the release of neurohor-
occurs in the cock and a relative regression of the right mones in the median eminence (neural portion) of the
duct occurs in the hen. A right oviduct may be present epiphysis (pituitary), which is linked to the midbrain.
in some raptors. The opening of the oviductal lumen These neurohormones are then carried via the blood-
into the cloaca often appears near the time of produc- stream to the anterior pituitary gland, inducing the syn-
tion of the first egg.30,34,53,58 thesis and subsequent release of luteinizing hormone
(LH) and follicle-stimulating hormone (FSH).
There is a period of time during fetal development when Luteinizing hormone stimulates gonadal activity and in
the testes are ambisexual due to extensive covering with combination with FSH stimulates ovarian development
a cortical crust. These cortical remnants normally disap- and testicular spermatogenises.23,37,54,55,70 See Ed. Note on
pear prior to hatch; however, they may remain and fur- page 522.
ther complicate visual sex identification. The seminifer-
ous tubules differentiate in the medullary portion of the Each circadian cycle includes a limited time period of
gonad. The ductus deferens develops from the meso- each day during which photoreceptors are particularly
nephric duct, while the epididymis arises from the sensitive to light. This stimulates a series of physiologic
mesonephros. The epididymis and ductus deferens ini- reactions. As daylight length increases each year, so
tially develop in both sexes, as does the oviduct. The does the opportunity for light to stimulate these recep-
male tubular structures normally regress in the female. tors during this limited time period. In addition, the
However, they have been reported to persist in some length of time these receptors are affected increases
passerines and domestic fowl, but are significantly with increasing daylight length (see Chapter 19,
smaller than the oviduct.23,35,58 Endocrine Considerations).23,37,55,70
Chapter 18 | E V A L U A T I N G A N D T R E A T I N G T H E R E P R O D U C T I V E S Y S T E M
521
During the late summer after breeding season has and crows lay a fixed number of eggs, while indetermi-
ended, the shortened daylight length stimulates the nate layers such as domestic fowl and Japanese quail
main molt. Gonadal hormones and tissue size decreases replace eggs that are lost. Continuous breeders lay
dramatically. Although the days are still relatively long, throughout the year. A rate of lay is the number of eggs
there is a photorefractory period that does not stimulate laid in a given time period. A sequence is a number of
gonadal hormone release and tissue growth. This pho- eggs laid on successive days, separated by pause days. A
torefractory period is best developed in migratory tem- clutch is a number of eggs laid during a sequence. A
perate zone species and is weak to absent in most tropi- longer sequence is associated with a shorter oviposi-
cal zone species. This may represent an adaptation for tion/ovulation cycle.30,31,34,52
scheduling a major molt and preparation for migration
by terminating reproductive activity while days are still During the non-breeding season, ovarian follicles nor-
long. The shorter days of winter inhibit gonadal growth. mally undergo atresia. Atresia is a process of regression
This is necessary to restore photosensitivity during the and resorption of a follicle. Two types of atresia have
spring, as gonadal tissue will not grow in response to been described: bursting and invasion. Bursting atresia
increasing day length unless there has been a prior occurs when the follicular wall ruptures and the yolk is
period of short daylight length.34,35,58 released into the coelomic cavity where it is usually
absorbed without any harm to the bird. Invasion atresia
Birds have developed several mechanisms to reduce involves granulosa and thecal cells invading the ovum
body weight, thereby conserving energy expended dur- and subsequent in situ yolk absorption. Early atresia is
ing flight. The reproductive tract (ovary, oviduct, testes noted when a vesicular lesion appears on the follicular
and ductus deferens) is greatly reduced in size during surface. This vesicular formation progresses until the
the non-breeding season, and eggs are laid and incu- entire follicle is covered. As the largest F1 follicle is
bated externally.34,35,58 absorbed, the other smaller follicles will progress in a
similar manner. Small follicles may be covered with con-
Physiology of the Female nective tissue, occasionally leaving a scar-like area. Large
When reproductively active, the ovary enlarges and folli- follicles may undergo cystic degeneration. If ovulation
cles form in a hierarchal manner. The primary or F1 fol- ceases suddenly, as may occur during trauma or stress,
licle is the largest and first in line to be ovulated. There developing follicles may become hemorrhagic, resulting
are several smaller follicles on the ovarian surface as in regression of the developing follicles. Aflatoxicosis
well. A stalk that contains smooth muscle with a blood also may cause follicular atresia. Aging hens may exhibit
and nerve supply suspends each large follicle.30,34,49,58 permanent ovarian involution, which is believed to be a
Gonadotropin secretion causes follicles to develop on normal physiologic process.30,31,34,73
the ovary in a hierarchal manner. As the breeding season
approaches, follicles undergo a period of rapid develop- Knowledge of the oviduct and its different anatomic
ment and growth. There is deposition of yolk protein regions is important in discerning pathologic conditions
and lipid from the liver; gonadotropins and steroid hor- of the oviduct and developing egg. The oviduct is divided
mones regulate this. The primary oocyte is surrounded into five parts: the infundibulum, magnum, isthmus,
by six layers of tissues: the oocyte plasma membrane, uterus or shell gland, and vagina. A mucosal layer of cili-
perivitelline membrane, granulosa cells, basal lamina, ated epithelium with unicellular mucous glands or gob-
and the theca interna and externa. These tissues have an let cells lines the wall of the oviduct. The submucosa has
endocrine role, providing communication between the mucosal folds that vary in height, thickness and tubular
ovary and oviduct with passage of each ovum. The nerve glands. The muscular layer has an inner layer of circular
supply is both adrenergic and cholinergic. Ovulation smooth muscle and an outer layer of longitudinal
occurs under the influence of several hormonal factors. smooth muscle.30,31,34,73
Meiotic or reduction division occurs approximately 2
hours preovulation, while the primary oocyte is still The infundibulum is divided into the proximal funnel
within the follicle. This yields a secondary oocyte and portion and a distal tubular portion. The funnel portion
first polar body, each with a haploid number of chromo- is where fertilization occurs. It has a thin wall with low
somes. Most birds have a meridional band or stigma on mucosal folds. This portion surrounds and engulfs the
large preovulatory follicles. This is where the oocyte ovum during ovulation. At the beginning and end of the
breaks through the follicular wall during ovulation.30,34,58 ovulatory cycle, the oviduct and ovary may not be syn-
chronized, resulting in ectopic ovulation also referred to
Ovulation occurs at a relatively fixed time period after as internal laying. This yolk and ovum may be resorbed
oviposition under several physiologic, neural and hor- without incident or may lead to coelomitis. The exact
monal controls. Determinant layers such as budgerigars mechanism by which coelomitis occurs after ectopic
ovulation is not well understood.17,30,31,34,73 Physiology of the Male

The testes are paired, ellipsoid- to bean-shaped organs
The tubular portion of the infundibulum is thicker,
that lie near the cranial pole of the kidney. The surface is
with taller branching folds. Underneath these folds are
covered with a fibrous tunic, the tunica albuginea. Each
branched, convoluted tubular glands that produce the
testicle is suspended by a short mesentery or mesor-
chalaza, which are fibrous bands that suspend the yolk
chium that protrudes into the intestinal peritoneal cavity
within the egg. A thin, dense layer of albumin is added
and is partially surrounded medially by the abdominal air
to surround the yolk. In some species, sperm host
sac. The testes change in size and color in response to
glands maintain sperm for fertilization for a variable
hormonal fluctuations that influence sexual activity. The
time period and are located within this portion of the
inactive testicles are often white to yellow due to accu-
infundibulum.17,30,31,34,73
mulation of lipid in the interstitial cells. In some species,
Large mucosal folds that result from numerous tubular the inactive testicles are black due to a large number of
glands distinguish the magnum histologically. It is the melanocytes. Active testicles are significantly larger and
longest portion of the oviduct. The majority of albumin paler due to the increased volume in the seminiferous
as well as sodium, magnesium and calcium are added tubules. The increased size is a result of increased length
to the egg by these glands. The release of albumin may and diameter of the seminiferous tubules, and numbers
be controlled by mechanical, neural and endocrine of Leydig or interstitial cells. Generally speaking, the
factors.17,30,31,34,73 increase in testicular size is a result of increasing serum
concentrations of FSH and LH. These physiologic
The isthmus follows and, in domestic fowl, is clearly processes occur during the nuptial or culmination phase
delineated from the magnum by a narrow translucent of the reproductive cycle.35,38,52,73 (Ed. Note: These results
band. This band is not present in psittacines. The isth- have not been verified since FSH was purified. Prior to
mus is relatively short and the mucosal folds are less the early 1990s, FSH was contaminated with LH
prominent. The tubular glands are unique in that they [Etches, R, University of Guelph, 2003]).
produce sulfur-containing proteins. These proteins are
incorporated into the shell membranes that are pro- Birds do not have septa that divide the testicles and
duced in the isthmus. A small amount of albumin is there are no mediastinal testes. Unlike mammals, the
added to the developing egg. Calcification is initiated in seminiferous tubules anastomose with each other. Each
the isthmus.17,30,31,34,73 seminiferous tubule is composed of a lining of sper-
matogonia and sustentacular or Sertoli cells. The sper-
During passage of the egg through the oviduct, the matogonia divide to form primary, then secondary sper-
majority of the time is spent in the uterus, or shell gland. matocytes. As these spermatocytes progress toward the
There are two portions: a short, narrow region which the lumen, they undergo a maturation process to become
egg traverses rapidly, and a pouch-like region where the spermatids, which then mature into spermatozoa or
egg spends the majority of the time. The mucosal lining sperm. This maturation process proceeds with the head
is characterized by a large number of leaf-like lamellar of each sperm embedded in the sustentacular cells. The
folds that press against the surface of the egg. This sustentacular cells extend the width of the epithelium to
increases the surface area to improve efficiency of calcifi- provide support for the developing spermatozoa. They
cation and plumping. “Plumping,” a process in which a are phagocytic and also may produce steroid hormones
large amount of water and solutes are added to the egg and bind testosterone.35,38,58
relatively quickly, occurs in the proximal short, narrow
region of the oviduct. It is in the pouch-like region that The spermatozoa detach from the Sertoli cells and travel
calcification of the shell is completed.17,19,30,31,34,73 down the seminiferous tubules when mature. In most
species, these tubules converge into a smaller number of
The vagina is separated from the uterus by the utero- short, straight tubules that continue as the rete testes.
vaginal sphincter. In most species the egg passes rapidly The rete testes is a meshwork of tubules embedded in
through the vagina to exit into the urodeum. However, connective tissue, located dorsomedially to each testicle,
in some species the egg may remain for a longer time adjacent to the epididymis. Both the rete testes and
period to allow for hardening of the shell. There are straight tubules are lined by sustentacular cells.35,38,58
sperm host glands at the uterovaginal sphincter for
sperm storage. Sperm from multiple male birds may be The Leydig, or interstitial, cells are located between the
stored and remain viable for long time periods. This may seminiferous tubules. They are light-colored and stain
be up to several months in the turkey. This allows for eosinophilic with hematoxylin-eosin stain because of the
the possibility of insemination of different ova of a single large concentration of smooth endoplasmic reticulum
clutch by different males.17,19,30,31,34,58,73 and cholesterol. The smooth endoplasmic reticulum is
523
involved in the conversion of cholesterol to steroid hor- The vent may be either a circular opening as in psitta-
mones, with testosterone and androstenedione being cines or a transverse slit as in Galliformes. The sphincter
the major androgens. These hormones stimulate the sec- muscle surrounds the opening and has an outer circular
ondary sex characteristics, including courtship, colora- and an inner transverse striated muscle layer. In addition,
tion, song, and the development and maturation of the there is a transverse muscle originating on the pelvic
tubules, particularly the ductus deferens.35,38,58 bone and/or caudal vertebrae that interdigitates with the
sphincter muscle surrounding the vent. Upon contrac-
The epididymis of the bird is concealed due to its dorso- tion of this transverse muscle, the vent is pulled ventro-
medial location on the testicle and its small size com- cranially, which is important during coitus. This muscular
pared to mammals. It is not divided into a head, body action allows the cloaca in the male bird to be directed
and tail, but is composed of several efferent ductules that over the female’s cloaca. The levator muscle originates
drain the rete testes and straight tubules. Several efferent on the ventral tailhead and inserts ventrally onto the vent
ductules drain into the main epididymal duct along its and/or the phallus. This muscle pulls the vent caudally
length. The epididymal duct is relatively short and after copulation and defecation.15,36,73
straight, and is lined by non-ciliated pseudostratified
columnar epithelium. The epithelium is secretory and The phallus may be intromittent as in ratites and Anseri-
provides some of the seminal fluid. Sperm may be stored formes, non-intromittent as in Galliformes, or absent as
in the epididymis or in the seminal glomus of more sea- in psittacines and passerines. The intromittent phallus
sonal birds. Some species have an appendix epididymis may be found in two forms: one form lacks a ventral cav-
that extends cranially into the adrenal gland. The efferent ity, and is found in ostriches, kiwis and tinamous; the
ductules of this tissue may secrete androgens following other form has a cavity and is found in emus, rheas, cas-
castration.35,38,58 sowaries and Anseriformes. The former type of phallus
consists of paired fibrolymphatic bodies with a dorsal
The epididymis continues distally as the ductus defer- sulcus to deliver semen. It lies on the floor of the cloaca
ens. The ductus deferens is closely associated with the and partially everts during micturition and defecation.
ureter in the dorsomedial coelom. In passerines, each Tumescence occurs by increased lymphatic flow and sta-
ductus elongates distally during the culmination phase sis into an elastic vascular body within the distal end of
of the reproductive cycle to form the cloacal promon- the phallus. Those phalluses with a ventral cavity also
tory, which can project into the cloaca. This protrusion are located on the cloacal floor, but are enclosed in a sac
gives the male external cloaca a pillar-like prominence or cavity. The proximal portion stays within the cavity
compared to a rounded profile in females; therefore, it and does not become engorged, while the distal portion
can be used for sex determination during the breeding everts when engorged with lymphatic fluid.15,36,73
season. Birds with a seminal glomus use it as the main
storage site for sperm. The ductus is composed of non- The non-intromittent phallus, as found in domestic fowl,
ciliated pseudostratified squamous epithelium and has is located on the floor near the lip of the vent. It consists
less secretory function when compared with the epi- of a median and two lateral phallic bodies. Lateral to the
didymis. There are no accessory sex glands in birds.35,38,58 phallic bodies are lymphatic folds located on the ventro-
lateral floor of the proctodeum. A lymphatic meshwork
Avian semen is derived in part from the sustentacular connects these folds and phallic bodies. Tumescence is
cells and epithelial cells that line the reproductive tract. a result of lymphatic flow through these structures. The
Lymph-like fluid is produced from lymphatic folds in the lymphatic folds and lateral phallic bodies accumulate a
floor of the proctodeum. This fluid appears to be harm- greater amount of fluid than the median phallic body,
ful to spermatozoa because of the presence of clotting resulting in eversion of the phallus and creating a
factors and high concentrations of chlorine and calcium. groove for delivery of semen. The phallus contacts the
Avian spermatozoa are either complex or simple. Complex everted oviductal opening where semen is deposited.15,36,73
sperm is found in passerines and simple sperm in other
species. Similar to mammals, each spermatozoon is com-
posed of an acrosome, head and tail. In simple sperma-
tozoa, the acrosome is attached to the head only at its Reproductive Disorders
most rostral point. The head is long and slender, and
the tail is long and moves in an undulating manner. In Avian reproductive disorders are a result of complex
complex sperm, the entire sperm is spiral in appearance combinations of hormonal, physiologic and behavioral
and moves by rotating along its longitudinal axis.35,38,58 actions reacting to photoperiods, food availability and
availability of nest sites.30,70 Environmental influences in
See Chapter 14, Evaluating and Treating the Gastro- captivity may result in the induction of reproductive and
intestinal System for a discussion of the cloaca. hormonal activity in several ways. Artificial lighting may
interfere with the normal photoperiod and annual light Therapy for chronic egg laying focuses on stopping egg
cycles, resulting in abnormal cycling.23 Food is typically production while altering any predisposing stimuli and
available ad libitum and is often high-fat, calorically correcting any secondary diseases that may be present.
dense seed, or foods high in simple carbohydrates such Pharmacologic, behavioral, nutritional, environmental
as corn and fruit. These foods may actually stimulate and surgical options are used alone or in combination
reproduction. Most pet birds are not intended for breed- depending on the needs of the individual patient.
ing and do not have mates. In some environments, pet Pharmacologic options have included medroxyproges-
birds may select an abnormal mate such as their human terone acetatea, levonorgestrelb, human chorionic
cohabitants or cage furniture. There may be a genetic gonadotropinc, norethindrone/mestranold, testosterone,
predisposition and lack of normal reproductive hor- leuprolide acetatee and tamoxifenf (Table 18.1). Med-
monal balance30,34,37 (see Chapter 3, Concepts in Behavior: roxyprogesterone acetate, though often effective, may
Section III, Pubescent and Adult Psittacine Behavior). cause serious side effects such as polyuria/polydipsia,
obesity, lethargy, hepatic lipidosis, diabetes mellitus,
Reproductively driven birds may display instinctual terri- hepatic cirrhosis and death.9,31,63 Levonorgestrel, another
torial and mate-related behaviors. These behaviors may synthetic progestin, has been evaluated only in
include, but are not limited to aggression, biting, mas- Japanese quail (Coturnix coturnix japonica) and may
turbation and excessive vocalization. These “undesir- carry the same side effects as medroxyprogesterone
able” behaviors may jeopardize their value as pets, acetate.72,77 Testosterone therapy interrupts the ovula-
diminishing the pet-human relationship and even result tory cycle, but has variable results and is contraindi-
in these birds losing their homes.30,34,37 cated in patients with liver disease.73 Norethindrone/
mestranol has caused severe hypertension in one Rouen
Reproduction is often not desired in pet birds. Egg duck (D. Zantop, personal communication, 2000).
production and hormonal cycling may lead to disease Human chorionic gonadotropin has demonstrated to be
processes of the reproductive system or systemic, a safer alternative with significantly fewer side effects;
endocrine and metabolic disorders. Therefore, avian however, it has not been consistently effective in man-
practitioners have sought medical and surgical methods aging these disorders and patients may become refrac-
to limit reproductive drive and hormone production.8,56,59 tory to treatment.34,44 Tamoxifen is a non-steroidal anti-
inflammatory agent used as an estrogen blocker to treat
CHRONIC EGG LAYING women with breast cancer. Tamoxifen was administered
to budgerigars presumed to be hens, but not actively
Chronic egg laying in pet birds occurs when a hen lays laying for 38 to 46 weeks.46 Leukopenia was a significant
repeated clutches or larger than normal clutch size with- side effect that resolved after therapy was discontinued.
out regard to the presence of a mate or accurate breed- An incidental finding in this study was the change in
ing season. This process often physically exhausts the coloration of the hen’s cere from brown to pink or
reproductive tract and is a serious metabolic drain, par- blue. This change implies that tamoxifen does have
ticularly on calcium stores, all of which may predispose some estrogen-blocking affects in birds. Leuprolide
the hen to egg binding, yolk coelomitis and osteoporosis. acetate is a long-acting gonadotropin-releasing hor-
Commonly affected species include cockatiels, finches mone (GnRH) analog. A single injection in women and
and lovebirds, however, any species may be affected. studied laboratory rodents results in an initial stimula-
Diagnosis of chronic egg laying is based on history and tion followed by a prolonged suppression of pituitary
physical examination. There typically is a history of the gonadotropins. In rats, this reduction in serum gonado-
hen laying large numbers of eggs with or without a pause tropin levels is achieved by reducing the number of
period in between clutches. A thorough history of the pituitary GnRH receptors. Repeated monthly injections
home environment will often reveal several reproductive result in receptor down regulation of GnRH pituitary
stimuli and a “mate relationship” with a member of the receptors, which causes a decreased secretion of
household or owner. Physical exam may reveal normal gonadal steroid hormones. Therefore, tissues and
findings, a palpable egg in the coelom, or other second- functions that depend on these hormones for main-
ary disease conditions such as a pathologic fracture sec- tenance become quiescent, and diseases resulting
ondary to osteoporosis. Serum chemistries may reveal from reproductive hormone production improve or
hypercalcemia, hypercholesterolemia and hyperglobu- resolve.16,33,50,51,78
linemia supportive of an ovulating hen. There may be a
hypocalcemia present if the hen’s calcium stores are Environmental stimuli should be altered, including
depleted, and particularly if she is consuming a low- decreasing the photoperiod to 8-10 hours of daylight
calcium diet such as seed9,31,33,65 (see Chapter 5, Calcium per day. Nest sites, toys and other items toward which
Metabolism). the bird has a sexual affinity should be removed from
525
Table 18.1 | Summary of Medical Therapy for

Reproductive Disorders
Therapy Dosages Comments
Leuprolide Acetatee 700-800*1 µg/kg IM Administered every 14
for birds <300 g days; 3 doses are usually
adequate
500 µg/kg IM for Stable in standard
birds >300 g freezer 9 months
Human chorionic 250-500 IU/kg IM Stable in refrigerator 60
gonadotropin*2,c on days 1, 3 and 7, days. If a second egg is
500-1000 IU/kg IM laid, repeat dose on day
3; if a third egg is laid,
repeat dose on day 7
Levonorgestrelh — Not recommended
Medroxyprogesteronea — Not recommended
Tamoxifenf 2 mg/kg PO QD Leukopenia
Arginine vasotocin 0.01-1.0 mg/kg IM Stable in standard
freezer
PGE (Prepidil Gel)g 0.025 ml/100 g May freeze into aliquots Fig 18.1| Ventrodorsal radiograph of a
0.2 mg/kg and thaw prior to budgerigar hen with polyostotic hyperostosis.
applied topically administration; relaxes Note the increased density of both femurs.
uterovaginal sphincter
while inducing uterine
contractions
PGF2alpha (Lutalyse) 0.02-1.0 mg/kg IM Does not relax utero-
lems should be corrected to improve the hen’s dietary
vaginal sphincter when plane to reduce the severity of metabolic drain.31,53,63
inducing uterine
contractions Dietary alteration and reduction of caloric intake does
Topically Applied to prolapsed appear to anecdotally reduce or stop egg production.
uterine tissue to stop
hemorrhage and shrink This nutritional effect is often achieved by converting
tissues the pet bird from a seed-based diet to a formulated one.
*1 Ed. Note: 1000 mg/kg has been used in recalcitrant cases. The exact reason for this effect is unknown, but it is
*2 Ed. Note: Should be administered with dexamethasone to avoid what
appears to be immune-based response to HCG. Can be given with common practice in poultry to reduce feed intake to
leuprolide acetate.
stop egg production and induce molting.56 Surgical salp-
ingohysterectomy may be elected or necessary if medical
the enclosure. Access to nesting environment or materi- therapy is not successful and if there is no intent to
als such as a box, other dark cavities, or shredded breed the particular hen. Laparoscopic salpingohysterec-
papers should be prohibited. In the event that a pet bird tomy may be performed as a preemptive measure on
is showing nesting behavior and laying eggs in a desig- juvenile birds to prevent egg production and its associ-
nated site, removal of eggs from the “nest” should be ated diseases. Any secondary disease conditions also
avoided for the normal incubation period for each should be appropriately treated.6,59,71
species to discourage the hen from laying further eggs to
replace those removed. Any perceived or actual mate
should be removed from the cage or room. In some
POLYOSTOTIC HYPEROSTOSIS
species such as the cockatiel, visual and auditory separa- Polyostotic hyperostosis differs from physiologic osteo-
tion from an actual or perceived mate may be necessary. myelosclerosis in that the latter condition occurs in non-
A “one-person bird,” which has a single household per- laying hens and cocks as a result of pathologic condi-
son who exclusively or primarily handles and cares for tions. Typically, radiographs reveal significantly increased
it, should potentially be viewed as having a “mate rela- bone density of the long bones and occasionally the ver-
tionship” with that person. This may serve as a trigger tebrae (Fig 18.1). The pathogenesis of polyostotic hyper-
for reproductively driven behaviors. Stimulatory petting ostosis is still unclear. Many affected birds exhibit con-
such as rubbing the pelvis, dorsum and cloacal regions current reproductive-associated activity or may suffer
and kissing the beak should be avoided. Feeding calori- from reproductive-associated disease conditions. In addi-
cally dense diets should be avoided, as mentioned previ- tion, increased medullary bone density does appear to
ously. Interactive behaviors that simulate a “flock rela- resolve radiographically with resolution of reproductive
tionship” should be encouraged such as the bird being drive or disease. Hepatic disease may play a role in this
handled by several people in the household. The cage condition due to the liver’s role in the inactivation of
location and furniture (toys, perches, food dishes) estrogen. However, a recent study does not support this
should be changed and rotated periodically to discour- theory, stating that budgerigars affected by polyostotic
age territorial behavior and limit reproductive drive in hyperostosis had no evidence of estrogen secretion or
response to a perceived “nest site.” Any nutritional prob- other endocrine disease.5,29,58,74
Figs 18.2a,b | Left lateral and ventrodorsal

radiographs of a 3-year-old egg-bound cockatiel.
The hen had been consuming a seed diet and was Fig 18.3 | Coelomic ultrasound of the same cock-
unable to perch for several days prior to presenta- atiel. Note the well-calcified egg in normal presen-
tion. The bird was thin (68 g), dehydrated and tation for oviposition (7.5-MHz probe).
hypocalcemic (6.2 mg/dl), and responded to sup-
portive care and arginine vasotocin. Egg produc-
tion was controlled after egg expulsion with
leuprolide acetate (750 µg/kg IM every 14 days for 3 injections) and alteration
of environmental stimuli. Diet was modified to include a 90% formulated diet.
EGG BINDING AND DYSTOCIA cia vary according to severity, size of the bird affected and
degree of secondary complications. Common signs
Egg binding is defined as the failure of an egg to pass
include acute depression, abdominal straining, persistent
through the oviduct within a normal period of time.
tail wagging, a wide stance, failure to perch, abdominal
Most companion birds lay eggs at intervals of greater
distension, dyspnea, and/or sudden death (Fig 18.3). An
than 24 hours, and individuals may vary further. This
egg lodged in the pelvic canal may compress the pelvic
variability may make it difficult to determine if there is a
blood vessels, kidneys and ischiatic nerves, causing circu-
problem in the early stages of this disease. Dystocia
latory disorders, lameness, paresis or paralysis. Pressure
involves the mechanical impedance to oviposition. The
necrosis of the oviductal wall may occur. Dystocia may
most common anatomic areas for this to occur are the
cause metabolic disturbances by interfering with normal
distal uterus, vagina and vaginal-cloacal junction.31,63,73
defecation and micturition, and cause ileus and renal dis-
Causes of egg binding may include chronic egg laying, ease, respectively. The severity of the patient’s condition
oviductal muscle dysfunction secondary to excessive egg can be estimated by the degree of depression and the
laying, calcium metabolic disease, vitamin E and sele- length of time clinical signs have been present.31,63,73
nium deficiencies, malnutrition, obesity, inadequate
Diagnosis of egg binding or dystocia in a severely com-
exercise and muscle strength, malformed eggs, mechani-
promised patient may be made based on history and
cal tears or damage to the oviduct, oviductal infections,
physical examination alone, and the patient may not be
systemic disease, genetic predisposition and environ-
stable enough to survive other diagnostic procedures.
mental stressors. Dystocia also may result when a devel-
Rapid diagnosis and therapy are crucial for a successful
oping egg in the distal oviduct obstructs the cloaca or
outcome. Physical examination may reveal depression,
causes oviductal tissue to prolapse. Oviductal torsion
lethargy, a thin or normal body condition, and dehydra-
and oviductal or abdominal masses compressing the
tion. There may be dyspnea or an increased respiratory
oviduct also may obstruct passage of an egg and result
rate due to compression of the caudal thoracic and
in dystocia. Breeding birds out of their natural season,
abdominal air sacs. The hen may not be able to perch,
egg-producing virginal hens and hens with a persistent
and may demonstrate pelvic limb paresis, paralysis or
right oviduct may be predisposed to egg binding or
cyanosis. An egg typically, but not always, is palpable in
dystocia.31,63,73
the caudal abdomen. Cranially located, soft-shelled and
non-shelled eggs may not be detected on abdominal pal-
Diagnosis pation. Palpable eggs may be located within the oviduct
Cockatiels, lovebirds, canaries and finches are most com- or ectopically within the coelom, and careful abdominal
monly reported to be affected and seem to present with palpation, cloacal examination, radiographs, coelomic
more severe clinical signs, possibly due to their small ultrasound, laparoscopy and/or laparotomy may be
size. Clinical signs associated with egg binding and dysto- required to determine the egg’s position.31,63,73
527
Fig 18.4a | Ventrodorsal radiograph of an eclectus Fig 18.4b | Ultrasound of the same bird
hen with a history of depression and inappetence. revealed a non shelled egg cranial to the shelled
Physical examination revealed a distended abdomen egg noted on the radiograph in Fig 18.4a.
and palpable egg in the coelom. Radiographs revealed
a calcified egg in the mid coelom.
Radiography and ultrasonography aid in evaluation of the Broad-spectrum antibiotics are indicated if it is suspected
position and characterization of the egg(s). There may be that the integrity of the oviduct has been compromised.
multiple eggs identified in the coelom due to an obstruc- Analgesics are indicated if the patient appears to be in
tion distally or secondary to motility disorders. Radio- pain or if clinical knowledge of the patient’s condition
graphs may reveal an egg in the coelom if the egg has a suggests that pain may be a part of the pathologic state.
visible shell. The egg is typically located in the distal ovi- Supportive care alone is often enough to allow oviposi-
duct, in the region of the uterus (see Figs 18.2a,b, Fig tion, although the hen should be monitored closely for
18.3). Osteomyelosclerosis of the femurs, tibiotarsi, radii, deterioration of her condition, which may require further
ulnas and/or spine may be visible, and a soft tissue den- intervention.40,63,73
sity suggestive of an enlarged ovary in the region of the
ovary may be noted, and is supportive of a reproductively Prostaglandin and hormonal therapy may be used to
active hen. A coelomic ultrasound will often reveal an induce oviductal contractions. This may result in expul-
egg and may identify soft-shelled or non-shelled egg(s) sion of the egg if the contractility of the oviduct is suffi-
that may not be identifiable on radiographs (Figs cient to expel the egg, the uterus is intact, the egg is
18.4a,b). Again, there may be several eggs visible within within the oviduct, and there is no obstruction such as a
the coelom. Follicles may be visible on the ovary, indicat- neoplastic mass, granuloma or egg adhered to the
ing the potential for further ovulation and egg formation. oviduct. Studies performed in poultry have found that
A hematologic analysis and serum chemistries are useful prostaglandin E2 (PGE2) and prostaglandin F2alpha
to identify any predisposing and secondary diseases. A (PGF2alpha) bind at specific receptor sites in the uterus
complete blood count may reveal a leukocytosis with a and vagina. The uterine myometrium appears to prefer-
relative heterophilia if there is a concurrent inflammatory entially bind PGF2alpha because it contains low-affinity
or infectious process. Serum chemistries may demon- and some high-affinity binding sites for PGE2 and spe-
strate elevated aminotransferase and creatinine phospho- cific high-affinity for PGF2alpha. Prostaglandin F2alpha
kinase due to skeletal muscle enzyme leakage from tissue binds at the shell receptor sites to cause a time- and
damage, or as a result of reduced food consumption and dose-dependent mobilization of cellular calcium in the
a hypermetabolic state. Hypercholesterolemia, hyperglob- presence of extracellular calcium, thereby causing uter-
ulinemia are supportive of an ovulating hen. Elevated ine muscle contraction. It has been demonstrated in
total and ionized calcium may be indicative of a cycling vitro that PGE2 is itself ineffective in calcium ion mobi-
hen. Hypocalcemia may be observed if a hen has been lization, but will enhance PGF2alpha-induced calcium
consuming a calcium-poor diet or has been laying exces- mobilization. This suggests that PGE2 may potentiate the
sive numbers of eggs, resulting in depletion of calcium
ability of PGF2alpha to cause uterine contraction. In the
stores31,40,60,73 (see Chapter 5, Calcium Metabolism).
vagina, high-affinity binding sites for PGE2 predominate.
It is possible that a high PGE2 concentration in the
Treatment vagina is needed to saturate high-affinity binding sites
Therapy varies with history, severity of clinical signs and and block PGF2alpha-binding sites. This allows for relax-
diagnostic test results. Supportive care should include ation of the uterovaginal sphincter and vagina. Due to
elevated environmental temperature, parenteral calcium the fact that fewer PGE2 high-affinity binding sites are
(only if indicated), fluid therapy and nutritional support. present in the uterus, they are not likely to interfere
with PGF2alpha binding and may potentiate the action

of PGF2alpha.27,28,63,67,68
When an egg is present in the uterus, the administration

of PGF2alpha and PGE2 will cause the concentration of
arginine vasotocin (AVT) to increase in systemic circula-
tion, however, PGF2alpha is the more potent stimulator
of AVT release. It is suggested that prostaglandins stimu-
late uterine contractions, which in turn stimulate the
release of AVT from the neurohypophysis, and that AVT
probably acts synergistically with PGF2alpha to increase
uterine contractions. Oxytocin and AVT appear to specif-
Fig 18.5 | Transabdominal ovocentesis and aspiration of egg
ically affect the uterus, inducing contractions. It is contents in a 7-year-old egg-bound cockatiel. Patient was anes-
important to note that PGF2alpha, oxytocin and AVT do thetized with isoflurane by mask induction. A 22-gauge needle
not cause relaxation of the uterovaginal sphincter while and 3-ml syringe were used to aspirate approximately 1 ml of
egg contents. The shell was passed approximately 4 hours pos-
inducing oviductal contractions. This may result in peri-
tovocentesis. Complete passage of the shell was confirmed by
stalsis of the egg, severe pain and/or rupture of the radiography.
uterus. Prior to their use it should be determined if the
uterovaginal sphincter is open. In addition, prosta-
motion. Potential complications may include retroperi-
glandin and hormonal therapy does require adequate
stalsis of the egg out of the oviduct into an ectopic posi-
calcium to be effective. As many of these patients are
tion within the coelom, rupture of the egg, oviductal
severely hypocalcemic due to either malnutrition or
trauma, oviductal laceration, oviductal avulsion, hemor-
chronic egg laying, supplemental calcium may be
rhage, and displacement of the egg or fragments into an
required prior to administration of these medica- ectopic position. If fertilization may have occurred and
tions.27,28,63,67,68 the egg may be fertile, it may be incubated if successfully
removed intact.31,63,73
PGE2 gelg may be applied to the uterovaginal sphincter
at a dose of 0.1 ml per 100-g bird. PGE2 causes relax- Ovocentesis may be performed to facilitate passage of an
ation of the uterovaginal sphincter while causing oviduc- egg. Aspiration may be performed through the cloacal
tal contractions and may be applied topically, thereby opening if the egg is distally located, or transabdominally
decreasing the incidence of systemic side effects. These if the egg is more cranially positioned. The egg is manip-
contractions may expel the egg within 15 minutes. ulated so that it is visible through the cloaca and a needle
Contact with PGE2 gel may cause altered menses and is inserted into the egg through the cloaca. The contents
induce spontaneous abortion in women. Therefore, it is of the egg are aspirated into a syringe, while the shell is
important to flush any excess from the cloaca after egg manually collapsed and the pieces expelled through the
expulsion, and to caution staff and clients regarding cloaca. (see Chapter 7, Emergency and Critical Care and
contact with any stool and/or urine produced. Prosta- Chapter 24, Diagnostic Value of Endoscopy and Biopsy).
glandin F2alpha, oxytocin and AVT also will cause If the egg cannot be visualized through the cloaca due to
powerful uterine contractions. Prostaglandin F2 alpha is a more cranial location, transabdominal ovocentesis may
administered parenterally, rather than locally, and is be performed (Fig 18.5). The egg is manually placed
more likely to cause systemic reactions such as hyper- directly against the abdominal wall so that other abdomi-
tension, bronchoconstriction and general smooth- nal organs are displaced and not damaged during aspira-
muscle stimulation.27,28,63,67,68 tion. A needle is inserted through the skin and abdomi-
nal wall into the egg. The egg contents are aspirated into
If supportive care and medical therapy fail to induce the syringe while the egg is manually collapsed. The
oviposition, then manual manipulation may be necessary. eggshell remnants are expelled through the cloaca, either
Massaging the abdomen and vaginal opening may relax naturally or with clinical assistance. It is important to
the vaginal sphincter and allow passage of the egg. It may confirm radiographically that these eggshell pieces have
be helpful to infuse lubricants into the cloaca to moisten been completely expelled. If these pieces are not
the tissues. Careful digital pressure applied to the cranial expelled within a reasonable amount of time, approxi-
portion of the egg and directed caudally may encourage mately 36 hours, it may be necessary to irrigate the
movement through the distal oviduct and cloaca. Using a oviduct through the cloaca or laparotomy approach. A
cloacal speculum, the vaginal opening of the oviduct can salpingohysterectomy may be performed if egg remnants
be dilated by inserting a blunt probe (eg, lubricated cot- are retained and the hen is not required for breeding.
ton-tipped swab) that is gently advanced in a twirling
529
Some clinicians advocate flushing the uterus postoviposi-

tion with saline, chlorhexidine or iodine to remove any
shell fragments and decrease the incidence of metritis.
Oviductal rupture, resulting in an ectopic egg, shell frag-
ments and yolk coelomitis, are possible complications of
ovocentesis.8,31,63,73 See Chapter 24, Diagnostic Value of
Endoscopy and Biopsy.
Prostaglandin treatment, manual delivery and ovocente-

sis are contraindicated in cases of ectopic eggs, oviductal
rupture, oviductal torsion and mechanical obstruction.
Complications that may require surgical intervention
include oviductal rupture with or without an ectopic
egg, oviductal necrosis, oviductal torsion, abdominal Fig 18.6 | Uterine prolapse, including partial prolapse of the
hernia or if the condition is interfering with defecation vagina and cloaca, in a 7-year-old cockatiel with a history of
chronic egg laying. Samples of affected tissues were taken for
and/or micturition. Medical therapy to reduce reproduc-
bacterial culture and sensitivity. Prolapsed tissues were irrigated
tive hormone levels and reproductive activity should be with sterile saline, dimethyl sulfoxide was applied and tissues
utilized to temporarily prevent further egg production. were reduced manually. Therapy included supportive care,
Surgical removal of an egg is required in cases of ectopic enrofloxacin (15 mg/kg PO q 12 h x 14 days), carprofen (2
eggs and dystocia, including oviductal rupture, oviductal mg/kg PO q 12 h x 3 days). Further egg production was con-
trolled with leuprolide acetate (750 µg/kg IM every 14 days for
torsion, or mechanical obstruction, or if medical treat- three injections) and alteration of environmental stimuli.
ment is not successful. If surgical intervention is neces-
sary, bacterial culture and sensitivity and histopathology
should be performed on oviductal tissue samples. clearing any bacterial infection and preventing further
Salpingohysterectomy may be considered to prevent fur- prolapse. It also is important to decrease reproductive
ther reproductive complications, and any predisposing hormone levels to prevent further egg formation,
and secondary diseases should be corrected.6,24,40,63,73 decrease the size of oviductal tissue and allow the repro-
ductive tract to rest. Broad-spectrum antibiotics and
OVIDUCTAL PROLAPSE anti-fungals should be initiated while bacterial and fun-
gal cultures are pending.8,31,63,69,73
Oviductal prolapse may occur secondary to any condi-
tion that causes chronic, excessive abdominal straining Salpingohysterectomy may be considered to prevent
such as normal physiologic hyperplasia, egg laying or recurrence. Predisposing factors should be corrected to
dystocia. An intracoelomic space-occupying mass also prevent recurrence and secondary diseases addressed
may induce prolapse of the oviduct. Predisposing factors (see Chapter 35, Surgical Resolution of Soft Tissue
may include abnormal or soft-shelled eggs, malnutrition, Disorders).
obesity, salpingitis and cloacitis. Typically, the uterus pro-
trudes through the cloaca, often with a partial prolapse
of the vagina and cloaca (Fig 18.6).31,63,73 UTERINE TORSION
Uterine torsion is usually diagnosed in the later stages
Rapid management is necessary to prevent necrosis of of the disease. Birds typically present with abdominal
these tissues. Any egg that may be present should be distension secondary to coelomitis. Early clinical signs
removed, all exposed tissues cleaned, irrigated and kept may include depression and anorexia following recent
well moistened to prevent desiccation. Topical anti- oviposition. A complete blood count often demonstrates
inflammatories such as dimethyl sulfoxide may be a leukocytosis with a relative heterophilia, and serum
applied, any lacerations should be repaired and all tis- chemistries show an elevated aspartate transferase
sues should be gently replaced. Temporary stay sutures and creatinine kinase. Diagnosis is usually made at
may be indicated to aid in preventing recurrence, as pro- exploratory laparotomy or laparoscopy. Many times,
lapse of the oviduct may recur and repeated replace- severe vascular compromise and necrosis of the oviduct
ment is often required. Bacterial culture and sensitivity is found, which requires salpingohysterectomy.1,6,24,71,73
of the prolapsed tissue should be performed to aid in
appropriate antibiotic therapy. Complete blood count,
serum chemistries, radiographs, ultrasonography and OVIDUCTAL IMPACTION
laparoscopy should be included in a complete diagnos- Oviductal impaction may occur following salpingitis,
tic evaluation to identify any predisposing and second- metritis or dystocia. Impactions may occur due to excess
ary disease conditions. Treatment should be directed at mucin or albumin, secondary to cystic hyperplasia of the
oviduct. Inspissated egg material also may cause obstruc- within the uterine portion of the oviduct. Metritis may
tion. Clinical signs may be vague and can include cessa- occur secondary to dystocia, egg binding, oviductal
tion of egg production, broody behavior without egg impaction, systemic bacterial infection and ascending
production, weight loss, anorexia, depression, constipa- infection. Salpingitis and metritis may cause abnormal
tion, diarrhea, abdominal distension, and reluctance to shell formation and impaired uterine contractions, and
walk or fly. A tentative diagnosis is made through history, may cause infections in chicks and embryos including
physical examination and supporting diagnostic tests. A embryonic death. Fatalities are often associated with
leukocytosis with or without a relative heterophilia may ovulation, egg binding or dystocia, oviductal rupture,
be noted. Serum chemistries may be supportive of an coelomitis and septicemia.8,63,73,75
ovulating hen. Radiographs and coelomic ultrasound
Clinical signs of salpingitis and metritis may be vague
may demonstrate a soft tissue density in the region of
and difficult to detect initially. In pet birds, these include
the oviduct, displacement of other coelomic viscera, loss
decreased egg production, infertility, abnormally shaped
of coelomic visceral detail or coelomic fluid if there is a
eggs and mild depression. More advanced cases may
concurrent coelomitis. Definitive diagnosis of oviductal
exhibit anorexia, lethargy, abdominal distension, oviduc-
impaction is often made at laparoscopy or laparotomy,
tal rupture, coelomitis and septicemia. There may be a
revealing an abnormal-appearing, enlarged oviduct with
leukocytosis with a relative heterophilia. Serum chem-
or without coelomitis and adhesions. In many cases, it is
istries may or may not be supportive of an ovulating
necessary to clean and repair or surgically remove the hen. Radiographs and ultrasonography may reveal an
oviduct. Surgery may be complicated if coelomic fluid enlarged oviduct. Laparoscopy may or may not identify
and/or adhesions are present.6,24,31,40,63,69,73 inflammation of the serosal surface of the oviduct. The
oviduct may be thin-walled, decreased in length or have
Bacterial culture and sensitivity should be performed on
vascular congestion. The lumen may contain fluid or fib-
specimens from the affected oviduct, and histopatho-
rinous exudates. Definitive diagnosis of salpingitis and
logic examination should be performed on biopsy sam-
metritis is based on cytology, bacterial and fungal cul-
ples. Treatment includes parenteral fluids, nutritional
ture and sensitivity, and biopsy with histopathologic
support, warmth and broad-spectrum antibiotics, pend-
analysis of a specimen from the oviduct.8,24,40,63,73
ing culture and sensitivity results. Medical or surgical
therapy to reduce reproductive hormone production Therapy of salpingitis and metritis is focused on correct-
and reproductive activity should be initiated, and envi- ing any underlying or contributing causes. Antibiotic
ronmental stimuli altered as discussed with chronic egg therapy for identified or suspected bacterial organisms
laying, to prevent recurrence. should be initiated pending results of bacterial culture
and sensitivity. Pharmacologic treatment and husbandry-
SALPINGITIS AND METRITIS related intervention, as discussed with chronic egg lay-
Salpingitis is defined as inflammation of the oviduct ing, should be initiated to prevent further hormonal
stimulation with subsequent egg production, which may
either by an infectious or non-infectious etiology, the
perpetuate or contribute to this disease. There should
latter being far less commonly reported. It is generally
be close follow-up including bacterial culture and sensi-
seen associated with airsacculitis, liver disease, pneumo-
tivity and fertility monitoring after treatment, as many
nia, systemic infections, and ascending infections of the
cases are difficult to resolve completely. It is important
oviduct from the uterus or cloaca. Excessive abdominal
to note that bacteria isolates from the cloaca are not
fat has been associated with salpingitis in domestic fowl.
equivalent to oviductal infectants, and cloacal bacterial
Some of the most commonly identified pathogens are
cultures should be interpreted carefully. Severe refrac-
Escherichia coli, Salmonella, Mycoplasma, Pasteurella
tory cases may require laparotomy to remove necrotic
and Streptococcus spp. Newcastle disease also has been
tissue and flushing of the oviduct with fluids and antibi-
associated with salpingitis in several species. In ground-
otics. Patients suffering from severe salpingitis may
nesting species such as Anseriformes and emus, non-
require salpingohysterectomy, or this may be elected in
lactose-fermenting, gram-negative bacteria such as
milder cases to resolve disease and prevent recurrence if
Pseudomonas aeruginosa, Proteus mirabilis and
the hen is not intended for breeding.6,63,71,73
Proteus vulgaris are commonly identified. Noninfectious
causes of salpingitis include trauma and inflammation
secondary to oviposition disorders, malnutrition and
CYSTIC HYPERPLASIA
OF THE OVIDUCT
foreign bodies. Salpingitis is most common in adult hens
but may occasionally occur in young birds as well.8,63,73,75 Cystic hyperplasia of the oviduct may occur from
improper formation of the left oviduct or secondary to
Metritis is a localized infection or inflammatory process an endocrine abnormality. Additionally, the vestigial right
531
Fig 18.8 | Coelomic ultrasound of an 8-year-old

African grey parrot. The patient had a history of
depression and inappetence. Physical examination
Fig 18.7 | Coelomic ultrasound. An ectopic egg and uterine revealed abdominal distension. Note the coelomic
laceration were noted on laparotomy, and a salpingohysterec- fluid and large ovarian cyst (7.5-MHz probe).
tomy performed. Note the calcified egg in the caudal coelom
and the ovum located more cranially (7.5-MHz probe). This
ovum could not be detected on the radiographs. The hen recov-
ered fully.
oviduct may become cystic and the associated ovary often anorexia, and abdominal distension secondary to
has cystic changes as well. Cystic hyperplasia often con- coelomitis or the deposition of egg or oviductal con-
tributes to salpingitis and egg binding. Clinical signs may tents. Radiographs and ultrasonography may reveal
include depression, anorexia, abdominal distension, osteomyelosclerosis, polyostotic hyperostosis, a soft
ascites and dyspnea. A tentative diagnosis is made tissue density in the region of the ovary, ovarian follicles,
through history, physical examination and supporting an enlarged or cystic oviduct, a shelled or non-shelled
laboratory tests, similarly to that of salpingitis and metri- egg, and coelomic fluid if a concurrent coelomitis is
tis. Radiographs may demonstrate an enlarged soft tissue present (Figs 18.7, 18.8). Diagnosis is confirmed at
density in the region of the oviduct. Ultrasonography may laparoscopy or laparotomy. The laceration may be
reveal an enlarged oviduct that may be fluid-filled or have repaired, depending on the integrity of the tissue,
obvious cysts present, with or without concurrent ovarian or salpingohysterectomy may be performed as a thera-
follicles or cysts. Laparoscopy may show a dilated oviduct peutic and preventive technique.6,24,31,40,63,73
filled with a white or brown mucoid fluid. Definitive diag-
nosis requires laparotomy with biopsy, cytology, histopath-
ECTOPIC OVULATION
ology, and bacterial culture and sensitivity.8,24,31,40,63,73
Ectopic ovulation may result from failure of the infun-
Therapy to stop ovulation should be initiated due to dibulum to retrieve an ovulated ovum, reverse peristalsis
increased risk of oviductal rupture during ovulation, of the oviduct or oviductal rupture. Ectopic ovulation
oviposition and possible hormonal contribution to the does not necessarily result in coelomitis. Internal laying
cystic state of the oviduct. If bacterial infection is sus- is actually a common occurrence in many avian species,
pected or documented by cytology and bacterial culture and the ova are usually resorbed without any problems
and sensitivity, appropriate antibiotic treatment is indi- whatsoever. Reverse peristalsis may be triggered by
cated. Salpingohysterectomy may be required to resolve obstruction of the oviduct, cystic hyperplasia, neoplasia,
the current problem or prevent future recurrences and malnutrition, trauma and stress. The ectopic ova may be
should be considered if the hen is not intended for resorbed without incident or may induce a severe
breeding, as complete resolution with medical therapy coelomitis.30,31,56,63,73
alone may be difficult.6,8,31,63,73
Clinical signs of ectopic ovulation may include transient
or persistent depression, inappetence and abdominal
OVIDUCTAL RUPTURE distension, especially if there is an associated coelomitis.
Oviductal rupture may occur secondary to dystocia or There may be a leukocytosis with a mature heterophilia.
oviductal disease. Prostaglandins, oxytocin, arginine Serum chemistries may demonstrate an ovulating hen.
vasotocin and ovocentesis may cause traumatic rupture Radiographs may reveal polyostotic hyperostosis and
of the oviduct. Clinical signs may include depression, one or multiple eggs in the abdomen. It is important to
Greg J Harrison
Fig 18.10 | Laparoscopic examination of
the African grey hen in Fig 18.8. Note the
Fig 18.9 | A cockatiel hen with a history of egg laying 3 months two ovarian cysts and several smaller follicles.
previous is showing depression and dyspnea. Note the severely
distended abdomen. Diagnosis was cystic ovarian disease.
note that an ectopic ova detected by ultrasound in the coelomic viscera. Ultrasound may reveal a fluid-filled
absence of clinical signs may resolve on its own with no cyst(s) in the area of the ovary or simply coelomic fluid
treatment, and any medical or surgical intervention may of an undetermined source. An ovarian cyst may be quite
be contraindicated. It may be difficult or impossible to large and may actually fold onto itself as it grows. There
determine if an egg is located within the oviduct or is may be normal ovarian follicles present as well (Fig
ectopic without laparoscopy or laparotomy, depending 18.10). Abdominocentesis with cytology and bacterial cul-
on its location within the coelom. If the egg is not laid ture and sensitivity should be performed in those patients
within a reasonable time period and/or the patient’s suffering from associated coelomitis. It is beneficial and
condition is declining, a laparotomy is indicated as an often necessary to perform a laparoscopic exam or
exploratory procedure. Ectopic eggs are removed by celiotomy with ovarian biopsy, especially for those
laparotomy, and any oviductal tear should be surgically patients with cysts that do not resolve with medical ther-
repaired or a salpingohysterectomy performed. Cytology, apy, as it is not uncommon for hens to develop ovarian
culture and sensitivity, and histopathology should be cysts secondary to neoplasia and oophoritis. Laparoscopy
performed in cases of oviductal rupture, cystic hyperpla- will reveal an ovarian cyst(s), and the contents may be
sia and neoplasia.8,31,40,63,73 aspirated during this procedure. Cytology of fluid aspi-
rated from these cysts is clear to straw-colored and of
low cellularity. However, it is important to practice
CYSTIC OVARIAN DISEASE
extreme caution during a laparoscopic exam and aspira-
Ovarian cysts have been known to occur in several pet tion, as fluid from the cyst or coelom may gain access to
bird species including cockatiels, canaries, budgerigars, the respiratory system through the entry hole in the
macaws, pheasants and domestic ducks. Cyst develop- abdominal air sac. Ovarian biopsy with cytologic analysis,
ment may be caused by endocrine disorders, anatomic histopathologic exam, and bacterial culture and sensitiv-
abnormalities on the ovary itself and pathologic condi- ity should be performed to identify any primary or sec-
tions of the ovary. A thorough history may reveal current ondary disease processes.14,40,63,73
or previous egg production, with an abrupt halt. Owners
may even report chronic reproductive behavior without Treatment goals include resolution of the cyst(s) and asso-
egg production or impaired reproductive performance ciated disease conditions such as coelomitis, oophoritis,
in breeding hens.8,14,73 ovarian granuloma and neoplasia. Abdominocentesis often
improves related dyspnea if there is coelomic fluid com-
Advanced cystic ovarian disease may cause depression, pressing the air sacs. Pharmacologic, behavioral, environ-
inappetence and weight loss. Abdominal distension, often mental and dietary intervention to reduce ovarian activity
due to secondary coelomitis, and related clinical signs are indicated as production of reproductive hormones
may be noted as well (Fig 18.9). A leukocytosis with a rel- may perpetuate ovarian cysts.14 Aspiration of cysts, salpin-
ative heterophilia, as well as a peripheral hypercalcemia, gohysterectomy and partial ovariectomy may be beneficial
hyperglobulinemia and hypercholesterolemia are com- for complete resolution.6,8,60,63,73 Cryosurgical destruction
mon findings. Radiographs may demonstrate polyostotic may be beneficial. Long-term resolution may be difficult
hyperostosis, a soft tissue density in the area of the ovary and patients suffering from cystic ovarian disease should
and/or oviduct, coelomic fluid and displacement of be regularly monitored for recurrence.8,14,63,73,78
533
Fig 18.12 | Coelomic ultrasound of the cockatiel

hen from Fig 18.11. Note the coelomic fluid and soft
Fig 18.11 | Ventrodorsal radiograph of a tissue density. Laparotomy revealed an oviductal
cockatiel hen with reproductive-associated granuloma, and the hen recovered fully in response
coelomitis. Note the severely enlarged to salpingohysterectomy and antibiotic therapy.
fluid/soft tissue density, cranial displacement
of the grit-filled ventriculus, obliteration/com-
pression of caudal thoracic and abdominal air
sacs, and increased density of both femurs.
REPRODUCTIVE-ASSOCIATED demonstrate polyostotic hyperostosis, soft tissue density

COELOMITIS in the region of the ovary and/or oviduct, coelomic fluid,
Reproductive-associated coelomitis may encompass egg abdominal and caudal thoracic air sac compression, or
yolk coelomitis, (previous egg related peritonitis) ectopic even an obvious shelled or non-shelled egg, or egg rem-
ovulation-associated coelomitis and septic coelomitis. nants leading to oviductal granuloma (Fig 18.12).
Coelomitis may be found in association with other dis- Contrast radiography may be helpful to illustrate organ
eases such as malnutrition, metabolic disorders and sys- displacement and locate any suspected space-occupying
temic infections. Cystic ovarian disease, salpingitis, metri- mass. Ultrasound may reveal coelomic fluid, ovarian folli-
tis, cystic hyperplasia, oviductal rupture, oviductal and cle(s), ovarian cyst(s), an ovarian mass, and oviductal
ovarian granulomas, septicemia, intestinal rupture and masses such as granuloma or neoplasia (Figs 18.13a,b).
neoplasia may cause associated coelomitis as well.8,31,73 Cytology of coelomic fluid may demonstrate a septic or
non-septic exudate, a transudate, or yolk or fat globules
Tentative diagnosis of reproductive-associated coelomitis if such material is present. Bacterial culture and sensitiv-
is made through history, physical examination and sup- ity should be performed on samples of coelomic fluid.
porting laboratory tests. The hen may have a history of Laparoscopy and/or laparotomy may be necessary to
egg production, which may have abruptly stopped. identify the causative etiology of coelomitis.8,31,40,63,73
Clinical signs may include transient or persistent depres-
sion, lethargy and inappetence. Patients with more Treatment of reproductive-associated coelomitis varies
advanced disease may suffer from weight loss, abdominal with type and severity of clinical signs. Many birds
distension, and dyspnea associated with coelomic fluid respond well to supportive care alone. Abdomino-
and air sac compression (Fig 18.11). It is important to centesis is not only supportive of diagnosis but thera-
note that not all patients with coelomitis will have identi- peutic as well, to relieve dyspnea due to air sac com-
fiable fluid present. Supportive diagnostic tests include a pression. Broad-spectrum antibiotics should be initiated
complete blood count, serum chemistries, radiographs, in cases of suspected or confirmed infectious coelomitis
coelomic ultrasound and analysis of any fluid recovered while waiting for sensitivity results on fluid obtained
from abdominocentesis including cytology, culture and from abdominocentesis. Corticosteroids may be indi-
sensitivity. A leukocytosis with a relative heterophilia, as cated in cases where an infectious etiology has been
well as a peripheral hypercalcemia, hyperglobulinemia excluded, but should be used judiciously due to poten-
and hypercholesterolemia compatible with pre- and tial serious side effects. Pharmacologic therapy may be
immediate postovulation may be noted. Many birds will used to stop further ovulation, reproductive hormone
actually be hypocalcemic due to calcium depletion subse- production and to reduce the size of the reproductive
quent to malnutrition or chronic egg laying. Some birds tract, which may perpetuate this condition.
may have egg yolk visible in their peripheral blood
smears as well as above the buffy coat in separated blood Once the coelomic fluid has decreased and the patient
samples and lipemia is common. Radiographs may is stable, it is beneficial to perform a laparoscopic
Figs 18.13a,b | Left lateral and ventrodorsal views of a 6-

year-old male budgerigar with a Sertoli cell tumor. Note the soft
tissue mass in the midcoelom and polyostotic hyperostosis of the
long bones.
examination. This allows direct visualization of the culture and sensitivity should be performed on fluid
ovary, oviduct and other organs to help confirm etiology recovered. Laparoscopy may demonstrate an enlarged,
such as a cyst, granuloma and/or tumor. Cytology and abnormal-appearing ovary, which may have associated
biopsy with histopathologic examination, and bacterial hypervascularization. Persistent or chronic oophoritis
culture and sensitivity should be performed on abnor- may progress to granulomatous disease, which may be
mal tissue. A celiotomy with or without a salpingohys- evident on ultrasound, laparoscopy and laparotomy.
terectomy may be necessary to biopsy or remove a mass, Definitive diagnosis is based on ovarian biopsy with
cystic oviduct or remove inflammatory debris from the histopathologic examination along with bacterial culture
abdomen, particularly if medical therapy alone is not and sensitivity.8,31,40,63,73
effective. It is important to note that during laparoscopy
Treatment of oophoritis includes broad-spectrum antibi-
or laparotomy there is a risk of fluid gaining access to
otics, pending sensitivity results. Egg binding is handled
the respiratory system via the incision through the
as previously described. As discussed for chronic egg lay-
abdominal air sacs, and often there are significant adhe-
ing, pharmacologic therapy to temporarily stop ovulation
sions between the oviduct and neighboring viscera due
should be initiated, as it does appear clinically that ovula-
to chronic inflammation.8,31,63,73
tion may perpetuate inflammation of the ovary. Laparo-
scopic exam, bacterial culture and sensitivity, and com-
OOPHORITIS plete blood count should be repeated until culture
Inflammation of the ovary results from neoplastic, results are negative and any leukocytosis has resolved.
mechanical or infectious causes. Infectious oophoritis Reproductive performance and general condition should
often occurs as a result of spread from adjacent organs or be carefully followed, as complete resolution may be dif-
septicemia, and is frequently bacterial in origin. Clinical ficult. Partial ovariectomy, usually performed with salpin-
signs may be vague and include anorexia, weight loss, gohysterectomy, may be beneficial in refractory cases if
depression, cessation of egg production, egg binding and the hen is not intended for breeding.8,31,63,73
sudden death. A diagnosis of oophoritis is made through
history, physical examination, radiography, ultrasonogra- OVARIAN AND OVIDUCTAL
phy, abdominocentesis with coelomic fluid analysis, NEOPLASIA
laparoscopy, laparotomy, and biopsy of the ovary with Ovarian and oviductal neoplasia is most commonly seen
bacterial culture and sensitivity and histopathologic in the budgerigar (Melopsittacus undulatus), cockatiel
analysis. Hematology may demonstrate a leukocytosis (Nymphicus hollandicus) and gallinaceous species.
with a relative heterophilia. Radiographs and ultrasound Clinical signs may include abdominal distension,
may demonstrate an egg or an enlarged soft tissue den- coelomic fluid, lameness, dyspnea, depression, inappe-
sity in the region of the ovary, ovarian follicle(s) and ovar- tence and chronic reproductive-associated behavior with
ian cyst(s), and there may be coelomic fluid present if or without egg production. Egg binding, oviductal
there is a concurrent coelomitis. If coelomic fluid is pres- impaction, ovarian cysts, abdominal hernia and coelomic
ent, abdominocentesis is beneficial both therapeutically fluid may be seen in conjunction with reproductive tract
and diagnostically. Cytologic analysis as well as bacterial neoplasia. This fact demonstrates the extreme impor-
535
tance of a complete diagnostic work-up. Alteration of non-infectious causes are associated with inflammation of
secondary sex characteristics such as a cere color change the testicles. Early clinical signs are vague and difficult to
may occur as well. Diagnosis is supported by history and detect, and may include infertility, mild depression and
physical examination, demonstration of enlargement in decreased appetite. As the disease progresses, the patient
the area of the ovary or oviduct on radiographs and may develop lethargy, inappetence and abdominal disten-
ultrasound, and biopsy with histopathologic examina- sion if a secondary coelomitis develops. Leukocytosis
tion of abnormal tissues. Lymphomatosis, adenocarci- with a relative heterophilia may be noted. Testicular
noma, leiomyosarcoma, leiomyomas, adenomas and enlargement may be noted on radiographs and ultra-
granulosa cell tumors have been reported.3,10,31,40,41,63,73 sonography, which is a normal condition for a normal
There have been anecdotal reports of treatment with male. There also may be notable enlargement, inflamma-
chemotherapeutic drugs such as carboplatin (D. Zantop, tion and hypervascularization on laparoscopy. Definitive
personal communication, 2000); however, no consistent diagnosis is made by cytology, bacterial culture and sensi-
results have been documented to date. Prognosis for tivity, and histopathologic examination of samples from
long-term recovery is grave, with no refereed reports of affected testis. Therapy includes broad-spectrum antibi-
successful treatment. Salpingohysterectomy with partial otics, pending sensitivity results.12,31,73
or complete ovariectomy may have value in select
patients.31,63,73 Cryosurgical ablation of the ovary and anti- TESTICULAR NEOPLASIA
angiogenesis therapy may prove beneficial.
Testicular neoplasia has been commonly documented in
the budgerigar (Melopsittacus undulatus) and is often
PARASITES unilateral. Clinical signs include abdominal distension
Ascarids and flukes have been reported to infect the and one-sided paresis, paralysis, or cyanosis and hypo-
oviduct from the cloaca by reverse peristalsis. Heavy thermia of the pelvic limb due to compression of the
infestation may cause soft-shelled and shell-less eggs, ischiatic nerve and blood vessels. The disease is often
and may result in salpingitis. Anseriformes are most advanced once clinical signs are evident. Definitive diag-
commonly affected. Ascarids and small flukes reportedly nosis is made by testicular biopsy and histopathologic
have been passed in eggs. Diagnosis is made by finding examination.13 Alterations of secondary sex characteris-
adult worms in the oviduct on celiotomy or necropsy, or tics such as cere color change from blue to brown may
by finding adult worms in eggs laid by affected hens. occur. Neoplasms reported include Sertoli cell tumor,
Fecal floatations should be performed, especially on seminoma, interstitial cell tumor and lymphosarcoma.
ground-dwelling species, and prophylactic anthelmintic Leiomyosarcoma and carcinoma have been reported to
programs may be helpful in preventing severe infesta- arise from the epididymis and ductus deferens.3,10
tions. If these parasites obstruct the oviduct, they Radiographs may reveal a soft tissue mass in the region
require surgical removal or salpingohysterectomy.73 of the testicles, air sac compression, and secondary sex
changes such as polyostotic hyperostosis (see Figs
18.13a,b). Treatment includes orchiectomy. Cryosurgical
OVERPRODUCTION OF EGGS ablation may be beneficial. Chemotherapy with carbo-
Safe numbers for egg production for different species are platin and O,P’-DDD (mitotane)21 has been anecdotally
not definitively documented. Nutrition and environmen- reported if the tumor is deemed incompletely or non-
tal conditions affect safe production levels. Free-ranging resectable, or if the patient is not a good surgical candi-
psittacines typically produce one to two clutches per date. However, no conclusive data have been reported
year; however, many captive psittacines produce far more to date regarding efficacy of chemotherapy.31,73
eggs than this. While many birds show no obvious side
effects, chronically overproducing hens may develop
CLOACAL PAPILLOMAS
reproductive tract disorders, as well as poor body condi-
Cloacal papillomas have been noted in New World
tion and feather quality. To improve long-term health in
psittacine species with green-wing macaws over-repre-
producing birds, egg production should be limited to
sented. To date the cause is unknown, but a herpes virus
two clutches per year in birds that show any signs of
etiology is strongly suspected7,22,39,57,62 (see Chapter 32,
poor health secondary to overproduction. It also is rec-
Implications of Viruses in Clinical Disorders). Clinical
ommended that all birds receive some rest period each
signs may include infertility due to mechanical obstruc-
year to prevent reproductive disorders from developing.73
tion, hematochezia, and straining to urinate and defecate.
Examination of the cloaca reveals one or several fleshy
ORCHITIS masses at the mucosal border. Inserting a lubricated swab
Infectious orchitis may occur from ascending infections, into the cloaca to evert the tissue facilitates cloacal exami-
hematogenous spread or infected adjacent organs. Rarely, nation (Fig 18.14). In addition, white vinegar applied to
Donald Zantop
Donald Zantop
Fig 18.14 | A 22-year-old yellow-naped Amazon parrot with a
history of depression, weakness and inappetence. Note the papil- Figs 18.15a,b |
lomatous masses at the mucocutaneous junction of the cloaca. Ventrodorsal and right
lateral radiographs of the
Amazon parrot in Fig
18.16. Note the severely
enlarged liver and caudal
displacement of the grit-
filled ventriculus.
Donald Zantop
Donald Zantop
Fig 18.16 | Coelomic ultrasound of the same
Amazon parrot. Note the severely enlarged liver
with increased echogenicity. Liver biopsy and
histopathologic examination revealed bile duct
adenocarcinoma (7.5-MHz probe).
the cloacal wall will significantly blanch papillomatous removal.18,61 Autogenous vaccines and cloacal mucosal
tissue, further assisting in identification. A thorough stripping have not met with consistent success.2,64
endoscopic exam of the cloaca should be performed to Imiquimodh, an immune response modifier used in
rule out obstruction of the gastrointestinal, urinary and humans for the treatment of anogenital warts, has been
reproductive tracts. It is important to perform a full exam- shown to decrease lesion mass and tenesmus, but it did
ination to detect oropharyngeal and laryngeal papillomas not cause remission of papillomatous tissue.43 It is impor-
and hepatomegaly. It is equally as important to perform tant when cauterizing papillomatous tissue with silver
complete blood count, serum chemistries, bile acids eval- nitrate to flush the area profusely with saline when suffi-
uation, radiographs including contrast studies, coelomic cient tissue is cauterized, otherwise normal cloacal tissue
ultrasound, and endoscopic exam of the coelom and will be cauterized. Topical medications such as dimethyl
cloaca. These tests are crucial to fully evaluate the sulfoxide and silver sulfadiazine cream should be applied
patient, as papillomas may occur at any site of the gas- to affected tissue after cauterization. Analgesics should be
trointestinal tract. Furthermore, bile duct and pancreatic administered postoperatively as well as antibiotics if
adenocarcinoma are associated with papillomatous dis- there is an associated cloacitis. Temporary spontaneous
ease.25,31,32,73,76 It is necessary to perform a liver and pan- remission has been reported. Recurrence is extremely
creatic biopsy for histopathologic examination to common and frequent re-examinations are necessary.31,73
rule out early bile duct and pancreatic adenocarcinoma Spontaneous regression has been reported.
upon diagnosis of cloacal papilloma (Figs 18.15a,b,
18.16). Cytology, culture and sensitivity are beneficial to Carboplatin chemotherapy has been reported to benefit
diagnose a secondary cloacitis. Histopathology of excised patients suffering from bile duct and pancreatic adeno-
or biopsied tissue will confirm the diagnosis.31,73 carcinoma, and does appear to be well tolerated.20,79
Therapy includes cauterization of papillomas with Affected birds should be separated from the non-affected
silver nitrate, cryosurgery, cloacotomy and laser surgical to prevent possible transmission.8,31,73 It is beneficial to
537
Fig 18.17 | Prolapsed cloaca in a 5-year-old male umbrella Fig 18.18 | The same umbrella cockatoo after manual cloacal
cockatoo. History included chronic masturbation and intermittent reduction and cloacopexy.
partial cloacal prolapse.
perform a thorough cloacal examination, particularly on the cloaca (D. Zantop, personal communication, 2003).
New World psittacines, during routine health examina- Salpingohysterectomy with partial ovariectomy or orchi-
tions, as affected birds should be isolated to prevent ectomy may be beneficial in those patients refractory to
potential spread to non-affected individuals. Healthy medical therapy. Broad-spectrum antibiotics should be
chicks have been raised from artificially incubated or fos- initiated, pending bacterial culture and sensitivity,
tered eggs from affected pairs.31,73 because primary and secondary bacterial infections are
common.8,31,63 See Chapter 3, Concepts in Behavior.
CLOACAL PROLAPSE
Cloacal prolapse may occur secondary to chronic strain- CLOACITIS
ing from masturbation, egg laying, space-occupying Cloacitis may result from both infectious and non-infec-
abdominal masses, and inappropriate weaning and tious processes. Cloacal prolapse, cloacal papillomas,
social behavior. Physical examination will reveal pro- cloacoliths and bacterial infections may cause inflamma-
lapsed tissue through the vent that may be intermittent tion of these tissues. This may result in secondary uro-
or persistent (Fig 18.17). Careful cleaning, irrigation and genital and/or gastrointestinal disease due to the
lubrication of prolapsed tissue are a necessity. Affected anatomic relationship to the cloaca. Cytology with
tissue should be examined for necrosis, and any adhered bacterial culture and sensitivity should be performed.
egg should be removed. Cytology and bacterial culture Appropriate antibiotics or anti-inflammatory therapy may
and sensitivity should be performed on prolapsed tissue be indicated. Dimethyl sulfoxide may be used to reduce
to aid in antibiotic therapy. A complete blood count, inflammation with no systemic side effects, and swab-
serum chemistries, radiographs, ultrasound and endo- bing the cloaca with petroleum jelly will prevent fecal
scopic exam of the coelom and cloaca are useful to and urate accumulation on the cloacal surface with sub-
determine any other predisposing cause.31,73 Chronic sequent irritation.73
reproductive-associated behavior and straining second-
ary to masturbation may respond to pharmacologic ther-
apy such as leuprolide acetate or environmental manipu-
CLOACOLITHIASIS
lation to decrease reproductive stimuli. Cloacopexy and Cloacolithiasis is infrequently noted in pet birds. It
the use of temporary stay sutures may be helpful in tem- may result from previous egg binding, infectious cloaci-
porary or permanent reduction. However, those proce- tis, malnutrition or neurologic disease of the cloaca.
dures interfere with movement of the cloaca and may Cloacoliths should be manually or surgically removed.
alter defecation and micturition4,66 (Fig 18.18). Ventplasty Cloacal cytology with bacterial culture and sensitivity
may decrease the vent opening and prevent further pro- should be performed. The identification of anaerobic
lapse if the vent has become flaccid (see Chapter 35, bacteria, notably Clostridia sp., is a common finding
Surgical Resolution of Soft Tissue Disorders). Clomipra- often associated with a fetid odor. Since routine aerobic
mine hydrochloride and phenylpropanolamine adminis- cultures will not isolate these organisms, Gram’s stains
tration has been anecdotally reported to contract the of the feces should be performed. Broad-spectrum anti-
vent orifice and assist in the resolution of prolapse of biotics should be initiated, pending culture results.
Improved nutrition through diet change should be initi- may demonstrate removal of one or several types of
ated. Patients should be monitored closely for recur- feathers, rough feather condition of any remaining feath-
rence, and prognosis for return to normal breeding per- ers, and the patient may become reproductively stimu-
formance is poor.73 lated during the examination. Serum chemistries panels
may reveal elevated serum calcium in hens (provided
CLOACAL NEOPLASIA they are not calcium deficient) and hypercholestero-
lemia. Radiography may demonstrate an enlarged
Cloacal carcinomas are infrequently reported in pet
gonad(s) and/or polyostotic hyperostosis. Ultrasono-
birds. An endoscopic examination of the cloaca should
graphy and laparoscopy may reveal ovarian follicles, ovar-
be performed, and the patency of openings into the
ian cysts, an enlarged oviduct or enlarged testicles. The
urodeum, proctodeum and coprodeum should be
diagnostic work-up must be extensive to rule out any
noted. Definitive diagnosis is made from histopathologic
other possible diseases. Serum estradiol, progesterone
analysis of biopsy samples. Neoplastic masses should be
and testosterone level tests are available, although nor-
surgically removed, with caution not to damage the
mal values are not known for every avian species.
openings to the gastrointestinal, urinary and reproduc-
Pharmacologic treatment, behavior counseling and envi-
tive tracts.3,41,42,73
ronmental changes to reduce reproductive drive and hor-
mone levels as discussed with chronic egg laying are rec-
OTHER CLOACAL DISEASES ommended. Response to treatment is important thera-
Other cloacal diseases include cloacal strictures and peutically and diagnostically. Treatment failures may be
excessive vent feathering. Cloacal strictures may be gen- due to the presence of non-reproductive-related disease
tly manually dilated with the use of a speculum. Excessive and concurrent disease. It is important to note that a full
feathering around the vent may cause infertility; prior to history and diagnostic work-up must be performed prior
breeding season, these feathers should be removed by to establishing a diagnosis of reproductive-related feather
trimming or pulling.73 disease. Many of these birds molt heavily after starting
therapy and this should not be interpreted as a deleteri-
REPRODUCTIVE HORMONE- ous side effect.8,11,48
RELATED FEATHER PICKING
Birds pick their feathers for several different reasons.
a. Depo-Provera, Upjohn C., Kalamazoo, MI, USA
Avian veterinarians often cannot elicit a cause from a b. Levonorgestrel, Sigma Chemical, St. Louis, MO, USA
complete history, physical examination and diagnostic c. HCG, Pregnyl Organon, Inc, West Orange, NJ, USA
d. Ortho-McNeal Pharmaceutical, Rantan, NJ, USA
work-up. In some avian patients, history may reveal e. Lupron Depot, TAP Pharmaceuticals Inc
f. Tamofen, Phone-Poulenc Rorer Canada Inc, Montreal Quebec, Canada
reproductive-related behaviors such as breeding, mastur-
g. Prepidil, Pharmacia and Upjohn, Kalamazoo, MI, USA
bating, regurgitation and failure to molt. Physical exam h. Imiquimod Aldara 5%, 3M Pharmaceuticals
References and HBD Int’l, Inc, 1999, pp 1125- testicular biopsy technique in the avian shell gland (uterus).
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Avian Medicine and Surgery. as the etiology of a cloacal papil- African grey parrot. Proc Assoc galerita). Proc Assoc Avian Vet,
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3. Antinoff N, et al: Smooth muscle 9. Bowles HL: Management of cystic depot (leuprolide acetate for like virus associated with a cloacal
neoplasia of suspected oviductal ovarian disease with leuprolide depot suspension) in the treat- papilloma in an orange-fronted
origin in the cloaca of a blue- acetate. Proc Assoc Avian Vet, ment of endometriosis: A ran- conure (Aratinga canicularis). J
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11(4):268-272, 1997. agement of female avian repro- Sterility 54:419-427, 1990. gland, circadian rhythms, and
4. Avgeris S, Rigg D: Cloacopexy in a ductive diseases. Proc Assoc Avian 17. Dorrestein GM: Physiology of the photoperiodism. In Whittow GC
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19_Endocrine.qxd 8/23/2005 11:57 AM Page 541
CHAPTER
19
Endocrine
Considerations
K. STORMY HUDELSON, BS, DVM, D ipl ABVP- Avian;
PAUL M. HUDELSON, BA, MA
Stress
Many things can be stressful, including isolation,20
weather change,101 separation from mate, forced exer-
cise,95 fear,68 starvation,67 handling,60 toxins and abnormal
physical conditions, such as infection, trauma and pain.93
Stress involves a cascade of physiologically adaptive
responses. These responses can be demonstrated in
altered behavior, such as aggression, escape attempts,
vocalizations, changes in feeding and drinking, feather
picking, repetitive movements and suppression of repro-
Greg J. Harrison
duction.79 These varied physiological reactions do not

constitute a uniform set of adaptive responses occurring
in a predictable temporal fashion (Fig 19.1).93 The most
Fig 19.1 | The European stork is a perfect example of birds reliable response to stress is an elevation in circulating
learning to modify stressors. corticosterone levels.93,60
In a set of experiments, the temporal association of

stress responses was determined. Juncos measured at
handling and again in 30 minutes demonstrated a four-
fold increase of corticosterone levels.60 In chickens given
a continuous infusion of adrenocorticotropic hormone
(ACTH), the corticosterone response was within 2
hours. Other significant indicators of stress were eleva-
tion of glucose by 12 hours; increased liver weight along
with increased hepatic lipid and decreased moisture by
18 hours; decreased relative weight of the spleen by 24
hours; elevated heterophil:lymphocyte ratio by 2 days;
decreased body weight and relative weight of the bursa
of Fabricius, as well as the weight of the thymus, by day
4; and decreased liver-soluble protein content by 12
days. Elevations in cholesterol, triglycerides, high-density
lipoproteins, corticosterone and glucose were found to
be reliable indicators of stress.111 Polydipsia and polyuria
were evident in chickens within 1 to 2 days of ACTH
infusion.94 Feed intake was slightly elevated over the
week of ACTH infusion; however, body weight was 20% Stress-induced immunomodulation has both beneficial
lower 1 week postinfusion at the end of the experi- and deleterious effects. Exogenous glucocorticoids or
ment.94 This was apparently due to a decrease in diges- increased circulating levels of corticosterone cause invo-
tion of proteins, carbohydrates, dry matter and gross lution of the thymus, bursa of Fabricius and spleen.35
energy. Fat digestion was unaffected. Digestion was With early destruction of the bursa, the bursal hormones
more affected than absorption and returned to control are not produced. This leads to a future stress hypore-
levels within 1 week. Post-ACTH infusion, as digestion sponsiveness.24 The composition of white blood cells
returned to normal, absorption of nutrients was moves toward an overall decrease in leukocytes, except
reduced. Losses of skeletal muscle from prolonged heterophils, leading to an increased heterophil:lympho-
gluconeogenesis by catabolism of muscle protein from cyte ratio.45 This decrease in leukocytes is partly due to
excess corticosteroids were not recovered by the end of the cells remaining in lymphoid organs.24 A decrease in
the experiment (1 week).94 lymphocytes causes an overall suppression in antibody
production.79 In addition, glucocorticoids decrease
Migratory birds undergoing a prolonged fasting period inducible cellular cytotoxicity, lymphoproliferation, T-cell
did not demonstrate elevated corticosterone levels until immunity, interleukin-2 and γ-interferon production.65
fat stores were depleted to less than 5% of body mass. At Taken together, these responses may increase suscepti-
that point, muscle catabolism occurred due to a moder- bility to viral and other infectious agents.45
ate elevation of corticosteroids. Further secretion of cor-
ticosterone is inhibited when additional stressors are Lymphocytes themselves secrete ACTH and therefore
encountered. This may be a means to continue migra- boost circulating corticosterone levels following anti-
tion by using muscle protein for energy while finding a genic challenge.81 The increase in corticosterone appears
suitable landing area at which to feed.67 Increased corti- to cause a shift to increased T-helper cells and decreased
costerone levels coupled with decreased fat stores stimu- T-suppressor cells in the spleen.81 Macrophages are acti-
late appetite and foraging.79 In non-migratory birds vated as they phagocytize an antigen. The activated
forced to exercise, corticosterone levels were elevated macrophages secrete interleukin-1. Interleukin-1
proportionally as the intensity of the exercise increased.95 increases secretion of corticotropin-releasing factor and
ACTH, and activates lymphocytes, which increase pro-
Corticosterone also affects various behaviors in birds. It duction of ACTH.81,82 Prolonged stress prior to antigenic
can cause an inhibition of territoriality, rearing of young stimulation may blunt the ACTH and interleukin-1
and behavior associated with breeding, without affecting response.15 The increased glucocorticoids cause the
luteinizing hormone or testosterone levels (see Table redistribution of circulating T-cells to secondary lym-
19.2).126 Severe stressors cause regression of the repro- phoid tissues where antigens may be sequestered.81
ductive system in chicken hens.106 Pharmacological doses
of corticosterone can induce a preovulatory surge of Some amount of corticosterone is important in the
luteinizing hormone and ovulation, whereas dexa- immune response. Corticosteroids cause enhanced lym-
methasone blocks ovulation, possibly because it sup- phocyte activity and the production of antibodies.
presses corticosterone.106 Corticosteroids and ACTH later act in a negative feed-
back manner to regulate and control the process of anti-
Fear behaviors are seen with increased corticosterone body production by inhibiting lymphocyte activities and
levels; they may be attenuated with vitamin C supple- reducing the responsiveness to stimuli.82 There is a sig-
mentation.68 Exogenous corticosterone induces protein nificantly lower corticosterone response postantigenic
catabolism and causes chickens to seek a high-protein stimuli in chicken strains that have autoimmune thy-
diet.68 Feather picking is associated with increased corti- roiditis or avian scleroderma (another autoimmune dis-
costerone levels.68 This suggests that some feather- ease).56 This lack of response would attenuate the nega-
picking behavior may be a stress response to protein tive feedback of corticosterones on ACTH and may allow
catabolism. for a more pronounced immune response causing the
autoimmune disease.
Glucocorticoids induce epinephrine synthesis while
ACTH stimulates epinephrine and norepinephrine The administration of dexamethasone has been shown
release.78,127 These catecholamines augment, through β- to depress ACTH and corticosterone for more than 24
adrenergic receptors, and suppress, through α-adrener- hours.56 In addition, both dexamethasone and pred-
gic receptors, the plasma corticosterone responses to nisone decrease body weight gain, the number of natu-
ACTH.96 Increased epinephrine stimulates glycogenoly- ral killer cells, the number of lymphocytes in the spleen,
sis, gluconeogenesis and lipogenesis. Norepinephrine production of interleukin-2 and γ-interferon by T-cells of
helps maintain blood pressure. the spleen.65 These steroids also cause splenic atrophy,
Chapter 19 | E N D O C R I N E C O N S I D E R A T I O N S
543
increased body fat deposition, decreased percentage of On the other hand, corticosterone depresses resistance
immunoglobulin-A and immunoglobulin-M-bearing B- to viral and Mycoplasma gallisepticum infections in
cells, decreased lymphoproliferation and increased sus- poultry.46 When chickens were given drugs to block the
ceptibility to Eimeria spp.65 adrenal gland’s production of corticosterone, fewer
deaths and more effective cell-mediated immunity were
The use of dexamethasone may cause more problems by seen to Newcastle disease and Mycoplasma gallisep-
not allowing for the natural effects of corticosterone. If ticum infections. Additionally, a rapid remission of
steroid administration could be beneficial to the patient, Marek’s tumors was demonstrated.47 Corticosterone and
the use of corticosterone or ACTH may be a better dexamethasone may decrease inhibin levels; this in turn
choice. When chickens infected with Streptococcus increases follicle-stimulating hormone, which may cause
faecalis were given corticosterone at 30 mg/kg in feed in follicle abnormalities.53 Handling birds could conceivably
combination with ampicillin, the chickens were able to exacerbate these diseases. Clinically, the use of mitotane
increase weight better than without corticosterone. (o,p’-DDD) has shown promise in controlling some neo-
Ampicillin alone did not alter the course of disease. plasias, viral infections and feather picking (G. Harrison,
Corticosterone alone was as good as the combination of personal communication, 2002).
ampicillin and corticosterone in most cases.48 Another Many clinical problems may be due to a stressful envi-
study demonstrated better resistance to Escherichia coli ronment (i.e., fatty liver disease, feather picking and
challenge exposure when corticosterone was given at 40 reproductive abnormalities). Many patients present with
mg/kg in feed.49 Pericarditis was reduced from 78% to liver disease. In theses cases, the liver may not be able to
7%. No antibiotics were given. Resistance to respiratory metabolize natural or exogenous glucocorticoids.
infections was improved in pigeons given corticos- Appropriate nutrition is imperative to the health of our
terone, because of improved tracheal mucociliary trans- patients; however, nutrition and other therapies cannot
port.72 Realizing that simply restraining a bird can elevate override conditions brought on by chronic stress. The
endogenous corticosterone tremendously, it may not be best therapy for many of the diseases we encounter
necessary to even treat with corticosterone, but simply should be directed toward the psychological well-being
to catch the bird several times.60 of our patients (Figs 19.2, 19.3 and Tables 19.1, 19.2).
Table 19.2 | Effects of Corticosterone

Table 19.1 | Causes of Increases Decreases
Corticosterone Elevation
• Feeding behavior • T3
• Immobilization • Fat stores • Territoriality
• Protein restriction • Gastric transit time • Growth
• Starvation • Muscle catabolism • Body weight
• Fear • Glucose • Circulating WBC
• Pain • Insulin (counteracted by down regulation of liver • Lymphoproliferation
• Increase in plasma osmolality receptors, thus causing insulin resistance) • Interleukin-2
• Oviposition • Involution of the thymus, bursa and spleen • γ-interferon
• Prostaglandins • Heterophil: Lymphocyte ratio • Inducible cellular cytotoxicity
• Low 3,5,3'-triiodothyronine (T3) • Trapping of leukocytes in secondary • Cell-mediated immunity
• Depressed liver metabolism of lymphoid organs • Antibody response
corticosterone • Susceptibility to viral infections, coccidiosis • Potassium excretion in renal
• Growth hormone and Mycoplasma spp. tubules
• Angiotensin II (See Fig 19.8) • Resistance to some bacteria • Absorption and digestion of
• Prolactin • Tracheal mucociliary clearance nutrients
• Parathyroid hormone • Fearfulness
• Catecholamines • Oral stereotypic behavior (feather picking,
• Serotonin polydipsia, pecking)
• Vasoactive intestinal peptide • Protein eating
• Activated immune cells • Sodium reabsorption in renal tubules
• Corticotropin-releasing factor • Level of sodium-linked water uptake across
• Arginine vasotocin the intestinal and hindgut mucosa
• Mesotocin • Catecholamines
• Adrenocorticotropin hormone (ACTH) • Cholesterol
• Melatonin • Triglycerides
• Progesterone • High-density lipoproteins
• Opioids • Liver size (due to hepatic lipogenesis)
• Exercise • Salt gland secretion of NaCl
• Lipolysis from adipocytes
• Free fatty acids
• Luteinizing hormone
• Glomerular filtration rate
Cold Trauma Stress
Hypothalamus
Age and
- fed state
TRH dependent CRF
- + +
+
MT
AVT
+ +
Somatostatin
TSH ACTH -
+
+
-
-
T4 T3 +
Corticosterone Serotonin
Aldosterone +
Epinephrine
Norepinephrine
TRH = thyrotropin releasing hormone CRF = corticotropin-releasing factor

TSH = thyroid stimulating hormone AVT = arginine vasotocin
T4 = thyroxine ACTH = adrenocorticotropic hormone
T4 = triiodothyronine + = stimulates
MT = mesotocin - = inhibits
Fig 19.2 | Hypothalamo-Pituitary-Adrenal Axis Hormones
Growth There are many hormones active during embryogenesis.

