Manul of Avian Disease

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AVIAN DISEASE MANUAL

SEVENTH EDITION
American Association of Avian Pathologists
Edited by M. Boulianne
with
M. L. Brash
B. R. Charlton
S. H. Fitz-Coy
R. M. Fulton
R. J. Julian
M.W. Jackwood
D. Ojkic
L. J. Newman
J. E. Sander
H. L. Shivaprasad
E. Wallner-Pendleton
P. R. Woolcock
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Seventh Edition Published by the

American Association of Avian Pathologists, Inc.
Copyright © 1979, 1983, 1989, 1996, 2000, 2006, 2012 by

All Rights Reserved
Printed by OmniPress
Library of Congress Control Number (LCCN)

2012940076
International Standard Book Number (ISBN)

9780978916343
Cover photo by Marco Langlois
Copies available from:

Additional information available at:
www.aaap.info/avian-disease-manual
AAAP, Inc.
12627 San Jose Blvd., Suite 202
Jacksonville, Florida 32223-8638
Email: [email protected]
Website: www.aaap.info
Preface to the 7th Edition iii
Preface to the 7th Edition

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The Avian Disease Manual has become the best selling publication of the AAAP. Its success is likely due to its ability to
deliver at a reasonable cost, concise yet complete information on commonly encountered diseases affecting poultry. Not
surprisingly, it has become an educational staple to North American veterinary and poultry science students, to those
interested in avian diseases, but also a most useful reference in developing countries.
The world of commercial poultry production is a rapidly evolving one, new pathogens regularly emerge, microorganisms
are reclassified and renamed, discoveries are being made, hence the need for regular re-edition of this manual. Putting
together a new edition, presented this new editor with the challenges of keeping the great teaching qualities of past
editions while updating the information and improving the format. This was made possible through a great team effort.
The current editorial committee is made up of newcomers and experienced members. They all have extremely busy
professional life, but all generously accepted to answer my call and share their knowledge and expertise. I would like to
thank them for their timely diligence in reviewing and updating their chapters. Naturally, we are also indebted to a number
of esteemed colleagues who, since the first edition in 1980, initially written by C.E. Whiteman and A.A. Bickford, provided
us with a solid heritage on which we keep building.
The manual is divided in various chapters grouping diseases by agent (viral, bacterial, fungal, etc…). Within each chapter,
diseases are listed alphabetically and the addition of an index will further help the reader to quickly locate the required
information. The Appendix contains tables, each of which lists the most common diseases of a single body system. Our
students have always appreciated the various tables and positively commented on the fact that you can quickly compare
diseases at a glance. To these tables, we have added two new ones: diseases of the ducks and diseases of the upland
game birds, to cover a wider spectrum of avian species. A poultry drug use list is also provided as a general guide, but
medication recommendations should always be carefully verified with the manufacturer’s label prior to use. Nowadays,
most of our students come from an urban background and have never seen a live chicken or turkey, let alone been on a
poultry farm. To fill this gap, as well as to put into perspective the work of a poultry veterinarian, a new chapter ‘’How do
we investigate a sick flock? ” was added to the manual. The necropsy chapter underwent major revision to include the
differential diagnosis procedure which goes on when a post-mortem examination is being performed.
Under the editorial guidance of Dr. Bruce Charlton, the previous edition incorporated the addition of electronic photos
available on a CD. The 7th edition has now included them in the text while enhancing its library content. After all, an image
is worth a 1000 words! Photos referenced in the text can be found after each disease section. The editorial committee
is deeply indebted to all the authors of the photographs for the exceptional quality and historic significance of the photos
in their collection. Special recognition needs to be offered to Dr. HL Shivaprasad (CAHFS, UC Davis) and Dr. HJ Barnes
(North Carolina State University) for their passion and amazing photo collection, and also to the numerous colleagues
who spontaneously accepted to go through their slides and photos to provide the readers with the highest quality images.
We also used select photos from the AAAP Slide Sets and want to extend our gratitude to their authors. Readers of
this manual are encouraged to investigate these sets and the book Diseases of Poultry for further excellent photos and
information. Although every attempt has been made to correctly credit authors and institutions of the photographs, we
apologize for any mistake that might inadvertently occur.
On a final note, I would like to thank the AAAP Board for their continuous support and willingness to endorse the editorial
committee suggestions, as well as recognize the hard work of Mr. Bob Bevans-Kerr, AAAP Executive Director. His
patience, availability and expertise in Photoshop and the editing process has made the whole process an enjoyable
experience.
Martine Boulianne, Editor

iv Avian Disease Manual
Table of Contents
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Preface to the 7th edition....................................................................................................................................................... iii
How do we investigate a sick poultry flock?.......................................................................................................................... 1

Written by Martine Boulianne
Viral diseases.......................................................................................................................................................................... 6
New parts and revision by Davor Ojkic, Marina L. Brash, Mark W. Jackwood and H.L. Shivaprasad
Bacterial diseases................................................................................................................................................................ 74
Revised by Richard M. Fulton, new sections on Campylobacter and E. cecorum by Martine Boulianne
Fungal diseases................................................................................................................................................................. 140

Revised by H.L. Shivaprasad
Parasitic diseases............................................................................................................................................................... 153

Revised by Steve H. Fitz-Coy
Nutritional diseases............................................................................................................................................................ 179

Miscellaneous diseases..................................................................................................................................................... 191

Diseases of the duck (table)............................................................................................................................................... 230

Written by Peter R. Woolcock and Martine Boulianne
Diseases of the game birds (table).................................................................................................................................... 235

Written by Eva Wallner-Pendleton
Appendix............................................................................................................................................................................. 238
Revised by Linnea J. Newman and Jean E. Sander
Poultry drug use guide....................................................................................................................................................... 263

Revised by Linnea J. Newman and Jean E. Sander
Necropsy of the fowl........................................................................................................................................................... 268

Written by Richard J. Julian and Martine Boulianne
Photos index....................................................................................................................................................................... 279
Index................................................................................................................................................................................... 293
Acknowledgements............................................................................................................................................................ 298
Contributing Authors........................................................................................................................................................... 299

How do we investigate a sick flock? 1
How do we investigate a sick flock? Flock visit

Reasons for visit
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Written by Martine Boulianne

A flock visit can be done either because there is a problem
and the owner has requested your presence, or as part
The approach to investigating a sick poultry flock is one of a routine health check. Compared to the other fields of
of population medicine. Not only do you need to look at veterinary practice, there is no real emergency in poultry
the flock as the unit of interest, but you must also closely medicine i.e., rare are the after hour calls. However, in
examine its immediate environment. Indeed, because the case of a marked increase in mortality, or in case of a
poultry is most often kept in barns, it closely depends on suspicious reportable disease, the veterinarian should visit
housing conditions to be healthy. The Koch’s postulate the affected flock as soon as possible.
‘one infectious agent, one disease’ thus can be remodelled
into this schematization: The most common reasons for a call to the poultry
veterinarian are the following: ‘increased mortality’,
Bird respiratory clinical signs, presence of diarrhea, lameness
or loss in performances. Due to the structure of the poultry
industry, a technician might be called first to later notify the
Environment Infectious agent veterinarian and maybe request his/her expertise.
Optimal environmental conditions, access to high quality
feed and water must therefore be provided for the bird ‘Normal mortality’
comfort, which in turn will translate in maximum efficiency In the case of an increased mortality, a greater number of
production and growth. birds than the usual expected daily rate die. This expected
daily mortality does vary according to the age of the flock,
In the coming chapter, emphasis will be put on the various the type of birds, the type of production and housing. For
parameters one needs to evaluate when visiting a sick example, a certain number of chicks/poults/ducklings
poultry flock. unable to find feed and water in the barn where placed
will die of starvation/dehydration once their yolk sac, hence
nutrient reserve, is exhausted.
The toolbox
Every veterinarian will tell you that essential instruments During the growth period some meat birds might also die
are the thermometer and stethoscope, all, but the poultry of a heart–related condition (sudden death syndrome in
veterinarian. In this case, a knife will be more useful. But chickens and turkeys, ascites in chickens and bilateral
an acute sense of observation, the ability to collect good cardiomyopathy of turkeys) or develop lameness. Inability
information when talking to the owner/animal caretaker to get to the feeder or the drinker will eventually lead to
and logical reasoning are as important, whatever the field dehydration/inanition. These animals should be killed
of practice, to determine the necessary course of action. humanely to end their suffering.
In the poultry veterinarian’s toolbox, you will find a necropsy Mortality is also expected in breeding/laying flocks, from
kit (e.g. necropsy knife, necropsy shears to cut bones, reproductive-related conditions (often associated with
enterotome to incise the gut, scalpel, forceps…), materials obesity), or again from lameness. Cannibalism is another
for sampling (e.g. needles and syringes, blood tubes, cause of death observed in many flocks.
sterile plastic bags and swabs, specimen containers with
and without 10% phosphate buffered formalin), possibly These are part of the so-called expected mortality in a
a microscope to look at Eimeria from gut scrapings, flock and this daily mortality is recorded on a chart which
various instruments to measure air and water quality, you must examine to determine the magnitude, onset and
and the appropriate gears (clean clothes or disposable duration of the problem.
coveralls, disposable plastic boots, head covering such as
a disposable bouffant, disposable gloves, hand sanitizer)
to comply with biosecurity measures.
2 Avian Disease Manual
The following mortality rates are provided as general guidelines and only apply to meat type birds kept in a closed barn
and laying hens kept in cages.
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Table 1. Expected mortality rates according to the bird type

Total end-flock
Type of bird Brooding period Growth
mortality
Broiler chicken ≤ 1% 0.5 bird/1000 birds/day ≤ 2.5%
(from 0 to 2 (between 2 and 4 weeks of age)
weeks of age) < 1 bird/1000 birds/day
(from 4 weeks and up)
Broiler turkey ≤ 2% 0.5 to 1/1000/day 4 to 6%
(from 0 to 2 (between 2 and 10 weeks of age) (broiler turkey)
weeks of age) 1 to 2/1000/day 6 to 12%
(from 10 weeks and up) (tom turkey)
Broiler breeder 1 to 2% ≤0.25/1000/day during growth 10%
(from 0 to 2 0.1% to 0.25%/ month during lay
weeks of age) (for a total of approx 6%
during that period)
Laying hen 1 to 2% ≤0.25/1000/day during growth 2 to 5%
(from 0 to 2 < 0.5% / month during lay
weeks of age)
Meat duck <2% 0.5 to 1/1000/day 3 to 7% when
(between 2 and 10 weeks of age) slaughtered at 7
1 to 2/1000/day weeks of age
(from 4 weeks and up)
Quail ≤0.25/1000/day
Guinea fowl ≤0.25/1000/day
Normal birds time of your visit once the stress caused by your presence
During the flock visit it is very important to closely observed has decreased.
the birds and look for unhealthy or sick birds. General
physical and behavioural observations provide a good Evaluating the body condition
indication. Healthy birds will be alert, active with bright Numerous growth charts are available and vary according
round and open eyes. Mature turkeys and laying chickens to the genetic, management system and feeding company.
should have a bright red comb. Birds should be clean with Such charts should be consulted to verify if the bird’s body
smooth feathers and bright neat scaly legs. Feces should weight and growth rate are within normal goals. One can
be well-formed, brown or grey with a white ‘cap’ (the also tell the body condition of a bird by palpating the breast
urates). During the visit you might also see on the litter, muscle. With the bird held by the legs in one hand in an
pale brown frothy feces which are from the ceca and can upside down position, use the palm of the other hand to
regularly be observed in the barn. palpate the protuberance of the keel, the development of
the breast muscles alongside that keel, and the convexity
Depending on the housing system, birds should be able to or concavity of the breast muscle contour. A nice growing
stand, walk, even run, scratch and sit only for short periods. bird will show a convex (rounded) contour of the breast
Turkeys and ducks do not scratch the litter and birds in with plump breast muscle and no protuberance of the keel,
cage cannot unless provided with a sand box. Chickens while an emaciated bird will show a marked concavity of
will quickly walk away from the unusual visitors while the breast contour caused by a prominent keel with barely
turkeys will follow them. Young broiler chickens will often no pectoral muscles being felt.
be found fighting i.e jumping at each other with spread
wings. Turkeys can show a belligerent behaviour to their
mates but will be hissing, walking slowly in the crowd with Clinical signs
fluffed up feathers, a blue colored head with an elongated Clinical signs will vary according to the disease and affected
snood. Breeder birds should be also found mating during a system(s) and will vary in severity. Not all birds in a flock
visit. Many birds but not all will be drinking and eating at the will exhibit clinical signs. Early in the course of the disease
only a few individuals might be affected and care should be Barn environment
taken to find them. As stated earlier, the quality of housing will greatly impact
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on the birds’ health. Poultry barns should provide clean

In general, sick birds are listless, will sit for long periods, feed and water, fresh air, protection against predators,
their head held close to the body, tail and possibly wings shelter from cold, rain, wind, sun and excessive heat; as
dropping. Comb and wattles may be paler and shrunken. well as a source of heat when birds are young. During the
Eyes will be dull and sometimes closed. They might visit, you can verify the most important elements using the
not drink nor eat, hence slowing/stopping growth and acronym F-L-A-W-S. F is for feed, L for light/litter, A for Air,
eventually losing weight. Anorexic chickens will often have W for water, S for Sanitation/safety/space/staff.
green colored feces (due to bile stain) which might stain
the feathers of the pericloacal area. Dehydrated birds will Feed. Feed and water are usually available at libitum in
show darker and thinner looking legs, they will feel lighter meat birds, but quantities are controlled in breeders and
and the skin will not move freely over the keel. If cold or layers. Feeders and drinkers must be located at the right
pyrexic, feathers will be fluffed, and birds will huddle in height to optimize access. Variations in feed consumption
corners or with others to keep warm. Uncomfortable chicks can be indicative of a disease, but also associated with hot
will initially be chirping loudly before becoming depressed and cold weather, the feed itself (energy, fiber, particle size)
if source of discomfort is not corrected. or with the birds’ needs (e.g. point of lay).
If a respiratory disease is suspected, early on the course Light. The lighting schedule and light intensity are very
of the disease, chickens will shake their head and scratch important parameters in laying birds, since light stimulates
it with their feet. As the disease progresses watery eyes egg production. In many meat type birds, daylength will be
and/or nasal exudate might be observed and will make the shortened early in life to control the growth rate.
birds look dirty with the dust and dirt adhering to the wet
feathers and beak. Swollen infra-orbital sinuses will affect Litter. The litter is a mixture of feces and bedding material.
the shape of the eye and might even force its closure. The latter should be made of absorbent material and in
Respiratory sounds can also be heard from a light ‘snick’ enough quantity for comfort. If too dry, respiratory problems
to loud rales. Birds do not have a diaphragm and will not will arise while a too humid litter might trigger intestinal and
cough. Severe respiratory difficulties might even cause skeletal pathologies. A litter is too humid if it keeps its shape
the bird to extend its neck and abdominal wall movements once you have squeezed a handful in your fist.
can be observed. If you want to hear the light snick sick
chickens make during a respiratory disease episode, you Air. One of the most important elements of managing the
can gently whistle and the chickens will stop cackling and environment inside a chicken barn is air quality and, in
will raise their head intrigued by this new sound. This trick particular, airflow. Ventilation in the majority of commercial
does not work in turkeys since they will respond to you with barns is mechanical and of the outmost importance
loud gobbles. since any power shortage will rapidly cause death due
to hyperthermia. Not only good ventilation will bring
If an enteritis is suspected, some birds might have dirty fresh air into the barn, but it will take out noxious gases
feathers around the vent that might be even soiled with (CO2, ammonia…), dust and humidity. Poor air quality
blood or sulphur colored feces depending on the infectious will increase in respiratory problems. Furthermore, if the
agent. These blood or sulphured colored feces will also be ventilation is poor, the litter will be more humid, creating an
found on the litter. ideal milieu for certain bacteria and parasites. You might
then end up with a coccidial challenge or lame birds. Barn
Lame birds will spend more time sitting, and will walk with temperatures are electronically controlled and monitored
difficulties, spreading their wings. Traumatic lesions will be with probes. There is a comfort zone at which growth is
observed on the ventral aspect of the carpo-metacarpal optimal. Since newly hatched birds are poikilotherm, a
joint as well as a sternal bursitis in chronically recumbent heat source must be provided. Since birds do not have
birds. Depending on the cause, joints might or might not be sweat glands and use evaporative cooling via their breath,
swollen and hot. The plantar surface of the feet might be temperature superior to 40oC are very uncomfortable and
dirty, crusted, cracked and/or reddened. might be lethal when more than 46oC.
When investigating a loss in performances, a reduced body Water. Drinking water should be of quality and present
weight, a higher feed conversion, a drop in egg production, in adequate quantity. Birds generally drink approximately
a decreased hatchability, flock results should be carefully twice as much water as the amount of feed consumed on
examined and compared to expected result in order to a weight basis. Any water restriction will impair feed intake.
define the problem perceived by the flock manager and Water consumption will often decrease a day or two before
answer the basic questions: who, what, when, where, the onset of clinical signs. Consumption is also closely
how? associated with environmental temperatures. For example,
during periods of extreme heat stress, water requirements Blood can easily be sampled from the brachial vein in
may easily quadruple. most birds, such as young and mature chickens, while
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the tibiotarsal vein is a good option for turkeys and ducks.

Sanitation. Information regarding cleaning, disinfection, Since the avian skin is very thin, it is easy to visualize the
pest control, downtime, as well as previous history of vein once a few feathers have been plucked and pressure
disease, routine and current medication, and vaccination applied proximally to the puncture site. Dampening the
program should be collected during the visit. Biosecurity skin with 70% alcohol will help to better define the vein.
measures should also be in place in order to minimize the
risk of disease introduction and spread. In most birds, a ½ to 1 inch, 21 to 22 ga needle (depending
on the size of the bird), with a 5 ml syringe, will suffice. Do
Space. Birds also need adequate space for movement not use a vacutainer for avian blood collection as the vein
and exercise, access to feeders and drinkers. Space will simply collapse, but apply a gentle steady negative
requirements vary with the species, type or breed of birds pressure on the syringe plunger to withdraw blood. Avian
that are raised, as well as the type of production system blood will easily coagulate during sampling.
used.
For most serological analysis, a 2 ml blood sample will be
Staff. An attentive and skilled farm manager and employee adequate. Blood should be collected aseptically in a vial
are of the outmost importance in the rearing and keeping and laid horizontally until it clots. Placing vials in warm
of a healthy poultry flock. Any changes to the management water right after collection will hasten the clotting, while
can adversely affect the birds. refrigeration will hinder the coagulation process. Sera can
then be transferred in vials, put on ice and shipped to the
Many books and extension services factsheets will provide lab. Never freeze sera if agglutination tests are planned
you with the appropriate information regarding the housing since this might cause false positive reactions.
criteria that must be respected in order to make the birds
comfortable. For some biochemical or other analysis requiring unclotted
blood samples, please enquire to the diagnostic lab as to
Conducting a necropsy the preferred anticoagulant (e.g. heparin, sodium citrate...).
Once you have closely observed the birds and their Samples should be sent as soon as possible on ice to the
housing conditions and look at the mortality chart and diagnostic laboratory.
other performance data, you have probably listed all the
possible differential diagnosis given the clinical facts. In Upon performing the necropsy, numerous tissues and
order to verify your hypothesis, you have the possibility of organs can be sampled depending on observed lesions. If
opening carcasses on the farm to verify for the presence bacterial cultures or viral samples are needed, they should
of lesions. The necropsy is essential to quickly observe be collected as aseptically as possible using sterile scalpel
the internal lesions, establish a differential diagnosis and blade (e.g. to collect joint/sinus exudates). Shipping whole
decide on the course of action. Ideally, necropsy should or parts of organs to the laboratory is also an option.
be performed on animals representative of the condition.
Indeed, the challenge of a good poultry diagnosis is to Tissues for histopathologic examination can be immersed
identify the most significant flock problem(s) rather than into 10% formalin (or other fixative), immediately after
focusing on individual bird pathologies. For large poultry death. Specimens should be small for a quick fixative
flocks, approximately five dead birds as well as five penetration and preserved in ten times their own volume.
individuals showing clinical signs should be selected for Ensure the container is tight and leak free for shipping
necropsy. Euthanasia of the sick birds should be performed purposes. (Alternative shipping: remove specimens
rapidly and humanely in accordance to ethical standards. from the jar and ship in a Ziploc bag with a paper towel
Necropsy procedures are described in another chapter of dampened in formalin to keep the tissue moist, but that will
the current manual. For further analysis and confirmation not crack or leak or spill in transit due to the sensitivity of
of your tentative/preliminary diagnosis, birds or samples shippers. Label the bags, of course).
should be sent to an animal diagnostic laboratory.
Feed samples should be collected from the feeders if a
problem with an ingredient, drug level, etc... is suspected,
Taking samples when there is feed refusal, or whenever mortality, drop
Some samples can be taken when birds are alive (e.g. in egg production, poor growth performances, are
blood samples, tracheal swabs...) or at post-mortem. Blood unexplained.
samples are usually collected for serology. Paired sera
taken two weeks apart will be desired if seroconversion to Water from the wells and from the end of the water line
some disease is expected. In adult birds, collecting eggs should be analyzed at least once a year to determine
will also serve this purpose since antibody titers can be microbiological and biochemical characteristics. Water pH
measured from the yolk.
and chlorine levels can be estimated with specific color

strips.
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If ventilation is suboptimal during the visit, ammonia,

CO2, relative humidity can easily be measured with
the appropriate instruments. Barn temperature can be
measured and comfort zones can be established with an
infra-red thermometer. Many barns are also equipped with
computer controlled ventilation systems monitoring and
logging minimal, maximal and mean barn temperatures as
well as relative humidity.
The visit report

The visit report should include farm/barn identification,
description of the problem (who, what, when, where, how...),
clinical observations, necropsy findings, conclusions and
recommendations based on available facts. A tentative
diagnosis can be offered pending further laboratory test
results. Confirmation should be given as soon as possible
via a phone call to the flock owner/manager or technician.
VIRAL DISEASES CLINICAL SIGNS

EEEV – neurologic disease and increased mortality have
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New parts and revision by Davor Ojkic, Marina L. Brash, been described in turkeys, pheasants, chukar partridges,
Mark W. Jackwood and H.L. Shivaprasad ducks and chickens. EEEV infection can also cause drop
in egg production in breeder turkeys.
ARBOVIRUS INFECTIONS WEEV – associated with neurologic disease in turkeys

in the past. WEEV was isolated from turkeys with egg
DEFINITION production drops in California in 1999.
Arbovirus is an abbreviation of “arthropod-borne virus”
which describes viruses that replicate in arthropods and HJV – Highlands J virus infection has been associated with
are then transmitted by blood-sucking to their hosts. neurologic disease in chukar partridges and egg production
drops in turkey breeders.
OCCURRENCE
WNV – Outbreaks of naturally occurring West Nile virus
Four arboviruses have been described in poultry and
infections have been reported in geese and domestic
farmed birds in North America: Eastern equine encephalitis
ducks (Fig. 1b). Affected ducks display general weakness
virus (EEEV) Western equine encephalitis virus (WEEV)
and inability to stand and increased flock mortality. Day-
Highlands J virus (HJV) and West Nile virus (WNV). This
old-chickens develop are susceptible and develop a
chapter is limited to arbovirus infections in North America.
neurologic disease following experimental inoculation.
Turkeys appear to be resistant.
HISTORICAL INFORMATION
EEEV – first identified in pheasants and pigeons in 1938.
LESIONS
WEEV – first identified in turkeys in 1957. Eastern Equine Encephalitis
1. Pheasants:
HJV – first recognized in blue jays 1960 in Florida. Gross lesions are not observed. Nervous lesions
histologically include vascular endothelial hypertrophy
WNV – first identified the northeastern US in 1999. (Fig. 1a), vasculitis, multifocal necrosis, perivascular
lymphoid cuffing, gliosis, degeneration of neurons and
meningitis or meningoencephalitis (Fig. 2a and 3a).
ETIOLOGY
Splenic fibrinous necrosis, myocardial necrosis (Fig.
EEEV, WEEV and HJV – genus Alphavirus, family
4a) and hepatic necrosis have also been reported.
Togaviridae. Viral particles are spherical, enveloped, 70
nm in diameter. Genetic material is positive sense single
Partridge: At necropsy, lesions include multifocal
stranded RNA.
myocardial necrosis and mottled enlarged spleens.
Histologically, nervous lesions include perivascular
WNV – genus Flavivirus, family Flaviviridae. Viral particles
lymphoid cuffing, gliosis, satellitosis and non-
are spherical, enveloped, 40-60 nm in diameter. Genetic
suppurative myocarditis.
material is positive sense single stranded RNA.
2. Turkeys:
EPIZOOTIOLOGY In young turkeys, brain lesions include lymphoid
1. The spread is seasonal when infected mosquitoes perivascular cuffing, neuronal degeneration and
transmit the infection among susceptible birds (and endothelial cell hypertrophy. With experimental
horses or people for EEEV, WEEV and WNV) while infections in young turkeys, at necropsy, lesions
feeding on them. Birds are important source of virus included dehydration, lack of feed in crops and
for mosquitoes because they carry a higher titer of thymic and bursal atrophy. Histologically, multifocal
virus than most mammals. myocardial, renal and pancreatic necrosis and thymic,
2. Cannibalism of viremic, sick, or dead birds by other splenic and bursal lymphoid depletion were reported.
susceptible birds may be an important method of In breeding hens, there is decreased egg production
transmission of virus within infected flocks. Also, with white, thin-shelled and shell-less eggs.
certain biting insects (gnats, deerflies, horseflies, etc.)
may transmit the virus mechanically. 3. Chickens:
With experimental infection, non-suppurative
3. Susceptible wild birds and poultry flocks can have myocarditis is the predominant lesion. Histological
transient infections and show no clinical signs. lesions of the brain were variable and included
Antibodies can be demonstrated in their sera. necrosis and mild lymphoid perivascular cuffing.
VIRAL DISEASES 7
Multifocal hepatic necrosis and splenic, thymic and CONTROL

bursal lymphoid depletion also may be observed. 1. Protect birds against insects by raising them where
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mosquitoes do not thrive, or by the use of screens,

Western Equine Encephalitis sprays, or other mosquito control methods.
No significant lesions have been described. 2. Avoid overcrowding and keep the houses or pens at a
comfortable temperature.
Highlands J Virus 3. Keep the houses rather dark and use only red light
1. Chukar Partridge bulbs.
Splenomegaly is a common finding at necropsy
whereas multifocal myocardial necrosis is occasionally TREATMENT
reported. Histologically, commonly reported lesions No treatment is available.
included multifocal myocardial necrosis with
mineralization and fibrinous splenic necrosis with ZOONOTIC POTENTIAL
lymphoid depletion and rare brain lesions which EEEV, WEEV and WNV are zoonotic agents.
include mild lymphoid perivascular cuffing, endothelial
cell hypertrophy and lymphocytic meningitis.
2. Turkeys
In experimental infections of young turkeys the
lesions identified are similar to those seen with EEE
infection and include dehydration, lack of feed in crops
and thymic and bursal atrophy. Microscopic lesions
include bursal, thymic and splenic lymphoid depletion,
with occasional splenic fibrinous necrosis. Multifocal
myocardial necrosis and mineralization and pancreatic
and renal necrosis is also described.
West Nile Virus

Enlarged, flaccid heart with mild pale streaking of
the myocardium is described at necropsy (Fig. 2b).
Histologically, there is multifocal nonsuppurative
myocarditis (Fig. 3b), splenic necrosis with lymphoid
depletion, pancreatic necrosis and occasionally mild
multifocal hepatic necrosis. Brain lesions include
nonsuppurative meningoencephalitis, perivascular
lymphoid cuffing, focal gliosis, neuronal degeneration
and satellitosis. Cerebellar lesions were those of
multifocal malacia of the grey matter with necrosis of
Purkinje cells and edema of the Purkinje cell layer.
DIAGNOSIS
1. Virus isolation is not recommended for routine
diagnosis for EEEV, WEEV and WNV because work
with these live agents requires level 3 biocontainment
facilities.
2. Antigen detection ELISA has been used for detection
of EEEV, WEEV and WNV, but more sensitive and
specific real-time RT-PCR methods are now available.
3. Immunohistochemistry (IHC) for EEEV (Fig. 5a) and
WNV (Fig. 4b and 5b) will reveal positive staining for
viral antigens in various tissues, such as myocardium,
intestines and brain, when used. Infections with EEEV,
WEEV and WNV are reportable in many jurisdictions.
Eastern Equine Encephalitis

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Fig. 1a Fig. 2a
Narrow predominantly lymphoid perivascular cuffs surrounding Meningoencephalitis in a EEEV affected pheasant. One can
vessels lined by hypertrophied endothelial cells in the brain of a observe low to moderate numbers of plasma cells, lymphocytes,
pheasant. heterophils within meninges.
Fig. 3a Fig. 4a
Multifocal gliosis, mild loss of Purkinje cells, neuronal necrosis Myocardial necrosis in a ring-neck pheasant affected with EEEV.
in a pheasant that died of EEEV.
Fig. 5a
EEEV antigen positive neurons and glial cells at
immunohistochemistry.
VIRAL DISEASES 9
West Nile Virus

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Fig. 1b Fig. 2b
General weakness and inability to stand in a WNV affected duck. Enlarged, flaccid heart with mild pale streaking of the myocardium.
Fig. 3b Fig. 4b
Myocarditis: histologic examination reveals degenerative cardiac Abundant staining for West Nile viral antigen present in the
myocytes with fibrosis and an infiltrate of predominantly myocardium of affected ducks (IHC, X100um).
mononuclear inflammatory cells (H&E, X100um).
Fig. 5b
Positive staining for West Nile viral antigen present in the brain of
affected ducks (IHC, X50um).
AVIAN ADENOVIRUS INFECTIONS drop syndrome - 1976 and quail bronchitis, are presented
in detail later in this section. Reports of other diseases
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DEFINITION attributed to adenoviral causation should be scrutinized

Adenovirus infections are common in poultry and some can closely for solid evidence of a definitive etiologic role.
be defined in terms of clinical and pathologic characteristics.
However, many adenovirus infections are either subclinical LESIONS
or associated with nondescript clinical syndromes. Lesions vary depending on the virus/syndrome involved
and are presented later in this section.
OCCURRENCE
Serologic surveys indicated that most poultry flocks have DIAGNOSIS
been exposed to infection with one or more adenoviral Routine diagnosis of infection is typically carried out
serotypes. Adenoviruses play a primary or secondary role by a combination of virus isolation and post-mortem
in a variety of syndromes including inclusion body hepatitis examination/histopathology, sometimes augmented with
and hepatitis/hydropericardium syndrome in chickens; electron microscopy or polymerase chain reaction.
hemorrhagic enteritis of turkeys; egg production declines
in laying chickens (egg drop syndrome—1976); bronchitis
CONTROL
in quail and other respiratory, arthritic, encephalitic, and
Licensed and autogenous vaccines are available in some
enteric syndromes including gizzard erosions, pancreatitis
countries.
and proventriculitis. However, the frequent presence of
these viruses even in healthy birds means that their role in
disease must be critically examined. TREATMENT
Not available.
The first recognized adenovirus infection of birds was quail ZOONOTIC POTENTIAL
bronchitis described in 1951. Human infection with avian adenoviruses has never been
documented. However, one controversial report has
suggested, based on a serological survey, a possible role
ETIOLOGY of an avian adenovirus in human obesity.
1. Adenoviruses are DNA viruses that replicate and
produce inclusion bodies in the nuclei of infected cells.
The viruses are non-enveloped and range in size from I. INCLUSION BODY HEPATITIS
70 to 90 nm.
DEFINITION
2. Adenovirus classification is not intuitive. The family Inclusion body hepatitis (IBH) is a disease of young chickens
Adenoviridae is divided into 5 genera and adenoviruses characterized by sudden onset, increased mortality and
infecting birds are in 3 genera; hepatitis accompanied with intranuclear inclusion bodies.
a. Aviadenovirus (previously known as Group I
Avian adenoviruses), OCCURRENCE
b. Siadenovirus (Group II Avian adenoviruses) FAdV-caused hepatitis has a worldwide distribution and has
and been described as IBH in North America, Europe, Australia
c. Atadenovirus (Group III Avian adenoviruses). and New Zealand and as hepatitis/hydropericardium
syndrome (HHS) in South America and Asia.
3. Fowl adenoviruses (FAdV), goose adenoviruses,
falcon adenovirus 1, duck adenovirus-2, pigeon Hepatitis associated with adenovirus infection has also
adenovirus-1 and turkey adenovirus-1 and -2 are been reported in turkeys, quail, pigeons, falcons and
in the genus Aviadenovirus. Turkey adenovirus-3 psittacines. Many other animal species such as snakes,
(Hemorrhagic enteritis) and raptor adenovirus-1 are dogs, chimpanzees and humans have their “own” hepatitis-
in the genus Siadenovirus. Duck adenovirus-1 (Egg associated adenoviruses.
drop syndrome virus) is in the genus Atadenovirus.
EPIZOOTIOLOGY HISTORICAL INFORMATION

Adenoviruses can be transmitted both vertically and 1. In 1963 hepatitis with inclusion bodies was described
horizontally. in chickens but the causative agent was not identified.
That outbreak probably was the disease we now call
IBH. In the early 1970s a similar disease occurred
CLINICAL SIGNS
in many flocks in Canada and the United States.
Diseases with well-established adenoviral etiologies,
namely inclusion body hepatitis, hemorrhagic enteritis, egg
VIRAL DISEASES 11
Adenovirus was isolated from an Indiana outbreak depressed and listless. In some outbreaks the clinical
and, eventually, from flocks in many other locations. signs are masked by other diseases in the flock.
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2. Historically, IBH occurred in immunologically deficient LESIONS

flocks as a consequence of earlier infection with IBD
1. The skin is pale and may be discoloured yellow (Fig.
or CIA virus. However, IBH is now recognized as a
1). Petechial and ecchymotic hemorrhages may be
primary disease and often does not require a preceding
present in the skeletal muscles of the legs.
immunosuppressive event.
2. The liver is swollen, enlarged, yellow to tan, and there
ETIOLOGY may be mottling with focal soft areas with petechial
1. Most commonly IBH cases involve FAdV8 and and ecchymotic hemorrhages under the capsule and
FAdV11, but sporadic cases associated with FAdV2 in the parenchyma (Fig. 2).
have been documented. 3. The kidneys frequently are swollen and pale or mottled
2. HHS has been associated with FAdV4. (Fig. 3).
3. Outbreaks of IBH are sometimes associated with 4. The bursa of Fabricius can be reduced in size.
immunosuppression or exacerbated if affected flocks 5. Microscopically, there is multifocal to locally extensive
are immunosuppressed. degeneration and necrosis of hepatocytes (Fig. 4) often
with the characteristic large basophilic intranuclear
EPIZOOTIOLOGY
adenoviral inclusions in the hepatocytes (Fig. 5) within
1. IBH can be transmitted both vertically and horizontally.
the foci of necrosis and elsewhere. The renal lesions
2. Egg-transmitted adenoviruses may remain inactive include membranous and membranoproliferative
in infected chickens or poults until maternal antibody glomerulitis and less frequently cortical tubular
wanes. Outbreaks in young birds (1-2 weeks) are degeneration and necrosis with intraluminal
typically associated with vertical transmission while inflammatory cells. In the bursa, there may be reduced
outbreaks in older birds are most often due to a follicular size with mild to moderate follicular lymphoid
horizontal transmission. When broilers from multiple depletion.
sources are mixed it is sometimes impossible to
determine the source of infection. DIAGNOSIS
3. In exposed birds the virus enters via the alimentary 1. In young, growing flocks a sudden increase in mortality
tract (and, in some cases, by the conjunctiva and is suggestive of IBH. Typical gross lesions and a history
nasal passages) and primary replication occurs in of prior outbreaks from the same parental flock(s) or
the nasopharynx and intestine. There is frequently on the premises are helpful.
a viremic stage in the infection with widespread 2. Histopathology – Demonstration of typical microscopic
dissemination of virus to secondary sites of replication. lesions in the liver, including the characteristic
As antibody is produced, viral activity wanes but the intranuclear inclusions, is required for a diagnosis of
virus may persist in a latent state in some organs. IBH.
4. There may be periods of virus reactivation throughout 3. Virus isolation – Isolation of FAdV from the liver of
life especially during episodes of immunosuppression affected chickens
or stress. 4. PCR – detection of FAdV DNA in the liver of affected
5. Exposure to one serotype does not confer immunity chickens
to other serotypes within the group or other groups. 5. Serology – Seroconversion to IBH-associated
Thus, birds can (and do) suffer repeated infections serotypes (FAdV2, FAdV8, FAdV11) can be detected
with antigenically unrelated adenoviruses. by a micro-neutralization assay. Group antigens can
6. Adenoviruses are relatively resistant to physical be detected by agar gel immunodiffusion or ELISA, but
and chemical factors and can remain infective in a these tests are of limited value because adenovirus
contaminated environment. infection is widespread and they do not differentiate
among non-pathogenic and pathogenic serotypes/
CLINICAL SIGNS strains.
1. A sudden marked increase in mortality is often the first
6. Genotyping - Analysis of the nucleotide sequences
indication of the disease. Mortality increases for 3-5
days, levels off for 3-5 days, and then decreases to encoding adenovirus hexon protein, the most
abundant viral surface protein that contains major
normal levels over another 3-5 days. Total mortality
antigenic determinants, has been used for genotyping
may be as high as 30% but is typically considerably
of fowl adenoviruses.
lower.
2. There are few specific signs. There may be pallor of the
comb, wattles, and facial skin. The affected birds are
CONTROL CLINICAL SIGNS