Insulin and insulin-like growth factors are reported to
Growth primarily involves cell proliferation, but also stimulate embryonic metabolism, growth and differentia-
may result from cell hypertrophy. The primary hormones tion.41 Some growth factors appear to have more specific
involved with growth are: growth hormone (GH), tri- actions in embryogenesis, though many seem to have
iodothyronine (T3) and insulin-like growth factor-1 (IGF- synergistic activity with IGF-1. Table 19.6 lists some of
1). Contradictions in the literature due to variable exper- the growth factors and their respective actions.
imental designs are exacerbated by the different actions
of various hormones, depending on age and nutritional As poultry moves into its rapidly growing phase at 3 to 4
status. Fig 19.4 demonstrates an overview of hormonal weeks posthatch, GH and IGF-1 levels peak and then
interactions. Tables 19.3-19.5 delineate what effects gradually decline to their minimum concentrations at
these hormones have on growth and body condition. about 8 weeks posthatch. During this period of rapid
growth, administration of exogenous GH or IGF-1
The reader should be aware that all available growth demonstrates no effect on growth rate.22,85 As endoge-
studies look at growth in poultry. There may be some nous nutrient partitioning is shifted toward greater fat
undiscovered variations among other species of birds. deposition, as seen with increasing age and cessation of
545
Dexamethasone ↑ insulin ↑ insulin resistance
Corticosterone
↑ fat deposits in liver
↑ n-3 fatty acids ↓ hepatic fatty acid synthase
↓ triglycerol (↓ further fatty acid

accumulation in liver)
Fig 19.3 | Fatty Liver
growth, exogenous GH is effective in decreasing fat and point, the excess GH may be bound by increased levels
increasing muscle formation.85 GH in adult birds is a of growth hormone-binding protein and GH-induced
potent lipolytic hormone and also increases blood glu- down regulation of growth hormone receptors.53
cose levels.22 There does not appear to be a diabetogenic Binding of GH may keep it from attaching to receptors,
effect, as seen in humans administered GH, possibly due but also may prolong its half-life.53
to increased sensitivity of peripheral insulin receptors.
GH also can block glucagon-induced lipolysis resulting β-adrenergic receptor agonists, epinephrine and norepi-
in antilipolytic activity. Exogenous GH, in 8- to 9-week nephrine also appear to have a significant role in growth
posthatch poultry, reduced feed intake and body weight and body composition. When clenbuterol (β-adrenergic
gain.119 The reduction of feed intake may be secondary receptor agonist) was given orally, growing chickens
to GH’s reduction of neuropeptide Y protein, a potent decreased their fat mass, while increasing their muscle
appetite stimulant.119 mass, weight gain and gain-to-feed-intake ratio.85 These
changes could be from a direct effect on muscle and adi-
In growing birds, GH decreases T3 degradation resulting pose tissue, modification of blood flow, central nervous
in elevated T3 concentrations.30 The effect of T3 is devel- system control of feed intake and/or action of other hor-
opmentally regulated. Exogenous GH produces a hyper- mones (ie, T3, corticosterone, insulin, GH).
thyroid response in late embryogenesis, newly hatched
and adult birds.29,75 This effect disappears during the The majority of information on growth in birds is still
rapid growth phase, most likely due to masking by high quite controversial, with many questions left unan-
endogenous GH and T3 levels.30,119 In mammals, GH must swered. Those answers found in poultry may have little
bind to two sites of the receptor, similar to antibody- to offer other species of birds.
antigen cross-bridging. Therefore, high levels of GH may
block signal transduction.37
Growth hormone receptors and growth hormone-bind- Thyroid

ing proteins also may play an important part in age-
related actions. In young birds, growth hormone recep- Thyroid hormones influence or are influenced by almost
tors are low, and GH and growth hormone-binding pro- all physiological, environmental and nutritional parame-
tein levels are high. Exogenous GH would have little to ters. When interpreting the literature, it is important to
no effect. In adult chickens, growth hormone receptors correlate the age of bird with the actual dose of drugs
are elevated and GH is low. In this case, exogenous GH used in the experimental design to interpret the data
may initially have stimulatory effects; however, at some correctly.
546
- more effective
Somatostatin
GHRH in adults
insulin
+
glucagon - TRH
- -
+
+ wers
in gro ? - -
- + - -
serotonin + - GH + TSH
species
dependent +
+ Corticosterone
age +
+ dep
end
melatonin ent -
+ +
T4 T3
-
Leptin IGF-1
+
-
-
Decreased feed intake IGF-2 and GH
(calorie and protein deprivation) Binding proteins
↓ T3 ↑ GH + ↓ somatostatin
GHRH = growth hormone releasing hormone TSH = thyroid stimulating hormone

GH = growth hormone T4 = thyroxine
IGF-1 = insulin-like growth factor-1 T3 = triiodothyronine
IGF-2 = insulin-like growth factor-2 + = stimulates - = inhibits
TRH = thyrotropin releasing hormone ? = possibly inhibits
-
Fig 19.4 | Growth Hormone
Table 19.3 | Growth Hormone Effects

Increases No Effect Decreases
• Differentiation and proliferation of target • Exogenous GH 2-24 days post hatch • Fat in adults
cells (i.e., muscle) - no effect on growth, feed intake, • Neuropeptide Y
• Glucose carcass protein, 8-9 weeks posthatch • Feed intake at 8-9 weeks post-hatch
• Fat in growing birds - no effect on IGF-1 levels • Muscle growth at 8-9 weeks old
• Insulin-like growth factor-1 in selected • Hypothalamic epinephrine
muscles of adults • Degradation of T3
• Exogenous GH: Fat birds between 3-5
weeks of age, lipolytic
Other birds lipogenic
Increase insulin and tryglycerides at
24 days of age
Increase tibia length between 2-24 days
of age
In adult birds, large increase in T3
• Large increase of T3 at late embryo early
hatch
• Conversion of thyroxine (T4) to
triiodothyronine (T3)
• Moderate increase of T3 at growth stage
due to decreased degradation of T3
547
Table 19.4 | Effects of Insulin-like Growth Factor-1 (IGF-1)

Increases No Effect Decreases
• Metabolism, growth, differentiation, • Exogenous IGF-1 has no effect on • Insulin
organogenesis of the embryo growth or protein synthesis rate • Insulin:glucagon ratio
• Fat in growing poultry • GH lipolysis in growing birds
• Glucose uptake • Muscle growth in chickens greater than
• Amino acid uptake and protein synthesis 8 weeks posthatch
• Inhibition of protein degradation • Muscle weight in 3-week-old chickens
• Proliferation of turkey and chicken • Glucose
myoblasts
• Peripheral tissue sensitivity to insulin
• Exogenous IGF-1 increases heart weight
and muscle breakdown in 3-week-old
chickens
Table 19.5 | Effects of Triiodothyronine (T3) on Growth

Increases/Stimulates Decreases Low Levels of T3
• Accretion of muscle protein during growth • GH • Increase GH
• Muscle mass and feather development in • IGF-1: may be age-dependent at low • Decrease skeletal, muscle and feather
growers dose development in growers
• Fat in growing birds • Decrease cardiac ventricle and pectoral
• Muscle mass due to decreased protein mass in growers
synthesis in non-growing birds
Table 19.6 | Growth Factors Involved with Embryogenesis

Increases/Stimulates Factors
Insulin-like Growth Factors (IGF) • IGF-1 most important (see Table 19.4)
Epidermal Growth Factor (EGF) • With IGF-1 and Fibroblast Growth Factor (FGF) stimulates proliferation of heart mesenchymal cells
Fibroblast Growth Factor (FGF) See EGF
Stimulates: • Muscle and bone development
• Differentiation of blastoderm cells into erythropoietic cells
• Proliferation of preadiposites
• Proliferation of chondrocytes with transforming growth factor-β (TGF-β)
• With IGF-1 proliferation of chicken myoblasts
Nerve Growth Factor (NGF) • Neural development
Transforming Growth Factor-β Includes several TGF-βs, e.g.: • Inhibin/Activin subunits
(TGF-β) • Bone Morphogenic Protein-4 (BMP-4)
• Glial Cell-Derived Nerve Growth Factor (GDNF)
• Muellerian Inhibitory Substance (MIS)
• Platelet-Derived Growth Factor (PDGF)
TGF-β Decreases: • DNA synthesis and melanocyte formation in neural crest cells
• Collagen production
Stimulates: • Expression of fibronectin
• Proliferation of chondrocytes with FGF and adiposites
• Limb formation
• Synthesis of non-collagen protein
• Muscle cell differentiation
Inhibin • Blocks release of follicle-stimulating hormone (FSH)
• With activin may play an antagonistic role in paracrine
regulation of embryonic gonadal steroidogenesis
Activin See Inhibin
• Stimulates release of FSH
• Determines right and left asymmetry
Bone Morphogenic Stimulates: • Osteoinduction
Protein-4 (BMP-4) • Gastrulation
• Neural crest cell apoptosis
Glial Cell-Derived Nerve Growth • Increase survival of motor neurons by reducing programmed apoptosis
Factor (GDNF)
Muellerian Inhibitory Substance • Muellerian duct regression in males
(MIS)
Platelet-Derived Growth Factor • Stimulates transformation of chicken myoblasts
(FDGF) • Inhibits differentiation
CRF TRH + VIP

- GH
-
+ + + +
age and fed
state dependent
+
ACTH TSH Prolactin

-
+ + +
-
- -
Corticosterone
T4 T3
+ -
+ Fasting
T4 = thyroxine
CRF = corticotropin-releasing factor GH = growth hormone T3 = triiodothyronine
ACTH = adrenocorticotropic hormone TRH = thyrotropin releasing hormone + = stimulates
VIP = vasoactive intestinal polypeptide TSH = thyroid stimulating hormone - = inhibits
Fig 19.5 | Thyroid Hormones
In chickens of all ages, thyroid stimulating hormone than T4.105 Figs 19.2, 19.4 and 19.5 elucidate some of the
(TSH) stimulates the release of predominately thyroxine pathways involved in thyroid regulation.
(T4) and lesser amounts of triiodothyronine (T3). Age
changes the mechanisms controlling TSH release and PHOTOSTIMULATION
the peripheral productions of T3. In the embryo, corti-
Increasing day lengths induce photostimulated repro-
cotropin releasing factor and thyrotropin releasing hor-
ductive activity and postnuptial molt. It has been sug-
mone may control TSH release.105 Thyrotropin releasing
gested that this onset of photostimulation combined
hormone stimulates the release of growth hormone
with endogenous thyroid hormones organize the events
(GH), which inhibits degradation of T3 through the
of seasonality.124 When American tree sparrows (Spizella
growing phase (see Growth section, this chapter).
arborea) were moved from short to long days, T4 along
Growing chickens respond differently to thyrotropin with circulating luteinizing hormone increased early dur-
releasing hormone when fasted. During a 1-day fast, thy- ing photostimulation, peaking between weeks 1 and 2.
rotroph cells increase their sensitivity to thyrotropin This was followed by luteinizing hormone-releasing hor-
releasing hormone and corticotropin releasing factor. mone and luteinizing hormone peaking between weeks
However, these cells do not release TSH because fasting 2 and 4. By week 6, gonad development was near maxi-
induces a decrease in thyrotropin releasing hormone mum. Thyroid activity peaked during copulation.25,97,123,124
secreted by the hypothalamus.40 Fasting also increases The postnuptial molt began at week 9 and ended by
corticosterone levels, which inhibit secretion of thy- week 18.97 A series of experiments on intact and variably
rotropin releasing hormone and, thus, TSH release. timed thyroidectomies concluded that thyroid-depend-
This was demonstrated in chickens with one injection ent gonadal growth was programmed during the first 7
of 40 µg of corticosterone.40 days of photostimulation. Photorefractoriness and initia-
tion of molt were programmed between 7 and 21 days
As chickens mature, they are less responsive to thy- of photostimulation.53 T3 failed to program birds for
rotropin-releasing hormone effects on TSH. TSH appears these events. This suggests that T4 directly or non-T3
to be more sensitive to circulating concentrations of T3 metabolites are the responsible hormones.124
549
Cases the test be validated for birds. The necessity of incubat-

Most reports of thyroid conditions in birds involved ing serum samples with proteolytic enzymes, and then
those genetically designed for hypothyroidism (ie, chick- precipitating with ethanol to avoid binding proteins in
ens of the obese strain, and white carneaux pigeons). the serum has been demonstrated.44 Without these extra
The only case of confirmed hypothyroidism in a steps, the test will be inaccurate.43 Another source of dif-
psittacine was reported in a scarlet macaw. This report ficulty is the lack of good reference ranges. With so
described contour feather loss, no indication of feather many variables capable of altering thyroid levels, it is
regrowth and excess subcutaneous fat. Skin biopsies important that those birds used for reference ranges be
demonstrated a catabolic state, a finding inconsistent fed, housed and cared for optimally.
with hypothyroid cases. A TSH stimulation test con-
T4 blood levels fluctuate normally during a 24-hour
firmed that the bird was hypothyroid. The bird
cycle, generally being higher in the night and during a
responded to thyroid hormone replacement in the water
fast.84 To measure T4 activity more accurately, a TSH stim-
at 0.015 mg/kg BID, which was later reduced to daily
ulation test is required. Recently, a stimulation test in
therapy.89 It was not clear if this was a lifelong therapy or
several genera of birds has been developed using syn-
was discontinued after the resolution of signs. If the bird
thetic human thyroid stimulating hormone.44 It was
was taken off thyroid medication and remained euthy-
found that a 0-hour baseline blood sample, TSH at 1.0
roid, it could have been due to a resolving thyroiditis,
IU/kg IM and a second blood sample in 6 hours gave
stressful environment and/or inadequate nutrition.
consistent results.
Goiter has often been associated with iodine-deficient
budgerigars. Another incidence of goiters was reported
in a goose flock of 2300 birds.66 Though geese feeding
on rapeseed meal develop goiters, rapeseed was not
Pancreas
part of this flock’s ration. The major pathological find-
ings were increased relative thyroid weight, fat accumu- ENDOCRINE-GLUCOSE REGULATION
lation, and retarded growth and plumage development. Glucose regulation is the primary endocrine function of
One group of birds was treated with iodine and another the pancreas. Effective glucose metabolism also main-
group was not. After 55 days, both groups improved. A tains normal protein and lipid metabolism. Neural, reti-
hunt for possible goitrogenic substance was not success- nal and adrenal tissues require glucose. The avian liver
ful.66 The two study groups were put in less dense envi- is the primary source of glucose to the plasma by its
ronments. This may have resulted in less stress, there- interaction with the pancreas. The pancreas releases the
fore less circulating corticosterone and less suppression proper ratio of insulin and glucagon. The combination
of thyroid activity. A recent report found a dispropor- of hormones and absorbed nutrients work together in
tional number of macaws with hyperplastic goiter. the liver to release products of digestion in dynamic
Seventy-five percent of these cases were in blue and gold response to the bird’s needs. After a bird feeds, plasma
macaws (Ara arauna). The cause was not determined.104 glucose and amino acid levels increase causing insulin
release from the pancreatic B-cells. Insulin aids hepatic
Avian muscular dystrophy in chickens has been treated
enzymes in glycogenesis. In the liver, protein synthesis
by thyroidectomy. Maintenance of low T3 plasma levels
and lipogenesis produce approximately 95% of lipids
with exogenous T3 replacement alleviated signs attribut-
through insulin stimulation. Thyroid hormones augment
able to the disease. These chicks demonstrated a large
the process. Insulin is therefore an anabolic hormone.
increase in T3 maximum binding capacity in dystrophic
muscles.73 In the fasting state, the liver is important for retrieving
energy sources and making them available. With lower
Cysts, adenomas and adenocarcinomas have been
blood glucose concentrations, insulin levels are low and
reported infrequently in several genera of birds. As
glucagon levels are high. At the liver, glucagon causes
intensive breeding and pollution with hormonally dis-
lipolysis, glycogenolysis and stimulates gluconeogenesis.112
ruptive chemicals increase, thyroid disease may be
Glucagon is therefore a catabolic hormone. The
reported more frequently.
glucagon insulin responses to food intake maintain sta-
ble blood glucose levels. A variety of species of birds
TESTING demonstrate only small declines during prolonged (5 to
Most available thyroid tests are designed for humans or 7 days) fasts.114 We have seen emaciated birds with only
dogs. These tests are not usually able to detect the rela- slightly decreased blood glucose. A study in migrating
tively low concentrations of T4 in the avian patient.43 garden warblers (Sylvia borin) found that glucose uti-
When testing for thyroid hormones, it is important that lization rate is reduced as food deprivation continues to
about 7 days. These experiments suggest that during and gallbladder secretions. They also are antilipolytic
migration, a period of prolonged fasting, glucose utiliza- and induce satiety via the central nervous system.55
tion may be supplanted by oxidation of fatty acids.113
EXOCRINE
Adipose, kidney and muscle tissues each play a role in
maintaining energy sources. The kidney can provide up Exocrine pancreatic secretions include trypsinogen, chy-
to 30% of glucose by gluconeogenesis. Adipose tissue is motrypsinogen, trypsin inhibitor, procarboxypeptidase,
important in providing lipids through lipolysis.39 During amylase and lipase. These enzymes are released into the
a catabolic state, muscle tissue itself may be broken duodenum and, along with gut peptides, further diges-
down (see Stress section, this chapter). tion. Trypsinogen and chymotrypsinogen are secreted in
an inactive form so as not to induce autodigestion.
Cholecystokinin, glucagon and a mixture of absorbed Enterokinase from the gut activates trypsinogen to
amino acids strongly stimulate, whereas glucose only trypsin. Trypsin, in turn, cleaves chymotrypsinogen to
weakly stimulates insulin release. Insulin enhances pro- chymotrypsin.
tein synthesis and is required for embryonic myogenesis
Factors influencing exocrine pancreatic enzyme secre-
and muscle structural proteins in adult birds. At the
tion include the following: feeding, distention of the
level of the muscles and adipocytes, insulin increases
proventriculus with peptones, gastrin-releasing peptides,
glucose transport carriers. These proteins increase the
increased cholecystokinin, vasoactive intestinal peptide,
transport of free glucose from the extracellular fluid
neurotensin, secretin, hydrochloric acid, vagus innerva-
across the cell membrane. Insulin aids transport of
tion and cholinergic agents.23,59,74,100,118
amino acids into cells. Insulin, or its hypoglycemic
effect, causes glucagon release and results in an increase Cholecystokinin influences the enzymatic content of
in free fatty acids. Therefore, insulin’s overall effects are pancreatic secretions except amylase.34,86 Secretin, and to
to remove glucose and amino acids from circulation, a larger extent vasoactive intestinal peptide, increase the
increase lipidemia and inhibit gluconeogenesis. aqueous component of pancreatic juices. Neurotensin
increases lipase and depresses amylase secretion.
Free fatty acids and cholecystokinin stimulate glucagon
Ingestion of lipids causes neurotensin release from
release from the pancreatic A-cells. In contrast to other
intestinal stores.33 Diets rich in carbohydrates increase
avian species, ducks also release glucagon in response to
amylase, fats increase lipase, and protein increases chy-
insulin and somatostatin. Glucose inhibits glucagon
motrypsin activity in pancreatic secretions.19,64 The
release. Glucagon suppresses leptin, a hormone that
release of some of the islet hormones occurs before
suppresses appetite, T3 and T4.3,83
nutrients are even absorbed into the bloodstream, allow-
Somatostatin controls the ratio of insulin to glucagon ing for rapid adjustments to maintain homeostasis.
released from the pancreas. Islet cells appear to be con-
tiguous with each other and share intra-islet extracellu- Exocrine Pancreatic Insufficiency
lar fluid. Somatostatin from pancreatic D-cells inhibits Exocrine pancreatic insufficiency in birds has been sug-
secretion from all other islet cells. Glucagon is the most gested by the observation of undigested food in the
sensitive and pancreatic polypeptides are the least sensi- feces, voluminous foul-smelling droppings, weight loss
tive to somatostatin. At the level of the gut, somatostatin and failure to thrive. With many cases of psittacine
decreases intestinal absorption of glucose and lipids. proventricular dilation presenting similarly, appropriate
This hormone’s actions allow a dynamic regulation of biopsies may be indicated to assist in diagnosis. Pancre-
gluco-homeostasis. atic insufficiency has been reported as a secondary effect
of a pancreatic adenocarcinoma.98 This yellow-naped
Absorbed nutrients stimulate D-cell somatostatin and A- Amazon (Amazona ochrocephala auropalliata) was pre-
cell glucagon activity. Increased glucose and amino acids sented with a 3-month history of weight loss and volumi-
stimulate B-cells (insulin) whereas glucose depresses A- nous foul-smelling droppings. Confirmation of pancre-
cells (glucagon). F-cells (pancreatic peptides) are stimu- atic insufficiency was made from fecal tests positive for
lated by cholecystokinin, secretin, gastrin and absorbed neutral and split fats and negative for trypsin. In addi-
amino acids. In summary, A-cells stimulate B- and D- tion, no elevation in blood triglyceride levels occurred
cells; D-cells inhibit A-, B- and F-cells. Pancreatic with oral corn oil administration until the oil was mixed
polypeptides from the F-cells are glycogenolytic without with pancreatic enzymes. The pancreatic adenocarci-
producing hyperglycemia. They also act to lower plasma noma was found on necropsy.98
glycerol, cholesterol, fatty acids and apolipoproteins,
while increasing triglyceride levels.105 Pancreatic polypep- Another case in a macaw was reported with feces con-
tides inhibit gut motility and gut, exocrine pancreatic taining starch and fat. The bird’s feces returned to nor-
551
mal with the addition of trypsin to the food. When tryp- Oral medications may have promise. Glipizide, a drug
sin was discontinued 6 weeks later, the feces remained that increases insulin release from β-cells, has been used
normal.90 A slightly acidic diet rich in peptones should successfully in some cases at 1 mg/kg PO BID (Echols,
increase pancreatic exocrine secretions. This may prove personal communication). Other oral medications that
a useful therapeutic adjunct to the addition of pancre- may be tried include thiazolidinediones, which enhance
atic enzymes to the food. peripheral insulin sensitivity, and α glucosidase
inhibitors, which delay glucose absorption from the gut.
Diabetes Mellitus and Pancreatitis Chicks with dexamethasone-induced hypocorticalism
demonstrated increased insulin sensitivity and attenu-
In most granivorous birds, hyperglycemia occurs with
ated glucagon responsiveness.70
normal insulin and increased glucagon levels, however,
some birds have been documented with low insulin lev-
els.90 Clinical signs attributable to hyperglycemia are
severe polyuria, polydipsia, increased appetite, and Pineal Gland
weight loss.90 Often there is a history of obesity and poor
nutrition. Hyperglycemia may be secondary to other The pineal gland is made of ependymal cells, photore-
diseases and often resolves when the underlying disease ceptor-like cells and neurons.17 The gland is located
is treated. Hyperglycemia in obese psittacines has between the two hemispheres of the telencephalon and
responded to low-fat diets and weight loss. Obese the cerebellum. This gland’s photoreceptive-like cells are
Quaker parakeets (Myiopsitta monachus) have been stimulated by light through pinopsen, a pineal-specific
found to have pancreatic necrosis.71 Those that survive photoreceptive molecule, making the pineal a major
have pancreatic insufficiency. A number of viruses, such component of the circadian pacemaking system.91,117 The
as herpes, pox and polyomavirus, may cause pancreatic pineal’s rhythmic synthesis and secretion of melatonin is
pathology.42 Birds on certain drugs (eg, medroxyproges- regulated by neural signals from sympathetic nerves.92 A
terone) have shown signs of hyperglycemia. second component of the circadian pacemaking system
consists of a self-sustained oscillator, which is an area of
It has been suggested that an amylase greater than 2000 the hypothalamic region possibly equivalent to the mam-
IU/L is diagnostic for pancreatitis. Lower values of amy- malian suprachiasmatic nuclei. The third component, at
lase may be more indicative of renal disease. Chronic least in some galliforms and columbiforms, are the reti-
stress causes chronic hyperglycemia with increased nae of the eyes.50,117 These three components work in
insulin levels and resultant insulin resistance. To evalu- concert to stabilize and amplify a self-sustaining circa-
ate a bird with hyperglycemia it is important to keep dian output. Light is the most powerful stimulus for the
environmental stressors to a minimum. Evaluating the circadian rhythm and also can affect the system via the
home situation and diet may indicate stress and/or nutri- extraretinal/extrapineal photoreceptors located deep in
tional issues. If possible, glucagon, insulin and amylase the brain (Fig 19.6).117 The relative contribution each part
should be evaluated along with evidence of persistent plays in keeping the rhythm differs between species and,
hyperglycemia. A urine dipstick in normal birds usually at times, within the same individual. The predominant
demonstrates negative or trace glucose. Radiographs and factor maintaining rhythm in the house sparrow is the
fecal Gram’s stains may aid in the search for any under- pineal gland, in the pigeon it is both eyes and pineal
lying diseases. gland, and in the Japanese quail it is the eyes.
Changes in the pacemaker are partly related to the

Treatment rhythmic synthesis and release of melatonin. These
If insulin levels are depressed, the bird may respond to changes may be important in environmental situations,
exogenous insulin. Insulin protocols are extrapolated such as mid-winter and summer in the high arctic where
from other species and are carried out in much the same conditions are constant, and also in the ever-changing
way as in mammals. Somatostatin was tried in a sulfur- conditions encountered during migration.50 In arctic
breasted toucan (Ramphastus sulfuratus) at 3 µg/kg SC mid-winter and mid-summer birds, and in migratory
BID. The bird improved clinically, but died acutely after birds, there is a reduction in melatonin amplitudes. This
4 months. The body was not presented for necropsy. reduction should result in a reduction in the degree of
During therapy, the bird maintained high glucose oscillation of the pacemaking system. A reduction in
(>1300 mg/dl) and glucagon (>3100 pg/ml) levels. It oscillation reduces the overall output of the pacemaker.
would be interesting to evaluate higher doses of somato- This should facilitate adjustments to altered environ-
statin.71 If glucagon is elevated, it would be interesting to mental conditions during migration, and in conditions
try antiglucagon serum. When anti-insulin serum was that are more constant, it may enhance entrainability to
used in chickens, glucose became extremely elevated.107 weak Zeitgeber influences.51
Light
- + -
+
Extraretinal/
Pineal extrapineal Photoreceptors Eye
Gland
Me +
lat in
on on
in elat
- - M +
-
Suprachiasmatic in day
Nuclei (SCN) + -
- +
- Superior Cervical
in day Ganglia
stimulates + inhibits -
Neuronal connections (dotted)
Fig 19.6 | Interactions of the Circadian Pacemaking System
Sometimes in constant conditions, the pacemakers are central thyroid-dependent mechanism that controls the
unable to sustain the persistent rhythm without periodic reproductive state in birds.11
melatonin input from the eyes or pineal gland, or peri-
odic neural input from the suprachiasmatic nuclei.117 The Melatonin helps to time migration and the hatching of
most powerful stimuli of synchronization of the circa- eggs, but does not fully coordinate reproductive activity
dian rhythm is periodic alteration of light intensity.2 with a favorable time of year.11 In non-tropical birds,
Light affects melatonin synthesis by entrainment of circa- photoperiod is the predominant proximate factor. With
dian melatonin rhythms and acute inhibition of mela- increasing photoperiod in the spring, secretion of
tonin synthesis.36 Light inhibition of melatonin causes luteinizing hormone releasing hormone (LHRH)
sleep impairment in pigeons.14 increases and results in gonadal maturation.61 Breeding
terminates while days are still long, due to induced pho-
Retinal photoreceptors appear to mediate light-induced torefractoriness. The gonadal regression during this time
suppression and photic entrainment in pigeons and is associated with a large decrease in LHRH. This sug-
Japanese quail.36 Dopamine stimulates retinal melatonin gests photoperiodic responses involve direct interactions
synthesis. Dopamine has shown to have a rhythm of between photoreceptors and LHRH neurons.31
release opposite to melatonin, that is, increased levels in
the day and decreased levels at night. Experiments have Melatonin synthesis also has been demonstrated in
demonstrated that the interaction of dopamine and Harderian glands, the gastrointestinal tract and retina.
melatonin are necessary for maintaining the anti-phase The extrapineal melatonin is only rarely released into
relationship between the two rhythms.36 the circulatory system. Presumably, it exerts its influence
locally.51,63 High concentrations of melatonin are found in
Melatonin also affects regulation of seasonal changes in enterochromaffin cells of the mucosal epithelium of the
immune function by enhancing cell-mediated immu- gastrointestinal tract.63 Pinealectomized pigeons were
nity.11 As discussed in the Song section in this chapter, found to have a 24-hour cycle of melatonin secretion in
melatonin also inhibits the neural plasticity of the song the gastrointestinal tract, with levels increased at night
control system.12,13,36 These seasonal regulations and the and decreased during the day.63 Melatonin receptors
action of melatonin appear to be modified by the same have been found in a variety of tissues, which suggests
553
direct actions of melatonin on the function of different

organ systems in response to internal and external
Song
stimuli.102 Over the last decade, there has been an increased inter-
est in the effects of hormones on behavior and changes
With the complex responses seen in birds due to dura-
in brain morphology. The complex learned behavior of
tion and intensity of light, it seems paramount that the
singing is expressed differently in the different sexes of
bird’s natural photoperiod be accommodated. This is
many species of birds. The current research suggests
true for the home environment as well as the hospital.
that steroid hormones can induce a neuroplasticity,
Night treatments should be done quickly, with an
which activates this behavior. This seasonal neuroplastic-
attempt not to shine light toward the head, because
ity is more dramatic in birds than in other vertebrates.
even a short duration of light exposure in the night can
throw the natural circadian rhythm off. In 24-hour clin- In many song birds, most notably the zebra finches
ics, it is important to keep cages covered during the nor- (Taniopygia guttata) and canaries (Serinus canaria), a
mal night duration. song control system (SCS) has been identified in the
brain. The higher vocal center, a part of this system,
THERMOGENESIS appears to be unique to the songbird suborder.4,21,88 This
center is implicated in the learning of new song, as well
The pineal gland influences thermoregulation. Pinealec-
as the production and perception of previously learned
tomy performed on some species caused increased core
songs.21,88 Several of the nuclei of the SCS contain high
body temperature and decreased tolerance to heat at
levels of androgen, estrogen, norepinephrine, and
night.18 This effect returns to normal with the adminis-
acetylcholine muscarinic and dopamine receptors along
tration of melatonin. Exogenous melatonin in intact
with acetylcholinesterase.99 In addition, fibers containing
house sparrows decreased core body temperature by
neurotransmitters (catecholamines), or neuropeptides
4.7°C within 30 minutes.16 Melatonin may be an effective
(vasoactive intestinal polypeptide, enkephalin, cholecys-
antipyretic. Melatonin facilitates sleep and acts to syn-
tokinin, substance P and Metenkephalin) are present.4,8,9
chronize the decrease in body temperature and meta-
bolic rate in order to reduce energy expenditure during Estrogenic metabolites of testosterone increase norepi-
inactive periods.14 nephrine and dopamine turnover in the SCS, suggesting
an interaction between the metabolites of testosterone
Another area of the brain that is involved in thermogene-
and these catecholamines.8,9 Androgen receptors in the
sis is the preoptic/anterior hypothalamic area (PO/AH)
SCS appear to be unique to song birds and the Anna’s
where warm- and cold-responsive neurons are found.32 A
hummingbird (Calypte anna), a non-song bird.38
number of neuroactive compounds have demonstrated
effects in this area. When acetylcholine, dopamine, sero- In the fall, when singing is not done to attract a mate,
tonin or norepinephrine were injected into the PO/AH daylight is decreasing and sex hormone levels are low. In
of pigeons, the birds demonstrated peripheral vasodila- the song sparrow (Melospiza melodia), evidence sug-
tion, inhibition of shivering and decreases in heat pro- gests that the autumnal singing involves estrogen acting
duction.58 Prostaglandin E2 injected into the hypothala- locally in the brain. The source of the neuroactive estro-
mus caused hyperthermia in pigeons and fowl, whereas gen is unknown, but does not appear to be from testos-
prostaglandin F2α caused hypothermia in fowl and hyper- terone of gonadal origin.110 The administration of testos-
thermia in pigeons.87 Arginine vasotocin reduces shiver- terone will increase song rate, whereas castration will
ing, body temperature and oxygen consumption, reduce, but not always eliminate, male-typical song,
whereas angiotensin-II has the opposite effects.54 depending on the species.1 Castrated song sparrows in
Thyroid hormones help to adjust the body temperature the wild sang at effective rates when territorial chal-
in response to the environment by increasing T3 levels in lenges occurred.125 Testosterone influences song quality.80
cold and decreasing T3 levels in warm surroundings.26 Studies indicate that it is the androgenic and estrogenic
This information implies that the hypothalamus is more metabolites of testosterone, through testosterone’s
an integrator of physiological inputs than a direct con- aromatization, that are required to completely restore
troller of thermogenesis. the full rate of singing.52 It appears that in zebra finches,
estrogenic metabolites of testosterone selectively pro-
It is clear that, under most situations, when a clinician is mote courtship song.121
faced with a “sick” bird (excluding head trauma), keep-
ing it warm is very important. If prostaglandins are Temperate zone wild male songbirds have seasonal
administered to the bird or the bird’s photoperiod is peaks of testosterone associated with increasing daylight
rearranged at this time, it would be prudent to monitor in the spring. At this time, increases in the volume of
for changes in the patient’s body temperature. song control nuclei occur.108,109 The song control nuclei
Testosterone
Changes in Song Song

Control Nuclei (SCN) Activation
1. Testosterone SCN Song

2. Testosterone Song SCN
3. Testosterone SCN
song
Fig 19.7 | Song Activation Models.
volume increase precedes the growth and development of explain the dissociation sometimes observed between
the reproductive system.116 Other environmental stimuli steroid-induced and seasonal changes in the song system
clearly play a role. Starlings in captivity, exposed to spring morphology and vocal behavior (Fig 19.7).
photoperiods, increased the volume of higher vocal center
Melatonin also may play a role in song system morphology
nuclei of the SCS, whereas males kept in outdoor aviaries
changes. The volume of the song control nuclei was stud-
in the spring had volume increases in the nuclei of most,
ied in castrated starlings held under different photoperi-
if not all of the SCS.10 It is possible that seasonal variation
ods to induce reproductive states characteristic of different
and/or steroid-induced changes in catecholaminergic affer-
seasons. Long days are associated with larger volumes of
ent input into the SCS are important in regulating changes
the higher vocal center nuclei than are short days.
in the vocal learning or production of song, as well as the
Melatonin administration attenuated the long day-induced
volume changes in nuclei of the SCS.
volume increases. The song system also was found to have
high densities of melatonin receptors.12,13 Long durations
A significant amount of research indicates the importance
of melatonin secretion in late fall and winter subdue the
of testosterone on the morphology of the SCS.
effects of testosterone. With long days, melatonin secre-
Testosterone can restore SCS development in castrated
tion decreases rapidly and testosterone increases. It is
males, corresponding to photoperiod changes in both
apparent that the interaction between many hormones
gonad and SCS size.1,108,109 Testosterone given to females
may fine-tune the activity of the SCS.
results in male-typical song behavior and increase in the
size of their song control systems.5,115 There also is evi- The SCS and behavior that induces singing are extremely
dence that the SCS can grow in response to photoperiods complex. Before administering hormones to induce
independent of testosterone.6 Recent data indicate that the singing, it is imperative that we learn more about this sys-
volume of SCS nuclei correlates with song performance in tem. More importantly, good nutrition and a good envi-
some cases. It may be that high rates of singing could ronment will allow the bird to sing when it is appropriate.
cause an increase in the SCS.7 Brain-derived neurotrophic A quiet bird out of breeding season may be a happy bird,
factor that promotes growth of the higher vocal center is with no need for male aggressive or territorial singing.
released by singing activity. This information helps to Conversely, compulsive singing may be a sign of stress.
555
From renal juxtaglomeruli

Renin Responds to sodium depletion
and chronic hypovolemia, but
not hypotension
+
Angiotensinogen Angiotensin I
Angiotensin II
ANP (chickens)
- -
Ca++ Somatostatin
PTH + -
+
ACTH Aldosterone (from adrenals)

+
+/- corticostreone
Serotonin +
+
Catecholamines
ANP = atrial natriuretic peptide ACTH = adrenocorticotropic hormone

PTH = parathyroid hormone + = stimulates - = inhibits
Fig 19.8 | Renin-Angiotensin System.
References and Rapid effects of photoperiod on 10. Benard DJ, Ball GF: Photo-
periodic condition modulates the
Derijk R: Neuroendocrine and
immunological mechanisms in
the volume of song control nuclei
Suggested Reading in American tree sparrows. The 5th effects of testosterone on song stress-induced immunomodula-
meeting of the Society for Research control nuclei volumes in male tion. J Steroid Biochem Molec
1. Arnold AP: The effects of castration European starlings. Gen Comp Biol 40:639-647, 1991.
on Biological Rhythms, Jackson-
and androgen replacement on Endocrinol 105:276-283, 1997. 16. Binkley S: Pineal and melatonin:
song courtship, and aggression in ville, FL, 1996.
11. Bentley GE: Unraveling the circadian rhythms and body tem-
Zebra finches. J Exp Zool 191:309- 7. Ball GF, Riters LV, Balthazart J:
enigma: the role of melatonin in peratures in sparrows. In Sheving
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20s1_Tumors Sec I.qxd 8/23/2005 12:16 PM Page 559
CHAPTER
20
Overview
of Tumors
Section I: Clinical Avian Neoplasia and Oncology
Section II: A Retrospective Study of Case
Overview of Tumors:
Section I
Clinical Avian Neoplasia and Oncology
TERESA L. LIGHTFOOT, DVM, D ipl ABVP-A vian
Avian neoplasias encountered in practice include cancer CUTANEOUS MASSES

of the skin, oral cavity, sinuses, liver, kidney, reproductive These may be pseudo-neoplastic conditions such as xan-
organs, bones, brain, vascular structures and connective thomas and lipomas, or neoplastic lesions.
tissue. External tumors may be detected by physical
examination and can often be diagnosed by needle aspi- Xanthomas
ration, wedge, punch or surgical biopsy. Internal neo-
These are generally friable, yellow-colored, fatty-appear-
plasias often require radiographs, ultrasound, endoscopy,
ing masses that may be located anywhere on the body,
and biopsy or exploratory surgery to identify, diagnose
but are often seen on the distal wing, in the sterno-
and determine the extent of the neoplastic processes.
pubic area and on the keel (see Chapter 13, Integument).
The origin of xanthomas is unknown, however, dietary
Treatment of neoplastic processes in birds is poorly doc-
improvement, including sufficient vitamin A or vitamin A
umented. Most reports of treatment protocols are either
precursors, has been noted to be curative in less
anecdotal or involve a single patient. Many reports are
advanced cases. Xanthomas tend to be very vascular and
not published, but are to be found in avian veterinary
surgical excision, when necessary, should be undertaken
discussion groups on the Internet.35,36,37
with due attention to hemostasis. Diffuse xanthomas
may be amenable to cryotherapy, but attention must be
The presentation in this text of these anecdotal treat-
paid to maintenance of the vascular supply.35
ments is problematic. Failure to include preliminary
information regarding efficacy and/or clinical response
Lipomas
may reduce the practitioner’s willingness and ability to
recommend treatment. However, future studies may These occur most frequently in budgerigars and are usu-
either reinforce these experimental protocols or they ally located on the keel or in the sterno pubic area. Most
early lipomas respond to modified diet therapy. Lipomas
may demonstrate a lack of efficacy or serious side effects
that cause clinical signs can be addressed via surgical
of these regimes. The ultimate decision will lie with the
excision. Malignant liposarcomas are rare in psittacines.33
knowledgeable practitioner and the well-informed client.
To date, the treatment of avian neoplasia has mirrored Mucoepidermoid Carcinomas

treatment in other domestic species. Generally, solid Mucoepidermoid carcinomas are rarely reported in birds.
tumors are best treated with surgical excision, while In humans, these tumors demonstrate variable degrees of
systemic neoplastic processes (ie, systemic lymphoma, malignancy and surgical resection is often curative.
metastatic conditions) are most effectively managed with Comparable grading of this type of neoplasia has not
use of systemic chemotherapy. Cases in which surgical been established in the avian patient (Figs 20.1.1, 20.1.2).
excision is incomplete or impossible may benefit from
alternative forms of local therapy, including external Fibrosarcomas
beam radiation (Cobalt 60 or linear accelerator), cryo- These can occur anywhere on the body, but are most
therapy, photodynamic therapy or hand-held radiation commonly seen in the oral cavity, associated with long
applicators. bones, or in the abdominal cavity (Figs 20.1.3, 20.1.4).
Chapter 20 | O V E R V I E W O F T U M O R S : S E C T I O N I
561
Lucy Bartlett
Lucy Bartlett
Fig 20.1.1 | Mucoepidermoid carcinoma. Fig 20.1.2 | Mucoepidermoid carcinoma after resection.
Fig 20.1.3 | Fibrosarcoma on the Fig 20.1.4 | Fibrosarcoma on the wing of Fig 20.1.5 | Squamous cell carcinoma
face of a budgerigar. a lovebird. of the rhamphotheca, and papillomatosis
in an older Timneh grey parrot.
Fibrosarcomas may be subcutaneous or more deeply complete excision is rarely accomplished. Radiation ther-
located in underlying tissue, and often appear fixed and apy has been attempted with some success, however,
proliferative with a nodular, red surface. They tend to be squamous cell carcinoma appears to be an exceptionally
locally invasive and often recur with conservative surgi- radioresistant tumor and long-term control is rare.
cal excision. Therefore, additional local treatment in the Anecdotal reports indicate that radioresistance may be
form of radiation therapy is often indicated for providing even greater in birds than in mammals.19,35 Strontium
long-term local control. As the metastatic rate in other therapy when tumor depth is not a limiting factor has
domestic species ranges from 5 to 15%, local disease shown some promise in selected psittacine cases.35
management is paramount, with metastatic control as a Distant metastasis is rare, therefore chemotherapy is not
secondary concern. Surgical excision followed by both commonly utilized. Photodynamic therapy (PDT) has
radiation and chemotherapy has been reported with been attempted in two reported cases. One case of a
some success in a few publications.14 Strontium radiation squamous cell carcinoma in the beak of a hornbill
therapy, although limited by depth of penetration, has showed a positive result in decreasing tumor size, but
been anecdotally reported as efficacious in several failure to eliminate the neoplasia.31 The second case
instances.35 demonstrated a positive response to PDT after each
treatment, but treatments were not able to be adminis-
Squamous Cell Carcinomas tered at regular intervals.28
These also may occur anywhere on the body, being most

prevalent at mucocutaneous junctions of the head (Fig NEOPLASIA OCCURRING IN THE
20.1.5), on the distal wing and on the phalanges. The MUSCULOSKELETAL SYSTEM
uropygial (preen) gland also may develop either adeno- Theoretically these include the benign lesions such as
carcinoma or squamous cell carcinoma. (Note that chondroma and hemangioma, and malignant tumors
Amazona spp. do not possess a preen gland). Squamous including osteosarcoma, chondrosarcoma and leiomyo-
cell carcinomas tend to be extremely locally invasive and sarcoma. Wide surgical resection or amputation are
Fig 20.1.6 | Chondroma on the leg of a Fig 20.1.7 | Gross appearance of the Fig 20.1.8 | The bird in Fig 20.1.11,
budgerigar. abdomen in a 9-month-old African grey showing hemangioma encompassing most
parrot with diffuse coelomic hemangioma. abdominal viscera.
generally the suggested methods of treatment, as (see Chapter 13, Integument). Although histopathologi-
benign lesions are often cured with complete excision cally benign, in at least one case in this author’s experi-
and a decrease in tumor burden can be accomplished ence, hemangioma occurred in a juvenile African grey
in malignant lesions. As tumors such as osteosarcoma (Psittacus erithacus) and involved the coelomic cavity,
carry high metastatic rates, additional therapies may be small intestine, liver, lung, air sacs and pericardium.
indicated. Extrapolation from canine and feline oncol- Complete surgical excision could not be accomplished
ogy may suggest other modalities such as radiation ther- and euthanasia was eventually required (Figs 20.1.7,
apy for additional local treatment and chemotherapy for 20.1.8). Treatment of a hemangiosarcoma with radiation
systemic control. therapy has been reported in one case.9
Chondromas Internal Carcinomas

Therapy for chondromas generally involves aggressive These are commonly reported in birds and include ovar-
surgical excision of the affected area (Fig 20.1.6). ian neoplasias (of various cell origins), renal carcinomas,
Radiation and chemotherapy may be considered. hepatic adenocarcinoma, hepatobiliary and pancreatic
adenocarcinoma (related to papillomas in Amazons),
Osteosarcoma splenic and gastric carcinomas. Papillary carcinomas of
Confirmation of osteosarcoma has rarely been reported air sac origin are locally invasive and may present as
in psittacines. Species and anatomic location predilec- external masses. Anecdotal reports exist indicating
tions have not been noted in psittacines. Documentation intralesional carboplatin therapy may be useful in ovar-
of classifiable radiographic changes consistent with ian and renal adenocarcinoma, generally following surgi-
osteosarcoma is not available for birds. cal debulking and confirmation of the neoplasia on
histopathology.18,34 Bile duct carcinoma also has been
A biopsy should be obtained from patients where radi-
treated with carboplatin successfully in one report.38
ographic bony lesions are present. Under inhalant anes-
Toxicity studies with cisplatin in cockatoos indicate that
thesia, a 22- to 20-gauge needle can be surgically intro-
psittacine tolerance for this drug may be greater than
duced into the bone. A sufficient sample is usually
that of mammals.8
obtained and subsequently retained in the hub of the
needle. The sample can then be dislodged with smaller Tamoxifen administration has not been evaluated for effi-
gauge wire and submitted. If a diagnosis of osteosar- cacy in cases of avian ovarian carcinoma, but anti-estro-
coma is received, amputation with follow-up chemother- genic activity was suggested and side effects were mini-
apy is the current recommended protocol extrapolated mal in one drug trial.17 GnRH agonistsa have been effec-
from canine medicine. tive empirically (dosed at 200-800 µg/kg), however, con-
firmation of neoplasia (as opposed to cystic ovarian dis-
INTERNAL NEOPLASIA ease) has not often been confirmed prior to therapy.16,20
Hemangiomas Doxorubicin (adriamycin) is commonly employed in the

These seem to occur more commonly than hemangiosar- treatment of carcinomas in human and canine patients.
comas in birds. Hemangioma may be internal or external The limiting toxic effects of doxorubicin include myelo-
and commonly appears as a red-purple, flat, firm lesion suppression and cardiac toxicity. To date, the degree to
563
which these concerns will apply to avian cancer patients

has not been determined. Anecdotal reports of both tox-
icity and efficacy of doxorubicin in avian patients are
currently inconclusive.34 Dosages of 50-60 mg/m2 have
been used with no adverse reactions. In several cases
there has been significant tumor regression (Goldsmith,
Lightfoot, unpublished data, 2004).
Carcinomas, generally diagnosed at necropsy, are often

found at the proventricular-ventricular junction. Death
from this neoplasia may be due to hemorrhage, perfora-
tion and sepsis or endotoxic shock, or inanition and
Lucy Bartlett
subsequent wasting. Metastasis to the lungs has been
confirmed in one case report.4
Biliary and pancreatic carcinomas are frequently diag- Fig 20.1.9 | Thymoma in a lovebird,
intraoperatively.
nosed in the genus Amazona and to a lesser degree,
Ara, in conjunction with internal papillomatosis.11,13 A
recent connection to a herpesvirus has been identified
(see Chapter 32, Implications of Viruses in Clinical with conditions related to the pituitary hormone(s) that
Disorders). Carboplatin has been used in several cases are affected. Usually, this will be pronounced polydypsia
with equivocal results, but with no apparent toxicity.7,35,38 and polyuria. Occasional presentations will be that of a
retrobulbar mass and subsequent exophthalmia.27 In
Surgical excision is the treatment of choice with solitary human medicine, surgical resection and radiation ther-
lesions of hepatic cell carcinoma in other species, and is apy (if needed) are utilized for treatment. Size and mon-
the only documented curative treatment in human medi- etary constraints make routine treatment by these meth-
cine. Combinations of chemotherapy and radiation ther- ods unlikely in our small psittacine patients.
apy have been used with equivocal results in people in
an attempt to prevent or limit metastatic disease. In Thyroid
widely disseminated hepatic carcinoma, palliative chemo- Budgerigars that are iodine deficient may develop non-
therapy is often employed. However, extrapolation from neoplastic thyroid hyperplasia that presents as a thyroid
people would indicate that this type of cancer is highly mass, often causing a change in the voice or a respira-
resistant to chemotherapy. The most commonly employed tory squeak.
chemotherapeutic agents in human medicine appear to
be doxorubicin and 5-fluorouracil (5-FU), however, Thyroid Tumors
mean survival times do not appear to be statistically These are not as common in birds as they are in domestic
improved in patients with widely disseminated disease. rabbits, but do occur (Fig 20.1.9). They may be intra-
The use of immunotherapy — including interferon, in thoracic or located in the area of the neck. In humans,
conjunction with cisplatin, doxorubicin and 5-FU — has classification according to cell type (medullary, cortical
shown the most promise to date in human patients. and mixed) is a prognostic indicator, with cortical
Unfortunately, interferon is limited in its usefulness by tumors having the highest incidence of recurrence and
cost and availability in veterinary medicine. The effi- malignancy. Thymoma and thyroid adenocarcinoma have
ciency of radiation therapy for carcinomas and other been reported in several psittacine species. Surgical exci-
neoplasias is largely unknown. However, tolerance of sion is the primary treatment recommendation. Adjuvant
radiation therapy has been anecdotally reported as radiation and chemotherapy protocols are being utilized
greater than anticipated. in human medicine. Cisplatin is used in many human
chemotherapy protocols for thymomas and thymic carci-
Endocrine Neoplasia nomas. Limited studies have shown that psittacines may
Neoplasia of endocrine origin is not frequently reported be tolerant of the common side effects induced by cis-
in birds. platin, and this agent may be useful in the treatment of
these neoplasias.
Pituitary Adenomas
These have been documented in multiple avian species, Pancreatic Neoplasias
but are most prevalent in budgerigars and cockatiels. Infrequent accounts of primary pancreatic neoplasia of
Affected animals may present with acute neurologic con- variable cell origin, not associated with internal papillo-
ditions (seizures/opisthotonos). They also may present matosis, have been reported.23
Lori Harrison
Lori Harrison
Fig 20.1.10 | Retrobulbar lymphoma in a young African grey. Fig 20.1.11 | Gross necropsy photo of the liver
from the African grey in Fig 20.1.10. A fine-nee-
dle aspirate of the liver demonstrated that the
lymphoma had spread to involve the hepatic
parenchyma.
Respiratory Neoplasia exist. Some of the chemotherapeutic agents listed may be

Primary respiratory neoplasia is uncommon in psitta- determined to be either ineffectual or contraindicated in
cines.12 An exception seems to be an intrathoracic neo- birds. As documentation of these variables occurs, it is
plasia reported in cockatiels. It is characterized by the hoped that protocols can be developed that will produce
inclusion of two cell types, having both mesenchymal more predictable results in the avian patient.
and epithelial cell components (see Section II of this Chemotherapy Protocols for Canine Lymphoma*
chapter). Few other primary pulmonary neoplasias have
(Current recommended canine dosages can be found in
been reported in the literature.2 Metastatic pulmonary
Plumb’s Veterinary Handbook).
neoplasia may occur, but it is not noted with the same
frequency as is documented in dogs.4 1. Oral Therapies
a. Prednisolone and cyclophosphamide
b. Lomustine (CCNU)
Lymphoma/Lymphosarcoma
2. Injectable Therapy
Numerous reports of exophthalmos in psittacines, par- a. COP-L Protocol
ticularly young African greys, have been diagnosed as i. L-asparaginase injection
retrobulbar lymphoma (Fig 20.1.10). Differential diag- ii. Oral prednisolone (tapering dose)
iii. Oral weekly cyclophosphamide
noses for this condition are pituitary adenoma and iv. Vincristine injections weekly IV
hyperplasia or adenoma of the Harderian gland. b. Single-agent adriamycin injections q 3 weeks IV
Lymphoma may have many presentations in pet birds, c. UW-Madison Cyclic Combination
much as it does in other companion animals (Fig i. L-asparaginase
20.1.11). Chemotherapy is the treatment of choice for ii. Vincristine
systemic disease, and surgery and radiation therapies iii. Cyclophosphamide
iv. Adriamycin
have been successfully employed in cases of solitary lym-
v. Prednisolone
phoma.6,35 To date, no evidence of retroviral activity has
Applicable testing (CBC, biochemistries, cardiac evalua-
been associated with psittacine lymphoma.
tion) should be performed to assess the initial and intra-
therapeutic health of the patient.
The clinician may find it useful to have access to current
protocols for lymphoma that are utilized in canine medi-
*It must be emphasized again that these protocols are
cine. Tracy LaDue, Diplomate ACVIM-Oncology and
designed for canine patients. Extrapolation to avian
ACVR-Radiation Oncology, of Florida Veterinary Specialists
patients must be undertaken with the knowledge that
in Tampa, Florida, US, has generously provided the fol-
efficacy and potential side effects have not been docu-
lowing abbreviated outline of therapeutic options and
mented.
chemotherapeutic agents. These protocols are NOT
established for avian patients, but are provided to give
the practitioner a point of reference when attempting to CHEMOTHERAPEUTIC AGENTS
design potential therapeutic regimes for birds with lym- Anticancer agents are typically broken into six categories
phoma. Again, species differences in response may well based on their mechanism of action.
565
1. Alkylating agents such as cyclophosphamide and Most anticancer agents have associated vomiting, diar-
lomustine prevent cell replication by covalently bind- rhea and bone marrow suppression as sequelae. It is
ing to the nucleotide bases of the DNA molecule. important to monitor patients for signs of dehydration
2. Antimetabolites will mimic purine, pyrimidine or or secondary infection as a result of chemotherapy
metabolite precursors of the nucleotide bases, result- administration. Some anticancer agents have particular
ing in non-functional DNA. toxicities known to that drug alone, such as sterile hem-
3. Steroids such as prednisone and prednisolone cause orrhagic cystitis due to cyclophosphamide metabolites in
lympholysis and suppress neutrophil function and dogs and people. Such toxicities are not well reported in
antibody production. avian species and should be monitored for accordingly.
4. Plant alkaloids such as vincristine bind to micro-
tubules to prevent normal formation and function of When confronted with a confirmed diagnosis of neoplasia,
the mitotic spindle. The antibiotics such as adriamycin a current literature search is warranted due to the rapid
intercalate between DNA base pairs to disrupt tran- advances and changes in treatment recommendations.
scription and also cause oxygen free radical damage. Consultation with a veterinary oncologist will increase the
5. Miscellaneous drugs such as the Platinol compounds likelihood of selecting an appropriate treatment regime
(cisplatin and carboplatin) also bind to bases of the and properly administering the chosen therapy.
DNA preventing replication, but have a bifunctional
ability with double attachment to DNA strands. Products Mentioned in Text
a. Depo-Lupron, Pharmaceuticals, Inc, Deerfield, IL USA, 800-622-2011
6. L-asparaginase hydrolyzes asparagine to aspartic acid
and ammonia, resulting in loss of an essential amino
acid for cell function.
References and 10. Hahn KA, Jones MP, Petersen MG: Adenocarcinoma in a Budgerigar. Parrot. J Avian Med Surg 9(4):263-
Metastatic pheochromocytoma in Exotic DVM 4(2):11-12 May 2002. 270, 1995.
Recommended Reading a parakeet. Avian Dis 41(3):751-4, 19. Manucy TK, Bennett RA, 28. Rosenthal K, et al: A Report of
1. Altman RA, et al (eds): Avian 1997. Greenacre C: Squamous cell car- Photodynamic Therapy for
Medicine and Surgery. Phila- 11. Hillyer EV, et al: Bile duct carci- cinoma of the mandibular beak in Squamous Cell Carcinoma in a
delphia, WB Saunders Co, 1997. noma in two out of ten Amazon a Buffon’s macaw (Ara ambigua). Cockatiel. Proc Ann Conf AAV
2. Andre JP, Delverdier M: Primary parrots with cloacal papillomas. J J Avian Med Surg 12(3):158-166, 2001, pp 175-176.
bronchial carcinoma with oseous Assoc Avian Vet 5(2):91-95, 1991. 1998. 29. Schmidt RE: Selected Neoplasia
metastasis in an African grey par- 12. Jones MP, Orosz SE: Pulmonary 20. Morrissey JK: Gastrointestinal of the Avian Integument. Exotic
rot (Psittacus erithacus). J Avian carcinoma with metastases in a Diseases of Psittacine Birds. Sem DVM Vol 4(2):13-14, 2002.
Med Surg 13(3):180-186, 1999. Moluccan cockatoo (Cacatua Avian Exotic Pet Med 8(2):66-74, 30. Sturkie PD, Whittow GC (eds):
3. Burgmann PM: Common moluccensis). J Avian Med Surg 1999. Sturkie’s Avian Physiology 5th ed.
psittacine dermatologic diseases. 15(2):107-113, 2001. 21. Orosz, SE, Ensley PK, Haynes CJ: San Diego, Academic Press,
Sem Avian Exotic Pet Med 13. Kennedy FA, Sattler-Augustin S: Avian Surgical Anatomy. Harcourt Brace and Co, 2000.
4(4):169-183, 1995. Oropharyngeal and cloacal papil- Philadelphia, WB Saunders Co, 31. Suedmeyer WK: Attempted
4. Campbell TW: Carcinoma of the lomas in two macaws (Ara spp.) 1992. Photodynamic Therapy of
ventriculus with metastasis to the with neoplasia with hepatic 22. Ottinger MA: Neuroendocrine Squamous Cell Carcinoma in the
lungs in a sulphur-crested cocka- metastasis. J Avian Med Surg Regulation of Reproduction in Casque of a Great Hornbill
too (Cacatua galerita), J Avian 10(2):89-95, 1996. Birds and Clinical Applications of (Buceros bicornis). J Avian Med
Med Surg 13(4):265-268, 1999. 14. Lamberski N, Theon AP: GnRH Analogues in Birds and Surg 15(1):44-49, 2001.
5. Clyde VL, Orosz SE, Munson L: Concurrent irradiation and intra- Mammals. Sem Avian Exotic Pet 32. Tell LA, Woods L, Mathews KG:
Severe hepatic fibrosis and bile tumoral chemotherapy with cis- Med 11(2):71-79 April, 2002. Basal cell carcinoma in a blue-
duct hyperplasia in four Amazon platin for treatment of a fibrosar- 23. Rae M: Endocrine Disease in Pet fronted amazon parrot (Amazona
parrots. J Avian Med Surg coma in a blue and gold macaw Birds. Semin Avian Exotic Pet Med aestiva), Avian Dis 41(3):755-9
10(4):252-257, 1996. (Ara ararauna). J Avian Med Surg 4(1):32-38 Jan 1995. Jul-Sep 1997.
6. Coleman CW: Lymphoid neopla- 16(3):234-238, 2002. 24. Ramos-Vara JA: Lymphosarcoma 33. Tully T: Liposarcomas In A Monk
sia in pet birds: A review. J Avian 15. Lennox AM: The Use of Aldara with plasmacytoid differentiation Parakeet (Myiopsitta monachus).
Med Surg 9(1):3-7, 1995. (Imiquimod) for the Treatment of in a scarlet macaw (Ara macao). J Assoc Avian Vet 8(3):120-124
7. Degernes LA: Multicystic biliary Cloacal Papillomatosis in Avian Dis 41(2):499-504 Apr-Jun Fall 1994.
adenocarcinoma in a blue-and- Psittacines. Exotic DVM 4(3):34- 1997. 34. Watson CL, Lucroy MD: Primary
gold macaw (Ara ararauna). J 35 July 2002. 25. Ritchie B, Harrison GJ, Harrison Appendicular Bone Tumors in
Avian Med Surg 12(2):100-107, 16. Lightfoot TL: Avian Common LR (eds): Avian Medicine: Dogs. Compend Contin Edu Pract
1998. Clinical Presentations: Neoplastic, Principles and Application. Lake Vet 24(2):128-138 Feb 2002.
8. Filippich LJ: Intravenous cisplatin Toxic, Viral and Miscellaneous. Worth, FL, Wingers Publishing, 35. www.vin.com, Member Search -
administration in sulphur-crested Proc Atlantic Coast Vet Conf, Inc, 1994. Species: Bird, Subject: Neoplasia
cockatoos (Cacatua galerita): 2001. 26. Ritchey JW, Degernes LA, Brown 36. www.exoticdvm.com
Clinical and pathologic observa- 17. Lupu CA: Evaluation of Side TT Jr: Exocrine pancreatic insuffi- 37. www.avianmedicine.net
tions. J Avian Med Surg 15(1):23- Effects of Tamoxifen in ciency in a yellow-naped Amazon 38. Zantop DA: Treatment of bile
30, 2001. Budgerigars, (Melopsittacus (Amazona ochrocephala) with duct carcinoma in birds with
9. Freeman KP: Radiation therapy undulatus). J Avian Med Surg pancreatic adenocarcinoma. Vet carboplatin. Exotic DVM 2(3):76-
for hemangiosarcoma in a 14(4):237-242 Dec 2000. Pathol 34(1):55-7 1997. 78, 2000.
budgerigar. J Avian Med Surg 18. MacWhirter P: Use of Carboplatin 27. Romagnano A, Mashima TY:
13(1):40-44, 1999. in the Treatment of Renal Pituitary Adenoma in an Amazon
20s2_Tumors Sec 2.qxd 8/23/2005 12:37 PM Page 566
Overview of Tumors:
Section II
A Retrospective Study of Case
MICHAEL M. GARNER, DVM, D ipl ACVP
The occurrence of various types of avian neoplasia has prevalence of neoplasia over the 7-year period was high-
been comprehensively reviewed.6 This section documents est in Anseriformes (ducks, geese, swans), Galliformes
the prevalence of neoplasms in 22 avian orders submit- (poultry, pheasants), Strigiformes (owls) and
ted to a specialty diagnostic service (Northwest ZooPath, Cuculiformes (cuckoos, turacos).
Monroe, WA) from 1994 to 2002. Cases were selected
based on histologic diagnosis. Cysts, hyperplastic Tables 20.2.3 and 20.2.4 list the tumor submissions by
processes, fibromatous polyps and poxvirus-related pro- type and biological behavior. The most common types of
liferative lesions were not included. Cases diagnosed as tumors were cutaneous squamous cell carcinoma, multi-
neoplastic based on cytology alone also were excluded. centric lymphoma, cutaneous soft tissue sarcoma, biliary
Although potentially reversible and not considered true adenocarcinoma and ovarian/oviduct adenocarcinoma.
neoplasms, adenomatous polyps and papillomas were
included because of the known association of these
lesions with concurrent neoplasia in psittacine birds.4 Neoplasia by Avian Order
Type, location, biological behavior and patient outcome
are addressed. Apparent trends for particular types of
neoplasms in some orders or species also are identified
PSITTACIFORMES
and discussed. For the purposes of this manuscript, Order Psittaciformes (parrots and related species) had
prevalence refers to a given percentage within the study 3545 representatives and 220 neoplastic processes
population, and the study population comprises the (prevalence = 6.2%) (see Table 20.2.2), slightly higher
cases submitted to the service. The prevalence of these than the average prevalence for tumor submissions from
neoplasms in the populations from which these birds other orders. Table 20.2.5 summarizes the most common
originated is not known. presentations of neoplasms within this order. Trend crite-
ria were based on total number of tumor types in a
Table 20.2.1 lists the tumor submissions by site and bio- species (two or more), and percent of total for all tumors
logical behavior. Skin was the most common site for in a species (10% or greater). Using these criteria, numer-
tumor development, followed by alimentary tract, repro- ous trends were observed within this order. For cock-
ductive tract and liver. In all locations except alimentary atiels (Nymphicus hollandicus), trends were identified in
tract, malignant tumors were more common than soft tissue sarcoma, squamous cell carcinoma, ovarian/
benign tumors; the large numbers of cloacal and oral oviduct adenocarcinoma, fibrosarcoma and seminoma.
papillomas and adenomatous polyps in psittacine birds For Amazon parrots (Amazona spp.), trends were identi-
account for this variation in behavior. fied for squamous cell carcinoma, cloacal adenomatous
polyp, cloacal papilloma and biliary adenocarcinoma. For
Table 20.2.2 summarizes total numbers of submissions macaws (Ara spp.), trends were identified for cloacal
and total numbers of tumors for each order. For the adenomatous polyp, cloacal papilloma and biliary adeno-
study period, 9574 avian samples were submitted, repre- carcinoma. For cockatoos (Cacatua spp.), trends were
senting 22 orders; 557 neoplastic processes were identi- identified for soft tissue sarcomas and cloacal adenoma-
fied, for an overall prevalence of 5.8%. The overall tous polyps. For budgerigars (Melopsittacus undulatus),
Chapter 20 | O V E R V I E W O F T U M O R S : S E C T I O N I I
567
Table 20.2.1 | Tumor Submissions by Table 20.2.3 | Epithelial, Gonadal and Bimorphic Neoplasmsa: Total Numbers,
Site and Biological Behavior Biological Behavior and Patient Outcome
Location Total Malignant Benign Tumor Tumor Invasive Lymphatic Meta- Death Death Excised Lost to
Type # Behavior invasion stasis Due to Due to follow
Skin 120 92 28
Tumor Other up
Alimentary 67 32 35
Malignant neoplasms
Reproductive 64 59 5
Squamous cell 48 48 1 4 16 0 3 29
Liver 54 45 9 carcinoma
Kidney 28 17 11 Biliary 29 29 0 5 28 0 0 1
Respiratory 20 20 0 adenocarcinoma
Intracoelomic 17 16 1 Ovarian/oviduct 28 28 2 9 19 2 0 7
adenocarcinoma
Pancreas 13 12 1
Renal 16 16 0 1 15 0 0 1
Endocrine 13 6 7 adenocarcinoma
Uropygial gland 8 7 1 Seminoma 15 15 0 0 5 8 3 3
Musculoskeletal 7 7 0 Pancreatic 13 13 0 7 13 0 0 0
Thymus 5 4 1 adenocarcinoma
Conjunctiva 5 2 3 Intracoelomic 12 12 0 5 12 0 0 0
adenocarcinoma
CNS 3 3 0
Hepatocellular 11 11 0 3 10 1 0 0
Spleen 2 1 1 carcinoma
Heart 2 2 0 Proventricular 10 10 0 4 10 0 0 0
adenocarcinoma
Air sac 9 9 1 4 8 0 0 1
Table 20.2.2 | Total Submissions and adenocarcinoma
Prevalence of Neoplasia by Order
Pulmonary 6 6 0 0 6 0 0 0
Order Cases Tumors % adenocarcinoma
Anseriformes 1024 119 11.6 Ventricular 5 5 1 1 5 0 0 0
adenocarcinoma
Strigiformes 131 13 9.9
Cloacal 4 4 0 0 1 0 0 3
Galliformes 783 74 9.4
adenocarcinoma
Cuculiformes 62 5 8.1
Sertoli cell tumor 4 4 1 1 1 3 0 0
Psittaciformes 3545 220 6.2
Bimorphic 4 4 0 1 4 0 0 0
Columbiformes 294 17 5.8 pulmonary tumor
Sphenisciformes 204 11 5.4 Thyroid 3 3 0 0 3 0 0 0
Phoenicopteriformes 265 13 4.9 adenocarcinoma
Coraciiformes 192 9 4.7 Interrenal cell 2 2 0 1 2 0 0 0

carcinoma
Unknown 44 2 4.5
Nephroblastoma 2 2 0 0 1 1 0 0
Gruiformes 249 11 4.4
Benign neoplasms
Falconiformes 272 10 3.7
Papilloma 21 0 0 0 0 2b 1 18
Ciconiiformes 307 11 3.6
Adenomatous 17 0 0 0 0 5c 1 11
Struthioniformes 111 3 2.7 polyp
Charadriiformes 240 6 2.5 Renal adenoma 12 0 0 0 6 6 0 0
Coliiformes 51 1 2.0 Hepatoma 4 0 0 0 2 1 0 1
Piciformes 198 4 2.0 Thyroid adenoma 4 0 0 0 1 3 0 0
Passeriformes 1441 27 1.8 Interrenal cell 3 0 0 0 0 3 0 0
Pelecaniformes 58 1 1.7 adenomad
Apodiformes 19 0 0.0 Biliary adenoma/ 3 0 0 0 0 4 0 1
cystadenoma
Procellariiformes 6 0 0.0
Granulosa cell 2 0 0 0 1 1 0 0
Gaviiformes 63 0 0.0 tumor
Caprimulgiformes 15 0 0.0 Folliculoma 2 0 0 0 0 0 1 1
Totals 9574 557 5.8
a. For all tumors represented two or more times in the study. Tumors represented only once not
included.
b. One psittacine cloacal papilloma was associated with concurrent fatal biliary adenocarcinoma, and
one psittacine ingluvial papilloma underwent transformation to fatal squamous cell carcinoma.
c. Four psittacine cloacal adenomatous polyps transformed locally to adenocarcinomas. Two
psittacines with cloacal adenomatous polyps had concurrent fatal biliary adenocarcinoma, and two
psittacines with cloacal adenomatous polyps had concurrent fatal pancreatic adenocarcinoma.
d. The function of interrenal cells (cells of the avian adrenal gland) is analogous to cortical cells of the
mammalian adrenal gland.
Table 20.2.4 | Mesenchymal Neoplasmsa: Biological Behavior and Patient Outcome

Tumor Type Tumor # Invasive Lymphatic Metastasis Death Due Death Due Excised Lost to
Behavior Invasion to Tumor to Other follow up
Malignant tumors
Lymphoma 40 40 0 36b 36 0 0 4
Soft tissue sarcoma c
36 33 1 4 15 2 6 13
Fibrosarcoma 19 19 0 0 6 2 1 10
Hemangiosarcoma 11 11 0 3 9 0 1 1
Osteosarcoma 6 6 0 1 5 0 1 1
Myelolipoma 5 5 0 0d 5 0 0 0
Nerve sheath 4 4 0 0 0 0 1 3
Melanoma 4 4 0 2 3 1 0 0
Thymoma 4 4 0 0 1 0 0 3
Liposarcoma 2 2 0 0 0 0 0 2
Lymphoproliferative disease 2 2 0 1* 2 0 0 0
Benign tumors
Lipoma 16 0 0 0 0 0 3 13
Hemangioma 8 0 0 0 1 1 2 4
Myelolipoma 2 0 0 0 0 1 1 0
*multicentric
a. For all tumors represented two or more times in the study. Tumors represented only once not included.
b. Lymphoma is generally a multicentric process. In 35 birds, the tumor was considered multicentric rather than metastatic, based on the
presence of neoplastic cells in at least two different tissue types. In only one dead bird with full tissue evaluation was lymphoma
detected in only one tissue (thymus). The remaining four cases were single tissue biopsies that were lost to follow-up, but also were
likely multicentric tumors. Two cases had apparent concurrent lymphoid leukemia, based on histologic evaluation.
c. Tumors were classified as soft tissue sarcomas if they were undifferentiated or had too much anaplasia to determine the cell of origin.
Likely differentials were fibrosarcoma, leiomyosarcoma, rhabdomyosarcoma, synovial sarcoma, neurofibrosarcoma, myxosarcoma and
amelanotic melanoma.
d. Intracoelomic myelolipomas were invasive and infiltrated many visceral tissues. It was difficult to determine if some visceral foci were
extensions of the invasive process or represented metastatic lesions.
Table 20.2.5 | Prevalence of Most Common Types of Neoplasms in Psittacine Birds

Species and Total # of Tumors
Tumor Type and Cockatiel Amazon Macaw Cockatoo Budgerigar Lovebird African Rosella
% of Total Psittacine Cases (220) (39) (30) (28) (25) (25) (19) Grey (8) (3)
Soft tissue sarcoma - 23 (10.5%) 6 (15%) 0 2 (7% ) 4 (16%) 4 (16%) 4 (21%) 1 (12.5%) 0
Squamous cell carcinoma - 22 (10%) 7 (18%) 3 (10%) 1 (4%) 0 5 ( 20%) 0 2 (25%) 2 (67%)
Cloacal adenomatous polyp - 15 (6.8%) 0 4 (13%) 4 (14%) 4 (16%) 0 0 1 (12.5%) 0
Ovarian/oviduct adenocarcinoma - 13 (5.9%) 7 (18%) 0 1 (4%) 2 (8%) 0 1 (5%) 0 0
Cloacal papilloma - 12 (5.5%) 0 4 (13%) 7 (25%) 0 0 0 1 (12.5%) 0
Fibrosarcoma - 11 (5%) 2 (5%) 0 0 2 (8%) 4 (16%) 2 (11%) 0 0
Biliary adenocarcinoma - 11 (5%) 0 4 (13%) 3 (11%) 0 0 1 (5%) 0 0
Lymphoma - 8 (3.6%) 0 2 (7%) 1 (4%) 0 1 (4%) 3 (16%) 1 (12.5%) 0
Seminoma - 7 (3.2%) 3 (7.6%) 0 1 (4%) 0 1 (4%) 0 0 0
Renal adenocarcinoma - 6 (2.7%) 0 0 1 (4%) 1 (4%) 4 (16%) 0 0 0
trends were identified for soft tissue sarcoma, squamous (Cacatua spp.), an African grey, a thick-billed parrot
cell carcinoma, fibrosarcoma and renal adenocarcinoma. (Rhynchopsitta pachyrhyncha) and a Patagonian conure
Interestingly, although lipomas are recognized as a com- (Cyanoliseus patagonus). This distribution is similar to
mon tumor in budgerigars,6,12 a trend was not identified that of retrospective studies of this condition.4,14 Malig-
in this analysis of submissions. This may be because clini- nant transformation of cloacal “papillomas” has been
cians easily recognize these tumors, thus biopsies are not described in psittacine birds.6,14 In this study, four cloacal
routinely submitted. For lovebirds (Agapornis spp.), adenomatous polyps (two macaws, one amazon parrot
trends were identified for soft tissue sarcoma, fibrosar- and one cockatoo) underwent local transformation to
coma and lymphoma. For African greys (Psittacus eritha- adenocarcinoma, although no metastases were seen.
cus) and rosellas (Platycercus spp.), trends were identi- Adenomatous polyps also were noted in the proventricu-
fied for squamous cell carcinoma. lus of a cockatoo and on the eyelid of a cockatiel. Two
cloacal adenomatous polyps were associated with con-
Cloacal Adenomatous Polyps and Papillomas current biliary adenocarcinoma and two with concurrent
Cloacal adenomatous polyps were common in Amazon pancreatic adenocarcinoma. Cloacal papillomas also
parrots and macaws, and also were seen in cockatoos were common in macaws and Amazon parrots, and one
569
was seen in an African grey. Concurrent or isolated GALLIFORMES

oral/choanal papillomas were occasionally seen. Only
Order Galliformes (chickens, turkeys, pheasants, pea-
one of the cloacal papillomas was associated with con-
fowl) had 783 representatives and 74 tumors (9.5%) (see
current biliary adenocarcinoma, and none were associ-
Table 20.2.2), considerably higher than the average for
ated with malignant transformation in the cloaca.
tumor submissions from other orders. Table 20.2.6 sum-
Proliferative lesions of the cloacal mucosa of psittacine marizes the most common presentations of neoplasms
birds are well recognized.4,6,14 Although typically referred within this order. Trend criteria were based on total
to as papillomas, there are different morphologic presen- number of a tumor type in a species (two or more), and
tations: a papilliform proliferation of squamous mucosal percent of total for all tumors in a species (10% or
epithelial cells resembling a typical papilloma; and an greater). Using these criteria, numerous trends were
adenomatous proliferation of glandular and villous observed within this order. For chickens, trends were
mucosa more typical of a polyp, perhaps best termed an identified for lymphoma, ovarian/oviduct adenocarci-
adenomatous polyp. Although the morphologic features noma and squamous cell carcinoma. These tumors are
of cloacal adenomatous polyps and papillomas differ, it is well recognized in poultry.2,10,11,16 Some of these tumors,
possible that these represent different morphologic vari- particularly the lymphoid malignancies, may have been
ants of the same disease process. Both have similar site associated with or induced by viral infection.2,10,11,16 The
and species predilections, and both are sometimes asso- only identifiable trend in pheasants was for interrenal
ciated with concurrent pancreatic and biliary malignan- cell adenoma, an otherwise uncommon tumor in birds.
cies. However, the distinction between cloacal adenoma- For guinea fowl, trends were identified for squamous
tous polyps and papillomas may not be purely academic. cell carcinoma, seminoma and hepatocellular carcinoma.
Based on this collection of the two cloacal phenotypes, The only trend identified in peafowl was lymphoma. For
the adenomatous polyps appear to have the most poten- turkeys, trends were identified for ovarian/oviduct ade-
tial for undergoing malignant transformation in the nocarcinoma and lymphoma. Herpesviruses and retro-
cloaca, and for being associated with concurrent pancre- viruses have been identified as important causes of neo-
atic or biliary neoplasia. Cloacal papillomas have been plasia in gallinaceous birds, particularly chickens and
associated with herpesvirus gene sequences.5,13 turkeys,2,10,11,16 and it is possible that viral oncogenesis
was a factor in many of the cases within this order; how-
Bimorphic Pulmonary Neoplasms of Cockatiels ever, serologic and other ancillary testing for viral causes
was not routinely performed on case submissions, so
Four separate cases of an unusual malignant pulmonary
viral status of affected birds was generally not known.
neoplasm were seen in cockatiels. The birds presented
with a history of dyspnea and usually had a radiographi-
cally apparent mass in the thoracic region of the coelomic ANSERIFORMES
cavity. Microscopically, the tumor involved the lung and Order Anseriformes (ducks, geese, swans) had 1024 rep-
spread by extension to serosal surfaces of viscera, espe- resentatives and 119 tumors (11.6%) (see Table 20.2.2),
cially heart and air sacs. One case of possible metastasis considerably higher than the average for tumor submis-
to the endocardial surface also was seen. The tumor sions from other orders. All the birds were adults or aged
appeared to arise within the pulmonary parenchyma, and most tumors likely occurred spontaneously. Trend cri-
around the parabronchi. These neoplasms have unusual teria were based on total number of a tumor type in a
cell morphology and are characterized by densely cellu- species (two or more), and percent of total for all tumors
lar sheets of round to elongate cells with large vesicular in a species (10% or greater). Using these criteria, only
to amphophilic smudged nuclei. The cells stain posi- two trends were identified: lymphoma and biliary adeno-
tively for mammalian vimentin, a mesenchymal cell carcinoma in ducks, although a broad spectrum of neo-
marker, and have cytoplasmic intermediate filaments plastic processes was represented in this group.
consistent with vimentin, suggesting that the cells are of
mesenchymal origin. The cells stain negatively for mam-
malian epithelial pan cytokeratins; however, desmo- PASSERIFORMES
somes, a feature of epithelial cells, are occasionally seen Order Passeriformes (songbirds) had 1441 representa-
between adjacent cells. The cell of origin is poorly tives and only 27 tumors (1.9%) (see Table 20.2.2), con-
understood, but the tumors appear to be “bimorphic” siderably below the average for other orders, suggesting
with mesenchymal and epithelial cell components. The that spontaneous neoplasia in passerine birds is rela-
nuclear characteristics of the neoplastic cells resemble tively uncommon. All birds were adults, a broad spec-
the inclusions caused by polyomavirus, but no virus has trum of neoplastic processes was represented and
been detected by electron microscopy, in situ hybridiza- tumors likely occurred spontaneously in most cases.
tion or PCR (M.M. Garner, unpublished data). One possible trend was observed: two mynahs had
Table 20.2.6 | Prevalence of Most Common Types of Neoplasms in Galliform Birds

Tumor Type Total # of Tumors per Species
and % of Total Galliform Cases
Chickena Pheasant Guinea fowl Peafowl Turkey
(74)
(37) (5) (8) (5) (10)
Lymphoma - 12 (16.2%) 6 (16%) 0 0 2 (40%) 4 (40%)
Squamous cell carcinoma - 9 (12.1%) 4 (11%) 0 3 (38%) 1 0
Ovarian/oviduct adenocarcinoma - 8 (10.8%) 6 (16%) 0 0 0 2 (20%)
Renal Adenocarcinoma - 4 (5.4%) 2 (5%) 1 (20%) 0 0 1 (10%)
Pancreatic adenocarcinoma - 4 (5.4%) 3 (8%) 0 0 0 1 (10%)
Seminoma - 4 (5.4%) 0 0 2 (25%) 0 1 (10%)
Interrenal cell adenoma - 3 (4.1%) 0 2 (40%) 0 1 (20%) 0
Hepatocellular carcinoma - 3 (4.1%) 1 0 2 (25%) 0 0
a. Includes chickens, roosters, jungle fowl
hepatic malignancies and concurrent hemochromatosis, with myelolipomas were from the same zoo.
suggesting iron storage in the liver may precipitate
malignant transformation in this species, as alluded to SPHENISCIFORMES
by other authors.8,9
Order Sphenisciformes (penguins) had 204 representa-
tives and 11 tumors (5.4%) (see Table 20.2.2), about
PHOENICOPTERIDAE average compared to submissions from other avian
Suborder Phoenicopteridae (flamingos) had 265 repre- orders. Over half of the tumor submissions (6, 55%)
sentatives and 13 tumors (4.9%) (see Table 20.2.2), were squamous cell carcinomas, occurring in four differ-
suggesting that the overall prevalence of neoplasia in ent species of penguins. These data suggest that, in gen-
the family/suborder is about average. Interestingly, liver eral, penguins may be predisposed to development of
tumors accounted for slightly less than half of the tumor this form of neoplasm.
submissions (see Table 20.2.1), suggesting that hepatic
neoplasia may be over-represented in captive flamingos. CICONIIFORMES
These birds typically store large amounts of iron in the Order Ciconiiformes (herons, storks, ibises, spoonbills,
liver7,15 and all the flamingos with hepatic neoplasia in New World vultures) (see Table 20.2.2) had 307 represen-
this study had iron deposition; however, no overt tatives and 11 tumors (3.6%), indicating the overall inci-
changes were noted morphologically in relation to the dence of neoplasia in this order was slightly below the
iron, such as cirrhosis seen in mynahs, toucans or birds submitted average. Eight of the tumor submissions were
of paradise,3,7,15 so the significance of the iron deposition in roseate spoonbills (Ajaia ajaja) and seven of the
relative to the neoplasia is undetermined. Two flamingos tumors in this species were focal or multicentric renal
had squamous cell carcinomas on the pads of the feet, adenomas, a tumor that was otherwise uncommonly
and had previous and ongoing protracted episodes of encountered in avian submissions. These data indicate
bumblefoot, which may have predisposed to neoplastic that roseate spoonbills may be predisposed to developing
transformation. this form of neoplasia. Although benign, four of these
tumors contributed directly to the cause of death.
STRIGIFORMES
Order Strigiformes (owls) had 131 representatives and 13 MISCELLANEOUS ORDERS
tumors (9.9%) (see Table 20.2.2), suggesting that overall Several orders had no apparent trends in neoplastic dis-
prevalence of neoplasia in this order may be relatively ease. These include Columbiformes (pigeons, doves),
high compared to other orders in the study. Six of the Gruiformes (cranes, related species), Falconiformes
owls were burrowing owls (Athene cunicularia), suggest- (eagles, hawks, falcons, Old World vultures), Charadrii-
ing that these birds may have a higher than average formes (shorebirds), Coraciiformes (kingfishers, mot
prevalence of neoplasia. Three hepatocellular neoplasms mots, hornbills), Cuculiformes (turacos, cuckoos), Pici-
were noted in this order, all in burrowing owls. Myelo- formes (woodpeckers, toucans, barbets), Struthioni-
lipoma, an unusual neoplasm in birds, appears to be formes (ratites), Coliiformes (mousebirds) and Pelecani-
over-represented in owls, occurring in three cases in the formes (pelicans, cormorants). Two birds of undeter-
study. All were intracoelomic neoplasms that were exten- mined species also had neoplastic processes. Four orders,
sively invasive and of undetermined origin. Interestingly, Gaviiformes (grebes, loons), Procellariiformes (fulmars),
the two affected snowy owls (Nyctea scandiaca) were Caprimulgiformes (tawny frogmouths) and Apodiformes
pen mates for most of their lives and died from these (hummingbirds) were represented in low numbers and
tumors within months of each other. All three of the owls had no neoplastic processes (see Table 20.2.2).
571
References and 5. Johne R, et al: Herpesviral, but Brentwood, TN, HBD Int’l, Inc, 13. Styles DK, Phalen DN,
no papovaviral sequences, are 1999, pp 1172-1199. Tomaszewski EK: Elucidating the
Suggested Reading detected in cloacal papillomas of 9. Panigrahy B, Senne DA: Diseases etiology of avian mucosal papillo-
1. Biggs PM: Lymphoproliferative dis- parrots. Arch Virol 147(10):1869- of mynahs. J Am Vet Med Assoc matosis in psittacine birds. Proc
ease of turkeys. In Calnek BW (ed): 1880, 2002. 199(3):378-381, 1991. Assoc Avian Vet, 2002, pp 175-
diseases of Poultry. Ames, Iowa 6. Latimer KS: Oncology. In Ritchie 10. Payne LN, Fadly AM: Leukosis/ 178.
State Univ Press, 1997, pp 485-489. BW, Harrison GJ, Harrison LR sarcoma group. In Calnek BW
2. Calnek BW, Witter RL: Marek’s (eds): Avian Medicine: Principles (ed): Diseases of Poultry. Ames, 14. Sundberg JP, et al: Cloacal papil-
Disease. In Calnek BW (ed): and Application. Brentwood, TN, Iowa State Univ Press, 1997, pp lomas in psittacines. Am J Vet Res
Diseases of Poultry. Ames, Iowa HBD Int’l, Inc, 1999, pp 640-672. 414-466. 47(4):928-32, 1986.
State Univ Press, 1997, pp 369-413. 7. Lowenstine LJ, Munson L: Iron 11. Reece RL, et al: Common 15. Ward RJ, et al: Hepatic iron over-
3. Gosselin SJ, Kramer LW: Patho- overload in the animal kingdom. necropsy findings in captive birds load in birds: Analytical and mor-
physiology of excessive iron stor- In Fowler ME, Miller RE (eds): Zoo in Victoria, Australia (1978-1987). phological studies. Avian Pathol
age in mynah birds. J Am Med and Wild Animal Medicine. Current J Zoo Wildl Med 23(3):301-312, 17:451-464, 1988.
Assoc 183(11):1238-1240, 1983. Therapy 4. Philadelphia, WB 1992.
4. Graham DL: Internal papilloma- Saunders Co, 1999, pp 260-268. 12. Reece RL: Tumors of unknown 16. Witter RL: Reticuloendotheliosis.
tous disease: A pathologist’s view 8. Macwhirter P: Passeriformes. In etiology. In Calnek BW (ed): In Calnek BW (ed): Diseases of
of cloacal papillomas – and then Ritchie BW, Harrison GJ, Diseases of Poultry. Ames, IA, Poultry. Ames, Iowa State Univ
some! Proc Assoc Avian Vet, 1991, Harrison LR (eds): Avian Medicine: Iowa State Univ Press, 1997, pp Press, 1997, pp 467-484.
pp 141-143. Principles and Application. 485-489.
21_Preventive Medicine.qxd 8/23/2005 12:47 PM Page 573
CHAPTER
21
Preventive
Medicine
and Screening
DAVID N. PHALEN, DVM, PhD, Dipl ABVP-Avian
We are all children at heart. When we want something,

we want it now and are willing to trust in fate if it means
that we can get it now. Many bird owners are like this.
They want a bird, so they buy it. They don’t necessarily
spend the time to research the source of the bird, and
often there is little money left over to make sure that
their purchase is healthy. Many people buy birds and
know very little about them, trusting in the information
provided by their friends, the Internet or the pet store.
As a result, husbandry-related diseases and infectious
disease still remain a critical problem for bird owners
and veterinarians.
Preventing the
Introduction of
Transmissible Diseases
EDUCATION
Preventive medicine is an essential element of avian
medicine, aviculture and pet bird ownership. Preventive
medicine begins with education. New bird owners
should be provided with a basic understanding of nutri-
tion, safe and adequate caging, household hazards,
hygiene and bird behavior. Improper nutrition, poor
caging, improper sanitation and improper or inadequate
socialization can all lead to disease — physical and psy-
chological — that can shorten the bird’s life or result in
significant lessening of its quality. Similarly, bird owners
and potential bird owners must be educated to the risk
factors that lead to the introduction of an infectious dis-
ease or the acquisition of a bird that is already sick.
The process of educating bird owners and potential bird for sick birds, the main facility for the breeding birds or
owners about bird health-related issues works best when pets, a kitchen, and if birds are being hand-raised, a
it is started before the bird is purchased. It begins at the nursery. A clean-up area separate from the kitchen is
grass roots level. Aviculturists, pet store owners and preferred. Obviously, pet bird owners and small hobby-
their employees have to educate themselves, assure that ists may only occasionally need a designated quarantine
their stock is healthy and provide accurate information area, hospital or nursery, whereas large breeding opera-
to their clients. Selling a healthy bird and providing the tions may need these facilities all the time. Likewise, the
information to keep it healthy will result in a satisfied actual physical structure of each component of the
client and repeat business. Veterinarians also must be aviary will vary enormously. In the home, a bathroom or
proactive. This means educating themselves, other vet- extra bedroom may serve as a hospital or quarantine
erinarians, clients and potential clients alike. Speaking to area. Large breeding facilities, on the other hand, might
local bird clubs, contributing to newsletters and bird mag- have separate buildings for some of these components.
azines, and being active in local and national avian veteri-
nary organizations are all part of preventive medicine. Other elements of aviary design can facilitate or reduce
the chances of disease transmission. Outdoor aviaries are
practical only in the warmer parts of the country, but
ACQUIRING BIRDS they have a number of important advantages. Rain and
The risk of disease drops dramatically if the person buy- wind naturally dilute pathogens, and freezing and direct
ing a bird researches potential sources of birds prior to sunlight also can inactivate some pathogens (Chapter 37,
purchase. It is reasonable for the buyer to ask a source Management of Racing Pigeons). On the other hand,
for references and to request to see the facilities where birds in outdoor aviaries are more likely to be attacked
the bird was raised. Aviculturists who are members of by raccoons and be exposed to sarcocystis from opos-
national organizations that promote bird breeding and sums. Parasites and mosquito-borne diseases also are a
education of their membership, such as the American risk with outdoor aviaries. The chances of disease trans-
Federation of Aviculture, are more likely to have a good mission can be reduced in indoor collections by making
preventive medicine plan in place. In the USA, avicultur- sure there is adequate ventilation and maximal separa-
ists can become certified as having the basic elements of tion of cages. If stocking density is high, especially if
a preventive medicine program through the Model cages are stacked on top of each other, then the chances
Avicultural Program. This or similar certification is a of disease transmission increase dramatically. Pacheco’s
good indication that the aviculturalist is making efforts disease and proventricular dilatation disease (PDD) are
to produce healthy birds. It also is a positive sign when examples of diseases that are more likely to occur in an
aviculturists or pet stores have an established relation- indoor aviary. Aspergillosis is a disease that is more likely
ship with an avian veterinarian. A great contribution to to occur in climates with high humidity or indoor collec-
the health of avicultural birds in the USA was the cessa- tions with poor ventilation.
tion of indiscriminate importation of wild-caught birds.
In other countries where the practice of wild bird Movement between these areas should be from the clean-
importation persists, contagious diseases still flourish. est place to the dirtiest. The kitchen is the cleanest area,
followed by the nursery, main collection of birds, hospital
and quarantine area. Keeping the traffic flow through the
COMBINING DIFFERENT facility to the minimum reduces the risk of disease trans-
SPECIES OF BIRDS fer. The traffic flow can be analyzed by drawing a floor
Risk of disease transmission is increased when birds that plan of a facility and using a pen to trace movement
originate from different parts of the world are combined. through it. The more complicated the movement pattern,
Aviculturists are strongly encouraged to focus on one the more chance for disease spread. It is often the case
group of closely related birds rather than raising a wide that a clean area has to be entered several times a day. In
variety of unrelated species. If many species of birds are large facilities with multiple workers, designating individ-
to be raised, separating them into different facilities by uals to work in specific areas can solve this problem.
genus or at least continent of origin may reduce disease When this is not possible, changing clothes or washing up
problems. well between areas should be considered. Restricting
access to the birds by the public and other bird owners
COMPONENTS OF THE also reduces the risk of disease transmission.
P H Y S I C A L F A C I L I T Y 30
Any multiple bird facility, including pet stores, should QUARANTINE
have specifically designated areas including a quarantine Quarantine will be effective only if the basic rules of
area for newly acquired birds, a separate hospital area quarantine are followed. The most important rule of
Chapter 21 | P R E V E N T I V E M E D I C I N E A N D S C R E E N I N G
575
quarantine is the “all in and all out” rule. One or more cause disease. These opportunistic organisms, however,
birds are brought into quarantine initially and no new cause disease only when they are allowed to reach high
birds are allowed into quarantine until the first birds concentrations or when other husbandry practices are
have left. The location of the quarantine facility or area less than ideal. Candida albicans, Aspergillus spp.,
also is important. Just keeping a bird in a separate cage Pseudomonas spp. and members of the Enterobacter-
is not good enough. Some degree of distance between iaceae are examples of ubiquitous opportunistic
the new bird and the previously acquired birds is neces- pathogens. Diseases caused by these organisms can be
sary. A separate building is ideal, but the garage, base- greatly minimized with proper hygiene. Whenever possi-
ment or bedroom also are acceptable. ble, food containers should be located so that they are
not contaminated with feces. Likewise, water sources
The proper duration of quarantine is a shifting target that should be designed and located to minimize contamina-
will vary to some degree with each circumstance. The tion from feces and food dunked in the water. Uneaten
longer the quarantine period, the more likely it is that a perishable foods should be removed from the cage before
disease problem will be recognized before a bird is intro- they have a chance to spoil. Water and food bowls should
duced into the flock. Thirty days is generally the mini-
be cleaned regularly and water sources such as automatic
mum quarantine period recommended for birds, but 45
drip systems should be regularly flushed and disinfected.
to 60 days is safer. Some aviculturists who are particularly
Cages should be designed so they are easily cleaned and
concerned about PDD may quarantine birds for 6 to 12
fecal and other organic material buildup does not occur.
months. For the quarantine to be meaningful, it has to
apply to all birds entering the collection, even those birds There are many misconceptions about sanitation and
that originated in that facility and are now returning. its importance. Many bird owners obsess about it. When
considering the degree of sanitation necessary for a pet
Applying quarantine procedures to all birds leaving and
home or aviary, it should be remembered that birds do
returning to the aviary can be onerous, especially for
not come from a sterile environment and a sterile envi-
those who show their birds. One solution to this prob-
ronment is not the goal. Many bird owners also obsess
lem is to select birds that will be shown that season and
about transmitting viruses among birds. The best way to
isolate them from the rest of the flock during the show
keep viruses out is to follow the above guidelines for
season. At the end of the show season, they can be quar-
preventing the introduction of these diseases. If a collec-
antined for a designated period of time and screened for
tion is not infected with viral disease(s), there is no
disease, if necessary, before being reintroduced into the
potential for viral transmission within that closed
collection.
collection.
NEW BIRD EXAMINATIONS Much time has been spent discussing which disinfectant
Having every new bird or group of birds acquired exam- is best. This focus on disinfectants ignores the most
ined and possibly screened for disease by an avian veteri- important part of sanitation, basic cleaning. Organic
narian is a critical element to a preventive medicine pro- material must be removed first before any disinfectant
gram. The extent of testing that might be done with a can be effective. It is in the organic material that the bac-
new bird will vary considerably according to the circum- teria can grow, parasite eggs are protected and viruses
stances. If a bird is going into a home where it will be the are at their highest concentration. In aviaries where
only bird, then testing is done to show that the bird is transmissible diseases are not a problem, cleaning is
healthy. If the bird is going into a multiple-bird household usually all that is necessary. Studies have shown that one
or aviary, testing is designed not only to make sure that of the best ways to sanitize food and water bowls is to
the bird is healthy, but also to determine as best as is pos- run them through the dishwasher. Syringes and other
sible if it is infected with diseases that could be intro- hand-feeding tools also are readily cleaned and for all
duced to a collection. practical purposes disinfected in the dishwasher. The
dishwasher should be separate from the home kitchen
dishwasher. If disinfectants are to be used, they should
be used after a surface is cleaned. They work best if they
Preventing Diseases by are left in contact with the surface for as long as possi-
Common Environmental ble. It is difficult or impossible to disinfect organic mate-
Pathogens rial, therefore, it is impossible to disinfect dirt floors and

very difficult to disinfect wood surfaces. Disinfectants
may be toxic, however, if viral diseases are or have been
SANITATION a problem in an aviary, disinfecting food and water con-
All environments contain organisms that can potentially tainers and environmental surfaces is indicated. Phenolic
disinfectants and bleach are effective against most screening tools that have a tremendous potential for
viruses and are the only disinfectants that work against abuse. It is generally assumed that parrots should have
viruses that do not have an envelope. Quaternary ammo- relatively few bacteria in swabs of their oral cavity and
nium and chlorhexidine-based disinfectants are effective cloaca, and that the predominate bacteria present on
only against enveloped viruses. these surfaces should be gram-positive rods and cocci.
The presence of large numbers of gram-negative bacter-
ial rods, clostridial spores or budding yeasts is consid-
ered to be abnormal. It has been the tendency of avian
Testing veterinarians to treat birds that have predominately
Examination and testing of birds has two goals. The first gram-negative flora of these areas. Likewise, when
is to make sure the newly acquired bird is healthy and Pseudomonas spp. or members of the Enterobacter-
does not have an infectious or non-infectious disease. iaceae such as E. coli are cultured, it has been common
The second is to make sure the bird is not subclinically practice to treat these birds.
infected with a disease that could be transmitted to other
Over time, however, it has become clear that this is not
birds in the owner’s aviary. There are two different types
the correct approach. The gastrointestinal flora is influ-
of testing. The first types are non-specific tests that pro-
enced by many factors. If the bird is not outwardly ill,
vide general information that suggests a bird is healthy or
the presence of the so-called “pathogenic bacteria” is
ill, but do not specifically identify the etiology. The sec-
more often a reflection of poor nutrition or other man-
ond types of tests are very specific and permit the identi-
agement problems than anything else and does not
fication of specific infectious agents. Because we cannot
mean that these organisms are causing this particular
test for all infectious agents, it is common to use both
bird a problem. In these instances, improving nutrition,
types of tests when evaluating a new bird.
hygiene or other management practices will result in the
Gram stain becoming normal again without treatment
NON-SPECIFIC ASSAYS (see Chapter 4, Nutritional Considerations).
The most important diagnostic assays in the broadest
manner of speaking are the history, examination of the The use of aerobic culturing to screen birds also can
bird in the cage and the physical exam (see Chapter 6, lead to false impressions. Many of the normal flora
Maximizing Information from the Physical Examination). found in the bird’s gut are anaerobes. When cultures are
However, it is the information derived from this phase of performed of cloacal swabs and feces, they are generally
the workup that will lead to the development of a test- sent in for aerobic culture. Under these circumstances,
ing plan, and will be important in the interpretation of only the facultative anerobes and the aerobic bacteria
the results of any diagnostics that may be done. grow, and the culture becomes skewed toward the
smaller numbers of Pseudomonas spp. and Entero-
Common non-specific diagnostic assays that are often bacteriaceae that may be present.
included in the new bird exam include the complete
blood cell count (CBC), chemistry panel, fecal wet The fecal Gram stain should be evaluated in light of the
mount and float, and oral and cloacal Gram stains and other findings in the individual bird. If the Gram stain is
culture. Plasma electrophoresis and even radiographs abnormal but the bird is otherwise healthy, management
are included as part of the new bird exam by some vet- problems may be the underlying cause of the abnormal
erinarians. Interpretation of these diagnostic assays is GI flora. Appropriate corrections to diet and husbandry
discussed in detail in other chapters and only a few com- can then be initiated. After these changes have been
ments will be made about these here. implemented for an adequate period (several weeks is
commonly employed), a fecal Gram stain should be
It has been the experience of the author that the CBC is a reexamined. If the bird has diarrhea or is showing other
very useful tool for screening the new bird. It rarely gives signs of illness and the Gram stain is abnormal, a culture
a definitive diagnosis, but if abnormalities in the CBC are may be indicated. Pending culture results, treatment
found it is a strong indication of an underlying health with appropriate antibiotic, anti-yeast or antifungal ther-
problem. The plasma electrophoresis also has consider- apy should be initiated.
able value, as alterations in this assay are found early in
the course of infectious diseases, often before the disease Salmonellosis is a problem that is rarely seen in parrots
becomes patent.6 Fecal wet mounts can reveal Giardia but is common in other species of birds. Currently,
spp. infections and are the best way to detect infections many facilities require that birds be screened for infec-
with Macrorhabdus ornithogaster (megabacterium).17 tion with Salmonella spp. prior to entry. It is fairly com-
mon for otherwise normal birds to have positive fecal
The Gram stain and fecal cultures are commonly used cultures. This poses a significant problem, as these birds
577
Table 21.1 | Diagnostic Assays for Psittacosis+

Assay Sample Effective in These Day Positive Specifics
Species of Birds after Infection
Serology*
Elementary body agglutination Serum or plasma Parrots Approx. 14 days Negative with successful treatment
Complement fixation Serum or plasma All species of birds Approx. 21 days May remain positive with successful treatment
Solid phase ELISA Serum or plasma Parrots, others? Unknown Not available in the USA
PCR* Whole blood and combined All species of birds Oral 5 days, blood 10 Rapidly negative after the onset of treatment
oral and cloacal swab days, cloaca 15 days
+ Commonly affected species include pigeons, doves and parrots (particularly budgerigars & cockatiels).
*A combination of the elementary body agglutination assay and PCR or the complement fixation assay and PCR is more sensitive than either test alone.
cannot be shipped and it is not known if they actually at the sampling site or in the laboratory can give false-posi-
are a health risk to other animals. Little work has been tive results. Obtaining a sample that contains the organism
done to determine the success of eliminating intestinal and getting it to the laboratory before it degrades also can
salmonellosis with antimicrobial treatment in exotic be a problem for some PCR-based assays. Likewise,
birds; it is known that this approach does not work in inhibitory substances such as antibiotics and the contents
poultry. Serotyping Salmonella isolates may be of some of droppings can cause false-negative results.
benefit, as certain serotypes are more commonly associ-
ated with disease in birds than others. Serology has been Not all PCR assays are created equal. Different laborato-
an extremely useful tool for the eradication of S. pullo- ries offer tests with differing levels of sensitivity. It is
rum in poultry. Serologic screening for salmonellosis in important to use a laboratory that has a long history of
other species has potential value.11 experience with avian samples.
There are limitations to the sensitivity and specificity of

SPECIFIC ASSAYS individual infectious agent testing. The practitioner must
In this day and age, we rely on two important types of remember that assays exist for only a select number of
diagnostic assays, serologic and polymerase chain reac- the potentially pathologic avian agents. Testing only for
tion (PCR) assays. Serologic assays detect antibodies to specific agents may not yield a diagnosis for an individ-
specific organisms. PCR assays detect the DNA or RNA of ual sick bird, nor is this testing sufficient to declare an
targeted organisms. Serologic assays have the advantage individual bird or a collection free of disease.
of being generally inexpensive and able to be performed
on an easily acquired sample (serum or plasma) that is PSITTACOSIS
inexpensively shipped to the laboratory. The disadvan-
Infection with Chlamydophila psittaci is common in pet
tages of serology are that these assays may not become
birds. Clinical signs vary from none to a mild respiratory
positive until 2 to 3 weeks after infection and may
disease to a severe multisystemic, often fatal, disease.
remain positive after the infectious agent is no longer
Psittacosis is particularly important in avian medicine
present. Other complicating factors related to serologic
because it can spread widely before it is recognized and
assays include non-specific substances in serum that can
because it is a zoonotic and reportable disease. Clinical
sometimes cause a virus-neutralizing assay to read posi-
signs and traditional diagnostic assays such as hematol-
tive at high concentrations of serum or plasma, and anti-
ogy, clinical pathology and radiology, while helpful, are
complementary substances that can invalidate the com-
generally insufficient to specifically diagnose this disease.
plement fixation assay. Virus neutralization assays have
the disadvantage of requiring that growing cells are
Serology
always available, and these assays typically take 3 to 5
days to run. Because of the time it takes to set up these The elementary body agglutination assay (EBA) is a
assays, they are generally performed only once a week. tried-and-true serologic assay that has been used for the
There are several serological assays that use a secondary past 10 years. It detects anti-Chlamydophila IgM. It can
antibody that is said to detect all avian immunoglobu- detect infected birds within 15 days of infection and
lins. This type of cross-reactivity is extremely unlikely generally is positive by the time a bird is showing signs
and this type of assay cannot be recommended.14 of illness (Table 21.1). Another advantage of this assay is
that it becomes negative with successful treatment. It has
PCR-based assays have the advantages of being extremely a few minor limitations. Rarely, a bird may develop signs
sensitive, able to detect pathogens in the early stages of of disease before the agglutinating antibodies are pro-
infection, and do not require viable microorganisms to duced. Also, rarely, a bird with chronic psittacosis may
document their presence in the sample. The sensitivity of be EBA negative. The EBA works very well for psittacine
these assays also is one of their limitations. Contamination birds, but may not work in all species, particularly doves
and pigeons. For doves and pigeons, the complement and M. genavense cause the majority of avian infections.
fixation assay (CF) is currently recommended.10,20 The time between infection and onset of clinical signs is
long, possibly several months. As a result, infected but
The CF test detects anti-Chlamydophila IgG that is present outwardly healthy birds may be introduced to a collec-
in blood a few days to a week after anti-Chlamydophila tion and infection disseminated widely before it is recog-
IgM. Therefore, there is a slight delay between when the nized. Mycobacteriosis is particularly common in captive
EBA and the CF become positive. The CF also may stay populations of grey-cheeked parakeets (Brotogeris
positive for an extended period of time after a bird has pyrrhoptera), canary-winged parakeets (B. versicolorus),
been successfully treated. To the best of the author’s Pionus spp., canaries (Serinus canarius), finches, the
knowledge at this time, only one laboratory offers the red siskin (Carduelis cuculatta) and waterfowl.
CF and EBA‡. The CF is a cumbersome test and is not Mycobacterial infections result in a multisystemic but
routinely run, so there may be a delay in getting results. slowly progressive disease that can present with many
possible signs. Because signs are rarely specific and
A solid phase enzyme-linked immunoassay (ELISA)a is
infection can remain inapparent for extended periods of
currently available, although not in the USA. This assay
time, ancillary diagnostic assays are needed.33
was found to compare favorably to the CF if the serum
sample produced a spot as dark or darker than the posi-
tive control (J. Grimes, personal communication, 1995). Detection of the Organism
Other serologic assays are offered, but have not been vali- Many mycobacterial infections colonize the intestinal
dated by peer-reviewed research. lamina propria and mycobacteria can be shed in the
feces. Acid-fast stains of the feces will reveal the organ-
PCR isms in some cases, but this assay has a very low sensitiv-
PCR testing for psittacosis is another excellent way to iden- ity and is of limited value as a screening tool. A PCR
tify infected birds. The organism can be detected in swabs assay‡‡ is now being offered that can detect mycobacteria
of the oral cavity as early as 5 days after infection, in cloa- in the feces. The major limitation with this assay is that
cal swabs by 10 days after infection and in the blood by 15 not all birds with avian tuberculosis are actively shed-
days after infection. The major disadvantage of the PCR is ding the organism, or they shed the organism in small
that birds that have been started on treatment before test- numbers or intermittently. A negative result with the
ing may be negative, and cloacal swabs that are heavily PCR assay, therefore, does not rule out the possibility of
contaminated with feces may interfere with this assay. The infection. The technology associated with PCR diagnos-
sensitivity of this assay is improved if both blood and com- tics for avian mycobacteriosis is developing rapidly and
bined oral and cloacal swabs are tested.1,8 this assay has significant long-term potential.33
No test is 100% sensitive. Therefore, if the greatest degree Serology

of sensitivity is sought, the PCR and the EBA and egg
Mounting evidence suggests that serology will be an
inoculation culture or tissue culture could both be per-
important tool for detecting birds with mycobacteriosis.
formed when screening parrots. PCR can be combined
At the time of this writing, however, serologic assays for
with the CF when screening doves and pigeons.
mycobacteriosis are still experimental. Successful sero-
Chlamydophila psittaci infections can occur in almost logic assays will have to be applicable to all species that
any species of caged bird. The author recommends test- are to be tested, and they will have to be able to detect
ing for this organism in most birds presented for new infection with the multiple species of mycobacteria that
bird purchase examinations. The author especially rec- infect birds. A complement fixation assay was developed
ommends testing cockatiels (Nymphicus hollandicus) as to detect mycobacterial antibodies. This assay had the
they can carry this bacterium and not demonstrate clini- advantage that it did not require species-specific reagents.
cal signs of disease. The few cases of human infections The complement fixation reaction, however, was very
the author has observed have been acquired from an cumbersome and required reagents that had a short
otherwise healthy pet cockatiel. Pigeons and doves are shelf life, making it impractical to use. Additionally, cul-
commonly infected with C. psittaci and should be rou- ture filtrate was used for this assay and it was necessary
tinely tested. to run multiple tests with antigens from each specific
serotype of M. avium in order to detect all of the
infected birds.18
MYCOBACTERIOSIS
Several mycobacterial species, including Mycobacterium Indirect ELISAs have been used successfully to detect
avium, M. genavense, M. fortuitum and M. tuberculosis, antimycobacterial antibodies in waterfowl and quail. The
cause mycobacteriosis in birds. Mycobacterium avium indirect ELISA, however, requires a specific secondary
579
antibody, limiting its usefulness to closely related disease is advanced. Radiographs, endoscopy and biopsy,
species. A blocking ELISA has been developed that cir- cytology and hematology are all valuable tools in the
cumvents the need for a specific secondary antibody. diagnosis of this disease. Even with all these assays, the
This assay has been tested in canaries, white-winged diagnosis of aspergillosis is often a difficult one.
wood ducks and quail with known or suspected M.
avium infections. At this point, there has been good cor- The diagnosis of aspergillosis has been most extensively
relation between infected birds and birds that are posi- studied in humans. Ancillary diagnostic assays used in
tive with this assay. Protoplasmic antigen from one people include PCR to detect Aspergillus DNA from
serotype of M. avium was found to cross-react with all blood, an ELISA to detect Aspergillus antigen and an
other serotypes tested. However, early work suggests ELISA to detect anti-Aspergillus antibody. These studies
that antibodies to other species of mycobacteria can be clearly indicate that even a combination of these three
detected only if their specific antigen is used.34 assays will not be adequate to detect many cases of
aspergillosis.4,5 The problem comes from the fact that
The immunological response of the host also may most people who contract aspergillosis are immunocom-
complicate the interpretation of serologic assays for promised. This also may be true in birds. If the infected
mycobacteriosis. The complement fixation assay was person’s immune system is adequate to contain the dis-
used to screen ring-necked turtledoves for infection. The ease and the organism is localized in a walled-off granu-
wild-type birds in this collection were all antibody posi- loma, then these individuals are found to produce anti-
tive, but the majority of the birds that had the white body. People with generalized disease are generally
color mutation were seronegative. It is not known if the severely immunocompromised and they do not produce
failure of an antibody response in these birds is limited antibody. In these people, Aspergillus antigen and DNA
to this particular color mutation or also may occur in are most likely to be found in the blood, but they are
other species and color mutations of birds18 (see Chapter not when the lesion is encapsulated. If the pathophysiol-
28, Implications of Mycobacteria in Clinical Disorders). ogy of avian aspergillosis resembles that seen in humans,
then none of these assays are likely to detect infection in
MYCOPLASMOSIS most infected birds. A combination of these assays may
Mycoplasmosis is a common disease of pigeons and be more specific, but false negatives are to be expected.
poultry, but occurs infrequently in companion birds with
the possible exception of cockatiels. The disease in Serology
pigeons and companion birds is characterized by con- Extended efforts have been undertaken to develop a
junctivitis and upper respiratory signs, and less fre- serologic assay for birds infected with Aspergillus spp.
quently pneumonia. Distention of the infraorbital sinus This work was pioneered at The Minnesota Raptor
with fluid or purulent material is common. PCR assays Center, which currently offers an ELISA assay for the
for Mycoplasma spp. have been developed and are
detection of anti-Aspergillus antibodies‡‡‡. Differing sec-
offered by many diagnostic laboratories. Some of these
ondary antibodies are used in this assay, depending on
assays will amplify DNA from all mycoplasmas, so that a
the species of bird to be tested. Using well-defined clini-
Mycoplasma sp. infecting a parrot could be detected
cal case material, the assay has been validated for use in
even if it was not one of the common poultry
several species of Falconiformes, but as designed does
pathogens. The disadvantage of this assay is that just
not work in owls. Immune suppression appears to
because mycoplasma is present in a lesion, it is not con-
accompany aspergillosis in raptors. Prior to treatment,
clusive proof that it is the cause of disease.
many raptors have little or no detectable antibody.
Successful treatment results in a subsequent rise fol-
ASPERGILLOSIS lowed by a decline in antibody titers. A failure of anti-
Aspergillosis is an infection of the respiratory system that body titers to rise with treatment or an increase in the
occurs sporadically in a wide range of birds (see Chapter titers without the expected decrease is considered to be
29, Implications of Mycoses in Clinical Disorders). Birds a poor prognostic sign. Thus a medium to high positive
from cold and dry climates are highly susceptible to antibody titer is highly suggestive of disease. However,
infection. Environments that are conducive to the envi- negative to low positive results are inconclusive.24
ronmental growth of Aspergillus spp. and environments Similar results were found in penguins with aspergillo-
that are poorly ventilated will result in an increased inci- sis.25 Birds with high antibody titers, high beta and
dence of aspergillosis. Disease can be localized to the gamma globulins, and albumen concentrations above
upper airways or the syrinx, or it may involve the air sacs 1.8 g/dl had a favorable prognosis. In contrast, birds
and lungs. Respiratory signs are a common feature of with low or undetectable antibody titers and albumin
this disease, but a bird may not manifest signs until the levels below 1.8 g/dl had a poor prognosis.
The accuracy of available serologic and antigen capture PBFDV agglutinates only red blood cells from a few
assays for the diagnosis of aspergillosis in parrots has species of cockatoos, this assay is not practical outside of
been inadequately studied. In one study, a commercially Australia.23
available ELISA for anti-Aspergillus antibodies and anti-
gen capture assay‡‡‡‡ was evaluated in seven birds with PCR
confirmed aspergillosis. Of these birds, only one was
Birds become viremic 7 to 14 days after infection with
found to be weakly positive with serology and three
PBFDV. If the birds are unable to mount an appropriate
birds were positive, two weakly, with the antigen detec-
immune response they will remain viremic. If they do
tion assay, suggesting that either parrots in this study did
mount an appropriate immune response they cease to
not make anti-Aspergillus antibodies and had little circu-
be viremic. Virus, however, may persist in the feathers
lating antigen, or that these assays were not sensitive.13 A
and possibly the skin, so that these birds are a potential
second study of ten birds found a higher percentage of
source of infection until their next molt. PCR is done on
sero- and antigen-positive birds; however, in neither
heparinized blood.7 If multiple birds are to be sampled,
study were non-infected birds tested, so the specificity of
care must be taken to prevent contamination between
these assays remains to be determined.16 Currently, the
samples. In most circumstances, birds that are PCR posi-
author does not recommend using any of the available
tive and have clinical signs of disease will remain posi-
Aspergillus assays for routine screening of parrots.
tive and are likely to die from their infection. Birds that
are positive but are not showing signs of disease should
PSITTACINE BEAK AND be retested in 3 months. If they are negative at that time
FEATHER DISEASE VIRUS (PBFDV) they are thought to be cured. Rarely, lories, lovebirds
PBFDV is a common infection of wild birds in Australia. and occasionally other species of parrots will develop
In the USA and possibly elsewhere, this virus is enzootic clinical disease, but will then recover and become virus
in many lovebird collections and also is seen to a lesser negative.
degree in budgerigar aviaries. Disease is seen in many
species of parrots, including African grey parrots, love- It has been suggested that it is important to differentiate
birds, budgerigars, lories, lorikeets, eclectus parrots and between the lory variant of PBFDV and the other vari-
cockatoos. Infection also occurs in Neotropical parrots, ants. The author does not agree with this conclusion.
but disease is rare and infections are transient in most Although the lory variant may behave somewhat differ-
cases. ently than other PBFDV variants, it is still pathogenic, so
the significance of a positive test is the same in a lory or
The sequence of the PBFDVs genome varies up to 16% any other parrot species, regardless of the variant.31
between isolates. This has diagnostic significance, as PCR
primers have to be designed in the conserved region of PBFDV infection in lovebirds (Agapornis spp.) may not
this virus (ORF1) if they are to detect all variants of this follow the same patterns as seen in other parrots.
virus.3,37 Recently, a specific variant of PBFDV has been PBFDV is widespread in commercial lovebird collections,
recognized in collections of lories in the USA. It also is but disease is rare. It is the author’s impression that
reported to occur in lovebirds.26 Its sequence and its rela- virus shedding may persist more than 3 months in birds
tionship to previously published sequences of the PBFDV that never show signs of disease.26
have not been reported. PCR primers derived from the
ORF1 also can detect this variant. Primers also have been AVIAN POLYOMAVIRUS (APV)
designed to differentiate it from other PBFDVs. Lories
APV is a common infection of a wide range of parrots.
with this infection may remain viremic for 6 months or
APV causes morbidity and mortality in nestling budgeri-
more without showing clinical signs. Lories that develop
gars (Melopsittacus undulatus), Indian ring-necked para-
clinical signs often die, but some will recover.31
keets (Psittacula krameri), lovebirds and many parrots.
Disease is less common in nestlings of other Old World
Serology parrots. Nestling budgerigars in aviaries with enzootic APV
Birds that become infected with PBFDV but do not become viremic within 7 days of hatch and are serologi-
develop disease have high antibody titers. Birds that do cally positive by 10 days after hatch. If they survive infec-
develop disease have low antibody titers or no antibody tion, fecal shedding may persist for 6 months or longer,
at all. A hemagglutination assay has been developed to but ceases at some point after the birds become sexually
detect serum antibodies to PBFDV. Serum antibody has mature. Although they stop shedding virus, infected
been detected within 1 to 2 weeks of exposure. This budgerigars will remain seropositive for life.15,16 Nestling
assay has been effectively used to study the prevalence parrots of other species become viremic within 2 weeks of
of PBFDV infections in wild Australian parrots. Because infection. They also develop virus-neutralizing antibody at
581
approximately 14 days postinfection. Antibody titers in appears that all species of parrots have the potential to
most species of nestlings that survive infection are main- become infected with and shed APV, so all birds that are
tained for 10 or more years and possibly for life. Viremia going into an aviary where they might expose nestlings
persists for 6 to 8 weeks in most cases. Fecal shedding should be tested. Nestlings that survive an outbreak of
begins shortly after the onset of viremia, but persists for APV are assumed to be shedding virus. Therefore, testing
as long as 12 to 16 weeks.21 In rare cases, viremia and fecal birds 4 months after the outbreak when virus shedding
virus shedding may persist for more than 10 months.7 The should have stopped, rather than immediately after the
duration of viremia and virus shedding in adult birds outbreak when virus shedding is expected, best uses the
infected with APV has been studied in only a limited num- owner’s resources.21
ber of birds. However, it appears that viremia and virus
shedding occurs only briefly in mature birds or not at Testing birds older than 16 weeks that are going into a
all.21 Viremia and virus shedding also are significantly single-bird household is of questionable value. If they
impacted by concurrent infections with PBFDV. Birds with test positive and are not sick, they will shed transiently
co-infections appear to shed APV continuously and may and stop shedding. If a bird is positive at 16 weeks, it
never clear the virus.16 has already been infected and will not generally become
clinically ill. It will continue to shed for some time and it
Serology should be isolated from other birds.
An excellent virus-neutralizing (VN) assay has been The author seriously doubts that the veterinarian will be
developed to detect antibodies that neutralize APV. In able to detect an infected bird that will subsequently come
this assay, virus is first incubated with two-fold dilutions down with disease as, in his experience, the onset of
of serum or heparinized plasma. The virus-plasma mix- viremia and the onset of disease occur very close together.
tures are then incubated with chicken embryo fibro-
blasts, the fibroblasts are washed and the cells are moni- When the value of testing blood was first recognized, it
tored for cytopathic effects (CPE). If CPE do occur at the was suggested that PCR of blood detected only frag-
highest concentration of serum, then the bird did not ments of DNA and that a positive did not reflect the true
have neutralizing antibody. If virus growth is inhibited infection status of the bird. It also was suggested that
and CPE do not occur, then the bird did have neutraliz- immunized birds that were blood PCR positive were pos-
ing antibody. In the author’s hands, this assay takes 5 itive because of DNA present in the vaccine. Both these
days to complete.15 assumptions have been proven to be false. Therefore, if
a bird is positive by blood PCR, it is infected with APV.19
Use of the APV VN If they test positive and do not have APV disease, they
Parrots infected with APV may begin shedding virus prior will shed transiently and then stop shedding.
to seroconversion and maintain high antibody titers many
years after they stop shedding virus. Therefore, the sero- P S I T T A C I D H E R P E S V I R U S E S ( P s HV s )
logic status of a bird is not a good indicator of virus shed- OR PACHECO’S DISEASE VIRUSES
ding. Sensitive PCR assays should be used in place of
PsHVs are the causative agent of Pacheco’s disease.
serology to detect virus-shedding birds. The APV VN has
Pacheco’s disease occurs in sporadic outbreaks in newly
some limited value in epidemiologic studies and could
formed and long-established parrot collections. Losses
be used to determine if APV had ever been in a collec-
can range from a single bird up to hundreds of birds.
tion. Under these circumstances the immunization status
Generally, birds that develop clinical Pacheco’s disease
of the birds should be considered. Nestlings do not pro-
die. There are four major genotypes of PsHVs. All are
duce virus-neutralizing antibody to the commercial APV
capable of causing Pacheco’s disease and genotypes 1, 2
vaccine. Therefore, antibody-positive nestlings have been
and 3 are capable of causing internal papillomas.32,35,36
infected with APV. Adult parrots do develop neutralizing
Outbreaks of Pacheco’s disease occur when carrier birds
antibody following immunization, but their antibody
expose naïve birds. The dynamics of each outbreak will
titers are typically low compared to those seen in birds
depend on the genotype of the virus and the species of
that survived infection.19
birds involved. In some collections, Pacheco’s disease
will not occur, but over time multiple birds will develop
Use of the APV PCR
papillomas.
Viremia may precede virus shedding and virus shedding
continues after the cessation of viremia; therefore, com- Macaws, Amazon parrots and some species of conures
bined oral and cloacal swabs and heparinized blood are most likely to be carriers of PsHVs. Infection preva-
should be submitted for PCR analysis. If blood is tested lence appears to be higher in imported wild-caught
alone, many virus-shedding birds will be missed. It birds. Infection also has been recognized in cockatoos
and African grey parrots, and under some circumstances able and include central nervous system disease, respira-
it also may occur in lovebirds and cockatiels. The list of tory signs, diarrhea and signs of pancreatic insuffi-
potential carrier species likely will grow as more is ciency.28,29 In a recent report of an outbreak of PMV-3 in a
learned about these viruses. Any bird that survives an pet store, the hemagglutination inhibition assay (HI) was
outbreak of Pacheco’s disease should be considered found to be a sensitive means of detecting infected
infected until shown otherwise. Mounting evidence sug- birds.14 Others have tried serologic methods for detect-
gests that parent-to-offspring transmission occurs. The ing subclinical infections of PMV-3 in Neophema and
offspring may remain asymptomatic or develop internal other species with little success.12,29 This discrepancy may
papillomatosis, depending on the genotype of the virus. It be due to the duration of the infection at the time serol-
appears that once a bird is infected they will be infected ogy is performed. In a recent study with PMV-1, low lev-
for life. This includes survivors of Pacheco’s disease that els of antibody were detected in African grey parrots.
were treated with acyclovir. These antibodies were detectable with an experimental
ELISA, but not with the HI. This assay is currently under
The key to preventing Pacheco’s outbreaks and internal development and may prove useful in the future.14 In
papillomatosis is keeping carrier birds out of the collec- disease outbreaks where PMV-3 is suspected, submission
tion or, if they are already in the collection, isolating them of proper samples for histopathology is currently the
from birds that are not infected. Studies to date show that most accurate method of confirmation.
PsHVs in carrier birds are present in significant concentra-
tions in the mucous membranes of the cloaca and oral
mucosa. Swabs of these surfaces can be tested by PCR.
Virus also may be detected in blood, but concentrations Applied Preventive
of virus are low in the blood and in one study blood PCR
was inconsistently positive, while mucosal swabs were
Medicine
more dependably positive. In rare individuals, birds have
been identified that are only blood positive. The biologi- TESTING NEWLY ACQUIRED BIRDS
cal significance of this is not known; until it is, it is recom- The ultimate decision as to what type of testing should
mended that both blood and combined oral and cloacal be done for a particular bird will depend on the specific
swabs be used for PsHV PCR.22 details regarding the source of the bird, species of the
bird, the aviary or home into which it is going, the
PCR resources of the owner and findings on physical exami-
Recently discovered sequence data has permitted the nation. Non-specific assays such as CBC, oral and fecal
development of a single PCR assay that can detect all Gram stain, protein electrophoresis, fecal wet mount
four genotypes of the PsHV (R. Dahlhausen, personal and fecal floatation can be applied to all birds. (Ed.
communication, 2003). Preliminary work with less ideal Note: In some practitioners’ experience, a negative fecal
primer sets suggests that PCR of blood and a combined flotation has not correlated with the absence of intes-
oral and cloacal swab will detect the majority of birds tinal parasites). Ascarids are commonly expelled from
unapparently infected with PsHVs. birds, especially those with previous exposure to warm,
outdoor environments, following the administration of
Serology an appropriate anthelmintic. This occurs in birds with
There are three major serogroups of the PsHV.9 Serotype negative fecal flotations, and routine deworming may be
1 contains genotypes 1 and 4, serotype 2 contains geno- advised in these situations (M. Wissman, personal com-
type 2 and serotype 3 contains genotype 3.36 It is clear munication, 2002).
that many birds that are infected with PsHVs are
Fecal and oral cultures are indicated if abnormalities are
seropositive. It still remains to be determined, however,
found on the Gram stains and birds show other evi-
if all birds infected with PsHVs will demonstrate positive
dence of illness. Chemistry panels are most likely to
serologic results. Preliminary evidence suggests that anti-
identify problems in older or unthrifty birds, but can be
bodies to one serotype inconsistently neutralize viruses
useful in detecting early disease or establishing baselines
of other serotypes.22 Therefore, if serology is to be used
for future reference, even in clinically healthy individu-
to detect PsHV-infected birds, multiple assays using all
als. Radiographs are relatively costly tests that can be
three viruses or their antigens will have to be run.
used for screening. Generally, however, they are used
only when there is some other indication of disease.
PARAMYXOVIRUS 3 (PMV-3) Currently, the choice of serologic and PCR-based testing
PMV-3 is a common cause of disease in the Australian is best tailored to the species and background of the
grass parakeets (Neophema spp.). Clinical signs are vari- bird being examined (Table 21.2 and Table 21.1).
583
Table 21.2 | Diagnostic Tests Used to Screen for Specific Infectious Diseases
Infectious Agent Assay Sample for Testing Species Commonly Infected Sensitivity Specificity
Mycobacteria PCR Feces Brotogeris spp., canaries, finches, Fair Good
red siskins, waterfowl
Serology Serum or plasma Experimental Experimental
M. ornithogaster Wet mount Feces Budgerigars, finches, cockatiels, Fair to poor Good if many organ-
parrotlets, lovebirds, lories, other isms present
PBFDV PCR Blood* Old World parrots Excellent Excellent
APV PCR Blood and swabs** Lovebirds, budgerigars, all parrots Excellent Excellent
recently exposed to other birds
Serology Serum or plasma Proof of previous or current Does not reflect virus-
infection shedding status
PsHV PCR Blood and swabs Macaws, Amazon parrots, conures, Excellent Excellent
others?
Serology Serum or plasma Unknown Unknown
PMV-3 HI+ Serum or plasma Neophema spp., others? Questionable in chronic infection Good
ELISA++ Serum or plasma Experimental Experimental
*Heparinized blood + HI: Hemoagglutination inhibition
**Combined oral and cloacal swab ++ ELISA: Enzyme-linked immunoassay
There is a saying: “Be careful for what you look for, by local bird clubs. These marts serve many valuable
because you may find it.” This is particularly applicable purposes. They provide an important outlet for the sale
to testing new birds. It is incumbent upon practitioners of birds and at the same time raise money for the spon-
to know everything that they can about the tests they are soring organizations. This money is used to help sup-
using so that if one does come back positive, it can be port the bird club and in many cases to fund research
properly interpreted. It also is important to correlate and conservation efforts. The bringing together of birds
test results with the entire clinical picture. If the testing from multiple premises into a confined area and the
results don’t make sense, then repeat those assays or handling of these birds by the general public, however,
have them performed by a different laboratory. results in the ideal opportunity for disease spread, the
most common of which is APV.
PREVENTIVE MEDICINE AND
There are preventive measures that can be taken that
THE VETERINARY HOSPITAL
will help to mitigate disease transmission at bird marts.
It is a common practice for veterinarians to board birds.
The most important is to limit sale of birds to those that
There is no doubt that this is a valuable service to the
are completely weaned. Weaned birds will rarely, if ever,
veterinarian’s clients, but it also poses challenges for the
develop APV disease although they are still susceptible
prevention of disease transmission. The greatest risk
to infection. Birds that are taken to a bird mart but not
occurs if birds of uncertain infection status are housed
sold should be quarantined away from the rest of the
in the same room. If all birds are screened for PBFDV,
breeder’s birds until they can be sold. A policy of not
APV, PsHVs and Chlamydophila psittaci before they are
letting anyone handle birds unless they have bought
allowed to board, then the risk of disease is diminished.
them also will reduce the spread of disease. Finally,
There is no test for birds that have the etiologic agent of
cages made of clear, hard plastic panels can be used to
proventricular dilatation disease, however, so the trans-
display birds that are for sale. Ideally, these cages would
mission of this disease cannot be prevented. Other
have a fan in the back that draws air out of the cage and
strategies for preventing disease transmission would be
a Hepa filter in the front to filter out potential pathogens.
to keep birds in isolettes or to house birds separately in
Even without these fans, cages made from clear plastic
different parts of the hospital.
panels are much better than wire cages. If nestlings are
Veterinarians see sick birds and therefore will have birds allowed at bird marts, then they should be confined to
with infectious diseases in their hospital. A protocol brooders or cages made from this material and taken
should be developed for every hospital for routine clean- out to the car or hotel room for feeding. Nestlings that
ing of the exam, treatment and hospital rooms and caging. are not sold must go into quarantine after the show.
Routine PCR testing of swabs of these environments can
be used to determine if the cleaning is effective. Boarding PREVENTIVE MEDICINE
birds should be housed separately from hospitalized birds. IN THE PET STORE
Pet store owners and managers who intend to sell birds
PREVENTIVE MEDICINE first need to consider what market it is that they wish to
AND BIRD MARTS reach. Budgerigars, cockatiels, lovebirds, canaries and
A common way for aviculturists to sell their birds is to finches appeal to one type of customer and come with
bring them to bird marts or bird fairs that are sponsored their own significant disease problems. The larger species
of birds appeal to other types of customers. Combining ease of nestling parrots. Lovebirds and budgerigars from
these birds can lead to additional health problems. many sources may shed this virus. The risk of APV disease
can be greatly reduced if stores buy only weaned birds.
It has been a common practice in the USA for individual Alternately, some stores may choose not to sell the
producers of cockatiels, lovebirds, budgerigars and smaller species of birds. If nestlings are to be present in
finches to sell their birds to buyers who combine birds the store, all the sources of all birds brought into the
from multiple sources and ship them to other sellers store need to be screened for APV. Setting up a separate
who distribute them to pet stores. This practice maxi- bird room that the public can look into but may enter
mizes the potential for disease transmission. Cockatiels only with supervision will help to keep customers from
supplied in this manner have a high incidence of psitta- bringing disease into the store. If a customer wants to
cosis. Similarly, lovebirds and budgerigars from these see a bird, they may be required to put on a clean smock
sources are commonly infected with APV, and lovebirds and gloves and possibly even dip their feet in a foot bath
are commonly infected with the PBFDV. When infected before entry into the bird room. If economics require
birds are mixed with birds from clean collections, dis- that nestlings that are still being hand-fed be purchased,
ease transmission is likely. When these birds come into a an alternate approach to keeping them healthy is to raise
pet store, not only may they be unhealthy, but they also and wean them in isolation away from the store.
are an important source of infection for other parrots
whose retail value may be much higher. The classic Psittacosis is very common in cockatiels and can occur in
example of this is APV outbreaks that occur in nestling any species of parrot. It can cause widespread disease in
macaws, conures and eclectus parrots 2 weeks after they pet store birds, requires a long treatment period, is a
are brought into a pet store. The tendency in these reportable disease in most areas and is transmissible to
circumstances is to blame the breeder who supplied the people. All sources of birds should be tested for this dis-
nestlings that died, but the problem lies with the ease.
budgerigars and lovebirds in the store that are actively
shedding virus and that fatally exposed these birds after Quarantine is another element of the preventive medi-
they entered the store. cine that can provide important dividends to the pet
store. All birds coming into the store should be isolated
It has been the author’s experience that pet stores have for some period of time before they are mixed with
healthier stock if they establish a relationship with one other birds in the store. If the incoming birds have been
or more local breeders and buy birds directly from exposed to disease, it is likely that they will begin show-
them. If the local breeder can see the possibility of a sus- ing signs during the quarantine period. It has been com-
tained market, they are more willing to spend money to mon practice for some distributors to treat some species
verify that their flock does not contain the common dis- of birds with tetracyclines for variable lengths of time
eases that can cause so many problems in the pet store. before they are sold. This can mask signs of psittacosis
Aviaries that supply birds to stores can be screened for but may not cure the birds. Once the birds are off med-
infectious diseases by environmental testing or testing a ication signs will often reappear. Money is a factor in any
random selection of birds. The specific types of screen- preventive health plan and a careful balance must be
ing tests should be tailored to the type of birds being established between cost of preventive medicine and its
purchased, and this protocol is best done with the assis- benefits. Careful consideration should be taken so that
tance of an avian veterinarian. Subsequently, if appropri- all preventive measures have a clear economic benefit.
ate biosecurity measures are maintained, the pet store
owners can feel assured that they are buying clean stock. Finally, if preventive measures are undertaken, the public
This requires some initial investment, but this invest- should be made aware of what is being done and birds
ment is spread out over many birds and is well worth it. should be sold as value-added products. For instance, if
extensive efforts are undertaken to acquire polyomavirus-
Other management techniques can be used to minimize free birds, then these birds should be advertised as such.
the risk of disease. First and foremost, a relationship When the consumer sees that one store is concerned
should be established with an avian veterinarian. The about infectious diseases and others do not place similar
veterinarian’s role is to provide advice that will help emphasis on them, the consumer will buy from that store,
minimize the risk of disease, but at the same time will even if the cost may be somewhat higher.
not result in huge expenditures. A general rule is that
any change should increase the pet store owner’s profit.
IMMUNIZATION AND
If it does not, then another approach should be taken.
PREVENTIVE MEDICINE
The two diseases that can substantially impact the pet Immunization for poxvirus, paramyxovirus-1 and salmo-
store are APV and psittacosis. APV is predominately a dis- nella can be important elements of disease control in rac-
585
ing pigeons. Poxvirus immunization also is advised for potential value and potential risks of the West Nile virus
canaries that are raised outdoors. The current parrot her- vaccine is minimal, it should probably be used only as a
pesvirus vaccine in the USA is a monovalent vaccine. The last resort. Screening in the enclosure of high-risk birds
exact serotype present in the current vaccine is not known and other mosquito control programs may be the safest
at the time of this writing. It is expected that this vaccine ways to prevent disease from the West Nile virus.
will protect against the serotype from which it is derived.
It is not known, however, if this vaccine will protect A discussion of the avian polyomavirus vaccine is
against other serotypes. In collections of birds where there included in Chapter 32, Implications of Viruses in
is a high risk of Pacheco’s disease, use of this vaccine may Clinical Disorders. The author believes that management
be indicated. A polyvalent vaccine that would protect practices are critical to the control of avian poly-
against infection with the three common serotypes may omavirus, and that there are few circumstances where
immunization would be helpful in its control.
someday be developed and could potentially protect
against Pacheco’s disease and internal papillomatosis.
Product Mentioned in the Text
The value of the equine West Nile virus vaccine in birds a. Immunocomb, Biolage Laboratories, Kibbutz Baled, Israel
remains to be proven. The author was not aware of

Resources
adverse reactions to the vaccine the first year that it was ‡ Texas Veterinary Medical Diagnostic Laboratory, PO Drawer 3040, College
used. However, a hemolytic anemia has been reported in Station, TX 77841, 979-845-3414
‡‡ Dr. Carlene Emerson, Department of Veterinary Microbiology and
lories that were immunized a year after the first set of Pathology, College of Veterinary Medicine, Washington State University,
immunizations. This problem, however, has not been Pullman, WA 99164-7040
‡‡‡ The Raptor Center, 1920 Fitch Ave, Saint Paul, MN 55108, 612-624-4969
seen in another collection of birds immunized 2 years in
‡‡‡‡ Avian and Wildlife Laboratory, University of Miami School of Medicine,
a row. Given that the current information about the Miami, FL
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9. Gravendyck M, et al: Antigenic Assoc Avian Vet, 1995, pp 65-68. Clinical signs, pathology and anti-
Suggested Reading diversity of psittacine her- 19. Phalen DN, et al: Avian poly- genic characterization Avian Dis
1. Andersen AA: Comparison of pha- pesvirus: Cluster analysis of anti- omavirus: More pieces to the puz- 42:418-422, 1998.
ryngeal, fecal, and cloacal samples genic differences obtained from zle. Proc Assoc Avian Vet, 1998, 29. Speer BL: A clinical look at the
for the isolation of Chlamydia cross-neutralization test. Avian pp 151-156. avian pancreas in health and dis-
psittaci from experimentally Pathol 25:345-357, 1996. 20. Phalen DN, et al: Diagnosis of ease. Proc Assoc Avian Vet, 1998,
infected cockatiels and turkeys. J 10. Grimes JE: Evaluation and inter- Chlamydia psittaci infections in pp 57-64.
Vet Diagn Invest 8:448-450, 1996. pretation of serologic responses cockatiels and Columbiformes. 30. Speer BL: Avicultural medical prac-
in psittacine birds to chlamydiosis Proc Assoc Avian Vet, 1999, tice: The nuts and bolts. Proc
2. Baghian A, et al: Production of a
and suggested complementary pp 13-17. Assoc Avian Vet, 1998, pp 347-355.
rabbit anti-cockatiel immunoglobu-
diagnostic procedures. J Avian 21. Phalen DN, et al: Viremia, virus 31. Strunk A, et al: Pathobiology
lin G and characterization of its
Med Surg 10:75-83, 1996. shedding, and antibody response and testing recommendations
cross-reactivities with immunoglo-
11. Grimes JE, Arzmendi F: during natural avian polyomavirus for psittacine circovirus 2 in
bulin G of other psittacine species.
Salmonella typhimurium agglu- infection in parrots. J Am Vet Med lories. Proc Assoc Avian Vet,
Avian Dis 43:48-54, 1999.
tinins in exotic bird sera in the Assoc 217:32-36, 2000. 2002, pp 45-47.
3. Bassami MR, et al: Genetic diversity
USA. J Vet Diagn Invest 7:270-274, 22. Phalen DN, et al: Diagnosis of
of beak and feather disease virus 32. Styles D, Tomaszewski E, Phalen
1995. parrots infected with Pacheco’s
detected in psittacine species in DN: Papillomas J Virol, submitted
12. Grund C, Grimm F, Kosters J: disease viruses. Proc Assoc Avian
Australia. Virology 20:392-400, 2001. 2003.
Serological studies on persistent Vet, 2001, pp 87-89.
4. Chan C, et al: Detection of anti- PMV-1 infection associated with 33. Tell LA, Woods L, Cromie RL:
23. Raidal SR, Cross GM: The
bodies specific to an antigenic cell PDD. Proc Assoc Avian Vet, 1999, Mycobacteriosis in birds. Rev Sci
haemagglutination spectrum of
wall galatomannoprotein for sero- pp 19-23. Tech Off Int Epiz 20:180-203,
psittacine beak and feather dis-
diagnosis of Aspergillus fumigatus 2001.
13. Ivey ES: Serologic and plasma pro- ease virus. Avian Pathol 23:621-
aspergillosis. J Clin Micro 40:2041- tein electrophoretic findings in 7 630, 1994. 34. Tell LA, et al: A multifaceted
2045, 2002. psittacine birds with aspergillosis. J 24. Redig PT, Orosz S, Cray C: The investigation into the diagnosis of
5. Costa C, et al: Real-time PCR cou- Avian Med Surg 14:103-106, 2000. ELISA as a management guide for mycobacterial infections in birds.
pled with automated DNA extrac- 14. Loudis BG: PMV-3 outbreak: aspergillosis in raptors. Proc Proc Assoc Avian Vet, 2002,
tion and detection of galactoman- Presentation, diagnosis and man- Assoc Avian Vet, 1994, pp 99-104. pp 61-63.
nan antigen in serum by enzyme- agement. Proc Assoc Avian Vet, 25. Reidarson TH, McBain J: Serum 35. Tomaszewski E, et al: Detection
liked immunosorbent assay for 1999, pp 223-227. protein electrophoresis and and heterogeneity of her-
diagnosis of invasive aspergillosis. 15. Phalen DN: Viruses. In Altman Aspergillus antibody titers as an pesviruses causing Pacheco’s dis-
J Clin Micro 40:2224-2227, 2002. RB, et al (eds): Avian Medicine aid to diagnosis of aspergillosis in ease in parrots. J Clin Micro
6. Cray C: Plasma protein electro- and Surgery. Philadelphia, WB penguins. Proc Assoc Avian Vet, 39:533-538, 2001.
phoresis: An update. Proc Assoc Saunders Co, 1997, pp 281-322. 1995, pp 61-64. 36. Tomaszewski E, Kaleta EF, Phalen
Avian Vet, 1997, pp 209-211. 16. Phalen DN: Avian polyomavirus: 26. Ritchie BW, et al: Documentation DN: Molecular phylogeny of the
7. Dahlhausen B, Radabaugh CS: My thoughts. Am Fed Avicul of a PBFD virus variant in lories. psittacid herpesviruses causing
Update on psittacine beak and Watchbird 25:28-39, 1998. Proc Assoc Avian Vet, 2000, pp Pacheco’s disease: Correlation of
feather disease and avian poly- 17. Phalen DN, Tomaszewski E, Davis 263-268. genotype with phenotypic expres-
omavirus testing. Proc Assoc Avian A: Investigation into the detec- 27. Romagnano A, et al: Aspergillosis sion. J Virol, submitted 2003.
Vet, 1993, pp 5-7. tion, treatment, and pathogenicity testing: Comparison of serologi- 37. Ypelaar I, et al: A universal poly-
8. Dahlhausen B, Radabaugh CS: of avian gastric yeast. Proc Assoc cal data. Proc Assoc Avian Vet, merase chain reaction for the
Detection of Chlamydia psittaci Avian Vet, 2002, pp. 49-51. 2002, pp 139-143. detection of psittacine beak and
infection in pet birds using a molec- 18. Phalen DN, et al: Serologic diagno- 28. Shihmanter EY, et al: Avian feather disease virus. J Clin Micro
ular-based diagnostic assay. Proc sis of mycobacteria infections in paramyxovirus serotype 3 isolated 16:141-8, 1999.
22_Hematology.qxd 8/23/2005 1:05 PM Page 587
CHAPTER
22
Diagnostic Value of
Hematology
JAIME SAMOUR, MVZ, P hD, D ipl ECAMS
Hematology is the discipline of medical science that

studies the blood and blood-forming tissues, and is cur-
rently considered an integral part of clinical laboratory
diagnostics in avian medicine. Hematology assays sel-
dom provide an etiological diagnosis, but they remain,
nevertheless, indispensable diagnostic tools to evaluate
health and disease in individuals, to monitor the prog-
ress of diseases, to evaluate the response to therapy and
to offer a prognosis.
The routine collection and processing of blood samples

allows the evaluation of the hematologic response to
disease. In addition, the creation of hematology data-
bases is important in establishing reference values for
various avian species.
In the past 15 years, significant advances have been

made in the use of hematology assays in the differential
diagnosis of pathologic conditions in avian species. This
appears to have developed parallel to other areas such
as nutrition, wellness examinations, anesthesia, surgery
and therapeutics.
The processing of hematology samples also has been

enhanced in recent years. In the past, automatic analysis
of avian blood samples was basically limited to total red
cell counts using the cell countersa that were available
and making manual adjustments of the thresholds and
current aperture settings. More recently, the analysis of
avian blood samples has received a significant boost
with the advent of more comprehensive and accurate
automatic analytical systems based on laser flow cytome-
try.b This methodology is based on the measurement of
scattered laser light, which fluctuates with the size of the
fore, total white blood cell counts and differential white

Table 22.1 | Materials Needed for Blood Sample
Collection
blood cell counts cannot be accepted as reliable in every
• Syringe, 1-ml or 3-ml, • Alcohol clinical case and in every species if the values were esti-
disposable • EDTA or heparin pediatric mated by laser flow cytometry. It is, therefore, highly rec-
• Needle, 27-gauge to 23- 0.5-ml or 1-ml blood ommended to re-evaluate these samples using manual
gauge, bent, disposable tubes, or sodium citrate methods. Clearly, the clinician must be fully familiar with
• Cotton tubes
the materials and methods of hematology analysis in
order to assess and understand the results.
cell, the complexity of the cell (eg, overall shape,
nucleus-to-cytoplasm ratio, granulation), and the size
and shape of the nucleus after blood cells are exposed
to a laser beam. The laser flow cytometry unit produces
Blood Sample Collection
a graphic display containing a total optical white cell It is essential that blood samples be obtained from avian
count, white cell differential count expressed in percent- species by or under the supervision of a veterinarian
age, absolute values and total red cell count, hemoglo- who is experienced with avian venipuncture. The assis-
bin measurement by the cyanmethemoglobin method, tant, if one is used, also should be comfortable with
thrombocyte count, and white cell count by cell-lysing restraint and handling techniques. The techniques used
impedance measurement of cell nuclei.14 However, the vary according to personal preferences and the species
use of laser flow cytometric technology in avian species being handled. Materials needed for blood sample col-
is not free from deficiencies. lection, ie, syringes, slides, tubes, should be labeled in
advance and readily accessible (Table 22.1).
There are certain pathological conditions in which the
presence of enlarged thrombocytes (commonly referred
to as megathrombocytes) in the blood film appear to be
METHOD
a characteristic hemoresponse. For instance, in the The total blood volume in clinically normal birds is in
houbara bustard (Chlamydotis undulata macqueenii), the range of 6 to 11 ml per 100 g of body weight.54
the mean thrombocyte measurements in birds undergo- Thus, a bird weighing 250 g would have approximately
ing chronic inflammation (severe shoulder injury as a 15 to 27.5 ml of blood, of which, in a clinically normal
result of repeated crashing against the enclosure wall) individual, up to 10% (1.5-2.7 ml) can be safely with-
were 9.22 ± 0.21 µm length and 8.10 ± 0.19 µm width drawn without having any detrimental effect on the
compared with 5.47 ± 0.12 µm length and 4.96 ± 0.10 patient. However, 0.2 to 0.3 ml of blood is generally suf-
µm width in clinically normal birds.9 The mean diameter ficient to carry out a comprehensive hematology exami-
of lymphocytes in clinically normal houbara bustards is nation in a bird.
7.7 µm;51 however, there are other species, such as the
In birds, blood samples are commonly collected using
kori bustard (Ardeotis kori), in which the presence of
the right jugular vein (v. jugularis dextra), as this is gen-
large and small thrombocytes in the same blood film
erally larger than the left jugular vein in most avian
appears to be normal.51 It is, therefore, probable that a
species (Fig 22.1a). Other preferred sites include the
sample containing megathrombocytes would yield a
basilic vein (Fig 22.1b) (v. cutanea ulnaris superficialis)
high lymphocyte count under an automatic analytical
and the caudal tibial vein (v. metatarsalis plantaris
system, as it would be impossible for even a sophisti-
superficialis) (Fig 22.1c).
cated unit to differentiate between lymphocytes and
megathrombocytes. When dealing with such species, the The methodology used for the collection of blood
software would require some adjustments in order to samples varies according to the species and the site
properly differentiate these cells. This would obviously selected (Fig 22.1d-h). For example, in long-legged
imply the need to carry out extensive calibration based birds such as large bustards, cranes and storks, the
on repeated manual assessments on a significant num- jugular or caudal tibial veins are very often used. In the
ber of samples. author’s opinion, blood samples should be collected
from the heart or the occipital sinus only if these birds
Furthermore, in certain species it is relatively common are under anesthesia and are to be euthanized. It is a
to find large and small lymphocytes in the same blood poor practice to collect blood samples from clipped
film.4,12,26,31,35 This phenomenon has been observed in nails, as cell distribution and cell content is invariably
many psittacine species. Clinically normal kori bustards, affected.
for instance, demonstrated a mean diameter for small
lymphocytes of 7.2 ± 0.12 µm, whereas the mean diam- The author prefers obtaining blood samples from most
eter of large lymphocytes was 10.7 ± 0.16 µm.31 There- bird species from 200 to 4000 g using a basilic vein
Chapter 22 | D I A G N O S T I C V A L U E O F H E M A T O L O G Y
589
Fig 22.1a | Right jugular being blocked in a love bird and a Fig 22.1b | The blocked basilic vein showing the torturous
syringe with a 27 ga needle that has been bent to allow nature of the vein making cannulation with a hypodermic nee-
venipuncture. dle difficult at best.
humerus to ensure a raised and well-defined vein. The

method of approaching the basilic vein dorsally by
entering under the adjacent tendon prevents hematoma
formation because the underlying tissue exerts pressure
on the venipuncture site when the needle is withdrawn.
It is essential to avoid sudden movements that can
alarm the bird and trigger a struggle, as this can easily
lacerate the vein and result in a hematoma or, worse, a
severe hemorrhage. After collection, a small ball of dry
cotton should be placed over the venipuncture site and
the wing closed to maintain pressure over the site for a
few seconds. It is strongly advisable to check the
Fig 22.1c | Caudal tibial vein in a love bird. venipuncture site before releasing the bird back to its
enclosure to ensure no post-collection hemorrhage has
occurred. Any sample that contains clots should be
while the bird is in dorsal recumbency, although most
rejected, as the processing of such samples would
practitioners in the US dealing with psittacine species
invariably lead to imprecise and therefore misleading
prefer jugular venipuncture. In most avian species, the
results.
optimal area for collecting a blood sample from a basilic
vein is along the medial section of the vein. The pre-
ferred side is from the right wing if the practitioner is STORAGE OF BLOOD SAMPLES
right-handed, while the left wing is the preferred side if After collection, the needle should be removed and the
the practitioner is left-handed. Venipuncture immedi- blood gently deposited into a 0.5 to 1.0 ml commercially
ately above the elbow joint is not recommended, as available pediatric blood storage tube containing the
hemostasis is difficult to achieve at this site in most anticoagulant agent ethylenediamine tetra-acetic acid
cases. The application of digital pressure with the thumb (EDTA) (1.5 mg/ml of blood) or lithium heparin (1.8
at the proximal humerus would help in raising the vein, mg/ml of blood). Squirting the sample through the
making it clearly visible running parallel to the external needle is a poor practice, as it may cause severe disrup-
aspect of the humerus. After separating the feathers and tion to the fragile blood cells. For general hematology
preparing the site with an alcohol swab, the bent needle analysis, EDTA is the anticoagulant of choice, as it is not
is gently inserted into the vein at an approximately 45° possible to estimate fibrinogen or to count white blood
angle. The sample can now be collected, taking precau- cells accurately in heparinized samples.
tion not to exert high negative pressure while withdraw-
ing with the syringe because this will invariably result in In some avian species, however, storing blood samples
the collapse of the vein. in tubes containing EDTA causes progressive red cell
hemolysis and is not recommended; in these cases, it is
While withdrawing the sample, it is recommended to preferable to use heparinized tubes. This is the case
continue maintaining pressure on the proximal with some species of Corvidae such as the jackdaw
Figs 22.1d-h | Small Birds - Basilic Vein
Fig 22.1e | Lancet used in a finger stick technique for blood

sampling for glucose analysis in humans. The lancet still has the
Fig 22.1d | The ventral surface of the wing of a cadaver with metal tip in place in the plastic cap.
the covert feathers removed to show the location for superficial
ulnaris vein lancing (arrow). Lancing the basilic vein in birds
under 100 gms avoids subcutaneous hematomas and the possi-
bility of death due to exsanguination. The site has a series of
natural depressions over the vein that serve to allow the blood to
pool. The depressions are formed by the insertion of the second-
ary feathers intermittently elevating and depressing the wing der-
mis just caudal to the border of the flexor carpi ulnaris muscle.
Fig 22.1g | The lancet readied at the site to lance the

superficial ulnaris vein.
Fig 22.1f | Lancet with the cap removed and the 1 mm tip
exposed.
Fig 22.2a | The improved Neubauer counting chamber and

the method for counting red blood cells. The total red blood cell
count is performed by counting the number of cells contained in
the 25 groups of 16 small squares (shaded) at the 4 corner
Fig 22.1h | The superficial ulnaris vein has been lanced and squares and center square in the central area of the chamber.
blood is being drawn into a micro capillary tube. A cotton ball is Closely ruled triple lines (illustrated in the drawing as thick lines)
applied to the site until hemostasis is achieved. separate these squares.
591
tubes is recommended when sending samples to a com-

mercial laboratory for processing using laser flow
cytometry.14,19
Commercially available collection tubes usually have

printed labels. A pencil or ballpoint pen is used to enter
the date and identification of the bird, preferably prior
to filling the tube with the collected blood sample.
Always remember the rule of thumb in clinical pathol-
ogy: label tubes, not lids.
TRANSPORTATION OF BLOOD
SAMPLES
Fig 22.2b | The counting system. Count cells that touch the In avian practice, hematology samples are commonly
center triple line (seen here as a thick line) of the rules to the
sent to commercial laboratories for processing (Table
left and bottom; do not count cells that touch the center triple
line of the rules to the right and top. 22.2). Therefore, it is essential to be familiar with and to
submit samples in full compliance with current local
mail and courier regulations.
Table 22.2 | Special Considerations When Submitting
Blood Samples to a Laboratory
• Seal the lid of the tube using waterproof tape in order to
prevent any leakage. Hematology
• Wrap the tube using an absorbent packing material, eg,
cotton, to soak up any potential leakage and to protect it
Laboratory Analysis
from breakage. Fasten it securely with tape, preferably
commercially available printed tape with the legend Although the hematology laboratory analysis described
“Pathological specimen. Fragile handle with care” or in this chapter were developed primarily for testing
similar tape. human blood and are in full compliance with the recom-
• The tube should then be placed within two leak-proof
plastic bags. Fasten the double wrapping securely with
mendations of the International Committee for
printed tape. Standardization in Hematology,34 these have been
• Place submission form in a separate plastic bag. adapted and used successfully in avian hematology.
• The package should then be placed within a postal- Ideally, laboratory analysis should be carried out within
approved commercially available transport container
made of aluminum, polystyrene, plastic or cardboard.
3 to 4 hours after collection. Many laboratories in the
• Attach recipient and sender labels directly to the con- USA request that a smear be made immediately and sent
tainer using tape, or place container within a padded along with the EDTA tube. If this is not possible, sam-
envelope and address it accordingly. ples should be refrigerated at 8 to 12° C or within a suit-
able container for processing within 24 to 48 hours.
Refrigerated samples are not ideal for hematology test-
Table 22.3 | Priorities When Processing ing, as the cells invariably suffer some changes. Only an
Hematology Samples experienced hematologist would be able to differentiate
• Blood film (differential, • White cell count (WBC) these changes from true hemoresponses to particular
white and red cell mor- • Hemoglobin (Hb) medical disorders. Samples should not be exposed to
phology, hemoparasites) • Red cell count (RBC) extreme environmental conditions or excessive shaking,
• Packed cell volume (PCV) • Fibrinogen
as this will affect the quality of the sample. Any form of
mouth pipetting with a Thoma pipette or any other
(Corvus monedula) and raven (Corvus corax); Gruidae pipette with or without tubing is not acceptable within
such as the black-necked crowned crane (Balearica clinical laboratory practices.
pavonina) and gray-necked crowned crane (Balearica
regulorum); Cracidae such as the black curassow (Crax The amount of blood available for testing from small
alector); Phasianidae such as the brush turkey (Alectura birds (eg, <80 g) is very often limited, making it impos-
lathami); Bucerotidae such as the crowned hornbill sible to carry out a full range of analyses. The clinician
(Tockus alboterminatus); and the ostrich (Struthio should bear this in mind and request the analysis in
camelus).3,25 Storing blood samples in sodium citrate order of priority (Table 22.3).
THE TOTAL RED BLOOD CELL

- 100
C O U N T ( R B C X 1 0 12 / L ) - 90
The total red blood cell count is in itself an important - 80

- 70
hematology assay, but it also is essential for the estima- Plasma
- 60
Fibrinogen
tion of mean corpuscular volume (MCV) and mean cor- B - 50
WBC, thrombocytes
puscular hemoglobin (MCH). Many laboratories prefer - 40
to estimate RBC using an automatic system, as this is RBC

- 30
C - 20
more precise than manual methods. The materials, solu-
- 10
tions and method described in Table 22.4, together with A -0
Fig 22.2a,b, apply to a manual technique.
Fig 22.3 | Hematocrit reader and method for estimating

HEMOGLOBIN ESTIMATION (H b g/dl ) packed cell volume. After centrifugation, position the capillary
tube on the rack. Align tube (at the bottom, with the demarca-
In avian species, estimation of hemoglobin is hampered
tion line between the sealing compound and the red blood cells)
by the presence of nuclei in the erythrocytes. Hemo- with line A. Slide the rack to the right or to the left, align the
globin estimation relies on the colorimetric measurement marginal meniscus at the top of the plasma column with line B.
of hemoglobin released after the lysing of the erythro- Position line C at the interface of the buffy layer and red cells,
and read value on the scale.
cytes. Hemoglobin can be estimated using automatic
methods or manual methods (Table 22.5). Commercial
laboratories that estimate hemoglobin using an automatic Mean Corpuscular Values (Red Cell Absolute Values)
hematology analyzer have to take into consideration the Mean corpuscular volume (MCV)
photometric interference of the free nuclei after lysing of Mean corpuscular volume (MCV) is the expression of the
the erythrocyte. In the manual method, it is essential to average volume of individual erythrocytes calculated
remove the nuclei from the preparation because its pres- with the following formula:
ence could yield unreliable results. The nuclei can be MCV = (PCV x 10)/RBC = MCV femto liters (fl)
deposited by low-speed centrifugation, but because some
Mean corpuscular hemoglobin (MCH)
hemoglobin remains attached to the nuclei, colorimetric
Mean corpuscular hemoglobin (MCH) is the expression
readings are commonly low. This can be overcome by of the average hemoglobin content of a single erythro-
estimating hemoglobin as cyanmethemoglobin using cyte calculated with the following formula:
alkaline Drabkin’s cyanide-ferricyanide solution or as oxy-
MCH = (Hb x 10)/RBC = MCH picogram (pg)
hemoglobin using ammonia solution. In both cases, the
estimation is carried out using a spectrophotometer at Mean corpuscular hemoglobin concentration
the absorbance reading of 540 nm. A calibration graph (MCHC)
should be made using commercially available hemoglo- Mean corpuscular hemoglobin concentration (MCHC) is
bin standards to express hemoglobin as oxyhemoglobin. the expression of the volume within the erythrocyte
Conversely, hemoglobin can be estimated directly as oxy- occupied by the hemoglobin and is calculated with the
hemoglobin using a commercially available hemoglobi- following formula:
nometer. This is the preferred method used and recom- MCHC = (Hb x 100)/PCV = MCHC (g/L)
mended by the author.
TOTAL WHITE BLOOD CELL COUNT
( W B C X 1 0 9/ L )
PACKED CELL VOLUME ESTIMATION The total white blood cell count (WBC) is one of the
P C V % ( H E M A T O C R I T H ct L/L) most important hematology assays in the assessment of
Packed cell volume (PCV) is an important hematologic health and disease in an individual. The WBC also is use-
assay because it provides an easy and objective way of ful because it is used together with the differential white
estimating the number of erythrocytes in the sample. It cell count to calculate the absolute number of each
also is essential for the calculation of the mean corpus- white blood cell within a blood sample. The materials,
cular volume (MCV) and mean corpuscular hemoglobin solutions and method described below, Table 22.6 and
Fig 22.4, apply to the technique.
concentration (MCHC). In avian species, PCV is best esti-
mated using the microhematocrit method described
(Fig 22.3). The use of plain microcapillary tubes is THE BLOOD FILM
preferable, since the same tube can be subsequently The examination of stained blood films is the single most
used to estimate fibrinogen. important assay in hematology analysis. An adequately
593
Table 22.4 | Manual Total Red Blood Cell (RBC) Count Hematology Test
c
Materials and Equipment Method
• Automatic dispenser, 0-50 ml • Label sample tubes using a permanent marker.
• Disposable sample tube with lid, 5 ml • Use an automatic dispenser to transfer 4 ml of either
• Micropipette, 20 µl and corresponding tip formol citrate solution or Natt and Herrick’s solution into
• Roller mixer sample tube.
• Plain capillary tubes • Wait for 5 minutes to allow working solution to reach
• Improved Neubauer hemocytometer and coverslip room temperature.
• Laboratory lens tissue • Aspirate 20 µl of whole blood from storage tube using
• Petri dish 8.5 cm diameter micropipette, wipe side of pipette tip carefully using tis-
• Filter paper 8.5 cm diameter sue and dispense on the side of sample tube to make a
• Toothpick dilution of 1:200.
• Distilled water • Avoid touching the distal opening of the pipette tip with
• Microscope, preferably with phase contrast capability the tissue, as this will cause capillary shift of blood into
the tissue.
Test Systems • Avoid immersing the pipette tip into the diluting fluid.
c
The Unopette 365851 system is probably the most popular This is a poor laboratory practice.
method used for manual red blood cell count in avian • Place sample tube in roller mixer and wait for 3 minutes.
species. It uses 10 µl of whole blood in 1.9 ml of 0.85% • Clean Neubauer hemocytometer and coverslip using a
saline, resulting in a 1:200 dilution. The two other com- dry, lint-free cloth or laboratory lens tissue.
monly used systems are based on using either formol • Place coverslip onto hemocytometer and slide gently over
citrate solution (Dacie’s fluid) or Natt and Herrick’s solu- it, making sure Newton’s rings (colored interference pat-
tion, depending on whether the examination is carried out tern) appear on both sides of the contact surfaces.
with or without phase contrast microscopy. Dacie’s formol • Withdraw a small aliquot of the diluted sample using a
citrate solution is the least known diluting fluid, but one plain capillary tube.
used and recommended by the author. • Fill up one side of the hemocytometer by touching gently
the intersection between coverslip and hemocytometer
Working Solutions with the loaded capillary tube. Avoid air bubbles and
underfilling or overfilling.
1. BD Unopette 365851c red blood count manual
• Place filter paper at the bottom of the Petri dish. Position
hematology test
two toothpicks on either side of the dish. Wet filter paper
2. Natt and Herrick’s solution lightly with distilled water. Rest hemocytometer on tooth-
(for use without phase contrast microscopy) picks. Cover Petri dish. Leave for 5 minutes for the cells
to settle down.
NaCl 3.88 g
• The hemocytometer is now ready for use.
Na2SO4 2.5 g • Count cells contained in the four corner and central
Na2HPO4 12 H2O 2.91 g squares in the mid section of the hemocytometer.
KH2PO4 0.25 g Following the “L” rule: count cells that touch the center
triple line of the ruling on the left and the bottom sides;
Formaldehyde 40% 7.5 ml
do not count cells that touch the center triple line of the
Methyl violet 2B 0.1 g ruling on the right and the top sides (see Figs 22.2a,b).
Distilled water to 1000 ml • Calculate red blood cell count using:
N/100 = RBC x 1012/L
Note: Allow solution to stand overnight. Filter before use.
Note: N = number of cells counted in 160 small squares.
3. Formol citrate solution or Dacie’s fluid
(for use with phase contrast microscopy)
Formaldehyde 10% 10 ml
Trisodium citrate 31.3 g
Distilled water 100 ml
Note: Refrigerate at 8 to 12° C.

Table 22.5 | Hemoglobin Estimation
Materials and Equipment
• Automatic dispenser, 0-50 ml • Toothpicks

• Disposable sample tube with • Cuvette, 10 mm2
lid, 5 ml • Laboratory lens tissue
• Micropipette, 20 µl and tip • Hemoglobinometer
• Roller mixer
Working Solution
Ammonia solution
Ammonia solution
4 ml
(0.88 specific gravity)
Distilled water to 1000 ml
Note: Refrigerate at 8 to 12° C.
Method Fig 22.4 | Improved Neubauer counting chamber and the

• Label sample tubes using a permanent marker. method for counting white blood cells. The total white blood cell
• Use an automatic dispenser to transfer 4 ml of ammonia count is performed by counting the number of cells contained in
solution into sample tube. 4 groups (shaded areas) of 16 large squares at the four corner
squares of the chamber. Closely ruled triple lines (illustrated in
• Wait for 5 minutes to allow working solution to reach
the drawing as thick lines) separate these squares.
room temperature.
• Aspirate 20 µl of whole blood from storage tube using
micropipette, wipe side of pipette tip carefully using tis-
sue and dispense on the side of sample tube.
• Avoid touching the distal opening of the pipette tip with
the tissue, as this will cause capillary shift of blood into
the tissue.
• Avoid immersing the pipette tip into the diluting fluid.
This is a poor laboratory practice.
• Place sample tube in roller mixer and wait for 3 minutes.
• Decant approximately 3.5 ml of the diluted blood
into cuvette.
• Remove cell nuclei jelly using toothpicks.
• Do not touch the clear reading walls of the cuvette
with bare fingers.
• Clean clear reading walls of cuvette using laboratory
lens tissue.
• Zero hemoglobinometer using ammonia solution Fig 22.5 | The slide-to-slide technique. Move spreader slide
as blank. backward to gently touch the drop of blood, allowing it to run
• Reading expressed as Hb g/dl. across the edge of the slide. Move forward to make smear. Move
slowly if blood runs slowly, move quickly if blood runs quickly.
prepared blood film provides the differential white blood clinicians is the coverslip-to-slide technique, as smudg-
cell count and absolute white blood cell count, the ing of blood red cells is generally minimized.
thrombocyte count and the hemoparasite examination.
Fixation and Staining of the Blood Film
Preparation of the Blood Film
It is commonly accepted that blood films can be pre-
Blood films can be made from a drop of fresh, non-anti-
pared and be fixed and stained at a later date. This is
coagulated blood directly from the tip of the syringe.
incorrect; blood films should at least be fixed immedi-
Conversely, films can be made from blood stored in
EDTA within 2 to 3 hours after collection. There are two ately after preparation, particularly if made in a hot and
generally accepted methods for the preparation of blood humid environment or under cold and freezing condi-
films in hematology: the slide-to-slide technique (Fig tions. Blood films should not be exposed to direct sun-
22.5, Table 22.7) and the coverslip-to-slide technique light, moisture of any kind or vapor from chemicals
(Fig 22.6, Table 22.8). A two cover-slip technique is not (formaldehyde in particular), as this would invariably
described here. The most popular method among avian affect cell morphology.
595
Table 22.6 | Total White Blood Cell (WBC) Count Hematology Test
Materials and Equipment Method

• Automatic dispenser, 0-50 ml • Label sample tubes using a permanent marker.
• Disposable sample tube with lid, 5 ml • Use an automatic dispenser to transfer 1.9 ml of 1%
• Micropipette, 100 µl and tip ammonium oxalate solution into sample tube.
• Roller mixer • Wait for 5 minutes to allow working solution to reach
• Plain capillary tubes room temperature.
• Improved Neubauer hemocytometer and coverslip • Aspirate 100 µl of whole blood from storage tube using
• Laboratory lens tissue micropipette, wipe side of pipette tip carefully using tis-
• Petri dish, 8.5 cm diameter sue and dispense on the side of sample tube.
• Filter paper, 8.5 cm diameter • Avoid touching the distal opening of the pipette tip with
• Toothpicks the tissue, as this will cause capillary shift of blood into
• Distilled water the tissue.
• Microscope, preferably with phase contrast capability • Avoid immersing the pipette tip into the diluting fluid.
This is a poor laboratory practice.
Test Systems • Place sample tube in roller mixer and wait for 3 minutes.
The Unopette 365877d system was originally developed for • Clean Neubauer hemocytometer and coverslip using a
the estimation of eosinophils in human hematology, but it laboratory lens tissue or dry, lint-free cloth.
has proved useful for determining the total white cell count • Place coverslip onto hemocytometer and slide gently over
in avian species. This system uses 25 µl of whole blood into it, making sure Newton’s rings (colored interference pat-
0.775 ml of 1% Phloxine B diluent resulting in a 1:32 dilu- tern) appear on both sides of the contact surfaces.
tion, and is the system used by most practitioners in the • Withdraw a small aliquot of the diluted sample using a
USA.3,19 The method described below is based on the use of plain capillary tube.
ammonium oxalate solution, which is the method used and • Fill up one side of the hemocytometer by gently touching
recommended by the author. the intersection between coverslip and hemocytometer
with the loaded capillary tube. Avoid air bubbles and
Working Solutions underfilling or overfilling.
1. BD Unopette 365877d eosinophil count • Place filter paper at the bottom of the Petri dish. Position
manual hematology testd two toothpicks on either side of the dish. Lightly wet filter
2. Ammonium oxalate solution 1% paper with distilled water. Rest hemocytometer on tooth-
picks. Cover Petri dish. Leave for 5 minutes for the cells
Ammonium oxalate 10 g
to settle down.
Distilled water to 1000 ml
• The hemocytometer is now ready for use.
Note: Refrigerate at 8 to 12° C. • Count cells contained in the four outer large squares of
the hemocytometer.
• Calculate total white blood cell count using:
N/20 = WBC x 109/L
Note: N = number of cells counted in 64 small squares.
Table 22.7 | Method for Slide-to-Slide Technique Table 22.8 | Method for Coverslip-to-Slide Technique
• It is highly recommended to use one-end-frosted micro- The only significant difference between this method and the
scopic slides to easily note the ID of the sample on the previous one consists of the following steps:
slide using a pencil. • Place a large rectangular coverslip over the drop of blood.
• Wipe slides clean with a lens tissue or lint-free cloth. • Pull the coverslip and the slide in opposite directions in
• Use a plain microcapillary tube to withdraw a small a steady but firm movement to create a uniform smear.
amount of fresh, non-anticoagulated blood directly from
syringe tip or EDTA tube.
• Place a small drop of blood (2 µl) at one end of a slide.
• Select a spreader slide and position it in front of the drop
of blood at about a 45° angle. The selected slide should
be free from any indentation. To test this, pass the
spreading edge over the edge of a fingernail.
• Gently move the spreader slide backward to touch the
drop of blood and allow the blood to run across the edge
of the slide.
• Gently drive the slide forward with a steady but firm
movement to create a uniform smear.
• It is always a good practice to make two good-quality
blood films.
Fig 22.6 | The coverslip-to-slide technique. Place coverslip

onto drop of blood. Apply gentle pressure downward. Move
slide and coverslip in opposite directions to make smear.
Fig 22.7 | A microcapillary tube after incubation and centrifu-

gation, and the measurements necessary for the estimation of
fibrinogen.
Fixation blood films. However, the results obtained with various

In general, freshly prepared blood films should be stains may be slightly different, and the selection of
immersed in absolute methanol within a Coplin jar for 5 stains is generally accepted as a matter of personal pref-
to 10 minutes immediately after preparation. Fixed erence. Commonly used stains include Wright stain,
blood films can then be stored within commercially Giemsa stain, Wright-Giemsa stain, Leishman stain,
available slide storage boxes (eg, under field conditions) Wright-Leishman stain, May-Grünwald stain and May-
and be stained at a later date. Blood films also can be Grünwald-Giemsa stain. In the author’s opinion, rapid
stained immediately after fixation. stains on their own, eg, Diff Quick and Rapid Diff, do
not produce adequate quality for the differentiation of
The importance of adequate fixation of blood films from subtle blood cell structures and those of hematozoa.
avian species cannot be overemphasized. The intracyto- This is particularly important with respect to the mor-
plasmic granules of the heterophils and basophils are phological characteristics of the granulocytes.
water soluble; therefore, blood films should be ade-
quately fixed before staining in order to preserve the Automatic slide stainers facilitate staining a relatively
large number of blood films at the same time, producing
integrity of these structures. A significant problem in
consistent results and eliminating variations that may
avian hematology is the presence of smudged red cell
occur with manual techniques. However, this type of
nuclei as a consequence of hemolysis in poorly fixed
equipment is relatively expensive to purchase and main-
blood films. This is one of the main reasons why clini-
tain and is more appropriate for high-volume commer-
cians and commercial laboratories are now inclined to
cial laboratories.
use stains that are prepared in absolute methanol (eg,
Wright-Giemsa stain, Leishman stain) and are used at full It is important that clinicians or laboratory technicians
strength so films are fixed and stained at the same time. recall the basic principles of hematology when staining
If absolute methanol within a Coplin jar is used for fixa- blood films. The pH of the stains should be checked
tion in your laboratory, it must be replaced as soon as it each time new stock is prepared. Some stains, particu-
begins showing chemical fatigue. This would depend on larly those prepared from powder, should be adequately
the number of slides fixed and the environmental condi- filtered. Glassware should be properly washed, rinsed
tions within the laboratory. with distilled water and dried thoroughly before use.
Many of the common artifacts on blood films are due to
Staining
careless preparation and improper methodology.
Most Romanovsky stains used for staining human and
mammalian blood films are suitable for staining avian The staining method currently used and recommended
597
Table 22.10 | Morphologic and Staining Characteristics of

Table 22.9 | Wright-Giemsa Staining Procedure Different Blood Cells
Working Stain Blood Cell Morphologic Staining
Characteristics Characteristics
• 3 g Wright stain powder
• 0.3 g Giemsa stain powder Erythrocyte Mature cells
• 5 ml glycerol Medium size, oval elon- Cytoplasm: uniform pale
• To 1000 ml absolute methanol (acetone free) gated shape, central oval orange to red-pink;
elongated nucleus Nucleus: purple-red,
• Filter and store condensed, clumped
chromatin
Method
Immature cells
• Prepare thin blood smears.
Smaller than mature cell, Polychromatic, cytoplasm
• Place on staining rack. round to semi-oval, pale to dark blue
• Flood smear with Wright-Giemsa stain, allow to stand for relatively larger nucleus
3 minutes.
Heterophil Medium size, round shape, Colorless cytoplasm, rod-
• Add equal amount of Sørensen’s pH 6.5-6.8 buffer, bilobed nucleus to cigar-shaped brick red
depending on batch stain. to pale blue granules
• Mix gently by blowing using a pipette until metallic green Eosinophil Medium size, round shape, Pale blue cytoplasm, round
sheen forms on the surface, allow to stand for 6 minutes. bilobed nucleus to oval brick red to pale
blue granules
• Rinse with buffer, allowing to stand for 1 minute for
Basophil Small size, round shape, Pale blue cytoplasm, vari-
differentiation.
unlobed nucleus able number of small,
• Wash copiously with buffer. medium and large dark
• Wipe the back of smear with tissue to remove excess stain. red-purple granules
• Prop in rack until dry. Lymphocyte Small to medium size, typi- Pale blue cytoplasm
cally round to triangular
shape, centrally positioned
large round nucleus; in
by the author is a slightly modified technique4 described general, 25 cytoplasm:75
nucleus; ratio, coarsely
in Table 22.9. condensed to highly
condensed chromatin
The placement of a coverslip using a commercially avail- Monocyte Large size, typically round Cytoplasm pale blue to
shape, eccentrically posi- pale gray
able mounting medium over the blood smear is tioned kidney-shaped
nucleus; in general 75
optional. Additionally, the mounting of blood films cytoplasm:25 nucleus ratio,
offers several advantages such as preventing scratching cytoplasm lace-like
appearance, often medium
during transport, protection against damage during size vacuoles, coarsely
condensed chromatin
excessive manipulation (eg, teaching material) and
enhancing visualization for optimal examination and Thrombocyte Small, oval to rectangular Cytoplasm colorless to pale
shape, nucleus oval to blue, large vacuoles,
photography. rectangular nucleus highly condensed
dark purple-red chromatin
Morphologic and Staining Characteristics of Red

Blood Cells, White Blood Cells and Thrombocytes Differential White Blood Cell and Absolute
White Blood Cell Count
Normal red blood cells appear elliptical and have ellipti-
For the differential white blood cell count and absolute
cal nuclei; the cytoplasm stains uniformly eosinophilic,
white blood cell count, the film should be examined
and the nuclei is dark purple in color (modified Wright-
thoroughly under high-power magnification, under oil
Giemsa stain).
(1000x). The recommended topographic site is on the
In general, the widely known “Romanovsky stains” con- shoulder of the blood film. The shoulder is the edge of
tain blue azure that reacts with acid groups, including the oval-shaped end of a smear. This is the area where
those of nucleic acids and proteins of the nucleus and the blood cells are in one layer and are slightly segre-
cytoplasm and eosin Y, which has a particular affinity for gated, thus facilitating examination.
basic groups of hemoglobin. When used in different
avian species, the slight variations observed may be the In general terms, 100 white blood cells should be
result of true species diversity or simply variations in the counted and classified according to the morphologic
materials and methods used from individual to individ- and staining characteristics. Counting is usually carried
ual or from laboratory to laboratory. out using a commercially available manual or electronic
differential cell counter. The differential white blood cell
Adequate knowledge of the morphology and staining count is expressed as a percentage of the individual cell
characteristics of the different blood cells is of the utmost group. The percentage of each cell group is then con-
importance for the differentiation and classification of verted into absolute numbers by reference to the total
those blood cells (Table 22.10 and Figs 22.8-22.43). WBC using the following formula:
(Percentage of white blood cell counted x total WBC)/100 =

absolute No. x 109/L Table 22.11 | Fibrinogen Estimation
Materials and Equipment Needed for

Thrombocyte Count Fibrinogen Estimation
Thrombocytes are usually counted while performing the • Microcapillary tube rack
differential white blood cell count. Valid and reliable • Microhematocrit centrifuge
results cannot be obtained if there is evidence of throm- • Microhematocrit reader
bocyte clumping. • Water bath 56° C ± 1° C
• Microcapillary tube holder
The absolute number of thrombocytes is estimated by • Microscope with measuring eyepiece
using the following formula: and stage Vernier scale
• Timer
(No. of thrombocytes counted/100) x WBC =
thrombocytes x 109/L Method (following estimation of packed cell volume)
Figs 22.44-22.48 and Tables 22.12-22.18 are offered as • Place microcapillary tube in tube rack.
references for interpreting hemotological findings. • Place loaded rack in water bath at 56° C for 3 minutes
(make sure the entire plasma column is immersed).
• Centrifuge microcapillary tubes again at 10,000 to 12,000
FIBRINOGEN ESTIMATION ( g/L) “g force” for 5 minutes.
Fibrinogen is a plasma protein essential for normal • Place microcapillary tubes in tube holder and, using the
blood coagulation, but also is one of the acute reactive microscope measuring eyepiece and the stage Vernier of
the microscope, take reading at the upper and lower limits
proteins that are detected in increased levels in associa-
of the protein layer and at the upper limit of the plasma
tion with medical disorders involving infection and column (see Fig 22.7).
inflammation (see Tables 22.11, 22.12 and 22.18). • Estimate fibrinogen with the following formula:
(B - A)/(C- A) x 100 = fibrinogen g/L
Hemoparasite Examination Note: It is essential to perform this analysis on blood stored in EDTA
Hemoparasite examination is carried out on thin, good- because the analysis would be invalidated if performed on samples
stored in heparin or on samples containing clots.
quality blood films. Prior to a differential white cell
count using high-power magnification (1000x), the
blood film should be examined under low-power magni- number of red cells containing hemoparasites (eg,
fication (eg, 200x or 400x) in order to detect large extra Haemoproteus spp., Babesia spp.). The number is then
cellular hemoparasites (eg, microfilariae), which could expressed in percentage and this usually constitutes the
be missed if the film is examined only under high-power degree of parasitemia.
magnification. The examination under low-power magni-
fication should concentrate on areas not commonly If hemoparasites are observed during routine examina-
examined under high-power magnification, eg, head and tion of the blood film under low- or high-power magnifi-
tail of the blood smear. The blood film should be exam- cation, it is imperative to immediately prepare additional
ined in full in a systematic way and following a consis- blood films. Ideally, a fresh blood sample should be
tent pathway. obtained to prepare these new blood films from non-
anticoagulated blood. This is of the utmost importance if
A blood parasite quantitative assessment should be car- a rare parasite is observed in the film. Blood films
ried out, in certain cases and under certain circum- should be fixed but unstained when sending them to
stances, by examining 1000 red cells (in the case of parasitologists, who have their own preferences for
intracytoplasmic parasitic forms) and determining the stains and staining procedures.
599
Unless specified otherwise, hematology images are from a saker falcon (Falco cherrug):
Fig 22.8 | Shown is a polychromatic erythroblast (pe) and poik- Fig 22.9 | The red cells in a bird with severe anemia show vac-
ilocytes (pc). The nuclear chromatin of the polychromatic ery- uolation (vc), hypochromia (hc) and polychromasia (plc). There
throblast is clumped and the cytoplasm is highly basophilic are some poikilocytes (pc) in the smear (modified Wright-Giemsa
(modified Wright-Giemsa stain). stain).
Fig 22.10 | The red cells in sickle cell anemia show sickling Fig 22.11 | Hypochromic (hc), teardrop-shaped red cells (tds)
(sc), vacuolation (vc), hypochromia (hc) and polychromasia (plc). and poikilocytes (pc) are illustrated (modified Wright-Giemsa
Some poikilocytes (pc) also are present (modified Wright-Giemsa stain).
stain).
Fig 22.12 | Erythroplastid (arrows) forms (modified Wright- Fig 22.13 | Poikilocytes (arrows) are seen in metabolic defects
Giemsa stain). and increased erythropoiesis. Polychromatic red cells (plc) are
produced in response to severe blood loss. These are larger than
normal cells (modified Wright-Giemsa stain).
Fig 22.14 | Shown are teardrop-shaped red cells (tds) and Fig 22.15 | Two normal heterophils (arrows). Heterophils are
polychromasia (plc). Teardrop-shaped cells are indications of tox- characterized by brick red, elongated intracytoplasmic granules
icosis (May-Grünwald Giemsa stain). and bilobed nuclei (modified Wright-Giemsa stain).
Fig 22.16 | In this eosinophil (arrow), note the numerous small Fig 22.17 | An eosinophil (arrow) from an eclectus parrot
and medium-sized, dark purple-colored granules located mainly (Eclectus roratus). Note the numerous small intracytoplasmic
in the periphery of the cytoplasm (modified Wright-Giemsa stain). granules widespread across the cytoplasm. The granules stain
dark purple in color (modified Wright-Giemsa stain).
Fig 22.18 | An eosinophil (arrow) from a kori bustard (Ardeotis Fig 22.19 | A slightly disrupted eosinophil (arrow) from a lesser
kori). Note the large, round, orange-colored granules character- sulphur-crested cockatoo (Cacatua sulphurea). The medium-sized,
istic of this species (May-Grünwald Giemsa stain). round granules are blue in color (May-Grünwald Giemsa stain).
601
Fig 22.20 | In this eosinophil (arrow) from a saker falcon (Falco Fig 22.21 | In this eosinophil (arrow) is seen a similar-staining
cherrug), the granules are not stained, giving the impression of artifactual difference, as in the previous figure. The granules are
numerous irregular vacuoles within the cytoplasm (May-Grünwald not stained, giving the impression of numerous vacuoles within
Giemsa stain). the cytoplasm (Diff Quik stain).
Fig 22.22 | These eosinophil (arrow) granules are well stained, Fig 22.23 | A basophil (arrow) is characterized by the presence
irregular in shape and size, stained purple or dark purple (modi- of large, round, dark purple granules widespread across the cyto-
fied Wright-Giemsa stain). The author highly recommends the plasm and an unlobed nucleus (modified Wright-Giemsa stain).
use of this stain for routine hematology.
Fig 22.24 | A normal monocyte (arrow) is a relatively large cell Fig 22.25 | A normal lymphocyte (ly) and a normal thrombo-
with a kidney-shaped nucleus and abundant, slightly opaque, cyte (th). Lymphocytes are regular round cells with a central or
blue-gray, “lace-like” cytoplasm (modified Wright-Giemsa stain). slightly eccentric nuclei, and with a varying amount of pale blue
cytoplasm (modified Wright-Giemsa stain).
Fig 22.26 | Two normal thrombocytes (arrows) from a kori bus- Fig 22.27 | Shown are a normal thrombocyte (th), normal lym-
tard (Ardeotis kori). Thrombocytes are round or irregular cells phocyte (ly) and a normal monocyte (mo) for comparison of
with completely dark purple and dense round or oval nuclei, and three different mononuclear cells. Thrombocytes and small lym-
clear blue-gray cytoplasm. In some species, a few cytoplasmic phocytes can be very similar. In order to differentiate between
projections can be observed. Sometimes it can be very difficult to them, the appearance of the nuclear chromatin has to be closely
differentiate between thrombocytes and small lymphocytes (May- examined (modified Wright-Giemsa stain).
Grünwald Giemsa stain).
Fig 22.28 | Two toxic heterophils (th) and a megathrombocyte Fig 22.29 | A toxic heterophil (arrow) showing loss of nuclear
(mth). One of the heterophils shows a lack of lobulation of the lobulation (left shift) and loss of cytoplasmic granulation. The
nucleus (left shift); both show loss of granulation and the cyto- granules are round, large and stained dark purple, and the cyto-
plasm is stained basophilic. The megathrombocyte is significantly plasm is basophilic (modified Wright-Giemsa stain).
larger than a normal thrombocyte. The cytoplasm is basophilic,
the nucleus cytoplasm ratio is increased and it has scalloped
cytoplasmic margins (modified Wright-Giemsa stain).
Fig 22.30 | A toxic heterophil (arrow) with a lack of nuclear Fig 22.31 | A toxic heterophil (arrow). The heterophil shows
lobulation (left shift) and loss of cytoplasmic granulation. Only a loss of nuclear lobulation (left shift) and loss of cytoplasmic gran-
few large, round, dark purple granules are present and the cyto- ulation. There are very few large, dark purple granules and the
plasm is basophilic (modified Wright-Giemsa stain). cytoplasm is basophilic (modified Wright-Giemsa stain).
603
Fig 22.32 | A toxic heterophil (arrow). The nucleus is seg- Fig 22.33 | A reactive monocyte (arrow). The cytoplasm is
mented into several fragments (right shift); the granules are not basophilic and the nuclear chromatin is coarse (modified Wright-
stained, giving the impression of numerous vacuoles within the Giemsa stain).
cytoplasm (May-Grünwald Giemsa stain).
Fig 22.34 | A toxic monocyte (arrow). The nuclear/cytoplasm Fig 22.35 | A normal lymphocyte (ly) and a normal thrombo-
ratio is increased, the cytoplasm stains basophilic and there are cyte (th) (modified Wright-Giemsa stain).
numerous vacuoles within the cytoplasm (modified Wright-
Giemsa stain).
Fig 22.36 | A megathrombocyte (arrow). Megathrombocytes Fig 22.37 | Haemoproteus tinnunculi (arrows) (modified Wright-
are larger than normal thrombocytes and can be confused with Giemsa stain).
small lymphocytes. The cytoplasm of megathrombocyte stains
basophilic and the nuclear chromatin is coarser (modified
Wright-Giemsa stain).
Fig 22.38 | Haemoproteus psittaci (arrows) from a green- Fig 22.39 | Babesia shortti (arrows) (modified Wright-Giemsa
winged macaw (Ara chloroptera). stain).
Fig 22.40 | Microfilaria sp. (modified Wright-Giemsa stain). Fig 22.41 | Leucocytozoon toddi (lct), Haemoproteus tinnunculi
(hpt) and normal heterophil (ht) (modified Wright-Giemsa stain).
Kendall Harr
M. Griener
Fig 22.42 | Leucocytozoon simondi from a Canada goose Fig 22.43 | Plasmodium vaughani schizont from a robin (Turdus
(Branta canadensis). migratorius).
605
Age-related Hematologic Changes