Live-licensed vaccine against FAdV8 has been used in 1. Sudden deaths are often the first sign of HE in a flock.
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Australia. Killed autogenous vaccines have been used with A concurrent drop in feed and water consumption may
various degrees of success. In North America autogenous be noted. Droppings containing fresh blood or melena
vaccines are typically bivalent and contain FAdV8 and can be seen, especially around waterers.
FAdV11. 2. A few birds exhibit signs of depression and have
bloody feces. Blood may be seen oozing from the
TREATMENT vent of dead or moribund birds or may be adhered to
Not available. feathers around the vent. Blood may be expelled from
the vent if the abdomen is squeezed. Most birds with
bloody feces die.
ZOONOTIC POTENTIAL
Not recorded. 3. The disease usually runs its course in a flock in 10-
14 days. Most mortality occurs over a 10-day period.
Mortality averages 5-10% but may exceed 60%.
II. HEMORRHAGIC
4. Outbreaks of colisepticemia often follow clinical and
ENTERITIS OF TURKEYS subclinical infections with hemorrhagic enteritis virus
DEFINITION 12 to14 days later. Colisepticemia may be the only
Hemorrhagic enteritis (HE) is a viral disease of young indication of prior HE subclinical infection.
turkeys characterized by sudden onset, depression,
LESIONS
bloody droppings, and variable but often high mortality.
1. Dead poults often appear pale due to intestinal blood
A subclinical form characterized by an enlarged, mottled
loss but are well fleshed with feed in their crops. The
spleen occurs and is more common than the acute form.
skin and feathers around the vent can be stained with
blood or blood stained feces.
OCCURRENCE 2. The intestinal tract, especially the duodenal loop, is
HE has a worldwide distribution and typically occurs in
distended, dark purple, and filled with hemorrhagic
6-12-week-old turkeys, but has been seen in poults as
content (Fig. 1). The intestinal mucosa, especially of
young as 2 weeks. It is rare in turkeys less than 4 weeks
the duodenum is congested, and may be covered with
of age, presumably because of maternal antibody.
a yellow layer of fibrinonecrotic exudates.
3. Early in the course of the disease, the spleen is
HISTORICAL INFORMATION typically very enlarged and mottled (Fig. 2) and as
HE in turkeys was first reported in 1937 but the cause the disease progresses, the spleen becomes smaller
was unknown. Only a few reports of the disease were and pale. Experimentally infected birds have splenic
published during the next 30 years. In 1972 the disease enlargement only during the first 4 days of illness.
was demonstrated to be caused by a viral infection. Since Lungs may be congested.
1970 there have been numerous reports on research and
field aspects of the disease and HE is recognized as a 4. Microscopically, early in the course of the disease,
common and important disease of turkeys. reticuloendothelial cells of the spleen contain
numerous large intranuclear adenoviral inclusions
and the condensed nuclear chromatin around the
ETIOLOGY inclusions often resembles a signet ring (Fig. 3). In
HE is caused by a turkey adenovirus, hemorrhagic enteritis later stages, the white pulp undergoes widespread
virus. necrosis and involution. Lymphoid depletion also
occurs in the thymus and the bursa of Fabricius.
EPIZOOTIOLOGY Intestinal lesions are most prominent in the duodenum
1. The virus is very resistant to environmental factors and with marked mucosal congestion, degeneration and
is shed in feces, hence the transmission route is fecal- exfoliation of the epithelium lining the villus tips and
oral. Infection frequently reoccurs on the same farm in hemorrhage from the tips of the villi into the lumen with
successive flocks. increased number of mixed mononuclear cells, mast
cells and heterophils in the lamina propria. Rarely,
2. There is no evidence of egg transmission.
intranuclear adenoviral inclusions are seen in the
3. Infection of turkeys with HE virus results in a transient epithelial cells lining the villi. In addition, intranuclear
immunosuppression, often involving secondary adenoviral inclusions can be seen in the liver, bone
colibacillosis. marrow, circulating white blood cells, lung, pancreas,
brain and kidney.
VIRAL DISEASES 13
DIAGNOSIS HISTORICAL INFORMATION

1. Typical history and gross lesions strongly suggest the This syndrome was first described as a unique problem
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diagnosis. Demonstration of intranuclear inclusions in laying hens in Holland in 1976, hence the initial name
in reticuloendothelial cells in the spleen or intestine egg drop syndrome-1976. It appears that the EDS virus
confirms the diagnosis unless the turkeys have was first introduced to chickens through a contaminated
received HE vaccine. vaccine.
2. The disease can be reproduced in 6-week-old or older,
susceptible poults by giving minced splenic tissue or ETIOLOGY
its supernate intravenously, orally, or intracloacally. EDS is caused by duck adenovirus-1 (DAdV-1) or egg drop
Typical intestinal content also will reproduce the syndrome virus.
disease when given orally or cloacally.
3. If known-positive antiserum and known-infectious EPIZOOTIOLOGY
splenic tissue are available, it is possible to use the The virus is spread both vertically and horizontally. Wild
agar-gel diffusion test to demonstrate antigen in the birds represent a potential source of infection, but this
spleen of an infected turkey or to demonstrate antibody mode of transmission appears to be less common. The
in the convalescent sera of recovered birds. primary site of virus replication is the pouch shell gland. In
4. HE must be differentiated from acute bacterial infected embryos or young birds the virus is latent until they
septicemia including colisepticemia, salmonellosis, fowl start laying eggs.
cholera and erysipelas. Gastrointestinal hemorrhage/
mucosal congestion may be associated with acute CLINICAL SIGNS
septicemic/viremic/bacteremic conditions. Intestinal Drop in egg production, loss of color in pigmented eggs and
coccidiosis should also be considered. HEV infection production of eggs with tin or no shells are early symptoms.
in growing turkeys results in immunosuppression Once established in a flock the egg shell-related problems
predisposing birds to secondary infections such as are less common, but birds typically fail to reach expected
Escherichia coli septicemia. production peaks. Infections of waterfowl are mostly
asymptomatic. However, outbreaks of an acute respiratory
CONTROL disease in goslings in Hungary and ducklings in Canada
1. Avirulent strains of HEV and related marble spleen have been described.
disease (of pheasants) virus are used as vaccines.
2. Vaccines are prepared as crude splenic homogenates
LESIONS
or are cell culture derived.
Gross lesions other than inactive ovaries and atrophied
TREATMENT oviducts are not seen in natural infections. Edema and
No treatment is available. Good care and management will swelling of the uterine mucosal folds and exudate in the
reduce mortality and economic loss. Radical changes in shell gland lumen have been described in experimentally
feed or management should be avoided. infected hens. With experimental infections, histologically,
oviduct changes include proprial edema, infiltration
of mixed mononuclear leukocytes (lymphofollicular
ZOONOTIC POTENTIAL aggregates in some cases) and heterophils changing to
Not recorded. predominantly mixed mononuclear cells in the later stages
of infection, atrophy of tubular glands, and degeneration/
III. EGG DROP SYNDROME desquamation and attenuation of uterine epithelium.
Intranuclear adenoviral inclusions may be seen in epithelial
DEFINITION cells of the uterus, isthmus, and vagina.
Egg drop syndrome (EDS) is an infectious disease of
laying hens caused by a hemagglutinating adenovirus Most descriptions of the pathology from naturally occurring
characterized by loss of color in pigmented eggs and disease outbreaks do not include the acute oviduct
failure to achieve production targets, or by production of inflammation or necrosis or the identification of viral
thin-shelled or shell-less eggs in otherwise healthy-looking inclusions as the lesions are transient.
birds.
DIAGNOSIS
OCCURRENCE Reduction in production with the occurrence of
EDS in chickens has not been described in North America, depigmented, soft-shelled eggs in the absence of other
but is present in Europe, Africa and Australasia. However, clinical signs should trigger consideration of EDS. Isolation
the causative agent of EDS appears to be widespread in its and identification of the virus is best achieved using EDS76-
natural host, waterfowl.
free embryonated duck or goose eggs or cell culture of CLINICAL SIGNS

duck or goose origin. 1. QB occurs with sudden onset of severe respiratory
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signs including tracheal rales, coughing, and sneezing.

Harvested allantoic fluid or cell culture supernatant can be Lacrimation, conjunctivitis, and neurologic disorders
checked for hemagglutinating activity, which is inhibited by may also be seen, but are less consistent signs.
specific EDS antiserum or viral DNA is detected by PCR.
2. The disease is most severe in young quail (under 4
weeks of age). Infections are milder or subclinical in
The hemagglutination inhibition test in suspect flocks is
birds over 8 weeks of age.
most helpful immediately after egg changes are observed
because many infected flocks do not have demonstrable 3. The incubation period of QB is 2-7 days, which
antibody during the growing period. explains the explosive spread of the disease in
susceptible flocks. Morbidity and mortality can be
substantial, ranging from 10 to 100% in young birds
CONTROL and the course of the disease in affected flocks varies
An inactivated vaccine has been successfully used
from 1 to 3 weeks.
against clinical EDS. Eradication programs can be used to
eradicate the disease. LESIONS
1. Excess mucus with thickening and roughening of the
TREATMENT mucosa are the major lesions in the trachea (Fig. 1)
No treatment is available. and bronchi. Air sacs may be mildly thickened and
cloudy. Ocular and nasal discharges are occasionally
noted. Lungs are congested. Multiple small pale foci
ZOONOTIC POTENTIAL are randomly distributed over the liver. The spleen
Not recorded. may be mottled and slightly enlarged.
2. Microscopically, tracheal and bronchial lesions
IV. QUAIL BRONCHITIS include epithelial deciliation, necrosis, exfoliation
and proliferation with epithelial cells containing large
DEFINITION basophilic intranuclear adenoviral inclusions. A mild
Quail bronchitis (QB) is an acute, contagious and
to moderate cellular infiltrate is in the lamina propria
sometimes highly lethal respiratory disease of bobwhite
composed of primarily lymphocytic/plasmacytic.
quail (Colinus virginianus) characterized by catarrhal
Luminal exudate is composed of exfoliating epithelial
tracheitis and airsacculitis.
cells frequently containing intranuclear adenoviral
inclusions, erythrocytes, a mixture of inflammatory cells
OCCURRENCE and necrotic cellular debris. Pulmonary lesions include
QB has been documented sporadically in captive quail focally extensive pneumonia. Liver has multiple foci of
throughout the United States. There is evidence suggesting necrosis with variable numbers of mononuclear cells
occurrence in wild quail as well. and fewer heterophils. Large basophilic intranuclear
adenoviral inclusions are often in the hepatocytes
HISTORICAL INFORMATION adjacent to the areas of necrosis or inflammation.
A respiratory disease (bronchitis) of quail caused by a virus 3. There is multifocal to locally extensive splenic lymphoid
was first described in 1951. necrosis with fibrin exudation and very mild leukocyte
infiltration and rare adenoviral inclusions. The severity
of the bursal lesions is variable and range from single
ETIOLOGY
cell lymphocyte necrosis with lymphoid depletion
The causative agent of quail bronchitis is fowl adenovirus-1.
and follicular atrophy to severe follicular lympholysis.
Intranuclear adenoviral inclusions are frequently in the
EPIZOOTIOLOGY mucosal epithelium.
1. The sources of the causative adenovirus are infected
breeders (via transovarial passage), carrier birds, DIAGNOSIS
contaminated feces, or fomites. 1. Acute respiratory disease with high mortality in young
quail chicks is highly suggestive of QB and is confirmed
2. Once established in a flock the QB virus spreads
histologically with a severe catarrhal tracheitis and
rapidly primarily by the fecal-oral route. Morbidity
bronchitis and respiratory epithelium containing the
usually reaches 100% in susceptible birds.
characteristic intranuclear adenoviral inclusions.
3. The disease frequently occurs in succeeding broods of
2. Isolation of the causative adenovirus confirms the
quail reared on contaminated premises owing in great
diagnosis of QB. Isolation is accomplished in 9-11-day-
part to the environmental resistance and persistence
of the causative adenovirus.
VIRAL DISEASES 15
old specific-pathogen-free embryonating eggs or cell TREATMENT

cultures. No treatment is available but increasing brooding house
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3. Serologic tests are of limited value unless flock temperature, elimination of drafts, and expanding floor
sampling is done on both an acute and convalescent space may be helpful as supportive measures in the face
basis to demonstrate definitive seroconversion of an outbreak.
CONTROL ZOONOTIC POTENTIAL

No licensed vaccines are available. Not recorded.
INCLUSION BODY HEPATITIS

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Fig. 1 Fig. 2
Jaundiced chicken dead with IBH. IBH in a chicken: the liver is swollen,
enlarged, tan, with mottling with
petechial hemorrhages under the
capsule and in the parenchyma.
Fig. 3 Fig. 4
The kidneys of this IBH chicken are markedly swollen, pale and At microscopy, presence of multifocal to locally extensive
mottled. degeneration and necrosis of hepatocytes.
Fig. 5
Microscopically, characteristic large basophilic intranuclear
adenoviral inclusions in the hepatocytes are observed.
VIRAL DISEASES 17
HEMORRHAGIC ENTERITIS OF TURKEYS

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Fig. 1
The intestinal tract of a turkey affected with HEV, especially Fig. 2
the duodenal loop, is distended, dark purple, and filled with Turkey affected with HEV: the spleen is typically very enlarged
hemorrhagic content. and mottled and the intestinal content is filled with hemorrhagic
content.
Fig. 3
Reticuloendothelial cells of the spleen containing large
intranuclear adenoviral inclusions.
QUAIL BRONCHITIS
Fig. 1
Excess mucus and necrotic exudate in the trachea of a quail affected
with QB.
AVIAN ENCEPHALOMYELITIS EPIDEMIOLOGY

(AE; Epidemic Tremor) 1. During the acute phase of infection in laying chickens,
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a period up to 1 month, some layers shed virus in some

of the eggs they lay. Although vertically transmitted AE
DEFINITION
may affect hatchability, many of the chicks will hatch
Avian encephalomyelitis (AE) is a viral infection of chickens,
and can show clinical signs of the disease as early as
turkeys, pheasants, and coturnix quail characterized in
the 1st day of age. The infected chicks will shed virus
young birds by ataxia progressing to paralysis and, usually,
in their feces resulting in horizontal spread to other
by tremors of the head and neck. Infected adults usually
chicks. Younger chicks tend to shed virus for a longer
show no signs.
period of time than older chicks.
2. The method of transmission of AE to susceptible adult
OCCURRENCE flocks is unknown but is probably via fomites. Multiage
Clinical outbreaks are usually observed in chickens and
farms are more likely to be infected than those with
most outbreaks are in 1-3-week-old chicks. Turkey poults,
single age groups.
pheasants, and coturnix quail are also infected naturally.
Experimental infection has been induced in ducklings, CLINICAL SIGNS
guinea fowl, and pigeon hatchlings. Infection can occur 1. In chicks, signs may be present at the time of hatch
in older birds but usually is clinically inapparent. AE is but usually occur between the 1st and 2nd week of
worldwide in distribution. age. Age resistance is marked if exposure is after 2-3
weeks of age.
HISTORICAL INFORMATION 2. In chicks, signs include dull expression, ataxia
1. In 1930 AE was first seen in 2-week-old Rhode progressing to paralysis and prostration (Fig. 1)
Island Red commercial chicks. Within a few years the and tremors of the head and neck. Tremor may be
disease was present in most of the other New England inapparent but often can be accentuated if the bird is
states and was referred to as “New England disease”. frightened or held inverted in the hand. Prostrate birds
Between 1955 and 1970 the disease was described are soon trampled and killed by the other birds.
successively in coturnix quail, pheasants, and turkeys.
3. The morbidity in chicks is quite variable but may
2. A nationwide testing program for AE antibody revealed go as high as 60%. If most chicks in the flock
that many chicken flocks in the United States have come from immune dams, morbidity is usually low.
antibody to AE virus. Mortality averages 25%. Few birds with signs recover
3. Hatcheries once replaced baby chicks that had completely. Those that survive often fail to grow or
AE or developed AE shortly after delivery. This produce eggs normally. Many survivors later develop a
practice caused considerable loss to the hatcheries. bluish opacity to the lens of the eye and have impaired
Vaccination of the breeders was first successfully vision (Fig. 2 and 3).
implemented in the 1950s and AE largely became 4. Layers seldom show signs when infection is going
controlled in commercial flocks by the 1960s. through the flock. However, good production records
often reveal a significant decline in egg production
ETIOLOGY generally lasting no more than 2 weeks.
1. AE is caused by a hepatovirus belonging to the
Picornaviridae family. There appear to be no serologic LESIONS
differences among isolates although they vary in their 1. Generally, there are no gross lesions. In chicks, whitish
tissue tropisms. All field strains are enterotropic but areas in musculature of the gizzard can sometimes be
some strains are more neurotropic than others and observed (Fig. 4). No gross lesions are seen in adult
pathogenicity varies. birds.
2. The virus can be grown in the yolk sac of chick 2. Microscopic lesions, if typical, have special diagnostic
embryos free of maternal antibodies and in a variety value. There is a disseminated, nonpurulent
of tissue culture systems. Embryo-adapted strains are encephalomyelitis with widespread and marked
not infectious by the oral route, are highly neurotropic, perivascular cuffing (Fig. 5). Two microscopic changes
and cause muscular dystrophy in inoculated embryos. are especially helpful: swelling and chromatolysis
3. Virus is present in the feces of infected birds and will of neurons (Fig. 6) in nuclei (nucleus rotundus and
survive there for at least 4 weeks. nucleus ovoidalis) in the midbrain and cerebellum,
and dense lymphoid aggregates in the muscle of the
4. The virus survives treatment with ether and chloroform
proventriculus (Fig. 7) and/or gizzard as well as the
and is fairly resistant to various environmental
myocardium and pancreas.
conditions.
VIRAL DISEASES 19
DIAGNOSIS CONTROL
1. In chicks, the history, age of the birds, and typical 1. Chicks from immune hens are usually protected by
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signs of central nervous system (CNS) lesions permit parental immunity during the critical first few weeks
a strong presumptive diagnosis. The diagnosis can after hatching. Breeding flocks can be vaccinated
often be strengthened by histopathologic examination. to provide maximum protection to their chicks.
Alternatively, the direct fluorescent antibody technique Although vaccination is usually conducted prior to
can be used to demonstrate AE viral antigen in infected the onset of lay, some killed vaccines can be used
chicks. during production. The embryo susceptibility test,
2. Isolation and identification of the virus from the brains which involves inoculation of AE into the yolk sac of
of infected chicks is possible but is time consuming and embryonated eggs from the breeders can be used to
expensive. Also, there must be a source of susceptible determine the immune status of the flock.
chick embryos and this usually necessitates a layer 2. Both killed and live vaccines are used for vaccination
flock that has never been exposed to AE. and are effective. Live virus vaccines must not be
3. Antibodies to AE can be detected as early as 4 days embryo adapted as they lose their ability to infect orally
postinfection and persist for at least 28 months. and can cause clinical disease when administered
Serologic assays include the ELISA, immunodiffusion parenterally. Live vaccine is given by the wing web
test, virus neutralization test, passive hemagglutinin stick method in combination with pox, via the drinking
test and the indirect FA test. Rising titers in sequential water, or by spray. Birds that will serve as breeders
samples are highly suggestive of active infection. should not be vaccinated until they are at least 8
weeks old. One vaccination is usually adequate for the
4. AE must be differentiated from other diseases that life of the bird. Live vaccines should be applied at least
cause signs of CNS disease in young birds. These 4 weeks prior to production; vaccines used in chickens
include: can be protective for turkeys.
Newcastle disease Mycotic encephalitis 3. Chicks from flocks that have been naturally infected
Arboviral infection Brain abscesses will probably receive enough parental immunity so that
Vitamin deficiencies Marek’s disease they will not develop the disease.
(E, A and Riboflavin) Toxicities
Equine Encephalomyelitis TREATMENT
Virus (salt, some pesticides, etc.) Treatment is of no value.
AVIAN ENCEPHALOMYELITIS
Fig. 1
Chicks with dull expression and paralysis due to AE.
Fig. 2
Surviving poult who has developed a bluish opacity to the
lens of the eye.
AVIAN ENCEPHALOMYELITIS
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Fig. 3
Marked bluish opacity to the len of the eye of an AE affected chicken
Fig. 4
(left) vs a normal eye (right).
Whitish areas in musculature of the gizzard of a chick.
Fig. 6
Fig. 5
Diffuse gliosis and central chromatolysis of neurons of one of the
Non-purulent encephalomyelitis characterized by
nuclei of the brain stem.
perivascular cuffing. Also note the gliosis and the
chromatolysis.
Fig. 7
Lymphoid aggregates in the muscle of the proventriculus.
VIRAL DISEASES 21
AVIAN INFLUENZA inhibition tests. Cross-protection does not occur between