Age-related hematologic findings in kori bustard (Ardeotis kori) chicks during their growth and development are presented
(Figs 22.44-22.48). Blood samples were collected from 16 clinically normal chicks at 1-month intervals. The tenth sampling
was obtained at 15 months of age.
The following is a collection of hematology values and an interpretation guide for the avian veterinarian:
Fig 22.44 | The RBC increased steadily for the first 4 months Fig 22.45 | The HB value followed a similar pattern as for
from 1.28 ± 0.06 x 1012/L at 1 month of age, increasing gradu- RBC, with a value of 7.5 ± 0.2 g/dl at the age of 1 month,
ally up to the age of 4 months to 2.06 ± 0.08 x 1012/L. After increasing to 12.1 ± 0.3 g/dl at 4 months of age. This value
this time, the RBC remained fairly constant. The RBC value at remained fairly constant until the age of 12 months, when it
the age of 12 to 15 months was 2.08 ± 0.06 x 1012/L. increased to 14.2 ± 0.4 g/dl.
Fig 22.46 | The Hct value continued to increase steadily from Fig 22.47 | The WBC count at 1 month of age was 8.78 ±
0.23 ± 0.7 L/L at 1 month of age to 0.399 ± 0.9 L/L at 5 0.45 x 109/L, increasing to 15.6 ± 0.7 x 109/L at 7 months, then
months of age and remained fairly constant until the age of 12 decreasing slightly to 14.5 ± 0.5 x 109/L at 9 months of age.
to 15 months, when the value increased to 0.47 ± 0.9 L/L.
Fig 22.48 | The fibrinogen value was 1.76 ± 0.18 g/L at 1

month of age, increasing steadily to 3.0 ± 0.2 g/L at the age of
7 months.
Hemoresponses
WBC, DIFFERENTIAL WHITE BLOOD CELL COUNT
Table 22.12 | Evaluating the RBC, HB, PCV and Red Cell Indices
Hematologic Findings Possible Causes
Polycythemia: Increased packed cell volume Absolute: Primary polycythemia
(PCV) or hematocrit (Hct) and red blood cell Polycythemia vera
count (RBC) Secondary polycythemia, reaction to hypoxia
Physiological: Adaptation to high altitudes
Pathological: Chronic circulatory or respiratory disease
(ie, COPD or asthma of macaws), iron storage disease, rickets
Hypoxic increase in erythropoietin production
Non-hypoxic, autonomous increase in erythropoietin production
Relative: Dehydration, different etiologies
PCV >56% or Hct >0.56 L/L Dehydration in most birds, relatively normal in small (<100 g)
psittacine and passerine birds, especially cockatiels
Anemia: Decreased PCV or Hct and RBC Absolute: Hemorrhage (trauma, coagulation disorders, ectoparasitism, endoparasitism); increased red
cell destruction (hemoparasites, some bacterial infections, autoimmune hemolytic anemia); decreased red
cell production (nutritional deficiencies, chronic infection, chronic renal disease, avian leukoses, toxicosis)
Relative: Overhydration
Low hemoglobin (Hb) value: Anemia in adult birds
(eg, <11.0 g/dl)
Low mean corpuscular hemoglobin con- Possible iron and other element deficiency
centration (MCHC) value: (eg, <29.0 g/dl)
Table 22.13 | Evaluating the Leukocytosis/Toxic Table 22.14 | Evaluating the Leukocytosis/Toxic
Heterophilia with Left Shift Heterophilia with Left Shift (cont)
Monocyte Count Possible Causes WBC and Monocyte Count Humoral Cellular Prognosis
Normal Infectious Differential Response to
Acute: Gram-negative septicemias. Tuberculosis Continued
(granulomas in Falconiformes and Presence of
Galliformes, but not in Psittaciformes, in Pathogen
these species exclusive accumulation of Normal Normal monocyte Additional abnormal- Poor
epithelioid cells [Gerlach, personal WBC/toxic count - acute ities-immature cells
communication, 2002]), coligranulomatosis, heterophils (left shift), anemia,
salmonellosis, yersiniosis and pasteurellosis and/or reactive bone marrow
Monocytosis Fungal: Aspergillosis, severe candidiasis lymphocytes damage, excessive
Parasitic: Trichomonaisis, capillariaiasis, maggot demand
infestations
Miscellaneous: Foreign body inhalation pneumonia, Monocytosis - No additional Excellent
focal peritonitis, chronic ulcerative chronic anemia abnormalities
lesions, old open wounds due to bone
Acute and chronic: Pox and herpesvirus infections, marrow damage =
chlamydophilosis depression/aplastic
Chronic: Granulomatous or purulent infections/ anemia
infestations
Note: Causes for bone marrow suppression and anemia include infec-
Monocytopenia Non-infectious tions such as viral, bacterial endotoxins in gram-negative septicemia,
Maggot infestation, burns, lead/smoke intoxication, neoplastic, toxic such as lead toxicosis, metabolic such as high estrogen
egg yolk peritonitis levels, emaciation.
Table 22.15 | Evaluating Leukocytosis/Heterophilia/ Table 22.16 | Evaluating Lymphocytosis with

Normal Heterophils Reactive Lymphocytes (seen rarely in species with a
Monocyte Serial Possible Causes of strong heterophilic leukogram)
Count Sampling Hemogram Changes Hematologic Findings Possible Causes
Monocytosis WBC reduced Healing of soft tissue damage Premature lymphoid Lymphoid leukosis; marked lymphocytosis
or bone fractures without the cells, mitotic figures, with or without immature cells indicates lym-
complications of severe infec- anemia phocytic leukemia, while marked lymphocy-
tion or necrosis, relative cell tosis with predominantly mature, small lym-
numbers depend on the phocytes with scalloped cell margins indi-
degree of chronicity cates lymphoid neoplasia
Normal WBC stays elevated Acute or chronic inflammation
Blood parasites with or Haemoproteus and Leucocytozoon spp.
monocyte without severe tissue necrosis
without lymphocytosis usually without manifesting clinical signs
count
and/or anemia with the exception of young birds; Babesia,
Return to normal within Stress Plasmodium spp. may cause life-threatening
24-72 hours in the condition with severe anemia and in some
absence of stressor cases lymphocytosis
Note: Monocytes are slow-reacting cells of the immune system, still Monocytosis Strong chronic stimulation of the immune
changing when other values are already close to normal levels. system, eg, chronic inflammation, chronic
viremias (leukopenia, lymphocytosis in
chronic viral antigen exposure), chronic
aspergillosis, immune-mediated diseases
607
Table 22.17 | Evaluating Leukopenia

Hematologic Findings Possible Causes
Toxic heterophils, immature cells, Final stage of immune response, severe bone marrow dam-
anemia, monocytosis, reactive age, gram-negative septicemia, infected wounds, circovirus
lymphocytes in psittacines, marked loss of skin, eg, burns, marked tissue
necrosis, smoke intoxication. Grave prognosis.
Normal morphology, Initial stage of stress
relative heterophilia, absolute
lymphopenia
Reactive lymphocytes, relative Acute viral infection (toxic heterophils in pox and her-
lymphocytosis, progressive or pesvirus infections)
intermittent leukopenia
Table 22.18 | Hematological Reference Values for Selected Avian Species

Hematology Assay Egyptian Vulture25 Common Buzzard25 Golden Eagle25 Saker Falcon50 Barn Owl25
(Neophron perc- (Buteo buteo) (Aquila chrysaetos) (Falco cherrug) (Tyto alba)
nopterus)
n=4 n=6 n=4 n = 25 n = 10
RBC x 1012/L 2.3 (1.9-2.6) 2.4 (2.2-2.7) 2.4 (1.9-2.7) 2.65 (2.0-3.9) 2.7 (2.2-3.0)
Hb g/dl 14.8 (13.3-16.5) 12.9 (11.6-14.6) 13.8 (12.1-15.2) 15.3 (13.3-21.2) 14.2 (12.7-16.4)
PCV % 43 (37-46) 38 (34-42) 41 (35-47) 47 (42-53) 46 (42-51)
MCV 190 (183-206) 159 (151-171) 174 (160-184) 183.1 (135.8-219.5) 176 (145-216)
MCH 67.7 (65.2-72.9) 53.8 (48.8-57.5) 58.9 (56.3-62.7) 60.7 (50.6-78.9) 51.1 (44.9-60.7)
MCHC 35.2 (35.0-35.5) 33.9 (31.4-36.0) 34.0 (32.3-35.9) 60.7 (50.6-78.9) 31.8 (28.9-34.9)
WBC x 109/L 7.6 (4.7-10.6) 9.1 (4.6-13.9) 13.1 (11.7-14.7) 33.2 (28.3-40) 16.6 (11.5-22.3)
Heterophils x 109/L 4.0 (1.2-5.5) 5.5 (2.3-8.8) 10.4 (9.5-12.7) 4.1 (2.1-5.9) 8.9 (5.2-12.5)
Eosinophils x 109/L 0.3-1.4 0.1-3.1 0.2-0.6 0 0
Basophils x 109/L 0 0.0-0.6 0.0-0.2 0 0
Lymphocytes x 109/L 2.5 (1.5-3.4) 1.7 (1.1-2.4) 2.2 (1.6-3.2) 1.3 (0.5-2.2) 5.0 (2.5-7.5)
Monocytes x 109/L 0.0-0.4 0 0 0.2 (0-0.6) 0
Thrombocytes x 109/L 13 (6-15) 27 (18-36) 14 (4-21) 0.41 (0.17-0.76) 33 (14-58)
Fibrinogen g/L 1.6 (1.0-1.9) 2.3 (1.3-3.3) 2.9 (2.0-4.1) 2.8 (1.7-4.7) 2.7 (1.9-3.3)
Hematology Assay Crowned Crane25 Greater Flamingo25 Rosy Flamingo43 White Stork25 Kori Bustard31
(Balearica regulorum) (Phoenicopterus (Phoenicopterus (Ciconia ciconia) (Ardeotis kori)
ruber) ruber ruber)
n = 33 n=9 n = 25 n = 16 n = 28
RBC x 1012/L 2.8 (2.4-3.1) 2.6 (2.3-2.8) 1.4 (1.1-1.8) 2.4 (2.1-2.7) 2.3 (1.74-2.95)
Hb g/dl 15.6 (11.9-18.8) 17.3 (15.9-19.6) 13.4 (9.2-17.6) 15.8 (14.4-17.7) 14.1 (11.9-15.9)
PCV % 47 (44-52) 50 (47-57) 47.8 (37.9-57.8) 45 (41-48) 47 (39.5-52.5)
MCV 171 (156-182) 193 (170-207) 326.6 (234.3-419.0) 189 (172-195) 208.5 (161.9-275.4)
MCH 64.3 (59.8-70.2) 66.2 (57.6-70.0) 91.5 (57.8-125.3) 67.2 (60.2-69.9) 62.4 (48-84.6)
MCHC 36.2 (34.5-39.2) 34.4 (33.5-35.2) 28.1 (20.4-35.8) 35.3 (31-36.9) 30.0 (29.7-34.9)
WBC x 109/L 11.1 (6.3-15.6) 2.4 (0.9-3.4) 8.7 (1.5-15.8) 10.8 (7-14.3) 7.3 (3.0-12.8)
Heterophils x 109/L 8.2 (4.1-13.3) 1.2 (0.2-3.0) 3.9 (1.0-11.4) 9.2 (5.1-14.9) 3.9 (0.9-9.25)
Eosinophils x 109/L (0.0-1.3) (0.0-0.4) (0.0-0.3) (0.0-0.7) 0.3 (0.0-1.1)
Basophils x 109/L (0.1-0.8) (0.0-0.4) (0.0-0.8) (0.0-0.5) 0.2 (0.0-0.8)
Lymphocytes x 109/L 1.6 (0.6-2.7) 0.9 (0.4-1.6) 5.2 (0.8-9.6) 0.8 (0.2-1.6) 2.2 (0.41-5.4)
Monocytes x 109/L (0.0-0.3) (0.0-0.2) 0.5 (0-1.8) (0.0-0.3) 0.6 (0.0-1.5)
Thrombocytes x 109/L 3.6 (5-18) 4 (2-7) — 19 (8-32) 5.5 (1.49-18.0)
Fibrinogen g/L — — — 2.3 (1.7-3.2) 2.42 (1.42-4.5)
Table 22.18 | Hematological Reference Values for Selected Avian Species (continued)
Hematology Assay Black-footed Humboldt African Grey Greater Sulphur- Scarlet Macaw25
Penguin25 Penguin55 Parrot25 crested Cockatoo25 (Ara macao)
(Spheniscus demersus) (Spheniscus (Psittacus erithacus) (Cacatua galerita)
humboldti)
n = 57 n = 14 n = 11 n = 25 n=7
RBC x 1012/L 1.74 (1.32-2.12) 1.8 3.3 (3.0-3.6) 2.7 (2.4-3.0) 3 (2.7-3.5)
Hb g/dl 16.8 (13.4-19.5) 15.0 15.5 (14.2-17.0) 15.7 (13.8-17.1) 16.8 (14.8-18.9)
PCV % 44 (36-51) 43 48 (43-51) 45 (41-49) 48 (46-52)
MCV 254 (232-273) 238.1 145 (137-155) 165.0 (145-187) 160 (143-175)
MCH 95.1 (87.2-104.3) 83.3 47.2 (41.9-52.8) 57.6 (53.8-60.6) 57.6 (51.1-64.2)
MCHC 37.8 (35.4-40) 34.8 32.5 (28.9-34) 34.9 (33.3-37.6) 35.9 (32.6-38.5)
WBC x 109/L 9.3 (3.5-16.3) 13.0 7.0 (3.3-10.3) 6.4 (1.4-10.7) 10.2 (6.4-15.4)
Heterophils x 109/L 8.1 (5.0-12.3) 8.0 4.9 (1.8-7.3) 3.7 (1-6.6) 8.0 (4.9-12.8)
Eosinophils x 109/L (0.0-0.2) 1.1 0 (0.0-0.2) 0
Basophils x 109/L (0.0-0.3) 0 (0.0-0.8) (0.0-0.9) (0.0-0.8)
Lymphocytes x 109/L 3.1 (0.8-5.2) 2.8 1.4 (0.7-2.1) 1.9 (1.0-3.6) 1.6 (1.2-2.2)
Monocytes x 109/L 0 0.6 (0.0-0.3) (0.0-0.2) 0
Thrombocytes x 109/L 11 (5-19) 18.3 22.0 (11-42) 13.0 (7-24) 22 (17-30)
Fibrinogen g/L 2.9 (2.2-3.7) — 2.2 (1.5-2.8) 1.4 (0.9-2.0) 1.7 (1.0-2.2)
Hematology Assay Kea25 Fisher’s Nicobar Pigeon47 Common Crowned Brown Pelican25
(Nestor notabilis) Lovebird250 (Caloenas nicobarica) Pigeon47 (Pelecanus
(Agapornis fischeri) (Goura cristata) occidentalis)
n=8 n = 16 n=9 n=5
RBC x 10 /L12
2.6 (2.3-3.1) 4.5 (3.8-5.3) 3.4 (2.6-4.3) 2.31 (1.95-2.6) 2.7 (2.6-2.8)
Hb g/dl 13.4 (10.6-16.9) 15.3 (13.0-17.7) 17 (12.7-19.7) 12.3 (10.6-14.7) 14.5 (14.3-14.8)
PCV % 40 (34-46) 53 (45-61) 50.7 (45-56) 37.6 (33.8-42) 46 (43-49)
MCV 154 (137-186) 124.5 (108-141) 149.8 (127.6-168.5) 158.7 (142.9-175.0) 168 (166-173)
MCH 51.2 (41.6-68.1) 34.5 (29.3-39.8) 50 (41.3-57.6) 50.8 (44.2-57.3) 53.4 (51.2-56.8)
MCHC 33.2 (30.4-37.0) 29 (25.7-32.3) 33.5 (28.3-36.1) 31.9 (27.9-38) 31.7 (30.4-32.9)
WBC x 109/L 16 (12.1-22.6) 3.5 (0.6-6.4) 4.23 (2-8.2) 17.7 (11.7-25.1) 11.9 (6.6-19.4)
Heterophils x 109/L 13.8 (9.4-20.1) 2.5 (0.1-4.9) 5.2 (4.2-7.1) 6.6 (5.5-7.8) 6.7 (4.0-9.5)
Eosinophils x 109/L (0.0-0.5) 0.15 (0.0-0.3) 3.7 (2.7-5.1) 0.2 (0.1-0.5) (0.0-0.2)
Basophils x 109/L (0.0-0.6) 0.2 (0.0-0.4) 0 (0.0-0.1) (0.0-.0.2)
Lymphocytes x 109/L 1.9 (1.1-2.7) 2.3 (0.6-4.1) 3.7 (2.7-5.1) 3.0 (1.8-4.0) 4.0 (2.5-7.0)
Monocytes x 109/L 0 0.2 (0.0-0.3) 2.1 (1-5) (0.0-0.02) (0.0-0.2)
Thrombocytes x 109/L 16 (11-24) 15 (5-25) — — 27.5 (17-38)
Fibrinogen g/L 1.5 (1.1-1.8) 2.45 (0.9-4.0) — — 2.9 (2.6-3.1)
Hematology Assay Ostrich52 Domestic Fowl20 Wood Duck45 Bar-Headed Stone Curlew52
(Struthio camelus) (Gallus domesticus) (Aix sponsa) Goose20 (Burhinus
n = 15 (Anser indicus) oedicnemus)
n = 18
RBC x 1012/L 1.7 3.2 (2.5-3.9) 2.79 (2.5-3.2) 2.86 (2.59-3.27)
Hb g/dl 12.2 12.6 (10.2-15.1) 14.95 (12.2-17.2) 14.4 (12.2-16.6)
PCV % 32 39.5 (30-49) 45.5 (43-56) 47 (44-58)
MCV 174 119.5 (104-135) 164.2 (155-187) 167.3 (149.9-196.2)
MCH 61 37.9 (32.0-43.9) 54.0 (47.8-60.7) 50.7 (43.7-57.1)
MCHC 33 33.2 (30.2-36.2) 32.9 (28.5-33.9) 30.3 (27.7-35.5)
WBC x 109/L 5.5 5.7 (1.9-9.5) 2.3 (3.1-12.0) 7.88 (2.45-12.6)
Heterophils x 109/L 6.2 4.0 (0.5-7.6) 8.4 (0.8-8.3) 5.99 (0.9-11.5)
Eosinophils x 109/L 0 0.9 (0.0-1.8) 0.5 (0.0-0.5) 0.6 (0.0-2.7)
Basophils x 109/L 0 0.5 (0.0-1.0) 0.4 (0.0-0.8) 0.19 (0.0-0.8)
Lymphocytes x 109/L 3.4 2.7 (1.2-4.2) 13.2 (0.5-4.2) 0.5 (0.2-1.3)
Monocytes x 109/L 0.2 0.5 (0.0-1.0) 1.0 (0.0-1.2) 0.4 (0.0-0.9)
Thrombocytes x 109/L — 18 (3-33) — (8-29) 8.9 (3.4-18.2)
Fibrinogen g/L — 2.7 (1.3-4.1) — (1.9-4.8) 3.3 (2.1-4.1)
609
Products Mentioned in the Text Acknowledgments

a. Coulter Counter ZF, Beckman Coulter Inc, Fullerton,
CA, USA www.beckmancoulter.com The author thanks HRH Prince Fahad bin Sultan bin
b. Cell Dyn 3500, Abbott Laboratories, Abbott Park, IL, Abdulaziz Al Saud for his support to the advancement of
USA www.abbottdiagnostics.com
c. BD Unopette 365851 red blood count manual hema- falcon medicine, and to Mr. Basil Al Abbasi, Director
tology test, Becton Dickinson Co, Franklin Lakes, NJ, USA www.bd.com
d. BD Unopette 365877 eosinophil count manual hema-
General, for his continuing interest in the clinical and
tology test, Becton Dickinson Co, Franklin Lakes, NJ, USA research program of the Falcon Specialist Hospital and
Research Institute; to Shinto K. John; Generoso
Dedication Quiambao; Dr. Jesus Naldo.
This chapter is dedicated to Dr. Christine M. Hawkey.
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10. D’Aloia M-A, et al: Normal hema- 24. Hauska H, Redig PT: Morphologi- ogy of the great bustard (Otis captive adult stone curlews
tology and age-related findings in cal changes in the white hemo- tarda). Avian Pathol 20:675-680, (Burhinus oedicnemus). Com
rufous-crested bustards (Eupodotis gram of raptors. Proc Assoc Avian 1991. Haem Int 8:219-224, 1998.
ruficrista). Com Haem Int 5:10-12, Vet, 1997, pp 205-208. 38. Lane RA: Avian hematology. In 53. Stewart JS: Husbandry, medical
1995. 25. Hawkey CM, Samour JH: The Rosskopf W, Woerpel R (eds): and surgical management of
11. D’Aloia M-A, et al: Normal hema- value of clinical hematology in Diseases of Cage and Aviary Birds ratites. Proc Assoc Avian Vet,
tology of the white bellied exotic birds. In Jacobson ER, 3rd ed. Baltimore, Lea and Febiger, 1989, pp 119-122.
(Eupodotis senegalensis), little Kollias GV Jr (eds): Contemporary 1996, pp 739-772. 54. Sturkie PD: Avian Physiology 2nd
black (Eupodotis afra) and Issues in Small Animal Practice. 39. Lind PJ, et al: Morphology of the ed. London, Bailliére, Tindall and
Heuglin’s (Neotis heuglinii) bus- London, Churchill Livingstone, avian eosinophil in raptors. J Cassell, 1965.
tards. Com Haem Int 6:46-49, 1988, pp 109-142. Assoc Avian Vet 4:33-38, 1990. 55. VanderHeyden N: Evaluation and
1996. 26. Hawkey C, et al: Normal and clin- 40. Maxwell MH: Avian blood leuco- interpretation of the avian
12. Dein FJ: Hematology. In Harrison ical hematology of captive cranes cyte responses to stress. World hemogram. Sem Avian Exotic Pet
GJ, Harrison LR (eds): Clinical (Gruiformes). Avian Pathol 12:73- Poult Sci J 49:34-43, 1993. Med 3(1):5-13, 1994.
Avian Medicine and Surgery. 84, 1983. 41. Maxwell MH, Robertson GW: The 56. Villouta G, Hargreaves R, Riveros
Philadelphia, WB Saunders Co, 27. Hawkey C, et al: Haematological avian basophilic leukocyte: A V: Haematological and clinical
1986, pp 174-191. changes in domestic fowl (Gallus review. World Poult Sci J 51:307- biochemistry findings in captive
13. Dorrestein GM: Cytology and gallus) and cranes (Gruiformes) 325, 1995. Humboldt penguins (Spheniscus
haemocytology. In Beynon PH, with Mycobacterium avium infec- 42. Maxwell MH, Hocking PM, humboldti). Avian Pathol 26:851-
Forbes NA, Lawton MPC (eds): tion. Avian Pathol 19:223-234, Robertson GW: Differential leuco- 858, 1997.
Manual of Psittacine Birds. 1990. cyte response to various degrees
Cheltenham, Glos, Br Small Anim 28. Hernandez M: Raptor clinical of food restriction in broilers,
23_Biochemistry.qxd 8/23/2005 1:26 PM Page 611
CHAPTER
23
Diagnostic Value of
Biochemistry
KENDAL E. HARR, DVM, MS, D ipl ACVP
Clinical chemistry, along with hematology and physical

examination, is the cornerstone of medical diagnosis of
disease in any species. Plasma biochemistry is especially
important in avian species, which frequently show mini-
mal overt clinical signs of disease, even when seriously
ill. Veterinarians, therefore, need accurate and useful
biochemical analysis to successfully diagnose and treat
avian species. The Clinical Laboratory Improvement
Amendments (CLIA) are the federal laws and regulations
that govern human diagnostic laboratories. No such gov-
erning policy exists in veterinary diagnostic medicine.
This results in variable methodology, protocol, and most
importantly, quality control, between veterinary labora-
tories. It falls to the veterinary clinician to ensure that
Fig 23.1 | A normal serum sample on the left and a lipemic the diagnostic laboratory being used maintains a high
sample on right.
standard of quality control and that results are accurate.
The clinician should develop a working relationship
with the laboratory of choice and must continually mon-
itor results for possible inaccuracy and error. Feedback
to the laboratory must occur to ensure that the labora-
tory personnel are aware of any errors and can correct
them. The laboratory used should be familiar with han-
dling avian samples. Modified techniques in the labora-
tory, such as the use of 10-µl microhematocrit tubes,
pediatric sample cups and dilution, can extend the sam-
ple and allow more data to be collected, especially from
the smaller avian patient. When choosing a laboratory,
the clinician also should consider its location, transport
issues and delayed processing of the sample. All of these
can cause artifactual change in the sample and decrease
ability to diagnose disease.
Concentrations of analytes represent a steady state of

input, consumption and partitioning. The body is always
in flux. Generally, pathologic conditions cause either an
increased or decreased concentration of various ana-
lytes. However, if both input and consumption are
Reference intervals generated by a laboratory represent

population reference intervals that are broader than the
reference interval generated when repeatedly sampling
an individual. Some individuals will regularly have con-
centrations in the low end of the population’s range and
some individuals will regularly have concentrations in
the high end of the population’s range. Therefore, an
individual may remain within the population reference
range even though there are abnormalities in the
patient.
In addition to accurate normal reference intervals, the

clinician must have knowledge of the sensitivity/speci-
J. Harvey
ficity and positive/negative predictive value of a test’s
ability to diagnose diseases specific to that species.
Fig 23.2 | 2.5% of the population is eliminated on each side of
the curve to generate a 95% reference interval. This increases Although a great deal is now known regarding avian
the likelihood that diseased patients are flagged as abnormal. It medicine, research into the diagnostic application, sensi-
also means that it is quite likely that a healthy patient will have tivity, specificity, and positive and negative predictive val-
one analyte that is mildly abnormal.
ues of biochemical analytes is still needed.
decreased or increased at the same time, the concentra- MEASURES OF THE

tion may remain in the normal reference interval even ACCURACY OF A TEST
though the patient is very ill. For example, the globulin Accuracy is how close the test approximates the true
fraction may remain within the normal reference interval value in the body. Precision measures how far from the
in a bird with marked enteritis because of increased pro- mean or average of replicate measurements a particular
duction of acute phase inflammatory proteins and anti- measurement lies (Fig. 23.3). Most laboratory techniques
bodies with concurrent loss of protein through a com- were designed for use in human medicine and are modi-
promised gastrointestinal tract. Interpretation of clinical fied for use in birds. Assessment of analytic accuracy and
chemistries must therefore be done on a case-by-case precision of a technique is very important when assess-
basis with knowledge of species-specific physiology. ing different mammalian species, not to mention differ-
ent kingdoms of animals. Any instrument error such as
In comparison to domestic species, it can be a challenge old bulbs, slight variation in machine temperature, varia-
to simply ascertain normal reference intervals for avian tion in reaction time or degraded reagents can cause
patients. Reference intervals for biochemical analytes are decreased accuracy and precision.
highly dependent on the machines, reagents and meth-
Sensitivity, specificity and predictive values are the meas-
ods used, and may vary significantly between different
ures of diagnostic accuracy. In medicine, sensitivity is the
laboratories. According to CLIA, each human diagnostic
likelihood that a diseased patient will have a positive test
laboratory must establish reference intervals for each
result in a population of individuals with the disease.
methodology validated within that laboratory in order to
Sensitivity is a measure of false negative values. To help
create a diagnostic range that can be used medically. A
remember the relationships note that the letter “N” is
minimum of 100 healthy individuals is sampled. A 95% present in sensitivity and false negative. Specificity is the
reference interval is created for normally distributed likelihood that a patient without the disease has a test
analytes using the formula, mean +/- 1.96 standard devi- value that remains within the reference interval in a pop-
ations. Therefore, the normal medical reference interval ulation of healthy individuals. Specificity is a measure of
used by clinicians excludes 2.5% of normal individuals at false positive values. Note that the letter “P” is present
the high and low ends of the range (Fig. 23.2). in specificity and false positive. The predictive value of a
Biochemical reference intervals for common species of test is determined by its measurement in a population of
psittacines (parrots), passerines (canaries and finches), healthy and sick individuals. A positive test result is
and galliformes (turkeys and chickens) have been estab- measured when the disease is present (positive predic-
lished by specialized laboratories, eg, California Avian tive value) and a negative test result is measured when
Laboratory, Citrus Heights, CA. Each laboratory analyzing the disease is not present (negative predictive value).
avian samples should develop species-specific and These can be mathematically determined using the for-
methodology-specific reference intervals. These are still mulas in Table 23.2. Tests that are highly sensitive fre-
lacking in some university and private laboratories. quently have a low specificity and vice versa. This does
Chapter 23 | D I A G N O S T I C V A L U E O F B I O C H E M I S T R Y
613
Fig 23.3 | Accuracy vs. Precision. When values are both precise and accurate, they are a tight cluster in the bull's eye. The precise val-
ues are all similar, but are some distance from the actual value. The accurate values are all within the third circle, with one almost
approximating the actual value, but are scattered around the bull's eye.
Table 23.1 | Statistical Analysis of a Diagnostic Test

carotenoid pigments; rarely, in severe disease states,
Formulas for the calculation of diagnostic sensitivity, diagnos- avian plasma may be truly icteric from bilirubin.39,49 Pink
tic specificity, positive predictive value and negative predictive or red plasma is usually indicative of hemolysis, though
value. TP = true positive, TN = true negative, FP = false posi- dyes from food should be ruled out. Green-tinged
tive, FN = false negative.
plasma is rarely observed, may be caused by biliverdin
TP
• Diagnostic sensitivity = TP+FN and is usually indicative of liver failure.23,31 When work-
TN ing with smaller species of birds, tuberculin or insulin
• Diagnostic specificity = TN+FP
TP syringes are frequently used, however, not all of these
• Positive predictive value = TP+FP syringes have detachable needles. Avian red blood cells
TN
• Negative predictive value = TN+FN are larger and deteriorate more quickly than mammalian
erythrocytes. This can make accurate analysis difficult
with ideal sample handling. Ejecting blood through a
not mean that the test is worthless. It simply means that 25-gauge or smaller needle can cause moderate to
it may have to be used with other tests to assess organ marked hemolysis that will invalidate many biochemical
function and disease. analysis.48 To avert this, attached needles can easily be
cut from the syringe using a pair of large veterinary nail
clippers or scissors before expelling the blood from the
syringe.
Sample Handling
HANDLING ANTICOAGULANT
In the USA, many exotic animal practitioners perform Prior to collection, the appropriate sample container is
venipuncture using a syringe that has been coated with labeled with the names of the owner, patient and the
injectable sodium heparin to prevent clot formation. signalment. Color-coded, rubber stoppered, evacuated
Experienced avian veterinarians working with experi- tubes are well standardized. Green-topped tubes contain
enced restrainers, who minimize trauma to the vessel heparin, which should be used for plasma chemistry
wall, can collect a high-quality sample without the addi- analysis in birds. Lithium heparin is the recommended
tion of sodium heparin. Reducing the amount of sodium anticoagulant, as sodium or potassium heparin can
heparin in the sample is desirable. If most of the heparin falsely increase the electrolyte values and skew anion
is expelled, it will minimally affect the sample. However, gap and acid base analysis. Ammonium heparin should
the amount of heparin actually retained may vary among not be used, as it significantly increases ammonia and
samples. Any droplets remaining may cause dilutional BUN concentrations. Heparin inhibits coagulation by
effects as well as interfere with some analytical tests such binding to antithrombin III and greatly accelerates the
as sodium and albumin. Samples for biochemical analy- inhibition of thrombin (factor II) by antithrombin III.
sis should be placed into a lithium heparin microtainer Factors VII (proconvertin) and X (Stuart Prower factor)
rather than a red-topped tube to avoid variable clotting also appear to be inhibited by the heparin-antithrombin
time and gelling of serum. Anticoagulant tubes must be III complex.
filled to the appropriate volume. A plasma separator also
can be used to increase plasma sample volume, though The disadvantage of heparin is that leukocytes do not
these tubes tend to be slightly more expensive. stain as well, and platelets and white blood cells clump
much more than they do in blood collected in ethylene-
Avian plasma samples are frequently yellow due to diaminetetra-acetic acid (EDTA). This leads to decreased
accuracy and precision in the complete blood count also may be indicative of underlying disease such as
(CBC) (see Chapter 22, Diagnostic Value of Hematology). hypothyroidism, diabetes mellitus, hyperadrenocorti-
Purple or lavender-topped tubes contain EDTA. Blue- cism, pancreatitis, or a primary lipid/lipoprotein disor-
topped tubes contain citrate and are used to harvest der. Lipemia causes refraction of light and therefore
plasma for coagulation analysis. Both citrate and EDTA causes error in many spectrophotometric and all refrac-
prevent coagulation by chelation of calcium (factor IV), tometric methods (see Fig. 23.1).
an electrolyte essential to coagulation. Neither purple-
nor blue-topped tubes are recommended for chemistry Lipid can be partially cleared by ultracentrifugation or
analysis because chelation of ions interferes with most precipitating agents (polyethylene glycol, liposol,
reactions. lipoclear). These techniques and clearing agents may
themselves induce artifact. Additionally, the removal of
Red-topped tubes lack anticoagulant and are used to har- lipid from a sample may in itself induce an artifact in
vest serum required in antibody, hormone, and other analytes of interest. For example, lipoproteins bind bile
protein analysis. At least 25% of avian serum samples will acids, which would be discarded along with the lipid fol-
form a proteinaceous gel when separated, significantly lowing ultracentrifugation. This may be one factor that
decreasing sample volume and occasionally completely contributes to the occasional measurement of decreased
preventing biochemical analysis. Additionally, time to clot postprandial values in comparison to fasted values. The
formation in avian species is variable, due in part to scattering of light due to lipemia will falsely increase the
greater dependence on the extrinsic coagulation cascade. postprandial bile acid measurement. Varying technique
The use of heparinized plasma therefore decreases vari- can therefore significantly alter bile acid values. This
ability in time to sample separation and improves the underscores the importance of contact with your labora-
chance of obtaining an adequate sample volume. tory to determine which technique is used and that the
techniques used are appropriate.
HEMOLYSIS
Again, technical support and literature should be
Hemolysis directly interferes with spectrophotometric reviewed for each machine. Wet chemistry analyzers are
absorbance readings and alters the pH of enzymatic reac- generally more impacted by lipemia than dry chemistry
tions. Constituents that are found in higher concentra- analyzers. Electrolytes measured by ion-specific elec-
tions within erythrocytes than in serum will be increased, trodes are not affected by lipemia, but electrolytes meas-
eg, aspartate aminotransferase (AST) and, potentially, ured by flame photometry are decreased.
potassium. Alteration in the enzymatic reactions may
appear randomly and cannot be predicted. Hemolysis Lipemia falsely increases all of the liver enzymes, alka-
can and should be monitored visually. Any sample that is line phosphatase, hemoglobin, MCHC, bile acids, total
more than very light pink should not be used diagnosti- bilirubin, glucose, calcium and phosphorous. Total pro-
cally. Additionally, if the sample is analyzed by an auto- tein measured by a refractometer is falsely increased, but
mated hematology analyzer, a mean cell hemoglobin con- the biuret method is minimally affected even by severe
centration (MCHC) that is greater than the reference lipemia. BUN and gamma glutamyl transferase (GGT)
range is an indication of possible hemolysis. may be increased or decreased depending on the
methodology. Albumin is generally decreased using
Artifactual change can vary between methods employed. bromcresol green methodology.
Technical support and literature should be reviewed for
each machine. Hemolysis in the sample falsely decreases
bile acids measurement by the colorimetric assay, while
radioimmunoassay (RIA) is unaffected. For many meth- Age
ods, hemolysis falsely increases alanine aminotransferase
(ALT), aspartate aminotransferase (AST), lactate dehydro- In general, non-protein nitrogen concentrations are
genase (LDH), creatinine, calcium, albumin, potassium, lower in young, growing animals, as most nitrogen is
amylase, creatine kinase (CK), hemoglobin, and MCHC. being consumed by growth. In neonatal eclectus parrots
A false decrease in triglycerides can occur. Glucose, mag- (Eclectus roratus), macaws and cockatoos, albumin,
nesium, phosphorus, cholesterol, alkaline phosphatase globulin and AST also have been found to be lower than
and lipase can be either increased or decreased depend- in adults. This is likely due to decreased production of
ing on the methodology.48 these analytes by the neonatal liver, combined with
increased utilization in the tissues that is needed for
growth. Additionally, it was found that calcium, sodium
LIPEMIA and chloride were decreased in chicks in comparison to
Lipemia may be present in postprandial samples, but adults. Alkaline phosphatase, a compound produced in
615
osteoblasts, is found in higher concentrations in grow- Diagnostic Value

ing animals. Blood phosphorus and potassium also are Healthy birds do not have ketones in their urine unless
found in increased concentrations in young birds due they have undergone strenuous activity, eg, migration.
partially to increased concentration of growth hormone, Measurement of ketone bodies in the urine is indicative
and mobilization for muscle and bone growth.11,12,13 of diabetes mellitus in most birds.
Albumin
Analytes Method
Most veterinary laboratories measure albumin using the
The following descriptions of analytes contain method, dye bromcresol green (bcg), which has not been vali-
physiology and diagnostic value sections. The method dated in companion avian species. Bromcresol green
sections are designed for practitioners who are running non-specifically binds protein. Binding of bcg causes
some values in their practice and, therefore, need to be increased color in the sample, which correlates with a
familiar with the method that they are using to analyze higher reported albumin concentration. It has been
plasma biochemical values. Different methods frequently demonstrated in dogs and humans that heparin can
will produce different results. The International cause false increases in albumin concentration due to
Federation of Clinical Chemists (IFCC) has standardized binding of fibrinogen.59 Avian albumin is markedly differ-
some test methods and these should be used. Analyzer ent in structure than mammalian albumin and binds bcg
manufacturers may sell alternate methods at reduced with decreased affinity. Comparison of gel electro-
prices to veterinarians, with the knowledge that they do phoresis and bcg have revealed that bcg results in lower
not meet current standards. The veterinarian should be concentrations reported than actually exist in the
aware of the appropriate method to use and the limita- patient.58 This error is caused in part by use of human
tions of interpretation in a species. Some artifacts and albumin standards and controls, which have different
drug interactions are discussed in the method sections, binding affinity for the dye than does avian albumin.
though these should not be considered to be complete This error in measurement may result in serious errors
listings of those interactions. Product specification when assessing hypoproteinemic syndromes such as
sheets for the methodology as well as technical support liver failure, protein-losing nephropathy and protein-los-
should be used as necessary. The sections on physiology ing enteropathy. At this time gel electrophoresis is the
discuss the function of the analyte in the body. The sec- recommended method of albumin determination in
tions on diagnostic value discuss clinical utility in birds. avian species.15,40,60 Bromcresol purple (bcp) also is com-
See also the Differential Diagnoses in Table 23.2. monly used in human laboratories and has different pro-
tein binding affinity for albumin.2,5,64 Bromcresol purple
Acetoacetate, Acetone (Ketones) may result in more accurate avian albumin measurement
and better diagnostic acuity. Further study is needed.
Method
Common urine test strips present in most practices use Physiology
the Rothera test in which alkaline nitroprusside turns Albumin, a small, approximately 65-kD protein, is the
purple in the presence of acetoacetate and, to a lesser most abundant protein found in plasma, most extravas-
extent, acetone. A third, relatively acutely produced cular body fluid, CSF and urine. Albumin’s synthesis by
ketone, 3-hydroxybutyrate, is not measured by this reac- the liver is primarily controlled by plasma oncotic pres-
tion. False negatives may occur if the patient is produc- sure. Albumin’s main function is the maintenance of col-
ing only 3-hydroxybutyrate. If diabetes is suspected and loid oncotic pressure in the intravascular and extravascu-
ketones are not measured, the urine should be lar spaces. Albumin also functions as a carrier protein to
rechecked in 48 hours. Some drug interactions may pro- transport a large number of compounds including cal-
duce false positives, including penicillamine, levodopa cium and administered drugs. Albumin levels are lower
and phenylketones. in chicks than in adults.
Physiology Diagnostic Value

Decreased glucose availability to the tissues results in Accurate assessment of albumin enables the practitioner
increased lipase activity in adipose tissue that catalyzes to assess hypoproteinemic disease such as liver failure,
long-chain fatty acids. These are catabolyzed to acetyl protein-losing nephropathy and protein-losing enter-
CoA that is metabolized to the ketones: 3-hydroxybu- opathy. This diagnosis may lead to alternate fluid therapy
tyrate, acetoacetate and acetone. These compounds are such as colloid (hetastarch) administration to prevent
excreted in urine and can be qualitatively measured in edema, which is rarely seen in birds, and ascites. A true
stressful physiologic or pathologic disease states. increase in albumin is pathognomonic for dehydration
Table 23.2 | Differential Diagnoses Based on Chemistry Abnormalities*
Albumin • Dehydration - generally accompanied by increased Aspartate • Hepatic damage (continued)

Increased globulin and total protein Aminotransferase - Infection [(bacterial, mycobacteriosis,
• Reproductive - mild increase observed in females (AST) (cont.) chlamydophilosis, polyoma virus, Pacheco’s
during egg formation Increased disease - herpes virus, adenovirus, reovirus, duck
virus hepatitis, Plasmodium, Trichomonas,
Albumin • Liver failure Histomonas (turkeys), Leucocytozoon (ducks and
Decreased - Cirrhosis/fibrosis geese), Atoxoplasma]
- Neoplasia - Toxic [(aflatoxin/mycotoxin, cottonseed
- Portosystemic shunt (Gossypium sp.), Crotalaria sp., oleander
- Amyloidosis (Nerium sp.), rapeseed (Brassica napus),
• Renal loss ragwort (Senecio jacobea), castor bean
- Glomerulonephritis/sclerosis (Ricinus communis)]
• Intestinal - Neoplasia
- Malabsorption/maldigestion • Primary
• Mycobacterial disease • Secondary
• Endoparasites - Artifactual
• Malnutrition (severe) • Erythrocyte leakage
• Exudative skin disease

- Burns Bicarbonate (CO2) • Compensated respiratory acidosis
- Large wounds Increased - Respiratory disease
- Vasculitis - Drugs (anesthetics)
- Frostbite • Small bowel obstruction
• External blood loss (subacute to chronic) • Gastric vomiting
• Inflammatory disease state - Obstruction
(seen with increased globulins) - Lead poisoning
- Septicemia
- Viremia Bicarbonate (CO2) • Metabolic acidosis
• Neonates - normally lower than adults Decreased - Dehydration
• Polyuria/Polydipsia - Renal failure
• Respiratory alkalosis
Alkaline • Bone isoenzyme - Tachypnea/panting
Phosphatase - Trauma - Excess anesthetic ventilation
Increased - Growth • Artifactual
- Osteosarcoma - Delayed analysis
- Osteomyelitis Bile Acids • Impaired liver function
• No hepatic-associated increase Increased - Lipidosis
currently documented - Biliary Stasis
- Infection (see AST)
Ammonia • Hepatic disease/failure - Inflammation
Increased - Cirrhosis - Neoplasia
- Neoplasia - Toxic (see AST)
- Polyoma - Hemochromatosis
• Artifactual - Cirrhosis/Fibrosis
- Hemolysis
Blood Urea • Prerenal azotemia
Amylase • Pancreatic Nitrogen - Dehydration (pigeons)
Increased - Inflammation/Infection Increased - Postprandial (some raptors)
- Neoplasia - GI hemorrhage
- Necrosis • Renal Failure
- Pancreatic duct obstruction (eg, egg binding)
• Zinc toxicity Blood Urea • Liver failure
• Enteritis Nitrogen • Neonates
• Renal disease (decreased filtration) Decreased • Diuresis
(mild to moderate increase) (Unlikely but can - Iatrogenic
be measured in - Physiologic
some species) - Pathologic
Anion Gap • Respiratory acidosis
Increased - Anoxia (anesthetic induced, other) Calcium • Reproductive (may be marked)
- Respiratory disease Increased - Physiologic increase in females
(chlamydia, aspergillosis, etc) - Pathologic
• Hyperglobulinemia (reproductive, inflammatory) • Hypervitaminosis D
• Metabolic acidosis (increased lactic acid and other • Primary hyperparathyroidism
unmeasured anions) • Renal secondary hyperparathyroidism
- Renal failure • Nutritional secondary hyperparathyroidism
- Gastrointestinal bicarbonate loss • Neoplasia
- Hypoperfusion/reperfusion - Lymphoma
- Shock - Osteosarcoma
• Diabetic ketoacidosis • Osteomyelitis
• Toxic • Granulomatous disease
- Ethylene glycol (mammals)
Calcium • Nutritional
- Others in birds
Decreased - Excess dietary phosphorus (seed)
Aspartate • Muscle damage - Hypovitaminosis D
Aminotransferase - Seizures - Dietary deficiency (severe)
(AST) - Trauma • Chronic egg laying
Increased - Capture myopathy (exertional rhabdomyolysis) - Egg-bound hen
- Intramuscular injection • Hypomagnesemia
• Hepatic damage • Hypoparathyroidism
- Drugs (cephalosporins, metronidazole, • Pancreatitis
trimethoprim sulfa, dexamethasone) • Malabsorption
- Hemochromatosis (iron storage disease) • Alkalosis
- Endocrine disease (diabetes mellitus,
hyperthyroidism)
- Hypoxia (cardiopulmonary in origin)
- Lipidosis (severe)
- Inflammation/Infection
617
Table 23.2 | Differential Diagnoses Based on Chemistry Abnormalities* (continued)
Chloride • Dehydration Lipase • Enteritis

Increased • Metabolic acidosis Increased • Pancreatitis
• Pancreatic neoplasia
Chloride • Gastric vomiting • Renal disease (decreased loss)
Decreased - Obstruction
- Lead poisoning Phosphorus • Renal disease
• Metabolic alkalosis Increased • Neonates
• Reproductive
Cholesterol • Reproductive - egg formation (cystic ovaries) - Egg formation (concurrent rise in calcium)
Increased • Nutritional/postprandial • Nutritional
• Cholestasis - Hypervitaminosis D
• Obesity - Increase dietary phosphorus
• Endocrine • Toxic
- Diabetes mellitus - Jasmine ingestion
- Hypothyroidism • Neoplasia
- Hyperestrogenism - Osteosarcoma
• Nephrotic syndrome • Inflammation
Cholesterol • Intestinal - Osteomyelitis
Decreased - Malabsorption/maldigestion • Artifactual hemolysis/delayed serum separation
• Liver failure • Primary hyperparathyroidism
• Starvation • Nutritional secondary hyperparathyroidism
• Neoplasia: PTH-like hormone
Creatine Kinase • Muscle damage
Increased - Intramuscular injection Phosphorus • Diabetic ketoacidosis
- Seizures Decreased • Dietary deficiency
- Capture myopathy
(exertional rhabdomyolysis) Potassium • Renal failure
- Myositis Increased • Diabetic ketoacidosis
• Sarcocystis • Severe muscle/tissue damage
• Toxoplasma • Dehydration
• Other parasitic • Drugs
• Bacterial - ACE inhibitors
- Hyperthermia - Potassium-sparing diuretics
- Hypothermia • Artifactual
- Vitamin E/Se deficiency - Collection in potassium heparin
- Trauma
• Surgical Potassium • Alkalosis
- Ischemia Decreased • Drugs
- Penicillins
Fibrinogen • Bacterial infection - Amphotericin B
Increased • Other inflammation - Loop diuretics
Fibrinogen • Liver failure - Insulin therapy
Decreased • Coagulopathy • Gastrointestinal loss
• Renal disease (chronic)
Gamma • Liver compromise
Sodium • Gastric vomiting (water loss)
Glutamyltransferase - Cholestasis
Increased • Intestinal fluid loss
(GGT) • Intrahepatic
• Renal failure
Increased • Extrahepatic
• Dehydration
- Neoplasia
• Biliary carcinoma Sodium • Diabetes mellitus
• Other biliary compromise Decreased • Gastric vomiting
• Intestinal sodium loss
Gamma • Artifactual hemolysis - Endoparasitism
Glutamyltransferase • Burns
(GGT) • Chronic effusions
Decreased - Egg yolk
Globulin • Dehydration (concurrent increase in albumin) • Psychogenic polydipsia
Increased • Inflammation • Renal failure (chronic)
• Egg formation • Artifactual
- Hyperlipidemia
Globulin • Neonatal
Decreased • Immunodeficiency Total Protein • Dehydration (albumin and globulin)
• Blood loss (subacute to chronic) Increased • Artifactual
• Protein-losing enteropathy - Hemolysis
Glucose • Endocrine Total Protein • Hemorrhage (chronic)

Increased - Diabetes mellitus Decreased • Intestinal loss
• Pancreatitis • Liver failure
• Stress • Renal loss
• Drugs • Immune suppression
- Glucocorticoids Uric Acid • Renal disease
- Progesterone Increased • Postprandial (carnivores)
• Dehydration (severe)
Glucose • Liver failure
Decreased • Starvation in small birds Uric Acid • Liver failure
• Neoplasia Decreased • Starvation
• Septicemia
Iron • Hemochromatosis
Increased • Inflammation
• Artifactual
- Hemolysis
Iron • Chronic blood loss
Decreased • Nutritional dietary deficiency*
*Ed. Note: Unlikely on formulated diet,
but possible on a seed/fruit.
and would indicate the need for administration of IV reaction oxidizes Nicoti Adenine Dinuleotide Hydrogen
crystalloid fluids. (NADH) to Nicotinamide Adenine Dinucleotide (NAD),
which can be optically measured at 340 nm.
Alkaline Phosphatase (ALP)
Meticulous precautions must be taken in sample han-
Method
dling to prevent false increases in ammonia concentra-
Numerous methods have been developed to determine
tion. Samples must be drawn cleanly, using an evacuated
ALP activity. The IFCC recommended method uses 4-
tube, and processed immediately for accurate results.
nitrophenyl phosphate (4-NPP) and 2A2M1P as a phos-
Poor venipuncture technique or increased exposure to
phate acceptor buffer at 37° C and absorbance at 405
air may result in increased ammonia levels. Probing for
nm. ALP catalyzes the hydrolysis of 4-NPP, forming phos-
a vein causes tissue damage that may elevate ammonia
phate and free 4-nitrophenol (4-NP) in an acidic solu-
levels. Drawing blood into a syringe and transfer of that
tion. Alkalinization causes conversion of colorless 4-NP
blood to a microtainer, or partial filling of an evacuated
to 4-nitrophenoxide ion, which is an intense yellow
tube allows subsequent entry of air that may cause
color. As veterinary laboratories may employ different
elevation of ammonia levels. Serum samples and
methods, normal reference intervals may be markedly
ammonium heparin may cause falsely elevated levels.
different. Caution should be used when assessing a
Production of ammonia by deamination of amino acids
patient using reference intervals from a textbook.
in the blood will occur once the specimen has been
Laboratory-specific reference intervals should be gener-
drawn. At 0° C, delays exceeding 15 minutes between
ated.
blood sampling and centrifugation can increase ammo-
Physiology nia concentrations.
Alkaline phosphatase is a glycoprotein dimer with sub-
Ammonia analysis are available on many dry chemistry
unit masses ranging from 40 to 83 kD. The protein’s
analyzers used in practice. Machines-specific reference
exact function is unknown. Mammalian and avian
ranges should be established, as different methodologies
isozymes of alkaline phosphatase have been identified in
will produce different reference intervals.
cell membranes in the liver (biliary epithelium), kidney,
intestine, bone (osteoblasts), as well as a steroid- Physiology
induced form in dogs. Isoenzymes from osteoblasts, The major source of ammonia is the gastrointestinal
duodenum and kidney have predominated in studies tract. It is derived from the hydrolysis of glutamine in
involving pigeons and domestic fowl.28,43,45 Very low levels the small and large intestine and from the action of bac-
of alkaline phosphatase have been identified in the liver terial proteases, ureases, and amine oxidases on digested
of pigeons and psittacines. Alkaline phosphatase levels food in the colon. Ammonia is converted to the less
are higher in chicks than in adults. toxic uric acid and urea in the liver.
Diagnostic Value Diagnostic Value

In mammals, alkaline phosphatase is of particular inter- Though plasma ammonia has not been validated in
est in two specific disease states: biliary disease frequently healthy or ill birds, some clinicians have observed up to
associated with cholestasis and bone disease associated a fourfold increase in blood ammonia values in birds
with increased osteoblastic activity. ALP does not with liver failure.
increase with simple hepatocellular damage. In avian
species at this time, marked increases in ALP have been Amylase
associated only with increased osteoblastic activity
Method
including traumatic, neoplastic and infectious disease
The three broad classifications of alpha-amylase
states. Further investigation into specific cholestatic and
(endoamylase) assays are saccharogenic, amyloclastic
biliary disease such as biliary carcinoma is warranted to
and chromogenic digestion of starch to glucose or malt-
assess the sensitivity and specificity of ALP in these bil-
ose. The most commonly used assay in veterinary labora-
iary diseases.
tories is the chromogenic alpha-amylase assay, which is
the most appropriate assay in the canine.35 This assay
Ammonia
detects the release of dyes bound to synthetic starch
Method substrates that are released as the starch is digested by
Both enzymatic and chemical methods are used to meas- amylase.
ure ammonia. Enzymatic assay with glutamate dehydro-
genase is the most frequently used method.52 Glutamate Physiology
dehydrogenase catalyzes the conversion of ammonium Alpha-amylases are calcium-dependent metalloenzymes
ion and 2-oxoglutarate to glutamate and water. This that catalyze hydrolysis of complex carbohydrates at
619
internal binding sites. The predominant sites of produc- addition of this coenzyme in the reaction. The conver-
tion are the pancreas and the duodenum. Trypsin in the sion of NADH to NAD can be optically measured at 340
small intestine degrades the enzyme, though some amy- nm. Reference intervals may vary slightly with variation
lase frequently is still detectable in the feces. Urinary of reagent concentration. AST is present in the cytosol of
clearance of this small, 55- to 60-kD protein also has erythrocytes and extended red cell exposure can cause
been documented in mammals. increased plasma AST concentration.
Diagnostic Value Physiology

Urine-to-serum ratios are used in human medicine to The aminotransferases, including AST (formerly gluta-
diagnose acute pancreatitis.26 Though this assay is fre- mate oxaloacetate transaminases, GOT) and alanine
quently used for the diagnosis of pancreatitis in humans, aminotransferase (ALT) (formerly glutamate pyruvate
it has decreased specificity and sensitivity in the dog. transaminases, GPT), are a group of enzymes that cat-
Validation of this assay for diagnosis of pancreatitis in alyze the interconversion of amino acids by transfer of
birds is needed. amino groups. A variety of tissues, predominately liver
and muscle, contain high aspartate aminotransferase.
Anion Gap The mitochondrial and cytosolic isoenzymes of AST are
Method approximately 90 kD in size.
This number is calculated from the following formula:
Diagnostic Value
Cations - Anions or
AST is not specific for hepatocellular damage, but is
(Sodium + Potassium) - (Chloride + Bicarbonate)
highly sensitive in detecting hepatocellular damage
Physiology caused by ethylene glycol in pigeons.40 Plasma AST activ-
The gap is generally around 15 mEq/L (mmol/L) in most ity returned to normal within 100 hours after doxycy-
species with some variation, and represents unmeasured cline-induced muscle trauma in pigeons. AST activity is
anions such as phosphate, sulfate, lactate, ketones, and currently considered to be a very sensitive but nonspe-
drugs such as salicylates and ethylene glycol metabolites. cific indicator of hepatocellular disease in other avian
If bicarbonate is not available, the total carbon dioxide species as well, and is used with the muscle-specific
value can be substituted. Generally, an increased anion enzyme creatine kinase (CK) to differentiate between
gap indicates acidosis. liver and muscle damage.16,30 ALT also is not liver-specific
in birds. Prolonged postinjection increases in ALT
Diagnostic Value decrease the diagnostic utility of this enzyme in the diag-
nosis of liver disease. ALT is therefore frequently omitted
Anion gap facilitates assessment of metabolic and respi-
from avian chemistry panels.
ratory acidosis. An increased anion gap should incite a
search for the cause of increased numbers of unmea-
Bicarbonate
sured anions.
Method
Acidemia causes an extracellular potassium shift as A common reaction used to measure bicarbonate is
hydrogen ions enter the cells; the more chronic the dis- based upon phosphoenolpyruvate carboxylase (PEPC)
order, the greater the intracellular potassium depletion. utilizing bicarbonate present in the sample to produce
When correcting the acidosis, potassium moves back oxaloacetate and phosphate. Malate dehydrogenase then
into the cell creating a potentially life-threatening catalyzes the reduction of oxaloacetate to malate, and
hypokalemia. Accurate assessment of the acid base status the oxidation of NADH to NAD. NADH oxidation can be
of patients with chronic respiratory disease is essential measured optically at 340 nm. Extended exposure of the
to provide appropriate fluid therapy and electrolyte sample to air (under-filled vials), late separation from
replacement. the cell fraction or a dehydrated sample can introduce
significant error in this measurement.
Aspartate Aminotransferase (AST)
Method Physiology
The IFCC has standardized this reaction to some extent Approximately 90% of carbon dioxide present in serum is
by limiting it to the rate-limiting reaction of L-aspartate in the form of bicarbonate. Therefore, measurement of
and 2-oxoglutarate catalyzed by AST to form oxaloac- total CO2 is frequently used in place of bicarbonate meas-
etate and L-glutamate. Oxaloacetate is then reacted with urement. This is different than pCO2, which represents
NADH in the presence of malate dehydrogenase to form the remaining small percentage actually present in the
L-malate and NAD. Pyridoxal-5’-phosphate is a required gaseous form. The combination of water and CO2 forms
coenzyme in the reaction and the IFCC recommends the weak acid carbonate, H2CO3, and its dissociated
Table 23.3 | Acid Base Imbalances and the Body’s absorption. They promote formation of polymolecular
Compensation aggregates known as micelles, which contain hydropho-
[H+] pH Imbalance Compensation bic lipid in the center and have a hydrophilic outer sur-
Respiratory acidosis ↑ ↓ ↑ pCO2 ↑ [HCO3-] face. Bile acids are absorbed in the distal small intestine
Metabolic acidosis ↑ ↓ ↓ [HCO3-] ↓ pCO2 into the plasma and recycled from the blood by hepato-
Respiratory alkalosis ↓ ↑ ↓ pCO2 ↓ [HCO3-] cytes (enterohepatic circulation).
Metabolic alkalosis ↓ ↑ ↑ [HCO3 ]-
↑ pCO2
Diagnostic Value
Bile acids are used to assess liver function.29,30,43 The clini-
forms, bicarbonate and hydronium ion, comprise one of
cian should be aware that RIA methodologies will gener-
the main buffering systems in animals. The Henderson
ally produce significantly lower numbers than enzymatic
Hasselbach equation, pH = 6.1 + log (HCO3- / H2CO3)
methods. Laboratories should be questioned to deter-
where 6.1 = pK for the HCO3-/H2CO3 buffer pair, is used
mine which methodology they are using. Generally,
to quantitatively analyze buffering by carbonic acid.
using the enzymatic method, >75 µmol/L suggests
Diagnostic Value hepatic insufficiency while >100 µmol/L is diagnostic for
The measurement of bicarbonate, usually in conjunction decreased liver function. Amazon parrots normally have
with sodium, potassium and chloride, is used in the slightly higher BA concentration than do other compan-
assessment of acid-base balance resulting from metabolic ion avian species.29 Decreased bile acids may occur as a
or respiratory disease. Respiratory acidemia is a common result of compromised intestinal absorption.
sequela in birds that have respiratory compromise or
are anesthetized. Unfortunately, it is currently rarely Bilirubin/Biliverdin
assessed or treated. See the Anion Gap section for infor- Method
mation and Table 23.3 for summaries of acid base assess- The most commonly used method for bilirubin measure-
ment. ment are based on the diazo reaction, first developed by
Ehrlich in 1883. Diazotized sulfanilic acid (diazo
Bile Acids (BA) reagent) reacts with bilirubin to produce two azodi-
Method pyrroles, which are reddish purple at neutral pH and
Radioimmunoassay (RIA) and enzymatic assay are the blue at low or high pH values. The fraction of bilirubin
two commonly used methods for bile acid determina- that reacts with sulfanilic acid in the absence of alcohol
tion. Liquid chromatography also can be used in is direct bilirubin (conjugated). Total bilirubin is deter-
research settings. RIAs measure non-sulfated, conjugated mined after the addition of alcohol, and indirect biliru-
bile acids.29 Though less affected by hemolysis, RIA, an bin (unconjugated) is determined by subtracting direct
antibody-based assay, will measure only an unspecified bilirubin from total bilirubin.
proportion of bile acids in different species. The enzy-
matic BA method, validated for canine, feline and At this time, biliverdin is measured only by high per-
human samples, measures the 3-alpha-hydroxyl group formance liquid chromatography (HPLC) for both clini-
present in most BAs. This test would be expected to best cal and research purposes.
approximate total BA concentration in most avian
Physiology
species. The value generated by RIA is generally lower
Bilirubin is the metabolic breakdown product of heme
than the enzymatic measurement.
derived primarily from senescent erythrocytes. There are
The pre- and postprandial sampling used in dogs and three types of bilirubin: unconjugated, conjugated and a
cats would likely be ideal for birds as well. However, the fraction irreversibly bound to protein. The unconjugated
crop has varying emptying times in different species, and portion of bilirubin is the most clinically important frac-
crop stasis is common in sick birds such that standardi- tion, as this is most likely to cause tissue damage. Birds
zation of postprandial sampling is impossible. If possi- have heme oxygenase, which converts the protopor-
ble, a fasted sample is preferred to eliminate random phyrin in heme to biliverdin;4 however, birds and rep-
postprandial increases in BA concentration. Fasting is tiles have significantly decreased hepatic production of
not necessary in species that do not have a gall bladder, biliverdin reductase that converts biliverdin to bilirubin.
such as pigeons, ostriches, and most parrots.48 Bacteria in the intestine may produce biliverdin reduc-
tase and bilirubin may be absorbed from the GI tract.
Physiology Additionally, though significantly decreased, hepatic
Bile acids are a group of amphipathic salts that act as biliverdin reductase is still present in some birds.49,61
detergent molecules both to facilitate hepatic excretion Bilirubin and biliverdin are detoxified via the glucuronic
of cholesterol and to solubilize lipids for intestinal acid pathway in the liver and excreted in bile.
621
Diagnostic Value ence and pH electrodes. Sensitive potentiometers meas-

Cholestasis and liver failure generally result in increased ure the voltage differential between electrodes, while
concentrations of biliverdin in birds. Bilirubin has been the microprocessor calibrates the system and calculates
previously dismissed as unhelpful in the diagnosis of calcium concentration and pH. Most of these units func-
liver disease. However, there are reports of increased tion at 37° C and so any significant temperature differen-
bilirubin in severe disease states.49 Diagnostic sensitivity tial will make them inaccurate. These units must be
and specificity should be further assessed. maintained with regular calibration and assessment of
controls.
Blood Urea Nitrogen (BUN)
Method Physiology
There are numerous enzymatic, chemical and electro- The ionized or free fraction of calcium is the freely dif-
chemical methods for measurement of urea with good fusible, biologically active fraction. It is generally very
specificity for the compound. Reference intervals will tightly regulated by all species. It has been shown to
vary with the methodology used. BUN levels are nor- increase mildly during active reproductive cycles in
mally low in birds and may be below the detectable limit oviparous species.33 Regulation of plasma calcium is
of some (but not all) assays used in the laboratory. achieved by interactions of parathyroid hormone, active
vitamin D and calcitonin.
Physiology
During protein catabolism, nitrogen in amino acids is Diagnostic Value
converted to urea in the liver by the action of the urea A general reference interval is 1.0 to 1.3 mmol/L used in
cycle enzymes. Though birds are predominately uri- avian species at University of California Davis. Free cal-
cotelic, with urea being a minor component of nitrogen cium concentration in normal laying hens was found to
excretion, many still have functional hepatic enzyme be 1.3 to 1.6 mmol/L.33 Species-specific values should be
action to drive the urea cycle. Additionally, bacteria in generated within the laboratory. There has been little
the gut may produce urea as well as ammonia, which work currently published on ionized calcium in disease
can be absorbed from the intestinal lumen. The majority in birds, but it will likely aid in differentiation of patho-
of urea is excreted through the kidneys, with some logic states such as renal disease, egg binding and mal-
excreted through the GI tract in bile and through the nutrition. Low ionized calcium in a symptomatic, possi-
skin. Urea is highly diffusible and, in addition to initial bly seizuring animal is an indication for well-monitored,
glomerular filtration, it moves passively through the intravenous calcium administration (see Chapter 5,
renal tubules. Calcium Metabolism).
Diagnostic Value
Prerenal azotemia may be observed in dehydrated Calcium (Total)
birds.36,37 In penguins, it appears that BUN is not Method
elevated postprandially, as was uric acid.34 On the Photometric measurement of total calcium is generally
other hand, peregrine falcons (Falco peregrinus) had used in veterinary diagnostic laboratories, though atomic
elevated BUN and uric acid when sampled 8 hours absorption methods also may be used in research facili-
postprandially.44 Renal disease also has been shown to ties. The two most common dyes used to bind calcium
cause azotemia.40 BUN and uric acid may be used are o-cresolphthalein complexone (CPC) and arsenazo
together — as separate pieces of the puzzle with history, III. The sample is acidified to release protein-bound and
physical exam, urinalysis and other more invasive diag- complexed calcium. In alkaline buffered solution, CPC
nostic tests — to adequately assess prerenal versus renal forms a red chromatophore when bound to calcium that
disease. Using decreased BUN concentration as an indi- can be measured at 580 nm. High magnesium concen-
cator of liver failure has not been assessed in avian tration, lipemia and hemolysis will increase and invali-
species, but may be possible in some species such as date results.
cockatoos.
Physiology
Calcium (Ionized/Free) The vast majority of calcium is stored in the skeleton as
Method hydroxyapatite. In blood, a large portion of calcium is
Ion-selective analyzersb capable of providing immediate free, generally a smaller portion is protein bound and
whole-blood determinations of free calcium, electrolytes the smallest fraction is complexed to anions. Oviparous
and blood gases are widely available. Calibration solu- species have remarkable variability of the protein-bound
tions, samples and wash solutions are pumped through and complexed portions due to estrogen-induced trans-
a measuring cell containing calcium ion-selective, refer- port of calcium-bound yolk proteins to the ovary.56
Diagnostic Value lized by pancreatic secretions, intestinal secretions, and

Calcium concentrations are dependent on the reproduc- bile to micelles and then to chylomicrons that are
tive cycle, sex and possibly season; separate reference absorbed into lacteals across intestinal villi. Transport of
intervals for each of these variables should be estab- cholesterol in blood occurs via lipoproteins as high-den-
lished for accurate clinical evaluation of calcium values. sity, intermediate-density, low-density, and very low-den-
sity lipoproteins. Higher density lipoproteins have
Absorption, excretion and compartmentalization all increased concentrations of cholesterol. Cholesterol is
affect increases and decreases in plasma calcium. synthesized and degraded in the liver (see Chapter 4,
Disease states affecting the reproductive, renal, and Nutritional Considerations, Section II Nutritional
digestive tract, as well as severe nutritive disorders may Disorders).
change calcium concentration.
Diagnostic Value
The relationship between plasma total calcium concen-
Cholesterol levels may be altered in a normal bird due
tration and total protein and albumin concentrations has
to oviparity, as well as postprandially. It should be noted
been evaluated in several bird species.3,38,46,62 Though cor-
that cholesterol can be elevated in oviparous reproduc-
relations between calcium, total protein and albumin
tively active females before eggs can be visualized on a
have been found in some species, they differ markedly
radiograph and may be accompanied by hyperostosis. In
between species. There are significant species differ-
captive psitticines, cystic ovarian disease is a common
ences in protein-calcium correlations such that general-
syndrome that presents with the above mentioned clini-
ized adjustment formulae will not be helpful in a clinical
cal and laboratory findings in the absence of egg-laying
setting where many different species are evaluated. Total
(see Chapter 18, Evaluating and Treating The Repro-
plasma calcium concentration, even if corrected for the
ductive System). When separated by plasma gel elec-
effects of protein binding, does not provide information
regarding ionized calcium concentration, the physiologi- trophoresis, the lipoproteins that transport cholesterol
cally active fraction. migrate predominately to the alpha and beta globulin
regions. Cholesterol levels are rarely diagnostic but may
In oviparous species, increased phosphorus and calcium be useful in determination of various disease syndromes
concentrations are observed during egg formation in (Table 23.3). HDL and LDL cholesterols are being investi-
females. Generally, these occur together and the cal- gated. Preliminary studies in birds show similar trends as
cium:phosphorus ratio stays above one in healthy indi- those seen in humans (Stanford, 2004).
viduals. If the calcium:phosphorus ratio is below one,
renal disease should be investigated. Creatine Kinase (CK)
Method
Chloride - See Electrolytes
Bioluminescent methods are most sensitive and use the
Cholesterol reaction of ATP (adenine triphosphate) with luciferin/
Method luciferase. Spectrophotometric methods are used most
There are numerous methods for lipid and cholesterol commonly in veterinary laboratories, ATP also is used as
determination, with significant laboratory variation. the rate-limiting component of the reaction. CK catalyzes
Enzymatic methods are most commonly used in veteri- the reaction between creatine phosphate and ADP (ade-
nary laboratories. Generally, cholesterol ester is reacted nine diphosphate) to form creatine and ATP at a pH of
with water in the presence of cholesteryl ester hydrolase 6.7 and the reverse reaction at a pH of 9. This is coupled
to form whole cholesterol and fatty acid. Cholesterol to a hexokinase-catalyzed reaction to form NADPH
then reacts with oxygen in the presence of cholesterol (reduced form of NADP). This conversion of NADP
oxidase to form cholest-4-en-3-one and hydrogen perox- (nicotinamide adenine dinucleotide phosphate) to
ide. Hydrogen peroxide is then measured in a peroxi- NADPH can be measured at 340 nm. Excess magnesium,
dase-catalyzed reaction that forms a dye that can be manganese, calcium, zinc, copper, citrate, nitrate,
measured at approximately 500 nm. iodide, bromide, malonate and L-thyroxine are
inhibitory to the reaction and result in decreased values.
Physiology
This 27-carbon, steroid alcohol is found in some concen- The addition of adenosine-5-monophosphate (AMP), N
tration in almost all cells and body fluids in animals, and acetylcysteine, EDTA and diadenosine pentaphosphate
at a much lower concentration as phytosterols in plants. (Ap5A) has been advocated to decrease changes in accu-
There is no cholesterol in plants. Cholesterol enters the racy due to the above compounds. Addition of these
intestine from three sources, the diet, bile and intestinal components will change the value reported and result in
secretions, and sloughed cells. Cholesterol is metabo- significant laboratory variation.
623
Physiology ance of cations and anions maintains pH and regulates

CK is a magnesium-dependent dimeric enzyme that cat- nervous, cardiac and muscular function. Anions and
alyzes the reaction of ADP and creatine phosphate (CrP) cations also are essential cofactors in numerous enzy-
to ATP and creatine in skeletal, cardiac and smooth mus- matic reactions.
cle, as well as brain. It is present in the cytosol and mito-
chondria of myocytes.
Diagnostic Value
Any disease that disturbs water homeostasis will disturb
Diagnostic Value electrolyte distribution and, therefore, plasma concen-
CK is increased for a short, <72-hour time period fol- tration. The success of electrolyte replacement therapy,
lowing myocyte damage or necrosis in birds.47 fluid therapy or any attempt to restore nervous, muscu-
Consideration should be given to the fact that all muscular or cardiac function is completely dependent upon
lar structures in the body may be involved in CK eleva- accurate assessment of electrolyte abnormalities.
tion, including skeletal muscle, cardiac muscle and, less
likely, muscle of the gastrointestinal tract. In mammalian Fibrinogen
species, hypothyroid patients frequently have marked Method
(three- to five fold) increase in CK. This has not been Heat precipitation is the most common method used in
reported in avian species at this time, but may exist. private practice settings and also is used commonly in
commercial laboratories. It is the least accurate method
Electrolytes - Chloride, Potassium, Sodium for measuring fibrinogen in mammals, and is generally
Methods considered an estimate and not a true measurement. It is
The most common method for measuring electrolytes in likely more inaccurate in birds. Protein is measured by
veterinary laboratories is the ion-specific electrode (ISE). refractometer in non-heated plasma and compared to a
An ion-specific membrane is reacted either directly with protein measurement in plasma heated to 57° C for 3
plasma and serum or indirectly with a large volume of minutes. The difference in plasma protein represents the
diluent, and then exposed to the membrane. The poten- precipitated fibrinogen. This is obviously not specific to
tiometer measures the change in electromotive force fibrinogen, as any refractile compound that precipitates
(charge) in comparison to a reference electrode. The will cause error. Birds, in comparison to mammals, fre-
microprocessor then compares the unknown sample to quently have increased quantities of refractile com-
a standard curve created from calibrators. pounds, such as glucose and lipid, which will increase
the error of this method.
This method is very different from the spectrophotomet-
ric methods generally used in smaller machines in prac- In veterinary diagnostic labs, a modification of the throm-
titioner’s offices. In this reaction, a specific ionophore bin test is used to more accurately measure fibrinogen. A
changes color upon binding to the electrolyte. These known, relatively dilute concentration of thrombin is
dyes are measured by a spectrophotometer. Actual val- mixed with fibrinogen. Thrombin enzymatically cleaves
ues that are generated by the two methods may be dra- fibrinogen to form fibrin, the final step in the coagulation
matically different and result in some difference between cascade. The fibrin formation rate is proportional to fib-
in-house and laboratory-generated reference intervals. rinogen concentration and can be calculated from tables.
The tables were derived in humans, and though they
ISE is less affected by hemolysis; however, hemolysis will work well in small animals, they markedly underestimate
result in significant differences in potassium concentra- fibrinogen concentration in horses. The modified throm-
tion (generally increased in most species) due to release bin test has not been validated in avian species.
from intracellular erythrocyte stores.
Physiology
Physiology Fibrinogen (coagulation factor I) is an acute-phase pro-
Water homeostasis in any organism is a fundamental tein, made by the liver, that is digested by thrombin to
dynamic function. The four major electrolytes’ primary form fibrin. Fibrin, when crosslinked, forms the back-
functions are: maintenance of osmotic pressure, electro- bone of the platelet clot.
neutrality and water distribution. In addition to the
main negatively charged ions (anions), bicarbonate and Diagnostic Value
chloride, that are used to calculate anion gap, phos- Fibrinogen is generally increased in non-specific inflam-
phates, sulfates, lactate, trace elements and proteins, all matory states. Fibrinogen concentration was increased
contribute to electrical neutrality and partitioning of above the reference interval in 77% of 89 birds, represent-
water. The positively charged ions (cations) are predom- ing 20 species, with confirmed bacterial disease.24
inately sodium and potassium, with contribution from Decreased fibrinogen may be indicative of end-stage liver
divalent ions such as calcium and magnesium. The bal- failure, but is most commonly detected in mammals with
disseminated intravascular coagulation (DIC). DIC is not carboxy-4-nitroanilide as the glutamyl donor and glycyl-
commonly evaluated in birds at this time. Further investi- glycine as the acceptor in a solution of hydrochloric acid.
gation is warranted. The nitrobenozoate produced is measured at 410 nm.
Other methods are still in use and may produce different
Galactose Clearance (GEC) values, therefore reference intervals may vary from those
Method values stated in available texts. Lipemia may increase or
Methods to determine GEC and blood galactose concen- decrease GGT, depending on methodology used.
tration in cockatoos have been described.30 The birds
were administered 0.5 g/kg of sterile galactose intra- Physiology
venously. Single-point galactose concentrations were GGT catalyzes the transfer of the gamma glutamyl group
best correlated with galactose clearance when sampled from a donor peptide to an acceptor compound. It is
at 80 minutes postadministration. Blood samples were present in serum and in low levels in the cell membrane
deproteinized within 90 minutes of collection by the of all cells except muscle in mammals. It may be
addition of 1 ml of 0.3 M perchloric acid to a 0.2 ml involved in glutathione metabolism and detoxification.
aliquot of blood. After centrifugation at 1500 g, the clear The primary source of plasma GGT is the biliary system,
supernatant was stored at -20° C for preservation until while significant levels of GGT of renal epithelium origin
galactose was measured using a commercial ultraviolet are found in the urine.
method coenzyme assay kitc. Galactose clearance was
calculated using the formula GEC (g/min)= (M-U)(tc=0 Diagnostic Value
+7) where M is the amount of galactose injected, U is Significant increases in GGT are due to obstruction of or
the amount of galactose excreted in urine, and tc=0 is the damage to the biliary tree including neoplasia, inflamma-
extrapolated time when concentration equals zero. A tion or cholelithiasis (stones). Hepatocyte damage alone
standard value of 6% urinary excretion was used will not significantly change plasma GGT concentration.
throughout, as the author determined previously in In mammals, GGT is a more sensitive indicator of biliary
cockatoos. At 80 minutes, the normal reference intervals damage than alkaline phosphatase. GGT has previously
were 0.05 to 0.55 g/L for single-point galactose concen- been thought to be insensitive in the diagnosis of “liver
tration and 0.86 to 1.52 g/min galactose clearance. disease,” which is likely due to the fact that it will not
Physiology become elevated in cases where the biliary tree is not
Galactose is a monosaccharide isomer of glucose that is compromised. Increased plasma GGT activity was found
converted to glucose in the liver through gluconeogene- in the majority of pigeons with experimentally induced
sis pathways for use as energy. Approximately 90% of cir- liver disease.47 Marked increases in GGT activity in birds
culating galactose is filtered from the blood by a healthy with bile duct carcinoma also have been reported.54
mammalian liver during the first pass effect. As hepatic
Although reference intervals have not been established,
function decreases, the portion of galactose filtered
GGT values of 0 to 10 U/L are considered normal at the
decreases and so the concentration of galactose meas-
ured would increase in disease states. Schubot Exotic Bird Health Center (College Station,
Texas, USA). GGT values appear slightly higher in older
Diagnostic Value Amazon parrots, which may have GGT values up to 16
Galactose clearance and galactose single-point concentra- U/L without other evidence of liver disease. These GGT
tions were evaluated during a prospective study on the values are higher than the reported reference intervals
effects of partial hepatectomy in cockatoos.30 In the study, for GGT47 of <3 or 4 U/L in most species except Amazon
galactose clearance appeared to be a more sensitive indi- parrots, which had a high normal value of 10 U/L.40
cator of hepatic insufficiency than plasma enzyme activi- Differences in methodologies for measuring GGT may
ties or BA levels, and were able to detect an 18% loss of account for the marked differences in reference intervals.
hepatic mass. Though single-point concentration was
never increased in animals with 18% hepatectomy, it is There are numerous reports of birds with bile duct car-
likely that this value would increase with more significant cinoma or cholangiocarcinoma in which no concurrent
liver dysfunction. The authors concluded that GEC has increase in GGT activity was reported.14,18,27,51 It is possi-
the potential to be a simple, sensitive method of screen- ble that GGT was not measured, since GGT activity
ing birds for decreased hepatic function. would be expected to increase in these hepatic diseases.
The authors did not indicate if GGT had been analyzed
Gamma Glutamyltransferase (GGT) in these cases. The clinical utility of GGT in the diagno-
Method sis of biliary conditions in birds has not been adequately
The IFCC reference method uses L-gamma-glutamyl-3 evaluated.
625
Globulin manufacturer’s insert. Results above that limit should be

Method written as >linear limit (#). It should be noted that
Globulin concentration is calculated by subtracting albu- many small handheld units guarantee only 20% coeffi-
min from total protein. Any error in albumin or total cient of variation, which means that the number
protein measurement will cause error in globulin con- obtained can vary as much as 20% from the actual glu-
centration. Globulins can be separated by plasma gel cose concentration in the sample.
electrophoresis. When the exact size of the protein of
Most veterinary laboratories use the hexokinase method
interest is unknown, as is commonly the case in veteri-
on a wet reagent analyzer, where NAD is measured at
nary medicine, the proteins are classified in the alpha,
340 nm after two reactions using hexokinase and glu-
beta or gamma globulin fraction, dependent upon
cose-6-phosphate dehydrogenase. This method has an
where they band on the gel.
upper limit of 1000 mg/ml in undiluted samples and
Physiology 2000 mg/ml with automatic dilution. It is therefore the
Any plasma protein that is not albumin or, in birds, preferred method in avian species.
transthyretin (pre-albumin) is classified as a globulin.
Lipemia and hemolysis can both increase the measured
Plasma globulins that have been identified in the band-
plasma glucose concentration.
ing pattern of birds are alpha-1-antitrypsin (alpha-1 glob-
ulin fraction); alpha-2-macroglobulin (alpha-2 globulin Physiology
fraction); fibrinogen, beta-lipoprotein, transferrin, com- There are species differences in the way that birds regu-
plement, and vitellogenin (beta-globulin fraction); and late blood glucose. The insulin content of the pancreas
immunoglobulins and complement degradation prod- of granivorous species is about one-sixth that of the
ucts (gamma globulin fraction).15 In oviparous females, mammalian pancreas, while glucagon content is about 2
vitellogenin and other proteins used in egg formation to 5 times greater.25 Pancreatectomy induces hypo-
can increase dramatically during reproductive activity. glycemic crisis in granivorous birds, but produces dia-
Thus, the globulin fraction increases more than the albu- betes mellitus in carnivorous birds.40 The finding sug-
min fraction, causing the Albumin:Globulin (A:G) ratio gests that while glucagon predominates in granivorous
to decrease physiologically in some female birds. birds, insulin may predominate in carnivorous birds.
Although diabetes mellitus in psittacines is attributed to
Diagnostic Value increased glucagon secretion, there have been reports of
In addition to egg formation causing increased globu- decreased insulin concentration in a diabetic African
lins, inflammatory disease states frequently result in gray (Psittacus erithacus) in comparison with a normal
increased globulins. Acute-phase proteins such as alpha- bird9 and positive responses to insulin therapy. It is
2-macroglobulin are produced in the liver in response to therefore possible that either glucagonemia or hypoinsu-
inflammatory cytokines. Generally in inflammatory linemia are responsible for diabetes in psittacines and
states, these acute-phase proteins and immunoglobulins other species.
increase while albumin, a negative acute-phase protein,
decreases. This results in a decreased A:G ratio. Gel elec- Stress hyperglycemia is induced in birds by high levels of
trophoresis allows the practitioner to examine the band- endogenous or exogenous glucocorticoids.
ing pattern and determine if the decreased A:G ratio is
due to acute or chronic inflammation or egg formation. Diagnostic Value
Banding patterns cannot be used to diagnose specific Stress hyperglycemia should be ruled out prior to a diag-
disease such as aspergillosis or chlamydophila infection. nosis of diabetes mellitus. Measurement of insulin and
glucagon levels in comparison to a control bird should
Decreased globulins result from decreased production be attempted to determine etiology of diabetes on a
such as in liver failure, or increased loss, most com- case-by-case basis. Etiologies of hypoglycemia should be
monly due to protein-losing enteropathy. ruled out using additional diagnostics. Consider the use
of a carbohydrate absorption test (xylene or glucose
Glucose challenge) to rule out underlying malabsorption/
Method maldigestion.
There are several methodologies used to measure glu-
cose that vary between the types of machines used. The Iron
normally high blood glucose level of many avian species Method
may fall above the linear range of measurement of some Care must be taken to ensure that anticoagulant collec-
handheld glucometers. The practitioner should know tion tubes do not contain iron, EDTA, oxalate or citrate
the linear limit of their glucometer, usually found in the that bind iron. Some iron methods require serum and
cannot assay plasma. Check with the laboratory prior to RIAs.21 Additionally, percentage iron saturation has not
submission. There are a variety of methods, including been evaluated in birds. Further study of iron status in
coulometry, colorimetry and atomic absorption spec- companion avian species may have the clinical benefit of
trophotometry, that are used to measure iron. Colometry eliminating invasive liver biopsies as a screening modal-
involves applying a voltage to a reaction and measuring ity for diagnosing hemosiderosis.
the amount of energy needed to drive the reaction. It can
be performed as a titration with another ion and is gener- Lipase
ally quite accurate in the measurement of iron. Atomic Method
absorption is unreliable due to matrix interference in Many lipase methods including titrimetric, turbidimetric,
serum. Through modification of the serum iron methods, spectrophotometric, fluorometric and immunological
total iron-binding capacity and serum transferrin also can techniques have been described, with no one method
be determined. Ferritin, the storage form of iron that is recognized as a gold standard. Differences in laboratory
generally measured to assess total iron stores in mam- values are likely due to differences in methodologies. Be
mals, is measured using antibody-based ELISA and RIA cautious when using reference intervals from the litera-
techniques that do not cross-react in avian species. ture to assess a patient.
Ferritin, therefore, cannot be measured at this time.
Physiology
Physiology Lipase hydrolyzes glycerol esters of emulsified, long-chain
All living organisms, except possibly Lactobacillus spp., fatty acids.55 Most lipase produced in mammals is pro-
require iron.57 Aside from meat-based products, most duced in the pancreas, however activity also is seen in gas-
ingested iron is in the less bioavailable ferric form. The trointestinal mucosa, leukocytes and adipocytes. Tissue
ferric form (Fe3+) can be reduced to the bioavailable fer- enzyme contributions have not been investigated in birds.
rous form (Fe2+) by intestinal bacteria. Free iron can cat-
Diagnostic Value
alyze free radical formation from oxygen and nitrogen,
In mammals, lipase concentration in plasma and effusive
and can therefore cause marked cellular and tissue dam-
fluid is most commonly used to investigate pancreatic
age. For this reason, plasma and intracellular iron are
disorders, usually pancreatitis. It is generally more use-
protein bound. The majority of iron in the body is
ful in acute forms of the disease, as more chronic lesions
bound in hemoglobin; however, iron also is bound to
are associated with increased parenchymal destruction
transferrin for transport in the plasma, ferritin and
that results in lower levels of lipase. Renal disease can
hemosiderin for cellular storage, and myoglobin in
result in mildly increased plasma levels due to decreased
muscle. Prior to egg laying, iron levels will increase 2 to
clearance, but increases are generally not as dramatic as
3 times normal in some species.28
with pancreatitic disease.
Diagnostic Value
Phosphorous
Serum chemistry results in birds with hemochromatosis
Method
may include increased liver enzyme activity, usually AST,
In the most common method used, phosphate reacts
which is believed to be due to iron-induced hepatocellu-
with ammonium molybdate to form a phosphomolyb-
lar damage.40 A few anecdotal case reports describe
date complex. The colorless phosphomolybdate can be
increased serum iron concentration in sick versus con-
measured photometrically at 340 nm or can be reduced
trol birds.40 Other studies found no significant correla-
to molybdenum blue and measured at 600 to 700 nm.
tion between serum chemistry values, serum iron con-
Measurement in the 340-nm range is more likely to be
centration, total iron-binding capacity and unsaturated
affected by hemolysis, icterus and lipemia.
iron-binding capacity with hepatic iron accumulation, as
assessed by histopathology and iron quantification.66 Common detergents are frequently contaminated with
However, the reference values used in one study were phosphate and it should be ensured that phosphate is
considerably higher than those used in domestic mam- measured using only new, unwashed equipment.
mals and human beings. Additionally, birds with possible Delayed plasma separation or hemolysis will significantly
inflammation (eg, leukocytosis, heterophilia and mono- alter plasma phosphorus levels.
cytosis) were included in the study.66
Physiology
Although serum ferritin concentration correlates signifi- Inorganic and organic phosphorus both have numerous
cantly with non-heme iron in the liver and spleen of vital roles in the body. Inorganic phosphate is com-
dogs, cats, horses and pigs, this correlation has not been plexed with calcium to form hydroxyapatite in beak and
explored in birds due to the species-specificity of anti- bone. This structural form also functions as a phosphate
body recognition and binding in ferritin ELISAs and storage compartment. The dissolution of phosphoric
627
acid in plasma is an important buffering system that one or more functions. An increase in plasma proteins
complements the carbonic acid buffering system. may be observed in egg-laying females.
Chemical energy in all cells depends on the high energy
bond in ATP and (guanosine triphosphate) GTP (both Diagnostic Value
triple phosphate molecules). Organic phosphate is an Though not adding information about specific disease eti-
essential component in phospholipid membranes and ology, total protein is important information used to estab-
nucleic acids, and is critical for several important lish supportive care. Decreased total protein may indicate
enzyme systems. the need for colloid (hetastarch) supplementation and
incite a search for an underlying protein-losing nephropa-
Diagnostic Value thy, enteropathy or liver failure. In cases of increased total
In oviparous species, increased phosphorus and calcium protein, reproductive activity should first be ruled out in
concentrations are observed during egg formation in females and then dehydration or an underlying inflamma-
females. Generally, these occur together and the calcium: tory disease state should be investigated.
phosphorus ratio stays above one in healthy individuals. If
the calcium:phosphorus ratio is below one, renal or other Uric Acid
disease (ie, primary or secondary hyperparathyroidism)
Method
should be investigated. Both hyperphosphatemia and
The most commonly used method is the uricase method
hypophosphatemia have been associated with renal dis-
where uric acid is catalyzed by uricase to allantoin. The
ease in birds. This electrolyte flux may represent acute
decrease in concentration of uric acid is measured at
and chronic forms of renal disease as in mammals.
approximately 285 nm.
Alkalosis will cause flux of phosphate into the cell and an
apparent hypophosphatemia. Some acidosis, such as dia- Physiology
betic ketoacidosis, results in catabolism of phosphorylated Uric acid is the major nitrogenous waste product of
compounds in the cell with excretion of phosphate at the birds. It is hypothesized that this has evolved due to
kidney and whole-body phosphorus depletion. oviparity.40 Embryonic and fetal development occur
within a closed compartment, the egg, that lacks diffu-
Total Protein sion of nutrients and waste. Uric acid is relatively inert
Method and substantially less toxic than ammonia or urea, thus
There have been several articles written on refractome- ensuring a viable hatchling. Uric acid (an oxidized form
ter versus biuret analysis of total protein.1,41,42,50 The of the purine, hypoxanthine) is synthesized predomi-
biuret method is a more specific chemical reaction nantly in the liver from purine metabolism, with a small
where peptide bonds are reacted with cupric ions to amount of synthesis occurring in the renal tubules.
form a colored product measured spectrophotometri- Approximately 90% of uric acid is secreted in the proxi-
cally at 540 nm. The total protein value determined mal convoluted tubules in the normal bird.20 This per-
using a refractometer is frequently inaccurate in com- centage can be markedly altered in pathologic condi-
panion avian species due to interference by high con- tions. Uric acid is passed to the cloaca and then may be
centrations of other light-refractive compounds in retropulsed to the rectum and ceca, where it may be
plasma, such as chromagens, lipids and glucose. Studies broken down by bacteria and reabsorbed.7,8
in chickens, turkeys and ducks have shown good corre-
lation between protein concentrations obtained by Diagnostic Value
refractometerd and biuret methods.1,50 These species tend Due to active renal tubular secretion, blood uric acid lev-
to have lower blood glucose values than most psittacines els are not notably affected by dehydration until GFR is
and smaller birds. Correlation studies in avian species decreased to the point that uric acid is not moved
with high blood glucose levels, such as pigeons, have through the tubules, which may occur in severe dehydra-
shown marked discrepancies between refractometer and tion. Raptors and penguins have higher reference values
biuret methods, however, a different brand of refrac- for uric acid, and marked increases in plasma uric acid
tometere was used, that may have contributed to the dif- concentration may be observed postprandially.34,44
ference in results.41,42 There is marked variation in nor- Therefore, sampling of carnivorous birds should be per-
mal blood glucose levels in avian species. The biuret formed after a 24-hour fast. Fasting also will decrease the
method is the most accurate method to quantify total likelihood of lipemia, which is frequently observed in
protein in the clinical setting, where samples from many postprandial samples. Contamination of the blood sample
different species may be evaluated. with trace amounts of urates from the skin of birds may
lead to extreme elevations in uric acid measurements.
Physiology Questionable samples should therefore be redrawn and
The body contains thousands of proteins each having the testing repeated. Once the above etiologies are ruled
out, renal disease should be assessed with urinalysis, radi- tein not reabsorbed in the proximal tubule is generally
ography, and/or renal biopsy (see Chapter 16, Evaluating precipitated with uric acid. Assuming there is no fecal
and Treating the Kidneys). contamination, normal avian urine should not contain
protein that can be detected on a urine dipstick.32
Urinalysis
Needle-shaped uric acid crystals also may be observed in
Osmoregulation is accomplished by contributions from
normal urine. Uric acid crystals polarize and can be
the kidneys, intestinal tract, salt glands and, to some
tested chemically using the murexide test. A drop of con-
extent, the skin and respiratory tract.19,20 Urine can be
centrated nitric acid is added to the crystals and heated
actively retropulsed from the urodeum to the copro-
to evaporation. A drop of ammonia is then added. If uric
deum of the cloaca and then to the rectum and poten-
acid is present, the liquid will turn a mauve color. Adding
tially the large intestine, where water can be reabsorbed
several drops of sodium hydroxide to a urine sample will
and electrolytes can be modified. This results in a
dissolve uric acid crystals. This can facilitate the identifi-
change in the specific gravity, electrolyte concentrations
cation of casts, bacteria and cells.
and bacterial contamination of urine.
Biliverdinuria, grossly apparent as green urates, is not a
Urinalysis is indicated when there is azotemia, uratemia,
normal finding and is most commonly caused by bile stasis
polyuria/polydipsia, hematuric abnormal urates, or geni-
due to liver compromise. It also may be seen in birds with
tourinary masses. Birds with renal pathology will fre-
hemolytic anemia. Biliverdinuria associated with nephrosis
quently have polyuria, resulting in a urine sample of
has been described histologically.53 The clinical significance
adequate volume for analysis. Avian urine is generally
of the described nephrosis is unknown. Prior to diagnos-
collected free catch by removal of cage paper and thor-
ing biliverdinuria, fecal contamination should be assessed
ough cleaning of the cage surface. A needle and syringe
by measuring urobilinogen with a urine dipstick. A posi-
or capillary tube can be used to aspirate urine from the
tive urobilinogen result supports fecal contamination.
cage bottom and minimize fecal contamination. Ureteral
catheterization has been performed, but, requires anes- Hemoglobinuria has been documented in heavy metal
thesia and is difficult.65 poisoning, specifically lead toxicosis, in Amazon, Electus
and African grey parrots secondary to intravascular
Normal urine has a clear fluid component. There is vari-
hemolysis.17 Ketonuria is not observed in normal birds.
ation in normal urine volume among species that are
Ketones have been found in the urine of migratory birds,
adapted to different food sources and environments.10,19
but otherwise support a diagnosis of diabetes mellitus.9,63
Specific gravity in most clinically normal birds has been
(See acetoacetate, acetone in the Analytes section).
reported as 1.005 to 1.020, and avian urine is generally
acidic.6 Normal urine sediment is generally composed of Even in free catch samples, culture and sensitivity are
uric acid precipitates and crystals, sloughed squamous indicated when bacterial infection (eg, pyuria) is sus-
epithelial cells, <3 WBC/40x field and <3 RBC/40x field, pected based on clinical presentation or urinalysis
and low quantities of predominantly gram-positive bac- results. Renal biopsy and culture also can be performed
teria. Bacteria present in normal samples are attributed if inflammation or infection is believed to involve the
to fecal contamination. kidney (see Chapter 16, Evaluating and Treating the
Kidneys).
The majority of uric acid in avian urine exists as a white
to light yellow colloidal suspension made up of small,
spherical conglomerates (urates) that range in diameter Products Mentioned in the Text
a. Vacutainer tubes, Becton Dickinson, Franklin Lakes, NJ, USA
from 0.5 to 15 µm.6 The urate precipitate is composed of
b. I-STAT, Heska Corporation, Fort Collins, CO, USA
uric acid, sodium and/or potassium, and protein. The c. Lactose/D-galactose assay kit, Boehringer Mannheim, Mannheim,
precipitate is not measured in the specific gravity of the Germany
d. AO Goldberg Refractometer, American Optical Corporation, Buffalo, NY,
urine supernatant, and therefore urine specific gravity is USA
lower in birds and reptiles than in mammals. Any pro- e. Atago Refractometer, Atago Corporation, Atago Ltd, Tokyo, Japan
References and 1989. 3. Bailey TA, et al: Age-related tion of heme oxygenase from
2. Assink HA, et al: The introduc- plasma chemistry findings in chick liver. Comparison of the
Suggested Reading tion of bromocresol purple for the buff-crested bustard avian and mammalian
1. Andreasen CB, et al: Determin- the determination of serum (Eupodotis ruficrista enzymes. Eur J Biochem
ation of chicken and turkey albumin on SMAC and ACA, gindiana). Zentralbl 189(1):155-166, 1990.
plasma and serum protein and the standardization proce- Veterinarmed 45B:635-640, 5. Brackeen GL, Dover JS, Long
conce628nt628rations by dure. J Clin Chem Clin 1998. CL: Serum albumin. Differences
refractometry and the biuret Biochem 22(10):685-692, 4. Bonkovsky HL, Healey JF, Pohl in assay specificity. Nutr Clin
method. Avian Dis 33:93-96, 1984. J: Purification and characteriza- Pract 4(6):203-205, 1989.
629
6. Braun EJ: Comparative renal distinctions in the physical exami- 38. Lumeij JT: Relation of plasma cal- 53. Phalen DN: The avian urinary sys-
function in birds, reptiles, and nation. In Ritchie BW, Harrison cium to toal protein and albumin tem: form, function, diseases.
mammals. Sem Avian Exotic Pet GJ, Harrison LR (eds): Avian in African grey (Psittacus eritha- Proc Assoc Avian Vet, 1990, pp 44-
Med 7:62-71, 1998. Medicine: Principles and cus) and Amazon (Amazona sp.) 57.
7. Braun EJ: Integration of renal Application. Lake Worth, FL, parrots. Avian Pathol 19:661-667,
54. Phalen DN, Homco L, Jaeger L:
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Suppl 3:70-74, 1989. infections. Avian Pathol 17:427- Wingers Publishing, 1994, pp Amazon parrots with bile duct
9. Candeletta SC, et al: Diabetes 432, 1988. 522-537. carcinomas. Proc Assoc Avian Vet,
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11. Clubb S, Schubot R, Joyner K: WB Saunders, 2001, pp 352-389. method for the determination of Calcium in Reproductive
Hematological and serum bio- 27. Hillyer EV, et al: Bile duct carci- total protein in avian plasma or Physiology: A Comparative Study
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24_Endoscopy.qxd 8/23/2005 1:35 PM Page 631
CHAPTER
24
Diagnostic Value of
Endoscopy
and Biopsy
MICHAEL LIERZ, D r med vet , MRCVS, C ertified Specialist Poultry-Avian
Medicine, Certified Species Conservation
Endoscopy has been used in avian medicine since the
1970s, primarily for determining gender in birds that are
not sexually dimorphic. With the advent of acceptable
inhalation anesthetics, the safety of this procedure has
increased while the stress to the patient has decreased.
Unless otherwise noted, the descriptions in this chapter
are of psittacine patients and related procedures using
rigid endoscopes (Fig 24.1).
M. Lierz, modified by Michael Pees
Endoscopes are fiberoptic probes that utilize magnifica-

tion to facilitate visual inspection of internal body struc-
tures. Endoscopy can complement imaging modalities
such as radiography and ultrasonography. Direct visuali-
zation of internal structures by the endoscope affords
numerous advantages as a diagnostic tool (Tables 24.1-
24.4). There are instances where the use of a semi-rigid
or a flexible endoscope is advantageous. Rigid endo-
scopes are available in a variety of viewing angles (Figs
24.3a-b).
While most endoscopic procedures are minimally inva-

sive, they do require anesthesia for restraint and pain
management. Endoscopic visualization performed by an
experienced practitioner carries minimal risk. However,
the risk increases when more invasive procedures
(biopsy, surgery) are performed (Table 24.5). In order to
minimize the risk to the patient and maximize the diag-
nostic information, the practitioner should become pro-
ficient with endoscopic location and visualization of
internal structures. Cadavers are excellent training tools,
as they allow immediate comparison between what is
visualized endoscopically and the actual organs or gross
necropsy (see Chapter 26, Diagnostic Value of
Necropsy).
Table 24.1 | Characteristics of Endoscopes

(see Figs 24.1, 24.2a-c)
Endoscopes Comments
Rigid • Best choice for primary scope
• 2.7 mm diameter, 30° viewing angle, 19 cm
length recommended
• 1.9 mm diameter provides acceptable imaging for
most patients and procedures
• 4.0 mm provides best imaging but is too large for
some avian patients
• Quality varies between manufacturers (Fig 24.1)
Flexible • Recommended for a second scope

• Preferred for evaluating proventriculus, ventriculus and
oviduct
• 3 mm diameter is most useful, has three ports to
accommodate the lens, fiberoptic light bundle,
instruments
• Quality differs between manufacturers (Figs 24.2a-c)
Fig 24.1 | Rigid endoscopes most commonly used in avian
Semi-rigida • 1.2 mm diameter ideal for small patients, endoscopy. Top to bottom: 1.9 mm 0°, 2.7 mm 30°, 4 mm 0°.
small orifices
• See Chapter 1, Clinical Practice, Fig 1.13
Note: Diameters of scopes do not include sheaths and their working
channels.
Table 24.2 | Light Sources

Light source Comments
Halogen: xenon • Gives the most light
Computed flash generator • Necessary for 35-mm slide
documentation
Light cable • Must be compatible with the light source
Otoscope handle • Portable scopes are available that attach
to otoscopes
• Less expensive, most provide adequate
Greg J. Harrison
illumination
Table 24.3 | Lenses for Rigid Endoscopes

Lense Comments
Single lens Lower-quality image Fig 24.2a | A flexible endoscope allows more maneuverability
Less expensive in viewing lungs and the gastrointestinal system.
Rod lens Best-quality image
More expensive
Table 24.4 | Viewing Angles for Rigid Endoscopes

(see Fig 24.3a-e) c
Angle Comments a
0° • Natural straightforward orientation
• Good for examination of the ear canal, oral cavity,
crop, trachea
Greg J. Harrison
• Superior for photodocumentation
Greg J. Harrison
30° • Forward oblique angle

• Allows visualization of a larger area by rotating the scope b
Table 24.5 | Surgical Equipment Used during Endoscopy Fig 24.2b | The 3-mm Fig 24.2c | The fiberoptic bundle
measurement of a small, (a) for light and visualization, the
• Small, curved mosquito hemostats • Tissue-handling forceps
flexible endoscope. air or flushing port (b), and an
• Scalpel, #15 blade • Needle holder
instrument port (c) of a 3-mm
• Small scissors • Suture
flexible endoscope.
Chapter 24 | D I A G N O S T I C V A L U E O F E N D O S C O P Y A N D B I O P S Y
633
K
OL
I
S
Fig 24.3 | a) The view as seen through a 2.7-mm 30° scope. Turning the scope around its optical axis, a panoramic view is possible.
b) Kidney (K), ovary (O), Ovarian ligament (OL) Intestine (I) and Spleen (S) seen with a 4-mm 0° scope. Only a straightforward view of the
organs is possible.
Table 24.6 | Endoscopic Accessories (see Figs 24.5a-b)

Accessory Comments
Flexible biopsy forceps • Must match working channel of
scope to allow use of forceps without
obstructing view
• 1.8 mm recommended
• Elliptical cup (deeper cuts)
• Round cup (recommended for testicular,
kidney biopsy)
Flexible grasping forceps • Removal of foreign bodies, granulomas
Infusion/aspiration needlea • 22-gauge flexible needle inside Teflon
catheterb
• Can be used in the working channel
Fig 24.4 | Basic equipment for endoscopic-guided multiple-
• Good for aspirating fluid from cysts and
entry surgery in birds. Top to bottom: monopolar sling, scissor, direct application of medications
grasping forceps, bipolar forceps for coagulations, trocars. (Figs 24.5a,b)
Software • Systems are available to store endo-
scopic images in medical records
Endoscopic-guided surgery • See Fig 24.4
equipment
Cleaning and sterilization • Follow manufacturer’s instructions
• Adequate time between patients is nec-
essary to properly sterilize all equipment
Most of the body can be examined using endoscopy. Apart

from the visual assessment, tissue sampling is possible
Preparation and
using the working channel and biopsy tools (Table 24.6). Contraindications
A sterile sheath is particularly valuable for microbiological
sampling (especially of the deeper respiratory system). Duration of pre-endoscopic fasting will parallel that of
The sheath prevents contamination of the sample. presurgical fasting for similar procedures. Longer fasts
may be required to facilitate visualization of abdominal
New surgical procedures using multiple endoscopes, organs. General anesthetic techniques and requirements
multiple sites and radical new instruments are being are discussed in Chapter 33, Updates in Anesthesia and
developed (Fig 24.4). The use of a flexible needle can Monitoring.
have multiple applications (Figs 24.5a,b).
Birds with bleeding dyscrasias are at heightened surgical
risk, especially when an organ biopsy is performed. The
Fig 24.5a | The Teflon tube of the flexible nee- Fig 24.5b | The flexible needle can be used for
dle is an excellent tool for the endoscopic-guided aspiration, biopsies, penetrations and applica-
application of medicine directly to lesions such as tion of medicine. Here, it is ready to penetrate a
this air sac granuloma. granuloma for a needle aspirate.
presence of cystic structures within the coelom, organo- may be entered (Figs 24.12a,b). Some clinicians prefer to
megaly or the presence of any fluid will complicate the enter between the ribs. This is best accomplished by
procedure and increase the risk to the patient. Fluid using a curved mosquito hemostat to elevate the ribs
should be carefully drained or reduced with diuretics prior to penetration. However, using this technique the
prior to endoscopy. Obesity often reduces the view in intercostal muscle is damaged, which is a disadvantage.
the body cavity, increasing the risk of organ damage. The direction of penetration should be toward the cra-
nial rib (remaining laterally positioned) to avoid the
liver. The scope is stabilized with the tips of the forefin-
Coelomic Laparoscopy ger and thumb while the hand rests on the table (Fig
24.13).
Studies
The scope is advanced between the legs of the forceps.
LEFT LATERAL APPROACH The air sacs will then be visible. Clear air sacs allow visu-
alization of the gonad, the adrenal gland, and the cranial
The endoscopic approach to the coelomic cavity depends
division of the kidney, through the abdominal air sac (Fig
on the diagnostic goal of the procedure (Fig 24.6) and
24.14). Cranial to this triad is the left lung. In larger
the results of previous imaging studies. The approach
birds, the scope may be advanced through the ostium
caudal to the last rib is ideal for exploration of the entire
between the lung and air sac to examine the bronchi
coelom (Fig 24.7). Due to the presence of an ovary in
(Figs 24.15-24.17). The medial lung, heart and liver can
most avian species on only the left side, approach from
the left is generally utilized to allow visualization of be seen as the scope advances cranially into the cranial
female reproductive structures (see the section on thoracic air sac.
gonads later in this chapter). The anesthetized bird is
The ureter, uterus, and ductus deferens are seen ventral
placed on its right side, with the left wing extended
to the kidney, and intestinal loops come into view if the
dorso cranially. The left leg may be pulled either cranially
scope is directed ventrally from the original entry site.
or caudally. The following description is for the approach
with the leg extended caudally (Fig 24.8). The proventriculus/ventriculus, liver and often the
spleen may be visualized when the scope is directed
Orientation to the surgical site is provided in Figs 24.9- cranioventrally. The punctured air sacs close rapidly and
24.11. A small incision is made in the skin, followed by a heal uneventfully. The skin incision can be closed with
caudal reflection of the muscle layers with curved for- sutures or tissue glue.
ceps. Penetration into the air sac is accompanied by a
palpable and sometimes audible pop. The use of blunt A similar approach to the coelom is made by entering
instruments for this penetration cannot be overempha- caudal to the pelvic limb, which is pulled cranially.
sized. Sharp instruments may damage underlying tissue. The incision is made caudal to the last rib. With this
The caudal thoracic air sac is most often penetrated, approach, there is less chance of entering the cranial
however, the abdominal or cranial thoracic air sacs also thoracic air sac.
635

Fig 24.6 | The various endoscopic entry sites overlying the artist’s rendition of bones
with colored areas representing the various air sacs encountered in endoscopy. Blue
represents the intraclavicular, yellow the cranial thoracic, green the caudal thoracic and
orange the abdominal air sacs.
Fig 24.7 | An artist’s rendition of the organs encountered in endoscopy from the left
lateral aspect. 1) heart 2) liver 3) trachea and lungs 4) proventriculus 5) ventriculus
6) intestines 7) kidney 8) spleen 9) adrenal-gonad area. The red star is a typical entry
location.

Greg J. Harrison
Fig 24.8 | Right lateral recumbency, left leg caudal. This bird is Fig 24.9 | The middle of a triangle formed by the spine (1), m.
malpositioned; not being in a true lateral, which is critical for iliotibialis (2) and last rib (3); the red arrow represents the most
organ relationships. Secondly, it can be seen that in this blue common lateral point of entry for laparoscopy.
crowned conure the area in front of the leg has a thick fat pad
(arrow) that has to be penetrated to reach the musculature.
636
Fig 24.10 | The muscle iliotibialis (a) overlies the point of Fig 24.11 | Using a curved forceps, the m. iliotibialis (a) is
entry, demonstrated on a dead bird with skin removed. reflected caudally and the underlying fascia is penetrated caudal
to the last rib (b), as is demonstrated here on a dead bird with skin
removed.
Figs 24.12a,b | Entering the body cavity caudal to the last rib usually places the scope into the caudal thoracic air sac (b). Changing
the route of penetration slightly, the scope is guided into the abdominal air sac (c) where the kidney (a) is located. One must penetrate
the confluent wall of the medial aspect of the caudal thoracic air sac and the left lateral wall of the abdominal air sac.
Fig 24.13 | Correct anchoring of the tip of the Fig 24.14 | View into the abdominal air sac.
scope. The hand should always be in contact with Kidney (a), ovary (b), intestine (c), adrenal gland
the bird while the wrist is rested on the table. (d), ureter and oviduct (e).
637
Fig 24.15 | The opening from the caudal thoracic Fig 24.16 | Lung tissue viewed from the caudal tho-
air sac into the lung (aperta) allows retrograde racic air sac. The bronchi and lung parenchyma are
endoscopy of internal structures of the lung. clearly visible.
Fig 24.17 | The endoscope has been advanced into Fig 24.18 | The ideal air sac is transparent. Minor
the horizontal secondary bronchi that branches from blood and lymph vessels are commonly visible in pet
the left or right primary bronchi. The honeycomb struc- and aviary birds.
ture of the lungs is seen. This view cannot be appreci-
ated via the trachea due to the diameter restrictions of
the syrinx, the fragility of the primary bronchi and the
acute angle at the origin of the secondary bronchi.
VENTRAL MIDLINE APPROACH ity, thickened walls and granulomas (Fig 24.20). These
changes may be due to infectious processes, or to
The bird is positioned in dorsal recumbency and a ven-
tral midline approach to the coelom is made. A layer of inhalation of respiratory irritants (ie, smoke, volatile
fat may be present just under the linea alba in the area chemicals). In some cases, a definitive diagnosis can be
directly caudal to the sternum. Care must be taken on made from visualization, cytology and/or biopsy of air
smaller birds not to inadvertently penetrate the duode- sac lesions (Figs 24.21a-c). Removal or debulking such
num or pancreas. The duodenum, pancreas and central lesions has been described using laser and radiosurgery
liver can be examined from this approach. via the endoscope.
Air Sacs Lungs and Bronchi
Normally the air sacs are transparent, although a few The lungs are dark pink with a prominent reticular pat-
vessels may be present (Fig 24.18). Fatty infiltrates may tern. Within the lungs, the anastamosing bronchi are visi-
be noted during routine examination without associated ble (see Figs 24.16, 24.17). Pneumonia will obscure the
pathology. Opacity and small vessels in the wall of an air normally well-defined parenchymal pattern of the lung.
sac are early signs of inflammation (Fig 24.19). Other A yellow discoloration of the lung tissue is often noted
abnormalities of the air sacs include increased vascular- with pneumonia (Fig 24.22). Anthracosis (focal black
Fig 24.19 | Prominent vessels in the air sac, opacity Fig 24.20 | Granulomas are forming in this case of
or small granulomas are signs of infections and/or air sacculitis.
irritation from environmental contaminants (smoke,
volatile chemicals).
Fig 24.21a | Fruiting aspergilloma in the air sac. Fig 24.21b | Active aspergilloma in an air sac with
This presentation carries a guarded prognosis. fluid exudate.
Fig 24.21c | Removal of an old aspergilloma using Fig 24.22 | Internal lung tissue of a bird with dysp-
a biopsy forceps. nea, viewed from the caudal thoracic air sac. Yellow
areas and the loss of the typical lung parenchyma are
signs of pneumonia. A biopsy to aid in specific diag-
nosis and treatment is highly recommended. The
black spots are soot (anthracosis) and can be found
in birds from smokers or cities.
639
Fig 24.23 | Post-traumatic hemorrhage of the lung. Fig 24.24 | The normal liver is a brown-red homo-
geneous color with a sharp border.
Fig 24.25 | A rounded liver border indicates an Fig 24.26 | Hematoma of the liver after trauma.
enlarged liver. A liver biopsy is often indicated to
identify the nature of the hepatomegaly.
spots) is regularly found in birds from cities, industrial color. The liver border tapers to an edge (Fig 24.24). A
areas or the homes of smokers (Fig 24.22). Bleeding from rounded liver border is not normal and may indicate
trauma can be diagnosed by endoscopic examination infection or hepatic lipidosis (Fig 24.25). The liver color
(Fig 24.23). changes to yellow with fatty liver. Focal bleeding in the
liver appears bright red, while hemosiderosis appears
Proventriculus, Ventriculus — Serosal Examination dark red that over time can turn black in color (Fig
24.26). Multiple white foci represent necrosis, abscesses
The proventriculus is an elongated, usually white organ
located in the ventral coelom, surrounded by the or neoplasia (Figs 24.27, 24.28). Pseudomembranous
abdominal air sac and the liver. The surface appearance infiltrates of the liver capsule and air sacs may also be
and size of the proventriculus are diagnostically impor- due to infection, inflammation or neoplasia (Fig 24.29).
tant. An enlarged proventriculus with a glossy surface Liver biopsies offer very valuable diagnostic information
might indicate proventricular dilatation disease (PDD). (see Chapter 15, Evaluating and Treating the Liver).
Focal bleeding may indicate foreign bodies or infections.
The ventriculus cannot always be visualized. In birds Heart and Pericardium
with a muscular ventriculus, abnormalities are seldom
The lateral approach through the caudal thoracic air sac
discernible endoscopically (see Chapter 26, Diagnostic
into the cranial thoracic air sac allows the visualization of
Value of Necropsy).
the heart and pericardium. Pericardial effusions can be
drained utilizing this approach. The normal pericardium
Liver is transparent (Fig 24.30a). A milky pericardium is the
The liver is a large organ of uniform brownish red result of pericarditis. The presence of fat at the heart
Fig 24.27 | White-yellow spots on the liver, diag- Fig 24.28 | Diffuse necrosis of the liver (histo-
nosed as abscesses. Neoplasias have a similar moniasis).
appearance.
Fig 24.29 | Yellow, caseated material present on Fig 24.30a | Liver (a), heart pericardium (b), heart fat
the liver and air sac due to a bacterial infection. (c), lung (d) as seen in a normal bird.
Kidney
The avian kidney is divided into three divisions. The
adrenal gland and gonad are present at the cranial pole
of the kidney (Fig 24.31). The ureter can be seen and, in
most cases, traced to the cloaca. The kidney is brown-
red-orange. Star-shaped collecting tubules filled with
urates are often visible on the surface. These structures
become hidden in swollen kidneys (Fig 24.32). Yellow to
white deposits on the surface of the kidney are often uric
Fig 24.30b | The aorta branching into the carotid acid crystals and may indicate renal gout (Fig 24.33).
artery is seen lying between the costal musculature,
These foci might occur due to dehydration as well. After
the base of the heart and the returning jugular vein.
rehydration the foci are eliminated, while in the case of
gout the foci are still present. Obesity can make the kid-
base and heart apex is normal. An absence of fat is a sign ney appear diffusely yellow. Abscesses or cysts may
of starvation or chronic disease. The main heart vessels appear as large yellow spots (Figs 24.34, 24.35). Neo-
are visible at the heart base as thick white tubes with reg- plasias or other gross abnormalities should be biopsied;
ular pulses (Fig 24.30b). The cardiac nerve supply can be assuming that the patient’s condition is sufficiently stable
found emanating from the thoracic vertebrae. (see Chapter 16, Evaluating and Treating the Kidneys).
641
a
c
b
Fig 24.31 | Kidney (a), adrenal gland (b) and testi- Fig 24.32 | A swollen kidney as seen in acute
cle (c). Apart from the clearly visible testicles, the nephritis. Note the lack of predominate stellate vas-
absence of a ligament crossing the cranial pole of culature pattern associated with the renal glomeruli.
the kidney represents a male bird. The lumpy nature
of the kidney surface is normal for swans.
Fig 24.33 | Uric acid deposits within the kidney. If Fig 24.34 | Renal cyst. Abscess or neoplasia are
this situation remains after several applications of possible differential diagnoses.
intravenous fluids, renal gout is likely.
Gonads
The left lateral approach is best for viewing gonads
K because hens generally lack a right ovary. Right ovaries
may be present in juvenile birds, especially in accipiters.
Gonads are present ventral to the cranial poles of the
kidneys.
DNA methods are available for sexing most monomor-

phic avian species and are less invasive than surgically
O sexing. Endoscopic sexing has the advantage of allowing
direct visualization and evaluation of the gonads and
other organs. Sexual function can be estimated and any
damage from sterilization or castration can be observed.
Fig 24.35 | Apart from the color changes of this The normal appearance of the gonads varies between
kidney (K), multiple yellow foci are visible. The typical species. The right side should be examined if the gonads
renal structure is no longer detectable. Histological
examination of a renal biopsy showed a pyelonephri-
are not clearly observed or discernible as to either ovary
tis. The ovary (O) has many involuted or testes, or if presumed abnormalities are present.
follicles. Gonads increase in size during sexual activity (Figs 24.36-
24.38). Gonads can be small due to stress, malnutrition,
Fig 24.36 | In juvenile birds, the rudimentary ovary Fig 24.37 | Secondary or tertiary follicles dramati-
on the right side still might be visible, sometimes cally increase in size during the reproduction cycle.
showing single follicles (arrow). The normal left ovary Pathological alterations such as inflammation or
is at the 9-11 position. neoplasias might lead to similar findings. A detailed
anamnesis indicating sexual display behavior may
indicate an active ovary. If a large follicle is very
close to the tip of the endoscope, the follicle can be
easily confused with a testicle.
b c
c a b
Fig 24.38 | A cluster of follicles makes identification Fig 24.39 | In juvenile birds, the ovary (a) might be
of the ovary (a) easy. More important is the detection difficult to detect. Only the suspensory ligament (c) at
of the suspensory ligament (b) of the ovary. It crosses the cranial pole of the kidney (e) characterizes the
the cranial pole of the kidney. Apart from sexing, female bird. Lung (d), adrenal (b). Small ovarian folli-
evaluation of the ligament is important to judge the cles are not an accurate estimation of age or repro-
possible breeding performance of the bird. Adrenal ductive ability.
gland (c).
lack of nesting stimuli or immaturity. birds, they will not lay eggs. A large uterus may indicate
previous egg laying or pathology. Inactive ovaries may be
Female Birds flat with a cobblestone appearance, while active ovaries
The ligamentum dorsale oviductus (suspensory liga- may appear as a cluster of spheres. The size and number
ment) from the ovary crosses the cranial pole of the kid- of visible follicles will vary with the age and reproductive
ney coursing toward the uterus (Fig 24.38). Lacking visu- status of the hen. Immature ovaries are sometimes diffi-
alization of a well-defined gonad, this ligament is the cult to distinguish from testicles. The ovary is generally
main evidence for sexing the bird as a female. The ovaries an off-white, yellowish color, but pigmentation (usually
can be difficult to detect in juvenile birds (Fig 24.39). black) occurs in some species (Fig 24.41). In addition,
When examining breeding birds this ligament must be the entire uterus should be evaluated.
carefully assessed. In cases where this ligament is dam-
aged or absent, the breeding performance of the bird is Male Birds
questionable (Fig 24.40). If this ligament is cut in juvenile In male birds there is no ligamentum dorsale oviductus
643
Fig 24.40 | The ovary (O) is clearly visible and the Fig 24.41 | Some avian species have melanistic
suspensory ligament is missing. This bird cannot be gonads, as is seen in this ovary.
recommended for breeding. The kidney (K) has just
been biopsied (arrow).
Fig 24.42a | The teste (1) is at the cranial pole of Fig 24.42b | Both paired teste are pictured here.
the kidney (2) and close to the adrenal gland (3). With increased size of the left testicle or opacity of air
sacs, the right testicle may be obscured from view.
(Figs 24.42a,b). The paired testicles are normally oval nal glands may be obscured. The adrenal glands are usu-
shaped with one to three faint vessels crossing the sur- ally located immediately cranial to the gonads. Changes
face. In birds with clear air sacs, both the left and right in size or increased vascularity of the adrenal glands may
testicles may be visualized from the left lateral approach. indicate stress or disease (Fig 24.46).
In some species the testicles are pigmented (eg,
Cacatua, some macaws and wading birds). The torturous Intestine
course of the ductus deferens makes it distinguishable
Visible pathologic changes of the intestinal serosal surface
from the ureter (Fig 24.43). The size of the testicles, epi-
are uncommon. Coelomic filarial worms are a rare finding
didymides and ductus deferens vary with the species,
in captive bred psittacines, but are regularly seen in birds
size, age and breeding condition of the individual bird
of prey (Figs 24.47, 24.48). The intestine has a smooth
(Fig 24.44). The breeding potential of a male bird nor-
surface covered with many vessels. The generally redish-
mally cannot be assessed by visual observation of the
gray color varies according to the intestinal fluid. White
male anatomy. If a reproductive problem is suspected, a
foci may be a sign of previous penetration by endopara-
testicular biopsy is suggested (Fig 24.45).
sites. Both thinning and thickening of the intestinal wall
are signs of enteritis. Thinning can be appreciated endo-
Adrenal Gland scopically from the visibility of intestinal contents.
Adrenal glands vary in color, size and shape (see Fig Necrosis of the intestine wall might be visible in cases of
24.42a). They may be confused with immature or inac- clostridiosis or coccidiosis. Enlarged ceca filled with
tive gonads. If the gonads are well-developed, the adre- caseous yellow material could indicate histomoniasis.
d
U
Fig 24.43 | Ductus deferens (d) and ureter (U) in a Fig 24.44 | Epididymis (E) of a sexually active male.
sexually active male.
K
a
b
Fig 24.45 | A testicle (T) with a structural abnormality Fig 24.46 | Enlarged adrenal glands (a) appear in
that would indicate the need for a biopsy. Kidney (K). cases of stress or diseases. Juvenile ovary (b).
Pancreas
Tracheoscopy Studies
The pancreas lies within the duodenal loop (Fig 24.49).
The pancreas is a white-yellow color with a homoge- TRACHEA AND THYROID GLAND
neous matrix. Color changes, glassy appearance or an
The trachea and thyroid gland can be approached via
uneven surface often accompany pathologies and may
the cervical branch of the cervicocephalic air sac, the
warrant biopsy (see Chapter 26, Diagnostic Value of
clavicular air sac or through the coelomic cavity. The thy-
Necropsy).
roid gland is visible as an elliptical pink structure
attached to the trachea near the syrinx (Fig 24.53).
Spleen Alterations in size or a shiny appearance are considered
Psittacine spleens are round, purplish and often speck- abnormal and a biopsy may be indicated.
led (Fig 24.50). The spleen is located at the dorsal aspect
of the proventricular/ventricular junction on the right ENDO-TRACHEAL EXAMINATION
side from a left lateral approach. Splenomegaly (immune Endoscopic examination of the tracheal lumen is accom-
response), yellow appearance (fatty spleen) and multiple plished by extending the patient’s neck and gently
white foci (necrosis) are possible pathological alterations advancing the scope through the larynx and down the
(Figs 24.51, 24.52). Chlamydophilosis and other bacter- trachea (Fig 24.54). Unless the procedure is very rapid,
ial diseases would be included in the differential. The an air sac breathing tube is necessary (see Chapter 33,
spleen can be biopsied utilizing the same precautions as Updates in Anesthesia and Monitoring). Many endo-
in mammals. scopes are equipped with a protective sheath. Removal
645
Fig 24.47 | Serratospiculum sp. in the air sac in a Fig 24.48 | The same bird as Fig 24.47 12 days
falcon. after treatment with ivermectin. The dead worm can
easily be confused with a bacterial infection.
a b
Fig 24.49 | The pancreas (P) identified in the duo- Fig 24.50 | Using the left lateral approach, the
denal loop (D). The pancreas should have a homo- spleen (a) is accessible from the abdominal air sac by
geneous structure and color. pushing the proventriculus in the caudal-ventral direc-
tion to expose the right side of the proventriculus. The
psittacine spleen is round and similar in color (red-
brown) to the kidney and liver. Intestine (b).
Fig 24.51 | Enlarged spleen of a bird with psittacosis. Fig 24.52 | Pale color changes and enlargement of
a spleen.
a
Fig 24.53 | The thyroid gland on the carotid artery Fig 24.54 | Performing a tracheobronchoscopy.
adjacent to the trachea as seen from the interclavicu- The neck of the bird must be fully extended. A
lar air sac. A laparoscopic approach may be used by beak speculum allows a better view and is safer
pushing the scope cranial, passing over the heart ven- for the scope in case the bird wakes up and
trally and following the trachea (a). The thyroid gland attempts to bite the instrument. Anesthesia can
(b) can be visualized. be delivered via an air sac tube.
Fig 24.55a | Normal trachea. Fig 24.55b | A case of severe tracheitis. The tra-
cheal rings appear distorted due to the mucosal
swelling, sloughing and hemorrhage.
of this sheath will decrease the scope’s diameter and bodies (Figs 24.56, 24.57). The tracheal diameter typi-
enable its introduction into the trachea of smaller birds. cally decreases toward the syrinx. The narrowed diame-
Unfortunately, this also increases the chance for damage ter and the tracheal bifurcation into the main stem
to the endoscope. An unsheathed 1.2-mm scopea can bronchi make this area particularly prone to fungal gran-
allow visualization of the trachea of birds the size of ulomas and foreign bodies. Some degree of post-exami-
canaries and finches (Fig 24.58). Without the sheath, the nation hyperemia of the trachea is normal.
tracheal lumen can be examined, but no instruments
Acute dyspnea warrants endoscopic tracheal examina-
can be introduced into the visual field in such a small
tion once the patient is stabilized. Hemorrhage of the
patient. Evaluation should be made of the tracheal color,
tracheal mucosa may be seen with polytetrafluoroethyl-
and mucosal texture. The mucosa of the trachea and the
ene toxicosis. More pronounced pathology would be
bronchi are light pink and glistening. The tracheal rings
expected in the lung parenchyma with this condition.
are clearly visible (Fig 24.55a). In cases of tracheitis, the
mucosa becomes red and swollen, making the rings less Respiratory parasites often can be visualized with the
obvious (Fig 24.55b). Tracheal exudates, when present, endoscope (Figs 24.57, 24.59). If mites are suspected
should be collected for cytology and culture. Possible and not visualized, swabbing the scope onto a sterile
abnormalities of the trachea include strictures, tumors, slide and examining the slide microscopically may reveal
inflammation, parasites, fungal granulomas and foreign tracheal mites.
647
Fig 24.56 | Foreign body (seed) in a trachea. The Fig 24.57 | Syngamus trachea in the trachea.
mucosa is irritated and swollen.
Greg J. Harrison
Greg J. Harrison
Fig 24.58 | Endoscopy of a canary trachea with a 1.2 mm Fig 24.59 | A canary tracheal mite under 100x. This mite was
semiflexible endoscopea. obtained from the endoscope tip. The mites in the trachea were
not visualized during endoscopy.
Pharyngoscopy and Upper to perform an infraorbital flushing technique also can be

entered endoscopically.
GI Studies
ESOPHAGUS, CROP,
OROPHARYNX PROVENTRICULUS, VENTRICULUS -
Sufficient anesthesia or restraint is necessary to prevent MUCOSAL EXAMINATION
damage to the endoscope by the bird’s beak. In addi-
Examination of the esophagus, crop and proventriculus
tion, the use of a beak speculum is advantageous. While
via the oral cavity is a common procedure (Fig 24.62). As
under anesthesia, the bird is held in a ventral recum-
the esophagus, crop (Fig 24.63) and proventriculus are
bency position and the neck is fully extended (Fig 24.61).
hollow organs, insufflation is necessary for visualization.
This position allows endoscopic examination of the
inner surface of the beak, oral cavity, choana, rhinal cav-
ity, tongue and larynx. The shape of the tongue differs
Table 24.7 | Common Oral Pathology in Psittacines
from species to species. The infundibular cleft should be
• Squamous metaplasia • Bacterial infection
free of swelling and debris. Check the entire oral cavity
• Keratinized debris • Oral papillomas: most
for signs of pathology (Table 24.7). • Blunting of choanal common in Ara spp.
papillae • Oral neoplasias:
RHINAL CAVITY • Plaques fibrosarcoma, squamous
• Fungal or yeast cell carcinoma
The rhinal cavity can be entered from the choana and colonization • Trauma
the turbinates examined. The operculum prevents the • Parasites: trichomonads • Ulcerations
passage of a scope through the nares. The points used
Fig 24.60 | For upper digestive system endoscopy, one uses Fig 24.61 | When performing a gastroscopy, the head of the
a sheath with a working channel, here with an endoscope bird must be in a position lower than the body. Aspiration of liq-
inserted. Hollow organs can be insufflated and flushed using liquids into the lungs is then easier to avoid. Tracheal intubation of
uids. Tubes for infusion liquids can be attached to the liquid-in the bird during anesthesia aids in the prevention of aspiration.
and liquid-out taps (a). The arrows demonstrate the direction of
the flow of liquids. A port for flexible instruments (grasping
biopsy forceps, needle, scissors or various brushes) (b) is shown
above the viewing eyepiece.
Fig 24.62 | Normal esophagus of a chicken. Fig 24.63 | Endoscopic view at the entrance of the
crop in a chicken. The oblong structure is the wall
between the esophagus and the crop. The other
opening is the entrance to the crop.
Prior to gastroscopy, a fasting period is important to let leading to a collecting container. The two taps allow
allow maximum viewing without the presence of food. accurate control of the amount of fluid within the diges-
Insufflation with air or sterile fluids is commonly used tive system, expanding the organs as needed for exami-
for positioning and advancement of the endoscope. nation. The fluid outlet is closed and the selected por-
Sterile fluids allow the flushing out of debris and subse- tion of the GI tract is dilated until good visualization of
quent dilation of the GI tract. This greatly aids in visuali- the mucosa is achieved. The fluid outlet is then opened
zation. It is important that the fluid be warm to the in order to flush out mucus and small particles. Opening
touch to avoid decreasing the body temperature of the the fluid inlet again can increase the pressure. To avoid
bird. A working channel is necessary to aim the washing aspiration, fluid should not be allowed to exit the diges-
solution. This working channel should have two taps, tive tract through the oral cavity, which could and often
one for fluids in and one for fluids out (see Fig 24.60). does lead to the contents being inhaled. Occlusion of
The third port is ideal to allow simultaneous passage of the scope and esophagus to retain the infused air or
a biopsy or grasping forceps. The fluid inlet is attached fluid in the crop can be easily accomplished by place-
to an infusion bag or bottle positioned at a higher eleva- ment of digital pressure on the scope and esophagus.
tion. A larger infusion tube is connected to the fluid out- Although the tracheal rings are solid in birds, caution
649
Fig 24.64 | Psittacine cloacal mucosa visualized Fig 24.65 | Urates (a) emanating from an ureter on
using liquid insufflation. the cloacal surface.
should be used to prevent restriction of normal airflow.

In addition, the bird should be positioned in ventral
Cloacoscopy Studies
recumbency with the head lower than the body. An
CLOACA
endotracheal tube should be in place (Fig 24.61).
The endoscope simplifies cloacal examination. Insuffla-
The mucosal surfaces of the esophagus and the crop tion is necessary for viewing to maintain an adequate
vary between species. The mucous membranes of the distance between the scope and tissues under examina-
tion. A soft rubber feeding tube may be used, with digi-
esophagus, crop and proventriculus are a homogeneous
tal pressure applied around the scope barrel to retain
pink (Fig 24.62). The mucosa of the esophagus is usually
the air or fluid.
smooth; the crop has furrows and the proventriculus
papillae (Fig 24.63). Focal dark red or bleeding areas are When performing a cloacoscopy, the bird is placed in
signs of irritation, which can be due to foreign bodies, dorsal recumbency and the endoscope is inserted with its
infections, ulcerations, or neoplasia. A yellow coating of working channel. Insufflation is usually done using fluid
the mucosa can be seen with trichomoniasis, candidiasis, (see description at Esophagus, Crop, Proventriculus,
the diphtheric form of avian pox or vitamin A deficiency Ventriculus - Mucosal Examination, above). Feces and
urine are almost always present and should be washed
or excess. If there is a loss of the proventricular mucous
out for optimal visualization. The mucosal surface is pink
membrane’s normal color it might be a sign of a wall
with ureteral papillae (Fig 24.64). Urine can be seen ema-
suggesting PDD. Biopsy of the proventriculus or the
nating from these ostia of the ureters (Fig 24.65).
crop and submission for histopathology may confirm a Hyperemic cloacal membranes are indicative of inflam-
suspected diagnosis of PDD. However the significant risk mation or infections. Rough and red raised areas (cauli-
of dehesience must be considered prior to obtaining a flower shape) are suggestive of papillomatosis. Inside the
proventricular biopsy. To evaluate the proventriculus in cloaca, the openings of the ureters, the rectum and, in
larger psittacines, it may be necessary to introduce the female birds, the uterus can be viewed. The oviduct can
scope through an ingluviotomy incision. A preferred sometimes be entered and the caudal chambers investi-
location for this incision is to the left and somewhat dor- gated. The occurrence of fresh blood within the feces is a
sally, to avoid postoperative pressure on the crop inci- clinical indication for cloacoscopy, as it may originate
from the cloaca, the intestine, the ureters or the uterus.
sion from ingesta. An area of reduced vascularity is ideal.
The scope is introduced and advanced carefully into the
thoracic esophagus, continuing caudally to the proven-
tricular lumen. This procedure is useful for proventricu- Otoscopy Studies
lar biopsies and retrieval of foreign bodies. A flexible
scope is mandatory to evaluate a fragile proventriculus EAR
(eg, normal lories, large macaws and all cases of PDD) In most species, feathers conceal the opening of the ear
or all ventriculi. canal. The external orifice can vary from <2 mm in small
Fig 24.66a | The brachial plexus is visible cranial- Fig 24.66b | Plexus sacralis dorsal to the kidney.
lateral to the heart.
Fig 24.67 | In case of a pansystemic airsacculitis

(here milky), the entrance of the scope is the site of
Fig 24.68 | In case of a grossly abnormal liver, a
choice for a biopsy.
biopsy should be performed at the liver border.
species and up to 6 cm in some large raptors. The nor-

mal tympanic membrane is clear and slightly convex.
Endoscopic-guided
Otitis externa is not a common finding in psittacines, Biopsies
but bacterial, fungal, neoplastic and allergic conditions
may occur. In raptors, common findings are bleeding Coordinating the endoscope and the biopsy instrument
into the ear canal from head trauma. can be challenging. The advent of sheaths that are now
provided with many endoscopes has simplified this pro-
cedure by allowing the biopsy forceps to approach the
site without changing the field of vision. The small size of
Nerve Studies the biopsy forceps used for these procedures usually pre-
cludes serious hemorrhage. Endoscopic-guided biopsies
The nerves of the brachial plexus are seen anterior and
lateral to the heart (Fig 24.66a) The sacral pluxus some- allow sampling of organs under direct visualization (Fig
times visible dorsal to the kidney (see Fig 24.66b). 24.67). In general, biopsies of the lung, air sac, liver, kid-
Ed Note: Harrison has used endoscopy to evaluate ney, spleen, gonads, proventriculus, ventriculus, thyroid
nerve damage. Muscles, nerves, vessels, tendons and lig- gland and mucosal membranes of esophagus, crop and
aments can be examined using the endoscope. In cases cloaca are possible using a biopsy forceps within a work-
of trauma, air or fluids can be injected subcutaneously ing channel. Aspiration biopsies are possible using a
to provide a path for the scope to follow anatomical long, flexible needle with a Teflon cover (see Table 24.6).
structures into the area of trauma. This technique Puncture of cysts, bone marrow biopsies or lavage sam-
could be useful to investigate brachial plexus evulsion, pling are the ideal uses for this needle. In case of a gen-
nerve transection, thrombi, emboli, and traumatic eral alteration of an organ, the biopsy should be taken
damage to soft tissue. from the organ’s border (Fig 24.68). Contraindications of
651
Fig 24.69a | For sterilization of the female bird, the Fig 24.69b | The appearance of the coagulated
oviduct can be obliterated using a bipolar coagulation section of the oviduct that will scar closed.
forceps. Surrounding tissues must be avoided.
a
Fig 24.70 | The dichotomy of when to perform Fig 24.71 | Endoscopic-guided multiple entry for
female reproductive surgery is amply demonstrated bipolar radiosurgery castration.
on the immature or involuted side of the question by
observing the intimate proximity of the ureter (a) to
the uterus (b) in this example. Avoiding collateral
biopsies are similar to those mentioned for endoscopy.
damage is imperative. The ureter should be observed
for movement of urates (arrows) seen moving during Endoscopic procedures, in particular tissue biopsies, lead
regular contraction cycles. While on the opposite end to changes in certain blood values;1 therefore, planned
of the spectrum, the mature or active uterus has up blood sampling must be performed before endoscopy.
to a centimeter of distance between these structures
in a bird as small as a cockatiel, allowing almost no
chance for neighboring tissue damage; hemostasis is
the challenge. Vessels increase in length but more
significantly in diameter and thickness, creating the Endoscopic-guided
imminent danger of life-threatening hemorrhage.
Some of these vessels are too large for casual coagu-
Surgical Procedures
lation or less than ideal vessel-clamping techniques,
resulting in oozing in the first case or loss of the clip Endoscopic-guided sterilization or castration is possible.
and hemorrhage in the latter. This might be indicated in chronic egg laying or birds
that are aggressive during breeding season. As castration
is quite complex, sterilization represents a quick and
easy procedure, as the gonads need not be removed.
This can be accomplished using electrosurgery with a
bipolar endoscopic forceps (Figs 24.69a,b). Performing
this procedure when the bird is sexually inactive reduces
the risk of hemorrhage. (Sterilization may hormonally
influence behaviors). In juvenile or hormonally inactive
females the challenge one is faced with is making the
distinction between the ureter and the quiescent tion of the air sac at the beginning of the laparoscopy.
oviduct. The ureter is marked by urates, or its regularly Perforations of the proventriculus may result in fatal peri-
occurring contractions (Fig 24.70). Administering intra- tonitis. If major bleeding occurs, electrocoagulation, oxi-
venous fluids will increase the likelihood of seeing dized regenerated cellulose or sterile sticks of cotton
urates pass down the ureter. wool can be used. The bird should be placed at a 45°
angle with the head elevated to prevent blood from
Endoscopic-guided obliteration of air sac granulomas or entering the lungs. This keeps the blood in the caudal air
papillomas in the cloaca is possible. Endoscopic-guided sacs. If a large entry site has been created, the site may
laser diodes have been used to obliterate granulomas need deep sutures to close the muscles and prevent sub-
within the trachea or air sac. Multiple-entry endoscopic cutaneous emphysema. Postsurgical closure of air sac
surgery has been developed for resection of tumors or defects is usually not necessary. If emphysema occurs, it
castrations (Fig 24.71). Instruments are guided into the should be punctured and deflated regularly until these
endoscopic field of vision using trocars. Laser or radio- defects close themselves. When performing endoscopy
surgery is helpful to maintain hemostasis. on multiple subjects sufficient sterilization time for the
equipment is imperative to avoid transmission of disease.
Complication During and Product Mentioned in the Text

a. Semi-rigid scopes, infusion/aspiration needle, Storz,
After Endoscopy www.karlstorzvet.com
b. 22-gauge aspiration needle within a teflon tube, Storz,
www.karlstorzvet.com
Hemorrhage is the main complication arising from
endoscopy. The kidney can be damaged during penetra-
References and (ed): Manual of Parrots, of prey and owls found injured HBD Int’l, Inc, 1999, pp 327-354.
Budgerigars and Other Psittacine and debilitated in Berlin and 10. Taylor M: Endoscopy. Proc Assoc
Recommended Reading Birds. West Sussex, UK, Brit Small Brandenburg. Veterinary Thesis, Avian Vet, 1990, pp 319-324.
Anim Vet Assoc, 1989. Free University of Berlin, Germany,
1. Lierz M, Ewringmann A, Goebel T: 4. Hochleithner M: Endoscopy. In 1999. 11. Taylor M: Endoscopic Examina-
Blood chemistry values in wild rap- Altman, et al (eds): Avian Medicine 8. McDonald SE: Endoscopic tion and Therapy of the Avian
tors and their changes after liver and Surgery. Philadelphia, WB examination. In Burr EW (ed): Gastrointestinal Tract. Sem Avian
biopsy. Berliner and Muenchener Saunders Co, 1997, pp 800-805. Companion Bird Medicine. Ames, Exotic Pet Med 8(3):110-114,
Tieraerztliche Wochenschrift, 1998, 5. Hochleithner M: Endoscopy. Proc IA, Iowa State Univ Press, 1987, pp 1999.
111, pp 295-301. Euro Conf Avian Med Surg, 1993, 166-174.
2. Baileys RE: Surgery for sexing and 12. Weber MA, et al: Benefits and
pp 162-166. 9. Taylor M: Endoscopic examination
observing gonad condition in complications of liver biopsy in
6. Kolias GV: Liver biopsy techniques and biopsy techniques. In Ritchie
birds. Auk 70:497-500, 1953. in avian clinical practice. Vet Clin BW, Harrison GJ, Harrison LR birds. Proc Assoc Avian Vet, 2001,
3. Eaton TM: Surgical sexing and North Amer 14(2):287-298, 1984. (eds): Avian Medicine: Principles pp 211-213.
diagnostic laparoscopy. In Price CJ 7. Lierz M: Investigations of birds and Application. Brentwood, TN,
25_Imaging.qxd 8/23/2005 2:22 PM Page 653
CHAPTER
25
Advances in
Diagnostic
Imaging
PETER HELMER, DVM, Dipl. ABVP-Avian
Advances in technology have resulted in many different

ways of producing and recording diagnostic images.
Conventional black and white radiographic images on
film continue to predominate, primarily due to wide-
spread access, ease of use, familiarity and relatively low
cost. Digital and computerized radiographic images are
not widely accessible in private practice. These latter
modalities produce a digital image that can be manipu-
lated with a computer to highlight detail and compen-
sate for less than ideal technique settings. Digital tech-
nology will become more affordable and more readily
available to the private practitioner in the future.
Radiographic Technique
The diagnostic value of a radiograph is directly propor-
tional to the quality of the radiograph. The small size
and fine detail of the avian patient necessitate excellent-
quality images. Multiple factors influence the quality of a
radiograph.20 These factors include motion, the speed of
the film, focal spot size, focal spot-to-film distance,
object-film distance, the use and type of intensifying
screen, and the use of a grid. No technique can maxi-
mize the benefits of all of these factors, but a reasonable
compromise can be obtained that results in radiographs
of high quality.
Motion, even in small amounts, results in significant

blurring of the image. In order to minimize this artifact,
patient restraint is required. Physical restraint of the
avian patient for radiography is rarely adequate. Proper
positioning of the awake patient is difficult. There is
Fig 25.1 | Mammography cassettea opened to reveal the single Fig 25.2 | Mammography filmb has a single-sided emulsion.
intensifying screen. When loading cassettes, the light side of the film should be in
contact with the white side of the cassette.
significant stress and risk of injury to the bird, as well as crystals makes them more likely to be exposed to x-rays
increased risk of radiation exposure for the handler. or light, thus they require a lower exposure to produce
Restraint in the form of inhalant anesthesia (isoflurane an image. However, the image will be less sharp than the
or sevoflurane) is strongly recommended. The risk of same image made on a “slower” film with smaller crys-
general anesthesia should be assessed for each patient, tals and a higher exposure. Intensifying screens are gen-
but usually this risk is far outweighed by the benefits of erally made of rare-earth crystals that fluoresce when
decreased patient stress, increased quality of the radi- struck by x-rays. Mammography cassettesa and filmb offer
ographs, less time spent by staff, less exposure to radia- an excellent combination for high-detail radiographs.
tion and fewer patient injuries. The initial cost of the screens is higher, but used screens
are often available at discounted prices through human
Respiratory motion is largely unaffected by appropriate imaging centers. Mammography film is more expensive
planes of anesthesia. Avian respiratory rates require rela- than standard radiographic film. Mammography cas-
tively short exposure times to eliminate the motion arti- settes have screens on only one side and mammography
fact. In practice, exposures of 0.01 to 0.05 seconds are film is single-sided emulsion. Proper loading of the cas-
routinely used. settes is essential. The dark side of the film faces the
dark side of the cassette and the light side faces the light
Other machine settings also influence radiograph qual-
side (Figs 25.1, 25.2). Most automatic processors can
ity. Selection of a smaller focal spot setting, if available,
routinely develop these films, though their non-standard
will result in sharper edge definition. Increases in the
size may create problems in some models. Mammo-
focal spot-to-film distance will positively affect detail;
graphy film is often still damp after the drying cycle as
however, the mAs (milliamperes seconds) or the kVp
programmed into most automatic processors. Care
(kilovolt peak) also must increase proportionately. A
should be taken to avoid damage to the developed film
compromise focal spot-to-film distance of 40 inches (100
and to provide for additional drying time. It also is
cm) is often used.
important to realize that mammography cassettes
Scatter radiation adversely affects the detail of radio- require a higher exposure setting than typical double-
graphs. This is particularly true when high-detail or mam- screened cassettes (Table 25.1). Non-screen film such as
mography screens are used. Close collimation of the pri- dental radiography film also provides excellent detail
mary beam around the areas of interest is important to and requires higher exposure settings.
decrease scatter. Birds are routinely positioned with the
film cassette on the tabletop. This decreases the object-
Table 25.1 | Technique Chart Used for Psittacines
to-film distance and maximizes detail. Grids are useful to
in the Author’s Practice Using Mammography
decrease scatter radiation when the thickness of the Cassettesa and Filmb
object being imaged is greater than 4 inches (10 cm); Time kVp
Species mA
however, few birds are thicker than this so grids are (in sec) (kilovolt peak)
rarely used. Budgerigar 300 1/10 40

Cockatiel 300 1/10 41-42
Film-screen combinations contribute significantly to Pionus/mini macaw 300 1/10 43
image quality and exposure settings. A “faster” film will Amazon/African grey 300 1/10 45
have larger silver halide crystals. The larger size of these Large cockatoo/macaw 300 1/10 48-50
Chapter 25 | A D V A N C E S I N D I A G N O S T I C I M A G I N G
655
Fig 25.4 | Routine positioning of an anesthetized bird for the

laterolateral projection.
Fig 25.3 | Routine positioning of an anes-

thetized bird for the ventrodorsal projection.
POSITIONING in these structures tend to be visible only in advanced

The principles of positioning the avian patient for radi- stages of disease. Magnetic resonance imaging (MRI) is a
ography are the same as for other species. At least two more sensitive tool for evaluation of these structures.16
views, 90° to each other, are suggested. Positioning may
The standard oblique views are left 75° ventral-right dor-
be maintained by taping the patient directly to the cas-
sal and right 75° ventral-left dorsal. The lateral view is
sette or to a radiolucent Plexiglas board. Masking tape is
obtained with the bird positioned in lateral recumbency
usually sufficient in the chemically immobilized patient
with the neck extended. Foam wedges are used to sup-
and has the advantage of not pulling out feathers when
port the skull such that the sagittal plane of the skull is
it is removed.
parallel to the film. For the ventrodorsal view, the
The basic views of the body are the laterolateral and the patient is placed in dorsal recumbency with the neck
ventrodorsal (Figs 25.3, 25.4). When assessing position- hyperextended such that the hard palate is parallel to
ing for the laterolateral view, the two femoral heads the cassette. Tape is used to secure the beak to the cas-
should overlie one another, the legs should be pulled sette. Additional views may be required on a case-by-case
caudally, the sternum should be parallel to the film and basis. Endotracheal tubes may interfere with interpreta-
the wings should be secured dorsally. In the ventrodor- tion of skull views, especially the ventrodorsal. If pathol-
sal view, the legs should be pulled caudally. Wings are ogy is suspected, the endotracheal tube can be removed
stretched and secured laterally, and the sternum should and an additional radiograph obtained.
directly overlie the vertebral column.
GASTROINTESTINAL
Standard views of the wing are the ventrodorsal (posi-
CONTRAST STUDIES
tioned as for the body) and the caudocranial view. The
Contrast studies of the upper and lower gastrointestinal
legs are evaluated with routine orthogonal lateral and
(GI) tract are often indicated based on suspicion of
anterior/posterior views.
space-occupying masses, ulceration, abnormalities in
Skull radiography is challenging due to overlap of multi- size or shape of coelomic organs, GI foreign bodies,
ple structures, and their complex relationships. In order alterations in GI motility or body wall abnormalities
to optimize interpretation of these films, lateral, ven- (Figs 25.5a-f).
trodorsal and oblique projections are suggested.15
Thirty percent weight to volume barium sulfate suspen-
Radiography of the skull is indicated for evaluation of sion is the most commonly used contrast medium.
bony structures, including identification of fractures, lux- Approximately 25 ml/kg given by gavage tube into the
ations, hyper- and hypocalcemia, and carcinoma.8 Sinuses crop is the suggested guideline. Iohexolc (240 mg
and soft tissue structures may be visualized, but changes iodine/ml) diluted 1:1 with tap water also may be used
a b c
d e
Fig 25.5| Normal barium series of a cockatiel.

f
Ventrodorsal and laterolateral images made prior to
barium administration, and at 30 and 60 minutes
postadministration. a) Plain film prior to barium
administration, ventrodorsal view. b) 30 minutes
postadministration of barium, ventrodorsal view.
c) 60 minutes postadministration of barium, ventro-
dorsal view. d) Plain film prior to barium administra-
tion, laterolateral view. e) 30 minutes postadministra-
tion of barium, laterolateral view. f) 60 minutes post-
administration of barium, laterolateral view.
at 25 to 30 ml/kg.4 approximately 3 hours, compared to approximately 1

hour with iohexol.c If barium is used, films are made at
A preliminary study comparing GI transit time of 5, 30, 60, 90, 120 and 180 minutes or possibly longer. A
psittacines restrained manually to those chemically
slightly different schedule of 1, 3, 15, 30, 60 and possi-
restrained with isoflurane revealed no significant differ-
bly 120 minutes is recommended if iohexolc is used.
ences between the two groups.11 Regardless of the type
Iohexolc also eliminates concerns of contrast material
of restraint used, great care should be taken to avoid
residue if endoscopy or surgery is indicated. If perfora-
contrast aspiration, especially in the early stages of the
study when the crop is distended. Precautions include tion is suspected or possible, iodinated contrast should
avoiding external pressure on the crop, maintaining the be used.
head in a slightly elevated position and intubation of
Retrograde or cloacally administered barium may be use-
anesthetized birds.
ful in detection of cloacal or colonic abnormalities such
The use of iohexolc results in significantly decreased GI as ulcerations or masses. Caution should be used to
transit time.4 The crop-to-cloaca transit time of barium is avoid barium entering the oviduct or ureters.
657
Ultrasound thesia is recommended for both procedures.
Ultrasonography uses the transmission and reflection of Ultrasound-guided hepatic FNA is accomplished using a
sound waves to produce an image. Organ visualization 22-gauge, 1-inch needle with a 6-inch extension set. A
in the avian patient is limited when compared to mam- study comparing FNA sampling techniques found that
malian species, as the ultrasound waves cannot pene- collecting multiple parenchymal samples with the needle
trate the gas-filled air sac system. However, there are under 0.5 ml of suction produced the most high quality
several applications for use of ultrasonography in the hepatic cells with the least hemodilution14. In this study
avian patient. of 27 normal Amazon parrots, no morbidity or mortality
was associated with hepatic FNA. Percutaneous ultra-
Due to the small size of most birds and the limited win- sound-guided hepatic biopsies may be obtained using a
dows of accessibility, the ultrasound transducer must 20-gauge Trucut needle. The depth of the biopsy will vary
have a small contact area or footprint. Sector transduc- with the size of the bird.
ers, producing a wedge-shaped image, are appropriate
as they tend to be smaller than linear transducers and Echocardiography in the avian patient is in its early
allow good maneuverability. Their disadvantage is a stages.9 The heart is usually visualized cranial to the liver
smaller field of view compared to a linear transducer. via the cranioventral acoustic window. Standardized
This is of minimal consequence when dealing with the imaging planes and chamber sizes have yet to be estab-
small avian patient. A transducer frequency of 7.5 MHz lished. Endocarditis, pericardial effusion, valvular insuffi-
or higher is recommended.9 ciency and cardiomyopathies may be diagnosed using
mammalian criteria as a guide (see Chapter 12,
There are three acoustic windows to the coelomic vis- Evaluating and Treating the Cardiovascular System).
cera of the avian patient: (1) the cranioventral approach,
on midline just caudal to the sternum; (2) the caudoven- The normal kidneys are not visible during ultrasound
tral approach, between the pubic bones; and (3) the lat- examination due to their anatomic position within bony
eral approach, in the flank area directly behind the last depressions of the pelvis and the surrounding abdomi-
rib on each side. Based on the size of the bird and the nal air sacs. Nephromegaly may be detected if the kid-
size of the transducer, not all of these windows may be neys extend beyond normal landmarks, as described in
accessible in each patient. radiographs discussed above, and can be characterized
as focal or diffuse. Ultrasound-guided renal biopsy has
While not always necessary, patients ideally should be
not been reported.
fasted for 2 to 4 hours prior to examination. Food and
gas within the gastrointestinal tract may impede visuali- Inactive gonads are not generally identified on ultra-
zation of other organs. Birds are restrained in dorsal sonographic examination. Active or enlarged gonadal tis-
recumbency, with the head and cranial coelom elevated sue can be evaluated with ultrasound. In the male, testes
with a 30° foam wedge to assist in visualization. Feathers enlarged due to seasonal, neoplastic or inflammatory
are either parted or plucked and wetted with a small conditions may be identified. A study of the normal
amount of isopropyl alcohol. Acoustic coupling gel is sonographic appearance of the reproductive tract of 52
applied to the skin to provide adequate contact between hens of various species identified 17 of 34 (50%) active
the transducer and the skin. In the non-pathologic state, ovaries, all in hens greater than 70 g body weight.9
liver, heart and active gonads (usually the ovaries) are Active ovaries were characterized by the presence of fol-
distinguishable. Spleen, normal kidneys and inactive licles in various states of development. Follicles are ini-
gonads are difficult to identify.9 tially round with indistinct anechoic or hypoechoic
inner structure. As development advances, the more
The indications for ultrasound include investigation of
echogenic yolk is visualized. The ovarian parenchyma,
superficial soft tissue masses, hepatomegaly, cardiac dis-
identified between follicles, has higher echogenicity and
ease, renomegaly, disorders of the reproductive tract and
identification of ascites. a non-homogeneous appearance due to the presence of
rudimentary follicles. As ova progress through the mag-
Hepatomegaly is commonly diagnosed with conven- num, they exhibit distinct separation of echogenic yolk
tional radiography. The normal liver should not extend surrounded by anechoic albumen. The hyperechoic shell
caudal to the sternum and has a characteristic coarse, is added in the uterus and is easily distinguishable. The
homogeneous echotexture similar to the mammalian shell prevents further examination of the inner struc-
liver.9 Hepatic disease can be focal or diffuse. The abnor- tures of the egg. Cysts of the ovary are visualized as
mal areas may be sampled by fine needle aspiration clearly defined, rounded, anechoic structures within the
(FNA) or biopsy for definitive diagnosis. General anes- parenchyma. Cysts may occur singly or in multiples.
658
Ultrasonographic examination is particularly valuable in

cases of suspected egg binding. Thin-shelled, non-
shelled, malformed and fully shelled eggs can be identi-
fied. Mineralized eggs are visible as round to oval struc-
tures of varying echogenicities resembling onion layers.
They are surrounded by anechoic to hypoechoic fluid.
Concurrent salpingitis should be suspected when oviduct
walls appear thickened. The inflammatory exudate in the
lumen of the oviduct may be anechoic to hypoechoic
(see Chapter 18, Evaluating and Treating the Reproduc- G
tive System).
Computed Tomography Fig 25.6 | Computed tomography image of a transverse slice

through the coelom of an Amazon parrot at the level of the
Computed tomography (CT) is a cross-sectional imaging lungs. The right lung is normal. The normal architecture of the
modality that uses x-rays to create a digital image or slice left lung is replaced by a cystic mass that was diagnosed as a
foreign-body-associated granuloma (G) on histopathologic
(Fig 25.6). that can be reformatted into additional planes
examination. The heart, keel and normal pectoral musculature
of view.2 Image densities are similar to conventional radi- are visible toward the top of the image.
ographs. The cross-sectional image eliminates overlying
structures so objects of interest are more accurately visu-
alized. CT is best suited for evaluation of bone and air- Advances in the technology of MRI have decreased the
filled structures. Soft tissue resolution is inferior to MRI time required for image acquisition, though general anes-
(see below). Reports of the use of CT include examina- thesia is routinely required. MRI studies usually take a
tion of the skull, sinuses and the lower respiratory longer period of time to preform than CT studies. The
tract.1,6,8,10 Machines vary in acquisition time and width of decreasing cost and increasing availability of this imaging
slice. Typically, the study can be performed in less than modality will increase its usefulness in avian diagnostics.
10 minutes. General anesthesia is required for the study.
Myelography
Magnetic Resonance
Techniques for myelography in avian patients have been
Imaging described.5 Indications include evaluation of the spinal
cord for compressive, traumatic or space-occupying
A review of the physics of magnetic resonance imaging
lesions. MRI should be strongly considered as an alterna-
(MRI) is beyond the scope of this chapter. Simplistically,
tive if feasible. In larger patients (1 kg and greater), a 25-
a strong external magnetic force is used to align certain
gauge needle is placed at the thoraco-synsacral junction
atoms within the body about a desired axis. The field is
and 0.8 to 1.2 ml/kg of non-ionic iodinated contrast
then turned off and the unit senses energy released as
medium is injected into the subarachnoid space (see
atoms return to their resting state.2 The image produced
Chapter 17, Evaluating and Treating the Nervous System).
is cross-sectional.
MRI is particularly useful for imaging soft tissue struc-

tures including the brain, spinal cord, coelomic organs Excretory Urography
and the upper respiratory tract. This MRI modality has
been evaluated in the diagnosis and management of Excretory urography (EU) is indicated for identification
chronic sinusitis in psittacines.16,17 In contrast to conven- of renal mass lesions, ureteral obstruction and abnor-
tional skull radiography, where identification of disease malities in renal excretion. The use of sodium diatri-
was limited to osseous changes or changes in pneumati- zoate (680 mg I/kg), iothalamate sodium (800 mg I/kg),
zation, MRI was successful in the identification of and meglumine diatrizoate (800 mg I/kg) has been
caseous plugs, granulomas, a mucocele and a polyp.16 reported without adverse effects.12 Contrast agents are
The accurate localization of these lesions within the warmed to body temperature prior to intravenous
sinuses permitted the planning of an optimal surgical administration, and radiographs are made at 1, 2, 5, 10
approach and drain placement for treatment. and 20 minutes. The technique has been described in
659
further detail.12 The absence of a renal pelvis and physio- Products Mentioned in the Text
logic variations in avian renal function limit the useful- a. Microvision Detail mammography cassette, Agfa, Greenville, SC, USA
b. Microvision Ci, Agfa, Greenville, SC, USA
ness of this procedure in birds. See Chapter 16, c. Iohexol, Omnipaque®, Amersham Health, 1-800-654-0118
Evaluating and Treating the Kidneys for further consider-
ations and alternate contrast agent doses.
References and Radiol Ultrasound 38(3):187-192,

1997.
ology and computed tomography.
Vet Radiol Ultrasound 34(3):382-
Application. Vet Radiol 31(4):218-
224, 1990.
Suggested Reading 6. Jenkins JR: Use of computed 390, 1993. 16. Pye GW, et al: Magnetic resonance
tomography (CT) in pet bird 11. Lennox AM, Crosta L, Buerkle M: imaging in psittacine birds with
1. Antinoff N, et al: Correlation
practice. Proc Assoc Avian Vet, The effects of isoflurane anesthe- chronic sinusitis. J Avian Med
between computed tomography
1991, pp 276-279. sia on gastrointestinal transit Surg 14(4):243-256, 2000.
and anatomy of the psittacine
7. Krautwald-Junghanns ME: Avian time. Proc Assoc Avian Vet, 2002. 17. Romagnano A, et al: Magnetic res-
sinus. Proc Assoc Avian Vet, 1996,
imaging. Proc 4th Europ Coll 12. McMillan MC: Imaging tech- onance imaging of the avian brain
pp 367-368.
Avian Medi Surg, 2001, pp 343- niques. In Ritchie BW, Harrison and abdominal cavity. Proc Assoc
2. Berry CR: Physical principles of
353. GJ, Harrison LR (eds): Avian Avian Vet, 1995, pp 307-309.
computed tomography and mag-
8. Krautwald-Junghanns ME, Kostka Medicine: Principles and Practice. 18. Rosenthal K, et al: Ultrasono-
netic resonance imaging. In Thrall
VM, Dorsch B: Comparative stud- Delray Beach, FL, HBD graphic findings in 30 cases of
DE (ed): Textbook of Veterinary
ies on the diagnostic value of International Inc, 1999, pp 246- avian coelomic disease. Proc
Diagnostic Radiology 4th ed.
conventional radiography and 326. Assoc Avian Vet, 1995, p 1.
Philadelphia, WB Saunders Co,
computed tomography in evaluat- 13. Newell SM: Radiology for the 19. Rosenthal K, et al: Computerized
2002, pp 28-35.
ing the heads of psittacine and avian patient/Y2K and beyond. tomography in 10 cases of
3. Drost WT: Basic ultrasound
raptorial birds. J Avian Med Surg Proc Assoc Avian Vet, 2000, pp intracranial disease. Proc Assoc
physics. In Thrall DE (ed):
12(3):149-157, 1998. 421-424. Avian Vet, 1995, p 1.
Textbook of Veterinary Diagnostic
9. Krautwald-Junghanns ME, Riedei 14. Nordberg C, et al: Ultrasound 20. Thrall DE, Widmer WR: Radiation
Radiology 4th ed. Philadelphia, WB
U, Neumann W: Diagnostic use of examination and guided fine-nee- physics, radiation protection, and
Saunders Co, 2002, pp 20-28.
ultrasonography in birds. Proc dle aspiration of the liver in darkroom theory. In Thrall DE
4. Ernst SE, et al: Comparison of
Assoc Avian Vet, 1991, pp 269- Amazon parrots (Amazona (ed): Textbook of Veterinary
iohexol and barium sulfate as gas-
275. species). J Avian Med Surg Diagnostic Radiology 4th ed.
trointestinal contrast media in mid-
10. Krautwald-Junghanns ME, 14(3):180-184, 2000. Philadelphia, WB Saunders Co,
sized psittacine birds. J Avian Med
Schumacher F, Tellhelm B: 15. Paul-Murphy JR, et al: Psittacine 2002, pp 1-19.
Surg 12(1):16-20, 1998.
Evaluation of the lower respira- skull radiography: Anatomy,
5. Harr KE, et al: A myelographic
tory tract in psittacines using radi- Radiographic Technic and Patient
technique for avian species. Vet
26_Necropsy.qxd 8/23/2005 2:32 PM Page 661
CHAPTER
26
Diagnostic Value of
Necropsy
MADELINE A. RAE, BS, DVM, MS, D ipl ABVP-A vian
Gross necropsy and postmortem diagnostic testing are

important parts of avian medicine, requiring a systematic
approach to the examination of organs and the collec-
tion of samples.
Necropsy examination functions as more than a way to

satisfy the curiosity of the client, breeder or attending
veterinarian — it provides important information that
can be used in the diagnosis and treatment of future
cases. Clinical signs and clinical pathologic findings are
often not definitively explained until necropsy.
Postmortem information can be invaluable in educating

clients regarding the seriousness of husbandry, nutri-
tional and infectious disease conditions, thereby pre-
venting them from making the same mistakes with sub-
sequent birds. For grieving owners, necropsy findings
can relieve them of some or all of the guilt associated
with the death of a beloved pet.
Necropsy findings are an integral part of the flock data-

base from which husbandry, management, treatment,
vaccination and quarantine recommendations can be
made.
In situations where the client may be dissatisfied with

treatment or outcomes, it is wise to have a veterinary
pathologist perform the necropsy. Developing a relation-
ship with a veterinary pathologist is also highly recom-
mended so that appropriate samples are submitted, opti-
mizing the chances of arriving at a diagnosis. The veteri-
nary pathologist should have training, experience and
interest in companion and free-ranging birds.
Preparing for the Necropsy METHOD OF EUTHANASIA

In some instances, it may be appropriate to euthanize a
The supplies needed for an avian necropsy are listed in sick bird in order to diagnose a flock problem. The
Table 26.1. Although bottles or jars of neutral buffered method of euthanasia is important to consider because
10% formalin should be available for the collection of many injectable agents can cause severe artifacts in tis-
specimens for histopathology, some cautions are in sues. If at all possible, barbiturates should not be
order. Ensure that formalin fumes do not contact tissues injected into the coelomic cavity, thoracic cavity or heart.
that are to be cultured for bacteria or viruses, as this can The barbiturates are very acidic and crystals readily pre-
compromise the culture accuracy. Make certain that for- cipitate, causing severe tissue destruction that may
malin fumes do not come in contact with blood or tissue obscure gross and histologic lesions. Even intravenous
cytological smears, as this can severely distort staining barbiturate solutions can cause intravascular erythrocyte
and interpretation. lysis and some tissue damage as the solution pools
within blood-filled organs.
A standardized necropsy form should be used and diag-
nostic specimen accession forms and instructions should Gas anesthetic agents seem to provide the least amount
be readily located. All specimen containers should be of tissue artifact (less muscle contraction artifact, no cell
clearly labeled with the appropriate information. A lysis). Once the gas agents anesthetize the bird, there is
refrigerator, a freezer, insulated shipping containers and the opportunity to collect antemortem blood samples
coolant packs should be available for appropriate han- for hematology, serum chemistries, hemoparasite detec-
dling and shipping of specimens. After the necropsy has tion, serology and toxicology. The gas anesthetic agents
been performed, the carcass can be frozen and saved for can then be followed with intravenous euthanasia
a period of time, as frozen tissues may be useful if initial agents, if needed, and the amount of injectable agent
testing is inconclusive. Have arrangements in place for necessary is usually quite reduced.
appropriate disposal of carcasses and infectious wastes.
PREPARING THE BODY

Table 26.1 | Supplies Needed for Avian Necropsy The necropsy should be performed as soon after death
• Gram scale as is possible. In order to prevent dry feathers from insu-
• Apron lating the body and delaying cooling, wet the feathers
• Mask
with a detergent and water solution. The detergent and
• Gloves
• Disinfectant water also decreases the dispersal of feather and fecal
• Necropsy checklist dust into the local environment, thereby decreasing the
• Scalpel handle and blades transmission of infectious agents.
• Scissors*
• Thumb forceps*
The body should be refrigerated, not frozen. Freezing
• Small rongeurs or toenail nippers for brain removal and
bone cutting
can create artifacts in the tissues that may seriously
• Ophthalmic scissors and forceps for small passerines, obscure histologic lesions. Postmortem autolysis also can
neonate and dead-in-shell obscure histologic lesions, so if necropsy cannot be per-
• Sturdy paper plates and/or plastic cutting board formed within 3 days, the body should be frozen, realiz-
• Microscope slides and coverslips
ing that histopathology is likely to be compromised.
• Blood and fluid collection tubes
• Sterile saline
• Sterile culturettes (aerobic and anaerobic) When shipping a cooled body, be sure the ice packs (or
• Sterile cotton-tipped applicators other frozen coolants) do not directly touch the body as
• Magnifying head loupe this may freeze the body tissues, especially in very small
• Good light source
birds. Wrap the ice packs in bubble wrap or newspaper
• Sterile sealable plastic bags or sterile plastic vials for
sample collection
to prevent freeze damage.
• Plastic screw-top jars containing 10% neutral buffered
formalin
• Sterile syringes and needles
GUIDELINES FOR OBTAINING
• Stains (Gram’s, Wright’s, Giemsa or Diff-Quik, acid-fast)
THE HISTORY
• Butane lighter or other heat source to heat-fix smears A detailed history should be obtained, just as the clini-
for acid-fast staining
cian would do upon seeing a live bird for the first time in
*Autoclave one set of scissors and forceps for collecting samples the examination room (Table 26.2) (see also Chapter 6,
aseptically.
Maximizing Information from the Physical Examination).
Chapter 26 | D I A G N O S T I C V A L U E O F N E C R O P S Y
663
Table 26.2 | Considerations for Obtaining History Information
• Start with the age of the bird and sex, in appetite and/or droppings. • How many other birds are in the home
if known. Breeders are often very inter- • How is water provided and how often or aviary and how many have died in
ested in having the sex of the dead bird is it changed? the last year? Are any other birds in
confirmed at necropsy. If the dead bird • Have feeding practices or the diet the household or aviary ill? Was the
is from a pair that is known to have changed recently? deceased bird in quarantine? Are any
produced fertile eggs, the knowledge • If this is a chick that is being hand-fed, humans in contact with the ill birds?
of the mate can be deduced from the obtain a detailed description of the • Have there been any recent changes in
confirmation of the dead bird’s sex. The feeding practices, brand of food with environmental conditions such as tem-
breeder then knows which sex of bird amounts and times per day, as well as perature changes?
to replace in the pair. any charts documenting weight loss • Have there been recent additions to
• Determine what the bird’s purpose is, or gain. the aviary or household?
whether it is a dear pet, a display bird • Is the bird allowed to fly freely within • Ask about the reproductive history of
or a breeder bird. the house? the bird, such as a recent history of
• It is important to obtain a detailed • Ask for a description of the cage and egg laying, dystocia or feeding of
description of the diet fed, and for how its placement within the house (eg, chicks.
long, including any supplements and near the kitchen where exposure to • Obtain a description of recent clinical
grit, brands used and their storage. toxic fumes may occur). signs noticed prior to death and their
Keeping a stored sample frozen in an • Is bedding material used and how duration.
airtight container may be useful. often is the cage cleaned? What • Ask about any other previous illnesses
Quality control by the manufacturer products are used for cleaning? or conditions. Were any medications or
and storage of formulated diets can be • Are there toys in the cage and does or treatments given to the bird? Be sure to
a problem. The resulting products may can the bird chew on them? ask about prescription medications as
be over-formulated or rancid, resulting • If this bird is from an aviary, a descrip- well as over-the-counter preparations.
in toxic levels over time. tion of the aviary and floor plan can be
• Determine if there have been changes very helpful.
PREVENTING CONTAMINATION It is important to collect samples of everything (all

Perform the necropsy in a well-lighted, well-ventilated organs, the grossly normal and abnormal). Labeling
area (preferably under a fume hood), and wear gloves, a sealable bags and formalin jars prior to the necropsy
mask and, if possible, a disposable apron. Aerosols from with the owner’s name and the tissues enclosed can
feathers, feces and exudates can be infectious. This is save time and prevent interruptions in the flow of the
particularly important with cases of chlamydophilosis necropsy.
and mycobacteriosis, which can be zoonotic. However, it
After the necropsy is completed, the decision of which
also is important to contain the feather dander and feces
samples to send and what tests to request can be made,
in cases of avian polyomavirus and psittacine circovirus
infections, so as not to contaminate the premises, your and at the very least, the diagnosis will not be cremated
clothing or other adjacent birds. with the carcass.
Disinfectant solutions should be readily available for

EXTERNAL EXAMINATION
clean-up after the necropsy, but neither these solutions
nor their fumes should come in contact with tissues The necropsy begins with an external examination.
being collected, as they may lyse cells and destroy Record the band number and scan for microchips; these
microorganisms needed for culture. can be removed, labeled and saved as proof of identifica-
tion. Weigh the bird using a gram scale and record the
weight on the checklist. Palpate for obvious fractures;
radiographs may be warranted in some instances.
Step-by-Step
Necropsy Procedure Examine the skin and feathers: often, feather abnormali-
ties may not be visible while the feather remains in the
The particular routine used for gross necropsy of birds follicle. For example, the concentric pinching of the
can vary, but what remains the same is that all organs feather shaft, seen in psittacine circovirus infection, may
and systems are examined, and the use of a checklist will not be visualized until the feather is plucked from the fol-
ensure this. Use the Necropsy Checklist (Table 26.3) to licle. Look for stress bars in the wing and tail primaries
document all findings, both normal and abnormal. Make (Fig 26.1). Collect multiple blood feathers, both plucked
this checklist a part of the medical record and send a and in the follicle, along with any skin lesions (Fig 26.2)
copy to the veterinary pathologist with any fixed tissues. and place them in formalin. Check for any signs of
Table 26.3 | Necropsy Checklist

Owner’s Name Date of Necropsy
Animal’s Name Date of Death
Species Euthanasia Method
Age Sex Body Weight at Necropsy
Band/Microchip # Tattoo?
Organ(s) Normal Abnormal Description

Skin/Feathers
Beak/Oral Cavity/Tongue
Eyes/Ears/Conjunctivae
Sinuses/Choana/Nasal Cavity
Skeletal muscle/Bones/Joints
Liver/Gall Bladder, if present
Spleen
Thyroids/Parathyroids
Trachea/Lungs/Airsacs
Kidneys/Adrenals
Testes/Ovary/Oviduct
Crop/Esophagus
Proventriculus/Ventriculus
Duodenum/Pancreas
Jejunum/Ileum/Ceca, if present
Colon/Cloaca
Bursa/Thymus
Brain/Meninges
Spinal Cord/Vertebrae/Nerves
Bone/bone marrow
Middle & inner ear
Heart/Great Vessels
Gut contents wet mount results:
Gut contents dried smear results:
Organ impression smear results:
Tissues in formalin:
Tissues frozen:
trauma or bruising. In neonates, closely examine the debris or exudate. Examine the conjunctivae and the
umbilicus for cleanliness and the adequacy of healing. nictitating membranes. In Columbiformes, these tissues
can be collected for Chlamydophila diagnostics, as they
Examine the unfeathered portions of the legs and the may contain elementary bodies.
feet for poxvirus lesions, bumblefoot, herpesvirus podo-
dermatitis and self-mutilation (Figs 26.3, 26.4). Examine The infraorbital sinuses should be opened as aseptically
the uropygial gland, found at the base of the tail in some as possible, and swabs or aspirates collected for cytology
species, and collect it for histopathologic evaluation, as and culture of bacteria, Mycoplasma and fungi (Figs
this can be a site of chronic inflammation and neoplasia. 26.7, 26.8). Bacterial sinusitis is quite common in
psittacines, but also occurs in passerine species, and
Evaluate the beak, both the external and the intraoral sur- caseous exudate is often seen (Fig 26.9).
faces (Fig 26.5). Open the mouth. Look at and under the
tongue for abnormalities. Look in the choanal slit for In cockatiels (Nymphicus hollandicus) with “lockjaw,”
mucus and exudate and for blunting of the choanal papil- sinusitis and temporomandibulitis are common, as well
lae (Fig 26.6). Salivary gland enlargement can occur at the as myositis of the mandibular muscles. The mandible
base of the tongue and can be due to hypovitaminosis A, and its attached muscles can be placed in formalin for
bacterial abscesses or, rarely, mycobacterial infections. histopathology. In these cases, bacteria such as Borde-
tella avium, Enterococcus, Escherichia coli and Entero-
The nares and ear canals should be clear and free of bacter may be isolated. It is important to indicate to the
665
Fig 26.1 | Dystrophic feathers from a sulfur-crested cockatoo

(Cacatua galerita) infected with psittacine circovirus. Note the
concentric pinching of the feather shafts.
Fig 26.2 | Dermal lymphosarcoma in a western screech owl

(Otus kennicottii).
Fig 26.3 | Cutaneous pox lesions of the feet in a red-tailed

hawk (Buteo jamaicensis).
Fig 26.4 | Avascular necrosis of the distal toes of a black- Fig 26.5 | Cutaneous pox involving the commissures of the
crowned night heron (Nycticorax nycticorax). mouth in a red-tailed hawk.
bacteriology laboratory that B. avium is suspected in formalin, decalcified if needed, and examined histo-
because this organism is somewhat fastidious and logically. Sometimes the nasal cavity epithelium may be
colonies may take longer to appear. Bordetella avium the only site of viral inclusions diagnostic for canarypox.
also may cause tracheitis, bronchitis and pneumonia in Cryptosporidial rhinitis and conjunctivitis also can be
cockatiels and rarely in other psittacines. diagnosed with this method.
Several Mycoplasma species have been implicated in

conjunctivitis and sinusitis in psittacines and passerines, COELOMIC CAVITY
but these require special media for isolation and are The coelomic cavity examination is begun by placing the
recovered uncommonly. In small passerines, cross- body in dorsal recumbency, incising the skin of the
sections of the nasal cavity and sinuses can be submitted abdomen and peeling it back caudally over the abdomen
Fig 26.6 | Normal choanal slit of a blue- Fig 26.7 | View of the avian skull with the Fig 26.8 | View of the infraorbital sinuses
fronted Amazon parrot (Amazona aestiva). lateral wall of the infraorbital sinuses cut in a blue-fronted Amazon parrot with the
Choanal slit (A), caudal palate containing away in a blue-fronted Amazon parrot. lateral wall removed. Infraorbital sinuses
salivary glands (B), choanal papillae (P), Exudate may accumulate in the temporo- (IS), zygomatic or jugal arch (Z).
palatine beak (C). mandibular joint (TMJ), especially in cock-
atiels. Ear (E).
and cranially over the pectoral muscle mass. Assess the

condition of the pectoral muscle, as this is a good meas-
ure of weight loss (Fig 26.10). Notice whether subcuta-
neous fat is present or absent and whether there is any
bruising or edema. Grasp the sternum with thumb for-
ceps and slightly elevate, maintaining tension on the
abdominal wall. Make a transverse incision with the
scalpel blade just caudal to the edge of sternum, being
careful not to lacerate the liver. Remove the keel and
pectoral muscles in one piece by cutting through the
ribs and shoulder girdle with scissors or rongeurs.
Liver and Spleen

Fig 26.9 | Spirochetes in a wet mount of exudate from the
Assess the size, color and consistency of the liver. Hepatic infraorbital sinuses of a cockatiel chick (Nymphicus hollandicus),
photographed under phase contrast.
margins should be sharp and not extend beyond the
caudal edge of the keel in an adult bird (Figs 26.11-
26.13). Note whether a gall bladder is present or absent,
as not all species have one. Assess the condition of the triculus and the ventriculus (Fig 26.14). Evaluate the size
air sacs and coelomic surfaces that are visible. If and shape of the spleen. Determining whether it is of
coelomic fluid is present, collect it with a sterile syringe normal size for the bird being necropsied requires some
for analysis. Aseptically collect samples of air sacs next, practice, so measuring the diameter can be helpful. The
since they are delicate structures that readily disappear spleen is round in some species, such as Psittaciformes
with further manipulation of the organs. Aseptically col- and Galliformes, and elongated or sock-like in Passeri-
lect liver samples: one sample each for bacteriology, formes and Columbiformes. Note the color and the pres-
virus isolation or DNA probe testing, Chlamydophila ence of any pale foci in the spleen. Collect the entire
testing and histopathology, and use any remaining tissue
spleen, dividing it into three samples: one for virology,
for toxicology and/or impression smears.
one for Chlamydophila diagnostics and one for histo-
Grasp the ventriculus, elevate and incise through the pathology. The spleen is the single most important sam-
attached membrane/air sac along the left margin and ple for the histopathologic diagnosis of avian polyoma-
rotate the ventriculus counterclockwise to find the spleen. virus infection, since this is where viral inclusions are
The spleen is nestled in the curve between the proven- most abundant.
667
Fig 26.10 | View of the normal pectoral Fig 26.11 | The liver extends beyond the Fig 26.12 | Marked hepatomegaly in a
muscles of a blue-fronted Amazon parrot caudal edge of the keel, indicating hepato- Lady Gouldian finch (Chloebia gouldiae). In
following removal of the skin. Crop (C). megaly in this mature red-tailed hawk with this case, the hepatomegaly was due to lym-
multiple mycobacterial granulomas in the phosarcoma, but a number of diseases can
liver. cause marked hepatomegaly in passerines.
Fig 26.13 | Cholangiocarcinoma in an Amazon parrot Fig 26.14 | Normal spleen in a blue-fronted Amazon parrot.
(Amazona sp.). This tumor can have a very pleomorphic gross Spleen (S), liver (L), proventriculus (P), ventriculus (V).
appearance. Heart (H).
Genitourinary black) in some species, most notably cockatoos. Note