subtypes.
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DEFINITION
Avian influenza (AI) is a viral disease characterized by EPIDEMIOLOGY
respiratory signs, depression and reduced feed and 1. Wild waterfowl and shorebirds are the major
water intake. In egg laying birds there is a decline in egg natural reservoir of AI viruses. Wild waterfowl are
production. asymptomatic, may excrete virus in the feces for long
periods, may be infected with more than one subtype,
There are many strains of AI viruses and generally they can and often do not develop a detectable antibody
be classified into two categories: low pathogenic (LPAI) that response. AI virus has been recovered directly from
typically causes little or no clinical signs in birds and highly lake and pond water used by infected wild ducks.
pathogenic (HPAI) that can cause severe clinical signs and/ Contact of these birds with range-reared commercial
or high mortality in birds. Those virulent AI viruses are also flocks is an important factor in some outbreaks.
classified as highly pathogenic notifiable avian influenza This source of infection often results in a seasonal
(HPNAI) viruses. Moreover, subtype H5 or H7 viruses with incidence in some states.
a hemagglutinin cleavage site similar to those in virulent 2. Two man-made reservoirs are live bird markets and
viruses are also considered HPNAI viruses, regardless of commercial swine facilities.
their virulence in vivo.
3. Live bird markets have existed in large cities, but they
The H5 and H7 isolates which are not highly pathogenic are an emerging phenomenon in some areas. They
and do not have the hemagglutinin cleavage site amino serve as a focal point for gathering and housing many
acid sequence similar to HPNAI viruses are classified species of birds that are then sold in or around large
as low pathogenicity notifiable avian influenza (LPNAI) cities. These facilities are often neither cleaned nor
viruses. depopulated. The continuous supply of susceptible
poultry in such markets enhances opportunity for viral
Non-H5 or non-H7 AIVs which are not highly pathogenic replication and mutation, and this in turn enhances the
are classified as low pathogenicity avian influenza (LPAI) opportunity for viruses to be carried back to susceptible
viruses. poultry flocks.
4. Swine have been known to be infected with swine flu
OCCURRENCE (H1N1) since the 1930s, but recently another subtype
AI viruses are spread worldwide in their hosts, wild (H3N2) has been spreading in swine populations.
waterfowl and shorebirds. AI outbreaks in commercial Transmission of influenza from swine to turkeys has
birds have also occurred throughout the world. In the past been documented.
HPNAI was relatively infrequent, but the ‘Asian’ H5N1 5. AIVs have been isolated from imported exotic birds.
has spread throughout 56 countries in Asia, Europe and These infected birds are a potential threat to cage
Africa between 2004 and 2010. HPNAI outbreaks caused birds, wild birds, and poultry.
by other subtypes (H5N2, H7N3 and H7N3) were less 6. Although waterfowl shed virus in their droppings
common during the same period. for long periods, most viral shedding from infected
gallinaceous poultry stops after seroconversion.
HISTORICAL INFORMATION Influenza virus is released in respiratory secretions
The most virulent form of AI was once called fowl plague and excretions and droppings of infected birds where
and was first documented in Italy more than 100 years ago. it is protected by organic material. The virus is labile
In the United States highly pathogenic AI first occurred in in warm conditions, but can survive for months in a
1924-1925. The current HPNAI/LPNAI/LPAI classification cold environment. Influenza virus has been isolated
has been updated in 2009. from turkey eggs and semen, but there is no evidence
of vertical transmission. Improper disposal of infected
eggs could potentially expose other susceptible birds,
ETIOLOGY
but such transmission has not been observed.
Avian influenza is caused by a type A influenza virus
belonging to the Orthomyxoviridae family. Influenza viruses 7. Once AIV is introduced into the poultry industry it is
have segmented RNA genome and two major surface transmitted from farm to farm by direct and indirect
antigens, hemagglutinin (H) and neuraminidase (N) that contact. AI viruses can be transmitted on contaminated
give rise to subtype names for specific viruses (eg. H4N6). shoes, clothing, crates, and other equipment and by
There are 16 hemagglutinins and 9 neuraminidases movement of birds and manure.
making 144 possible virus subtypes. Influenza viruses are
subtyped by hemagglutination inhibition and neuraminidase
CLINICAL SIGNS DIAGNOSIS

1. Most outbreaks are caused by LPAI viruses. The 1. History, signs, and lesions may be suggestive of LPAI,
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LPAI signs vary greatly and depend on many factors, but are similar to other diseases.
including the age and species, the virulence of 2. Confirmation of suspect AI cases requires laboratory
the virus, concurrent infections, and husbandry. In tests such as serology (AGID and/or ELISA) and virus
most outbreaks, signs are predominantly those of a detection (real-time RT-PCR and/or virus isolation).
respiratory disease with coughing, sneezing, rales,
lacrimation, sinusitis (Fig. 1), and depression. In egg 3. Rapid testing by an influenza A cross-reactive real-
layers decreased egg production and quality are seen. time RT-PCR test is typically carried out first. Reactive
samples are then subjected to H5 and H7 subtype-
2. In young growing turkeys the disease may be specific real-time RT-PCR tests.
subclinical or severe, particularly where secondary
infection with live Pasteurella vaccine, E. coli, or 4. Confirmation of HPNAI requires molecular
Bordetella occurs. Outbreaks in egg laying turkeys characterization of the virus and/or inoculating
often reduce production markedly and frequently are susceptible chickens with the virus.
associated with abnormal eggshell pigmentation and 5. Influenza virus usually can be isolated in chick embryos
quality. from tissue or swab samples of trachea, lung, air sac,
3. Morbidity and mortality are highly variable, depending sinus exudate, or cloaca. Viruses from some species
upon the same factors that determine clinical signs such as geese may not grow well in embryonated
noted above. chicken eggs. The virus hemagglutinates chicken red
blood cells.
4. HPAI is a severe form of influenza usually seen in
chickens. Viruses of high pathogenicity may cause 6. Serological tests can be used to demonstrate
fatal infections preceded by few signs. Onset is seroconversion between acute and convalescent sera.
sudden, the course is short, affected birds are quite ill, 7. Influenza must be differentiated from other poultry
and mortality may approach 100%. Signs may relate diseases including Newcastle disease, other
to the respiratory, enteric, or nervous systems. There paramyxovirus infections, mycoplasmosis, chlamydial
may be diarrhea, edema of the head and face (Fig. 1), infections, and fowl cholera. HPNAI should be
or nervous disorders. differentiated from velogenic viscerotropic Newcastle
disease. Because AI viruses causing highly pathogenic
LESIONS AI are considered exotic, they are reportable and
1. With LPAI outbreaks in poultry there is mild to confirmation by virus isolation is essential.
moderate inflammation of the trachea, sinuses (Fig. 2),
air sacs (Fig. 3) and conjunctiva. In laying birds there CONTROL
often is ovarian atresia (Fig. 4) and involution of the 1. Prevention of LPAI is largely through prevention of
oviduct or egg yolk peritonitis (Fig. 5). Fibrinopurulent exposure to influenza viruses by direct or indirect
bronchopneumonia (Fig. 6) can occur with secondary contact with waterfowl and shorebirds, live bird
infection. Various degrees of congestive, hemorrhagic, markets and swine farms.
transudative, and necrotic lesions have been
2. Once LPAI non-H5 or non-H7 virus is introduced into
described.
the poultry industry, control is largely dependent on
2. In HPNAI infection, gross lesions in chickens are the voluntary, industry efforts since there are no official
most extensive and severe. Fibrinous exudates may state eradication programs.
be found on the air sacs, oviduct, pericardial sac, or on
3. Routine serologic monitoring of blood or egg yolk
the peritoneum. Small foci of necrosis may be apparent
antibody is used in areas where AI has been a problem.
in the skin, comb, and wattles or in the liver, kidney,
This effort provides early detection of an outbreak
spleen, or lungs. Indications of vascular damage
and permits other measures such as isolation and
often include congestion, edema, and hemorrhages at
sanitation to be used early.
many sites.
4. Reporting outbreaks to industry personnel who are in
3. Classical lesions of HPNAI in chickens include
direct or indirect contact with poultry is necessary so
cyanosis and edema of the head (Fig. 7 and 8),
that appropriate measures can be taken.
vesicles and ulceration on the combs, edema of the
feet, blotchy red discoloration of the shanks (Fig. 9), 5. Voluntary isolation of infected flocks is the responsibility
petechiae in the abdominal fat and various mucosal of the owner and is necessary to prevent transmission
and serosal surfaces, and necrosis or hemorrhage in to other flocks. Rigorous measures to prevent the
the mucosa of the gizzard and proventriculus (Fig. 10). contamination of and control the movement of people
and equipment are required in order to stop this
4. Lesions of HPNAI in turkeys are not well described,
disease.
but encephalitis and pancreatitis have been reported.
VIRAL DISEASES 23
6. Different states and industries take different approaches

to the next step. Controlled marketing of flocks after
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they have recovered from infection is common in

the turkey industry. In some broiler producing states,
voluntary destruction of infected flocks is encouraged.
7. Rescheduling flocks is necessary to make sure there
is no active AI virus on the farm before another flock
is placed.
8. History has proven that prevention of HPNAI is based
on successful control of H5 or H7 LPAI.
9. H5 or H7 LPNAI results in a response that varies
according to the response plan developed by each
state. Generally all outbreaks of H5 or H7 LPAI will
result in a rapid aggressive response, although the
means that are used to bring it under control will vary
according to species involved, density and the state
plan.
10. H5 or H7 HPNAI results in a uniform response plan
under the direction of government agencies and there
also will be input from public health, occupational
health and pollution control agencies.
11. All outbreaks of influenza should be reported
immediately to the state veterinarian or other
appropriate health authorities.
12. Vaccines - Immunity is hemagglutinin subtype specific.
Because birds are susceptible to all 16 hemagglutinins,
preventive vaccination is not practical. Once an
outbreak occurs and the subtype is identified, however,
vaccination is a tool that may be used to help bring
the infection under control. Because influenza viruses
are unstable, little research has been done on live
influenza virus vaccines for poultry. Killed, injectable
and recombinant vaccines are available against H3,
H5 and H7 subtypes.
TREATMENT
There is no effective treatment. However, good husbandry
may reduce losses from secondary infections.
ZOONOTIC POTENTIAL
Although infection of humans with AIV is rare, human
cases caused by avian influenza subtypes H5, H7 and H9
have been documented.
A pathogenic H5N1 virus that spread in poultry and wild

birds over most of Asia and parts of Europe and Africa has
caused 247 confirmed human deaths from 2003 - 2010.
Some H1N1 and H3N2 influenza virus strains that circulate

in swine and humans can also infect birds and vice versa.
AVIAN INFLUENZA
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Fig. 1
Turkey affected with LPAI showing sinusitis. Fig. 2
Cross-section of the head of a LPAI affected turkey
showing the fibrinopurulent exudate filled sinuses.
Fig. 3
Airsacculitis in a LPAI infected Fig. 4
turkey. Atretic ovarian follicles.
Fig. 5 Fig. 6
Egg yolk peritonitis in a LPAI positive laying hen. Bronchopneumonia in a LPAI positive turkey.
VIRAL DISEASES 25
AVIAN INFLUENZA
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Fig. 7 Fig. 8
Edema of the head in a HPAI infected layer. Subcutaneous edema of the head.
Fig. 10
Fig. 9 Proventricular hemorrhages.
Blotchy red discoloration of the shanks in a HPAI positive layer.
AVIAN METAPNEUMOVIRUS EPIDEMIOLOGY

1. Turkeys and chickens appear to be natural reservoirs
INFECTION
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of aMPV, but limited studies have found the evidence of

aMPV infection in several species of wild and domestic
DEFINITION birds. Whether the virus persists in recovered turkey
Avian metapneumovirus (aMPV) infection is a highly flocks is also unknown. The virus has been detected
contagious infectious respiratory disease of turkeys and in oviduct tissue, and neonatal infection has been
chickens characterized by coughing, swollen sinuses, nasal observed, but no proof of egg borne transmission has
discharge and lowered feed and water consumption. The been shown.
disease caused by aMPV infection was originally referred
to as avian pneumovirus infection or turkey rhinotracheitis 2. The virus is transmitted by direct contact between
in turkeys and as swollen head syndrome in chickens. infected and susceptible birds and is believed to be
transmitted by indirect contact including exposure
to aerosol droplets or to virus-contaminated boots,
OCCURRENCE clothing or equipment. Airborne transmission has been
1. aMPV infections have been described throughout demonstrated in the laboratory, but such transmission
most of the world. Only Canada and Australia appear from farm to farm is unproven.
to be free of aMPV infection. No chicken aMPV cases
have been reported in the U.S.A. CLINICAL SIGNS
2. There are four subtypes of aMPV, A, B, C and D. In the 1. The clinical signs are variable and depend on the
U.S.A. all isolates have been type C. age, gender, concurrent infections, and management
factors. In young turkeys, clinical signs include nasal
3. The virus has been isolated from turkeys in many discharge (Fig. 1), foamy conjunctivitis, swollen
parts of the world. Experimental studies have shown infraorbital sinuses (Fig. 2) with submandibular edema
chickens, ducks, guinea fowl and pheasants to be (Fig. 3). As clinical signs subside birds may begin to
susceptible. Serological studies have detected die. Mortality rates in market turkeys range from nil to
antibody in ostriches and herring gulls. Using RT- 80%, but death is usually due to secondary infections.
PCR, APV RNA has been detected in geese, coots, Condemnation rates are usually elevated if turkeys are
sparrows, swallows, starlings and an owl. A seasonal infected within two weeks of processing.
incidence with peaks in the spring and fall has been
observed. 2. Turkey breeder hens may have a decline in egg
production of 10 to 30% and lay increased numbers
HISTORICAL INFORMATION of cull eggs. Mortality in breeders is usually 0 to 2%
1. Turkey rhinotracheitis caused by aMPV was first but may be higher if live Pasteurella vaccine has been
identified in South Africa in the late 1970s. used in the flock.
2. In the U.S.A. aMPV was first identified in Colorado 3. In chickens aMPV infection may be subclinical and/
turkeys in 1997. Subsequently the disease was or associated with other agents in swollen head
detected serologically, using an ELISA developed syndrome (Fig. 4) and egg production problems.
at the National Veterinary Services Laboratories, in
Minnesota turkeys in the spring of 1997. It is likely that LESIONS
the infection was present in Colorado and Minnesota 1. In mature female turkeys, a marked decrease in egg
prior to 1997. It has remained in Minnesota turkeys production with increased production of eggs with
infecting 40 to 50% of the flocks each year since 1997, poor shell quality and increased numbers of birds
and there has only been limited spread to neighbouring with peritonitis and uterine prolapsed are described.
states. Experimental infections produced a watery mucoid
nasal discharge and increased amounts of tracheal
ETIOLOGY mucus in addition to egg peritonitis and production of
1. aMPV is an enveloped, single stranded RNA virus, poor quality and abnormal eggs. Secondary bacterial
member of the genus Metapneumovirus of the infections may increase the severity of the lesions with
Paramyxoviridae family. aMPVs have a fusion (F) airsacculitis, pericarditis, perihepatitis and pneumonia.
protein and a glycoprotein (G) as surface antigens. 2. Microscopically, with experimental infections,
2. The virus is present in respiratory secretions and focal deciliation, epithelial necrosis, hyperemia
excretions of infected birds where it is protected by and submucosal inflammation with a mixture of
organic material. The virus is susceptible to detergents mononuclear cells of the nasal mucosa and transient
and disinfectants. However, the virus can remain deciliation of the tracheal mucosa have been described.
infective for long periods of time under cool and moist 3. In chickens, the infection has been associated with
environmental conditions, e.g. in poultry litter for three secondary Escherichia coli infection with subsequent
days at 20 to 25°C and for 14 to 30 days at 8°C. development of swollen head syndrome which
VIRAL DISEASES 27
presents yellow gelatinous to heterophilic exudates testing of choanal swabs can provide early detection
in the subcutaneous tissues of the head and swollen so that other control measures can be instituted.
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periorbital and infraorbital sinuses. Transient localized

inflammation of the upper respiratory tract has been TREATMENT
observed. No treatment is available. Reduced density, increased
supplemental heat and good management conditions are
DIAGNOSIS associated with reduced financial loss due to the disease.
1. The history and signs of coughing, nasal discharge Antibiotic treatment has been used to reduce the effects of
and swollen sinuses may be suggestive of aMPV concurrent bacterial infections.
infection but are similar to other respiratory infections.
Confirmation of the diagnosis requires laboratory tests.
2. The virus is difficult to isolate from swabs or tissues
of affected birds so other laboratory tests used are:
immunohistochemistry on formalin fixed turbinate
tissues (Fig. 5), RT-PCR to detect viral RNA in tracheal
swabs, choanal swabs or turbinates, and ELISA to
detect pneumovirus-specific antibodies.
3. Avian pneumoviruses are difficult to isolate, but once
recovered from affected birds aMPVs grow in embryos
and tissue culture systems. Unlike other members
of the paramyxovirus family, pneumoviruses do not
hemagglutinate.
CONTROL
1. The reservoir of metapneumovirus in nature is not
known but wild birds are suspected. Whether or
not infected flocks remain a source of virus for their
whole life is also not known, but they should be
considered a potential source for life. Prevention of
metapneumovirus infection requires preventing the
introduction of the virus by direct or indirect contact
from these possible reservoirs (wild birds and infected
flocks).
2. Limited studies indicate that there might be partial
cross protection between APV types.
3. Since the disease is spread by direct and indirect
contact, strict biosecurity and a good sanitation
program are imperative. A minimum biosecurity
program for controlling aMPV would include:
4. Crews that handle birds (vaccination, moving, live haul,
insemination) must be controlled. Crew members
should wear disposable or freshly laundered clothing
including footwear.
5. Equipment that moves from farm to farm and comes
in contact with poultry or birds (rendering, moving,
live haul trucks and dumpsters, loaders, vaccination
equipment) should be washed with detergent and
disinfectant.
6. Poultry facilities should be wild bird proofed.
7. A live attenuated vaccine is available in the Midwestern
USA. Killed autogenous oil emulsion vaccine has been
used after live vaccines in turkey breeders.
8. A routine monitoring program is suggested for
areas where aMPV infection has been a problem.
Serological screening of blood samples and PCR
AVIAN METAPNEUMOVIRUS INFECTION

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Fig. 1 Fig. 2
Turkey poult with nasal discharge. Sinusitis in a turkey affected with avian metapneumovirus.
Fig. 3
Fig. 4
Submandibular edema in a young turkey. Note the dyspnea.
Swollen head syndrome in a 29 day-old broiler chicken.
Fig. 5
Immunohistochemical findings for nasal turbinates, showing
peroxidase staining of viral antigen in the epithelial surface of a
turkey poult exposed to metapneumovirus.
VIRAL DISEASES 29
AVIAN NEPHRITIS VIRUS DIAGNOSIS

1. A presumptive diagnosis can be made based on
INFECTION IN CHICKENS
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clinical signs, mortality patterns combined with gross

and microscopic lesions in young chicks.
DEFINITION
Avian nephritis virus (ANV) is an astrovirus that causes 2. Virus can be difficult to isolate. It can be isolated in
infection of the kidneys in young chickens. The infection 6-day-old chicken egg embryos by inoculation through
is acute, highly contagious but usually subclinical in nature yolk sac route and in chicken embryo kidney cells.
characterized by nephritis and urate deposits in the kidneys 3. Other techniques such as RT-PCR,
and abdominal viscera. immunofluorescence, ELISA and electron microscopy
have been used to diagnose ANV.
OCCURRENCE CONTROL AND TREATMENT
ANV was first reported from Japan and the disease or the Currently there are no control or treatment measures that
antibodies have been reported in Europe and USA. are available and biosecurity implementation may help
limit the spread of the virus.
ETIOLOGY
ANV has been classified as an astrovirus distinct from Duck
Hepatitis type 2 and 3, turkey and chicken astroviruses.
Astroviruses are non-enveloped single-stranded positive
sense RNA icosahedral virus, 28-30 nm in diameter that
may exhibit five or six pointed star-like surface when
viewed by electron microscopy. ANV has been placed in
a new genus Aviastrovirus in the family Astroviridae. There
are genetic differences among various isolates of ANV.
EPIDEMIOLOGY
Transmission of ANV appears to be by direct contact with
infected birds. Vertical transmission of the virus has also
been suggested.
CLINICAL SIGNS
1. The only clinical sign reported due to ANV in 1-day-old
chicks is transient diarrhea but not all birds will show
this. But some of the characteristic lesions develop in Fig. 1
chicks up to 4 weeks of age. Chick suffering from ANV showing
enlarged and pale kidneys with increased
2. Runting stunting of chicks and decrease in body urates.
weights are observed.
3. Mortality can range from negligible to 6 %.
LESIONS
1. Grossly the chicks suffering from ANV may show
enlarged and pale kidneys with increased urates (Fig.
1).
2. Visceral urate deposits (gout) in the pericardium,
capsule of the liver, abdominal cavity, subcutaneous
tissues, etc… can be observed.
3. Histologically, degeneration and necrosis of the
epithelial cells of the proximal convoluted tubules
and dilation accompanied by lymphocytic interstitial
nephritis with tophi formation can be observed. Tophi
and associated inflammation can also be observed in
various other organs.
AVIAN VIRAL TUMORS effective in preventing the disease. However, sporadic

losses and the fear of increased virulence of the virus have
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DEFINITION kept MD among the most important poultry diseases.