Reflect the ventriculus and the intestinal tract to the right the degree of development of the ovary and oviduct. Is
side of the bird to view the adrenals, gonads and kidneys, there follicular development? If so, record the general
leaving the unopened gastrointestinal tract for last to size of the follicles. Is the oviduct hypertrophied?
avoid contamination of the other abdominal organs. The
adrenals are often obscured by active gonadal tissue, so it Open the oviduct to look for exudate and tumors, and
is easier to collect the cranial division of the kidney with collect samples for bacteriology and histopathology as
the adrenal and gonad(s) attached for histopathology. needed. Neoplasms of the oviduct may occur in the
Adrenalitis is sometimes noted in unexplained death and mucosa or myometrium. Testicular tumors are common
may be the only abnormality in some psittacines with in budgerigars (Melopsittacus undulatus) and ducks (Fig
proventricular dilatation disease (PDD).
26.15), but seasonal testicular enlargement also occurs.
Sex the bird visually. In most species, only the left ovary In some species, such as in many passerines, this enlarge-
and oviduct develop in females, but both testes develop ment can be mistaken for neoplasia; histopathology can
in male birds. The gonads may be pigmented (brown or usually distinguish between these two changes.
Fig 26.15 | Seminoma of the testes in a mallard duck Fig 26.16 | Dissection displaying kidneys, reproductive
(Anas platyrhynchos). structures and lung from a normal blue-fronted Amazon
parrot. Lung (L), ovary, immature (O), cranial division (Cr),
middle division (M) caudal division (Ca) of the kidney,
salpinx or oviduct (S).
The kidneys are nestled in the renal fossae of the syn-

sacrum, with the lumbosacral plexus lying deep to the
caudal divisions of the kidney bilaterally (Fig 26.16). The
ureters run down the ventral surface of the kidneys. In
addition to the kidney/adrenal/gonad tissue collected as
described above for histopathology, aseptically collect
additional renal samples for virology, toxicology and bac-
teriology (if exudate is present).
In small birds (under 30 g), one can make an en bloc

excision of the kidneys still in situ within the synsacrum
and place this in formalin. After fixation, renal dissection
is easier and/or the synsacrum can be decalcified and
cross-sections of kidney together with bone can be cut.
After removal of the kidneys, evaluate the lumbosacral Fig 26.17 | View of the thoracic inlet, thorax and cranial
plexus, especially in cases of pelvic limb weakness or abdomen following removal of the keel and pectoral mus-
malfunction. Samples of these nerves can be collected in cles of a blue-fronted Amazon parrot. Thyroids (Th) are
located cranial to the heart on either side of the trachea
formalin for histopathologic evaluation.
(Tr), close to the carotid arteries. The parathyroids are
located at the caudal margin of the thyroids and are barely
visible in normal birds.
THORACIC INLET
Move to the thoracic inlet region. Identify the thyroids
and parathyroids, located cranial to the heart and adja-
ered. Parathyroid hypertrophy is usually the only gross
cent to the carotid arteries bilaterally, and collect them
pathologic lesion found in the hypocalcemia syndrome
for histopathology (Fig 26.17). Goitrous changes were
of African grey parrots (Psittacus erithacus).
once quite common in budgerigars, but are less so with
the advent of commercial diets. Hyperplastic goiter has
In young birds, multiple pale lobules of thymic tissue
been reported in juvenile macaws recently, but the cause
can be found along the cervical region, from the jaw to
is currently unknown. Lymphocytic thyroiditis also may
the thoracic inlet (Figs 26.18, 26.19). Thymic tissue can
be seen histologically, especially in Amazon parrots
be collected for virology and histopathology. Thymomas
(Amazona spp.). Thyroid tumors are uncommon, but
occasionally are seen as circumscribed, fairly encapsu-
seem to be observed most often in cockatiels, where
they tend to be very vascular. lated masses; they tend to be slow growing, undergoing
cystic degeneration with large areas of hemorrhage.
Normal parathyroids are barely visible. When they are Thymic tissue is usually quite difficult to detect in adult
prominent, metabolic bone disease should be consid- birds.
669
Fig 26.18 | Left lateral view of

the neck of a normal young blue-
fronted Amazon parrot revealing
multiple lobules of thymic tissue
along its entire length from the jaw Fig 26.19 | Right lateral view of the neck Fig 26.20 | Visceral gout in a red-tailed hawk
to the thoracic inlet. Thymus (Th), of a young blue-fronted Amazon parrot with severe deposition of urates in the pericar-
crop (Cr). revealing multiple lobules of thymic tissue dial sac and in the perihepatic membranes. This
along its entire length from the jaw to the is a very important gross lesion for the practi-
thoracic inlet. Thymus (Th), trachea (Tr). tioner to recognize, because the urates may dis-
solve out of the tissue when placed in formalin.
A smear of the white material can be examined
under polarized light to reveal the typical urate
crystal structure. Trachea (T), liver (L), heart (H).
Cardiac Cardiomyopathy, usually the dilative form, can occur in

birds. The cause of the cardiomyopathy is often obscure
Examine the heart, pericardium and great vessels.
Visceral gout can cause the deposition of white, mucoid by the time it becomes a clinical problem, but myocar-
urate material in the pericardial sac (Fig 26.20). View a dial degeneration and fibrosis are often seen histologi-
smear of this material under polarized light to confirm cally. After removing the heart and great vessels, open
the presence of uric acid crystals. It is very important to the heart in the direction of blood flow, using water to
recognize the gross appearance of visceral gout, because rinse away blood and clots. (See Chapter 12, Evaluating
formalin fixation may dissolve the uric acid crystals and and Treating the Cardiovascular System for measure-
they may not be visible on histopathology (crystals do ments of the heart). Look for thrombi, valvular endo-
not dissolve if fixed in ethanol, but this is usually not a carditis lesions and pale areas in the myocardium.
practical fixative for other reasons). Congenital cardiac anomalies are rarely diagnosed.
Suppurative pericarditis can be caused by a variety of Open the great vessels to look for atherosclerosis, which
bacteria such as Pasteurella and Chlamydophila. may involve the aorta, pulmonary artery or carotids.
Cytologic examination of the pericardial exudate may Atherosclerosis is characterized grossly by yellowish,
reveal the causative organisms. Portions of the pericar- raised, intimal plaques, but occasionally may be so
dial sac can be included in the tissues used for Chlamy- severe that the carotids are completely obstructed.
dophila diagnostics. Hydropericardium is a common Mineralization of the great vessels also may occur in
finding in avian polyomavirus infection in juvenile association with atherosclerosis or may be related to
psittacines. renal disease and hypervitaminosis D.
Prior to removing the heart from the thoracic cavity, heart Atherosclerosis is most commonly seen in African grey
blood can be collected using a sterile syringe and needle parrots, where it can be mild to moderate, but also in
for bacteriology. Smears of heart blood can be stained obese, older Amazon parrots, older macaw species (Ara
with Wright’s stain and examined for hemoprotozoa and spp.) and captive raptors, where it can be so severe that
microfilaria, or Gram’s stained to look for bacteria. it results in acute death (Fig 26.21). Atherosclerotic
ORAL CAVITY AND

GASTROINTESTINAL TRACT
Cutting through the mandible at one of the lateral com-
missures allows access to the caudal pharynx and visuali-
zation of the glottis (Figs 26.22, 26.23). The larynx and
trachea can then be opened down to the tracheal bifur-
cation, looking for hemorrhage, exudate, foreign bodies,
granulomas, and parasites such as respiratory mites or
Syngamus nematodes. Laryngeal papillomatosis can
occur in the pharynx and may occlude the glottis
(Fig 26.24).
Tissue samples should be collected for histopathology

and virus isolation, as well as bacteriology and fungal
Fig 26.21 | Atherosclerotic plaques on the luminal surfaces of
the great vessels of the heart in an Amazon parrot (Amazona culture if warranted. Fungal tracheitis, especially at the
sp.). Note the smooth, glistening luminal surfaces of the normal syrinx, can be diagnosed by cytologic examination of
heart on the left. exudate or granulomatous material, fungal culture
and/or by histopathology. Rarely, mycobacterial organ-
lesions also may be found in the coronary arteries, but isms can cause syringeal granulomas.
usually these lesions are discovered upon histopathologic
examination. Atherosclerosis is a commonly missed diag- In canaries, Enterococcus faecalis can cause chronic
nosis because the vessels are not opened and examined. tracheobronchitis; culture of the tracheal lumen is nec-
essary for diagnosis. Viral tracheitis is rare in psittacine
It is best to place most of the heart in formalin so that birds, but a herpesviral tracheitis, bronchitis and airsac-
multiple sections can be cut for histopathologic evalua- culitis have been reported in Neophema parrots. Canary-
tion. Pale foci or streaks can indicate degenerative pox can produce a severe tracheobronchitis with intracy-
myopathy related to vitamin E/selenium deficiency, or toplasmic inclusions. A severe, chronic tracheobronchitis
myocarditis associated with septicemia or viral diseases can be seen with Bordetella avium in cockatiels; this
such as West Nile virus or PDD. Petechial and ecchy- organism also is often associated with the “lockjaw” syn-
motic epicardial hemorrhages are commonly seen in drome of sinusitis and temporomandibulitis.
cases of acute death from avian polyomavirus.
Esophagus and Crop

Lungs
Going back to the pharynx, the cut can extend down-
Examine the lungs in situ prior to removing them. Avian
ward the length of the esophagus and into the crop,
lungs are fixed in place within the avian thoracic cavity
looking for lacerations, punctures, peri-esophageal
and are not freely moveable. Removal requires gentle
teasing of the lung tissue away from the ribs. The avian abscesses and other abnormalities. In game birds, the
lung is one tissue in which gross lesions may appear esophagus and crop may exhibit moderate to marked
quite significant, but upon histopathologic evaluation thickening and mucus production due to capillariasis. A
turn out to be just passive congestion. Conversely, wet mount scraping from the crop can reveal the typical
grossly normal lungs may contain significant histologic bipolar capillarid ova. In juvenile psittacines, thickening
lesions. So, it is wise to always include lung for histo- and “Turkish towel” appearance of the crop mucosa is
pathology, even if it appears grossly normal. Collect a often due to candidiasis, and either a wet mount smear,
portion of the lung for bacteriology and virology and cytology or Gram’s stain of a crop mucosal scraping can
place the rest in formalin for histopathology. Because be diagnostic (Fig 26.25).
lesions can be focal or multifocal, it is best to include a
Trichomonads can be found in wet mounts from the
large portion of at least one lung for histopathology.
oral cavity and/or crop of Columbiformes and raptors,
In canaries and mynahs, a Wright’s-stained impression but also may occasionally be found in the crops of
smear of lung (along with impressions from liver and budgerigars and passerines. The crop contents can be
spleen) is very important in detecting the monocytic collected in a plastic bag and frozen, if there is any sug-
form of atoxoplasmosis, as Atoxoplasma organisms are gestion of toxin ingestion. A large section of crop, to
not usually visible on histopathology. Sarcocystis organ- include a large vessel and adjacent nerve, should be col-
isms, bacteria and fungi also can be seen in impression lected for histopathology, since PDD lesions are often
smears of the lung. closely associated with the nerves.
671
Fig 26.22 | Cutting through the mandible allows opening of Fig 26.23 | Normal glottis from a blue-fronted Amazon parrot.
the entire oral cavity and better visualization in a blue-fronted Tongue (T), glottis (G).
Amazon parrot.
The bursa is important in diagnosing psittacine cir-

covirus, especially in young African grey parrots that
die acutely without feather lesions, since the bursa may
be the only site where viral inclusions are found.
Circoviral inclusions also can be found in the bursa of
young pigeon squabs dying from a variety of secondary
infections. Lesions in the bursa are often non-specific
as to etiology, but can indicate the acuteness or
chronicity of stress.
Proventriculus and Ventriculus

Open the distal esophagus with scissors, continuing
on into the proventriculus and ventriculus. Evaluate
the stomach contents for amount and any foreign
material. Washing the contents into a bowl or strainer
can allow the food material to be rinsed away, leaving
metallic and other foreign bodies behind. Collect and
Fig 26.24 | The glottis of this Fig 26.25 | Severe crop mycosis
lilac-crowned Amazon parrot in a cockatiel chick. freeze the contents for possible toxicologic analysis.
(Amazona finschi) is occluded by Rinse the mucosa with water and make wet mount
laryngeal papillomatosis. and dried smears of mucus and/or mucosal scrapings.
Do not separate the proventriculus and ventriculus.
At this point, the esophagus distal to the crop can be
transected. Caudal traction of the distal esophagus and The isthmus (the junction between the proventriculus
sharp dissection of the mesenteric attachments can be and ventriculus) is a common site for avian gastric
utilized to remove the entire gastrointestinal tract. yeast (formerly known as megabacteria); its suggested
new name is Macrorhabdus ornithogaster (see
Bursa of Fabricius Chapter 30, Implications of Macrorhabdus in Clinical
Disorders) (Fig 26.26). Grey-cheeked parakeets (Broto-
Continue the dissection to make a circular incision
geris pyrrhopterus) seem to be prone to the develop-
around the vent, leaving a margin of intact vent skin and
ment of gastric carcinoma at the isthmus and the gross
the bursa of Fabricius attached to the tract. The bursa is
lesions are often unexciting. Collect a large specimen
present in young birds usually less than 6 to 12 months
of proventriculus, isthmus and ventriculus (all in one
of age and is located dorsal to the cloaca. The bursa piece if possible), containing at least one large serosal
should always be collected when it is present and nerve and blood vessel, for histopathology.
divided in half. Submit one half in formalin for histo-
pathology and save the other half for virology and/or In small birds, the entire proventriculus and ventricu-
DNA probe testing. lus can be placed in formalin. A large specimen
Fig 26.26 | Large gram-positive organisms consistent with the

yeast Macrorhabdus ornithogaster (formerly known as mega-
bacteria) are seen in a Gram’s-stained smear of intestinal con-
tents from a cockatiel. Note the size difference between these
Fig 26.27 | Marked dilatation of the proventriculus (P) in a
fungal organisms and the smaller gram-positive bacilli.
macaw (Ara ararauna) with proventricular dilatation disease
(PDD). H= heart, V= ventriculus.
allows multiple sections to be examined by the veteri- vive the initial insult may develop severe pancreatic atro-
nary pathologist in the search for nerves and plexi. phy and fibrosis. Inclusion body pancreatitis can be seen
Dilatation of the proventriculus and/or ventriculus is a with herpesvirus and adenovirus infections. Lympho-
hallmark gross lesion of PDD, but in juvenile psittacines plasmacytic pancreatitis in Neophema parrots is associ-
being hand-fed, these organs also may be dilated as a ated with paramyxovirus infection. Pancreatic necrosis
normal finding. Histopathology is required to differenti- also is a common lesion in West Nile virus infection.
ate between PDD and normal juvenile underdevelop-
ment of the proventriculus and ventriculus (Fig 26.27). Vacuolar changes and necrosis of acinar cells may be
seen in zinc toxicosis, but these lesions can be readily
Foreign body penetration of the ventricular wall can obscured by even mild postmortem autolysis. The pan-
occur in any species, but is most common in waterfowl creas concentrates zinc in the acinar cells and should be
and ratites. Nutritional muscular dystrophy (degenera- collected for toxicologic analysis, along with liver and
tive myopathy) can be seen in some species as white kidney, to diagnose zinc toxicity. Collect a sample of pan-
streaks in the ventricular muscle as a manifestation of creas for virology. Also submit in formalin a transverse
vitamin E/selenium deficiency. Endoventricular mycosis section through the duodenal loop with pancreas
(fungal invasion of the koilin lining of the ventriculus) attached, as this helps to identify the duodenum.
can be seen histologically and is a common finding in
debilitated passerines, despite the usually unremarkable Yolk Sac
gross appearance.
In neonate, the yolk sac and stalk should be evaluated
for the degree of absorption. In psittacine and passerine
Duodenum and Pancreas
chicks, the yolk sac is usually quite tiny by 3 days after
Open the outflow tract from the ventriculus and pro- hatching. Collect a sterile sample of the yolk material for
ceed into the duodenal loop. The largest limb of the culture and place the rest of the yolk sac (wall and con-
pancreas lies in the duodenal loop mesentery while the tents) into formalin. Yolk sacculitis and yolk sac reten-
small splenic lobe of the pancreas is located adjacent to tion are common problems in neonatal ratites.
the spleen. Pancreatic lesions are fairly common histo-
logically, but gross lesions may not be very striking. The
Intestines
pancreas also is one of the first organs to undergo post-
mortem autolysis. Continue opening the intestine through the jejunum
and ileum to the ceca (if present in the species) and
Quaker parrots (Myiopsitta monachus) are prone to the colon. Collect sections of intestine for histopathology.
development of acute pancreatic necrosis of unknown Opened intestinal sections are usually best, as this gives
etiology. Fat necrosis and serositis may accompany pan- the mucosa a chance to fix rapidly (Fig 26.28). Do not
creatitis and pancreatic necrosis. Quaker parrots that sur- disturb the mucosa by scraping or handling, as artifacts
673
Fig 26.29 | Fibrino-suppurative enteritis in a tufted puffin

(Fratercula cirrhata).
bacteriaceae, are common infectious agents in psittacines

and passerines. In addition, Campylobacter spp. and
Yersinia pseudotuberculosis are more common in
canaries and exotic finches. Campylobacter organisms
usually require special media and microaerophilic incu-
Fig 26.28 | Intestinal volvulus in an ostrich (Struthio camelus). bation conditions, so it is wise to alert the bacteriology
laboratory when this organism is suspected.
can confuse or obliterate the histologic diagnosis. Multifocal granulomas or thickened areas of bowel can
be indicative of mycobacteriosis. These sites should be
Wet mounts of intestinal contents (usually two different
collected for histopathology, and special acid-fast tissue
sites) are helpful in diagnosing parasitic and bacterial
stains can be applied to paraffin sections to demonstrate
problems. Wet mounts should be examined for parasite
the organisms. Alternatively, impressions or scrapings
ova and oocysts, as well as flagellates, yeast and motile
from these sites can be stained with a rapid acid-fast stain
bacteria. Sections of bowel can be tied off with string or
for a quick, presumptive diagnosis. Sections of affected
suture and submitted for culture. In some cases, both aer-
bowel can be collected for mycobacterial culture.
obic and anaerobic culture may be warranted (Fig 26.29).
Intestinal neoplasia is fortunately uncommon in birds,
If necrotic lesions are encountered in the intestinal
but needs to be included in the differential diagnosis of
mucosa, clostridial disease should be considered. Quail
thickened or proliferative bowel lesions.
disease caused by Clostridium colinum is a common
problem in quail, and typical “button ulcers” can be Flagellate protozoa and coccidial organisms also may
seen in the intestines as well as “crateriform” necrotic produce enteritis. Flagellates (including Giardia spp.
lesions in the liver. Clostridial enteritis, usually caused and Cochlosoma spp.) are diagnosed by fresh wet
by Clostridium perfringens, is becoming more com- mount smears of intestinal contents, but they are nearly
monly recognized in psittacines, especially nectar eaters impossible to diagnose on histopathology. Coccidiosis
such as lories and lorikeets. Clostridial organisms in can be diagnosed by wet mount smears of intestinal
large numbers can cause acute necrohemorrhagic enteri- scrapings and by histopathology. Nematode and cestode
tis. Finding large gram-positive bacilli, with or without parasites are uncommon in domestically raised
spore formation, as the primary organism on a Gram’s- psittacines and passerines, but geographic pockets of
stained smear of intestinal contents gives a presumptive these parasites may exist and should always be consid-
diagnosis that should be followed by anaerobic culture ered (Fig 26.31). These parasites are still common in
(Fig 26.30). Because exposure to oxygen in the air can
ground-feeding and feral or wild birds.
inhibit clostridia, it is wise to tie off a loop of unopened,
affected bowel with string or suture and place it in a
Ceca
sealable bag with the air evacuated prior to sending it
for anaerobic culture. Many species of birds do not possess ceca. Psittacines do
not. Passerines and Columbiformes have tiny vestigial
A wide variety of other bacteria can cause enteritis and ceca composed of lymphoid tissue, while Galliformes,
septicemia. Gram-negative organisms, especially Entero- Anseriformes and ratites possess large bilateral ceca.
Fig 26.30 | A Gram’s-stained smear of intestinal contents from Fig 26.31 | Tapeworms attached to the intestinal mucosa of a
a lory (Trichoglossus haematodus) that died of acute necrohem- great horned owl (Bubo virginianus).
orrhagic enteritis. Clostridium perfringens was isolated from the
intestinal tract. Note the large gram-positive rods with sub-
terminal spores.
These should be opened to look for cecal worms and

their contents should be included for culture. Cecal con-
tents should be included in culture for Salmonella,
especially in Galliformes.
Colon
Colon contents should start to look like fecal material as Fig 26.32 | Cloacal papillomatosis is seen in a lilac-crowned
one moves toward the cloaca. Open the cloaca to look Amazon parrot. The cloaca has been opened caudally to cra-
for papillomatous lesions, cloacoliths, trauma, inflamma- nially.
tory lesions and neoplasia (Fig 26.32).
In summary, intestinal samples should include the fol- spinal cord. Cut the vertebral column with cord in situ
lowing: wet mounts from at least two different sites, into 2- to 3-cm pieces and fix in formalin overnight. This
smears for Gram’s stain and possibly acid-fast stain, con- process will allow easier removal using rongeurs, with
tents for aerobic and possibly anaerobic bacteria or minimal damage to the less fragile, fixed spinal cord. In
Campylobacter culture, tissue for histopathology and very small birds, cross-sections of the cervical vertebral
ingesta for virology (direct electromicroscopy, virus isola- column with the spinal cord in situ can be decalcified
tion and/or DNA probes), and toxicology. and examined histologically.
In birds with head tilt or neurologic disease, especially

NEUROLOGIC Neophema parrots and exotic finches, fix a large portion
The brain and spinal cord can be very important in the of the petrous temporal bone containing the middle ear.
diagnosis of some diseases, especially PDD. The dorsal This bone can later be decalcified by the veterinary
calvarium should be carefully removed with rongeurs pathologist and sectioned to examine the middle ear for
(Fig 26.33). Visualize the brain in situ for any obvious inflammation and viral inclusions associated with
abnormalities such as abscesses, which should be cul- paramyxovirus infections. Congestion of the vascular
tured. Remove the brain by inverting the skull and tran- sinuses in the bones of the skull is a common finding,
secting the ventral and cranial attachments (Fig 26.34). but it is significant only if there also is corresponding
Collect a portion of the forebrain for virology and toxi- subdural hemorrhage or bleeding of brain parenchyma.
cology, and fix the rest of the brain in formalin. In
neonates, the brain is so soft that making a cut through The eyes can be removed and fixed in formalin if there
the dorsal skull and placing the entire calvarium con- is any suspicion of blindness, ocular or neurologic dis-
taining the brain in situ into formalin is recommended. ease. Dissection through some orbital bone may be
After fixation, the brain will harden somewhat and it can required for removal. Remember that the avian eye has
be removed more easily without damaging it. bony scleral ossicles, which may make their sectioning
somewhat more difficult. The globes can be transected
A similar procedure can be followed for the cervical at the optic nerves or dissection can be carried out
675
Fig 26.33 | View of the dorsal surface of calvarium of a Fig 26.34 | Dorsal surface of a normal brain from a blue-
psittacine bird with congested vascular sinuses (S). fronted Amazon parrot.
Fig 26.35 | View of the ventral surface of the brain from a Fig 26.36 | A pituitary tumor in a budgerigar (Melopsittacus
blue-fronted Amazon parrot. Pituitary (P), optic lobes (O), brain- undulatus).
stem (BS), optic chiasm (C), optic nerves (N).
through the ventral calvarium to keep the optic nerves thy and Sarcocystis infection can be diagnosed histologi-
and chiasm intact and attached to the brain. On the ven- cally (Fig 26.37). Open the joints of the pelvic and tho-
tral surface of the brain near the optic chiasm is the racic limbs and look for exudate; collect synovial fluid
pituitary (Fig 26.35). Tumors of the pituitary have been with a sterile syringe for bacterial and mycoplasmal cul-
reported in budgerigars and cockatiels (Fig 26.36). ture, although exudate also can be caseous.
Articular gout can be diagnosed by examining the exu-

MUSCULOSKELETAL date on cytology or by histopathology. The lesions of
Bone marrow can be collected by aspiration of the degenerative joint disease, periarticular proliferation and
femur and smears made and stained for cytologic evalua- proliferative synovitis are fairly common in the joints of
tion. Collect a segment of femur using rongeurs and the feet, but also may occur in the shoulder, stifle and
place it in formalin. Once fixed, the previously fragile hock. Any bone or joint lesions demonstrated radi-
bone marrow can be dissected out and examined histo- ographically should be opened and sampled for culture
logically. Leukemic or aplastic processes can be diag- and histopathology (Fig 26.38).
nosed from bone marrow samples, and circovirus inclu-
sions also may occasionally be seen histologically. The flexibility of bones (eg, tibiotarsus, ribs) can be used
in the assessment of the adequacy of mineralization. The
Samples of skeletal muscle should be collected for bones should break with an audible snap if mineraliza-
histopathology. Muscular lesions may include trauma, tion is normal. The rachitic “rosary” at the costochondral
hemorrhage, degeneration, mineralization, and injection or costovertebral junctions and deformation of the keel
or vaccine site reactions. Myositis, degenerative myopa- or other long bones are obvious lesions of metabolic
Fig 26.37 | Pale areas in skeletal muscle from an emu Fig 26.38 | A proliferative osteosarcoma involving the right leg
(Dromiceius novaehollandiae) with degenerative myopathy. The and pelvis of a peach-faced lovebird (Agapornis roseicollis).
heart muscle appears grossly normal.
bone disease. Sections of bone, especially areas of the

metaphyses and epiphyses, can be examined histologi-
Ancillary Testing of
cally for metabolic bone disease. Samples Collected at
Ratites are prone to developing angular limb deformities.
Necropsy
The “rubber rhea” syndrome is often due to hypophos- After the necropsy has been concluded, the remaining
phatemic rickets. Other ratite limb deformities can be parts of the carcass can be placed in a sealable plastic
multifactorial, but nutritional imbalances in calcium, bag and frozen until diagnostic testing has been com-
phosphorus and vitamin D3, growth rates and problems pleted. Examine wet mounts of intestinal contents and
with substrates are often implicated. Flock problems with crop or oral cavity scrapings as quickly as possible in-
limb deformities in ratites can be investigated through house for parasite ova, oocysts, motile flagellates, yeast
feed/forage analysis and bone ash analysis. and motile bacteria.
SMALL BIRDS AND DEAD-IN-SHELL MICROBIOLOGY

Stain impression smears from organs and bone marrow,
Necropsy of very small birds and neonates (under 15 g)
smears of exudate, or cells from fluid analysis with a
is challenging. One can open the coelomic cavity and
Wright’s stain and examine for cell types and microor-
thorax and fix the entire body in formalin; opening the
ganisms, including bacteria and fungi. If bacteria are
ventriculus as well is recommended for best fixation.
seen on the cytologic preparations, a stained smear can
The veterinary pathologist can then carry out dissection.
be destained and restained with Gram’s stain, or another
It is very difficult to get good fixation of tissues in birds
smear can be stained. If macrophages with “ghost
weighing more than 20 g, so this technique should not bacilli” are seen on the cytologic preparation, an acid-
be used for them. fast stain is in order to attempt to demonstrate myco-
bacterial organisms.
Dead-in-shell and egg necropsies can be performed, but
there are limited lesions and testing available. Open the A Gram’s stain of the colonic contents can be performed
egg as aseptically as possible at the air cell end. Collect in-house to provide a quick evaluation of the presence
samples aseptically for bacterial culture, virology and of abnormal bacterial populations, and then followed up
DNA probes. Assess gestational age and positioning of with culture. This type of Gram’s stain is especially
the embryo or chick. Then place the embryos and mem- important in detecting possible clostridial organisms,
branes in formalin. Histopathologic diagnosis is often which would then prompt an anaerobic culture. Avian
limited by autolysis, since the eggs often remain in the gastric yeast also can be detected in fecal smears or from
incubator for a period of time after embryonic death. scrapings of the isthmus stained with cytologic stains.
Histologic examination of the blastodisk can help deter-
mine if the eggs are truly infertile or whether early Composite Samples
embryonic death occurred post-fertilization. A collection of liver, spleen and air sac can be submitted
677
for Chlamydophila diagnostics. A Gimenez or Macchia- submitted, as this can depend on the particular virus or
vello stain can be performed on impression smears of air antigen and upon the particular laboratory’s technique.
sac, liver and spleen for the demonstration of elemen-
tary bodies. In Columbiformes, conjunctiva and nictitat- PARASITOLOGY
ing membrane should be included, as elementary bodies
Direct wet mounts of intestinal contents and crop or
may be confined to this location in these species. Fluore-
oral cavity scrapings prepared and examined at the time
scent antibody and chlamydial culture may be available
of necropsy are invaluable in the diagnosis of trichomo-
at certain laboratories, and some also can perform a
niasis in pigeons, raptors and budgerigars; cochlosomia-
DNA probe for Chlamydophila on a swab from the com-
sis in finches and canaries; and giardiasis in cockatiels
bined surfaces of liver, air sac and spleen.
and other psittacine and passerine species. Many of
Tissues, exudates or swabs can be submitted to diagnos- these organisms dry up easily, so examination should be
tic laboratories for bacterial, mycoplasmal or fungal cul- performed promptly. Examination of these wet mounts
ture as indicated. With the exception of samples for under dark field or phase contrast, if available, may
Campylobacter, which does not survive freezing well, make the detection of flagellates and motile bacteria eas-
these samples can often be frozen if not sent for culture ier. Inoculating Diamond’s media and submitting the
immediately. media for incubation can attempt culture of some tri-
chomonad parasites.
Special media is required for the culture of Mycoplasma
Microscopy of whole parasites such as nematodes, ces-
spp. Alert the bacteriology laboratory if fastidious organ-
todes, flukes and acanthocephalans may provide mor-
isms such as Campylobacter spp. and Bordetella avium
phology that can point to the classification of the para-
are of interest in the particular species or individual bird,
sites, plus characteristic ova may be visible within the
as these organisms often require special media and incu-
helminths. An acid-fast or auramine stain can be per-
bation parameters. DNA probe testing for Salmonella
formed on smears for the detection of Cryptosporidium
spp. is available at some laboratories. An antibiotic sensi-
oocysts, which can be found in the intestine, conjunc-
tivity tailored to drugs used in pet avian species also can
tiva, nasal cavity or bursa.
be requested if other birds on the premises are at risk.
A stained smear of the heart blood or lung impression
Mycobacterial culture is required for accurate speciation
can be examined for microfilaria and hematozoa such
of acid-fast organisms, and special media and handling
as Plasmodium, Hemoproteus and Leucocytozoon.
are necessary. Once Mycobacterium isolates are grown
Wright’s-stained impression smears of lung, spleen and
on solid media, some laboratories are capable of speciat-
liver are especially important in canaries and finches for
ing the organisms by the use of DNA probes and may
the diagnosis of the monocytic form of atoxoplasmosis,
offer antibiotic sensitivity testing for mycobacterial
as these organisms may not be visible histologically.
isolates.
Rarely, flagellates can be demonstrated in impression
Fungal culture may be requested in cases of suspected
smears from the lung, trachea, sinus and conjunctiva,
mycoses and is often required for accurate identification
which are not readily visible histologically. Other proto-
of the species involved. Antifungal sensitivity testing is
zoal parasites such as Sarcocystis, Toxoplasma and Leuco-
available at specialized mycology laboratories.
cytozoon can be found in impression smears of organs.
A pool of parenchymal tissues (liver, spleen, air sac,
lung, kidney, brain and bursa if present) and a separate HISTOPATHOLOGY
pool of intestinal contents should be refrigerated or Select a group of formalin-fixed tissues with lesions or
frozen for possible virus isolation or DNA probe testing. a group of tissues that commonly contain histologic
A combination swab from heart blood and the cut sur- lesions that could lead to diagnosis and submit them for
faces of liver, spleen, lung, kidney and bursa can be histopathology. This commonly includes tissues such as
submitted for DNA probe testing for viruses such as liver, spleen, air sac, kidney, lung, trachea, heart, bursa,
psittacine circovirus and avian polyomavirus. Fluorescent brain, duodenum/pancreas and proventriculus/ventricu-
antibody techniques on frozen sections of tissue may be lus. Save the remaining formalin-fixed tissues in case the
available for certain viruses. diagnosis is not made with the first set of tissues.
Polymerase chain reaction (PCR) tests are available for This second set of tissues may include spinal cord, bone
the detection of certain viruses, such as West Nile virus, marrow, nasal cavity, skin and feathers, bone and joint,
on fresh or frozen tissues. It is important to contact the middle and inner ear, eyes, tongue, skeletal muscle, thy-
individual laboratory so the most appropriate tissues are roid, parathyroid, adrenal, esophagus, crop, jejunum,
ileum, colon, ceca, gall bladder, ovary, oviduct, testes, Iron storage disease is most commonly seen in toucans,
thymus, nerve (ischiatic, brachial plexus) and beak. toucanettes, mynahs and birds of paradise; the condition
is rare in psittacines, although there is emerging evidence
The veterinary pathologist may recommend special diag-
that lories and lorikeets may be prone to iron accumula-
nostics such as stains for acid-fast organisms, fungi, bac-
tion. The special histologic stain, Perl’s Prussian blue,
teria, iron or copper, depending on what is seen on the
can provide qualitative information about the amount of
routine hematoxylin- and eosin-stained sections. In spe-
cial situations, tissues may be embedded in plastic so iron in the liver, but, again, quantitative levels are
that electron microscopy can be performed. Direct elec- detected by toxicologic analysis.
tromicroscopy also can be performed on intestinal con-
Poisonous plants can be found in the digestive tract and
tents or tissue homogenates. In situ DNA hybridization
techniques on paraffin-embedded tissues are available submitted to a botanist or university botany department
for certain viruses such as Pacheco’s herpesvirus, aden- for identification. The plants or wood can be frozen
ovirus, avian polyomavirus, psittacine circovirus and until submission to prevent the breakdown of toxic prin-
paramyxovirus. ciples. Ingestion of fertilized plants can result in nitrate
toxicity, and samples of these plants can be analyzed for
Immunohistochemical stains can detect certain antigens the amount of nitrates present.
from bacteria, fungi, viruses and parasites in paraffin-
embedded tissues, and these techniques also can be uti- Polytetrafluoroethylene (PTFE or non-stick coatings) and
lized to detect some cell markers in the diagnosis of other toxic inhalation products are rarely detectable in
tumors. Gene sequencing of certain microorganisms tissues, and the diagnosis is usually made by a history of
(Clostridium perfringens, for example) in formalin-fixed,
exposure, the presence of pulmonary edema and hemor-
paraffin-embedded tissues is available at some diagnostic
rhage, and the exclusion of other causes of death. There
laboratories.
is a wide variety of items commonly found in the house-
hold that can give off PTFE fumes, including non-stick
TOXICOLOGY cookware and appliances such as self-cleaning ovens and
Toxicologic testing requires some idea of what toxin is electric grills.
being considered. This information often comes from
the history and histopathologic findings. Contacting the Birds also can be sensitive to other inhalants such as car-
toxicology laboratory is essential for submission of the bon dioxide, carbon monoxide and fumes from glues,
most appropriate tissues and amounts. resins, plastics and paints. Mycotoxins may be implicated
in the case of multiple birds suffering liver damage.
The most common toxins tested for are heavy metals
Aflatoxins can be detected in foodstuffs, but usually by
such as lead and zinc. Usually liver and kidney are
required for this analysis, although zinc also accumulates the time chronic liver damage is evident, the offending
in the pancreas preferentially. Heavy metals also can be foodstuff is often no longer available. In the case of
detected in foreign bodies, water and feed. Copper accu- acute toxicosis, samples of the feed should be frozen
mulation in the livers of swans can be demonstrated along with liver and kidney, pending further investiga-
qualitatively with special histologic stains for copper, but tion. Contact the toxicology laboratory for specimen
quantitative levels require toxicologic analysis. requirements and costs.
27_Chlamydophila.qxd 8/24/2005 11:13 AM Page 679
CHAPTER
27
Update on
Chlamydophila
psittaci
A Short Comment
THOMAS N. TULLY, JR, DVM, MS, D ipl ABVP-A vian , D ipl ECAMS
Chlamydophila psittaci is a zoonotic intracellular bacte-

rial organism that causes the diseases psittacosis in
humans and avian chlamydiosis in avian species. Clinical
signs often associated with a psittacosis (human) infec-
tion include generalized “flu-like” symptoms to more
severe pneumonia and complicating health issues. Avian
chlamydiosis will present as non-specific clinical signs in
a companion bird patient (Fig 27.1). These non-specific
signs can include ocular, nasal or conjunctival irritation
and discharge, anorexia, depression, dehydration, bright
green urates and diarrhea (Fig27.2). Many avian species
have been diagnosed with C. psittaci, but it is the com-
panion bird species where this disease is the greatest
public health concern.
Fig 27.1 | A bird infected with C. psittaci organism may not
have clinical signs. This condition can occur in small birds such It is often difficult to confirm a diagnosis of avian chlamy-
as this blue budgerigar.
diosis because of the intracellular life cycle of the organ-
ism, prophylactic treatment of patients with appropriate
antibiotics but using inappropriate doses and treatment
periods, and the periodic shedding of elementary bodies
(the infectious form of the disease). The difficulty to con-
firm avian chlamydiosis cases encourages the veterinarian
to use multiple testing methodologies. Testing methods
that can be used either individually or preferably in com-
bination include pathology, antibody testing (direct com-
plement fixation and elementary-body agglutination) and
antigen testing (enzyme-linked immunosorbent assay,
immunofluorescent antibody tests, polymerase chain
reaction amplification technology on choanal/cloacal
Fig 27.2 | This lutino cockatiel has the upper respiratory signs
swabs and blood). Prior to sample submission, the diag-
associated with avian chlamydiosis. The bird tested positive for
the disease. Additional therapies may be needed to treat sec- nostic laboratory should be contacted for recommenda-
ondary infections that arise as a result of the primary disease. tions on proper sample collection, labeling, packaging
27_Chlamydophila.qxd 8/24/2005 11:13 AM Page 680
and shipment of the sample material. A breakdown in and the proper tests are used to confirm the presence of
sample handling or shipment delay can adversely affect the disease. Early communication to a client about the
the reliability of C. psittaci test results. ability of this organism to resist improper treatment and
the consequences of discontinuing treatment will often
There are several treatment options available to treat lead to owner compliance with antibiotic administration.
suspected or confirmed avian chlamydiosis cases. The In hopes of protecting birds and bird owners in the
treatment options are based on doxycycline as the drug future, research is currently being conducted to improve
of choice and being administered in the most appropri- C. psittaci diagnostic testing and to develop a vaccine to
ate way for the patient(s) to receive a therapeutically protect birds from infection if exposed to the infectious
effective dose for the duration of the 45-day treatment elementary bodies.
regimen. There have been recent advances in using
doxycycline hyclate powder from opened capsules as a See Chapter 1, Clinical Practice for location the com-
seed coating for budgerigars or mixing the powder in pendium of psittacosis control from the CDC. See
water for larger birds.1 Oral doxycycline (monohydrate Chapter 21 Preventative Medicine and Screening for a
or calcium) or intramuscular injections of specific for- review of diagnosis and preventive measures.
mulationsa can be effective treating the individual bird or
group of birds that will tolerate the stress of capture and Product Mentioned in the Text
drug administration on a regular basis. a. Vibrovenos formulation, Pfizer Laboratories, London
Chlamydophila psittaci is a public health concern and References

can be a deadly, expensive disease within an aviary or to 1. Smith KA, Eidson M, Johnston WB, et al. Compendium of measures to
control Chlamydophila psittaci (formerly Chlamydia psittaci) infection
the individual companion bird. Although difficult to among humans (psittacosis) and pet birds, 2002. Compend Contin Educ
Pract Vet 24:328-335, 374-378, 2002.
diagnose, avian chlamydiosis can be diagnosed and
2. TullyTN: Update on Chlamydophila psittaci, Seminars in Avian and
treated if there is an understanding of the available tests, Exotic Pet Medicine, vol 10, No 1 (January) 2001, pp 20-24.
28_Mycobacteria.qxd 8/23/2005 2:08 PM Page 681
CHAPTER
28
Implications of
Mycobacteria
in Clinical Disorders
CHRISTAL G. POLLOCK, DVM, D ipl ABVP-A vian
Avian mycobacteriosis is generally a disease of captive

populations. In the past, most cases were believed to
have been caused by Mycobacterium avium and M.
intracellulare. More recently, however, the atypical
organism, M. genavense, has emerged as a significant
cause of disease. Although the incidence of disease is
relatively rare, the potential for avian mycobacteriosis to
spread to humans makes this subject pertinent for avian
veterinarians. In this chapter, aspects of avian mycobac-
teriosis, including clinical presentation, therapeutic
options, zoonotic potential and diagnostic tests with
promising new molecular techniques such as deoxyri-
bonucleic acid (DNA) probes, will be covered.
Mycobacterium spp.
Mycobacterium avium and M. intracellulare are fre-
quently grouped together as the Mycobacterium avium
intracellulare (MAI) complex or Mycobacterium avium
complex (MAC). Twenty-eight seeknown serotypes of
MAI exist.56 The more pathogenic serotypes 1, 2 and 3
belong to the M. avium group.20,54 Serotypes 4 to 28
make up the M. intracellulare group, which is consid-
ered relatively avirulent.31,56,77 Historically, these two
species were considered the cause of avian tuberculosis,
and they still play an important role in avian mycobacte-
riosis today.
The atypical organism, Mycobacterium genavense, is an

important cause of mycobacteriosis, especially in com-
panion birds.38,40-42 In a recent survey of necropsied pet
birds in Europe, M. genavense was the predominant
mycobacterial species isolated.49 Mycobacterium gena-
vense is a fastidious organism only recently identified. It
is most closely related to M. simiae and was first isolated
from immunosuppressed human patients.10,19,84 Addi-
tional atypical mycobacteria isolated from companion bacterium spp. into mucosal or dermal lesions, or by
birds in rare instances include M. fortuitum, the use of contaminated needles.36,83
M. gordonae and M. nonchromogenicum.38,41,70,79
HOST IMMUNE RESPONSE
There also are rare reports of disease caused by Myco-
bacterium tuberculosis or M. bovis.80 All avian species The presence of humeral antibodies does not appear to
studied have been relatively resistant to M. bovis.13 Myco- protect against the development of avian mycobacterio-
bacterium tuberculosis has been reported only in com- sis.20,82 In the mammal, cell-mediated immunity is much
panion parrot species.29,36,77,80 There are no case reports, more important, and this also may be true in the bird.
as yet, of M. tuberculosis in passerines or free-ranging Studies evaluating growing layer hens inoculated with
psittacines.13,48 Infection is probably secondary to close Mycobacterium butyricum found that dietary linoleic
contact with infected humans.31,48 Mycobacterium tuber- acid may boost cell-mediated immunity.69
culosis was cultured from a green-winged macaw (Ara
chloroptera) 3 to 4 years after active tuberculosis was
diagnosed in two human occupants of the household.85 Clinical Disease
INCIDENCE
Pathogenesis of Disease The distribution of avian mycobacteriosis is worldwide,
although most reports of disease are from northern
SOURCE OF INFECTION hemisphere’s temperate zones. The incidence of avian
mycobacteriosis is reportedly uncommon in some coun-
Mycobacterium is a ubiquitous environmental sapro-
tries, such as Japan.49,68
phyte most commonly found in soil with heavy fecal
contamination or other organic debris.31 High levels of
mycobacteria also might be found in surface water or in SIGNALMENT
marshy, shaded areas.20,77 Although wild birds are a possi- Adult birds, 3 to 10 years of age, are most frequently
ble source of infection, they are probably not an impor- diagnosed with avian mycobacteriosis.20,51,80 There is
tant source of disease for captive birds.6,18,43,77 The preva- probably no gender predilection, although some reports
lence of mycobacteriosis is low (usually <1%) in most suggest a slightly higher incidence of disease in the
free-ranging populations.24 female bird.42,77,80
Avian mycobacteriosis has been reported in virtually all

TRANSMISSION avian taxonomic orders, however, susceptibility varies
Avian mycobacteriosis is usually transmitted by the inges- (Table 28.1). The greatest incidence of disease has been
tion or inhalation of soil or water contaminated by feces, in captive collections of waterfowl, parrots, songbirds,
or, less commonly, by urine.29,82 Raptors might become and ground-dwelling birds such as farmed ratites and
infected by ingesting infected prey. A mechanical arthro- small poultry flocks. Reports also are common in the
pod vector is a rare mode of transmission. Vertical trans- wood pigeon (Columba palumbus) and free-ranging
mission also is possible, however, avian mycobacteriosis waterfowl. Orders Falconiformes and Gruiformes also
is generally associated with an immediate halt in repro- are considered susceptible.6,16,20,24,27,41,43,44,49,59,60,77,80
ductive activity.77
Species considered relatively resistant to avian mycobac-
teriosis include rooks (Corvus frugilegus), turtle doves
Pathogenesis
(Streptopelia risoria), turkey (Meleagridis spp.) and
The primary site of entry and initial colonization of guinea fowl (Numida meleagris). Although the flamingo
mycobacteria is the intestine. Subclinical bacteremia formerly was considered fairly resistant to avian
quickly follows and the organism spreads to the liver mycobacteriosis, an epidemic was reported in lesser
through the portal circulation. The absence of lymph flamingos (Phoeniconaias minor) in 1993. More than
nodes in the bird then allows mycobacteria to spread 18,500 birds died over a 3-month period.45,77
hematogenously to distant parenchyma such as the
spleen, bone marrow, skin and lungs.29,36,80
CLINICAL PICTURE
Disturbance of contaminated surface water might lead to There are three forms of avian mycobacteriosis, which
the inhalation of aerosolized mycobacteria and direct have been historically described as classical, paratubercu-
colonization of the respiratory tract. Focal skin disease lous or diffuse disease. The most common form of dis-
probably occurs secondary to the inoculation of Myco- ease in the avian patient involves granulomatous lesions
Chapter 28 | I M P L I C A T I O N S O F M Y C O B A C T E R I A I N C L I N I C A L D I S O R D E R S
683
Table 28.1 | Species Highly Susceptible to Avian Table 28.2 | Incidence of Granulomatous Lesions with
Mycobacteriosis1,6,12,16,17,22,24,27,29,39,41,43,44,46,49,59,60,62,75,77,80,86,87,88 Avian Mycobacteriosis29
Order Species Usually
Common
Absent
Anseriformes • White-winged wood duck (Aix sponsa)
• Sea ducks (Somateria fischeri, Clangula hyemalis, Charadriiformes (gulls, shorebirds) ✓
Melanitta spp.)
Ciconiiformes (bitterns, herons, egrets, ibises) ✓
Columbiformes • Wood pigeon (Columba palumbus)
Cuculiformes (cuckoos) ✓
Falconiformes
Falconiformes (hawks, eagles, falcons) ✓
Galliformes • Partridge (Alectoris spp., Lerwa sp., Ammoperdix spp.,
Tetraogallus spp.) Galliformes (fowl) ✓
• Pheasants (Phasianus colchicus) Gruiformes (coots, cranes, rails) ✓
• Quail (Coturnix japonica)
Piciformes (toucans) ✓
Gruiformes • Cranes (Grus spp., Balearica spp., Anthropoides spp.)
• Rails (Rallus spp., Laterallus jamaicensis) Strigiformes (owls) ✓
• Gallinules (Porphyrula spp.)
• Coots (Fulica spp.) Anseriformes (waterfowl) ✓
Passeriformes • Canaries (Serinus canarius) Columbiformes (pigeons, doves) ✓

• Sparrows (Passer domesticus) Coraciiformes (hornbills, kingfishers) ✓
• Hooded siskin (Spinus sp.)
• Lady Gouldian (Chloebia gouldiae) Passeriformes (songbirds) ✓
Psittaciformes • Amazon parrots (Amazona spp.) Amazona ochro- Psittaciformes (parrots) ✓
cephala auropalliata, Amazona farinosa,
Amazona aestiva
• Grey-cheeked parakeet (Brotogeris pyrrhopterus)
• Budgerigar (Melopsittacus undulatus)
• Horned parakeets (Eunymphicus cornutus)
• Pionus (Pionus sp.)
• Ring-necked parakeets (Psittacula)
Fig 28.1 | Granulomatous intestinal lesions in a mallard duck Fig 28.2 | Multifocal granulomatous lesions in the liver of a
(Anas platyrhynchos) caused by Mycobacterium avium intracellulare. sandhill crane (Grus canadensis) caused by Mycobacterium spp.
in the gastrointestinal tract (Fig 28.1) and liver (para- develops. The presentation of wasting with an increased
tuberculous) (Fig 28.2). Classic avian mycobacteriosis is appetite can lead to the incorrect presumptive diagnosis
associated with tubercles in many organs such as the kid- of proventricular dilatation disease. Additional non-spe-
ney, liver and spleen, while diffuse disease may be associ- cific signs of illness might include poor feather quality,
ated with diffuse enlargement of affected organs.24,29,80 lethargy, weakness and pallor.51 Chronic or intermittent
diarrhea may also be observed.12,29,80
Granulomatous lesions are common in birds of prey but
rare in pigeons and doves, waterfowl and most parrots Abdominal distension due to enlargement of the liver or
(Table 28.2).29 Diffuse mycobacteriosis has been most small intestines also might be detected. Ascites is rare,
commonly reported in Coraciiformes, such as the king- although it has been reported in Canada geese (Branta
fisher (Alcedo spp.), and Passeriformes.32,61 canadensis), mute swans (Cygnus olor), tundra swans
(Cygnus columbianus) and some parrots.86
Granulomatous Intestinal Disease
Granulomatous intestinal or paratuberculous disease is Musculoskeletal Disease
associated with muscle wasting and emaciation. Initially Reports in the literature describe anywhere from 2 to
the bird will display a good appetite, but anorexia later 93% incidence of bony lesions in avian mycobacteriosis.
Dr. Nancy Boedeker

Dr. Carol Canny
Fig 28.3 | Granulomatous nodules within the skin of a lovebird Fig 28.4 | An irregular, firm, fleshy mass in the choana of a
(Agapornis roseicollis) caused by Mycobacterium spp. blue-fronted Amazon parrot (Amazona aestiva) caused by
Mycobacterium spp.
Acute or chronic lameness, which might be shifting leg in ANTEMORTEM DIAGNOSTICS

nature, may be observed due to granulomatous lesions in Antemortem diagnosis of mycobacteriosis is difficult due
bones or joints. The carpometacarpal and elbow joints to the wide variety of possible clinical signs and physical
are most commonly involved, and skin overlying the examination findings. A strong index of suspicion for
affected joints might be thickened and ulcerated.29,80 avian mycobacteriosis can be based on signalment, clini-
cal findings consistent with disease, profound leukocyto-
Respiratory Disease sis, organomegaly and the cytologic presence of acid-fast
Granulomas within the lungs or compression of air sacs bacteria. Serologic techniques such as enzyme-linked
secondary to hepatomegaly can lead to dyspnea or exer- immunosorbent assay (ELISA) also may prove helpful in
cise intolerance. Additional signs of respiratory disease selected cases and are described in the following section
are rare with avian mycobacteriosis, although focal nod- on serology. A definitive diagnosis of mycobacteriosis
ules have been reported within the infraorbital sinus, relies on histologic identification or culture of the organ-
nares and syrinx.14,71,85 ism. Molecular techniques, such as DNA probes and
nucleic acid amplification, also are promising in the aid
of diagnosing avian mycobacteriosis.
Skin Disease
Tubercle formation within the skin also is rare. Dermatitis,
Minimum Database
diffuse, non-pruritic thickening associated with xan-
thomatosis, as well as pale, soft, subcutaneous masses Minimum database results are variable. The complete
have been reported in association with avian mycobacte- blood count might reveal a marked heterophilic leukocy-
riosis (Fig 28.3).25,29,80 tosis, monocytosis, thrombocytosis and elevated fibrino-
gen. Chemistry panel results often are unremarkable,
although liver enzymes may be mildly to moderately ele-
Ocular Lesions
vated, and albumin levels may be decreased. Early in the
Granulomatous lesions may be associated with the eye- disease process, a polyclonal gammaglobulinopathy also
lids, nictitating membranes, retrobulbar tissue and might be detected.35,77,80
pecten.1,62,71,77,85 There also is one report of keratitis asso-
ciated with avian mycobacteriosis.74
Imaging
Radiographic findings can include hepatosplenomegaly
Miscellaneous Lesions
and dilation of intestinal loops with gas (Fig 28.5).80
In rare reports, granulomas have been found within Gastrointestinal contrast radiography may demonstrate a
the oropharynx (Fig 28.4), larynx or external auditory thickened and irregular small intestinal wall. Granulomas
canal.1,29,85 Endocrine abnormalities such as reproductive may be identified within the bones, lungs or coelom,
failure might occur secondary to an infection in the however, these lesions are more difficult to identify in
adrenal glands, pancreas or gonads.80 Avian myco- the bird, since they do not calcify as in mammals.77
bacteriosis also might be associated with neurologic
signs due to involvement of the spinal cord, brain or Radiographic findings involving bone might include lysis
vertebral column.52,77,80 and/or sclerosis consistent with osteomyelitis, osteophy-
685
A suggestive diagnosis of avian mycobacteriosis may be

based on identification of the organism in cytologic sam-
ples; however, the acid-fast stain is not a specific test,
because non-pathogenic mycobacteria can be transient
gastrointestinal inhabitants or environmental contami-
nants. Therefore, positive acid-fast cytology should be
confirmed by culture, histopathology or DNA probe
analysis.
Serology
Serologic tests available include hemagglutination (HA),
complement fixation (CF) and ELISA. These tests are
highly species-specific and they are available for only a
limited number of species.
HA is a rapid, easy-to-perform assay run on whole blood

or serum. The use of fresh whole blood might produce
more sensitive (true positive) results than whole blood
in EDTA or serum. Species-specific antigen is required
Fig 28.5 | Widening of the cardiohepatic silhouette on
a V/D radiograph due to hepatomegaly caused by avian for reliable results. HA has been of some use in water-
mycobacteriosis in an Amazon parrot (Amazona sp.). fowl, domestic fowl, raptors and cranes.21,35
ELISA is a sensitive, albeit labor-intensive, test that

tosis around arthritic joints, pathological fractures and requires at least 24 hours before results are available.
endosteal bone densities.77 Anatomic regions most com- Highly species-specific antigen is required. For instance,
monly affected include the midshaft region of long a sensitive and specific ELISA exists for mycobacteria in
bones, such as the humerus, tibiotarsus and ulna, and feral barnacle geese (Branta leucopsis).16,19,21,28,77
the ribs and sternum. There are rare reports of lesions
involving the vertebrae and femur.80 In an unusual case CF titers of 1:20 or greater have been used to confirm
report, chondritis, osteitis and osteomyelitis were infection or exposure to Mycobacterium avium infection
described in the nasal bone of a wood duck (Aix in grey-cheeked parakeets (Brotogeris pyrrhopterus).58
sponsa) with mycobacteriosis.27
Culture
Ultrasonography and alternate imaging methods, such as
Culture has several practical limitations. Mycobacterium
computed tomography, also are potentially useful diag-
is only intermittently shed, and careful sample collection
nostic modalities.
is necessary to prevent environmental contamination.
Mycobacteria are difficult to culture, and no growth
Laparoscopy
occurs even when proper protocols are followed. If
Laparoscopy is an extremely useful technique for identi- growth does occur, at least 2 to 4 weeks are required for
fying lesions on the serosal surface of the liver, spleen, visible colonies to appear and up to 8 weeks of incuba-
intestine, lung and air sacs. Granulomas may be visual- tion is required. Some strains of M. avium require up to
ized as white, yellow or tan round masses, which are 6 months before colonies are identifiable.
soft and easily biopsied.80
Use of a radiometric culture methoda reduces the length
Cytology of time needed for culture. This acidic culture medium
is especially useful for isolation of the fastidious Myco-
A large number of mycobacteria must be present (5 x
bacterium genavense. In one study, only 3 out of 34 M.
104/ml) before the organism can be visualized micro-
genavense isolates grew on conventional solid media,
scopically; therefore, fecal acid-fast stains serve as a poor
while the acidic culture medium supported growth of
screening tool. The Ziehl-Neelsen stain is the standard
23/34 isolates.41,43
method for identification of acid-fast organisms. A modi-
fied Ziehl-Neelsen stain utilizes peanut oil to reduce
damage to the mycobacterial cell wall. Mycobacteria DNA Probes
appear pink-red with the Ziehl-Neelsen stain. Myco- The DNA probe assay is a rapid method for identifying
bacterium tuberculosis is rod-shaped, while M. avium various species of Mycobacterium grown in culture.
can appear almost coccoid or as long, beaded rods.3,77 Although a very sensitive (95%) and specific (100%) test,
686
the currently available gene probeb is not sensitive Intestinal Lesions

enough to directly detect acid-fast bacilli in specimens.3 Distension or thickening of the intestines is an extremely
common finding in granulomatous intestinal disease.
Polymerase Chain Reaction Intestinal mucosa also may display a “shaggy carpet”
appearance caused by prominently thickened or clubbed
Molecular techniques may be used to identify organisms
villi.77 Proventricular lesions also may be identified.37
grown not only on culture media but also identified
within fecal, biopsy or necropsy samples, including for- Granulomas
malin-fixed paraffin-embedded sections.4,34,47 Polymerase Tubercles are frequently white, tan or yellow in color,
chain reaction (PCR) methodsc, based on the amplifica- and they might range in size from miliary foci to nodules
tion and sequencing of the small subunit 16S rRNA gene several centimeters in diameter. Granulomas are most
of mycobacteria, have been used to identify M. avium, commonly located within the intestinal wall, liver,
M. bovis and M. genavense.9,47,56,60,76 spleen and bone.11,24,49,53,77 Granulomas also might be
found in subcutaneous tissue as well as a variety of
One study comparing the sensitivity and specificity of
other viscera such as the kidney.46 Tubercle formation
various samples found that fecal specimens had the
within the skin and lungs is rare.25,29
highest sensitivity by PCR (77.8%). Processing fecal spec-
imens with the zwitterionic detergent, C18-carboxypropy- Miscellaneous Lesions
lbetaine (CB-18), also might increase the sensitivity of Additional lesions that might be identified with avian
test results.78 mycobacteriosis include the following: proliferative or
lytic bony lesions (secondary pathologic fractures are
Intradermal Skin Testing possible),77 dermatitis or diffuse thickening of the skin
associated with xanthomatosis,80 and pulmonary necrosis
Intradermal skin testing has been used for decades in
or ulceration.24,53 A single fluid-filled pulmonary cyst has
poultry in the diagnosis of mycobacteriosis. A small vol-
been reported in a cockatoo.57 An extremely unusual
ume (0.1 ml) of avian purified protein derivative tuber-
manifestation of mycobacteriosis was reported in fairy
culin (PPD) is injected into the wattle or comb and
bluebirds (Irena spp.) with granulomatous cardiopul-
assessed 48 to 72 hours later.7,55,77
monary arteritis.50
Unfortunately, intradermal testing has proven unreliable
in a number of avian species including pigeons, geese, Histologic Findings
quail and raptors. In these species, intradermal skin test- The most common findings reported include granuloma-
ing is frequently associated with false negatives, espe- tous enteritis, splenitis or hepatitis with variable amounts
cially in the early and late stages of disease. Testing has of acid-fast bacteria. A marked accumulation of
been attempted on skin over the hock, vent, wing web macrophages also may be identified within the dermis,
and eyelid. The skin just behind the ear also has been mucous membranes and subserosa of the peritoneum
utilized in ratites.29,77 and airsacs.24 Granulomatous intestinal lesions can also
be associated with expansion of the intestinal villi by dif-
POSTMORTEM DIAGNOSIS fuse granulomatous infiltrate and proliferations of epithe-
lial cells within the glands of Lieberkuhn.29,83
Gross Findings
Large numbers of acid-fast rods are found in lesions
The gross necropsy findings of avian mycobacteriosis
caused by Mycobacterium avium, while M. bovis and
vary widely. Non-specific findings might include muscle
M. tuberculosis tend to be found in relatively small
wasting, loss of subcutaneous and intracoelomic fat and
numbers.80
discolored, poor-quality feathers. There may be no sig-
nificant gross findings in the diffuse form of myco- Granulomas generally do not possess a region of central
bacteriosis.59,80 calcification or an extensive necrotic center.80 The
necrotic regions that are identified in avian mycobacterial
Organomegaly
granulomas are surrounded by epithelioid cells, multi-
Hepatosplenomegaly is one of the most consistent nucleated giant cells and lymphocytes.38,53 Non-caseous
findings in songbirds and grey-cheeked parakeets granulomas may contain large macrophages with highly
(Brotogeris spp.) with mycobacteriosis.11,63 Some birds vacuolated cytoplasm and numerous acid-fast bacteria.60
may also demonstrate an enlarged, pale, firm liver due
to amyloid deposition, which may eventually lead to The diffuse form of avian mycobacteriosis is more diffi-
hepatic rupture and hemorrhage.77 Polycystic livers and cult to recognize at necropsy, because organomegaly
cystic granulomas have been reported in waterfowl.63 may not be observed. Instead, a diffuse infiltration with
687
Table 28.4 | Multi-Drug Therapy5,8,66,81,82

Table 28.3 | Anti-mycobacterial Drugs5,8,66,81,82
Drug Therapy
• Aminoglycosides - • Isoniazid Rifabutin-Ethambutol-Clarithromycin
Amikacin, Aminosidine, • Macrolides -
Rifabutin 15 mg/kg PO q 24 h
Kanamycin, Streptomycin Azithromycin,
• Clofazimine Clarithromycin Ethambutol 30 mg/kg PO q 24 h
• Cycloserine • Pyrazinamide Clarithromycin 85 mg/kg PO q 24 h
(allometrically scaled)
• Dapsone • Rifamycins -
• Ethambutol Rifabutin, Rifampin Rifabutin-Ethambutol-Azithromycin*
• Ethionamide • Tetracyclines - Rifabutin 15 mg/kg PO q 24 h
• Fluoroquinolones - Doxycycline Ethambutol 30 mg/kg PO q 24 h
Ciprofloxacin, Azithromycin 43 mg/kg PO q 24 h
Enrofloxacin or
Ethambutol 56-85 mg/kg PO q 24 h
Azithromycin or 43 mg/kg PO q 24 h or
large, foamy histiocytes may be seen. 23,32,61
Clarithromycin 85 mg/kg PO q 24 h
Rifampin-Ethambutol-Clofazimine
Rifampin 45 mg/kg PO q 24 h
THERAPEUTICS
Ethambutol 30 mg/kg PO q 24 h
Humane euthanasia is recommended for birds diagnosed Clofazimine 6 mg/kg PO q 24 h
with mycobacteriosis. Birds infected with Mycobacterium Rifampin-Ethambutol-Isoniazid**
avium may continuously shed large numbers of organ- Rifampin 45 mg/kg PO q 24 h
isms into the environment.77,81 This potential zoonotic Ethambutol 30 mg/kg PO q 24 h
risk is especially important in households with immuno- Isoniazid 30 mg/kg PO q 24 h
suppressed individuals, such as those on chemotherapy, Rifampin-Ethambutol-Streptomycin

Rifampin 15 mg/kg PO q 12 h
the very young, the elderly and human immunodefi-
ciency virus (HIV)-positive. Any humans in contact with
Streptomycin 30 mg/kg IM q 12 h
an infected bird should consult a physician for evaluation.
Rifabutin-Ethambutol-Enrofloxacin
Surgery Ethambutol 30 mg/kg PO q 24 h
Enrofloxacin 30 mg/kg PO q 24 h
Surgical excision may be possible and perhaps even
Rifabutin-Ethambutol-Ciprofloxacin
curative for discrete nodules in the skin, subcutaneous
tissue or periocular tissue. Medical management is indi- Ethambutol 30 mg/kg PO q 24 h
cated for disseminated avian mycobacteriosis when treat- Ciprofloxacin 80 mg/kg PO q 24 h
ment is deemed appropriate. Ethambutol-Cycloserine-Clofazimine-Enrofloxacin (raptors)
Medical Management Cycloserine 5 mg/kg PO q 12 h

Clofazimine 1.5 mg/kg PO q 24 h
There are numerous drugs with anti-mycobacterial activ- Enrofloxacin 10-15 mg/kg PO, IM q 12 h
ity (Table 28.3). Mycobacterium avium isolated from Lamprene-Seromycin-Myambutol
human patients has been reported sensitive to azithro- Lamprene 1.5 mg/kg PO q 24 h
mycin, clarithromycin, ciprofloxacin, rifabutin, rifampi- Seromycin 10 mg/kg PO q 12 h
cin, amikacin, clofazimine and ethambutol. Doxycycline Myambutol 40 mg/kg PO q 12 h
has shown efficacy against atypical mycobacterium like With advanced cases give
M. fortuitum.81 Ciprofloxacin 20 mg/kg PO q 12 h

or
Enrofloxacin 15 mg/kg PO q 12 h
or
Multi-drug therapy should be employed in the treat- Streptomycin 20-40 mg/kg IM q 12 h
x 7-10d
ment of avian mycobacteriosis. Numerous successful
*Lower doses have been reported
combinations have been reported in the literature **Drugs are mixed into a dextrose powder, then mixed into a small
amount of food and given PO q 24 h.
(Table 28.4).8,65,66,75,81,82 Due to the intracellular nature of
the pathogen, its slow growth, and the bacteriostatic
activity of most anti-mycobacterial drugs, an extended vival rates. Mycobacterium vaccae was used in a small
course of treatment lasting 4 months or longer is rec- trial in captive waterfowl; however, results were incon-
ommended. clusive.11
Immunotherapy has been a useful adjunct for treatment

of human tuberculosis patients.72,73 Administration of CONTROL AND PREVENTION
killed M. vaccae has some immunomodulatory effects Mycobacterium is extremely stable in the environment. It
and has been associated with an improvement in sur- is highly resistant to environmental extremes and might
survive for months or years in contaminated soil and sur- cobacterial activity include alcohol, aldehydes, halogens,
face water or less commonly in feed, feathers or dis- peroxygens and phenols (Table 28.5).67 The use of reed
carded food.24 biofiltration systems to remove contamination from
water also is being investigated.77
There are no absolute means for control of avian tuber-
culosis. Quarantine and surveillance programs must
Vaccination
strive to identify and eliminate infected animals.
Providing complete, balanced nutrition and utilizing There are only rare reports of vaccination against myco-
good sanitation practices will minimize the impact of dis- bacteriosis in birds. The bacille Calmette-Guérin (BCG)
ease. Stressors such as overcrowding also must be mini- vaccine, a human product directed against Myco-
mized.26 bacterium tuberculosis, was tried in poultry but was
found to be of little benefit.33 A vaccine against
Mycobacterium avium also has been given to poultry
Identification and Elimination
and, more recently, captive waterfowl in Britain.54,64
of Infected Animals
The poultry industry has relied on the use of intrader-
mal skin testing to identify and then eradicate affected ZOONOTIC POTENTIAL OF AVIAN
birds. Unfortunately, this screening test has not proven MYCOBACTERIOSIS
useful in the exotic avian species studied to date.30,40,51,77 Are birds that live in close proximity to people a poten-
In a zoological or aviary setting, an extended quarantine tial source of tuberculosis? Although the incidence of M.
period of 3 to 6 months should be considered.40,43 During avium infection in human acquired immunodeficiency
this time, screening tests should include physical exami- syndrome (AIDS) patients is increasing,40 these mycobac-
nation, hematology, serum biochemistry, acid-fast fecal terial strains are thought to be environmental in origin.
smears and serology in those species for which it is avail- Studies using DNA probes have shown that avian strains
able. Laparoscopy, fecal culture and PCR testing also of M. avium rarely infect people.2 Birds and humans are
should be considered. probably exposed to the same environmental sources of
mycobacteria.31
If birds with confirmed mycobacteriosis are not eutha-
nized, they must be kept permanently separated from
other birds. Birds that were in contact with mycobacte- CONCLUSION
ria-positive individuals also should be quarantined for 1 Avian mycobacteriosis may be caused by MAI or atypical
to 2 years. During this time, periodic retesting every 6 to mycobacteria such as M. genavense. Birds usually are
12 weeks for mycobacteriosis is recommended.26,77 exposed to mycobacteria through soil or water contami-
nated by feces. Clinical disease varies with the species
Removal or Prevention of Tuberculosis and strain of Mycobacterium spp., the species of bird
in the Environment affected and the route of transmission. Classically, how-
ever, mycobacteriosis is a disease of the gastrointestinal
To reduce the risk of exposure to mycobacteria, carefully
tract and liver in the bird. While identification of disease
consider cage design and sanitation. Prevent contact
relies on intradermal skin testing in poultry, this has not
with wild birds. In aviaries or zoological collections, one
proved useful in other avian species. Ancillary testing in
should consider solid, non-porous flooring and other
nongallinaceous birds should include a complete blood
easily disinfected surfaces instead of dirt substrate.
count, imaging, laparoscopy, cytology, serology and PCR
Footbaths should be utilized to minimize the potential
testing. A definitive diagnosis is based on culture or
introduction of mycobacteria into the enclosure.23,43
histopathology. Euthanasia is recommended for affected
Tuberculosis is more resistant to disinfectants than other birds. Control should focus on identification of affected
non-spore-forming bacteria.77 Compounds with antimy- birds through quarantine and use of appropriate screen-
ing tests. Avoiding dirt flooring may reduce exposure to
infectious material. Instead, utilize non-porous, easy-to-
Table 28.5 | Anti-mycobacterial Compounds5,8,66,81,82
• Alcohol • Peroxygens clean surfaces, appropriate disinfectants and footbaths.
• Aldehydes - • Phenolics
Formaldehyde, • Chemosterilizing gases -
Glutaraldehyde, Ethylene oxide, Beta- Products Mentioned in the Text
Succinaldehyde, Glyoxal propiolactone a. BACTEC System, Becton Dickinson, Diagnostic Instrument Systems, Inc,
• Halogens - Sparks, MD, USA, www.bd.com/clinical/products/mycob
Chlorine-releasing b. AccuProbe System, GenProbe Inc, San Diego, CA, USA,
www.gen-probe.com/prod_serv/mycobac_accuprobe.asp
agents, Iodine-releasing
c. Roche Molecular Systems, Branchburg, NJ, USA,
agents
www.roche-diagnostics.com/ba_rmd/products.html
689
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29_Mycoses.qxd 8/23/2005 2:00 PM Page 691
CHAPTER
29
Implications of
Mycoses
ROBERT D. DAHLHAUSEN, DVM, MS
Mycotic infections are relatively common in avian

species. Many fungal agents exist in the environment as
soil-borne saprophytes. Most birds are exposed to them
in their normal habitat or aviary environment without
effect. Nutritional disorders in parrots, stress of captivity
in raptors and incubation-related disorders in hatchling
galliforms, along with other causes of impaired immune
function and environmental factors conducive to fungal
proliferation, can cause disease to occur. Respiratory
tract aspergillosis and alimentary tract infections due to
Candida and other yeasts are the most frequent forms
of fungal disease observed. The early diagnosis and suc-
cessful management of systemic fungal disease can pres-
Fig 29.1 | New methylene blue stain of Aspergillus conidio-
ent a diagnostic and management challenge to the avian
phores from an air sac sample obtained at endoscopy.
practitioner. Advances in diagnostic methods, improved
knowledge of therapeutic agents and better manage-
ment practices have reduced the morbidity and mortality
associated with these agents.
Aspergillosis
Aspergillosis is a non-contagious, opportunistic infection
referring to any disease condition caused by members of
the fungal genus Aspergillus. The organism is an oppor-
tunistic, angio-invasive fungus that may act as an aller-
gen, colonizer or invasive pathogen. It can produce both
acute and chronic disease varying in spectrum from local
involvement to systemic dissemination. It is the most
frequent cause of respiratory disease and the most
commonly diagnosed fungal disease in pet birds.70 It
also is considered the most common, non-traumatically-
induced medical problem in free-ranging birds of prey.92
The disease is known to occur in a wide variety of cap-
tive and free-living birds. Almost all avian species should
be considered as potential hosts susceptible to formulated diet (G.J. Harrison, personal communication,
Aspergillus infection.2 2003) (see Chapter 4, Nutritional Considerations).
Aspergillosis is the most commonly occurring respiratory

EPIDEMIOLOGY disease in captive wild birds.95 Of the psittacine species,
Aspergillus spp. are ubiquitous fungi commonly found the African grey parrot (Psittacus erithacus) and pionus
in nature in the environment, soil and feed grains. They parrots (Pionus spp.) are reported to have an increased
are distributed worldwide and proliferate in environ- susceptibility to the development of disease.9 Localized
ments with high humidity and warm (>25° C) tempera- infection of the nasal passages is observed in Amazon
tures.62 Moldy litter, grain and bedding material contami- parrots, possibly due to the higher incidence of hypovit-
nated with feces are common media for fungal growth. aminosis A in this species.9 Raptorial species at particu-
Aspergillus fumigatus is the most commonly isolated larly high risk of developing aspergillosis include
species from birds with aspergillosis, followed by goshawks (Accipiter gentilis), rough-legged hawks
A. flavus and A. niger.22,56 Aspergillus clavatus, (Buteo lagopus), immature red-tailed hawks (Buteo
A. glaucus, A. nidulans, A. oryzae, A. terreus, A. ustus jamaicensis), golden eagles (Aquila chrysaetos) and
and A. versicolor are among the other species less com- snowy owls (Nyctea scandiaca).39,92,95 Gyrfalcons (Falco
monly isolated. rusticolus) are believed to be especially susceptible to
Aspergillus infection39,42,92,95. Among waterfowl, a higher
DISEASE PREDISPOSITION incidence of aspergillosis is seen in swans (Cygnus spp.).
Captive penguins (Sphenisciformes) also are extremely
Susceptibility to disease is greatly increased when the
susceptible to developing the disease. In these species,
immune system is impaired. Immunosuppression is the
the increased incidence of aspergillosis may reflect envi-
major factor predisposing birds to the development of
ronmental and husbandry deficiencies occurring in cap-
opportunistic Aspergillus infections. Aspergillus spores
tivity and/or increased species susceptibility.
are widespread in the environment, and many birds may
carry them in their lungs and air sacs until immunosup-
pression or stress triggers clinical disease (Fig 29.1). ASPERGILLUS PATHOGENESIS
Aspergillus spp. are widespread in nature. Birds are
Stress alone (a strong immune suppressor) or other fac-
exposed to fungal spores on a regular basis, and many
tors related to confinement, poor husbandry practice,
carry them in their lungs and air sacs without ill effect.
malnutrition, pre-existing disease and the prolonged use
The nature of disease that occurs is thought to depend
of antibiotics and steroids increase the predilection to
on the resistance of the avian host and the number and
disease.73,95 Overpopulated, poorly ventilated and dusty
distribution of fungal spores.8 Healthy birds exposed to
aviary environments lead to pulmonary and air sac dis-
high concentrations of spores can be resistant to infec-
ease. Research has confirmed a causal relationship
tion, whereas immunocompromised patients can
between high concentrations of Aspergillus spp. spores
become severely affected by minimal exposure.48,122
in the environment and aspergillosis. Damp feed or bed-
ding in warm, humid environments and poor ventilation Aspergillosis is usually contracted as the result of a sus-
allow for a high concentration of Aspergillus spores to ceptible host inhaling fungal spores. Oral ingestion of
develop.87 Corncob and walnut shell litters can grow spores from moldy feeds may also occur. The fungus is,
Aspergillus spp. in aviary environments. Inhalation of however, capable of penetrating broken skin and
large numbers of spores may occur. Birds exposed to eggshells and can infect developing embryos during the
the organism in quantities sufficient to establish a pri- incubation process.
mary infection have developed acute disease. There is
often a correlation between poor husbandry and a high In birds, aspergillosis is predominantly a disease of the
concentration of spores. Eucalyptus leaves, which have lower respiratory tract that usually occurs secondarily to
been promoted as a “natural” insect repellent, are often other disease or immunosuppressive processes. Acute
heavily contaminated with this fungus. Acute, severe, and chronic forms of the disease can occur. Infections
untreatable aspergillosis has been associated with their may be localized or diffuse, depending upon the distribu-
use.43 Aspergillosis is a common sequela to other respiration and growth of fungal organisms. Initial lesions occur
tory tract disease. A predominantly seed diet, with sub- mainly in the lungs and air sacs, although the trachea,
sequent malnutrition including vitamin A deficiency, can syrinx and bronchi also may be affected. Infections may
lead to squamous metaplasia of the oral and respiratory spread from the respiratory tract to pneumatized bone or
epithelium and the establishment of fungal growth.73 enter the peritoneal cavity by direct extension through
The incidence of fungal disorders is negligible in an the air sac walls. The organism may reach various other
avian practice where the majority of parrots are fed a tissues by vascular invasion and embolism. The fungus
Chapter 29 | I M P L I C A T I O N S O F M Y C O S E S I N C L I N I C A L D I S O R D E R S
693
Acute Disease
Acute aspergillosis is a fatal respiratory disease character-
ized by variable morbidity and high mortality. It is usu-
ally seen in young and newly captive birds and occurs
when an immunocompromised host inhales an over-
whelming number of spores. Onset of clinical disease is
rapid and followed by death within several days. Affected
birds may show dyspnea, cyanosis, lethargy, anorexia,
polyuria, polydipsia and sudden death. A white mucoid
exudate and marked congestion of the lungs and air sacs
occur. Numerous, diffusely distributed foci of pneu-
monic nodules also may be variably present.
Fig 29.2 | Miliary lung nodules due to inhalation of Aspergillus

Acute aspergillosis has been reported to occur in
spp. spores.
psittacine chicks.116 Most are septicemic and acutely
depressed when illness is observed. In addition to
can infect any organ. Aerogenous and hematogenous dis- tachypnea, dyspnea and vomiting, abdominal enlarge-
semination result in diffuse, systemic disease.49 ment due to ascites formation frequently develops. The
disease is rapidly fatal with few chicks surviving long
In the acute disease, whitish mucoid exudates of fungal enough to develop pulmonary granulomas.
growth are present in the respiratory tract. Marked con-
gestion of the lungs and thickening of the air sac mem- Mycotic Tracheitis
branes occur. Miliary foci of inflammation develop Mycotic tracheitis refers to a form of aspergillosis local-
around sites of fungal growth and result in the forma- ized in the trachea, syrinx and major bronchi.59 The
tion of micronodules (Fig 29.2).66,120 These predominate pathogenesis is similar to that for acute aspergillosis in
in the caudal thoracic and abdominal air sacs and an immune-compromised host with exposure to numer-
peripheral lung fields. In the chronic form of the disease, ous fungal spores. Colonization may occur anywhere
multiple nodules may coalesce into plaques and larger along the length of the trachea, but is most often found
granulomatous lesions. Sporulating fungal colonies may at the level of the syrinx and tracheal bifurcation (Fig
develop in the center of these lesions, with extensive 29.3).87 Granuloma formation causes a progressive course
adhesions forming between the air sac membranes, of life-threatening obstructive airway disease (Fig 29.4).
lungs and abdominal viscera. A change in vocalization may be present and is highly
suggestive of lesions in the syrinx.87 Birds also may pres-
Some Aspergillus spp. produce mycotoxins that are ent with a rapid onset of severe dyspnea, open-mouthed
immunosuppressive and may be involved in the patho- breathing, gurgling respirations or a cough.45,121 Sudden
genesis of the disease. Some mycotoxins also possess death also may occur.
carcinogenic activity. Of these, aflatoxin is well known
and may induce hepatocellular carcinoma or hepatic Chronic Disease
fibrosis with subsequent cirrhosis when ingested. Afla-
Chronic aspergillosis is the more commonly observed
toxins are most commonly associated with Aspergillus
form of the disease. It generally occurs in older birds
flavus and may contaminate feeds such as peanuts.77 that have been in captivity and is the result of long-term
malnutrition and stress.8,59 Previous disease, prolonged
DISEASE antibiotic or corticosteroid therapy and other stress fac-
tors are contributory. Some form of immunosuppression
Clinical signs associated with aspergillosis are variable
is implicated in the chronic disease.95 This form is often
and depend upon such factors as the pathogenesis of
seen in species like the African grey parrot, pionus par-
initial infection, location of lesions, organ systems
rot and Amazon parrot.
involved and host immune defenses. The disease may be
either localized or diffuse and often causes a progres- Chronic forms of the disease can be quite subtle in
sive, debilitating illness with high mortality. Aspergillosis onset, and early clinical signs are often non-specific. A
predominantly affects the upper and lower respiratory change in behavior, reduced level of activity and
tract, however, any organ system may be involved. Both decreased appetite may be observed. In some instances,
acute and chronic forms of infection are commonly rec- exercise intolerance and weight loss, even in light of a
ognized in birds. good appetite, are the only signs noticed.73 Birds with
Fig 29.3 | Granuloma (arrow) of the syrinx in a Fig 29.4 | Aspergillus granuloma (arrow) occluding the left
blue-headed pionus parrot (Pionus menstruus). bronchus in an African grey parrot (Psittacus erithacus).
The owner noted a characteristic change and
weakness in vocalizations several days prior to
finding the bird deceased.
lower respiratory tract involvement may exhibit variable tract often presents as a chronic rhinitis and sinusitis in
respiratory compromise, depending upon the nature and psittacine birds. Distension of the infraorbital sinus and
extent of the lesions present.53 With the exception of the periorbital soft tissue swellings may be present. Birds
acute form and mycotic tracheitis, lower respiratory tract may exhibit a unilateral or bilateral nasal discharge that
aspergillosis is often inapparent. Respiratory signs are can be serous to purulent in character.87 Formation of
usually absent until the disease is extensively devel- rhinoliths and oronasal granulomas may occur and often
oped.87 Tachypnea and dyspnea are not commonly obstruct the upper airways, causing wheezing respira-
observed until late in the disease process.59 tory sounds. Secondary bacterial sinus infections are
common. In psittacines, obstruction of the connection
Hepatic signs (biliverdinuria and hepatomegaly) and between the right and left nares may occur with Asper-
renal signs (polyuria, polydipsia and renomegaly) may gillus rhinitis. This obstruction may be due to the pres-
be present. Ascites also may occur. Gastrointestinal ence of caseated debris or bony deformation from
involvement (regurgitation, diarrhea and abnormal chronic infection.
droppings) is less frequently observed.
Aspergillus air sacculitis is the most frequently encoun- Central Nervous System
tered form of the disease with extension to the lungs Encephalitic and meningoencephalitic lesions may occur
commonly occurring.87 Aspergillomas may be found with disseminated aspergillosis. Necrotizing aspergillosis
throughout the entire respiratory tract but most com- with dissemination of thrombi to the brain and spinal
monly occur in the posterior thoracic and abdominal air cord is often associated with ataxia or paralysis, incoor-
sacs (Figs 29.5, 29.6). In advanced cases, changes occur dination, tremors and torticollis.73,95 A trumpeter swan
in the respiratory rate and effort and in vocalization. (Cygnus buccinator) with ataxia, incoordination and
Dyspnea and tachypnea in an unstressed bird, tail bob- heart murmur had cerebral aspergillomas and Aspergillus
bing, open-mouthed breathing and audible respiratory granulomas in both ventricles of the heart.5
sounds are indications of advanced lower respiratory
tract disease.24,59,87,112 Although auscultation is less valu- Ocular Mycoses
able in avian patients than in mammals for evaluation of
Fungal infections of the eye are rare in birds but have
respiratory tract disease, abnormal crackles or clicking
been reported in numerous species.22,56 Aspergillus fumi-
noises can indicate air sac involvement.24
gatus was isolated on conjunctival culture from a blue-
The time from onset of clinical signs to death ranges fronted Amazon parrot (Amazona aestiva) with mycotic
from less than 1 week to over 6 weeks.73 Aspergillus keratitis.56 It was implicated as a cause of severe blephar-
hyphae are tissue- and angio-invasive and can cause res- itis and dermatitis of the eyelids in a falcon/gyrfalcon
piratory hemorrhage and acute death in affected birds at hybrid (Falco peregrinus X Falco rusticolus) and kerati-
any stage of the disease process (Fig 29.7). tis in chickens.1,10 Most reported occurrences result from
the extension of preexisting upper respiratory infec-
Localized aspergillosis involving the upper respiratory tions, although ocular trauma and corticosteroid therapy
695
are other predisposing factors.10,56,64 Affected birds may

show blepharospasm, photophobia, severe periorbital
swelling and conjunctival hyperemia.22,56 Corneal epithe-
lial erosions and stromal necrosis may result in perfora-
tion of the cornea or panophthalmitis, resulting in func-
tional loss of the eye.56 Characteristic signs with recent
stress and/or poor nutrition should make aspergillosis a
strong presumptive diagnosis.
ASPERGILLUS DIAGNOSIS
Antemortem diagnosis of aspergillosis is challenging and
often requires several diagnostic methods.15,79 A pre-
sumptive diagnosis is often based upon the clinical his-
tory, physical exam, clinical impression, complete blood
count, radiography and endoscopy. History of a previous
stressful event, an immunosuppressive disease or treat-
Fig 29.5 | Aspergillus fumigatus granuloma ment and/or exposure to spore-laden environments is
exhibiting conidiophore growth in the lung and air supportive. Clinical signs, especially dyspnea, weight
sacs of an African grey parrot (Psittacus erithacus).
loss, exercise intolerance and chronic debilitation, also
suggest aspergillosis; however, a definitive diagnosis
requires confirmation of the organism by cytology, cul-
ture, histopathology or DNA testing.8,15,59 Demonstration
of the causal agent consistent with the clinical disease
and observed lesion(s) is the diagnostic goal.
Hematology and Serum Chemistry

Aspergillosis generally causes a significant heterophilic
leukocytosis (25,000 cells/µl to 100,000 cells/µl), which
may be associated with both acute and chronic dis-
ease.15,18 White blood cells are often very reactive and a
left shift may be present. Heterophils often exhibit
degranulation and other toxic signs. Reactive lymphocyte
Fig 29.6 | Fungal granuloma in avian lung tissue, central area
of necrosis with fungal hyphae. PAS fungal stain. changes also occur and may result in a marked lym-
phopenia, especially in Amazon parrot species.44 A mono-
cytosis is often observed in chronic forms of the disease.19
A non-regenerative anemia due to the chronic inflamma-

tion of the disease is often present. Lack of an appropri-
ate bone marrow response may be evidenced by the
absence of polychromasia, reticulocytosis, macrocytosis
and/or anisocytosis.60 Psittacosis and mycobacteriosis can
induce similar hemograms.
Serum biochemistry analysis may show an increase in

aspartate aminotransferase (AST), lactate dehydrogenase
(LDH) and serum bile acids if liver involvement is pres-
ent. Hypoalbuminemia and hypergammaglobulinemia
also are characteristic of the disease.87
Fig 29.7 | Mycelial growth of Aspergillus fumigatus throughout
Plasma protein electrophoresis may help support the
an avian pulmonary granuloma. PAS fungal stain.
diagnosis of aspergillosis in psittacine birds but is not
specific for this disease. Observed changes in the plasma
protein electrophoretograms are indicative only of a
non-specific inflammatory response.
696
In one study, most (6/7) birds exhibited moderate to

marked decrease in the plasma albumin to globulin
ratio.58 Some (3/7) birds showed a moderate to marked
increase in β-globulin concentrations. Affected birds may,
however, demonstrate normal values for these indices.
Serology
Aspergillus antibody titers have only a moderate predic-
tive value in disease diagnosis. The indirect ELISA assay
(The Raptor Center, University of Minnesota) measures
Aspergillus antibody levels and has shown useful correla-
tion with clinical infections in raptor species, although
false-negative results can occur.95 The test requires
species-specific antibody conjugates and is most useful in
these species. In a report of falconiform birds with con-
firmed aspergillosis, 43% (10/23) of the birds had moder-
ate to marked antibody titers, whereas 22% (5/23) had Fig 29.8 | Radiograph of an Aspergillus granu-
loma (arrow) in the air sac of a blue and gold
negative titers.93 In contrast, all 112 owls described in the
macaw (Ara ararauna).
same report had negative antibody titers despite con-
firmed aspergillosis in some of these birds. In a study of
captive penguins (Spheniscus humboldti, Spheniscus Radiology
magellanicus, Pygoscelis adeliae) with confirmed Radiographic evaluation can demonstrate the distribution
aspergillosis, many birds had markedly increased titers and severity of mycotic lesions in the lungs and air sacs
and only 20% had negative antibody titers.96 but is usually of limited diagnostic value until late in the
disease process. Although mycotic air sacculitis with gran-
A negative antibody titer in an infected bird may be
uloma formation is well documented in a variety of avian
explained either by a lack of reactivity between the test
species, lesions are usually advanced before becoming
conjugate and patient immunoglobulins or by a lack of radiographically apparent.24,87,112 A bronchopneumonia
patient humoral response (immunosuppression). Lack with marked parabronchial patterns is one of the more
of humoral response also has been attributed to seques- common radiologic findings.73 The fibrinous air sacculitis
tration of the infection site.26 In raptors, indirect ELISA associated with aspergillosis allows for radiographic visu-
values in the mid to high range help confirm the diagno- alization of the air sac walls.87 Asymmetry, hyperinflation
sis when aspergillosis diagnosis correlates with the clini- or consolidation of the air sacs may be evident. A nodular
cal signs shown by the patient.93 A positive result means air sacculitis with focal air sac densities is often seen and
active infection, long-term exposure or previous infec- occurs primarily in the abdominal and, less often, tho-
tion antibody.95 The test should be utilized with hematol- racic air sacs. Single or multiple soft tissue densities in
ogy, endoscopy, radiology, and tracheal or air sac culture the air sacs or lungs are most often granulomas but
in potential aspergillosis cases. With treatment, the anti- should be considered non-specific (Fig 29.8).73 Although
body titer generally rises, and with successful treatment intraluminal granulomas of the syrinx, trachea and main
then falls to undetectable levels. Failure of the titer to stem bronchi are fairly common, they are seldom visual-
rise or subsequently drop with treatment is a poor prog- ized radiographically. The syrinx is often obscured by
nostic sign.15 soft tissue and bone.87 Fungal air sacculitis usually causes
plaque-like and nodular granulomatous lesions in the
Aspergillus antibody testing is probably less useful in air sacs. Even after the successful resolution of clinical
psittacine species. In a report documenting the sensitiv- Aspergillus infection, lungs and air sacs may remain
ity of serologic testing in detecting aspergillosis in thickened and irregular and appear abnormal both radio-
psittacine birds, Aspergillus antibody and antigen ELISA graphically and via endoscopic examination.
titers in infected birds were weakly positive.58 The inci-
dence of weakly positive antigen titers in clinically nor- Computed tomography (CT) scans provide a detailed
mal birds is reported to be high, making these results image of all parts of the respiratory tract and are useful
difficult to interpret clinically.26,58 Currently, there is no for demonstrating small lesions that are not visible on
hematologic test that can reliably detect aspergillosis in radiographs and for visualizing lesions in the infraorbital
psittacine birds.58 sinus, retrobulbar area, trachea and main stem bronchi.87
697
Fig 29.9 | Aspergillus spores and avian red blood cells from a Fig 29.10 | Hyphal elements and spores of Aspergillus fumiga-
clinical sample obtained during diagnostic endoscopy. tus in Gram’s-stained clinical specimen collected at endoscopy.
A concurrent hepatomegaly and renomegaly may be ylene blue stain.95 Microscopic evaluation often reveals
visualized on radiography or detected by abdominal long, dichotomously branched (~45°), septate hyphae,
palpation.59 2.5 to 4.5 µm in diameter. Fruiting bodies with spores
also may be identified (Fig 29.10).
Endoscopy
Air sac consolidation and granulomas can obscure radi- Confirming the Diagnosis
ographic detail in the coelomic cavity. Lesions are often Histopathology and fungal culture can be used to
best observed by endoscopy, which is an efficient way to demonstrate the organism in clinical samples and are
detect and sample fungal plaques in the trachea, syrinx important in providing a confirmed diagnosis of the dis-
or lower respiratory tract.94,109 ease. DNA probe testing of clinical specimens also can
validate the diagnosis. Tracheal swabs or air sac swabs
The trachea (depending on species and the size of scope and granuloma biopsy specimens obtained at endoscopy
being used) can be visualized down to the level of the can be tested specifically for A. fumigatus.a Genus-
syrinx with both rigid and flexible endoscopes. Depend- specific probes can be used to test for Aspergillus spp.
ing on the extent of the disease and chronicity of the in general. Research on the use of DNA probe testing of
condition, air sacs that are normally thin and transparent whole blood samples suggests that this may be helpful
may be thickened, cloudy or covered with exudate. Early in providing a confirmed diagnosis of the disease.
in the disease process, prominent vascularity of the air
sacs may be the only observable abnormality.95 Fungal air
sacculitis usually causes plaque-like, coalescing and TREATMENT
nodular granulomatous lesions in the air sacs. Plaques Amphotericin B
vary from white to yellow in color to green to black on
Amphotericin Bb is an amphoteric polyene macrolide
the surface, owing to the development of conidia and
anti-fungal agent.72 Its mechanism of action is to bind
fungal spores.97 The observation of typical lesions by
ergosterol, the principal sterol present in the cell mem-
endoscopy with biopsy sample collection for cytology,
brane of sensitive fungi.65 It has a wide spectrum of activ-
histopathology or fungal culture can provide a confirmed
ity, being fungicidal to both Aspergillus spp. and Candida
diagnosis of aspergillosis. Endoscopy is useful in evaluat-
spp., and to other fungi including Blastomyces, Coccid-
ing the extent of infection and monitoring progress dur-
ioides, Histoplasma, Sporothrix and Mucor spp.
ing treatment94 (see Chapter 1, Clinical Practice and
Chapter 24, Diagnostic Value of Endoscopy and Biopsy). Amphotericin Bb has been used to treat both systemic
and topical fungal infections in birds.38 It can be adminis-
Cytological Evaluation tered intratracheally, intravenously, in sinus flushes and
Cytologic evaluation of clinical samples can aid the diag- through nebulization. Parenteral use quickly establishes
nosis of aspergillosis. Choanal swabs, infraorbital sinus fungicidal concentrations, making it a frequent choice for
aspirates, tracheal and air sac swabs and washings may initial therapy. The drug is eliminated by the kidneys and
reveal Aspergillus hyphae and spores (Fig 29.9).8 Squash is used for only short duration due to the risk of induced
preparations of wet mount clinical specimens are pre- nephrotoxicity. A dose of 1.5 mg/kg IV is administered
pared and stained with lactophenol cotton blue or meth- q8h for a period of 3 to 5 days and in combination with
itraconazolec, fluconazoled or terbinafinef orally.38 respiratory tissue levels.70