The viral neoplastic diseases of chickens and turkeys,
although previously considered a “complex”, are actually ETIOLOGY
distinct disease entities. In some cases a single tumor 1. Marek’s disease virus is a cell-associated alpha
virus strain can induce multiple disease syndromes, thus herpesvirus of subgroup a3. The herpesviruses
causing indecision whether these neoplasms should be associated with MD are classified into three
classified by etiology or by lesion type. Furthermore, some serotypes. Serotype 1 isolates are ubiquitous in
of the lesion types are so rare as to be of little concern. chickens and pathotypes vary from very virulent
plus (vv+) (oncogenic) to nearly avirulent (mild).
In an attempt to simplify this situation, we will consider Serotype 2 isolates are common in chickens and are
here only the four neoplastic disease syndromes that nononcogenic. Serotype 3 isolates, also known as
have economic importance: Marek’s disease, a common turkey herpesvirus, are ubiquitous in turkeys and are
lymphoproliferative disease of chickens caused by an nononcogenic. The three serotypes have considerable
alpha herpesvirus; avian leukosis/sarcoma, common antigenic cross-reactivity.
retroviral diseases characterized by lymphoid or other 2. The serotype 1 virus can be grown in cultured chick
neoplasias and lowered egg production in adult chickens; kidney cells prepared from 1-3 week old chicks and
reticuloendotheliosis, a nondefective retrovirus which in duck embryo fibroblasts. It produces a distinct
causes a runting disease and a chronic lymphoma in cytopathic effect with intranuclear inclusions in
turkeys, chickens, and a variety of other avian species; those cells. Embryonal chick kidney cells and chick
and lymphoproliferative disease, a retrovirus-induced embryo fibroblasts are less effective for low-passage
disease of turkeys characterized by chronic lymphomas virus. Serotype 2 and 3 viruses can be isolated and
that although not yet reported in the United States, is propagated in chick embryo fibroblasts. The virus is
found elsewhere and must be considered in a differential usually tightly bound to living cells and in this form
diagnosis. is very labile, but cell-free virus is released from the
feather follicle epithelium and is relatively resistant to
I. MAREK’S DISEASE environmental factors. Both cell-associated and cell-
free viruses are susceptible to a number of common
DEFINITION disinfectants.
Marek’s disease (MD) is a herpesvirus-induced neoplastic
disease of chickens characterized by infiltration of various EPIDEMIOLOGY
nerve trunks and/or organs with pleomorphic lymphoid Infected chickens shed virus-containing feather follicle
cells. dander, which is a source of infection for other chickens
by the respiratory route. Infected carriers may or may not
be clinically ill, and carrier birds can sporadically shed virus
OCCURRENCE throughout their lifetimes. The disease is very contagious
Marek’s disease is important primarily in chickens, to a
and infectious dander can be disseminated over long
much lesser degree in quail, and has been rarely observed
distances. Although excretions and secretions of infected
in turkeys, pheasants and jungle fowl. Turkeys and other
chickens may contain virus, dander containing infectious
species have limited susceptibility. The disease most
enveloped virus particles is the most important means
commonly occurs in young, sexually immature chickens
of transmission. Transmission of the virus through the
2-7 months old, but can occur at virtually any age beyond
egg does not occur. Hatchery transmission through shell
3 weeks. The disease occurs throughout the world and
contamination is also unlikely due to adverse environmental
virtually all flocks are exposed to the causative virus.
conditions for the virus.
HISTORICAL INFORMATION CLINICAL SIGNS

A report in 1907 by a Hungarian veterinarian, Jozsef
Clinical signs occur in chickens affected with MD but are
Marek, of paresis in roosters is the first description of the
of little help in establishing a diagnosis. Birds with visceral
disease now called MD. The disease was first reported in
tumors are depressed and often cachectic prior to death.
the United States in 1914. Although forms of MD were an
Birds with lymphoid infiltration of peripheral nerves may
important cause of mortality in chickens prior to 1950, a
demonstrate asymmetric partial paralysis (Fig. 1) and / or
sudden increase in mortality in the late 1950s and 1960s
dilation of the crop due to vagus nerve paralysis. Blindness
accelerated research. Reliable experimental transmission
is associated with lymphoid infiltration of the iris (Fig. 2).
was achieved in 1962 and the causative herpesvirus was
Clinical signs usually do not appear prior to 3 weeks of age
isolated and identified in 1967. Vaccines became available
and peak between 2 and 7 months.
for use in the United States by 1970 and have been very
VIRAL DISEASES 31
LESIONS 2. The most common vaccines consist of turkey

1. At least four different lesion patterns are recognized: herpesvirus (HVT), a serotype 3 virus as a cell-
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gross enlargement (Fig. 3) and/or yellowing and associated preparation, or a bivalent vaccine consisting
loss of cross-striations of peripheral nerves (Fig. 4); of turkey herpesvirus and a serotype 2 virus (SB-1 or
discoloration of the iris (Fig. 5); enlargement of feather 301 B). Attenuated serotype 1 vaccines (CVI988, RM1
follicles (Fig. 6) with reddening (skin leukosis); and and 648A80) are also used. Care must be taken in
visceral tumors (Fig. 7) involving the liver (Fig. 7&8), handling cell-associated vaccines as they are highly
heart (Fig. 7&9), spleen (Fig. 8), gonad, kidney (Fig. susceptible to adverse environmental conditions.
10), proventriculus (Fig. 11), and other organs and 3. Genetic differences associated with the major
tissues. Visceral tumors are the most frequent lesions, histocompatibility (B) complex can aid both in resistance
but combinations of lesion patterns are common. to MD as well as the response to vaccination.
2. Microscopically, the lymphomas are characterized by
a mixture of pleomorphic lymphocytes (Fig. 12). Some TREATMENT
of these probably are true tumor cells that carry T-cell There is no effective treatment for MD. Birds with tumors or
surface antigens and a MD tumor-associated surface multiple skin lesions are condemned at slaughter.
antigen (MATSA). Others are probably host cells
reacting against viral or tumor antigens and represent II. AVIAN LEUKOSIS/SARCOMA VIRUSES
both T- and B-cells.
DEFINITION
DIAGNOSIS The avian leukosis (ALV)/sarcoma group are retrovirus-
1. A diagnosis can usually be made after careful caused, neoplastic diseases of semimature or mature
consideration of the history, the ages of the birds chickens. Strains of this group are classified by the
affected, and the location of the neoplastic lesions in pathological lesion they cause and by their subgroup. The
a generous sample of typically affected chickens. Few most common, lymphoid leukosis (LL) is characterized
epornitic diseases resemble MD with the exception of by a gradual onset in a flock, persistent low mortality, and
lymphoid leukosis and reticuloendotheliosis. neoplasia of the bursa of Fabricius with metastasis to
2. Marek’s disease often occurs in 2-5-month-old many other internal organs, especially the liver, spleen,
(sexually immature) chickens but can also occur after and kidney. A relatively new strain of ALV, “J”, probably
the onset of egg production. Outbreaks after the onset resulting from the recombination of endogenous and
of egg production in vaccinated stock have been called exogenous viruses, primarily causes myeloid leukosis
“late Marek’s” and are often associated with newer, (myelocytomatosis).
more highly virulent vv+ pathotypes.
3. Characteristics of MD lesions of importance in OCCURRENCE
differential diagnosis include nerve involvement Lymphoid leukosis associated mortality is most common
(when present), the absence of bursal lesions or, in chickens 16 weeks of age or older. The disease is
rarely, diffusely thickened bursas, and pleomorphic worldwide in distribution and widespread in the United
lymphocytes comprising lesions, some of which States. Virtually all flocks are considered to be exposed
exhibit MATSA and only few of which are positive for to the virus but infection rates within some flocks have
immunoglobulin M (IgM). The ubiquitous nature of MD decreased due to efforts at eradication by primary breeder
virus renders virology and serology of little value in companies. Overall, the incidence of LL is low (1 or 2%),
diagnosis. although occasional heavy losses can occur. A higher
incidence of bursal disease virus may be associated with a
CONTROL reduced incidence of LL. With ALV-J, meat-type chickens
1. Commercial flocks are usually immunized via appear to be more susceptible than layers.
injection at 18 days of embryonation or at hatching.
Care must be taken to insure that an effective dose
is administered to every embryo or chicken. Because
The first report of LL is attributed to Roloff in 1868. However,
immunity from vaccination is not fully developed for
the disease was not well characterized until a basis for its
7-10 days, it is crucial to minimize early exposure. This
separation from MD was established in 1962.
requires careful sanitation and disinfection, particularly
because MD virus survives well for months in poultry
houses. Revaccination is not necessary and immunity ETIOLOGY
is usually life-long. Appearance of the disease at Avian leukosis is caused by a family of retroviruses known
older ages has been attributed to immunodepression as avian leukosis viruses (alpha retroviruses), which have
due to environmental stress or infection with the vv+ been classified into 10 subgroups—A, B, C, D, E, F, G,
pathotype. H, I and J. In the United States, subgroup A viruses are
most common and are most frequently associated with LL
with ALV-J myelocytomatosis next in frequency. Subgroup not otherwise be obvious. Myelocytomatosis (Fig. 4) is
B viruses are occasionally isolated, whereas subgroups C most common with ALV-J; however, other tumor types
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and D are rare. Subgroup E viruses are common and are such as hemangiomas (Fig. 5) can also be seen.
considered «endogenous» because they are derived from 2. Microscopically, the neoplastic cells in lymphoid
proviral genes permanently integrated into the host cell tumors are uniformly lymphoblastic and the cells are
DNA; they rarely are associated with neoplasms. Subgroup pyroninophilic. Also, they are nearly all positive for
F, G, H and I viruses primarily cause leukosis in species surface immunoglobulin M (IgM). The tumors originate
other than chickens. The viruses produce a group-specific from bursal lymphocytes (B-cells) in which the proviral
antigen that can be detected in albumen of eggs and body DNA of the virus integrates during the process of
tissues or fluids. ALV-J viruses have extensive antigenic replication at a site in the host cell genome close to the
variation within the strain. The avian leukosis viruses can c-myc gene, a normal host cell gene with homology to
be cultured in chicken embryo fibroblasts but most produce an oncogene present in avian retroviral strain MC29.
no cytopathology and are detected by antigen tests. Simple Activation of this oncogene is believed to be the
tests for antigen detection are available and are used in primary event in starting the neoplastic process.
eradication programs in breeders. Antibody tests are also
available and are used to monitor the status of flocks from DIAGNOSIS
which the virus has been eradicated. 1. Lymphoid Leukosis can usually be diagnosed after
careful consideration of the age of the affected
EPIDEMIOLOGY chickens, the course of the disease and the pattern of
Egg transmission is an important mechanism of spread mortality in the flock, and the location of gross lesions
of avian leukosis viruses. The frequency of infected eggs in a moderate number of typically affected chickens.
is usually low but chicks hatched from infected eggs are Involvement of the bursa of Fabricius is nearly always
permanently viremic (immune tolerant), do not develop present, although the lesions may not be detected
antibody, have an increased risk of death from LL, may without incision of the organ and examination of the
lay fewer eggs, and will probably shed virus into their own epithelial surface. In contrast to MD, bursal tumors
eggs thus perpetuating the infection. Chickens also can are intrafollicular, generally causing a more nodular
become infected by contact exposure, particularly with enlargement (Fig. 6). The characteristic tumor cell has
ALV-J, which is efficient at horizontal transmission. In meat B-cell and IgM surface markers. Molecular methods
type chickens, ALV-J viremia negative/antibody positive are available in research laboratories to detect in the
birds can shed virus and post hatch infected birds become DNA of tumor cells the proviral DNA of ALV located in
tolerant shedders. Some chickens, particularly those of close proximity to the c-myc gene.
greater susceptibility due to endogenous virus infection 2. Diagnosis is made more difficult because the lesions
or absence of maternal antibody, may transmit virus to of LL often appear similar to those of MD, and can
progeny as a result of contact infection soon after hatch. appear identical to those induced experimentally
by reticuloendotheliosis virus. Because ALV is very
CLINICAL SIGNS widespread in chickens, virological and serological
Chickens with LL may present with nonspecific or no clinical methods offer little help in confirming a diagnosis.
signs of disease. Many birds with tumors are unthrifty or 3. Diagnosis of ALV-J is achieved by gross and
emaciated and have pale combs and wattles. Enlargement histopathologic examination of tumors and by virus
of the abdomen may result from massive enlargement of isolation from cloacal or vaginal swabs or tumors.
the liver. Some birds with tumors can be detected prior Although PCR tests have been developed, the virus
to death by palpation of an enlarged and lumpy bursa of mutates frequently requiring the production of new
Fabricius by insertion of a finger into the cloaca. Birds with primers.
skeletal myelocytomatosis may have observable masses
on the shanks, head and thorax. Osteopetrosis of the long CONTROL
bones (Fig. 1) or “boot” shanks may occur. Flocks with high 1. With LL, because egg transmission is so important and
infection rates experience depressed egg production. the disease is not very contagious, eradication is the
preferred method of control. Most of the eradication
efforts have been conducted by the primary breeding
LESIONS companies. Many breeders of egg-type chickens have
1. There are no unique external lesions. Lymphomas reduced markedly the rate of congenital transmission
(Fig. 2) are seen in many organs in chickens 16 weeks in their primary breeders and grandparent stocks
of age or older, but are especially common in the liver, through a program of testing dams prior to egg
kidney, ovary, and bursa of Fabricius (Fig. 3). The production and removal of those considered likely to
white-to-gray neoplastic lesions can be diffuse or are transmit virus to progeny. Some breeders have flocks
sometimes focal. If the bursa of Fabricius is incised, from which the virus apparently has been eradicated.
small nodular lesions can often be detected that would Commercial progeny from such breeders should have
VIRAL DISEASES 33
lower infection rates and thus should experience less to infection. All isolates are of a single serotype, but minor
tumor mortality and greater egg production. subtype differences have been noted.
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2. Although LL is not a disease of commercial broilers,

ALV-J is a problem and breeders have made significant EPIDEMIOLOGY
progress in their eradication programs. However, due The virus is transmitted horizontally. Mosquitoes have been
to the efficient horizontal transmission of ALV-J, control incriminated as passive carriers. Fowl pox viruses have
by eradication is more difficult. also been found to harbor infectious REV. Transmission
3. Genetic resistance to infection with subgroup A viruses through the egg has also been identified, but usually
is common in meat-type chickens, but quite rare in occurs at a very low rate.
egg-type chickens. When present, this resistance
offers an alternative approach to control. CLINICAL SIGNS
4. There is no vaccine that can protect against tumors The runting syndrome, usually induced by inoculation of
and mortality. Congenitally infected chicks are chicks at 1 week of age or less with RE virus-contaminated
immunologically tolerant and cannot be immunized. biologics, produces severe stunting and a feather
Vaccines to immunize parent stock where ALV has abnormality characterized by compression of barbules
been eradicated is being considered as a means to to the shaft in its proximal portion. Signs associated
provide maternal immunity to progeny. with chronic lymphomas are few but birds may become
depressed prior to death.
TREATMENT
There is no effective treatment for LL. LESIONS
1. The runting syndrome is characterized by severe
III. RETICULOENDOTHELIOSIS (RE) atrophy of the thymus and bursa of Fabricius. The
birds are immunodepressed and may show lesions
DEFINITION of concurrent infections. Generally no tumors are
Reticuloendotheliosis (RE) is a term used for a variety noted but some birds may have enlarged nerves,
of syndromes caused by retroviruses that may be either proventriculitis, enteritis, and anemia.
defective or nondefective for replication in cell culture. Only
2. The chronic lymphoma syndrome as produced
a runting syndrome and a chronic lymphoma, both caused
experimentally in chickens with nondefective RE virus is
by nondefective RE virus, are of economic importance.
identical in all respects with lymphoid leukosis. A different
lymphoma has been induced experimentally in certain
OCCURRENCE chicken strains that closely resembles MD because of
Nondefective RE virus is not ubiquitous, but infection is nerve lesions, tumors in the liver (Fig. 1), thymus, and
fairly widespread in chickens and turkeys, particularly heart, and its occurrence as early as 6 weeks of age.
in the southern region of the USA. The disease is Chronic lymphomas in species other than chickens are
uncommon. Runting disease has been associated with characterized by tumors of the liver and spleen, but
the use of RE virus-contaminated vaccines in chickens. bursal tumors are not particularly common.
Chronic lymphomas occur naturally in turkeys, including
wild turkeys, ducks, quail, pheasants, geese, peafowl, DIAGNOSIS
prairie chickens and chickens but are rare. Exportation of 1. A diagnosis of RE is probably best made on the basis of
seropositive birds to some countries is not permitted. typical lesions and demonstration of infection with the
causative agent by virus or antibody tests. Currently,
the PCR test, an immunoperoxidase plaque assay,
HISTORICAL INFORMATION and an enzyme immunoassay are available.
A virus was isolated from a field case of turkey lymphomas
in 1958 that, after rapid serial passage in chickens and 2. In chickens, the disease must be distinguished
turkeys caused high neoplastic mortality within 3 weeks. from both LL and MD. Thus far, however, naturally
Although this isolate, strain T, has been considered a occurring chronic lymphomas in chickens have not
prototype, it is not typical of field strains. Other isolates from been documented. The runting syndrome must
ducks and chickens were recognized in 1974 to comprise be distinguished from other immunodepressive
a family of RE viruses. conditions, especially infectious bursal disease and
chicken infectious anemia.
ETIOLOGY 3. In turkeys, the disease must be distinguished from
RE virus is a retrovirus with an unusually wide host range. It lymphoproliferative disease in countries of occurrence.
can be grown in cells from chickens, ducks, turkeys, quail, This can usually be accomplished by noting the age
and other species, even some mammalian cells. It infects of onset, the absence of greatly enlarged spleens, the
a variety of avian species. Non avian species are resistant uniform lymphoblastic morphology of the tumor cells
on histology and detection of viral nucleic acid using DIFFERENTIAL DIAGNOSIS

PCR assays. OF AVIAN TUMORS
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The differential diagnosis of tumors in chickens and turkeys

CONTROL
is difficult and requires an adequate history and a careful
No methods for control or treatment have been reported,
postmortem examination of a representative sample of birds
most likely because of low rates of vertical transmission,
with typical lesions. In some cases, additional tests such
and the sporadic incidence and the self-limiting nature of
as histology, immunofluorescent tests for surface antigens,
the disease. Strict sanitation and insect control may help
in situ hybridization tests and molecular techniques (PCR)
prevent infection from environmental sources. Eradication
will be helpful. The characteristics in the following table
programs patterned after those developed for LL may be
may be helpful in arriving at the correct diagnosis.
useful in breaking the egg transmission cycle.
Chickens Turkeys
Characteristic MD A
LL RE B
RE LPD
Gross lesions
Liver +++ +++ +++ +++ +++
Spleen +++ +++ +++ +++ +++
Nerves +++ - ++ +++ +
Skin +++ + + + +
Gonads +++ +++ +++ +++ +
Heart +++ + +++ ++ +
Bursa + +++ +++/-- +++ +
Intestine + ++ +++ +++ +++
Lungs +++ ++ ++ ++ +++
Kidneys +++ +++ +++ +++ +++
Histology
Pleomorphic cells + - -/+ - +
Uniform blast cells - + +/- + -
Antigens
MATSA + - - ? ?
IgM + +++ +/- ? ?
B-cell + +++ +/- ? ?
T-cell +++ + -/+ ? ?
Age of occurrence (months)

Peak time 2-7 4-10 2-6 4-6 2-4
Limits >1 >3 >1 >4 >2
A
Abbreviations: MD = Marek’s disease, LL = lymphoid leukosis, RE = reticuloendotheliosis, LPD = lymphoproliferative
disease.
B
Two experimental syndromes are recognized: a bursal lymphoma with characteristics similar to LL, and a nonbursal
lymphoma with characteristics similar to MD.
VIRAL DISEASES 35
MAREK’S DISEASE
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Fig. 1 Fig. 2
Typical partial paralysis associated with peripheral nerve Iris infiltration.
involvement in Marek’s Disease.
Fig. 4
Fig. 3 Enlarged sciatic nerve at the bottom with swelling and loss of cross-
Enlarged sciatic plexus on the right. striations compared to a normal sectioned sciatic nerve at the top.
Fig. 6
Fig. 5 Skin leukosis: enlarged feather follicles due to lymphoid infiltration.
Ocular lesions of MD. Note the normal eye (right) with a well-
defined pupil and well-pigmented iris while the MD affected
eye (left) has a discolored iris and irregular pupil as a result of
mononuclear cell infiltration.
MAREK’S DISEASE
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Fig. 7 Fig. 8
Visceral lymphomas in the liver and the Visceral lymphomas: diffuse hepatic and splenic
heart occurring as focal, nodular growths enlargements on the left vs normal liver and spleen
of varying sizes. on the right.
Fig. 9 Fig. 10
Multiple lymphomas in heart. Renal tumor.
Fig. 12
Fig. 11 Section of a nerve of a chicken with MD; infiltration of rapidly
Proventricular tumor. proliferating pleomorphic lymphoid cells between the neurons.
VIRAL DISEASES 37
AVIAN LEUKOSIS/SARCOMA VIRUSES

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Fig. 1
Fig. 2
Bones on the right are affected with osteopetrosis.
Visceral tumors involving liver, heart and
spleen.
Fig. 3 Fig. 4
Visceral tumors involving the bursa of Fabricius, kidneys and Myelocytomatosis.
ovary.
Fig. 5 Fig. 6
Hemangioma in a ALV-J positive broiler breeder. Transformed LL bursal follicle at the bottom with normal appearing
follicles in the remainder of the bursa of Fabricius.
RETICULOENDOTHELIOSIS (RE)
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Fig. 1
Gross lymphoma in the liver.
VIRAL DISEASES 39
CHICKEN INFECTIOUS ANEMIA 3. Morbidity and mortality rates depend on various

(CIA; Chicken Anemia Virus; Chicken viral, host and environmental factors and concurrent
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infection with other agents. Uncomplicated CIA may

Anemia Agent; Blue Wing Disease) only cause low mortality and poor performance. When
complicated with other factors mortality can be 30% or
DEFINITION even higher.
Chicken infectious anemia (CIA) is a disease of young
chickens characterized by aplastic anemia, generalized 4. Early infections with CIAV can interfere with vaccination
lymphoid atrophy, subcutaneous and intramuscular against Marek’s disease or infectious bursal disease.
hemorrhage, and immunodepression. LESIONS
1. Marked thymic atrophy is the most consistent lesion
OCCURRENCE (Fig. 2).
CIA is ubiquitous in all major chicken-producing countries 2. Fatty yellowish bone marrow, particularly in the femur,
in the world. is characteristic (Fig. 3).
3. Bursal atrophy can also be seen in a small number of
HISTORICAL INFORMATION birds.
CIA virus (CIAV) was first isolated by Yuasa in Japan in
1979. It has also been called chicken anemia agent, 4. Hemorrhages in the mucosa of the proventriculus,
chicken anemia virus, and parvovirus-like virus. The subcutis, and muscles may also be observed (Fig. 4).
clinical signs and lesions previously described as blue wing 5. Secondary bacterial infections may occur and include
disease, anemia-dermatitis syndrome, and hemorrhagic gangrenous dermatitis or blue wing disease if the
anemia may have been caused by CIAV. wings are affected (Fig. 5).
6. Histologically, there is marked thymic lymphoid
ETIOLOGY depletion (Fig. 6) and marked atrophy of all cell lines in
1. CIAV is classified into genus Gyrovirus of the family the bone marrow (Fig. 7). The bursal lymphoid follicles
Circoviridae. are mildly to severely depleted (Fig. 8) and spleen and
2. Viral particles are non-enveloped and are other tissues with lymphoid aggregates are variably
environmentally very resistant. depleted. There may be histological evidence of
secondary bacterial infections including gangrenous
3. They have a diameter of approximately 25 nm and dermatitis.
contain a single-stranded circular DNA genome.
4. Although viral isolates may differ at a molecular level DIAGNOSIS
antigenic or pathogenicity differences have not been 1. A presumptive diagnosis is based upon clinical signs
reported. and gross lesions.
2. Isolation in cell cultures (MDCC-CU147 or MSB1) and
EPIDEMIOLOGY identification of the virus from most tissues, buffy coat
1. All ages are susceptible to infection but clinical cells, and cloacal contents.
disease is typically seen only during the first 2 to 4
weeks. However, age resistance may be delayed by 3. Serologic assays to detect antibodies such as
simultaneous infection with infectious bursal disease the ELISA, virus neutralization test, and indirect
virus. immunofluorescence.
2. The virus is spread both vertically and horizontally. 4. PCR is the test of choice for identification of CIA virus
The most important method of transmission is vertical in cell cultures and chicken tissues.
from infected hens. Antibody-negative chicks are most CONTROL
susceptible to clinical disease. CIA virus also easily Best prevention is by immunization of breeder flocks prior
spreads via feces among birds in a population. to the onset of egg production (between 13-15 weeks of
CLINICAL SIGNS age but no closer to egg production than 4 weeks).
1. The only specific sign of CIAV infection is anemia
characterized by hematocrit values ranging from 6 to TREATMENT
27% (normal hematocrit values are generally 29-35%) No treatment is available.
(Fig. 1).
2. Nonspecific clinical signs include depression, pale ZOONOTIC POTENTIAL
tissues, depressed weight gain, and secondary None reported.
bacterial, mycotic, and viral infections.
CHICKEN INFECTIOUS ANEMIA

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Fig. 2
Severely atrophied thymus in a chick affected with CIA compared to
a normal thymus (top).
Fig. 1
Hematocrit tubes showing low
Packed Cell Volume (15 to 22%)
in 3 naturally infected chickens
with CIA compared to a normal
hematocrit (35%) on the left.
Fig. 3 Fig. 4
Pale yellow, fatty bone marrow in the femur of a chick infected with Petechiae and ecchymotic hemorrhages on the pectoral muscles in
CIA compared to a normal bone marrow (top). two chicks with hemorrhagic syndrome probably secondary to CIA.
Fig. 6
Fig. 5 Thymus: atrophy of lobules and loss of distinction between medulla
A 15-day-old chick with dermatitis, naturally and cortex with chick infected with CIA compared to normal on the
infected with CIA. left (H&E, 9,5X).
VIRAL DISEASES 41
CHICKEN INFECTIOUS ANEMIA

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Fig. 7 Fig. 8
Bone marrow: severe hypoplasia of both erythroid and myeloid Bursa of Fabricius: a plica showing lymphoid depletion and
cells and replacement by adipose tissue in a chick infected with CIA increased interstitium in a chick infected with CIA compared to
compared to normal on the left (H&E, 12,6X). normal on the left (H&E, 30,2X).
DUCK VIRUS ENTERITIS 3. The virus grows best on the chorioallantoic membrane
(DVE; Duck Plague) of 9-14-day-old embryonated duck eggs or on duck
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embryo fibroblasts. Initially it does not grow in chicken

eggs although it can be adapted to them. The virus also
DEFINITION can be isolated in ducklings, with Muscovy ducklings
Duck virus enteritis (DVE) is an acute herpesvirus disease
being the most sensitive.
of ducks, geese, and swans characterized by weakness,
thirst, diarrhea, short duration, high mortality, and by 4. The virus produces intranuclear inclusion bodies in a
lesions of the vascular, digestive, and lymphoid systems. variety of cells in the host.
EPIZOOTIOLOGY
OCCURRENCE 1. The virus can be transmitted horizontally from infected
1. Wild and domestic ducks, geese, and swans (order to susceptible bird by direct contact or through contact
Anseriformes) are affected. All age groups and many with the contaminated environment (particularly water).
varieties are susceptible; however, mostly adults are Natural infection is limited to ducks, geese, and swans.
affected. The blue-winged teal is the most susceptible
2. A carrier state for as long as 1 year has been
and the pintail duck is the least susceptible.
demonstrated in wild ducks. And there is some
2. In the United States the disease has occurred in New evidence that carrier birds under stress shed virus
York, Pennsylvania, Maryland, California, and South intermittently, thus exposing susceptible birds.
Dakota. The disease has been reported in Canada as
3. Because viremia occurs in affected birds, arthropods
well as the Netherlands, France, China, Belgium, and
feeding on those birds may transmit the disease.
India. Because wild waterfowl are migratory, it seems
However, this method of transmission is unproven.
likely that the disease may occur in other countries that
have migratory waterfowl. 4. Vertical transmission has been reported experimentally.
HISTORICAL INFORMATION CLINICAL SIGNS

1. The disease was first observed in the Netherlands in 1. In young commercial ducklings, signs appear 3-7 days
1923. Initially it was mistaken for avian influenza but in after exposure. Ducklings have diarrhea, a blood-
1942 it was clearly differentiated from avian influenza stained vent, dehydration, and a cyanotic bill. Death
and was termed duck plague. Subsequently the usually occurs in 1-5 days.
disease was identified in many other countries. 2. In domestic breeder ducks there is a marked drop in
2. In 1967 DVE appeared in white Pekin ducks raised egg production (25-40%) a sudden, high persistent
commercially on Long Island, New York. It also was mortality. Sick birds show inappetence, weakness,
identified in wild waterfowl. An effort to eradicate ataxia, photophobia, adhered eyelids, nasal discharge,
the disease in the domesticated white Pekin duck extreme thirst, prolapsed penis, and watery diarrhea.
appeared to be successful. They soon become exhausted and unable to stand.
They then maintain a position with their head down
3. Multiple outbreaks of DVE have been recognized in
and drooping outstretched wings. Tremors may be
California and it is classified as a reportable disease in
apparent. Morbidity and mortality are usually high but
this state. In the spring of 1973 the disease appeared
vary from 5 to 100%. Most birds that develop clinical
in congregated wild waterfowl in South Dakota
signs die. Wild waterfowl are said to have similar signs.
and resulted in the death of approximately 48,000
They often conceal themselves and die in vegetation
waterfowl, mostly ducks.
near the water.
4. DVE is now considered to be enzootic in North America.
Prior to the 1973 outbreak, DVE was considered LESIONS
an exotic disease by the USDA. It is being watched 1. Hemorrhages are present at many sites and there may
with interest because of its ability to kill congregated, be free blood in body cavities, gizzard, or intestine.
susceptible waterfowl. Hemorrhages often occur on the liver, in the mucosa
of the gastrointestinal tract (including the esophageal-
ETIOLOGY proventricular junction), throughout the heart, in the
1. The etiologic agent is a herpesvirus. Although strains pericardium and ovary. There may be edema in the
vary in pathogenicity, all appear to be identical cervical region.
immunologically.
2. There is severe enteritis. There may be elevated,
2. The virus is nonhemagglutinating. This differs from crusty plaques in the esophagus, ceca, rectum,
the viruses causing Newcastle disease and avian cloaca, or bursa of Fabricius. In young ducklings the
influenza, which do hemagglutinate and which must esophageal mucosa may slough.
be differentiated in diagnostic work.
VIRAL DISEASES 43
3. There is hemorrhage and/or necrosis in the annular TREATMENT

bands or discs of lymphoid tissue along the intestine. There is no effective treatment.
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The spleen is usually of normal or reduced size.

4. Initially the liver may be discolored and contain
petechial hemorrhages. Later it may be bile-stained
and contain scattered small, white foci as well as many
hemorrhages.
5. Microscopically there may be intranuclear inclusion
bodies in degenerating hepatocytes, epithelial cells of
the digestive tract, and in reticuloendothelial cells.
DIAGNOSIS
1. Typical signs and lesions, along with epizootic losses,
are highly suggestive of duck plague. The diagnosis
can be strengthened if intranuclear inclusion bodies can
be demonstrated or if the virus can be demonstrated in
the tissues through fluorescent antibody tests.
2. The virus should be isolated and identified for
confirmation. The virus will grow initially in embryonated
duck eggs but not in chick embryos. Using known
antisera to DVE, the virus can be identified by a
neutralization test.
3. Retrospectively, it is possible to identify an outbreak
of DVE if acute and convalescent sera are used to
demonstrate an increasing antibody titer to duck
plague virus. However the antibody response to
natural infection can be low and transient.
4. DVE must be differentiated from duck viral hepatitis,
pasteurellosis, Newcastle disease, avian influenza,
coccidiosis, and other causes of enteritis.
CONTROL
1. Owners should prevent cohabitation or contact of
their waterfowl with wild waterfowl. All appropriate
quarantine and sanitary practices should be followed
to prevent disease.
2. All suspected outbreaks should be reported
immediately to state authorities. They, with federal
authorities, will decide how an outbreak is to be
handled. In commercially raised waterfowl, outbreaks
were once controlled by combining slaughter with
indemnification and by the application of quarantine
measures. Presently, slaughter with indemnification
has been discontinued and vaccination has been
authorized on certain premises.
3. Both killed and live attenuated vaccines are available
for prevention but approval by animal health authorities
is required before they can be used. It has not been
authorized for general use.
4. A monitoring system for detection of DVE has been
established in the United States. Suspected outbreaks
should be processed through official state or federal
diagnostic laboratories.
DUCK HEPATITIS EPIZOOTIOLOGY

(DH, DHV, Duck viral hepatitis) 1. DHV type 1 is a highly contagious disease. The virus
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is excreted by recovered ducklings for up to 8 weeks

after onset of infection. Susceptible ducklings can be
DEFINITION
infected by direct contact with infected ducklings or
Duck hepatitis (DH) is a peracute, rapidly spreading viral
their contaminated environment. The virus can survive
infection of young ducklings characterized by a short
for 10 weeks in contaminated brooders and for 37
duration, high mortality, and by punctate or ecchymotic
days in feces. DHV type 2 is transmitted via both the
hemorrhages in the liver. Three different viruses are known
oral and cloacal routes. Survivors excrete virus for up
to cause DH.
to 1 week postinfection. DHV type 3 is similar to but
less severe than DHV type 2.
OCCURRENCE 2. Wild birds have been suspected of acting as
Duck Hepatitis virus (DHV) type 1 occurs primarily in
mechanical carriers of virus over short distances. The
commercially raised Pekin ducklings and is seen almost
viruses do not appear to be transmitted through the
exclusively in ducklings less than 5 weeks of age. Natural
egg and there are no known vectors of the disease.
outbreaks have not been reported in other species. The
disease is probably present in all major duck-raising areas CLINICAL SIGNS
of the world. DHV type 2 is seen exclusively in the United
Kingdom and affects ducklings up to 6 weeks of age. The DHV type 1
United States is the only country in which DHV type 3 1. The incubation period is very short, often around 24
has been observed. Ducklings up to 5 weeks of age are hours in experimental infections, and morbidity is close
susceptible to DHV type 3. to 100%. Onset of disease and spread within a flock
are very rapid and most mortality occurs within 1 week
of onset.
A disease that probably was DHV type 1 first appeared 2. Affected ducklings at first are slow and lag behind the
in New York in 1945. A similar disease, called duck viral flock. Within a short time they squat with their eyes
hepatitis, appeared on Long Island in 1949 and killed an partially closed, fall on their side, kick spasmodically,
estimated 750,000 ducklings. Subsequently, the disease and soon die. They often die in the opisthotonos
was reported in many other states and from many position (Fig. 1). Death often occurs within 1 hour of
countries throughout the world. In the United States the the appearance of signs.
disease remains one of the major diseases of the duck- 3. Mortality is age related and occurs as follows: ducklings
raising industry. DHV type 2 was first reported in DHV type less than 1 week old—up to 95% mortality; ducklings
1-vaccinated ducklings in Great Britain in 1965. In 1969, 1-3 weeks old—up to 50% mortality; ducklings over 4
DHV type 3 was reported to occur in DHV type 1-immune weeks and older ducks—negligible mortality.
ducklings on Long Island. 4. In older or partially immune ducklings, signs and
losses may be so limited that the disease may go
ETIOLOGY unrecognized.
1. The etiologic agent of DHV type 1 is an enterovirus
in the family Picornaviridae. It is chloroform resistant DHV type 2 and 3
and does not hemagglutinate; features that help Affected ducklings die within 1-2 hours after the onset of
separate it from most other viral diseases of ducks. clinical signs. Clinical signs usually appear within 1-4 days
The virus is rather stable and difficult to eliminate from postinfection. Signs include convulsions and opisthotonos.
contaminated premises. Serologic variants of DHV Mortality ranges from 10 to 50% and nearly all birds with
type 1 have been reported. clinical signs die. DHV type 3 is similar to DHV type 1 but
mortality is rarely over 30% and morbidity is higher.
2. DHV type 2 has been identified as an astrovirus. As
with DHV type 1, the virus is fairly resistant. DHV type
3 is also caused by an astrovirus, but it is unrelated to LESIONS
DHV type 1. 1. The lesions observed with all three viruses are similar.
3. DHV type 1 can be isolated from affected livers 2. The cadaver may be in opisthotonos, the position in
in embryonated chicken or duck eggs, 1-day-old which many of the ducklings die.
ducklings, or duck embryo kidney or liver cell cultures. 3. The liver is swollen and contains punctate or diffuse
DHV type 2 is difficult to isolate, whereas DHV type hemorrhages (Fig. 2). The kidneys may be swollen
3 can be isolated on chorioallantoic membranes of and the spleen enlarged. Microscopically, there may
9-10-day-old duck embryos. be areas of hepatic necrosis, bile duct proliferation,
4. DHV stimulates a high degree of immunity in ducklings and some degree of inflammatory response (Fig. 3).
that survive infection and in inoculated adult ducks.
VIRAL DISEASES 45
DIAGNOSIS TREATMENT
1. The sudden onset, rapid spread, short course, and There is no treatment for the disease.
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focal, hemorrhagic hepatitis in young ducklings