Combined nebulization therapy with clotrimazolee or
terbinafine also is suggested (see Chapter 9, Therapeutic Itraconazolec is marketed as capsules containing coated
Agents). lactose granules, which are soluble only at low pH.
Dissolution of these granules in acid solutions results in
Sinus and tracheal aspergillosis are more difficult to improved bioavailability and higher blood itraconazolec
treat. Intratracheal use of amphotericin Bb at 1 mg/kg levels following oral administration in avian patients.61,83
q8-12 h has been described as supplemental treatment Absorption also is enhanced when the drug is adminis-
for these infections. Topically, the drug can be very tis- tered with a fatty meal.82 It is recommended that itra-
sue irritating and must be diluted in water (saline inacti- conazolec beads from a 100-mg capsule be divided into
vates amphotericin Bb) to reduce the risk of iatrogenic five equal parts of 20 mg each. Each 20-mg aliquot is dis-
sinusitis or tracheitis.59 Nebulization with amphotericin solved in 0.4 ml of 0.1 N HCl. The resulting solution is
Bb has been reported to cause severe bronchoconstric- diluted to a final concentration of 5 mg/ml by the addi-
tion in horses.13 Amphotericin Bb has been used in nebu- tion of orange juice.61 For avian dosing, the drug is
lization and sinus flushes for 20 years in avian species administered by gavage with food. Itraconazolec also is
with good success and no clinical complications. available in a 10 mg/ml liquidc for oral administration
that avoids any concern with sufficient dissolution or
Itraconazole suspension.
Itraconazolec is one of the most widely used antifungal
agents in birds and is especially effective in combination Other Agents
with nebulized clotrimazolee and/or intravenous ampho-
Fluconazoled is effective against aspergillosis although
tericin Bb.40,81,95 It has greater efficacy than ketoconazolei
generally less so than itraconazolec. It is rapidly
or fluconazoled against Aspergillus spp. and has less
absorbed with high bioavailability after oral administra-
potential toxicity than amphotericin Bb.47,95,115 It has been
tion. The drug is widely distributed to the extracellular
used effectively to treat aspergillosis in raptors,
space, making it useful for treating mycoses of the eye
psittacine birds and waterfowl, and is a recommended
and central nervous system.71 Aspergillus keratomycosis
treatment of choice in these species.38,40,81,95
in a blue-fronted Amazon parrot was treated with oral
Itraconazolec is eliminated by hepatic metabolism and is and topical fluconazoled.56 A dose of 5 to 15 mg/kg PO
generally well tolerated during long-term use.83 The q12h is recommended in most psittacine species.21
effective drug dose and potential for adverse effects is
Clotrimazolee and enilconazolek are relatively insoluble
variable among avian species. In most psittacine species,
and useful against aspergillosis only at sites that can be
effective serum concentrations are attained when ther-
treated topically with the drug or reached by inhalation
apy is initiated at 5 to 10 mg/kg PO twice daily for 5
or nebulization. Miconazolel is effective for treating fun-
days, then once daily for the duration of treatment.82,87
Temporary anorexia and lethargy were the only side gal keratoconjunctivitis when used in an ophthalmic
effects observed in an orange-winged Amazon parrot form with frequent medication intervals (q3-4h).4,14,41,56
(Amazona amazonica) treated with 5 mg/kg itracona-
Terbinafine hydrochloridef is a synthetic allylamine anti-
zolec for 1 year.83 African grey parrots are reportedly
fungal agent that is fungicidal against a wide variety of
more sensitive to itraconazolec and may exhibit adverse
dermatophytes, molds and fungi. The drug’s efficacy is
drug effects at normal dosage levels. One report sug-
similar to or more effective than amphotericin Bb and
gests that the drug may have contributed to several
itraconazolec against Aspergillus spp., and has been used
deaths in this species.83 A dose of 2.5 to 5.0 mg/kg PO
to treat aspergillosis effectively in psittacine species.28 In
q24h is recommended for use in African grey parrots.87
addition to its fungicidal property, terbinafinef has good
Itraconazolec is safe in raptors when dosed at 10 mg/kg ability to penetrate mycotic granulomas. It is readily
per day PO for 3 to 6 months duration.61 Hawks treated absorbed after oral administration and has a low poten-
at this level reached steady state plasma levels within 2 tial for adverse side effects. No signs of toxicosis were
weeks, with effective organ tissue levels adequate to observed during prolonged drug administration in
treat most fungal infections.61 Poor distribution in the psittacine birds.28 The drug has proven very useful as an
respiratory tissues after oral dosing in pigeons has been alternative treatment for avian aspergillosis, especially in
reported, which might limit applicability in this species.70 cases where more conventional therapies have been inef-
A dose of 6 mg/kg q12h in pigeons achieves effective fective. The combination therapy of terbinafinef at 10 to
plasma concentrations; however, a comparatively higher 15 mg/kg PO q12-24h with iatraconazolec is a safe and
dose of 26 mg/kg PO q12h is needed to attain effective very effective treatment for systemic avian fungal disease.
699
Nebulization Therapy Cannulae also may be used to induce and maintain

Aerosolization therapy is used to augment systemic treat- anesthesia during tracheal, syringeal or oral surgery. For
ment by delivering drugs directly to the respiratory tract. suspected tracheal granulomas, an open-end tom cat
Target tissues receive high concentrations of the drug catheter can be used to obtain clinical samples and for
while minimizing systemic exposure.13 In addition, hepatic suction therapy to cannulate the tracheal lumen. Trache-
first-pass metabolism following oral administration is cir- otomy, through a ventral midline incision centered over
cumvented.13 Clotrimazolee supplied as a 1% solution can the thoracic inlet, may be used to access granulomas in
be used for nebulization therapy at 30 minutes q24h.63 the tracheal lumen.30,89 If the granuloma is at the level of
However, a 15% aqueous suspension can be com- the syrinx, blunt dissection through the interclavicular air
pounded, which appears to be more effective than the sac or an alternative left lateral approach may provide
commercial form (P. Redig, personal communication, needed access.89 A clavicular osteotomy may be necessary
2003). Terbinafine hydrochloridef nebulized as a 1 mg/ml to improve surgical access to the syrinx in some birds.89
aqueous solution (20 minutes q8h) was effective in resolv-
Fungal granulomas of the lower respiratory tract are
ing a non-responsive respiratory aspergillosis in a 6-year-
often resistant to medical therapy.24,87,112 Surgical resec-
old Congo African grey parrot (Psittacus erithacus).28
tion of these masses has been recommended; however,
A commercially available disinfectantg is useful for treat- little has been published about techniques and their
ment of birds within their quarters or en masse when respective success.24,89,109 Attempts at surgical removal are
nebulized at a 1:250 aqueous dilution. Nebulization often incomplete due to the location of granulomas
therapy q12h for 3 to 12 weeks has been successful in within the respiratory tract and the need to minimize
the treatment of aspergillosis in a 12-week-old Congo trauma to adjacent structures.53 Endoscopy allows access
African grey parrot and effective in combination with to most of the lower avian respiratory tract with minimal
itraconazolec for raptorial species.7,107 It also can be used trauma and is an alternate approach for removing these
to fog aviary rooms and pigeon lofts to reduce the level lesions.109 A detailed knowledge of the avian air sac sys-
of fungal contamination in these premises107. tem and competence with the rigid endoscope is a pre-
requisite before attempting this procedure53 (see chapter
Surgical Treatment 24, Diagnostic Value of Endoscopy and Biopsy).
Treatment of respiratory aspergillosis is clinically chal- A recent report describes endoscopic debridement and
lenging. Granulomatous lesions may occlude vital respi- laser ablation as a viable alternative to conventional sur-
ratory pathways or prove resistant to therapy because of gery in the management of lung and air sac granulomas.53
poor drug penetration into the encapsulated lesions.24,87,112 A gallium-aluminum-arsenide diode laser, employing flex-
If nebulization and systemic administration of antifungal ible fibers passed through the operating channel of the
agents is not effective, surgical debulking of granulomas rigid endoscope, was used to ablate remaining granulo-
may be necessary.87 For infections of the sinus cavities, matous tissues in the air sacs after endosurgical debulk-
trephination of the frontal sinuses permits direct access ing.53 A small volume of amphotericin Bb was used to ster-
to granulomas for debridement and topical application ilize the remaining lesion. Greater clinical success was
of medications in an otherwise inaccessible site.87 achieved by endosurgical debridement and laser ablation,
compared with conventional surgical exploration and
Rhinitis or sinusitis of Aspergillus origin may require
removal of granulomas or medical therapy alone.53
enzymatic therapy to dissolve the caseated debris and
allow flushing of the affected area with the appropriate
Summary
antifungal agent. Both hyaluronidase and trypsin-based
flushes have been used for this purpose. In treating aspergillosis, proper supportive care includ-
ing heated environment, fluids and nutritional support
Tracheal and syringeal granulomas may precipitate life- are essential. Because affected birds are severely com-
threatening respiratory tract obstructions. Granulomas promised, the risk of secondary bacterial infections is
often form just proximal to or at the bifurcation of the significant. Antibiotic therapy is indicated. Prolonged
trachea. Birds can effectively ventilate through cannulae antifungal therapy for periods up to 4 to 6 months is
placed in the clavicular, caudal thoracic or abdominal air often necessary for treatment success.
sacs.33,51,98,101 These can provide an alternative airway in
emergency cases of tracheal obstruction and can be used Patients should be closely monitored for clinical
for both short- and long-term duration. They can be left improvement and observed for any signs of toxicosis
in place for periods of up to 1 week, but should be during this period. Treatments are usually continued for
removed when possible to prevent iatrogenically 1 month after the complete blood count has returned to
induced air sacculitis.89,101 normal.87 Aspergillosis is a preventable disease. Proper
Fig 29.11 | Candida albicans in an avian fecal Gram’s stain. Fig 29.12 | Candida albicans exhibiting mycelial growth in a
Yeast in this form proliferates in the lumen of the digestive tract fecal Gram’s stain from a cockatiel (Nymphicus hollandicus).
and is responsive to topically acting antifungal agents (nystatinh). Yeast in this form is tissue invasive and requires systemic anti-
fungal therapy for proper treatment.
diet and husbandry practices to reduce stress and pro- crop stasis, inappetence and poor digestion of food.
vide good hygiene will reduce factors that predispose to Droppings are often abnormal, appearing brownish in
the development of this disease. color and watery. Affected chicks do not grow or gain
weight well and appear stunted.
Lesions vary in severity. They consist of thickening of the

Candidiasis digestive tract mucosa with increased mucous and
pseudomembranous patches. The choanae may become
Candidiasis in birds, also known as thrush, moniliasis or
abscessed with formation of a diphtheritic membrane in
sour crop, refers to infections by yeasts of the genus
the oropharynx as mycelial growth develops.102 Whitish
Candida. C. albicans is the most commonly implicated
plaques may be evident under the tongue, in the mouth
species, although C. parapsilosis, C. krusei, and C. tropi-
and most frequently in the crop. In advanced cases,
calis also may cause disease.103
stomatitis and palpable thickening of the ingluvies are
C. albicans is an opportunistic yeast and not regarded as present. Endoscopic examination of affected membranes
a primary pathogen. Small numbers of the non-budding of the oropharynx, crop, esophagus, proventriculus and
organism are commonly found in the digestive tract of ventriculus may reveal white-grey to grey-green, thick-
normal birds and considered normal flora in healthy ened and diphtheritic membranes. A characteristic
pigeons.102 Host defense mechanisms and bacterial flora “Turkish towel” thickening of the crop lining is evident
keep numbers of the organism controlled. Candida spp. in advanced cases.
can proliferate and cause disease when digestive tract
Diagnosis is made by identifying the organism on wet
flora are severely suppressed. In most cases, the infec-
or Gram’s-stained smears from lesions in the oral cavity,
tion is endogenous in origin, occurring secondarily to
crop or cloaca (Fig 29.11). Crop washings and fecal
stress, immunosuppression, inadequate nutrition, poor
samples also may be used. Candida albicans grows as a
sanitation, debilitation or in birds that have been exten-
budding yeast cell, oval in shape, 3.5 to 6.0 x 6.0 to 10.0
sively treated with antibiotics.
µm in size. High numbers of budding yeast confirm the
This disease is most often seen in psittacine neonates diagnosis. The presence of elongated pseudohyphae
and cockatiels. Yeasts gain entry into the host by the oral suggests more severe infection with deeper tissue
route.102 The organisms can be transmitted from the par- involvement (Fig 29.12). The organism can be cultured
ent bird to chicks during regurgitative feeding. The on mycological agar with cycloheximide and chloram-
infection also may be spread throughout the nursery phenicol at 37° C for 24 to 48 hours. Growth appears as
population by the use of contaminated fomites and feed- shiny and convex round colonies measuring 3 to 5 mm
ing utensils. in diameter, pearl white to light cream in color.
Candidiasis affects the mucocutaneous areas of the body Differential diagnoses for inflammation of the upper gas-
and gastrointestinal mucosa, particularly of the orophar- trointestinal tract include bacterial stomatitis, trichomo-
ynx, crop and esophagus. Affected birds are depressed niasis, capillariasis and nutritional disorders (see
and may exhibit delayed crop emptying, regurgitation, Chapter 4, Nutritional Considerations).
701
TREATMENT sents a new genus of ascomycetous yeast called Macro-

Correction of the diet and husbandry are necessary for rhabdus ornithogaster.91,110 The clinical condition in
successful treatment of candidiasis. Nystatinh is the first birds is more properly referred to as macrorhabdosis.
drug of choice for yeast infections confined to the ali- The reader is referred to Chapter 30, Implications of
mentary tract. It is not absorbed from the digestive tract Macrorhabdus in Clinical Disorders in this text for
and is effective for oral or topical use only. Nystatinh is detailed discussion on this topic.
fungistatic in action and must come in contact with the
organism to be effective. Oral lesions may not respond if
the drug is administered by gavage tube beyond this site
of infection. The drug also can be applied directly to
Mycotic Dermatitis
lesions of the mucous membranes in the oropharynx. Fungal dermatitis is rarely reported in birds, even
The recommended dose of 290,000 units/kg PO q8-12h though fungi such as Trichophyton and Aspergillus spp.
is safe and effective for use in psittacine neonates.21 For have been recovered from the feathers, skin and eyes of
flock treatment, nystatinh can be added to the drinking healthy birds.32,122 Infections of the integument caused by
water at 100,000 IU/L.102 Candida albicans, Rhodotorula, Microsporum gallinae,
Aspergillus, Rhizopus, Malassezia and Mucor species
Severe yeast infections may be refractory to nystatinh have been described.17,25,85,118 Skin and feather lesions
therapy. If the organism is resistant to nystatinh or is in associated with Aspergillus have been recognized in
the hyphal stage, having penetrated the wall of the pigeons and psittacine birds.111 Aspergillus and
digestive tract, systemic antifungals are indicated. Alternaria spp. also have been associated with epider-
Fluconazoled or ketoconazolei are the systemic drugs of mal cysts in the domestic chicken.108 Other reports of
choice. Fluconazoled is one of the most effective antifun- fungal dermatitis include Trichophyton in canaries
gal agents for the treatment of tissue-based yeast infec- (Serinus canarius), Microsporum gypseum in budgeri-
tions. A dose of 5 to 15 mg/kg PO q12h is recommended gars (Melopsittacus undulatus), Microsporum gallinae
for most avian species.21 It also is effective against ali- and Cladosporium berbarum in chickens (Gallus
mentary tract yeast when added to the drinking water at gallus) and Candida species in gallinaceous birds.66,105,111
50 mg/L.102 Ketoconazolei also can be used to treat sys-
temic yeast infections at 10 to 30 mg/kg PO q12h. It can Favus, commonly referred to as “avian ringworm,”
be added to the drinking water at 200 mg/L for flock describes a mycotic dermatitis found primarily in gallina-
treatment of pigeons.102 ceous birds. It consists of white, crusting lesions of the
face, comb and wattles that can extend to the feathered
Itraconazolec has been used in the successful treatment portion of the head. Microsporum gallinae is the agent
of candidal tracheitis in a blue and gold macaw (Ara most often involved, although M. gypseum and Trich-
ararauna) and candidal infection of the uropygial gland ophyton simii also have been isolated.
in a king penguin (Aptenodytes patagonicus).55 Some
Candida spp. are, however, extremely resistant to itra- Correction of diet and husbandry issues combined with
conazolec.114 The drug is unlikely to achieve therapeutic topical and oral systemic miconazolel therapy is usually
concentrations at 5 mg/kg and should be used at the efficacious in treating mycotic dermatitis in affected
higher dose of 10 mg/kg PO q24h. birds.
Oral chlorhexidinej at 10 to 20 ml per gallon drinking

water for 3 weeks can be used for flock control of
Candida infections but generally will not eliminate Cryptococcosis
them. Mild cases of candidiasis may respond to
Cryptococcosis is most commonly caused by infection
acidification (see apple cider vinegar in Chapter 9,
with Cryptococcus neoformans var. neoformans, an
Therapeutic Agents).
encapsulated saprophytic fungus with worldwide distri-
bution. Cryptococcus neoformans var. gatti is more geo-
graphically restricted because of an ecological associa-
Macrorhabdosis tion with the river red gum (Eucalyptus camaldulensis)
and other eucalyptus trees.34 The organism is commonly
Clinical disease caused by the organism historically found in soils contaminated with bird droppings.68
known as Megabacterium has been referred to as
megabacteriosis, Megabacterium-associated disease and While cryptococcosis is a rare disease of birds, dissemi-
proventricular disease in birds.6,36 More recent studies nated infection has been reported in the green-winged
have confirmed that the organism is a fungus and repre- macaw (Ara chloroptera), Moluccan cockatoo (Cacatua
moluccensis), thick-billed parrot (Rhynchopsitta zoo specimens. The soil-borne organism Histoplasma
pachyrhyncha) and North Island brown kiwi (Apteryx capsulatum has worldwide distribution and is endemic
australis mantelli).23,27,35,54,100 Infections may involve the in the eastern and central USA. It is commonly associ-
respiratory tract, digestive tract and central nervous sys- ated with fecal material from pigeons and gallinaceous
tem, producing necrotic granulomatous lesions and a birds, and has the potential to grow within dirt sub-
characteristic thick, pale, gelatinous exudate. The lower strates of enclosed aviaries.8 Histoplasma infections in
temperature of the upper respiratory tract makes it more birds produce disease signs similar to those seen with
susceptible than other areas of the body to initial colo- Cryptococcus spp. infections. An initial pneumonia can
nization with Cryptococcus.23 Upper respiratory tract progress to disseminated disease with the formation of
involvement can produce facial granulomas that distort necrotic granulomas. Histoplasmosis was identified as
the rhamphotheca.20,27,31 A chronic rhinosinusitis resem- the cause of an osteomyelitis and mineralized soft tissue
bling a neoplasm of the rhamphotheca was described in granuloma of the shoulder and antebrachium in a
a Major Mitchell’s cockatoo (Cacatua leadbeateri) and Moluccan cockatoo.119 The infection should be consid-
was due to C. neoformans var. gatti.90 An encephalitis or ered part of the differential diagnosis of granulomatous
meningitis also may occur, causing blindness or paralysis respiratory disease in avian patients. Diagnosis is based
in affected birds.23,35 on culture of the organism and histopathologic examina-
tion of tissue samples.
Diagnosis of cryptococcosis should be based on cytology
and histopathology in combination with culture rather
than culture of nasochoanal swabs or washes alone.90
Cryptococcus neoformans var. neoformans and var. gatti Mucormycosis
may be carried asymptomatically in the upper respira-
tory tract. Wright’s-stained smears of gelatinous material The order Mucorales includes a number of saprophytic
often reveal aggregates of encapsulated yeast organisms fungi that have been implicated as possible avian patho-
measuring 6 to 10 µm within 8- to 12-µm non-staining gens. They have been implicated as an etiologic agent of
capsules.90 meningoencephalitis in birds.11,86 Hyphal invasion of cere-
bral blood vessels and dissemination of an Absidia sp. in
Veterinarians must use extreme caution when handling the cerebrum was identified as the cause of progressive
clinical materials that may contain Cryptococcus spores. neurologic defects culminating in seizures in a chattering
Most human infections occur through contact with con- lory (Lorius garrulus).80 Other clinical syndromes
taminated exudates, fecal material and non-clinical described include air sacculitis in a pigeon (Columba
infected or diseased birds.74,78 While human infection sp.), pneumonia in a rock hopper penguin (Eudyptes
with C. neoformans var. neoformans is well recognized crestatus) and a group of rock ptarmigan (Lagopus
in immunosuppressed patients, infection with C. neofor- mutus), and an osteolytic mass involving the ribs and air
mans var. gatti is commonly associated with otherwise sacs of a penguin (Sphenisciformes).12,50,67,84 The feeding of
healthy and immunocompetent individuals.68,106 damp, germinated seed has been implicated in dissemi-
nated mucormycosis causing alimentary granulomas in a
Antifungal agents such as amphotericin Bb, fluconazoled
group of canaries (Serinus canarius) and nephritis in an
or itraconazolec have been suggested as treatment for
African grey parrot; glossitis in an African grey parrot;
cryptococcosis.23 Fluconazoled administered orally at a
myocarditis in an Australian parakeet (Psittacula sp.);
dosage of 8 mg/kg q24h for 2 months was successful in
and nasal infection in waterfowl.16,29,75 Absidia corymb-
resolving bilateral nasal cryptococcosis in an African grey
ifera is the pathogen most often isolated, although
parrot, but the lesions recurred 3 years later.31
Mucor and Rhizopus spp. also are identified.66
Although cryptococcosis is a rare disease of birds, the
Antemortem diagnosis of mucormycosis is difficult
zoonotic potential associated with this infection is signif-
because the organisms do not culture well from clinical
icant. Veterinarians must be aware of this disease when
samples.69 Histopathology of biopsy specimens is more
diagnosing and treating upper respiratory disease in
reliable in confirming the diagnosis.80
birds and must remember to discuss the zoonotic poten-
tial of this infection with their clients.
No effective treatment of mucormycosis in birds has
been reported. Amphotericin Bb is the single most reli-
able agent used in humans.
Histoplasmosis Other antifungal medications including nystatinh, 5-fluor-
Histoplasmosis is an infectious but not contagious cytosinem, clotrimazolee and miconazolel are reported to
mycotic disease that has been reported in poultry and have no consistent in vivo activity against the Mucorales.69
703
Dactylariosis c. Sporanox, Janssen Pharmaceutical Inc, Titusville, NJ 08560, USA

d. Diflucan, Pfizer Inc, New York, NY, USA
e. Lotrimin, Schering, Schering Corporation, Kenilworth, NJ 07033, USA
f. Lamisil, Novartis Consumer Health, Inc, Summit, NJ 07901-1312, USA
Dactyloriosis is a fatal encephalitis of poultry caused by g. F10, Health and Hygiene Ltd, PO Box 347, Sunning hill 2157, South
Dactylaria gallopava. The organism grows in old saw- Africa, www.healthandhygiene.net
h. Nystatin oral suspension, Lederle Standard Products, Pearl River, NY
dust and wood shavings. Infection involves the central 10965, USA
i. Nizoral, Janssen Pharmaceutica, Titusville, NJ 08560, USA
nervous system, causing torticollis, incoordination, j. Nolvasan, Fort Dodge Animal Health, Fort Dodge, IA 50501, USA
tremors and sternal recumbency. The respiratory system k. Enilconazole, Janssen, Titusville, N.J. 08560
l. Miconazole, Janssen, Titusville, N.J. 08560
is a less commonly involved site. The signs and lesions m. 5-fluorcytosine, Rocké Pharmaceuticals, Nutley, N.J. 07110
of dactylariosis resemble those caused by aspergillosis.
Culture can be used to differentiate the infection.
Resources Mentioned in the Text

a. Veterinary Molecular Diagnostics, Inc, 5989 Meijer Dr, Suite 5, Milford,
OH 45150, USA, 513-576-1808
b. Fungizone, Bristol-Meyers Squib Company, Princeton, NJ 08543, USA
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Med Surg 9:162-174, 1995.
62. Jordan FTW: Fungal diseases. In Medicine and Surgery. Phila- Vet, 1995, pp 61-64.
Jordan FTW (ed): Poultry delphia, WB Saunders Co, 1997, 97. Richard JL, et al: Recent studies 113. Ungerechts N: Radiographic
Diseases 3rd ed. Philadelphia, pp 323-331. on aspergillosis in turkey poults. signs of proventricular infection
Bailliere Tindall, 1990, pp 216- 80. Orcutt CJ, Bartick TE: Mucor- Mycopathologia 87:3-11, 1984. with “megabacteria.” J Avian
225. mycotic meningoencephalitis and 98. Rode J, Bartlow S, Ludders J: Med Surg 4:203, 1990.
63. Joseph V, Pappagianis D, Reavill pneumonia in a chattering lory Ventilation through an air sac 114. Van Cutsem J, Van Gerven F,
DR: Clotrimazole nebulization for (Lorius Garrulus). J Avian Med cannula during tracheal obstruc- Janssen PAJ: Activity of orally,
the treatment of respiratory Surg 8:85-89, 1994. tion in ducks. J Avian Med Surg topically, and parenterally
aspergillosis. Proc Assoc Avian 81. Orosz SE, Frazier DL: Antifungal 4:98-102, 1990. administered itraconazole in the
Vet, 1994, pp 301-306. agents: A review of their pharma- 99. Rossi G: Histological and treatment of superficial and
64. Kern TJ: Exotic animal ophthal- cology and therapeutic indica- immunohistochemical findings deep mycoses: Animal models.
mology. In Gelatt KN (ed): tions. J Avian Med Surg 9:8-18, in proventricular mucosa of Rev Infect Dis 9:15-32, 1987.
Veterinary Ophthalmology 3rd ed. 1995. chickens experimentally infected 115. Van Cutsem J, Janssen PAJ: In
Philadelphia, Lippincot, Williams 82. Orosz SE, et al: Pharmacokinetic with “megabacterium.” Proc vitro and in vivo models to
& Wilkins, 1999, pp 1273-1305. properties of itraconazole in blue- Euro Soc Vet Pathol, 2000, p study the activity of antifungals
65. Kerridge D: Mode of action of fronted Amazon parrots 156. against Aspergillus. In Vanden
clinically important antifungal (Amazona aestiva aestiva). J 100. Rosskopf WJ, Woerpel RW: Bossche H, MacKenzie DWK,
drugs. Adv Microbiol Physiol 27:1- Avian Med Surg 10:168-173, 1996. Cryptococcosis in a thick-billed Cauwenbergh G (eds):
72, 1998. 83. Orosz SE, et al: The effects of for- parrot. Proc Assoc Avian Vet, Aspergillus and Aspergillosis.
66. Keymer IF: Mycosis. In Petrak ML mulation on the systemic avail- 1984, pp 281-288. New York, Plenum Press, 1987,
(ed): Diseases of Cage and Aviary ability of itraconazole in pigeons. 101. Rosskopf WJ: Surgery of the pp 215-227.
Birds 2nd ed. Philadelphia, Lea & J Avian Med Surg 9:255-262, avian respiratory system. Proc 116. Van Der Hayden N: Aspergillosis
Febiger, 1982, pp 599-605. 1995. Amer Coll Vet Surg, 1988, pp in psittacine chicks. Proc Assoc
67. Kon VM, Linton AH: Mucor- 84. Panigrahy B, et al: Candidiasis in 373-382. Avian Vet, 1993, pp 1-6.
mycotic infection of birds. Vet Rec cockatiel nestlings and mucormy- 102. Rupiper DJ: Diseases that affect 117. VanHerck H, et al: A bacterial
73:1008, 1961. cosis in a pigeon. Avian Dis race performance of homing proventriculitis in canaries
68. Kwon-Chung KJ: Cryptococcosis. 23:757-760, 1979. pigeons. Part II: bacterial, fun- (Serinus canaria). Avian Pathol
In Kwon-Chung KJ, Bennett JE 85. Pass DL: The pathology of the gal, and parasitic diseases. J 13:561-572, 1984.
(eds): Medical Mycology. avian integument: A review. Avian Avian Med Surg 12:138-148, 118. Van Sant F: Impression cytology:
Philadelphia, Lea & Febiger, 1992, Pathol 18:17, 1989. 1998. New insights into avian skin
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69. Lehrer RI, et al: Mucormycosis. Proc Assoc Avian Vet, 1992, pp and therapeutic management of pp 139-141.
Ann Intern Med 93:93-108,1980. 420-432. candidiasis in falcons in Saudi
119. Vaughn S: What is your diagno-
70. Lumeij JT, Gorgevska D, 87. Phalen DN: Respiratory medicine Arabia. J Avian Med Surg 16:129-
sis? J Avian Med Surg 10:33-35,
Woestenborghs R: Plasma and tis- of cage and aviary birds. Vet Clin 132, 2002.
1996.
sue concentrations of itracona- No Am Exotic Anim Pract 3:423- 104. Scanlan CM, Graham DL:
zole in racing pigeons (Columba 452, 2000. Characterization of a gram-posi- 120. Wallach JD, Boever WJ: Diseases
livia domestica). J Avian Med 88. Phalen DN, Tomaszewski E, Davis tive bacterium from the proven- of Exotic Animals. Philadelphia,
Surg 9:32-35,1995. A: Investigation into the detec- triculus of budgerigars WB Saunders Co, 1983, pp 856-
71. Luttrull JK, et al: Treatment of tion, treatment, and pathogenicity (Melopsittacus undulatus). 946.
ocular fungal infections with oral of avian gastric yeast. Proc Assoc Avian Dis 34:779-786, 1990. 121. Ward FP, Fairchild DG, Vuicich
fluconazole. Amer J Ophthalmol Avian Vet, 2002, pp 49-51. 105. Shivaprasad HL: Poultry ophthal- JV: Pulmonary aspergillosis in
119:477-481, 1994. 89. Pye G: Surgery of the avian respi- mology. In Gelatt K (ed): prairie falcon nest mates. J Wildl
72. Lyman CA, Walsh TJ: Systemati- ratory system. Vet Clin No Am Veterinary Ophthalmology 3rd ed. Dis 6:80-83, 1970.
cally administered antifungal Exotic Pet Med 3:693-713, 2000. Philadelphia, Lippincot, Williams 122. Wolf ED, Amass K, Olsen J:
agents. A review of their clinical 90. Raidal SR, Butler R: Chronic rhi- & Wilkins, 1999, pp 1177-1207. Survey of conjunctival flora in
pharmacology and therapeutic nosinusitis and rhamphothecal 106. Speed B, Dunt D: Clinical and the eye of clinically captive
applications. Drugs 44:9-35, destruction in a Major Mitchell’s host differences between infec- exotic birds. J Am Vet Med Assoc
1992. cockatoo (Cacatua leadbeateri) tions with the two varieties of 11:1232-1233, 1983.
73. McMillian M, Petrak M: Retro- due to Cryptococcosis neofor- Cryptococcosis neoformans. 123. Wolff, PL, Petrini KR, Kolmstetter
spective study of aspergillosis in mans var. gatti. J Avian Med Surg Clin Infect Dis 21:28-34, 1995. C: An outbreak of aspergillosis
pet birds. J Avian Med Surg 3:211- 15:121-122, 2001. 107. Stanford M: Use of F10 in in crested wood partridges
215, 1989. 91. Ravelhofer-Rothenender K, et al: Psittacines. Exotic DVM 3(4)18, (Rollulus roulroul). J Zoo Wildl
74. Micalezzi C, Persi A, Parodi A: Untersuchungen zur taxo- 2001. Med 23:108-112, 1992.
30_Macrorhabdus.qxd 8/23/2005 1:50 PM Page 705
CHAPTER
30
Implications of
Macrorhabdus
DAVID N. PHALEN, DVM, P hD, D ipl ABVP-A vian
History and Identification

of the Organism
The information available about macrorhabdosis (aka
megabacteriosis, virgamycosis, avian gastric yeast) in
birds is confusing for those unfamiliar with the literature
and sometimes equally as confusing for those who are.
The organism was originally thought to be a yeast
because of its staining characteristics.3 Subsequently, Van
Herck, et al, concluded that it was a bacterium, as they
were unable to demonstrate cytoplasmic organelles or a
nucleus. They did, however, show nuclear-like structures
in Giemsa-stained organisms but interpreted them to be
Fig 30.1 | Macrorhabdus ornithogaster stained with calcofluor “granules.”23 Scanlan and Graham reported isolating a
white M2R and viewed with ultraviolet light (380-420 nm). bacterium from the stomach of budgerigars using stan-
dard microbiological techniques. The isolated bacterium,
however, was smaller than the organism in vivo and was
not characterized by periodic acid-Schiff (PAS) or silver
stains.20 Attempts by other investigators to grow this
organism with standard microbiological isolation tech-
niques have been unsuccessful. However, Gerlach
reported isolation of this organism on MRS medium, a
medium used for growing fungi, but was unable to
maintain it past a few passages.8 Huchzemeyer, et al, also
reported isolating an organism from the proventriculus
of ostriches using MRS agar. This organism had the same
biochemical properties as the one isolated by Scanlan
and Graham, but was smaller than those seen histologi-
cally, and its ability to stain with PAS and silver stains
was not reported.9
More recent work suggested that the “megabacterium” M. ornithogaster also can infect mammals.19 The organ-
was, in fact, a yeast. In vivo trials showed that the isms used in these experiments, however, appear to be
“megabacterium” was susceptible to amphotericin B but bacteria and not M. ornithogaster, and there is no
not to antibacterial antibiotics.4 It also stained strongly evidence at this time to suggest that it is a pathogen of
with calcofluor white M2R (Fig 30.1) and blancophor BA, mammals.
stains that bind to chitin and cellulose, products not
found in bacteria.11,16 It grows, albeit slowly, in cell cul-
BUDGERIGARS
ture media supplemented with dextrose, fetal calf serum
and antibacterial antibiotics. A nucleus was demon- Filippich describes two clinical presentations in the
strated by electron microscopy, and in situ hybridization budgerigar. In the acute presentation, apparently healthy
with a pan eukaryote rRNA probe was positive.17 Prior to birds suddenly go off feed, regurgitate ingesta (which
conclusive determination of the genus and species to may be blood stained), and die within 1 to 2 days. In the
which the organism belonged, it was temporarily called more common chronic form, affected birds typically
avian gastric yeast. Tomaszewski, et al sequenced the appear to be hungry and spend considerable time at the
ribosomal DNA of this organism and used this informa- food dish. Instead of eating, however, these birds are
tion to prove that it was a novel anamorphic ascomyce- grinding their food but not ingesting it. Regurgitation is
tous yeast that belongs in its own new genus.22 common, and fresh or dried saliva is often found on the
tops of affected birds’ heads. Undigested seeds may be
Originally, it was proposed that it be named Virgamycosis present in the droppings. Diarrhea with or without
avigastricus, but this name was not accepted. Subse- melena also may be present. These birds go through
quently, it has been named Macrorhabdus ornithogaster.22 a prolonged period of weight loss (going light) where
they appear unthrifty and eventually die. If the affected
budgerigar colony is sufficiently large, there will always
SIGNS OF INFECTION be a few birds in the collection that will be showing
There are mixed opinions about whether M. ornitho- these signs. Birds with clinical signs of infection are
gaster can cause disease. Many investigators consider it reported to have decreased packed cell volumes and low
to be a pathogen, while others have described it as a sodium, chloride, phosphate, glucose, cholesterol and
commensal.8,20 The truth probably falls in between. It is aspartate aminotransferase values. When there was gas-
clear that under some, perhaps most, circumstances, tric ulceration, markedly low total protein concentrations
infection with M. ornithogaster does not result in clini- were observed. Contrast radiography revealed, in some
cal signs. It is equally clear that certain individual birds birds, a dilated proventriculus and an increased transit
will show signs that can be attributed to infection with time. In one aviary, mature birds with a mean age of 2.7
this organism, and that the prevalence of disease may be years were most commonly affected.5,6 Although clinical
high in some collections and perhaps in some species of signs are more common in middle-aged budgerigars,
birds. Whether this represents variation in the patho- infection begins very early in these birds and the author
genicity of different strains of M. ornithogaster or differ- has seen large numbers of organisms in the isthmus of
ing susceptibilities of the affected birds is not known. nestling budgerigars that were only 12 days old. It is criti-
cal to note that other diseases in budgerigars also can
cause similar signs; these include candidiasis of the crop
or ventriculus, a bacterial ventriculitis, trichomoniasis,
Host Range enteritis, heavy metal poisoning and neoplasia of the
stomach.
Macrorhabdus ornithogaster has a wide host range
and a worldwide distribution. It was first described in
canaries and has subsequently been identified in captive- PARROTLETS
raised and free-ranging finches.3,6,13,23 The prevalence of Parrotlets appear to have an acute onset of disease where
infection in budgerigar aviaries is high, and the percent- they develop regurgitation and may have melena (D.
age of infected birds in aviaries where it is enzootic may Zantop, personal communication). Infection and disease
range from 27 to 64%, as judged by fecal shedding.1,4,5 appear to be most common in the green-rumped parrot-
let, especially its color mutations.14
Macrorhabdus ornithogaster also is commonly found in
parrotlets, cockatiels and lovebirds.5,10,14 Filippich reports
that it is seen in several species of captive Australian par- LOVEBIRDS
rots.5 Macrorhabdus ornithogaster also is reported in Regurgitation and weight loss were seen in two flocks of
ostriches, chickens, turkeys, geese, ducks and two species lovebirds. Organisms believed to be M. ornithogaster
of ibis.8,10,12,21 It is suggested that organisms thought to be were found in significant concentrations in the drop-
Chapter 30 | I M P L I C A T I O N S O F M A C R O R H A B D U S I N C L I N I C A L D I S O R D E R S
707
Fig 30.2 | Unstained M. ornithogaster. The organism on the Fig 30.3 | Gram stain of M. ornithogaster. Only the cytoplasm
right is typical. The Y-form on the left is rarely seen. stains. Often many of the organisms will stain only faintly or not
at all with Gram’s stain.
pings of these birds. Psittacine beak and feather disease rate in infected birds was reduced compared to non-
also was found in affected birds and may have played a infected controls, suggesting that M. ornithogaster may
role in the ability of M. ornithogaster to cause disease in have an important economic significance if introduced
them (T. Lightfoot, personal communication, 2003). It into poultry flocks.15
should be noted, however, that psittacine beak and
feather disease virus infection is widespread in
lovebirds, so this may have been a coincidental finding.
Detection
CANARIES AND FINCHES Macrorhabdus ornithogaster is a long, straight, narrow
Signs of disease in canaries and finches are poorly rod that is 3 to 4 µm wide and 20 to 80 µm long (Fig
defined. Most bird owners first recognize that there is 30.2). It will occasionally branch, but this is rare (Fig
a problem when a bird is found dead. Typically these 30.2). The longer organisms are actually chains of 2 to 4
birds are thin, suggesting a chronic course of disease cells, but the septations between cells are not readily
that was unrecognized by the owner.3,23 observed. They are gram-positive, but many organisms
will not pick up the stain or will only pick up the cyto-
plasm and not the thick cell wall, and therefore will stain
OSTRICHES faintly or not at all (Fig 30.3).
Disease in ostriches associated with M. ornithogaster
was described in 10-day-old to 12-week-old chicks. Birds Similarly, M. ornithogaster stains poorly and variably
appeared normal but ceased growing and lost weight. with quick stains used for cytology.22 Also, it has been
Eventually they became weak and died. Birds had soiled the author’s impression that the organism is easily
vents and were anemic. Diarrhea was observed in some washed off slides during the staining process.
birds while others had dry, pelleted stools. Mortality
Short of a proventricular scraping or flush, there is no
rates varied from 40 to 80% in affected flocks.9
definitive way to detect M. ornithogaster infections in the
live bird. Many, probably most, sick birds with macro-
CHICKENS rhabdosis will shed large numbers of organisms in their
Two reports describe signs that were seen in flocks of droppings. These organisms are best observed by making
chickens naturally infected with M. ornithogaster. In the an unstained wet mount of a dropping and examining it
first report, birds were stunted and prone to eat litter under the microscope at 100x and 400x magnifications.
and pick at each other.10 In the second report, stunting Reducing the diameter of the stage diaphragm will make
also was seen along with increased mortality and poor the organisms easier to see (Fig 30.4). Shedding in birds
laying performance. All but one of the birds in the sec- that are not showing signs of illness is highly inconsis-
ond study had significant concurrent diseases, making it tent. Examination of five or more droppings may be nec-
difficult to know if M. ornithogaster acted as a primary essary to find even a few organisms, and in some birds
or secondary pathogen.21 Experimental infection with M. shedding will not be detected at all. The opposite also is
ornithogaster in white leghorn chickens did not result true, in that an occasional asymptomatic bird will shed
in clinical signs of disease. However, the feed conversion large numbers of organisms. Additionally, fecal screening
organism. Previous reports suggesting that M. ornitho-

gaster is susceptible to antibacterial antibiotics were
erroneous, as the organism they tested was not M.
ornithogaster.18,20
Evidence suggests there are mixed benefits to treating an

entire flock of birds for M. ornithogaster. This would
require that amphotericin B be given by gavage to every
bird twice a day for 30 days. Additionally, it would
require that the environment be extensively cleaned and
disinfected; to date it is not known which disinfectants
are effective against M. ornithogaster. With these con-
straints, flock treatment is not likely to result in a flock
cure. Filippich, however, suggested that treatment did
Fig 30.4 | Wet mount of a scraping from the gastric isthmus of a result in a significant reduction of birds that were shed-
budgerigar with a heavy infection of Macrorhabdus ornithogaster.
ding the organism.6 Culling positive birds without treat-
The aperture stage condenser was narrowed to increase contrast.
ment did not result in a reduction of shedding. How-
ever, it was suggested that culling positive birds after
is complicated because feces contain debris that may be treatment might be of some benefit, as these birds may
mistaken for M. ornithogaster.14 Macrorhabdus ornitho- be infected with amphotericin-resistant strains.
gaster stained with calcofluor white M2R is readily visual-
ized with a fluorescent microscope with excitation barrier An alternate approach to eliminating the infection from
filters (380-420 nm) (see Fig 30.1). Unfortunately, this a flock is to incubator-hatch and hand-raise the young.
technique is not commonly available.11 Experimentally, it has been shown that if budgerigar
eggs are pulled from the parents and cleaned, and the
chicks are not allowed to have contact with the egg or
infected birds after hatching, infection does not occur.
Treatment Options Hand-feeding nestling day-old parrotlets and budgeri-
and Interruption of gars and keeping them isolated from other birds is not
an easy task, but may be one that a breeder is willing to
the Infection Cycle do if this organism is a problem in a flock of valuable
breeding birds.
The only antimicrobial tested to date that was effective
against M. ornithogaster is amphotericin B.4,14 Treatment Based on the virtual impossibility of treating large flocks
was effective only at a dose of 100 mg/kg by gavage twice for M. ornithogaster, the author recommends treatment
a day for 30 days. A water-soluble preparationa when of birds showing signs and selectively breeding birds
given for 14 days was not effective. A strain of M. that do not demonstrate signs of disease. Clinical experi-
ornithogaster resistant to amphotericin B has been iden- ence suggests that some budgerigars may have a herita-
tified in Australia.14 It is not known how widespread ble resistance to infection (L. Filippich, personal com-
resistance to amphotericin B may be. Initial reports in munication, 1997).
chickens suggested that fluconazole (100 mg/kg q 12 h)
showed some promise for treating this organism. Subse- It was thought that M. ornithogaster may cause a change
quent testing showed that this dose was highly toxic to in the pH of the stomach. While this seems very unlikely
budgerigars and that mortality was seen even when the given that M. ornithogaster has little or no impact on
dose was reduced to 10 mg/kg q 12 h. A dose of 10 the acid-secreting cells of the proventriculus, it has led
mg/kg q 24 h was less toxic but was not effective.14 A sin- some to speculate that administering agents that would
gle report suggested that nystatin was effective for treat- acidify the stomach may be effective in its treatment. A
ing M. ornithogaster in a small group of goldfinches.4 controlled study testing this hypothesis failed to show
Nystatin, however, was not effective in budgerigars in efficacy of an orally administered acidifying agent.4
Australia.7 Iodine preparations, lufenuron, ketoconazole,
terbinafine or itraconazole also were not effective against
M. ornithogaster in other trials.14 Macrorhabdus
ornithogaster shedding ceased when a Lactobacillus sp.
Findings at Necropsy
was administered by gavage in treated budgerigars.7 The Gross necropsy findings are not specific. Birds are typi-
birds were not necropsied, so it is not known if they cally thin to emaciated and have little or no body fat.
were cured or just temporarily stopped shedding the There may be ulceration of the ventriculus, proventricu-
Chapter 30 | I M P L I C A T I O N S O F M A C R O R H A B D U S I N C L I N I C A L D I S O R D E R S
709
ulceration there will be a heterophilic response. It is nor-

mal for budgerigars, particularly nestling budgerigars, to
have mild to moderate lymphoplasmacytic aggregates in
the lamina propria of the proventriculus and isthmus.
These findings should not be interpreted as a response
to M. ornithogaster infection. It is possible, however, that
these aggregates may become larger and more extensive
in some infected birds. Baker found a significant mono-
nuclear cell infiltrate in the mucosa of budgerigars with
macrorhabdosis. Birds with chronic disease also showed
evidence of goblet cell hypertrophy and fibrosis of the
submucosa. Glandular cysts were seen occasionally.1
The microscopic lesions in infected chickens resemble

Fig 30.5 | Hematoxylin and eosin-stained section of the gastric those described by Baker in the budgerigar. The normal
isthmus, demonstrating the “log-jam” appearance of Macro-
lymphoplasmacytic aggregates found in the lamina pro-
rhabdus ornithogaster in situ.
pria and submucosa are markedly expanded, resulting in
a prominent widening of the folds of the glands of the
lus or both. Most often the distal proventriculus and isthmus.12,15,21
isthmus, the narrow zone of the stomach between the
proventriculus and the ventriculus, is slightly dilated and It is important to note that infections with M. ornitho-
has a thin wall. Perforation of the proventriculus is gaster are common and are often present in birds that
reported in some cases. Thick, opaque mucous secre- die from other causes. Finding M. ornithogaster without
tions may cover the mucosa of the proventriculus and evidence of koilin disruption and ulceration makes it
isthmus.1,5,6 Microscopically, the organism is found on the unlikely that it was the cause of death.
surface of the glands of the isthmus and the transitional
There are reports that M. ornithogaster can be found
koilin. When present in large numbers, these organisms
in the intestinal tract and very rarely in other organs.8
penetrate between the isthmus glands and invade the
There are bacteria that can have a similar appearance to
transitional koilin of the isthmus and the koilin of the
M. ornithogaster; therefore, if it is suspected that organ-
ventriculus (Fig 30.5). When the organisms penetrate to
isms outside the stomach are in fact M. ornithogaster,
the level of the isthmus glands, there is usually a signifi-
sections should be stained with a chitin-specific stain to
cant accompanying disruption of the koilin. Additionally,
prove that they are not bacteria.
isthmus glands appear to atrophy or undergo necrosis.
Varying degrees of inflammation were observed in differ-
ent studies. In the author’s experience, inflammation in
a. Amphotericin-B, Megabac-S, Vetafarm, Wagga Wagga, Australia, www.veta-
the budgerigar often is absent or minimal. If there is farm.com.au
References and tricular/ventricular disease in 13. Pennycott TW, et al: Causes of Vet Path, 2000, p 156.
psittacines and passerines. Proc death of wild birds of the family 19. Rossi G: Possibility of infecting
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1. Baker JR: Clinical and pathological 293. 143:155-158, 1998.
lated from birds. Vet Rec 147:371-
aspects of “going light” in exhibi- 7. Filippich LJ, Perry RA: Drug trials 14. Phalen DN, Tomaszewski E, Davis
371, 2000.
tion budgerigars (Melopsittacus against megabacteria in budgeri- A: Investigation into the detec-
gars (Melopsittacus undulatus). tion, treatment, and pathogenicity 20. Scanlan CM, Graham DL:
undulatus). Vet Rec 116:406-408,
Aust Vet Pract 23:184-189, 1993. of avian gastric yeast. Proc Assoc Characterization of a gram-posi-
1985.
8. Gerlach H: Megabacteriosis. Sem Avian Vet, 2002, pp 49-51. tive bacterium from the proven-
2. Davis A, Phalen DN: Sensitivity and
Avian Exotic Pet Med 10:12-19, 15. Phalen DN, Moore R: Experimen- triculus of budgerigars (Melopsit-
specificity of wet-mount examina-
2001. tal infection of white-leghorn tacus undulatus). Avian Dis
tion for the detection of budgeri-
9. Huchzermeyer FW, Henton MM, cockerels with Macrorhabdus 34:779-786, 1990.
gars infected with Macrorhabdus
Keffen RH: High mortality associ- ornithogaster (megabacterium).
ornithogaster. Forthcoming. 21. Schulze C, Heidrich R: Mega-
ated with megabacteriosis of Apr-Jan 47(2) 254-260. Avian Dis,
3. Dorrestein GM, Zwart P, Buitellaar proventriculus and gizzard in 2003. bacteria-associated proventriculi-
MN: Problems arising from disease ostrich chicks. Vet Rec 133:143- 16. Ravelhofer K, et al: Megabakte- tis in poultry in the state of
during the periods of breeding and 144, 1993. riosen bei verscheidenen vogel- Brandenburg, Germany. Dtsch
rearing canaries and other aviary 10. Lublin A: A five-year survey of spezies. DVG Tag Vogelkr 9:95- Tierärztl Wschr 108:264-266,
birds. Tijdschr Diergeneeskd megabacteriosis in birds of Israel 104, 1998. 2001.
105:535-543, 1980. and a biological control. Proc 17. Ravelhofer-Rotheneder K, et al: 22. Tomaszewski EK, et al: Phylo-
4. Filippich LJ, Herdrikz JK: Assoc Avian Vet, 1998, pp 241-245. Taxonomic classification of genetic analysis identifies the
Prevalence of megabacteria in 11. Moore RP, Snowden KF, Phalen “megabacteria” isolates originat- “megabacterium” of birds is a
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76:92-95, 1998. novel anamorphic ascomycetous
transmission of so-called cus undulatus). Tierärztl Prax yeast, Macrorhabdus ornitho-
5. Filippich LJ, O’Boyle DA, Webb R, megabacteria in budgerigars 28:415-420, 2000.
et al: Megabacteria in birds in gaster, 534: 1201-1205. Int J Sys
(Melopsittacus undulatus). J 18. Rossi G: Histological and
Australia. Aust Vet Prac 23:72-76, Evol Micro, 2003.
Avian Med Surg 15:283-287, 2001. immunohistochemical findings in
1993. 12. Mutlu OF, et al: Proventriculitis in proventricular mucosa of chick- 23. Van Herck H, et al: A bacterial
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Megabacteriosis and proven- Tierärztl Prax 25:460-462, 1997. “megabacterium.” Proc Eur Soc Pathol 13:561-572, 1984.
31_Toxins.qxd 8/23/2005 3:41 PM Page 711
CHAPTER
31
Implications of
Toxic Substances
JILL A. RICHARDSON, DVM
Birds are curious in nature and certain dangerous

objects may be attractive to them (Fig 31.1). As most pet
birds have clipped wings, remain caged or have limited
activity outside their cages, toxicosis are not common.
However, birds with free household access or free-rang-
ing birds are most at risk of becoming exposed to toxi-
cants. With any potential toxicosis, proper and prompt
treatment including stabilization and decontamination is
essential. Supportive care is also a critical factor in the
Greg J. Harrison
full recovery of the bird.
Assessing the condition of the bird is the initial step in

Fig 31.1 | A lutino cockatiel with excessive yellow feather managing potential toxicosis. This assessment should be
pigmentation commonly seen in nutritional disorders. performed quickly and in a manner that will limit stress
Helga Gerlach first proposed that consumption of foreign to the bird. Sedation with isoflurane or sevoflurane gas
bodies is mediated by nutrient imbalances. Since that time,
anesthesia may be required to limit stress or when deal-
the use of formulated diets has become much more preva-
lent. Practitioners have empirically noted a concomitant ing with fractious birds. Toxic birds are prone to both
and precipitous decline in foreign body ingestion. active and passive regurgitation, and care must be taken
to prevent aspiration. To help decrease stress, birds
should be examined and maintained in a quiet, warm
environment.1 The assessment should include an evalua-
tion of the respiratory rate and effort, capillary refill time
and general attitude (see Chapter 6, Maximizing Infor-
mation from the Physical Examination). The examination
of a bird that is unconscious, in shock, seizuring or in
cardiovascular or respiratory distress must be conducted
simultaneously with stabilization measures (see Chapter
7, Emergency and Critical Care).
Stabilizing the bird is a life-saving priority.1 Once the

animal is stabilized, a comprehensive history of the bird
including exposure history can be obtained. Common
presentations of birds that require stabilization include
dyspnea, cyanosis, severe depression, emaciation, severe
diarrhea, seizures and hemorrhage.1 Minimal handling
is imperative with dyspneic birds in order to decrease
Greg J. Harrison
Gwen Flinchum
Fig 31.2 | Fluids being given subcutaneously to a Fig 31.3 | Lavaging the digestive system with warmed
toxic duck. saline via a crop tube. If lavage is contraindicated, the
liquids can be used to dilute toxins and/or aspirate flu-
ids in the crop that may contain toxins
oxygen requirements. Dyspneic birds should be placed follow-up examinations are warranted with exposures to
in a cage supplemented with oxygen before and during corrosive agents or if clinical signs of redness, pain or
examination.1 A diuretic may be indicated with the pres- ocular discharge occur.
ence of pulmonary edema.1
Anti-convulsant therapy such as diazepam at 0.6 mg/kg

ORAL EXPOSURES
IM should be given if the bird is seizuring.7 Intravenous, Dilution with milk or water in combination with demul-
intraosseous or subcutaneous fluids may be needed if cents is recommended in cases of corrosive ingestion.
the bird is severely dehydrated (Fig 31.2). Close monitoring is recommended following ingestion
of corrosive agents, which can lead to tissue necrosis
and inflammation of the mouth, esophagus and crop.
Severity of injury depends on the concentration and
Decontamination duration of contact.
Preventing absorption of the substance is an important Never induce emesis in a bird. Emesis is considered
step in treating a toxicosis. unsafe in birds, due to the potential of aspiration and
ineffectiveness of emetic medications.10 Crop lavage may
DERMAL EXPOSURES be considered with recent ingestion of toxicants (Fig
31.3). Contraindications to performing a crop lavage
With light dermal exposures, the bird can be gently
spritzed with a solution of mild liquid dishwashing deter- include ingestion of corrosive substances or petroleum
gent and warm water, softly rubbed and then spritzed distillates. With ingestion of corrosive agents, gastric
with plain warm water to remove soap. This process can lavage is not recommended.3,4 Instead, oral dilution with
be repeated as needed, making sure all soap is removed. milk or water is preferred.3,4 Dilution is most effective if
it is performed early. Sedation is recommended for
A thorough bathing may be indicated with heavy expo- frightened or fractious birds. Isoflurane or sevoflurane
sures. Following the bath, the bird should be lightly pat- gases are the optimal anesthetic agents, and an endotra-
ted dry, kept warm and monitored for signs of hypother- cheal tube should be inserted during the process to pre-
mia. Removal of the toxicants from the feathers is con- vent aspiration. To lavage the crop, body-temperature
traindicated if the bird is seriously ill; always stabilize saline is gently flushed into the crop and aspirated
the patient first. With corrosive or irritating substances, repeatedly (3-4 times).10
the bird’s skin should be monitored for redness,
swelling or pain. Activated charcoal is considered a non-specific adsorbent
that binds to many substances through weak forces, and
prevents their systemic absorption. It is not an effective
OCULAR EXPOSURES adsorbent for corrosive substances, petroleum distillates
With ocular exposures, the bird’s eyes should be gently or heavy metals.3,4,6,15 Activated charcoal can be given to
flushed with tepid tap water or with physiologic saline. birds with a dosing syringe, an eyedropper or lavage
The use of an eyedropper to gently administer the flush tube, although extreme caution must be used to avoid
is recommended in small birds. Fluorescein staining and aspiration. Dosage of activated charcoal in most species
Chapter 31 | I M P L I C A T I O N S O F T O X I C S U B S T A N C E S I N C L I N I C A L D I S O R D E R S
713
Greg J. Harrison
Greg J. Harrison
Fig 31.4 | Psyllium is high in mucopolysaccharides and forms a Fig 31.5 | Inexpensive pet carriers are often made from hard-
slick mass that can sweep the digestive tract free of a multitude ware cloth. This metal wire is always toxic to chewers as it is
of toxins. Using more than 2% concentration can lead to gastro- high in lead and zinc. This 27-year-old Amazon traveled safely
intestinal blockage by this hydroscopic mass. Given with in such a carrier its entire life. The owner was lucky this did not
balanced electrolytes and dextrose it will simultaneously act to kill the bird.
rehydrate the patient.
is 1 g/kg (or 1-3 mg/g body weight).3,4

Common Hazards
Cathartics are substances that enhance the elimination
of activated charcoal, but should be used cautiously in HEAVY METALS
birds. Cathartics can be added to solutions of activated
Zinc
charcoal, or premixed combinations are available. Never
use cathartics when the bird is dehydrated. Bulking Sources of zinc include hardware such as wire (Fig 31.5),
agents can be useful in removing small solid objects screws, bolts, nuts, and USA pennies. Pennies minted
from the bird’s gastrointestinal tract, such as lead paint since 1983 contain 99.2% zinc and 0.8% copper and one
chips. One half teaspoon of psyllium (Fig 31.4) mixed penny contains approximately 2440 mg of elemental
with 60 cc baby food gruel has been suggested as a bulk- zinc.15 The process of galvanization involves the coating
ing agent for birds, and can be administered with a dos- of wire or other material with a zinc-based compound to
ing syringe or eyedropper.10 Use extreme caution to prevent rust. Owners often are not aware of galvaniza-
avoid aspiration. The mixture may be repeated to ensure tion on the wire used for making cages (Fig 31.6). Food
complete removal of the objects. Peanut butter also and water dishes also may be galvanized and sufficient
zinc may leak into the water or food to create toxicity.
has been recommended as a bulking agent.10
(Ed. Note: In tracking cases of zinc toxicity over 7
The bird should be monitored closely during treatment.
years, computer records indicate that in 82 cases of
Routinely evaluate vital signs and the parameters most
zinc toxicity, approximately half of the clients denied
likely to be affected. Preventive measures such as gastric
any potential exposure of their birds to zinc or other
protection or antibiotics may be needed. Additional
heavy metal. The idea that a bird out of its cage is truly
measures such as nutritional and hydration support are
“supervised” is overrated. Also, powder-coated cages
key components for full recovery. Daily maintenance
made outside of the USA, especially in China, have been
fluid requirements in most birds are 50 ml/kg per day.1
known to use zinc to expedite setting of the powder
It is extremely important to maintain the bird’s nutri-
coating [F. VanSant, personal communication, 2000]).
tional requirements. Hospitalized birds eating voluntar-
ily can be fed their normal diet. Tube-feed ill birds that Although the exact toxicologic mechanisms of zinc in
are not eating, unless vomiting or delayed emptying of birds or other animals is not known, zinc toxicosis can
the crop is present.1 Good nursing care should be given affect the renal, hepatic and the hematopoietic tissues.
until the bird completely recovers. The propensity for Clinical signs of zinc toxicosis in birds may include
hypothermia in a bird that is ill for any reason should polyuria, polydipsia, diarrhea, weight loss, weakness,
be considered and external heat and humidity provided anemia, cyanosis, seizures and death.2,16 An under-
as required. reported clinical sign of zinc toxicity is polydipsia with
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 31.6 | Two sources of zinc: a USA 1- Fig 31.7 | Placing a bird un- Fig 31.8 | Lead used to balance automobile
cent coin and a galvanized metal cage anesthetized in a paper bag is wheels and fishing weights are modern sources
tray. The zinc in the tray has oxidized to its often a safe and accurate way to of lead toxicosis.
most toxic form — a pure white powder — diagnose metal toxicosis.
evident at the margin of the rust and the
galvanization.
passive regurgitation of water when the bird is handled. (see also Chapter 14, Evaluating and Treating the
Mild anemia also is frequently encountered. Concurrent Gastrointestinal System). Activated charcoal is not indi-
marked elevations in the total WBC are noted in the cated, as it is of little benefit in binding zinc.15 Bulk
majority of cases of heavy metal toxicosis. Whether this cathartics, psyllium (sodium sulfate 125-250 mg/kg),
is a true infection or an inflammatory response is not peanut butter, mineral oil and corn oil may aid in the
documented, so treatment with antibiotics will depend removal of zinc objects from the GI tract. The use of
on the practitioner’s evaluation. However, the presence chelators may not be necessary in cases where prompt
of a high WBC should not convince the practitioner that removal of the zinc source is accomplished. If chelation
the discovery of metal in the ventriculus is not the pri- therapy is instituted, careful monitoring of renal parame-
mary etiology of illness. ters is important for the duration of therapy. Elevated
uric acids in heavy metal poisoning and a decrease with
Diagnosis therapy have been reported (E. Odberg, personal com-
Radiography of the abdomen may reveal the presence of munication, 2001). The following chelating agents have
metallic objects in the gastrointestinal tract. This need been suggested for zinc poisoning in birds: Ca EDTA 35
not be a properly positioned radiograph, but rather can mg/kg BID, IM for 5 days.7 If needed, the second course
be done as a stress-free scan for the presence of metal in of therapy is given after a 5- to 7-day waiting period.
the ventriculus (see Chapter 1, Clinical Practice for “bag If/when the bird is able to tolerate oral medication, D-
rad” scan) (Fig 31.7). Serum zinc levels may be obtained penicillamine (Cuprimine) can be administered orally at
using blood collected from plastic syringes (no rubber 55 mg/kg BID PO for 1 week.7 A second course of 1-
grommets) and stored in royal blue-top vacutainers or week therapy can be given, if needed, after a 1-week
directly into vacutainers with appropriate needle to min- rest. Succimer, (2, 3 dimercaptosuccinic acid) at 25 to 35
imize contamination with exogenous zinc.15 In general, mg/kg for 5 days per week for 3 to 5 weeks also has
blood zinc levels of >200 µg/dl (2 ppm) are considered been used to treat zinc toxicosis in birds.7 In addition,
to be diagnostic.16 The pancreas is considered to be the treatment for symptomatic animals should include blood
best tissue for postmortem zinc analysis.2,16 Pancreatic tis- replacement therapy as needed, parenteral fluids and
sue zinc levels greater than 1000 µg/g are suggestive of a good nursing care such as force-feeding or hand-feeding.
zinc toxicosis.16
Treatment Lead
It is imperative to remove the sources of zinc from the Sources of lead include paint, toys, drapery weights,
gastrointestinal tract. Removal of zinc-containing foreign linoleum, batteries, plumbing materials, galvanized wire,
bodies via endoscopy or proventriculotomy/enterotomy solder, stained glass, fishing sinkers (Fig 31.8), lead shot,
may be required. The success of the removal process can foil from champagne bottles and improperly glazed
be assessed with radiographs. Since most zinc items bowls.4,16 Lead is considered to be the most commonly
swallowed by pet birds are galvanized iron, the use of reported of avian toxicosis with acute toxicities more
magnets attached to an enteral tube is an effective common in captive birds and chronic in free-ranging
means of removing ferrous items that are zinc coated12 birds (Fig 31.9).
715
Greg J. Harrison
Greg J. Harrison
Greg J. Harrison
Fig 31.9 | Pelicans are presented
with fishing lines and hooks swallowed
Fig 31.10 | Peregrine falcons are Fig 31.11 | Blue-winged teal and other water
or tangled in their extremities. Radio-
carnivorous and can consume prey birds can dabble in tidal marshes or ponds that
graphs for lead are always indicated
that were shot with lead-containing may contain decades-old hunting remnants from
to ensure a bird with a lead weight in
pellets. Radiographs are indicated. lead shot.
its digestive system is not released.
Raptors can ingest lead shot from preying on animals both considered to be effective chelating agents in avian
that have been shot with or have ingested lead shot (Fig species.4 Succimer has been reported to decrease blood
31.10).20 Lead toxicosis also has been documented in an lead concentration by 87% when given at a dose of 30
Amazon parrot that had been fed portions of game birds mg/kg PO BID for 7 days minimum, with no apparent
that contained lead shot.18 Between 1983 and 1986, the adverse secondary effects, however, a dose of 80 mg/kg
National Wildlife Health Center examined 1041 mori- resulted in death.9 The therapeutic dose of succimer in
bund or dead waterfowl and diagnosed lead poisoning in pet birds is 25 to 35 mg/kg PO BID 5 days a week for 3 to
approximately 40% (Fig 31.11).5 Although lead shot has 5 weeks.7 Calcium EDTA is considered the preferred ini-
since been banned for hunting waterfowl, spent shot is tial chelator for lead toxicity in birds and is given at a
still present in waterways.20 Ingestion of 1 to 3 lead shot- dose of 35 mg/kg BID, IM for 5 days, off 3 to 4 days, and
gun pellets has been reported to be lethal to waterfowl.4 repeated if needed.7 Fluid therapy is recommended to
prevent renal effects from Ca EDTA during treatment.11
Lead affects multiple tissues, especially the gastrointesti- Penicillamine and diethylene triamine pentaacetic acid
nal tract, renal and nervous systems. Lead combines (DTPA) have also been used to treat avian lead toxicosis.7
with erythrocytes in circulating blood, increasing RBC
fragility, anemia and capillary damage. It also can cause Since lead can be immunosuppressive, broad-spectrum
segmental demyelination of neurons and necrosis of antibiotics may be indicated.4 In addition, good support-
renal tubular epithelium, GI tract mucosa and liver ive care including seizure control is recommended until
parenchyma. Clinical signs seen in psittacine birds full recovery.
are often vague and may include lethargy, weakness,
anorexia, regurgitation, polyuria, ataxia, circling and Nicotine Products
convulsions.4 In some species such as Amazons, hemo-
Tobacco products contain varying amounts of nicotine
globinuria also may be noted.11
(Table 31.1), with cigarettes containing 3 to 30 mg and
cigars containing 15 to 40 mg.15 Butts contain about 25%
Diagnosis
Radiography of the abdomen may reveal evidence of
metal in the ventriculus. Blood levels of lead are helpful Table 31.1 | Nicotine Content
in confirming lead toxicosis in birds with suspicious of Common Sources of Nicotine
Nicotine Product Nicotine Content
radiographic changes.19 Whole blood levels greater than
Cigarettes 3-30 mg per 1 whole cigarette
0.6 ppm are viewed as diagnostic for lead toxicosis when
Cigarette butts .75-7.5 mg
accompanied by appropriate clinical signs.19 The baso-
Cigars 15-40 mg
philic stippling and cytoplasmic vacuolization of red
Moist snuff 4.6-32 mg/g
blood cells are not always seen with lead poisoning in Dry snuff 12.4-15.6 mg/g
avian species.19 Chewing tobacco 2.5-8.0 mg/g
Nicotine gum 2-4 mg per piece
Treatment Transdermal patches 15-114 mg per patch
Removal of lead particles via bulk diet therapy, endoscopy Nicotine nasal sprays 10 mg per ml
or surgery is recommended. Succimer and Ca EDTA are Nicotine inhaler rods 10 mg per cartridge
716
of the total nicotine content. Nicotine also is found as a coated metal cooking sheet and the perch was then
natural form of insecticide. Signs develop quickly in later placed in the bird’s cage.
most species, usually within 15 to 45 minutes, and
include excitation, tachypnea, salivation and emesis. A V O C A D O (Persea americana)
Muscle weakness, twitching, depression, tachycardia,
The toxic principle in avocado is persin, and leaves,
dyspnea, collapse, coma and cardiac arrest may follow.
fruit, bark and seeds of the avocado have been reported
Death from nicotine toxicosis occurs secondary to to be toxic to birds and various other species.10,15,17
respiratory paralysis.15 A less serious but common Several varieties of avocado are available, but not all
response to cigarette smoke deposition on the feathers varieties appear to be equally toxic. In birds, clinical
is feather-destructive behavior. effects seen with avocado toxicosis include respiratory
distress, generalized congestion, hydropericardium,
(Ed. Note: One timneh grey that expired at 21 years of
anasarca and death.10,17 Onset of clinical signs usually
age reportedly had lived its entire life with a heavy
occurs after 12 hours of the ingestion, with death occur-
smoker. The histopathologic diagnosis of multiple
ring within 1 to 2 days of the time of exposure.10 Small
masses in the lungs was carcinoma, but was not defi- birds such as canaries and budgies are considered to be
nitely labeled as bronchiogenic). more susceptible, however, clinical signs have been
observed in other species. Treatment for recent avocado
Inhalants ingestion includes decontamination via crop lavage and
The avian respiratory tract is extremely sensitive to activated charcoal; bulking diets may help prevent
inhalants. Any strong odor or smoke could potentially absorption. Close monitoring for cardiovascular and pul-
be toxic (Table 31.2).17 Polytetrafluoroethylene (PTFE)- monary signs should follow. With symptomatic animals,
coated cookware or cooking utensils can emit toxic treatment with humidified oxygen and minimal handling
fumes when overheated (>280° F).17 Clinical signs may may be required. Diuretics may be helpful in cases with
include acute death, rales, dyspnea, ataxia, depression pulmonary edema.4
and restless behavior.2,10 Hemorrhage and edema in pul-
monary tissues leads to respiratory failure and death. POISONOUS PLANTS
Prognosis is usually guarded to poor. Treatment for The following is a partial list of plants that have been
inhalation toxicosis includes the administration of oxy- shown to cause toxicity in small animals. The severity of
gen, rapidly acting corticosteroids, diuretics, analgesics, signs or toxicity of these plants in birds has not been
parenteral antibiotics and topical ophthalmic antibiotic thoroughly studied.
ointment.1 A bronchodilator may be needed for bron-
chospasms1 (see Chapter 7, Emergency and Critical Care Potentially Cardiotoxic Plants
for an updated therapy). In most cases, prognosis is
• Lily of the valley (Convallaria majalis)
guarded to poor.* • Oleander (Nerium oleander)
• Rhododendron species
*Ed. Note: The first-time heating of several new non-
• Japanese, American, English and Western yew
stick pans is a frequent finding with PTFE toxicosis. (Taxus spp.)
One empirical report (Beckett, personal communica- • Foxglove (Digitalis purpurea)
tion, 2001) had a bird indirectly exposed days later • Kalanchoe species
when a wooden perch had been “sterilized” on a PTFE- • Kalmia species
Plants That Could Cause Kidney Failure

• Rhubarb (Rheum spp.) - leaves only
Table 31.2 | Examples of Noxious Inhalants
• Some non-stick surfaces (pots, pans, cookware, irons,
Plants That Could Cause Liver Failure
ironing boards)
• Heating elements on reverse cycle air conditioners • Cycad, Sago, Zamia palms (Cycad spp.)
• Gasoline or other volatile gas fumes • Amanita mushrooms
• Any source of smoke
• Automobile exhaust Plants That Can Cause Multisystem Effects
• Carbon monoxide
• Self-cleaning ovens and drip pans for ranges • Autumn crocus (Colchicum sp.)
• Aerosol sprays • Castor bean (Ricinus sp.)
• Cleaning products such as ammonia or bleach
• Paint fumes Plants Containing Calcium Oxalate Crystals
• Fumigants
• Candles with lead wicks, scented plug-in items
Peace lilies, Calla lilies, philodendrons, dumb cane,
717
Greg J. Harrison
Greg J. Harrison
Fig 31.12 | Houseplants need to be considered as potential Fig 31.13 | A poinsettia plant growing wild in the rare species
toxicants, especially in birds with livers stressed by nutritional breeding aviary in Tenerife, Spain.
disorders.
Greg J. Harrison
Greg J. Harrison
Fig 31.14 | A lantana plant in the same aviary as in Fig 31.13. Fig 31.15 | A budgie has been oiled by an ill-informed owner.
mother-in-law, and Pothos plants contain insoluble cal- to 48 hours has resulted in 100% recovery. Lack of mor-
cium oxalate crystals. These crystals can cause mechanical tality also has lead to a lack of histopathology, so any
irritation of the oral cavity and tongue of birds when plant additional toxic effects other than oral irritation have
material is ingested. Clinical signs usually include regurgi- not been documented [TTL]).
tation, oral pain, dysphagia and anorexia. The signs are
rarely severe and usually respond to supportive care. Aviculturists need to be sure potentially toxic plants are
avoided in the plantings of the aviary (Figs 31.13, 31.14).
• Peace lilies (Spathiphyllum spp.)
• Calla lily (Zantedeschia aethiopica)
• Philodendron (Philodendron sp.) OIL-CONTAMINATED BIRDS
• Dumb cane (Dieffenbachia sp.) Oil spills are not an uncommon problem for aquatic
• Mother-in-law plant (Monstera sp.) species of birds. According to California’s Oiled Wildlife
• Pothos (Epipremnum sp.) Care Network, bird survival is dependent upon many
factors, including the speed of recovery and the species’
(Ed. Note: A common presentation in cockatiels appears susceptibility to toxicity and captive stress.13 The first
to be oral irritation from ingestion of small amounts of step when treating oiled birds is to stabilize the animal
Pothos or philodendron species of plants (Fig 31.12). and provide a warm (approximately 27° C) and stress-
In this editor’s practice, more than 15 cockatiels have free environment.13 Common presenting clinical signs
presented over the course of 20 years with documenta- include respiratory distress and seizures.13 Following ini-
tion of recent chewing on leaves of these plants and tial stabilization, a thorough exam should be performed.
almost immediate production of clinical signs. The Most affected birds are hypothermic, hypoglycemic,
birds appear acutely depressed and anorectic, but still hypoproteinemic and lethargic on presentation.13
in good body weight. Examination of the tongue will Anemia also has been reported.13,14 Symptomatic care
reveal pronounced erythema, sometimes with obvious including nutritional support should be provided as
ulceration, and hypersalivation. Supportive care for 24 needed.
Greg J. Harrison
Greg J. Harrison
Fig 31.17 | The insectivorous passerine, such as

this painted bunting, is seldom seen when ill.
Fig 31.16 | When presented When presented for rehabilitation, pesticide toxic-
to a rehabilitation center, an ity should be investigated.
insectivorous raptor, the bur-
rowing owl, should have pesti-
cide toxicity investigated to doc-
ument this common but seldom
proven condition.
With oil contamination, feathers lose the ability to insu- In 1999, a massive die-off of white pelicans (Pelecannus
late, which can result in hypothermia1 (Fig 31.15). Oil erythrorhynchos), wood storks (Mycteria americana),
also can interfere with the animal’s buoyancy.13 Oil can great egrets (Ardea albus) and great herons (Ardea hero-
be removed from the feathers once the animal is stable dias) occurred on the shore of Lake Apopka in Central
using dishwashing detergent in warm baths. The temper- Florida. The University of Florida and USA Fish and
ature of water used should be 106° F, and water should Wildlife eventually detected the chemicals DDT,
be softened to 2 to 3 grains of hardness to help com- toxaphene and dieldrin in lethal levels in these fish-eat-
pletely remove oil and prevent mineral crystallization in ing birds. These pesticides are believed to be carcino-
the feathers.13 Following thorough rinsing, the bird must genic and were banned in the 1970s and 1980s; however,
be placed in a warm environment and allowed to dry. the chemicals can persist for decades in soil and animal
Multiple baths may be needed, however, repeat wash- tissue.
ings because of incomplete oil or soap removal are asso-
ciated with increased mortality.13 Other recommenda- It was the nation’s worst pesticide poisoning in decades.
tions for care include the use of lactulose at 0.3 ml/kg Over 800 documented great white pelicans were killed
PO q 12 h, papaya enzymes, 1 tablet PO q 12 h, aggres- by this toxic exposure, and the extrapolated number of
sive fluid therapy for feather-eating species and warm- dead created great concern for the survival of this species
water exercise pools.13 in North America. However, political and legal concerns
kept the problem from being widely publicized.
Pesticides have tremendous residual potential. Their pro-

Editor’s Comments longed half-lives, combined with the general lack of both
infrastructure and funding for testing and detection of
While documentation of environmental toxins is hard pollutants, make it likely that a great deal more expo-
to prove as the cause of death in wild birds, one must sures to toxic pesticides will occur in many species than
strongly suspect pesticides when seeing insectivorous is suspected or reported.
birds like burrowing owls (Fig 31.16), the painted
bunting (Fig 31.17) and related birds presented to reha- As veterinarians, we have an opportunity to be cognizant
bilitation centers with clinical signs consistent with toxi- of this dangerous potential, to appropriately diagnose
city. When the literature on pesticides is studied (see ref- and treat these toxicities in individual birds, and also to
erence 9 in Chapter 11, Low-Risk Pest Management), it report suspected toxicities to responsive authorities,
seems rather obvious the veterinary profession is com- requesting and expecting an appropriate investigative
monly missing pesticide toxicosis. response.
719
References and Arch Environ Contam Toxicol, 11. Lightfoot TL: Common Avian 16. Pushner B, St. Leger J, Galey FD:
35(3):506-512, 1998. Medicine Presentations II. Normal and toxic zinc concentra-
Suggested Reading 6. Buck WB, Bratich PM: Activated Proceeding Notes. Western tion in serum/plasma and liver of
charcoal: Preventing unnecessary Veterinary Conference 2002. psittacines with respect to genus
1. Agnes AE: Critical Care of Pet
death by poisoning. Food Animal 12. Lumeij JT: Gastroenterology. In differences. J Vet Diagn Invest
Birds: Procedures, Therapeutics,
Practice. Veterinary Medicine Avian Medicine: Principles and 11(6):522-527, 1999.
and Patient Support. In Veterinary
January 1986:73-77. Application. Brentwood, TN, 17. Richardson JA, et al: Managing Pet
Clinics of North America, Exotic
7. Carpenter JW, Mashima TY, HBD International Inc, 1999, p Bird Toxicosis. Exotic DVM 3:1
Animal Practice. Philadelphia, WB
Rupiper DJ: Exotic Animal 503. 2001, pp 23-27.
Saunders Co, 1:1 1998, pp 11-42.
Formulary 2nd ed. Philadelphia, 13. Mazet JAK, et al: Advances in 18. Riggs SM, Puschner B, Tell LA:
2. Bauck L, LaBonde J: Toxic diseases. WB Saunders Co, 2001. Oiled Bird Emergency Medicine Management of ingested lead for-
In Altman RB, et al (eds): Avian 8. Dumonceaux G, Harrison G: and Management. J Avian Med eign body in an Amazon parrot.
Medicine and Surgery. Philadel- Toxins. In Avian Medicine: Surg 16(2):146-149, 2002. Vet Human Toxicol 44(6):345-
phia, WB Saunders Co, 1997, pp Principles and Application. 348, 2002.
14. Newman SH, et al. Haemato-
604-613. Brentwood, TN, HBD logical changes and anaemia asso- 19. Ritchie BW: Diagnosis,
3. Beasley VR., Dorman D: Manage- International Inc, 1999, pp 1030- ciated with captivity and petro- Management, and Prevention of
ment of toxicosis. Vet Clin North 1052. leum exposure in seabirds. Common Gastrointestinal
Amer 20:2, 1990, pp 307-338. 9. Hoogesteijn AL, et al: Oral treat- Compar Haematol Int 9:60-67, Disease. Atlantic Coast Veterinary
4. Beasley VR, et al: A Systems ment of avian lead intoxication 1999. Conference 2002.
Affected Approach to Veterinary with meso-2,3-dimercaptosuccinic 15. POISINDEX editorial staff: 20. Shimmel L, Snell K: Case Studies
Toxicology. Urbana, IL, University acid. J Zoo Wildl Med 34(1):82- (Toxicologic Management: in Poisoning- Two Eagles. Semin
of Illinois Press, 1999, pp 27-69. 87, 2003. Nicotine, Zinc, Avocado). In Avian Exotic Pet Med 8(1):12-20,
5. Beyer WN, et al: Retrospective 10. LaBonde J: Toxicity in Pet Avian Rumack BH, et al (eds): POISIN- 1999.
study of the diagnostic criteria in a Patients. Semin Avian Exotic Pet DEX System vol 100. Englewood,
lead-poising survey of waterfowl. Med 4(1):23-31, 1995. CO, Micromedex, 2003.
32_Viruses.qxd 8/23/2005 2:50 PM Page 721
CHAPTER
32
Implications of
Viruses
DAVID N. PHALEN, DVM, P hD, D ipl ABVP
The past 15 years have seen remarkable growth in the

understanding of the viral diseases of companion and avi-
culture birds. Molecular-based and traditional investiga-
tive and diagnostic tools allowed scientists to discover
and understand the biology of many of the viruses that
cause the common diseases seen in these birds. This
information resulted in the development of management
strategies that, when implemented, mitigate or com-
pletely eliminate the risk of several viral diseases. Unfor-
tunately, we still lack critical information on a number
of viral diseases and diseases thought to be caused by
viruses. Additionally, not all bird owners are aware that
they should apply what has been learned, and many are
unwilling to do so. Therefore, viral diseases are still a sig-
nificant threat to captive populations of birds.
Diagnostic Assays Used to

Detect Viral Infections
SEROLOGY IN THE LIVE BIRD
Historically, serologic assays were used to screen large
groups of animals to determine if a disease agent was
present in the flock or herd in question. If a significant
number of animals tested positive, then there was suffi-
cient proof that the infectious agent was present and
management changes were made accordingly. We ask
much more from serology in pet bird and aviary medi-
cine. We ask that each assay applied to a single sample
tell us if the bird is or is not currently infected with
whatever agent we are interested in; unfortunately, this
is often not possible. Birds in the early stages of infec-
tion may not have had time to develop antibody. Assays
that detect immunoglobulin M (IgM) will not become
positive for 7 to 14 days after infection, while assays that detect both IgM and IgY as long as they are neutralizing.
detect immunoglobulin Y (IgY) may take an additional 7 In this assay, serum or plasma is diluted and each dilu-
days before they are positive. The other major limitation tion is incubated with a specific concentration of live
of serology is that many birds remain seropositive after virus. The virus-serum mixture is then incubated with
they are no longer infected with the virus and, without cells that are susceptible to infection. The cells are moni-
proper knowledge, a practitioner or bird owner could tored for several days. If antibody is present in the
be misled into believing that a serologically positive bird serum and neutralizes the virus, cytopathic effects (CPE)
was actively shedding virus. to the cells are prevented. If the serum does not contain
antibody, CPE occurs at all dilutions of serum. The anti-
Sadly, it must be noted that serologic and other diagnos- body titer is defined as the reciprocal of the highest
tic assays for avian infectious diseases have been and are serum dilution that results in a 50% or 100% reduction
still being offered commercially that are meaningless or in CPE.
their meaning is not known. For a diagnostic assay for
any infectious disease to be valid, it must be tested rigor- The biggest disadvantages of the VN are that it requires
ously in controlled infection trials or by the compilation that live cells be available and the assay itself takes 3 to 5
and careful analysis of clinical data obtained from natu- days. As a result, most laboratories will do this assay
rally infected animals. The accuracy of assays that have only once a week, and the turnaround time may be as
not been presented and preferably published in a peer- long as 2 weeks.
reviewed journal is suspect until proven otherwise.
POLYMERASE CHAIN REACTION
Enzyme-linked Immunoassay (ELISA) (PCR) IN THE LIVE BIRD
The ELISA detects antibodies from test plasma that react PCR has been the single most important advancement in
with viral antigens. To do this, the assay depends on a the detection of subclinical virus infection of birds. PCR
specific secondary antibody that can recognize the anti- detects viruses by amplifying a portion of the viral DNA,
body of the bird being tested. If a single species is being or viral RNA converted to DNA, to detectable levels.
tested and a secondary antibody to that species is avail- Blood, oral and cloacal swabs, tissue swabs and even
able, the ELISA is an excellent assay. Cross-reactivity environmental swabs can be used in this assay. Which
between secondary antibodies made to the antibody of samples need to be examined for each virus will depend
one species of bird and the antibodies of other birds, on the virus and the stage of infection at the time of
however, will vary. Therefore, an ELISA using anti- sampling. Development of a PCR assay requires know-
Amazon parrot antibody may work for all species of ledge of the DNA or RNA sequence of the virus to be
Amazons and with careful controls may be applied to all detected. It also is necessary to know the variations in
species of parrots. It is, however, not likely to work in the sequences of the specific viruses. If there is consider-
divergent species, such as passerines or ducks. able genetic variability but little biological variation
within a virus, it may be critical to develop an assay that
Hemagglutination Inhibition Assay (HI) can detect all of the viruses. On the other hand, if signif-
Several avian viruses, including the psittacine beak and icant biological variation is correlated with genetic differ-
feather disease virus, avian influenza and the paramyx- ences, it may be important to develop multiple PCR
oviruses, when added to red blood cells of the appropri- assays that can differentiate among the genetic variants.
ate species will cause them to agglutinate. If the viruses
PCR assays are highly sensitive, but not all PCR assays
are mixed with diluted serum containing antibodies to
are equally sensitive. When screening birds for avian
that virus, hemagglutination may be inhibited. HI can
polyomavirus, psittacid herpesviruses and the psittacine
then be used to detect and quantitate circulating anti-
beak and feather disease virus, it is important to use PCR
body. This assay is highly sensitive; however, non-specific
assays that have the highest level of sensitivity. The most
hemagglutins and hemagglutin inhibitors occur in the
sensitive assays typically use a nested or semi-nested
serum of birds, complicating this assay. At times this assay
PCR reaction that produces labeled amplification prod-
may prove cumbersome, as some viruses will agglutinate
ucts that can be detected with an automated system. The
the cells of some species and not others. If the necessary
sensitivity of the PCR assay also can be a disadvantage.
species are rare, this assay becomes impractical. Evidence
Contamination of the sample at the time of collection or
suggests that the HI may not detect antibody in birds
at the laboratory can result in false-positive results. It
chronically infected with paramyxovirus 3.
takes contamination with only one infected cell to cause
a sample to become positive. Contamination is much
Virus Neutralization Assay (VN) more likely to occur when multiple birds are sampled.
The VN is a very sensitive and specific assay and can This technology is rapidly advancing, and it is certain
Chapter 32 | I M P L I C A T I O N S O F V I R U S E S I N C L I N I C A L D I S O R D E R S
723
that the ability to screen for many more diseases soon variants of this virus have been identified, and the DNA
will be available. Likewise, the cost and convenience of sequence of these variants differs up to 11% compared
these assays will greatly improve. to the originally sequenced variants. Studies in Australia
have not shown a host specificity for any one of these
POSTMORTEM DIAGNOSTICS FOR variants or an indication that one variant is more patho-
VIRAL INFECTIONS genic than others.4 Work in the USA has identified a vari-
ant that is commonly found in lories and lorikeets.35 The
Many viruses leave a characteristic histologic pattern of
biology of this virus in lories may differ somewhat from
disease in their victims. Therefore, if the whole bird or a
other PBFDV variants in other species.42 Genetic varia-
complete set of fixed tissues is submitted to the patho-
tion in these viruses has significant implications for test-
logist, a diagnosis can often be made based on the pres-
ing. In order to detect all PBFDV variants, PCR assays
ence of specific histologic lesions, such as patterns of
must be designed to detect conserved areas of these
necrosis, the inflammatory response and the presence of
viruses that are identical in all of them. Alternately, mul-
viral inclusion bodies. When inclusions cannot be found
tiple assays that are variant-specific must be used.35,53
or the inclusions are not specific, macerated fresh tissue
and even formalin-fixed tissue can be examined for virus Infected birds shed virus in feather and skin dander, feces
particles using electron microscopy. Virus isolation some- and crop secretions. Transmission has been postulated to
times is necessary to detect specific viruses. Viruses can be result from inhalation of the virus, ingestion of the virus
isolated in embryonated chicken eggs and in primary cell or possibly by movement of the virus across the bursal fol-
cultures. Virus isolation often requires multiple blind pas- licular epithelium. Vertical transmission also has been
sages before the virus is detected, and the whole process postulated; however, the overall role that vertical trans-
may take one to several weeks. Not all viruses grow read- mission plays in the dissemination of beak and feather
ily in eggs or cell culture, so a negative finding does not infection remains uncertain. Naturally occurring disease
conclusively rule out the possibility of a viral infection. predominates in juvenile and young adult birds. Whether
birds become persistently infected and develop disease
Molecular-based diagnostic assays have greatly improved
depends on the age and species of the bird exposed and
the pathologist’s ability to detect infectious agents in
possibly the specific variant of the infecting virus.
necropsy specimens. Fresh tissues from birds that die
with viral infections typically contain high concentra- Virus replication occurs in a wide range of tissues, includ-
tions of virus. This virus is readily detected by PCR, if an ing the thymus, bursa of Fabricius, crop, esophagus, intes-
assay for that virus is available. Formalin-fixed tissues tine, skin and feathers. Virus also has been identified in
also can be examined for virus DNA. However, formalin circulating leukocytes. Feather dysplasia results from
degrades DNA into small pieces; therefore, it is best to virus-induced necrosis and disruption of the epidermal
screen tissues that have been fixed for only a short time collar, intermediate basal epidermis and feather pulp, and
or have been fixed and then imbedded in paraffin within thrombosis and hemorrhage within the feather pulp.
2 or 3 days. Selecting PCR primers that amplify a short Damage to the germinal epithelium of the beak is similar,
segment of the viral DNA also will increase the chance of resulting in the observed gross changes. Necrosis of the
detecting the viral DNA in formalin-fixed tissues. In situ bursa, thymus and possibly circulating leukocytes results
hybridization and in situ PCR are techniques where the in varying degrees of immune suppression. Diseases
viral DNA actually can be detected in thin sections of for- caused by opportunistic pathogens are common in
malin-fixed tissues. These assays have only limited avail- PBFDV-infected birds.36
ability and have a reduced sensitivity as compared to
PCR of fresh tissue; however, they have important appli- Clinical disease may develop within 2 to 4 weeks in
cations under some circumstances. exposed nestling parrots, but prolonged incubation peri-
ods of months and possibly even years are more likely
when young adult birds are infected. Virus can be
DNA Viruses detected in the blood before clinical signs are observed.
In one report, virus could be detected in an experimen-
tally infected bird 2 days after infection. The onset of
CIRCOVIRUS: PSITTACINE BEAK viremia may be longer in naturally infected birds.
AND FEATHER DISEASE VIRUS
(PBFDV)
Clinical Presentation
Applied Biology Species Distribution
PBFDV is a non-enveloped DNA virus. Its single-stranded Psittacine beak and feather disease (PBFD) occurs in a
genome appears to code for seven proteins. Multiple wide range of wild and captive parrots, particularly the
cockatoos, eclectus parrots (Eclectus roratus), budgeri- fracture, leaving underlying necrotic debris and bone.
gar (Melopsittacus undulatus) and lories and lorikeets Necrosis of the palatine mucosa causes it to separate
from Australia, the Pacific Islands and Southeast Asia. from the beak (Fig 32.2). The resulting space fills with
African parrots, including the African grey parrot caseous material. Beneath the caseous material is bone.
(Psittacus erithacus) and lovebirds (Agapornis spp.), These lesions are painful and birds may become partially
also are highly susceptible to infection and disease, and or completely anorectic. Secondary infections of the
infection has been found in the wild African parrots. beak and oral cavity are common. A pathologic process
Infection in Neotropical parrots in captivity occurs at a similar to the one occurring in the beak also may affect
low to moderate rate, but disease is rare. A small num- the nails of the feet. These lesions, however, generally
ber of macaws and Amazon parrots and a single pionus are not a significant manifestation of PBFD.
parrot have been reported with PBFDV.24 PBFDV infec-
tions in wild Neotropical parrots are not documented. If the beak lesions are not severe, birds can live with the
PBFD for many years. However, the vast majority of
Signs in Cockatoos these birds die, either from their primary lesions or from
PBFDV causes chronic progressive disease in birds older secondary infectious diseases within 6 to 12 months
than 8 to 10 months. The large majority of birds with the after onset of the signs. Mounting evidence suggests that
chronic form of PBFDV first develop lesions between 6 birds with PBFD have significant alterations in their
months and 3 years of age. The first signs of PBFDV are immune function. As a result, opportunistic pathogens,
subtle. A lack of powder on the beak may be the first eg, yeasts and other fungi, both gram-positive and gram-
indication that powder down feathers are diseased. Some negative bacteria, cryptosporidia and avian polyoma-
birds will present with a history of a delayed molt. Close virus, are common complications and often terminal
inspection of these birds will generally reveal at least a manifestations of PBFD. A survey of cockatoos with
few dysplastic feathers. Both down and contour feathers PBFD showed that most have high concentrations of
are affected, but the disease may predominate in one or avian polyomavirus in their skin and would be expected
the other. Initially, diseased feathers are widely scattered to be continuously shedding this virus.
and are associated with the pattern of molt. As the dis-
ease advances, all feather tracts will become involved, Acute PBFD in nestling cockatoos may begin with non-
generally in a somewhat symmetrical fashion (Fig 32.1). specific signs such as depression and regurgitation.
In advanced cases, only down feathers, a few scattered Feather lesions develop rapidly and are extensive. These
contour feathers or no feathers at all may remain. lesions may be identical to those seen in the chronic
form of PBFD, or more often, annular constricting bands
Affected feathers show varying degrees of dysplasia. near the base of the feather develop simultaneously in
Hyperkeratosis of the feather sheath is common, result- numerous feathers (Fig 32.3). These feathers break off
ing in sheath thickening and retention. Growing feathers easily and may bleed. They also tend to be loose in the
are short and may be pinched off either at their proxi- follicles and are easily pulled out. An understated feature
mal ends or near their base (clubbing). Thinning of the of this disease is the discomfort of the nestling. The dam-
rachis and recent and previous hemorrhage within the aged feathers are painful and these birds do not want to
feather shaft is common. In some feathers there is so be handled. Like the chronic form of PBFD, an early sign
much disruption of feather growth that the sheath con- of infection is reduced powder on the beak. This last sign
tains only a disorganized mass of keratin. Mildly affected is not specific because young cockatoos do not always
feathers may show bowing, have transverse dystrophic groom themselves as intensively as the adults and will
lines and fracture at any location along their length. routinely have less powder on their beaks. Advanced
beak lesions rarely have time to develop, as the acute dis-
Beak lesions are common in the sulphur-crested ease is often rapidly fatal. As with the older birds, the rate
(Cacatua galerita), Major Mitchell’s (C. leadbeateri), of disease progression varies. Infection studies suggest
Moluccan (C. moluccensis) and umbrella cockatoos (C. that rapidly fatal disease is likely to occur in umbrella
alba), little corella (C. sanguinea) and galahs (Eolophus and sulphur-crested cockatoos, whereas a more chronic
roseicapillus). They are less frequent or entirely absent form of the disease can be expected in galahs.
in other species. These lesions may occur at any stage of
the disease but are seen most commonly in birds with PBFD was rampant in wild-caught cockatoos imported
advanced disease. Early changes in the beak are the into the USA and Europe prior to 1992. Importation has
result of hyperkeratosis of its superficial layer. These ceased or is dramatically diminished; as a result PBFD in
changes cause beak elongation and overgrowth. Longi- cockatoos has become rare. Circumstances are entirely
tudinal fissures develop subsequently. In the terminal different in Australia, where the disease is common in
stages of the disease, the distal portion of the beak will the wild and infected wild-caught birds sold as pets.
725
Bob Dahlhausen
Bob Dahlhausen
Bob Dahlhausen
Fig 32.3 | A nestling Moluccan

cockatoo with the acute form of
psittacine beak and feather disease.
All growing feathers are involved.
Fig 32.1 | A cockatoo with generalized Fig 32.2 | Necrosis of the junction of the Many are seen to have hemorrhage
feather dysplasia characteristic of rhinotheca and the oral mucosa in a cocka- within their shafts.
psittacine beak and feather disease. too with advanced psittacine beak and
feather disease.
Signs in African Grey Parrots are only transiently infected. When disease does occur
Acute PBFD also occurs in juvenile African grey parrots. in lovebirds, it is most common in young adult birds.
In experimentally infected birds, non-specific systemic These birds appear unthrifty, they may shed feathers
signs preceded feather lesions. Dystrophic feathers iden- and not regrow them, or they may have a delayed molt.
tical to those seen in cockatoos also occur in African Dystrophic feathers may predominate, be scattered or
grey parrots. Additionally, newly formed contour feath- absent entirely. Some of these birds survive for many
ers that would normally be gray will sometimes be red. months or years, and some will recover and may elimi-
Red coloration of contour feathers, however, is not spe- nate the virus. It has been reported that the lory variant
cific for PBFD. Not all African grey parrots with PBFD of PBFDV may be common in lovebirds.
have demonstrable feather lesions. A rapidly fatal form
Encephalitozoon hellem is a common infection in love-
of PBFD was described in 7-week-old to 9-month-old
birds and a potential zoonotic disease. The prevalence
African grey parrots. Birds typically presented with an
of E. hellem shedding is significantly higher in lovebirds
acute onset of crop status, regurgitation and weakness.
infected with PBFDV.3
Feather loss was present in 3 of 14 birds. Total white
blood cell counts fewer than 1000 cells/µl were com- Signs in Budgerigars
mon. An acute, often massive, liver necrosis also was a PBFDV infection is enzootic in some budgerigar breed-
common finding, although changes in serum chemistry ing facilities, but it is not as widely disseminated as it is
findings did not consistently correlate with the degree of in the lovebird. Most affected birds are fledglings. In the
liver disease. Most of these birds died or were eutha- author’s experience, diffuse feather changes similar to
nized within 2 weeks of presentation.36,37 those seen in cockatoos are uncommon. Instead, many
of these birds have normal feathering except for the
Signs in Lovebirds
complete absence of primary and secondary wing feath-
PBFDV infection is extremely common in lovebirds. Up ers (Fig 32.4). The owners refer to these birds as runners
to 40% of the lovebird samples submitted to one labora- or creepers. These lesions are not specific for PBFD, and
tory for genetic probing were positive. A survey of com- identical feather abnormalities are caused by avian poly-
mercial lovebird producers in Texas found that 60% of omavirus infections. PBFDV and polyomavirus infections
the facilities sampled had PBFDV in their collections. in budgerigars also can occur concurrently.
Many, possibly most, PBFDV infections in lovebirds do
not result in clinical disease. The dynamics of PBFDV Signs in Eclectus Parrots
infection in lovebirds have not been studied extensively, PBFD in the eclectus is very similar to that in the love-
but it appears that asymptomatically infected lovebirds bird. Dystrophic feathers may or may not be present, but
specific signs and inapparently infected birds using a PCR

assay of heparinized blood. In capable hands, this is a
highly sensitive and specific assay. Birds with clinical
signs of PBFD that are positive by PCR have a guarded
prognosis. With supportive care, some will live many
years with the disease. Uncommonly, clinical signs will
resolve in some birds and they will subsequently become
virus-negative. Birds infected with the lory variant may be
more likely to survive infection. Histopathologic examina-
tion of biopsies from PBFD birds also can be used to con-
firm the clinical diagnosis. Clinically normal birds with a
positive test result represent birds in the early stages of
infection or birds with a transient subclinical infection or
a sample that was contaminated at the time of collection.
Fig 32.4 | A budgerigar with “French molt.” There is incom-
plete development of the primary wing feathers and the tail Clinically normal birds with positive test results should
feathers. These lesions are the result of either psittacine beak be retested in 90 days. Lories infected with the lory vari-
and feather disease, avian polyomavirus or a concurrent infec- ant have remained positive for over 6 months without
tion with both.
showing signs of disease. It is critical to remember that
all positive birds are actively shedding virus whether they
feather quality of clinically affected birds is poor. Many are showing signs or not. Also, birds that no longer have
of these parrots are unthrifty and are plagued with other virus in the blood may continue to shed virus in their
infectious diseases. Fatal polyomavirus infections in feather and skin dander until their next molt.
adult eclectus parrots have been correlated with concur-
Before the PCR-based assay was developed, diagnosis of
rent PBFDV infections.
PBFD was made by histopathologic examination of
Signs in Lories plucked growing feathers or biopsies of feathers and
PBFD appears to be relatively common in free-ranging feather follicles. Characteristic changes in the growing
Australian rainbow lorikeets (Trichoglossus haemato- feather and its follicle and the presence of virus-induced
dus). Fledgling lorikeets with typical dysplastic feather intranuclear and intra-cytoplasmic inclusion bodies
lesions are found walking on the ground. Histology of (basophilic globule cells) are considered diagnostic.
these birds reveals characteristic bursal lesions. Similar inclusion bodies are irregularly found in other
Approximately one-third of these birds die before their tissues. In the African grey and eclectus parrots, feather
first molt, another third have persistent feather abnor- lesions may not be present. In birds without feather
malities, but the remaining birds go on to molt and lesions, the clinician often does not suspect PBFD. As
develop normal feathers (L. Filippich, personal commu- inclusion bodies may be found only in the bursa, sub-
nication, 1997). A similar disease has been described in mission of a complete set of tissues is necessary for an
lory and lorikeet collections in the USA. Some of these accurate diagnosis.36
birds never develop signs, while others develop tran-
sient feather disease and still others develop persistent CONTROL
feather lesions and other manifestations of PBFD.35
With the advent of a sensitive and specific diagnostic
Signs in Neotropical Parrots assay for PBFDV, control of this disease has been greatly
PBFDV infection in New World parrots has been docu- simplified. All new birds should be tested for the virus at
mented in 3 to 5% of samples submitted for PBFDV the time of purchase. Alternately, testing can be delayed a
screening in one laboratory. Disease in these birds, how- month to permit a recently exposed bird time to become
ever, is extremely rare. Clinically affected birds have viremic. The most conservative method would be to test
feather lesions essentially identical to those of cocka- initially after purchase and repeat the test in 30 days.
toos. Also like the cockatoos, disease has been seen in Testing of new birds is of no value unless all other birds
both adult and nestling birds. Resolution of the clinical in the aviary also are tested. Although expensive, testing
signs has been documented in some of these birds. all birds in valuable collections of at-risk species can avert
future catastrophic loses. Birds with a positive test result
should be immediately removed from the aviary, as they
DIAGNOSIS
are sources of massive amounts of virus.
When typical clinical signs are observed, they strongly
support the diagnosis of PBFD. PBFDV infection can be The cost of testing individual birds can make it difficult
confirmed in birds with clinical disease, those with non- to persuade pet store owners and private individuals to
727
test all lovebirds and budgerigars. If private owners are and a PCR assay capable of detecting the virus in tissue
unwilling to test these birds but have other birds at risk has been developed. Using this assay, it was shown that
at home, they should be discouraged from keeping them. the Columbid circovirus, as it is now called, is wide-
Rather than test individual birds coming into a collection, spread in European racing pigeons. It is highly likely
pet stores can require that their sources swab their aviary that it is present in flocks of feral and domestic pigeons
or holding areas for PBFDV before birds are purchased worldwide. Like PBFDV, Columbid circovirus also can be
from them. PBFDV is believed to be highly resistant to detected in the blood of live birds.14
commonly used disinfectants; therefore, aggressive clean-
ing is necessary to eliminate it from a contaminated envi-
ronment. Following cleaning, PCR of environmental AVIAN POLYOMAVIRUS (APV)
swabs can be used to determine if a facility has been ade-
Applied Biology
quately cleaned. Routine environmental testing in veteri-
nary hospitals is recommended. A vaccine for PBFDV is APV is widespread and can be found in most countries
not available at the time of this writing. of the world where psittacine birds are raised. It is a non-
enveloped DNA virus that codes for six proteins. Some
CIRCOVIRUS INFECTION degree of genetic variation has been identified in APV
IN THE CANARY but it is relatively small, and it is assumed that all APV
A disease with high morbidity and mortality has been variants have the same host range.29 The route of natural
reported in nestling canaries (Serinus canarius). infection has never been experimentally verified, but
Affected birds have a distended abdomen and an infection has been induced through the respiratory route.
enlarged gall bladder. Exudate in the air sacs also is Given the rapid spread of this virus at bird sales and in
reported. Canary fanciers refer to the disease as “black the nursery, natural infection through the respiratory
spot,” as the enlarged gall bladder can be observed system is likely. In the budgerigar, the virus replicates in
through the nestlings’ skin. Lesions characteristic of cir- a wide range of tissues, including growing feathers, skin,
covirus infections in other birds are present in these liver, spleen, renal tubular epithelium, heart and cere-
canaries, as are the characteristic intranuclear and cyto- bellum. Clinical signs and necropsy findings are largely
plasmic inclusion bodies. Diagnosis is most readily made associated with tissue distribution of virus replication.
in birds 10 to 20 days old. The partial DNA sequence of Disease in budgerigars is confined to nestlings. Not all
a novel circovirus — named the canary circovirus — was budgerigars die with APV infection, and surviving birds
amplified from a flock of canaries experiencing a high shed virus in skin and feather dander and in droppings.24
degree of mortality. Gross lesions were confined to
petechial hemorrhages in two of four birds examined. Most non-budgerigar parrots are assumed to be suscepti-
Microscopic examination of the tissues was not done. ble to APV infection. Disease, however, typically is limited
This sequence information will permit more extensive to nestling parrots. Macaws, conures and eclectus parrots
studies of this virus in the future.46 are over-represented, although diagnosis of this disease
has occurred in most psittacine species (Fig 32.5). Birds
CIRCOVIRUS INFECTIONS IN become viremic sometime between 1 week and 10 days
COLUMBIFORMES after infection. Disease, if it is going to occur, develops
A circovirus infection also has been documented in 10 to 14 days after exposure. It is characterized by gener-
pigeons. Unlike the disease seen in psittacine birds, it is alized hemorrhage, moderate to massive hepatic necro-
not usually associated with abnormal feathering. Signs sis, and an immune-complex glomerulopathy. Character-
are rarely specific, and birds generally have other dis- istic karyomegalic changes and intranuclear inclusion
eases as well. Chlamydophila, mycoplasma, adenovirus bodies are typically found in macrophages and other
and herpesvirus infections and systemic bacterial infec- antigen processing cells, including the mesangial cells of
tions have all been described in pigeons with circovirus the glomerulus. The vast majority of birds with these
infection. It is possible that this virus is immunosuppres-
lesions die. Adult birds and nestlings that are infected
sive and weakens the pigeon’s immune system to a
but do not develop disease will remain viremic for a vari-
point that other diseases develop47 (see Chapter 13,
able period of time and shed virus in their droppings,
Integument).
and possibly in feather dander and skin, before becom-
Diagnosis is made by finding basophilic globule cells in ing virus-negative. Most infected birds clear the virus
tissue sections. A complete set of tissues, including the after several weeks to several months and, although they
bursa in the young bird, may be necessary to detect this maintain a persistent antibody titer, are not thought to be
virus by histopathology. This virus has been sequenced persistently infected.30
Reprinted with the permission of the American Federation of Aviculture.

Fig 32.6 | A nestling macaw
with avian polyomavirus dis-
ease. Note the extensive
Fig 32.5 | Age distribution of nestling macaws, conures, and eclectus parrots with
petechial and ecchymotic hem-
avian polyomavirus disease, from the literature and birds submitted to the Schubot
orrhage and pale musculature.
Exotic Birds Health Center.2, 5
Clinical Presentations APV in Non-budgerigar Parrots

Non-budgerigar parrots are susceptible to APV. Some are
APV in Budgerigars
highly susceptible to disease, while others rarely, if ever,
Budgerigar breeders first detect this problem in their
develop disease. APV disease in these birds occurs at
flocks when there is a sudden increase in the number of
different ages in different birds. In conures, deaths typi-
dead nestlings in the nest boxes. The nestling mortality cally occur in birds less than 6 weeks of age. Deaths in
rate often is high and may approach 100% when the macaws and eclectus parrots occur in birds 14 weeks and
virus is first introduced to an aviary. If there is no inter- younger (see Fig 32.5). Most, possibly all, of the nestlings
vention in subsequent breeding seasons, mortality rates lost are being hand-fed. Infected nestlings appear healthy,
will decline but production will always remain depressed. show very few premonitory signs and then die suddenly.
The signs of APV disease in budgerigar nestlings are When signs do occur, they precede death by only a few
somewhat variable. Most often, the young birds experi- hours. Observant owners may notice delayed crop emp-
ence an abbreviated course of disease. At death, birds tying, weakness and a generalized pallor or bruising
are found to be stunted and have abnormal feather under the skin in the preceding hours before death.
development, skin discoloration, abdominal distension, Yellow discoloration of the urates is another rare observa-
ascites, hepatomegaly with localized areas of necrosis tion. Occasionally, complete blood count and serum
and scattered areas of hemorrhage. In some outbreaks, chemistry tests can be performed prior to death. Increases
the virus attacks the cerebellum and these birds will in the liver enzyme aspartate aminotransferase are
have head tremors. Death predominates in birds that are expected. Near death, birds have a marked thrombocyto-
10 to 20 days old.25 penia. Birds that die are typically in excellent body condi-
tion. Additional findings commonly include generalized
Not every budgerigar nestling infected with APV dies. pallor with subcutaneous and subserosal hemorrhage
Some never show signs. Other nestlings will fail to and enlargement of the spleen and liver (Fig 32.6). Less
develop their primary and secondary wing feathers and commonly, ascites and pericardial effusion may be present.
tail feathers (see Fig 32.4). These birds have been
APV in Lovebirds
referred to as runners or creepers, and this form of the APV disease in lovebirds is distinct enough to merit
disease has been described as French molt. PBFDV or a special attention. As in the budgerigar, this disease
combination of APV and PBFDV can cause identical occurs in nestling birds, and inclusion bodies can be
lesions. It is possible that one or more additional dis- found in multiple organs. Unlike the budgerigar, birds
eases may cause similar feather disease. Not all budgeri- up to 1 year of age also can be affected. This unusual
gars appear to be equally susceptible to infection and dis- age susceptibility has not been fully explained. However,
ease. In one study in the United States, English budgeri- in at least some of these older birds, concurrent infec-
gars were rarely found to be infected with APV, although tion with PBFDV also is occurring and may permit APV
they were housed with other birds shedding the virus. disease in a bird that would otherwise be resistant to it.
729
APV in Nestling Cockatoos gesting that stress may play a role in the pathogenesis of
A unique presentation of APV disease occurs in nestling disease.
cockatoos. These birds present at an age of 4 to 8 weeks
with a history of difficulty breathing. Physical examina- Diagnosis
tion reveals a severely dyspneic bird that is underweight Testing Inapparently Infected Birds
and may be stunted in its growth. These birds have all The goal of testing is to detect inapparently infected
the appearances of a bird that has aspirated food. Most birds that are shedding virus and to keep them from
of these birds die. Necropsy reveals heavy, wet lungs that exposing other birds. Budgerigars, when infected as
may not float in formalin. Histologically, there is a severe nestlings, shed virus for 6 or more months. Larger species
generalized interstitial pneumonia with huge numbers of parrots, when infected as nestlings, become viremic
of inclusion bodies in what are believed to be type II for 4 to 8 weeks and shed virus from 6 to 16 weeks.
pneumonocytes. Preliminary sequence data suggests that Viremia and virus shedding have rarely been detected for
this form of APV disease is caused by a specific APV vari- as long as 10 months. Birds infected with PBFDV and APV
ant. This variant is still capable of causing the classic may shed virus continuously. To detect virus-shedding
form of APV disease in other susceptible species.32 birds, both blood and a combined oral and cloacal swab
are examined by PCR. Testing blood alone is not recom-
Post-APV Edema and Ascites Syndrome mended, as viremia ceases before virus shedding ends.
Some birds that have APV disease survive. An unknown Limited studies have been done on the duration of virus
percentage of these birds go on to develop ascites and shedding in adult birds. However, it appears that after
generalized edema. They still appear bright and alert and exposure, viremia and virus shedding are absent or
may continue to eat and empty their crops, but they are greatly abbreviated as compared to nestlings.25,28
edematous and have a fluid-filled peritoneum. The fluid
is a transudate or modified transudate and does not con- All birds infected with APV develop a detectable virus-
tain inflammatory cells. These birds do not improve and neutralizing (VN) antibody titer within 2 to 3 weeks. The
either die or are euthanized. Histologic lesions include a presence of antibody has no bearing on virus shedding,
sclerosis of the glomeruli and regenerative lesions in the as antibody-positive birds continue to shed virus for
liver. It is suspected that the edema and ascites syndrome many weeks. Also, once a bird develops antibody, most
is secondary to hypoproteinemia, either from a failure of will maintain a high antibody titer many years after they
albumen production in the liver or a loss of protein from have stopped shedding virus. Even though virus shed-
the kidney. Viral inclusion bodies are rare or absent in ding cannot be predicted by serology, serology still has
these birds. This disease very closely resembles the viral some value in the control of APV. Serology can be used
serositis lesions described in nestling parrots with east- to screen young budgerigars and lovebirds coming out
ern equine encephalitis and may be mistaken for it. of an aviary or returning from the show circuit. If they
These birds are still loaded with APV, and PCR of blood are coming from an aviary and are seropositive, they
or cloacal swabs in the live bird or blood or a liver swab have been recently infected with APV and are most likely
in the dead bird will be strongly positive.32 shedding virus. If birds that have been on the show cir-
cuit are seronegative after a 2-week quarantine, they are
APV in Adult Parrots not infected with APV.
APV readily infects adult parrots. Most infections, proba-
bly greater than 99.9% of them, are completely asympto- Postmortem Diagnosis of APV Disease
matic. These birds become infected, shed virus for a few Gross and microscopic lesions seen in birds that die
weeks or do not shed virus at all, and do not show signs with APV infection are characteristic. Spleen, liver, lung
of illness. APV disease, however, has been documented and kidney are essential tissues to provide to the pathol-
in adult birds. Disease in these birds resembles that seen ogist. These birds are viremic at the time of death, and
in the nestling. An atypical form of a progressive virus swabs of any tissue will be positive by PCR. Immuno-
encephalopathy also has been reported in two cocka- fluorescent staining of impression smears and in situ
toos. Why rare adult birds or groups of birds develop hybridization also can be used to confirm infection if
disease is not known in all cases. In many cases, how- other histologic findings are inconclusive.36
ever, adult birds that die with APV disease have concur-
rent PBFDV infections. PBFDV is believed to be immuno- Prevention and Control of APV25
suppressive, allowing APV to cause disease in a bird that The key to prevention of APV disease is to make sure
would normally be refractory to infection. APV disease that birds that are shedding virus are not introduced
does uncommonly occur in adult parrots that do not into an aviary or that materials that might be contami-
have concurrent PBFDV infections. In the author’s expe- nated with APV are not brought into the aviary. Testing
rience, these deaths typically occur in pet stores, sug- can be an important part of a prevention plan. Excellent
PCR assays have been developed to detect infection in Prevention and Control in Lovebird Collections
the live bird. Serology can be used to determine if a bird The sad state of the matter is that both PBFDV and APV
has been infected in the past but does not adequately are enzootic in many lovebird aviaries. Oddly, disease in
predict the virus-shedding status of the bird. these birds is often rare. Shedding, however, occurs in
young lovebirds and may be continuous in birds that are
Control in Budgerigar Aviaries
concurrently infected with PBFDV. Breeders who wish to
If a prevention program for APV infection is to be insti-
have a lovebird collection that does not have APV should
tuted in a budgerigar aviary, the first step is to make sure
first test their birds for infection. Again, serology using
that it is not already there. The virus is readily detected
the virus neutralization assay or PCR of swabs from the
by PCR in the environment of aviaries where the infec-
environment or blood and combined oral and cloacal
tion is enzootic. Alternately, blood and combined oral
swabs of individual nestlings and fledglings will readily
and cloacal swabs can be used to test nestlings and
detect virus. To prevent the introduction of APV to a
young adult birds. A virus neutralization assay can be
lovebird aviary, a representative number of each lot of
used to detect antibodies to APV. Most birds in an aviary
incoming birds is tested by serology or PCR. Alternately,
with enzootic APV will be seropositive.
environmental swabs are used to verify that the aviary
Exhaustive efforts are required to keep APV out of a from which the birds originate is free of APV.
budgerigar collection. The movement of birds on and off
Prevention and Control in Aviaries Breeding
the property must be carefully restricted. All new birds
Non-budgerigar Parrots
coming onto the property should be seronegative or
PCR-negative. Alternatively, environmental swabs of their Outbreaks of APV do not occur in adult breeding birds,
aviary of origin can be tested by PCR. If the aviary is a they occur exclusively in nurseries. Outbreaks occur
commercial aviary, dealers, feed salespeople, delivery when birds with inapparent infections, generally nest-
trucks and other bird breeders should be banned from lings, are introduced to the nursery. If the following
the aviary entirely. Young birds taken to the bird dealer rules are followed, APV outbreaks in the nursery are
and rejected should not be returned to the aviary. Food extremely unlikely. Breeders of the larger species of par-
should be purchased directly from the feed mill so that rots should not breed cockatiels, lovebirds or budgeri-
it is never in contact with other birds. If the aviary is pri- gars. If they must breed these species, they must test
marily breeding show budgerigars, then all birds going them thoroughly to make sure they are not infected with
to the show should be quarantined until the end of the APV. The breeder should raise only the chicks that they
show season and tested by serology or PCR before they produce. If they must raise chicks from other sources,
are returned to the breeding colony. these birds must be quarantined and tested by PCR
before they are brought into the nursery. Extensive and
Budgerigars are not the only birds that can bring APV repeated environmental testing of the aviary of origin
into a collection. Lovebirds and possibly cockatiels may be substituted for individual bird testing. Any bird
(Nymphicus hollandicus) also can be sources. Devastating that leaves the nursery and is in direct or even indirect
outbreaks have occurred in budgerigar operations when contact with other birds must not be allowed back into
lovebirds have been introduced into previously closed the nursery. Adult birds coming into the aviary also
budgerigar colonies. should be quarantined and tested for APV. Ideally, peo-
ple taking care of the nursery would not take care of the
Elimination of APV from a budgerigar collection is chal- adult birds. Often, this is not possible. In these situa-
lenging, but not impossible. The first critical step is to stop tions, cleaning up and changing clothes before working
breeding. The infection cycle is perpetuated by the con- with the nestlings is recommended.
stant presence of infected nestlings, fledglings and young
adult birds. These birds shed virus for up to 6 months or APV outbreaks in the nursery are devastating. In most
more after infection, seeding the environment with virus. cases, once APV is introduced to a nursery it spreads
Chicks are then exposed immediately upon hatch and the rapidly, so that by the time the first case is recognized
cycle continues. Once breeding is stopped, all birds that most of the nestlings are already infected. This concept
have not been used for breeding should be removed from is important for two reasons. First, vaccination at this
the property. Adult birds should be moved to a temporary point will do no good. Second, testing during the out-
environment and the aviary totally disinfected. Nest boxes break will prove only that the virus is widely dissemi-
can be cleaned and painted but are better off destroyed nated. To save money, the aviculturalist should be
and replaced with new boxes. All wood surfaces should encouraged to reserve testing to determine when shed-
either be discarded or cleaned and painted over. After a 6- ding has stopped and the chicks can be sold.
month hiatus, the adult breeding stock can be returned
to the clean aviary and set up for breeding again. Little can be done to keep exposed chicks from becom-
731
ing infected with APV in most nurseries. However, tions about this vaccine and its ability to protect against
efforts should be made to improve hygiene, decrease APV infection. The vaccine is to be given to nestlings that
density of birds and use individual syringes for hand- are 4 weeks of age or older and is thought to provide
feeding individual chicks. The most important element protection to nestlings 2 weeks after the second vaccine,
in the control of APV outbreaks is to stop bringing or by the age of 8 weeks. From the dynamics of the dis-
babies into the nursery. Chicks can be left in the nest to ease, however, most birds cannot be immunized early
be raised by the parents or pulled and sent to another enough in life to be protected. An additional concern is
facility to be raised. It remains unclear why, but parent- that VN antibody was not detected in nestlings immu-
raised chicks (excepting lovebirds and budgerigars) are nized with this vaccine, and immunization of adult birds
not reported to develop APV disease. Surviving chicks resulted only in low antibody titers.28 Clinical trials that
will shed virus for 8 to 14 weeks, rarely as long as 16 claim to show that the vaccine stopped outbreaks of APV
weeks. The older the chick at the time of exposure, the disease in nurseries did not study control flocks where
shorter the period of virus shedding. Chicks should be the vaccine was not used. If new nestlings were not
negative by PCR of blood and a combined oral and cloa- added to a nursery experiencing an outbreak, deaths
cal swab before they are sold. PCR of the oral and cloa- would stop on their own within 2 to 4 weeks of the first
cal swab is critical, as viremia ceases before shedding death.34 Claims that immunizing already infected birds
stops. will result in a shortening of the duration of virus shed-
ding are not documented.
After the outbreak has stopped, a close inspection of the
aviary must be done. Birds that might be shedding virus APV is, by and large, a completely preventable disease
need to be identified and tested or eliminated from the through appropriate management strategies and selec-
aviary. Extensive cleaning and disinfection of the nursery tive testing. As a result, the author stresses these avenues
also will have to be done. In aviaries where the underly- of control and does not recommend immunization.
ing source of disease has been eliminated, subsequent
breeding seasons can be free of the disease. APV Infection and Disease in Non-psittacine Birds
One or more APV strains can infect non-psittacine birds.
Preventing APV Disease in the Pet Store Several species of passerines have been documented to
The pet store is one of the most common places where have classical APV disease. In the author’s experience,
APV outbreaks occur. Most pet stores get their birds from flocks of Gouldian finches (Chloebia gouldiae) are per-
multiple sources. They sell budgerigars, lovebirds and haps at greatest risk. Again in the author’s experience,
cockatiels, the three species that are most likely to be mortality is limited to nestling and young adult finches
shedding virus, and many stores will acquire susceptible during one breeding season but is not seen again in the
species when they are still nestlings. To avoid disease, pet following year. Surviving birds have moderate levels of
stores can use several strategies. The easiest and best antibody that will neutralize a lovebird-derived APV. APV
method for preventing APV disease in the pet store is to DNA was detected in the tissues of one finch with PCR
buy only weaned nestlings. These birds will be old primers derived from the psittacine APV sequence, sug-
enough that, if infected with APV, they will not develop gesting that this bird was infected with a psittacine vari-
disease. If unweaned nestlings are to be purchased, they ant. However, other studies suggest that another signifi-
should be raised outside of the store until weaned. If cantly different virus also may infect passerines.
nestlings must be in the store, they should be separated
from all other birds, and have a person designated to There is a single published report of a rhamphastid
take care of only them and no other birds. The public dying with an APV disease. The bird was a green aracaris
should not be allowed to handle these birds. Stores that (Pteroglossus viridis). The virus sequenced from this
sell high-value nestling parrots should consider limiting bird was found to be nearly identical to those derived
their bird sales to these birds only and not selling love- from psittacine birds. It was speculated that the original
birds, budgerigars and cockatiels. Establishing long-term source was a cockatoo. In this study, in-contact birds,
relationships with breeders also can reduce the risk of including zebra finches (Poephila guttata), a kookaburra
disease transmission. Breeders supplying pet stores (Dacelo novaguineae) and a Lady Ross turaco
should be encouraged to develop a preventive medicine (Musophaga rossae), became seropositive but did not
program to develop and maintain APV-free flocks. develop disease.19
Immunization APV Infection in Free-ranging Birds

A commercial APV vaccinea is available in the USA. Its There is strong evidence that APV infection occurs in
value as a tool in the prevention of APV disease is con- wild birds on multiple continents. A high prevalence of
troversial. The author’s research has raised several ques- anti-APV antibody was found in free-ranging greater
sulphur-crested cockatoos in Australia.33 APV disease has cells in parrots that die with other diseases. These lesions
not been reported to occur in wild Australian birds, but are most common in lovebirds and budgerigars.21,36
a disease with characteristic APV lesions was induced in
A fatal adenovirus infection causing hepatitis is described
a cockatoo infected with a preparation of PBFD virus
in the nestlings of Senegal parrots (Poicephalus sene-
derived from the feathers of a wild bird, suggesting that
galus) and related species. The disease occurs sporadi-
APV was present in these tissues and was copurified with
cally within aviaries. In one collection, the disease
the PBFD virus.33 Recently, APVs were identified in five
occurred in 3 out of 4 years in offspring from a single
buzzards (Buteo buteo) and a falcon (Falco tinnunculus)
pair of Senegal parrots. Affected nestlings typically pres-
in Europe. Genetically, the sequence of the falcon virus
ent acutely ill or are found dead. Grossly, the liver is dis-
was nearly identical to other APV variants of psittacine
colored red-black, and scattered yellow-gray areas may
origin and the virus in the buzzard amplified with PCR
be present. Multifocal hepatic necrosis and the presence
primers derived from the sequence of the original APV
of large, darkly basophilic intranuclear inclusion bodies
isolated from a budgerigar. Because of autolysis in the
within hepatocytes characterize this disease.36
buzzards, the histologic lesions associated with this dis-
ease could not be characterized.17 The author has seen adenovirus infections in several
mixed flocks of finches. Typically, clinical signs are not
Preliminary evidence that APV may occur in wild birds
observed. Concurrent diseases, such as candidiasis and
in North America also exists. A house sparrow (Passer
atoxoplasmosis, were common. Poor hygiene and high
domesticus) was found to have a glomerulopathy with
stocking density may have played roles in these deaths.
characteristic APV-like inclusions within mesangial cells
and PAS-positive deposits within the mesangium and
Pigeon Adenovirus
glomerular capillaries.24
Adenoviruses in pigeons cause two distinctly different
Goose Hemorrhagic Polyomavirus diseases. The first occurs in pigeons less than 1 year old
and may be associated with the onset of the racing sea-
A genetically distinct polyomavirus with limited homol-
son. This virus replicates predominately in the intestinal
ogy to the avian polyomavirus has been implicated as
epithelium, causing villus atrophy. Many birds will
the cause of the hemorrhagic nephritis and enteritis of
develop disease. Signs are those of acute severe enteri-
geese in Europe. Little is known about the importance
tis, diarrhea and vomiting. Severely affected birds die,
of this virus in waterfowl, but it may be widespread, as
but many uncomplicated infections resolve within 1
the histologic lesions that it is reported to cause are
week. A common complication of this adenovirus infec-
not specific.13
tion is an Escherichia coli overgrowth of the intestinal
tract. These birds have persistent diarrhea, lose condi-
PAPILLOMAVIRUSES tion and will die if not aggressively treated. E. coli over-
Diseases caused by papillomaviruses in birds have been growth of the intestine also can result in septicemia and
described only in wild European finches and imported sudden death. Mild to moderate hepatic necrosis may
African grey parrots. The African grey parrots had papil- occur in some infections and contribute to the clinical
liferous plaques of the commissures of the beak, eyelids signs and duration of the disease.
and face that became more extensive over the course of
A second adenovirus causes massive hepatic necrosis.
the year the birds were monitored. Lesions in European
All ages of birds are susceptible. Disease, however, is
finches predominate on the legs and feet; lesions of the
sporadic in a flock and spreads slowly. Signs of infection
face are rare. These lesions should be differentiated
include vomiting and biliverdin-stained urates; however,
from those caused by poxviruses.43
most birds die before signs are recognized. Birds show-
ing signs die within 24 to 48 hours.
ADENOVIRUSES
Diagnosis for both adenovirus infections can be made
Adenoviruses in Companion Birds only at necropsy. Treating for dehydration and secondary
Adenovirus infections and disease in companion birds are bacterial infections can mitigate mortality in birds with
rare. They have been associated with hepatitis, acute the enteric adenovirus infection.8,52
necrotizing pancreatitis, conjunctivitis and a multisystemic
disease in lovebirds. However, recent reports of these dis- PSITTACID HERPESVIRUSES
eases have been lacking. Adenovirus-associated encephali- (P s HV s )
tis also is a rare disease that has not been recently
reported. Characteristic basophilic intranuclear inclusion Applied Biology
bodies are infrequently seen in renal tubular epithelial PsHVs are alpha herpesviruses that are the causative
733
agent of Pacheco’s disease (PD) and internal papillo- remains to be proven. There is no evidence that persist-
matosis of parrots (IP). The PsHV1 virus contains three ently infected birds will subsequently develop PD.
major serotypes. Two additional serotypes (serotypes 4 However, some persistently infected birds will develop
and 5) are described, but they are each represented by IP. Which birds will develop IP may depend on the
only a single virus isolate. It is unclear if 5th serotype is species of the bird, the genotype of the virus and as yet
a PsHV1 or an entirely different herpesvirus. There are undetermined factors.
four major genotypes of PsHV1. The viruses in geno-
types 1 and 4 comprise serotype 1, the viruses in geno- Most persistently infected birds are readily detected by
type 2 comprise serotype 2 and the viruses in genotype PCR analysis of blood and combined oral and cloacal
3 comprise serotype 3. The single serotype 4 isolate is a swabs. These birds will be consistently positive with
genotype 4, but appears to have evolved into a unique repeated samplings.31 Even though PsHVs are continu-
serotype.49 A new herpesvirus, PsHV2, has been discov- ously present in the mucosa of persistently infected birds,
ered. This virus has been identified in mucosal tissues field data suggest that actual virus shedding or the degree
from Congo African grey parrots and a single blue and of virus shedding may fluctuate over time. Species persist-
gold macaw. Most birds were not showing signs of dis- ently infected with PsHVs include the macaws, Amazon
ease, however this virus was found in a mucosal papil- parrots, some of the Aratinga conures and the Patagonian
conure (Cyanoliseus patagonus). Increasing evidence
loma in one African grey parrot and cutaneous papil-
also suggests that cockatiels, lovebirds, cockatoos and
loma from another.
possibly other species may be persistently infected with
The study of the complexity of these viruses and the corone or more PsHVs. Wild-caught birds that have passed
relation between genotype and pathotype is still in its through a quarantine station, parent-raised chicks of wild-
infancy, but patterns are beginning to unfold. Current caught birds and birds that have survived an outbreak of
sequence data has allowed the development of PCR PD are at highest risk for persistent infection.
primers that can detect all of the viruses discovered to
The incubation period for PD typically ranges from 5 to
date. This discovery allowed investigators to determine
14 days. Virus replication occurs in a number of organs,
that the PsHVs that cause PD persist in the mucous
and birds are viremic. Inclusion bodies are most often
membranes of the oral cavity and cloaca and can be
found in the liver and spleen and to a lesser extent the
inconsistently detected in the blood.31,49,50
crop, small intestine and pancreas. Necrosis of the
Based on these data, the following epizootiologic picture infected cells, particularly hepatocytes, accounts for the
is proposed. Transmission between birds occurs when a clinical signs.36
naïve bird is exposed to the oral secretions, droppings or
vomitus of a persistently infected bird. The route of infec- Clinical Presentation
tion can be by ingestion or contact with conjunctival or PD occurs almost exclusively in psittacine birds. Disease
respiratory mucous membranes. The outcome of infec- is most common in avicultural collections, quarantined
tion will depend on the genotype of the virus and the birds and pet stores. The most common clinical presenta-
species of bird exposed. Genotypes 1, 2 and 3 are highly tion is a dead bird that died with little or no advanced
pathogenic to Amazon parrots. In Europe, genotype 4 evidence that it was ill. PD occurs most frequently in
PsHV also kills Amazon parrots, but this virus is not mixed collections of parrots that contain Amazons,
found to cause PD in Amazon parrots in the USA.49 In macaws and conures, particularly Patagonian and Aratinga
contrast, genotype 4 is the most common cause of PD in conures. The onset of the breeding season or recent
macaws and conures. Cockatiels, cockatoos and other changes in the aviary may predispose to virus shedding
Pacific species of birds are relatively resistant to PD, but and PD outbreaks. Clinical signs may precede death in
when they do develop disease, any of the four genotypes macaws and less frequently in other species. Signs are
may be responsible. African grey parrots are susceptible non-specific and include lethargy, depression and
to genotypes 2, 3 and 4. Genotype 1 has not been found anorexia. Profuse sulfur-colored (biliverdin-stained)
in African grey parrots with PD, but the number of urates are another non-specific but consistently reported
African greys tested to date is small, so this should be sign. Regurgitation, bloody diarrhea and terminal central
considered only a preliminary finding. nervous system signs are infrequently reported. Duration
of clinical signs ranges from a few minutes to a few days.
Birds that become infected with PsHVs and either do not Only a few birds are known to survive infection once
develop PD or do develop PD but are treated and sur- clinical signs develop. Elevation in the serum aspartate
vive will become persistently infected and will remain amino transferase concentrations and a marked leukope-
persistently infected for life. There is a possibility that nia are reported in these birds. Radiographically, hepato-
some subclinical infections may result in a cure, but this megaly, splenomegaly and renal enlargement also are
documented. The number of affected birds can vary from ence, mortality stops within 24 hours after the initiation
a single isolated case to hundreds.24 of flock treatment. Treatment options include adminis-
tration of acyclovir in the drinking water (1 mg/ml) and
To the author’s knowledge, the only documented natu- food (400 mg/quart of seed) simultaneously or by gavage
rally occurring case of Pacheco’s disease in a non- (80 mg/kg q 8 h). A higher oral dose of 330 mg/kg q 12
psittacine bird occurred in a keel-billed toucan (Ram- h also has been recommended. The necessary length of
phastos sulfuratus). Lesions in this bird and a second treatment is not known. The author treats flocks for 7
keel-billed toucan experimentally infected with Pacheco’s days and birds with signs of disease for 2 weeks.23
virus were characteristic of the psittacine infection. In
another toucan (species not reported), a disease resem- Preventing virus spread is another important aspect of
bling Pacheco’s disease was described. Herpesvirus viri- bringing a Pacheco’s disease outbreak under control.
ons were identified in the tissues of this bird; however, Traffic through the aviary should be minimized and
fluorescent antibody-staining of the tissues with a hygiene improved. Additionally, barriers between cages
Pacheco’s virus-specific antibody was negative. can be erected, or cages can be moved farther apart.
Intensive cleaning efforts may result in the increased
Diagnosis aerosolization and further dissemination of the virus.
Diagnosis in the live bird is difficult and rarely made. Immunization in the face of an outbreak is of question-
History, signs and laboratory findings are strongly sug- able benefit, as protective antibody titers would not be
gestive of PD but are not specific. These birds are expected for 2 weeks after vaccination.
strongly positive on PCR of combined oral and cloacal
swabs and blood but usually die before the samples can Prevention and Control
be analyzed. In the author’s experience, once a bird is Control measures fall into three categories: savvy man-
confirmed to have disease and owners know what to agement practices, testing and immunization. Given that
look for, they will detect the early stages of the disease some conure species have repeatedly been implicated in
in birds, often in time to save them with treatment.24, 36 the outbreak of this disease, these birds should not be
kept in a mixed collection. General concepts, such as a
Most birds that die are well muscled and may have closed aviary, proper quarantine procedures and acquisi-
recently ingested food. Common gross lesions include tion of birds from reputable sources, will help to mini-
hepatomegaly, splenomegaly, renal swelling and serosal mize the likelihood of Pacheco’s virus being introduced
and epicardial hemorrhage. The affected liver may be to an aviary. Adequate spacing between cages and limit-
uniformly pale yellow, resembling the appearance of a ing human traffic in the aviary also are important pre-
diffuse lipidosis (Fig 32.7), have a diffuse mottling, or ventive measures. Outbreaks are less likely to occur in
have scattered, irregularly shaped, discolored foci. In outdoor aviaries.
many birds, liver lesions are not observed grossly. Less
commonly, submucosal hemorrhage of the intestines Testing is becoming an increasingly practical means of
with or without intraluminal blood also may be present. preventing the introduction of PsHVs into a collection.
Because of the acute nature of this disease, gross lesions Persistently infected birds are readily detected by PCR of
may be entirely absent in some birds. blood and combined oral and cloacal swabs. Birds that
are at highest risk for being persistently infected are
Histologically, hepatic necrosis is present in the vast those that have survived PD outbreaks and wild-caught
majority of the cases. Varying degrees of splenic lymphoid parrots and chicks raised by wild-caught parrots. Macaws,
hyperplasia and necrosis, pancreatitis and enteritis also Amazon parrots, Patagonian conures and Aratinga spp.
occur. Eosinophilic and, less frequently, basophilic conures commonly are demonstrated to be infected per-
intranuclear inclusion bodies are found in the liver on sistently.
the margins of the necrotic areas and in bile duct epithe-
lium. Inclusions will sometimes be present in the spleen, A single Pacheco’s disease virus vaccinec is currently
intestinal epithelium, crop and pancreas. Although these being marketed in the USA. The serotype of the virus in
lesions are characteristic for PD, the diagnosis can be ver- this vaccine and its ability to protect against all serotypes
ified by PCR of tissue swabs, staining impression smears of PsHVs are not known. Immunizing parrots in mixed
with specific fluorescently labeled anti-Pacheco’s virus collections of high-risk birds may be beneficial.
antibody and in situ hybridization.
Internal Papillomatosis of Parrots (IP)
Treatment Clinical Manifestations
Mortality in Pacheco’s virus outbreaks can be minimized IP is a disease that primarily affects macaws, Amazon
by prophylactic use of acyclovirb. In the author’s experi- parrots, hawk-headed parrots and, less commonly,
735
Fig 32.7 | An eclectus parrot with Pacheco’s Fig 32.8 | Extensive papillomatous changes to
disease. The liver has a diffuse yellow mottling the cloacal mucosa of an Amazon parrot.
that is caused by extensive hepatic necrosis.
Although many cases do not present with this
lesion, the presence of this lesion should alert
the practitioner or pathologist to the possibility
that they are dealing with Pacheco’s disease.
conures. Most lesions are confined to the oral and cloa- ished as compared to other birds without this disease. The
cal mucosa, although lesions also may be found in the chronic irritation associated with cloacal lesions and
conjunctiva, nasal lacrimal duct, bursa, esophagus, crop, repeated surgeries to remove the lesions may result in
proventriculus and ventriculus. Cloacal lesions are the cloacal strictures. Birds with diffuse lesions of their upper
most common manifestation of IP in Amazon parrots digestive system often develop a wasting disease that may
and generally are present in the macaw as well. Oral resemble proventricular dilatation disease.
papillomas are common in macaws. Of the macaws, the
A small to moderate percent of birds with IP will go on
green-winged macaw (Ara chloroptera) is prone to
to develop bile duct or pancreatic duct carcinomas. Signs
develop the most widely disseminated form of IP. In
of bile duct carcinomas are not specific. Birds typically
these birds, lesions generally are present in both the
lose body condition, appear unthrifty and may have an
cloaca and oral cavity and may extend into the esopha-
overgrown beak. Elevated gamma glutamyl transferase
gus, crop and even the proventriculus and ventriculus.
levels have been reported in birds with advanced
Less frequently, blue and gold (Ara ararauna) and scar-
lesions. Bile duct carcinomas are readily demonstrated
let macaws (Ara macao) and, uncommonly, an Amazon
with ultrasonography and appear as hyperechoic round
parrot will develop this diffuse form of IP.23
to irregular masses. Infection with PsHV genotype 3 may
predispose to the development of bile duct carcinomas.
Owners usually first recognize that their bird has IP when
they see blood in the bottom of the cage from an ulcer- Treatment
ated cloacal papilloma or when the papilloma prolapses Birds with cloacal papillomas are often in pain, so it has
through the cloaca (Fig 32.8). Oral lesions may be exten- been common practice to remove all or part of these
sive but rarely result in clinical signs. Papillomatous lesions lesions. Cryotherapy, electrocautery, chemical cautery,
are rarely static; they wax and wane and may disappear laser surgery and sharp dissection have all been used. In
entirely. Often, the only indication that IP is present is a the experience of the author, removing part of a lesion
slight roughening of the cloacal mucosa or a thickening of will often cause the remainder to regress; these lesions
the choanal edges and blunting of the choanal papillae. If generally return, however. To minimize the risk of stric-
the lesions do not spontaneously resolve, each time they ture formation, surgery is limited to a small portion of the
recur they generally are more severe. The lesions in some cloaca or not done at all. Carboplatin has been used in a
birds will be consistently present. Birds with IP may live few birds to treat bile duct carcinomas (B. Speer, personal
for many years and even be reproductively successful. The communication, 2001) (see Chapter 35, Surgical
general life expectancy of these birds, however, is dimin- Resolution of Soft Tissue Disorders).
Prevention monly in some birds with Pacheco’s disease, and this

Mounting evidence strongly suggests the viruses that could be mistaken for Amazon tracheitis.
cause PD are the same viruses that cause IP.18,27,43,44,48
Depending on the genotype of the viruses and the DUCK VIRUS ENTERITIS (DVE)
species involved, however, these viruses can disseminate
This herpesvirus has caused massive die-offs of wild
through a collection without causing Pacheco’s disease.
ducks on several occasions in the USA. In Texas, the dis-
The first clue that the virus is there is when birds begin
ease is seen on a smaller scale in the early summer on
to develop papillomas. Transmission can occur from par-
small community or golf course ponds. Generally, these
ent to offspring and between cages of birds. Trans-
ponds are densely populated with semi-domestic ducks.
mission is much more likely to occur if cages are in
A common factor in most of the outbreaks is the pres-
close proximity and birds are housed indoors. A meticu-
ence of Muscovy ducks on the pond. There is a signifi-
lous physical examination of birds before entry into a
cant amount of controversy surrounding this virus and
collection coupled with a PCR assay for PsHVs will
what to do when an outbreak occurs. In the past,
detect infected birds.
attempts were made to euthanize all ducks on the pond
Treating birds with anti-herpesvirus drugs will not cure in an effort to eliminate the carrier birds. This approach
them of infection and does not appear to impact the to control is rarely practical and almost certainly will
course of IP. These viruses presumably persist in a non- offend some members of the local community. Addition-
replicating form and are not susceptible to these drugs. ally, genetic-based tests now support the idea that this
virus is widespread in wild waterfowl. At this point, the
best method of control is to limit the density of ducks
Cutaneous Plaques and Papilliferous
Lesions of the Foot maintained on ponds and, if possible, prevent the intro-
duction of Muscovy ducks onto these ponds.38
Herpesvirus virions are documented in proliferative
lesions on the feet of macaws and cockatoos. These
lesions show some species-specific variations. Lesions in PIGEON HERPESVIRUS (PHV)
cockatoos tend to be papilliferous, while those of PHV has a worldwide distribution and is a particular
macaws are raised, depigmented plaques. These lesions problem in racing pigeons, as birds are exposed when
regress if treated topically with acyclovir. The sequence closely housed with birds from other lofts prior to each
of a herpesvirus from a plaque from the foot of a macaw race. When the virus is first introduced to the loft, many
was found to closely resemble that of the PsHVs that birds will be affected. Signs include depression, reluc-
cause PD and IP.48 tance to move, protrusion of the third eyelid, conjunc-
tivitis, vomiting, rhinitis, dyspnea, anorexia, weight loss
MISCELLANEOUS HERPESVIRUS and loose green droppings. Characteristic gray to yellow
INFECTIONS IN COMPANION BIRDS oral and pharyngeal diphtheritic plaques mark this
disease. Birds that survive infection appear to remain
An infection resembling a herpesvirus infection is
infected for life. Virus shedding increases during the
described in Gouldian, melba (Pytilia melba) and purple
breeding season, resulting in infection of squabs. Infected
grenadier (Uraeginthus ianthinogaster) finches. Clinical
squabs become carriers but disease does not occur, pos-
signs include weight loss, anorexia, dyspnea, severe con-
sibly because of passive transfer of antibody.8,23 Egg trans-
junctivitis and, less commonly, a head tilt. Mortality ranges
mission of PHV does not occur, and fostering eggs from
from 25 to 100%. Gross and microscopic lesions are
infected flocks under hens that are not infected may
found in the conjunctiva, trachea and air sacs.40
break the infection cycle.23
A herpesvirus has been isolated from English budgeri-
gars in Europe. Its presence has been correlated with POXVIRUSES
reduced hatchability and is believed to be transmitted
Applied Biology
vertically.
There are many poxviruses. Each poxvirus has its own
A virus believed to be a mutation of the infectious laryn- host range, a range that may include one or several
gotracheitis virus of chickens has been observed to species of birds. Examples of poxviruses with a limited
cause a severe upper respiratory and tracheal disease host range include the canary poxvirus, which affects
in Amazon parrots and Bourke’s parakeet (Neophema only canaries and canaries hybridized with other species,
bourkii). The duration of this disease is variable, but and the parrot pox that appears to be confined to South
clinical signs have been reported to last up to 9 months. American parrots. A mynah poxvirus appears to affect
This disease is reported in the USA, but if it occurs in only mynahs, but mynahs may be susceptible to the star-
the USA, it is rare. Additionally, tracheitis occurs uncom- ling poxvirus.24,51 In contrast, poxviruses brought into
737
Hawaii in non-native species have had a devastating infections of these lesions are common. Extensive oral
impact on native Hawaiian forest birds. Fowl pox can lesions and tracheal lesions may obstruct airflow and
cause disease in a number of gallinaceous birds and cause asphyxiation. Mortality in canary aviaries is often
appears to be the cause of pox lesions seen in ostrich high. If treated aggressively, some of these birds will sur-
chicks in the USA.39 vive but may have persistent ocular lesions. Wet pox
sometimes may accompany dry pox.
Poxviruses require an injury to enter the body. Mosqui-
toes are the most common vectors for poxviruses, allow- Systemic pox occurs in canaries as an acute onset dis-
ing the virus to enter the body through a bite wound. ease. Chemosis, depression, anorexia and dyspnea char-
When wild-caught nestling blue-fronted Amazon parrots acterize this disease. Birds die within a few days. If they
were held in quarantine, incompletely sanitized hand- survive, they will develop cutaneous lesions. Necropsy
feeding utensils were believed to spread the virus from findings include air sacculitis and pneumonia.
one bird to the next. Generally, canary outbreaks occur
in birds that are housed outdoors, but conspecific aggres- Diagnosis
sion and cannibalism also may result in rapid dissemina- The gross appearance of the lesions in the appropriate
tion if latently infected birds are present in the flock. species is highly suggestive of the disease. Biopsies of
Rarely, aerosolized virus in feces or feather dander may mucous membranes and cutaneous masses will reveal
directly infect respiratory epithelium. the classic large eosinophilic intracytoplasmic inclusion
bodies (Bollinger bodies) (Fig 32.10). Impression smears
Clinical Presentation of these lesions also may reveal these inclusion bodies.
The practitioner is most likely to see this disease in Because the lesions often ulcerate, inflammatory cells,
canaries and chickens housed outdoors and in free-rang- bacteria and yeasts are likely to be present in scrapings
ing birds and young domestic pigeons. Historically, dis- and impression smears.
ease was seen in nestling blue-fronted Amazon parrots
held in quarantine. This problem is not seen in captive- Treatment
raised birds and, because the importation of these birds The poxviruses themselves cannot be treated. In the
has essentially ceased, this manifestation of disease is no mild form of the disease, treatment is generally not nec-
longer seen in the USA. essary. Severe lesions may cause the birds to stop eating.
In these cases, supportive care (tube-feeding and fluids)
Three forms of disease are recognized. The so-called dry is indicated. Ulcerated lesions may become infected and
pox is the most common disease manifestation. In this antibiotic therapy is indicated in these birds. Vitamin A
form of the disease, lesions are most commonly seen supplementation also is suggested to be therapeutic.
around the face (especially the eyelid and commissures Surgical removal of pox lesions will only cause scarring
of the mouth), on the feet and under the wings (Fig 32.9). and should not be attempted.
Lesions are raised, smooth to nodular, and may ulcerate.
Lesions may be small and clinically insignificant to exten- Prevention and Control
sive, deforming lids and even the beak. Extreme cases Poxviruses are transmitted by insect bites or by inocula-
result in lesions that may appear neoplastic. Secondary tion into abrasions on the skin or mucous membranes.
superficial bacterial and fungal infections occur in ulcer- Raising birds indoors or screening the aviary best con-
ated lesions. Conjunctivitis and keratitis are common trols infections in canaries. A canary pox vaccined is avail-
when there is extensive lid involvement. Extensive lesions able. Immunization of pigeons with the pigeon pox vac-
also may impair vision, resulting in the birds not being cine also is an important means of control. Racing
able to find food. The lesions develop rapidly over the pigeons are immunizede no less than 6 weeks before the
course of several days, but take up to 6 weeks to regress. racing season begins, as the vaccine is live and will cause
When they do begin to regress, they regress rapidly. the birds to show some signs of illness.
Wet or mucosal pox is a second manifestation of some

poxvirus infections. It is seen in canaries, lovebirds,
mynahs and imported blue-fronted Amazon parrots. RNA Viruses
The disease in canaries is characterized by a unilateral
or bilateral blepharitis, chemosis and conjunctivitis. PARAMYXOVIRUS 1 (PMV-1) EXOTIC
Typically, there will be considerable ocular discharge and NEWCASTLE DISEASE VIRUS
the eyelids will swell shut. Diphtheritic lesions of the
oral cavity and trachea develop subsequently. These Applied Biology
lesions cause the birds to stop eating, and secondary Nine serogroups of avian paramyxoviruses are recognized.
Fig 32.9 | The dry form of pox in a chicken. Fig 32.10 | Hematoxylin and eosin-stained section of an avian
pox lesion. The round eosinophilic intracytoplasmic inclusions are
characteristic of those produced by poxviruses.
Within each paramyxovirus serogroup there may be many movements of fighting cocks from Mexico. Infected chick-
strains. PMV-1 or the Newcastle disease virus strains are ens shed virus through their respiratory system and feces.
defined immunologically, genetically and by their patho- Inhalation of the virus may be an important means of
genicity to chicken embryos or chicks. Velogenic viruses transmission when birds are in direct contact. Movement
are highly pathogenic to chickens. These viruses can be of the virus between flocks results from the movement of
divided into those that cause predominately hemorrhagic infected birds and the movement of the virus on contam-
lesions of the digestive tract — viscerotrophic velogenic inated vehicles and other equipment, clothes and feed
Newcastle disease virus (VVND) — and those that cause sacks. END can colonize the conjunctiva of the human
predominately respiratory and central nervous system eye where it can persist for at least 48 hours, but it is not
lesions — neurotropic velogenic Newcastle disease virus known if this plays a role in END dissemination. Vertical
(NVND). Less pathogenic forms that primarily cause dis- transmission of virus is not believed to play an important
ease in young chickens are called mesogenic pathotypes, role in END dissemination.
and those that cause little or no disease in the chicken
are called lentogenic pathotypes. The virulence of PMV-1 Clinical Presentation and Diagnosis
virus for chickens does not consistently reflect the viru- END in Poultry
lence of the virus in other species, as VVND may cause END is as likely to appear in small, privately owned
only mild signs in companion birds, and mesogenic collections of chickens as it is in large poultry opera-
viruses have caused devastating outbreaks of disease in tions. Therefore, it is entirely possible that private
wild birds. The two most important PMV-1 viruses that practitioners will be presented with chickens with this
the practitioner confronts are the highly pathogenic reportable disease.
VVND strain known as exotic Newcastle disease virus
(END) and pigeon paramyxovirus.1,24 The first indication of END in a flock of chickens may be
the sudden onset of mortality with few antemortem signs.
Signs are generally non-specific and may involve the gas-
EXOTIC NEWCASTLE DISEASE
VIRUS trointestinal tract, respiratory system, central nervous sys-
tem or a combination of these systems. Sneezing, cough-
END is a highly virulent virus that has a devastating ing, nasal discharge and dyspnea, swelling around the
impact on poultry worldwide. It has been excluded from eyes and the head, green diarrhea, depression, weakness,
many nations in the world by strict laws governing the muscle fasciculations, torticollis, paralysis and sudden
movement of birds. In the USA, all birds entering the death are all listed as signs associated with the 2003 out-
country are required to go through a 30-day government- break in the southwestern USA. Birds with these signs
monitored quarantine. Random birds and birds that die should be immediately reported to local regulatory veteri-
in quarantine are tested for END. Illegal movements of narians. Necropsies of these birds are not performed in
parrots across the Mexican border have been responsible the clinic but at official diagnostic facilities.
for limited outbreaks of END in the USA in the past. The
2003 outbreak occurring in California, Nevada, Arizona Gross lesions also can be extremely variable. However,
and Texas is speculated to have resulted from illegal lesions that are highly suggestive of END include hemor-
739
rhagic lesions of the conjunctiva, esophagus, proven- onto the premises, including food, has not been
triculus, small intestines, ceca and cloaca. Tracheal hem- exposed to other birds.
orrhage may be a significant lesion in birds infected with
certain strains. Birds with CNS signs may not have gross There is no desire on the part of regulatory veterinarians
lesions. to unnecessarily kill companion birds. Therefore, in the
USA, consideration is given to the specific circumstances
END in Parrots of the home or the aviary before action is taken. For max-
END has entered the USA on several occasions in smug- imum protection, birds are housed indoors. If this is not
gled parrots. Although the entry was along the USA- possible, they should be housed in a way that keeps out
Mexico border, often the disease was not recognized
all wild birds and rodents. A fence preventing loose
until these parrots had made it to northern states.
neighborhood birds from entering the facility is critical. It
Outbreaks have typically been associated with nestling
is highly recommended that all exotic bird owners not
yellow-naped (Amazona ochrocephala auropalliata) and
keep poultry, or if they do, that the poultry be confined
double yellow-headed Amazon parrots (A. ochrocephala
to a cage and isolated the same way the companion birds
ochrocephala). Signs are not specific and include depres-
are isolated. Food and water dishes are covered so the
sion, anorexia, weight loss and diarrhea. Respiratory
signs may or may not be present. Ataxia, torticollis, droppings of wild birds cannot contaminate them. An
opisthotonus, head bobbing, chorea and paralysis may effective biosecurity protocol as described is critical. If
occur in birds surviving the acute form of the disease. END is found in close proximity to an aviary, the aviary is
The development of neurologic signs in a sick bird should likely to be quarantined. Owners will then be required to
alert the veterinarian that he or she may be dealing with follow specific quarantine measures, including having
END. Recovery can occur, and recovered birds may shed their birds swabbed twice at a 15-day interval. If END is
virus for months to years. If this disease is suspected, a found in a flock, the birds will be euthanized. For more
regulatory veterinarian should be immediately contacted. detailed information see the California Animal Health
and Food Safety Services Web site at www.cdfa.ca.gov.
Prevention and Protection Immunization of companion birds with Newcastle dis-
The first line of defense against END is controlling the ease vaccines intended for poultry is not recommended.
movement of birds into a country. When this fails and It also should be noted that immunized poultry still may
the disease infects poultry, the situation is catastrophic. contract END, and their vaccination status will not
Under these circumstances, efforts are made to isolate impact the outcome of the flock if they are exposed.
the virus to a specific geographic area by stopping the
movement of birds. Then a door-to-door campaign is
PMV-1 IN PIGEONS (PPMV-1)
undertaken to identify and slaughter all flocks with the
disease. An extensive public education effort is necessary Applied Biology
to keep this disease from spreading. In affected areas,
Pigeon paramyxovirus-1 (PPMV-1) was first recognized in
breeders of companion birds are significantly impacted.
the early 1980s and has since disseminated throughout
Bird shows and sales are banned, and movement of
the world. It is found in feral pigeon populations and is a
birds out of the quarantined areas is prohibited.
significant problem in racing pigeon flocks. Evolution of
Veterinarians in the quarantined areas and in areas this virus has resulted in changes in its virulence and
where the disease has the potential of spreading will be clinical manifestations. PPMV-1 is not restricted to
asked by aviculturists what they can do to protect their pigeons and has been identified in feral Eurasian collared
flocks. The most important means of preventing END is doves (Streptopelia decaocto).45 The strain of virus identi-
to maintain a closed flock. This means that no birds are fied in these doves, however, appears to be adapted to them
introduced to the aviary until the outbreak is under con- and varies somewhat from that found in pigeons.8,24,45
trol. If owners are outside of the quarantine area and
must bring in new birds, these birds are isolated in a Clinical Presentation and Diagnosis
separate facility for 30 days before being introduced into
a flock. A veterinarian should examine all birds showing PPMV-1 may present in two ways. In the first, neurologic
any sign of disease. A closed colony also means restricted signs predominate. Ataxia and torticollis are the most
access to the public. In quarantine areas, visitors who common signs. The second presentation is polyuria with
own birds or might have been around birds should be or without neurologic signs. In both forms of the dis-
completely barred from the facility. Footbaths should be ease, many birds in a loft will show signs and mortality
placed at the entranceway to the aviary, and every effort can be high. Affected birds should be submitted for
should be made to make sure that anything brought necropsy to verify the infection.
Prevention EASTERN EQUINE

PPMV-1 is disseminated by contact with other pigeons. It
ENCEPHALITIS (EEE)
is particularly common for it to be introduced to a loft The importance of EEE in parrots is unclear. EEE was
when pigeons are raced, as the birds are in close contact implicated in a disease of 7- to 12-week-old macaws.
with birds from other flocks prior to the race. Immuniza- The birds showed varied signs from sudden death to
decreased appetite with abdominal distention. Grossly,
tion with a PPMV-1 vaccinef at least 6 weeks prior to the
serositis with extensive abdominal effusion was noted.
racing season is recommended on a yearly basis.
Histologically, hepatic disease, interstitial pneumonia
and lymphocytic proventriculitis were consistent find-
OTHER PARAMYXOVIRUSES ings. This disease has been termed polyserositis. It is the
author’s experience that this disease is extremely rare.
Paramyxovirus 2 (PMV-2)
However, edema and ascites occur with some degree of
PMV-2 rarely causes disease in companion birds. It has frequency following APV infections, and this disease and
been associated with contact with wild passerine birds, its associated lesions may be mistaken for polyserositis.
particularly finches, and should be considered a differ-
ential for birds that are showing respiratory signs. WEST NILE VIRUS (WNV)
Applied Biology
Paramyxovirus 3 (PMV-3)
WNV is a flavivirus that is a member of the Japanese
PMV-3 has been recognized in multiple nations around
encephalitis virus complex. WNV can be divided into
the world, but its basic biology is poorly understood. It
two lineages. Lineage 1 has a wide distribution. It has
appears to cause subclinical infections in some birds and
been isolated from Africa, Europe, the Middle East,
it is these birds that are responsible for the spread of India, Australia and the USA. Lineage 2 is confined to
infection. Disease is reported most frequently in Neo- Africa. Recently, outbreaks of WNV have occurred in
phema species, lovebirds, cockatiels and Amazon parrots, France, Romania, Italy, Russia and Israel. The outbreak
although recently the disease also has been seen in African in Israel was atypical because the virus had an apparent
grey parrots. Signs of infection may be non-specific and increased virulence for humans and birds. A strain of
precede death by 24 to 48 hours. Birds with a longer WNV essentially identical to the strain found in Israel
duration of signs will develop CNS signs resembling was first identified in New York City in 1999. By the time
those seen with END. In some cases, respiratory signs of this writing, it has spread widely and has been identi-
also may occur. Chronic infections in Neophema species fied in the majority of states in the USA and in several
often result in chronic pancreatitis. These birds have provinces in Canada. It is expected that it will continue
voluminous stools that contain undigested starch and fat. to expand its range into Central and South America in
PMV-3 infections also are reported in finches with signs the coming years.15,20
of diarrhea, dysphagia, conjunctivitis and dyspnea.22,24
Birds are the primary vertebrate host for WNV. Mosqui-
Antemortem diagnostic assays have not been consis- toes, particularly the members of the genus Culex, are
tently effective in identifying birds with disease and the insect vectors. It has been postulated that hippo-
boscid flies also may be vectors of WNV, but this has not
asymptomatically infected birds. Traditionally, birds
been experimentally tested (M. Taylor, personal commu-
infected with PMVs will produce antibodies that will
nication, 2002). After ingesting blood from a viremic
inhibit virus-induced agglutination of red blood cells.
bird, the virus is amplified in the digestive tract and sali-
This may be true in some parrots with acute PMV-3, but
vary gland of the mosquito. Bird infection occurs when
may not be true in chronic infections. Current efforts to
an infected mosquito bites a bird. After a bird is infected,
develop an ELISA assay to detect chronically infected
it remains viremic from 4 to 7 days. The magnitude of
birds may help to resolve this issue. Molecular-based the viremia depends on the species infected. Crows,
technology also may prove to be beneficial in the diag- magpies, house sparrows (Passer domesticus) and other
nosis of these infections. passerines appear to develop the highest concentrations
of virus in the blood and have the longest duration of
AVIAN INFLUENZA viremia. WNV may persist in the skin after the cessation
of viremia, allowing mosquito infection for an as-yet-
Avian influenza is a rare disease of companion birds. It is
undetermined period of time after infection.
reported to cause non-specific signs as well as signs
related to the central nervous system. It is readily recov- Preliminary studies suggest that consumption of animals
ered from swabs of the cloaca and trachea. infected with WNV and even ingestion of infected mos-
741
quitoes will result in infection in some species of birds. Prevention

Close contact also can result in viral dissemination WNV has created panic in the general bird-owning popu-
between birds. Virus can be found in the oral cavity and lation in the USA and has been of great concern to
cloaca of infected birds for 9 or more days after infec- wildlife and zoo veterinarians. Many zoo veterinarians
tion, and it is a reasonable hypothesis to assume that it have elected to use the West Nile virus vaccineg for horses
is present in saliva and droppings. WNV persists in the to vaccinate birds. The equine dose is 1 ml. Experimental
tissues of some species that survive for as long as 14 immunization using a 0.5-ml dose given twice 2 weeks
days after infection. Experiments have not been done to apart did not induce an antibody response in cockatiels. A
show if it persists longer than this.16 full 1.0-ml dose given three times, 3 weeks apart, did
induce an antibody titer in some but not all birds immu-
Clinical Presentation nized at the Houston Zoo (J. Flanagan, personal commu-
nication, 2003). Adverse reactions to the vaccine were not
WNV can infect and is believed to have caused death in a
noted. A hemolytic anemia, however, has been reported
wide range of species. Birds particularly susceptible to
in lories immunized 1 year after their first set of immu-
disease caused by WNV include crows, blue jays (Cyan-
nizations the year before. Similar problems have not been
cocitta cristata), magpies, accipiters, red-tailed hawks
noted at the Houston Zoo in birds that have been immu-
(Buteo jamaicensis) and several species of northern
nized 2 years in a row (J. Flanagan, personal communica-
owls. Ruffed grouse (Bonasa umbellus), gulls, house
tion, 2003). Given that it is not known how protective this
sparrows, robins (Turdus migratorius) and mourning
vaccine is for birds and that at least one institution has
doves (Zenaida macroura) make a significant number seen adverse effects that may be linked to immunization
of reported cases, but reported disease in these species with it, use of this vaccine should be considered a last
is less than 10% of that reported for crows. Naturally resort when other mosquito control options are not avail-
and experimentally infected geese appear to be sensitive able. An immunization schedule that has been used has
to disease from WNV. Chickens, turkeys and at least been to give a 1-ml dose of the vaccine every 3 weeks for
some species of psittacine birds appear to be relatively three immunizations. The vaccine can be divided and
refractory to disease. given in multiple sites in smaller birds.
WNV infection has a seasonal distribution in temperate Disease in psittacine birds is rare; therefore, immuniza-
climates. The first cases are seen in the spring and then tion of psittacine birds is not recommended at this time.
continue through the summer. A short course of Concerned pet owners should keep their birds indoors
lethargy followed by death may be the only signs seen. in the warmer months of the year.
Other birds, however, develop signs of central nervous
system disease, including ataxia, tremors, weakness, REOVIRUS
seizures and abnormal head postures prior to death.
A reovirus was found to be one of several pathogens
Anisocoria and impaired vision also were noted in some
causing a complex of diseases in recently imported
birds. Observations by practitioners suggest that some
African grey parrots, but also was seen in several other
birds may show mild signs of illness and then recover.41
species including cockatoos.6 Because imported wild
birds are rarely seen in practice today in the USA, this
Diagnosis disease has essentially disappeared. Wild-caught African
Necropsy findings suggestive of WNV disease include grey parrots are, however, still imported into Europe,
intraosseous hemorrhage of the calvaria and hemor- and this disease continues to be a problem there.
rhage of the meninges, mucosa and serosa of the gas-
trointestinal tract. Splenomegaly is minimal to marked. Clinical Presentation
Focal, linear, or diffuse myocardial pallor also may be The signs of disease have varied to some degree with the
present. Microscopic lesions of the brain, heart, pan- specific outbreak. Signs in outbreaks seen in the USA
creas, intestines and spleen are highly suggestive of WNV included depression, weakness, weight loss, edema of
disease. Infection can be confirmed by isolating the virus the legs and head, and paralysis. Anemia, leukopenia
from oral and cloacal swabs, brain, heart, kidney, liver, and elevated liver enzymes also are reported. More
lung and spleen or PCR of these tissues. recent outbreaks in African grey parrots imported into
Italy showed respiratory signs, including coughing, nasal
Neutralizing virus antibody is detected in the majority of discharge and increased lung sounds. The disease had a
birds within 14 days of infection. Plaque reduction prolonged course and affected birds died. Australian
assays and hemagglutination inhibition assays are used king parrots also were affected with this disease, but
to detect antibodies to WNV.15,16,41 these birds died suddenly.
Natural reovirus infections are often complicated by con- experiencing an outbreak of PMV-3 infection: these find-
current infections with multiple other infectious agents, ings were strengthened by the discovery of antibodies to
including bacteria, Aspergillus spp. and other viruses. PMV-1 in birds with PDD, and isolation of a low virulent
Each of these pathogens contributes to the clinical pic- strain of PMV-1 from the spinal cord of 6 of 32 parrots
ture of disease. with PDD.11,12,22 It is hoped that the slow but steady
progress made by investigators working with this disease
Diagnosis will soon lead to the discovery of its etiologic agent.
Diagnosis in the live bird is probably impossible. How-
Clinical manifestations of the disease are the result of a
ever, this disease should be suspected in recently
lymphoplasmacytic inflammation of the nerves of the
imported wild-caught African grey parrots and birds that
gastrointestinal tract and brain, spinal cord and periph-
are in contact with them. Gross lesions include enlarge-
eral nerves.5 Lesions also may be found in the heart and
ment of the liver and the kidney, with focal depressed
adrenal gland. Lesions are rarely diffuse and are variable
discoloration of the capsular and cut surfaces of the liver.
in their severity. As a result, clinical signs of disease vary
Serosal hemorrhages, enteritis and renal enlargement
from case to case.
occur less commonly. Lesions from other pathogens also
may be present. Histologic lesions are not specific, and
virus isolation is necessary to confirm reovirus infection. Clinical Presentation and Diagnosis
PDD occurs most frequently in African grey parrots,
Control macaws, Amazon parrots, cockatoos and conures, but it
There is no means of control for this disease other than is possible that all parrot species are susceptible.24 It also
to stop importing wild-caught African grey parrots. may occur in non-psittacine birds, as a disease with simi-
Isolation of imported African grey parrots from other lar lesions has been observed in Canada geese, a red-
imported species may prevent some losses. tailed hawk and flamingos. There is no sex predilection
for PDD. The median age of onset of PDD is 3 to 4 years,
but birds as young as 10 weeks and as old as 17 years
RETROVIRUSES have been documented with lesions consistent with
Retroviruses are important causes of disease in water- PDD. Domestically raised and imported birds are equally
fowl and gallinaceous birds. Documentation of retro- susceptible to disease. The incubation period for this
virus diseases in companion birds is lacking. disease is not known but may be long, as birds isolated
from contact with other birds for up to 2 years still have
developed this disease.
Diseases Thought to be The number of birds affected by PDD in a collection, the
Caused by Viruses rapidity with which it spreads through a collection and
the clinical signs of disease can vary significantly. Birds
PSITTACINE PROVENTRICULAR with the most common form of the disease present with
DILATATION DISEASE (PDD) what the owner considers to be an acute onset of dis-
ease. There may be a history of regurgitation, anorexia
Applied Biology and the presence of undigested seeds in the droppings.
PDD is a disease of unknown etiology, but circumstantial Physical examination, however, reveals an emaciated
evidence suggests that one or more viruses cause it. bird. Often the ventriculus can be palpated in the
Numerous clinical reports document the spread of PDD coelomic cavity caudal to the edge of the sternum.
through a collection after the introduction of birds that Radiographically, the proventriculus is often massively
subsequently develop disease. Inoculation of tissue dilated, filling the left side of the coelomic cavity (Figs
homogenates derived from a bird with PDD induced a 32.11, 32.12). Typically, it develops a “J” shape causing
histologically identical disease in experimentally infected the ventriculus to be displaced to the right and ventrally
birds. Viruses and virus particles have been identified in (Fig 32.13). Ultrasound will demonstrate a widely dis-
a number of birds with PDD. Several viruses have been tended proventriculus and ventriculus. Muscle contrac-
identified in birds with PDD or in flocks where PDD was tions typically are weak, and there is a failure of the
a problem. These include eastern equine encephalitis, junction between the proventriculus and ventriculus to
enterovirus, coronavirus, reovirus, avian paramyxovirus close. Contrast studies show distention of the proven-
1 and paramyxovirus 3.9,10,12 The potential role of triculus and ventriculus and often the proximal duode-
paramyxoviruses as the cause of PDD has been strength- num. Transit time of the contrast material is markedly
ened by the development of lesions identical to those reduced. Various permutations of this disease may occur,
seen in PDD in a flock of Neophema spp.. They were and dilation of the crop, ventriculus, proventriculus or
743
Fig 32.11 | Lateral radiograph of an eclectus parrot reveals Fig 32.12 | In this ventral dorsal radiograph of the eclectus
proventricular dilatation disease (PDD). Note the massively dis- parrot in Fig 32.11, the hugely distended proventriculus fills the
tended proventriculus. left lateral coelomic cavity.
duodenum may be seen alone or in combination.
CNS signs may be absent, occur in combination with the

gastrointestinal signs, or be the only presenting signs.
CNS signs may have an acute onset or be very slowly
progressive. They may reflect disease of the brain or the
spinal cord, and recent evidence suggests that they also
may reflect lesions of the lower motor neurons. Ataxia
that may be slowly progressive, proprioceptive deficits,
paresis and less commonly paralysis, head tremors and
rarely seizures have been reported in birds with PDD. Fig 32.13 | In the gross necropsy of a eclectus with PDD in Figs
32.11 and 32.12, note the massively distended proventriculus
Clinical pathologic findings are not specific but typically that extends laterally beyond the edge of the left liver lobe. The
ventriculus is displaced to the right and ventrally.
reflect the fact that these birds are starving. High uric acid
levels were seen in one of the author’s cases, because the
bird’s neurologic disease prevented it from reaching the to years. However, there are times when only an individ-
water bowl and drinking. Overgrowth of the digestive ual bird is affected. Uncommonly, there are outbreaks
tract with yeast and gram-negative bacteria occurs as the where multiple birds develop disease within a very short
result of gastrointestinal stasis. Initial attempts at diagnos- period of time.
ing this disease by serology and electron microscopy of
the feces have subsequently been discontinued. As common as this disease is, there are other diseases
that can cause nearly identical signs.2 Gastrointestinal
Demonstrating characteristic lesions in a crop biopsy can signs identical to those seen in PDD can be caused by
make a definitive diagnosis of this disease. Not all birds neoplasia of the intestines, intestinal foreign bodies
with PDD have crop lesions, so failure to find lesions in and even massive worm burdens that cause intestinal
a biopsy does not rule out the disease. It is suggested obstruction. Emptying of the proventriculus and ventri-
that biopsying the right cranial ventral aspect of the culus appears to be inhibited as long as the intestinal
crop, while making sure that it contains a blood vessel, tract is distended. As a result, proventricular dilatation
will increase the probability of a lesion being found.10 occurs in cases of lower bowel obstruction. Inflammatory
Biopsy of the proventriculus is not indicated, as the disease and neoplastic diseases of the ventriculus and
proventriculus will already be diseased and is likely to proventriculus also can cause gastrointestinal stasis.
dehisce. A partial thickness biopsy of the ventriculus to Another common cause of gastrointestinal stasis is heavy
get a section of the splanchnic nerves is safe but is metal poisoning. Heavy metal poisoning is commonly
rarely done. associated with central nervous system signs as well. A
chronic wasting disease caused by internal papillomato-
The progression of PDD through a flock cannot be pre- sis also resembles PDD.
dicted. Typically, once it is recognized in the flock, addi-
tional birds will develop disease in the following months PDD should be considered as a differential in any bird
with CNS disease. Traumatic injuries, heavy metal poi- SEASONAL MORTALITY IN GREAT-
soning, neoplasia, viral, bacterial and fungal infections of BILLED PARROTS
the CNS, nutritional deficiencies and hydrocephalus are A disease of unknown etiology is killing great-billed par-
additional diseases that can cause similar signs. rots (Tanygnathus megalorhynchos ) in the USA.26 A sur-
vey of great-billed parrot owners suggests that this dis-
Treatment ease has killed approximately 50% of the great-billed
parrots housed in the southern USA during the period
Celecoxibh, a COX-2 inhibitor, has been advocated as a of 1995 to 2000. The disease occurs predominately in
treatment for PDD.7 Controlled trials with this drug for Gulf Coast States from July to October. Other species
the treatment of PDD have not been done, but careful that have had similar signs of this disease include the
clinical reporting suggests that celecoxib does cause mealy Amazon parrot (Amazona farinosa) and lories.
regression of the signs of PDD, and birds that otherwise The disease occurs typically in outbreaks, with multiple
would have died are still alive up to 2 years after treat- birds developing signs over a period of 1 to 4 weeks.
ment. Successful treatment appears to be more likely if Both hand-fed nestling parrots and adult parrots are sus-
PDD is diagnosed before the bird is extremely debili- ceptible. Birds housed outside are primarily affected, but
tated. The recommended treatment protocol is to make disease also has occurred in indoor birds.
a suspension of celecoxib in lactulose and to administer Clinical signs of this disease are dramatic. Gastrointestinal
10 mg/kg orally once a day for a minimum of 6 weeks or motility ceases, so birds stop eating. They may have diar-
until the signs resolve completely. Although lactulose rhea or no droppings at all. Even liquid diets do not pass
was the first agent used to suspend this drug, others through the digestive tract. Affected birds rapidly become
may work just as affectively. Anecdotal information sug- dehydrated. Birds die within 1 to 3 days, despite aggres-
gests that other COX-2 inhibitors also may be effective. sive therapy. One case did survive after 2 weeks of treat-
ment, during which time the bird lost nearly 50% of its
Additional supportive care will need to be supplied to body weight before its digestive tract began to function
these birds in addition to celecoxib treatment. Birds that again. Intussusception of the intestines occurs in a signif-
are dehydrated should be given fluids. Liquid diets icant number of cases, resulting in bowel strangulation
sometimes will pass through the digestive system while and necrosis. Blood counts and clinical chemistries show
solid diets will not. Secondary yeast and bacterial infec- a moderate drop in the total white blood cell count, con-
tions also should be treated. centration of the blood from dehydration, an imbalance
of electrolytes, elevation in muscle enzymes and an eleva-
tion in uric acid, indicating severe dehydration or pri-
Prevention and Control
mary kidney disease or a combination of both.
Until the etiologic agent of this disease is identified and
an appropriate test for that agent is developed, preven- Consistent specific necropsy findings do not occur. Given
the seasonality of this disease, an insect-borne virus has
tive measures will depend on conservative management
been suspected to cause this disease. However, repeated
practices. A detailed history of the source of all new
virus isolation attempts have been unsuccessful. Investi-
birds and long quarantine periods (>6 months) will
gators are currently examining the possibility that a
reduce the risk of introducing this disease. Historical
clostridium toxin may be causing this disease.
findings suggest that this disease is more likely to spread
in indoor collections. Keeping breeding birds outdoors
EPIZOOTIC RESPIRATORY
when possible and maximizing hygiene, ventilation and
NEOPLASIA OF COCKATIELS
cage separation in indoor aviaries may reduce the risk of
Rapidly growing tumors of the air sacs and lungs occur
PDD transmission.
in cockatiels. Multiple birds in a collection may be
affected over a period of several years. The most com-
The diagnosis of PDD in a collection can be a devastat-
mon clinical sign is the sudden onset of severe dyspnea,
ing blow to the aviculturalist. Remember, however, that
although observant owners may see the signs develop
sooner or later most large collections of birds that have
over the course of several days. By the time the birds are
been assembled from multiple sources will have a case severely dyspneic, restraint for physical examination or
of PDD. Isolating birds in contact with birds that have radiographs can be life threatening. If the bird can be
had PDD may prevent dissemination. Incubator-hatching radiographed, masses will be seen either in the lung or
eggs and hand-raising these chicks in isolation also may lungs or in an air sac. These are highly invasive tumors
break the infection cycle, although this has not been and will penetrate through adjacent vertebrae, com-
proven scientifically. pressing the spinal cord. When this occurs, birds present
745
with a progressive or sudden onset of paresis or paraly- aviaries, but APV DNA has not been identified in these
sis of the legs. Attempts to treat these tumors have not tumors.
been reported.24
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they may outwardly appear as lipomas. The appearance f. Paramyxovirus 1 Vaccine, Maine Biological Laboratory, Waterville ME, USA,
of the nuclei of the neoplastic cells resembles the 207-873-3989, www.mainebiolab.com
g. West Nile Virus Vaccine, Fort Dodge Laboratories, Fort Dodge, IA, USA,
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of APV disease has been documented in some of these h. Celebrex, Pharmacia, Pfizer, www.celebrex.com
References and diagnose pigeon circovirus infec- omavirus: More pieces to the native and exotic birds during the
tion in vivo. J. Virol Meth 104:55- puzzle. Proc Assoc Avian Vet, 1999 outbreak in New York City,
Suggested Reading 58, 2002. 1998, pp 151-156. New York. Vet Pathol 37:208-224,
1. Alexander DJ: Newcastle disease 15. Johnson DJ, et al: Detection of 29. Phalen DN, et al: Genetic diversi- 2000.
and other avian Paramyxoviridae North American West Nile virus in ty in twenty variants of the avian 42. Strunk A, et al: Pathobiology and
infections. In Calnek BW (ed): animal tissue by a reverse tran- polyomavirus. Avian Dis 43:207- testing recommendations for
Diseases of Poultry 10th ed. scription-nested polymerase 218, 1999. psittacine circovirus 2 in lories.
Ames, Iowa State University Press, chain reaction assay. Emer Infect 30. Phalen DN, et al: Viremia, virus Proc Assoc Avian Vet, 2002, pp 45-
1997, pp 541-569. Dis 4:739-741,1998. shedding, and antibody response 47.
2. Antinoff N: It isn’t always PDD: 16. Komar N, et al: Experimental during natural avian poly- 43. Styles D, Phalen DN, Tomas-
Three cases with proventricular infection of North American birds omavirus infection in parrots. J zewski E: Elucidating the etiology
enlargement. Proc Assoc Avian with the New York 1999 strain of Am Vet Med Assoc 217:32-36, of avian mucosal papillomatosis
Vet, 2001, pp 35-37. West Nile virus. Emer Infect Dis 2000. in psittacine birds. Proc Assoc
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KF: Prevalence of microsporidial 17. Johne R, Müller H: Avian poly- parrots infected with Pacheco’s 44. Styles D, Tomaszewski E, Phalen
shedding in asymptomatic love- omavirus in wild birds: Genome disease viruses. Proc Assoc Avian DN: Psittacid herpesviruses in
birds: Evidence for a potential analysis of isolates from Falconi- Vet, 2001, pp 87-89. mucosal papillomas of Neo-
emerging zoonosis. J Avian Med formes and Psittaciformes. Arch 32. Phalen DN, et al: Genetic diversi- tropical parrots. Manuscript in
Surg, in press, 2003. Virol 143:1501-1512, 1998. ty of avian polyomaviruses: preparation. 2003.
4. Bassami MR, et al: Genetic diver- 18. Johne R, et al: Herpesviral, but Clinical implications. Proc Assoc 45. Terregino C, et al: Character-
sity of beak and feather disease no papovaviral sequences, are Avian Vet, 2001, pp 171-172. ization of Newcastle disease virus
virus detected in psittacine detected in cloacal papillomas of 33. Raidal SR, et al: A serologic sur- isolates obtained from Eurasian
species in Australia. Virology parrots. Arch Virol 10:1869-1880, vey for avian polyomavirus and collared doves (Streptopelia
20:392-400, 2001. 2002. Pacheco’s disease virus in decaocto) in Italy. Avian Pathol
5. Berhane Y, et al: Peripheral neuri- 19. Lafferty SL, et al: Avian poly- Australian cockatoos. Avian Pathol 32:63-68, 2003.
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Avian Pathol 30:563-570, 2001. viridis). Avian Dis 43:577-585, genicity, and efficacy of an inacti- novel circovirus of canaries. Avian
6. Conzo G, et al: Reovirus infection 1999. vated avian polyomavirus vaccine. Pathol 30:321-325, 2001.
in two species of Psittaciformes 20. Lanciotti RS, et al: Complete Amer J Vet Res 59:143-148, 1998. 47. Todd D, et al: Evaluation of poly-
recently imported into Italy. Avian genome sequences and phyloge- 35. Ritchie BW, et al: Documentation merase chain reaction and dot
Pathol 30:43-47, 2001. netic analysis of West Nile virus of a PBFD virus variant in lories. blot hybridization tests in the
7. Dahlhausen B, Aldred S, Colaizzi strains isolated from the United Proc Assoc Avian Vet, 2000, pp diagnosis of pigeon circovirus
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qxd 8/24/2005 11:23 AM Page I

TERESA L. LIGHTFOOT, BS, DVM

Spix Publishing, Inc.,

Library of Congress Control Number: 2005922214

Clinical Avian Medicine (2-volume set) ISBN: 00-9754994-0-8

Production: Zoological Education Network

Cover Design: Jean Coffinberry

Proofreading: K. Stormy Hudelson, DVM, Dipl ABVP-Avian, Paul Hudelson

Indexing: Ann Truesdale, DVM

Administrative Assistants: Lesley Flahie, Patty Wolf

Technical Assistance: Chris Lane

Printing and Binding: Four Colour Imports

Advertising and Sales: HBD Intl Inc. www.harrisonsbirdfoods.com

©2006 Spix Publishing, Inc., Palm Beach, Florida

Last digit is the print number: 9 8 7 6 5 4 3 2 1

MARCELLUS BÜRKLE, DVM

CARL D. CHENEY, PhD

PETER COUTTEEL, DVM

LORENZO CROSTA, DVM

ROBERT D. DAHLHAUSEN, DVM, MS

BOB DONELEY, BVSc, FACVSc (Avian Health)

M. SCOTT ECHOLS, DVM, Diplomate American Board of Veterinary Practitioners (Avian)

THOMAS M. EDLING, DVM, MSpVM

GWEN B. FLINCHUM, BS, MS, DVM

SUSAN G. FRIEDMAN, PhD

MICHAEL M. GARNER, DVM, Diplomate American College of Veterinary Pathologists

STACEY GELIS, BSc, BVSc (Hons), MACVSc (Avian Health)

PHOEBE GREENE LINDEN, BA, MA

KENDAL E. HARR, DVM, MS, Diplomate American College of Veterinary Pathologists

LORI DANIELLE HARRISON, DVM

PETER HELMER, DVM, Diplomate American Board of Veterinary Practitioners (Avian),

CLAUDIA HOCHLEITHNER, Dr med vet

MANFRED HOCHLEITHNER, Dr med vet, Diplomate European

JAN HOOIMEIJER, DVM

PAUL M. HUDELSON, BA, MA

JACK J. KOTTWITZ, DVM

MARIA-ELISABETH KRAUTWALD-JUNGHANNS, Prof Dr med vet, Dr habil,

ANGELA M. LENNOX, DVM, Diplomate American Board of Veterinary Practitioners (Avian)

KEATH L. MARX, DVM

DEBRA McDONALD, PhD, BSc (HONS I)

ROBERT D. NESS, DVM, Certified in Chiropractic (American Veterinary

ESPEN ODBERG, DVM

JOANNE PAUL-MURPHY, DVM, Diplomate American College of Zoo Medicine

MICHAEL PEES, Dr med vet, German Veterinary Specialist for Birds/Reptiles

DAVID N. PHALEN, DVM, PhD, Diplomate American Board of

SIMON R. PLATT, BVM&S, MRCVS, Diplomate American College of Internal

CHRISTAL G. POLLOCK, DVM, Diplomate American Board of Veterinary

DIANA POST, VMD

MADELINE A. RAE, BS, DVM, MS, Diplomate American Board of Veterinary

PATRICK T. REDIG, DVM, PhD

JILL A. RICHARDSON, DVM

PETER SANDMEIER, Dr med vet, Diplomate European College of Avian

JAIME SAMOUR, MVZ, PhD, Diplomate European College of Avian

ROBERT E. SCHMIDT, DVM, PhD, Diplomate American College of

MICHAEL STANFORD, BVSc, MRCVS

JENS STRAUB, Dr med vet, German Veterinary Specialist for Birds/Reptiles

LINDA TIMOSSI, DVM

LIZ WILSON, CVT