suggest a diagnosis of DHV.
2. DHV type 1 can usually be isolated in embryonated
chick or duck embryos or 1-day-old susceptible
ducklings. Once the virus is isolated, it can be
identified by serum neutralization using known
hepatitis antiserum. Identification is also possible
by inoculation of the virus into both susceptible and
immune ducklings. DHV type 2 can be identified
through electron microscopy on liver or blood. DHV
type 3 cannot be isolated in chicken embryos and is
difficult to reproduce in ducklings. The chorioallantoic
membranes of duck embryos are the preferred route
of inoculation. A direct fluorescent test on duckling liver
has been reported.
3. The disease must be differentiated from duck viral
enteritis, Newcastle disease, and avian influenza. In
contrast to the viruses of DHV, the viruses causing
those diseases are susceptible to chloroform; also Fig. 1
Duckling affected with DVH, dead in the opisthotonos position.
the viruses of influenza and Newcastle disease
hemagglutinate erythrocytes.
CONTROL
DHV type 1
1. In the initial stages of outbreak, all susceptible
ducklings should be inoculated intramuscularly with
duck hepatitis viral antiserum. One inoculation should
be adequate if the antiserum is potent. A potent
antiserum can be made from the blood of naturally
or experimentally infected ducks. The blood can
be collected at slaughter and the sera harvested.
Antibodies for prophylactic use may also be obtained
from the yolk of eggs produced by immune breeders,
or from the eggs of chickens hyperimmunized with the
virus.
2. Unexposed ducklings can be actively immunized using
Fig. 2
a chicken embryo-adapted apathogenic vaccine. Enlarged liver with petechial to
However, young ducklings with parental immunity may diffuse hemorrhages.
not respond to vaccination.
3. Many duck breeders prefer to vaccinate their breeding
stock at 3-4-month intervals to maintain a high
antibody titer. Those birds then will transmit antibody
through their eggs to the progeny. The progeny will
usually be protected through the critical early weeks
of life. Breeder birds should be vaccinated at least 2
weeks before their eggs are to be saved for hatching.
Both live and inactivated vaccines are available.
DHV type 2 and 3

Vaccines for breeders are in the experimental stage
only. Strict biosecurity procedures must be employed.
Information concerning vaccines or antiserum can be
obtained by contacting the Duck Research Laboratory, Fig. 3
Eastport, Long Island, NY 11941. Microscopic lesions in the liver of a duckling affected with DVH.
Note the massive liver cell necrosis and hemorrhage.
FOWL POX birds but these are not practical for routine diagnosis.
(Pox; Avian Pox) Restriction endonuclease analysis of DNA has been
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successful in differentiating strains.

DEFINITION 4. Recovery from poxvirus infection usually results in
Fowl pox is a slow-spreading viral disease of chickens, a strong, enduring immunity to later exposure to the
turkeys, and many other birds characterized by cutaneous same virus. Also, in turkeys and chickens vaccination
lesions on unfeathered skin of the head, neck, legs, and is usually quite effective in preventing pox. Recently,
feet and/or by diphtheritic lesions in the mouth, upper however, several outbreaks of fowl pox have occurred
digestive and respiratory tracts. in vaccinated chickens.
5. Virus is present in lesions and in desquamated scabs.
OCCURRENCE Poxvirus is quite resistant to environmental factors and
Among poultry, pox occurs frequently in chickens and persists in the environment for many months.
turkeys. Among other birds, pigeons, canaries, and 6. Most poxviruses stimulate the formation of inclusion
psittacines are frequently infected and the disease is seen bodies in infected epithelium. Cytoplasmic inclusion
occasionally in many wild birds. Perhaps all birds are bodies (Bollinger bodies) contain elementary bodies
susceptible. The disease occurs in all age groups except (Borrel bodies). Bollinger bodies are quite large and
the recently hatched and is worldwide in distribution. readily identified microscopically.
EPIDEMIOLOGY
HISTORICAL INFORMATION 1. The virus-containing crusts (scabs) formed on the skin
Fowl pox is an ancient disease and in the distant past
are desquamated into the environment. Virus persists
was mistakenly thought to be related to small pox and
in the environment and may later infect susceptible
chicken pox of man. The characteristic pox inclusion
birds by entering the skin through minor abrasions.
bodies (Bollinger bodies) and the smaller elementary
Mechanical transmission via cannibalism is thought to
bodies within them (Borrel bodies) were studied by Drs.
play a significant role in some outbreaks. Respiratory
Bollinger and Borrel, respectively, in 1873 and 1904. In the
tract infection can result from inhalation of aerosolized
United States, pox has been a common and frequently
feathers and scabs containing virus.
reported disease of poultry. In recent years there has been
increased interest in pox in wildlife and caged birds, which 2. Certain mosquitoes, and possibly other blood-
are being submitted to diagnostic laboratories in increasing sucking arthropods, can transmit virus from infected
frequencies. to susceptible birds. Mosquitoes remain infective for
several weeks. Mosquito-transmitted outbreaks may
result in rapid spread.
ETIOLOGY
1. Fowl pox is caused by a large DNA Avipoxvirus of the 3. Poxvirus infection can result from mechanical
family Poxviridae. Many strains of virus are recognized transmission from toms to turkey hens via artificial
and naturally infect the species given in their name. insemination.
Some common examples are:
CLINICAL SIGNS
fowl poxvirus (type species) quail poxvirus 1. In poultry, onset often is gradual and the disease may
turkey poxvirus mynah poxvirus go undetected until cutaneous lesions are numerous
pigeon poxvirus psittacine poxvirus and obvious in the flock. The disease spreads slowly
canary poxvirus and severe outbreaks may last many weeks. Turkey
pox infection is generally more chronic than fowl pox
2. Poxviruses appear to be closely related, however,
infection. Canaries can have systemic infection with
strong host specificity is found with most poxvirus
high mortality. Signs vary somewhat with the two
strains. In some instances, exposure to one of the
overlapping forms of pox:
viruses in the group engenders immunity to that virus
and one or more of the other viruses in the group. A. Cutaneous form
Poxvirus isolates from Hawaiian forest birds (alala This form predominates in most outbreaks. Birds
and apapane poxvirus strains) are more related to often show few signs other than a mild to moderate
each other than to fowl poxvirus indicating genetically reduction in rate of gain, a temporary loss in egg
distinct poxviruses in this region. Perhaps all strains production, or a lack of flock vigor. Mortality is low
are host-modified variants of what was once a single if the disease is uncomplicated.
virus.
3. The various strains of avian poxvirus are B. Diphtheritic form
morphologically identical. Strain classification has Lesions in the upper respiratory or digestive tract
traditionally depended upon the cross-protection test in may result in dyspnea or inappetence, respectively.
VIRAL DISEASES 47
Lesions in the nasal cavity or conjunctiva lead usually done when the birds are 4 weeks of age but
to nasal or ocular discharge. Mortality is low can be done at any age if necessary. Pullets should be
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to moderate and is often due to suffocation or vaccinated 1-2 months before production begins.
starvation and dehydration. 2. Chickens and pigeons usually are vaccinated by the
wing web-stick method. An applicator with two slotted
LESIONS needles is dipped in vaccine and thrust through the
1. Cutaneous lesions vary in appearance according to wing web. Turkeys may be vaccinated by the wing
whether the papule, vesicle, pustule, or crust (scab) web route but lesions may be transferred to the head
stage is observed. In most outbreaks the terminal from the vaccination site. Vaccination by a drumstick-
reddish brown to black scab stage (Fig. 1) is present stab method when the birds are 2-3 months old is the
on at least some of the birds presented for diagnosis. recommended route. Turkeys retained as breeders
Papules, the initial lesions, are light-colored nodules should be revaccinated.
in the skin. Vesicles and pustules are raised, usually 3. Pigeon pox vaccine is now widely used in chickens
yellow. Occasionally, small papilloma-like lesions either alone or in combination with fowl pox vaccine.
occur. Lesions usually occur on the unfeathered skin Chickens purchased as replacements for layers should
of the head (Fig. 2) and neck but may occur around the be revaccinated if the initial vaccination occurs prior
vent or on the feet or legs (Fig. 3). Cage birds and wild to 10 weeks of age. Pigeon pox vaccine can cause
birds often have lesions on the feet or legs and these severe reactions in pigeons if not applied properly.
may appear as horny growths.
4. Turkeys are usually vaccinated with fowl pox vaccine.
2. Diphtheritic lesions are raised, buff to yellow plaques Turkey pox, quail pox, and canary pox vaccines are
on mucous membranes. They usually predominate in commercially available when circumstances indicate
the mouth (Fig. 4) but may be present in the sinuses, that these strains are the causative agents. Fowl and
nasal cavity, conjunctiva, pharynx, larynx, trachea (Fig. pigeon pox vaccines are not cross-protective with
5), or esophagus. Diphtheritic lesions often accompany these strains. Fowl pox vaccine should not be used to
cutaneous lesions but may occur alone in some birds. vaccinate pigeons.
3. Turkey pox (Fig. 6) has been observed in turkeys 5. Vaccination produces a small lesion (“take”) at the site
previously vaccinated with fowl pox vaccine. of vaccination. A generous sample of the birds should
Occasional birds develop lesions on the conjunctiva, be examined for vaccination lesions about 5-7 days
mouth, and upper digestive tract. Economic loss is after vaccination. Takes caused by turkey pox vaccine
often due to poor feed conversion. generally appear later (8-10 days after vaccination)
4. Microscopically, epithelial hyperplasia (Fig. 7) with than those caused by fowl pox. A large percent of those
eosinophilic cytoplasmic inclusion bodies (Fig. 8) and birds should have takes or revaccination is necessary.
surrounding inflammation are observed whether the 6. Broilers are not vaccinated unless there is pox in the
lesion is cutaneous or diphteric. area. Broilers may be vaccinated with a mild tissue
culture fowl pox vaccine administered subcutaneously
DIAGNOSIS
at 1 day of age. This vaccine does not produce a
1. Typical skin lesions are very suggestive of the disease.
visible take, but may result in a small number of birds
The diagnosis can be confirmed by demonstrating
that exhibit central nervous system (CNS) signs at
intracytoplasmic inclusion bodies in stained sections
4-12 days postvaccination. In ovo injection of this
or in scrapings of the lesions.
vaccine may magnify the number of chicks exhibiting
2. Typical skin lesions can be reproduced in a susceptible CNS reactions.
bird of the same species. Ground lesion material
7. Control cannibalism with proper beak trimming and
should be inoculated into scarified skin or empty
reduced environmental light intensity.
feather follicles and should produce a typical pox
“take” at the application site in about 5-7 days. 8. Fowl pox is currently being employed as a vector for
recombinant vaccines.
3. Virus-containing lesion material will produce pocks
on the dropped chorioallantoic membrane of TREATMENT
embryonated chicken eggs. The lesions contain typical There is no satisfactory treatment for pox.
intracytoplasmic inclusion bodies.
4. Some poxvirus strains, particularly turkey pox, may not
have demonstrable inclusion bodies in tissue sections.
Electron microscopy may be helpful in these cases.
CONTROL
1. Pox can be prevented in chickens, turkeys, pigeons,
canaries, and quail by vaccination. Vaccination is
FOWL POX
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Fig. 1 Fig. 2
Terminal reddish brown to black scab stage Pox lesions on the unfeathered skin of the head of a hen.
of a fowl pox infection in a broiler breeder
chicken.
Fig. 4
Fig. 3
Diphtheritic pox lesions in the mouth of a naturally infected
Cutaneous pox lesion (foot) in an
chicken.
experimentally infected bird.
Fig. 5
Fig. 6
Diphtheritic pox lesions in a naturally infected hen showing a
Young turkey affected with dry pox.
tracheal plug.
VIRAL DISEASES 49
FOWL POX
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Fig. 7 Fig. 8
Microscopic lesions of the trachea showing epithelial hyperplasia Microscopic lesions showing ballooning degeneration and
and inflammation. Note the presence of necrotic cells in the lumen. characteristic eosinophilic cytoplasmic inclusion bodies in infected
cells.
HEPATITIS E VIRUS EPIDEMIOLOGY

(HEV or Hepatitis-Splenomegaly 1. Transmission of Avian HEV appears to be by fecal-oral,
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but experimentally the disease has been reproduced

Syndrome in Chickens)
by oronasal route of inoculation.
DEFINITION 2. In the field, transmission occurs readily within and
Hepatitis E Virus causes a disease known as Hepatitis- between chicken flocks.
splenomegaly (HS) syndrome in both layer and broiler-type 3. Embryonic chicken eggs can be infected by the
chickens. It is characterized by increased mortality and intravenous route.
decreased egg production. Dead birds have hemorrhagic
livers, with clotted blood around the liver or abdominal CLINICAL SIGNS
cavity and splenomegaly. The disease has been seen in 1. Clinical signs due to HS are non specific and consist
the USA, Australia, Canada, Europe, and China and is also of anorexia, depression, pale combs and wattles and
probably present in other parts of the world. soiled vents.
2. Some birds can die suddenly without exhibiting any
OCCURRENCE clinical signs.
HS syndrome was first reported in western Canada in 3. The morbidity and mortality in the field can be low.
1991, and since then has been recognized in the United Mortality can be 1 % per week lasting for 3 to 4 weeks.
States, Australia and Europe. The disease has been called
4. Egg production drops are above normal, but can be
by many names in the US and Canada; weeping liver
significant in some affected flocks, as high as 20 %.
disease, necrohemorrhagic hepatitis, necrotic hemorrhagic
In broiler chickens small eggs with thin and poorly
hepatosplenomegalic syndrome, chronic fulminating
pigmented shells can be observed.
cholangiohepatitis and necrotic hemorrhagic hepatitis
splenomegaly syndrome. In Australia, the disease is called LESIONS
Big Liver and Spleen (BLS) disease. 1. Reported gross lesions include hemorrhages in the
abdominal cavity and/or on the livers (Fig. 1), as well
ETIOLOGY as red fluid within the abdominal cavity.
HS is primarily caused by Hepatitis E virus (HEV) distantly 2. Livers can be enlarged, friable, and stippled with
related (58 to 61 % with the helicase gene) to human and mottled white, red or tan foci. Subcapsular hematomas
swine Hepatitis E viruses. Hepatitis E virus is a spherical, can be seen occasionally in the liver.
non-enveloped, symmetrical virus of about 32-34 nm in
diameter. It is a single-stranded, positive sense RNA virus 3. Spleens can be severely enlarged and mottled white
that has been placed in a new family Hepeviridae and genus (Fig. 2). Ovaries are often regressing.
Hepevirus. There are genetic differences among various 4. Microscopically, liver lesions range from multifocal
isolates of Avian HEV isolated from different geographic to extensive hepatic necrosis and hemorrhage (Fig.
regions such as Australia, the USA and Europe. Avian HEV 3), with infiltration of mononuclear inflammatory cells
has also been isolated apparently from clinically normal around portal triads. Infiltration of lymphocytes in and
chickens. around the blood vessels in the liver is a characteristic
lesion of this syndrome. Microscopic lesions in the
It has been determined that there is a 79 % nucleotide spleen include lymphoid depletion, hyperplasia
sequence (in the helicase gene) similarity between avian of mononuclear phagocytic system cells and the
Hepatitis E viruses that cause HS and BLS. The syndrome accumulation of eosinophilic material in and around
is most common in laying hens between 30 and 72 weeks small arteries and in the interstitium of the vascular
of age, with the highest incidence occurring between 40 sinuses. Similar eosinophilic material can also be
and 50 weeks of age. Leghorn hens in cages are typically present in the interstitium of the liver (Fig. 4). This
affected and on some farms HS frequently reoccurs. The material is usually positive for amyloid using Congo
disease is endemic in chicken flocks in the US. Serological red stain (Fig. 5).
studies in the US revealed that 71 % of the flocks and 30
% of chickens are positive for avian HEV antibodies. About DIAGNOSIS
17 % of chickens less than 18 weeks of age and about 36 1. A presumptive diagnosis can be made based on
% of adult chickens are positive for avian HEV antibodies. clinical signs, mortality patterns combined with gross
Antibodies to BLS have also been demonstrated in and microscopic lesions. However, gross lesions of HS
chickens in the US. can appear similar to hemorrhagic fatty liver syndrome
(HFLS) of chickens. With HS syndrome the livers tend
not to be fatty both grossly and microscopically and
amyloidosis is not seen with HFLS.
VIRAL DISEASES 51
2. Virus can be isolated in chicken egg embryos by CONTROL AND TREATMENT

inoculation through intravenous route but it is not Biosecurity implementation may help limit the spread of the
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practical as this method is difficult and many embryos virus. Currently there is no treatment available to control
may die by this technique. Negative stain electron HS. One study suggested that immunization of chickens
microscopy to detect 30 to 35 nm virus particles in with avian HEV recombinant ORF2 capsid protein with
the bile or the feces in chickens suffering from HS aluminum as adjuvant can induce protective immunity
syndrome can also be used. against avian HEV infection.
3. Immunohistochemistry (IHC) on tissues can also be
used for diagnosis.
4. Serology by ELISA and AGID are other methods that
can be used for diagnosis of HS.
5. Currently, the diagnosis of avian HEV is made primarily
based on the detection of virus RNA by RT-PCR either
in the feces or liver samples.
Fig. 3
Acute hemorrhage with architectural disruption of hepatocellular
cords and hepatic sinusoids (H&E).
Fig. 1
Enlarged and hemorrhagic liver
from a 63-week-old chicken
with hepatitis E virus infection.
Fig. 4
Photomicrograph of a liver from a chicken infected with HEV
showing accumulation of homogeneous eosinophilic material,
amyloid, in the interstitium stained with H&E.
Fig. 2
Two enlarged and mottled white spleens from 56-week-old chickens
with hepatitis E virus infection. the spleen on the left is of normal
size.
Fig. 5
Congo red stain positive shows orange colored amyloid (on the left)
and apple green birefringence property of amyloid under polarizing
filter (on the right).
INFECTIOUS BRONCHITIS 2. The virus may persist on contaminated premises for

(IB) approximately 4 weeks or longer under favorable
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conditions. Susceptible birds brought on the premises

during that interval may contract the disease.
DEFINITION
Infectious bronchitis (IB) is an acute, highly contagious 3. A few birds may periodically shed the virus for
viral disease of chickens characterized by respiratory months after infection. Intermittent virus shedding
signs (gasping, sneezing, coughing, and nasal discharge), can contaminate the environment and be a source of
severe renal disease associated with nephrotropic strains, infection for susceptible chickens.
and a marked decrease in egg production. 4. Vertical transmission has not been documented.
OCCURRENCE CLINICAL SIGNS

1. IB occurs naturally only in chickens. All ages are Baby chicks
susceptible, assuming they have not had prior 1. Signs include coughing, sneezing, rales, and nasal
exposure to the virus or are not passively immune. and ocular discharge (Fig. 1). Morbidity is virtually
100%, although severity of signs varies. Signs can
2. The disease is present in all countries where chickens
develop within 48 hours postinfection.
are raised in large numbers. In the United States the
disease occurs frequently and throughout the year, 2. There is weakness, depression, and huddling near
even in vaccinated flocks. heat sources.
3. Mortality in young chicks is usually negligible unless
the disease is complicated by other infectious agents.
1. In 1930, IB was first observed in young chicks. By the
Nephrogenic strains may cause high mortality.
1940’s, IB was a serious disease of laying flocks causing
marked loss in egg production. Nephropathogenic IB Laying chickens and broilers
was first observed in the 1960s. 1. Coughing, sneezing, and rales are common. Seldom
2. The virus was first isolated by Beach and Schalm in is there nasal or ocular discharge.
1936 and multiple serotypes were first reported in 2. Egg production drops markedly (up to 50%). Effects
1956. on production can last 6-8 weeks or longer. Eggs are
3. Vaccination became commercially available in the often soft-shelled or misshapened (Fig. 2). Egg albumin
1950’s and is currently practiced worldwide. may be watery. Low egg quality and shell irregularities
may persist long after an outbreak of IB. Chickens that
ETIOLOGY had IB or a severe reaction to IB vaccine when less
1. IB is caused by a coronavirus. The virus is fairly labile than 2 weeks of age may suffer permanent damage to
and can be destroyed by many common disinfectants. the oviduct resulting in poor-to-no egg-laying capacity.
2. Most IB virus (IBV) without enzyme treatment do not 3. Chickens that have IB or a severe reaction to IB
hemagglutinate erythrocytes as do Newcastle and vaccination may develop airsacculitis, due to an
influenza viruses. increased susceptibility to secondary infectious
3. There is considerable antigenic variation among agents (especially Escherichia coli or Mycoplasma
IBV strains and many serotypes of the virus have gallisepticum). This complication can be very severe
been identified. Common serotypes (Connecticut, and may accentuate respiratory signs, especially in
Massachusetts, Arkansas 99, DEO72 and GA98) are young chickens.
used in US vaccine preparation. There is little or no 4. Mortality associated with swollen pale kidneys and
cross-protection among different serotypes. urolithiasis (Fig. 3) is induced by nephrotropic IBV
4. Some IBV strains have a distinct predilection for renal strains in pullets and even in mature birds.
tissue and these nephrotropic strains can induce
significant mortality.
LESIONS
1. There is mild to moderate inflammation of the upper
5. IBV has a high mutation rate, making diagnosis and respiratory tract (Fig. 4). There may or may not be
control very difficult. airsacculitis (Fig. 5). Severe airsacculitis is manifested
as a marked thickening and opacity of the air sac
EPIZOOTIOLOGY membranes and often is accompanied by exudate in
1. Transmission of IBV is by inhalation of virus-containing
the air sacs. Airsacculitis can result in high mortality in
droplets expelled by infected chickens. Aerosol
young, growing birds, especially if husbandry is poor.
transmission apparently can occur over considerable
Older birds are usually more resistant.
distance. Spread of infection throughout a flock is
explosively rapid.
VIRAL DISEASES 53
2. The kidneys sometimes are swollen and the ureters CONTROL

and tubules contain uric acid crystals, especially in 1. Modified live IBV vaccines are used in young chickens
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young birds, including broilers. for prevention. Vaccines are effective only if they
3. Yolk material frequently is present throughout the contain the homologous serotypes in a given area.
peritoneal cavity and the ovarian follicles appear Typically a prime at one-day of age followed by a
flaccid. These lesions are not specific for IB but boost at around 2 weeks of age are given, particularly
accompany many acute diseases of layers. in birds with maternal immunity. Polyvalent bronchitis
vaccines are typically used but can cause more severe
4. In layers that had IB or a severe vaccination reaction vaccine reactions in naive chicks. IBV vaccine is often
while less than 2 week old, there may be abnormalities combined with Newcastle vaccine in the same vial but
of the oviducts (particularly the middle third) in some can cause interference with the Newcastle vaccine if
birds. Oviducts may be hypoplastic or cystic and such not commercially prepared as a combination vaccine.
birds may deposit yolks or fully formed eggs in the Vaccines are generally applied via the drinking water
abdominal cavity and are referred to as internal layers. or by spray. Utmost care needs to be taken to preserve
5. Histologically, tracheitis is characterized by an the vaccine integrity as the vaccine virus can be prone
edematous mucosa, cilia loss, rounding and sloughing to inactivation under adverse conditions.
of epithelial cells and presence of inflammatory cells 2. Vaccinated birds should be watched carefully for
(Fig. 6). Kidney lesions are those of an interstitial possible onset of airsacculitis following vaccination.
nephritis (Fig. 7). If signs or lesions of airsacculitis are detected, broad-
DIAGNOSIS spectrum antibiotics added to the feed or water will
1. Tests of paired acute and convalescent serum can usually minimize the airsacculitis and reaction.
be very useful in demonstrating a specific immune 3. Killed virus vaccines (oil emulsion base) are now
response. Several procedures including serum-virus widely used. They are administered by injection
neutralization (VN), enzyme-linked immunosorbent (subcutaneous or intramuscular) to breeders or layer
assay (ELISA) and modified hemagglutination replacement pullets from 14 to 18 weeks of age. They
inhibition (HI) are available, but only VN and to some induce high and sustained antibody levels.
extent HI tests (due to cross-reactions) are serotype
specific. TREATMENT
4. No effective treatment of IB is known although broad-
2. For diagnosis it is necessary to isolate and identify spectrum antibiotics may control the complications.
the IBV type. Isolation is usually is done in 9-12-day- If there are no complications of IBV infection or
old embryonated eggs. Trachea, lungs, air sacs, and vaccination, medication following vaccination or
kidneys are good sources of virus. In infections beyond infection is not recommended.
1 week duration, cecal tonsils and cloacal swabs can
sometimes be productive. The type of the virus can 5. For baby chicks with IBV, it may be helpful to increase
be determined by VN testing, HI tests, monoclonal the room temperature, encourage the birds to eat by
antibodies, and RT-PCR and sequencing. using a warm moist mash, and correct any apparent
management deficiencies.
3. Nine to 12-day-old embryonated eggs inoculated
with supernatant containing IBV develop lesions that
are useful in diagnosis. The mesonephros of living
embryos surviving 5-7 days postinoculation contains
excessive urates. IBV causes dwarfing and stunting of
some inoculated chick embryos. Also, the amnion and
allantois are thickened and closely invest the embryo.
After initial isolation it may be necessary to passage
the virus three to five times to obtain embryo lesions.
Similar embryo lesions can be observed with some
lentogenic strains of Newcastle virus.
4. All most all IBV isolates do not hemagglutinate
erythrocytes naturally, but will hemagglutinate if
treated with neuraminidase. Newcastle virus and
avian influenza virus can hemagglutinate erythrocytes
without any prior treatment.
5. The fluorescent antibody technique or electron Fig. 1
microscopy can be used on tracheal samples for rapid Chick with ocular discharge.
diagnosis of IB but do not differentiate the serotype.
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Fig. 2
Misshapened and softshelled eggs from IB positive broiler breeder Fig. 3
hens. Kidney lesions associated with IB caused
by a nephrogenic strain.
Fig. 4
Mild inflammation of the Fig. 5
upper respiratory tract, note Mild and acute airsacculitis in a broiler chicken. Note the foamy
the foamy exudate in the exudate in the abdominal airsac.
laryngeal area.
Fig. 6
Viral tracheitis characterized by cilia loss, mucous gland depletion,
and mucosal epithelial degenerative changes including hyperplasia,
and inflammatory cell infiltration. Fig. 7
Tubulointerstitial nephritis in a chicken infected with a nephrogenic
IBV strain.
VIRAL DISEASES 55
INFECTIOUS BURSAL DISEASE contaminated houses and for weeks in water, feed,
(IBD; Gumboro Disease) and droppings. It can be transmitted by fomites. It has
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some susceptibility to formalin and iodide disinfectants.

Invert soaps with 0.05% sodium hydroxide may kill
DEFINITION IBD virus.
Infectious bursal disease (IBD) is an acute, contagious, viral
disease of young chickens characterized by inflammation EPIZOOTIOLOGY
followed by atrophy of the Bursa of Fabricius and variable 1. The virus spreads rapidly from infected chicks and
degrees of immunosuppression. from contaminated premises or fomites to susceptible
chicks. The disease is highly contagious.
OCCURRENCE 2. Vertical transmission of IBD virus has not been
IBD occurs in all of the major poultry-producing countries documented and there is no evidence for a carrier
of the world. Clinical signs are variable and are generally state.
more severe in birds 3-6 weeks old. However, IBD may
3. The lesser meal worm (Alphitobius diaperinus) harbors
occur in chickens as long as they have a functional bursa
the virus for weeks after an outbreak and may transmit
of Fabricius (1-16-weeks of age). Birds infected at less
it to susceptible birds. This worm lives in poultry litter.
than 3 weeks of age do not have clinical signs. However,
destruction of the bursa results in immunosuppression. 4. The incubation period is very short with clinical signs
The younger the bird at the time of infection, the more evident 2-3 days post exposure.
severe the immunosuppression, resulting in a high degree 5. Subclinical infection (before 3 weeks of age) is
of susceptibility to subsequent pathogens. Once a premise economically important due to suppression of humoral
has been contaminated with IBD virus, the disease tends immunity and subsequent secondary infections.
to recur, usually as a subclinical infection. The virus is lymphocidal (immunoglobulin-bearing
lymphocytes) and severely damages the bursa of
In turkeys, subclinical infection with IBD virus occurs Fabricius. The thymus, spleen, and cecal tonsils are
without immunosuppression. However, there is no known also damaged but less severely.
disease associated with IBD viral infection. IBD viruses
from turkeys are serologically distinct from those isolated 6. It has been demonstrated that IBD can severely
from chickens. Ducks can also be subclinically infected damage the humoral responsiveness of susceptible
with no apparent immunosuppression. chicks when they are infected at less than 3 weeks
of age. Those chicks then do not respond properly
when vaccinated against other diseases. There is
HISTORICAL INFORMATION evidence that inclusion body hepatitis and gangrenous
A disease caused by infectious bursal disease virus dermatitis occur frequently in such flocks. Some live
(IBDV) was first described in Gumboro, Delaware in vaccines may have a similar potential for damage as
1962, hence the IBDV-related clinical problems and field infections.
associated conditions are often referred to as “Gumboro
7. The passive transfer of maternal antibodies to baby
disease”. The immunosuppressive effects of IBD were first
chicks is very important for the prevention of early
reported by Allan in 1972. For years IBD was successfully
infections with the virus. Breeder flocks must receive
controlled with “classic” vaccines based on early IBD
vaccines or field exposure to the virus followed by
isolates. Variant strains of serotype 1 IBD were found in
booster vaccinations to stimulate high levels of maternal
the Delmarva region in the 1980’s. In the United States
antibody. Progeny from well-immunized breeder flocks
the disease is a persistent problem in the broiler industry
may resist infection for 2-3 weeks. Passive immunity
despite vaccination. Very virulent strains of IBD have been
will interfere with vaccinations and it is necessary to
reported in The Netherlands, Africa, Asia, South America
vaccinate chickens after maternal immunity has fallen
and the United States.
to a point that the vaccine will overcome the lower
levels of maternal antibody.
ETIOLOGY
1. IBD is caused by a double-stranded RNA virus CLINICAL SIGNS
belonging to the genus Avibirnavirus of the family 1. Clinical disease is observed only in birds infected after
Birnaviridae. The viral genome has two double- 3 weeks of age. There is a sudden onset, particularly
stranded RNA segments. The virus may be propagated with the first outbreak. There may be tremor or
in chicken embryos or chicken embryo cell cultures. unsteadiness. There is depression, anorexia, ruffled
Two serotypes exist, with only serotype 1 being feathers, and a droopy appearance (Fig. 1) that
pathogenic. resembles coccidiosis.
2. The virus is very resistant to environmental factors 2. Diarrhea and dehydration are usually present.
and many disinfectants. It can persist for months in Occasionally there is voiding of blood and straining
during defecation. Vent picking is common and may 2. PCR, paired serologic testing with rising titers using
be self-inflicted. the ELISA, agar-gel precipitin, or virus neutralization
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3. Morbidity is very high. Mortality is usually low although can be used to confirm the diagnosis.
it can be substantial (approaching 30%) if husbandry is 3. PCR and various molecular typing assays, antigen-
poor or if strains are particularly virulent. Mortality in a capture enzyme immunoassay with monoclonal
flock has usually peaked and receded within a week of antibodies and virus neutralization assay can also be
onset. IBD tends to be more severe in leghorn strains used to differentiate among serotype 1 subtypes.
than in broiler stock.
CONTROL
LESIONS 1. Vaccination of breeders to confer immunity to progeny
1. In the acute phase, the bursa is very enlarged with is an effective method of reducing the disease in
subserosal edema (Fig. 2) and mucosal to transmural young chicks. Vaccination programs typically include
petechial (Fig. 3) to ecchymotic hemorrhage. Caseous “priming” with live vaccines and “boosting” with
exudate may be found in the lumen of the bursa as a inactivated oil-emulsion vaccines to produce high and
result of the extensive necrosis and inflammation of the long-lasting levels of antibody in breeders.
bursal follicles during the acute phase of the disease 2. Chicks can be vaccinated against the disease but
(Fig. 4). The swelling recedes by the 5th day and the timing the vaccination in maternally immune chicks
bursa atrophies rapidly until 8-10 days post infection can be difficult. When maternal antibodies wane, use
(Fig. 5). There is increased mucus in the intestine. of “hot” vaccines in nonimmune chicks may result in
2. Petechial and echymotic hemorrhages are common in bursal atrophy. Vaccination with milder vaccines will
thigh (Fig. 6) and pectoral muscles and, sometimes at not be effective in birds with high levels of maternal
the junction of the proventriculus and gizzard. antibody. Therefore, knowledge of passive antibody
3. Kidneys may be swollen and the ureters may contain levels and correct timing are necessary for successful
urates. The spleen can be slightly enlarged and vaccination.
contain small pale foci. 3. An in ovo immune complex vaccine is available that
4. Necrotic lesions/atrophy may also be found in other results in decreased vaccine pathogenicity without
lymphoid tissues such as the thymus, Harderian loss of immunogenicity.
gland, cecal tonsils and Peyer’s patches, particularly 4. Sanitation programs are rarely successful due to the
with highly virulent IBD strains. highly resistant nature of the virus.
5. Microscopically, in the bursa there is marked lymphoid
TREATMENT
follicle necrosis with heterophil rich cellular infiltrates,
Good husbandry may reduce the severity of the disease.
edema and hyperemia (Fig. 7) followed by atrophy and
interfollicular fibroplasia (Fig. 8). Transient lymphoid
necrosis occurs in the spleen, thymus, cecal tonsils ZOONOTIC POTENTIAL
and Harderian gland. The renal lesions are non- None reported.
specific with tubular casts of protein and sometimes
heterophils and are likely secondary to dehydration.
6. Some variant strains of the virus cause few clinical
signs and minimal gross acute changes in the
bursa. However, these variant strains may induce
follicular lymphoid necrosis without the inflammatory
component and rapid bursal atrophy and severe
immunosuppression.
7. IBD infection results in immunosuppression, so
birds are more susceptible to secondary infections
such as gangrenous dermatitis, IBH, coccidiosis,
etc. Historically, IBH was preceded by an
immunosuppressive infection such as IBD but recently
IBH has been recognized as a primary disease.
DIAGNOSIS
1. In an acute outbreak in susceptible chicks, the short
course and bursal lesions are very suggestive of IBD.
Signs and lesions can be less apparent in subsequent
outbreaks and in chicks with parental antibody.
VIRAL DISEASES 57
INFECTIOUS BURSAL DISEASE

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Fig. 1 Fig. 2
Broiler chicken showing depression, ruffled feathers, and a droopy Swollen and edematous bursa. By the 2nd or 3rd day postinfection,
appearance. the bursa is covered with a gelatinous yellowish transudate.
Fig. 3 Fig. 4
Enlarged bursa with mucosal petechiation. Caseous exudate in the lumen of
the bursa as a result of the extensive
necrosis and inflammation of the
bursal follicles during the acute
phase of the disease.
Fig. 5
Bursas of Fabricius showing edema (on the right) and atrophy (on
the left). The middle bursas are showing some degrees of subserosal Fig. 6
edema. Petechial and echymotic hemorrhages in thigh muscles.
INFECTIOUS BURSAL DISEASE

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Fig. 7
Microscopically there is marked lymphoid follicle necrosis with
heterophilic infiltration, edema and hyperemia of bursa (on the
right). The bursa on the left is normal. Fig. 8
Microscopic lesions showing atrophy and interfollicular fibroplasia
of the bursa.
VIRAL DISEASES 59
INFECTIOUS LARYNGOTRACHEITIS LESIONS

1. Infected birds often have blood exuding from the
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DEFINITION nostrils, mouth or staining the feathers of the face and

Infectious laryngotracheitis (ILT) is an acute viral disease of neck. With milder strains of ILT virus, only swollen
chickens, and, rarely, pheasants and peafowl characterized eyelids (Fig. 3) and ocular and nasal discharge may
by marked dyspnea, coughing, gasping, and expectoration be seen.
of bloody exudate. 2. Lesions are most common in the nasal turbinates,
sinuses, conjunctiva, larynx and trachea. Lesions are
OCCURRENCE variable and depend upon the virulence of the virus.
ILT is worldwide in distribution. Most outbreaks in chickens There may only be edema and congestion of the
occur in broilers more than 4 weeks of age or in mature conjunctiva, nasal and sinus epithelium and reddening
or nearly mature chickens, although all age groups are of the tracheal mucosa with serous or mucoid
susceptible. exudates. With more pathogenic strains of ILT virus,
the tracheal mucosa will be congested, hemorrhagic
and roughened with mucoid or mucohemorrhagic or
ETIOLOGY fibrinonecrotic exudates (Fig. 4) sometimes with the
ILT is caused by a DNA virus belonging to the genus formation of tracheal casts (Fig. 5) that can result
Iltovirus of the family Herpesviridae. The virus is sensitive in tracheal occlusion and death from suffocation.
to many disinfectants and is not highly resistant outside of Inflammation may extend into the primary bronchi and
the host. There appears to be only one immunologic strain, airsacs.
although strains vary considerably in pathogenicity.
3. Microscopical lesions are those of epithelial erosion
and ulceration of the conjunctiva, nasal turbinates
EPIZOOTIOLOGY and sinuses, larynx, trachea and primary bronchi with
Some recovered chickens and vaccinated chickens formation of multinucleated syncytial cells containing
become carriers and will shed virus for long periods of the characteristic eosinophilic intranuclear herpesvirus
time or much later can shed virus following stress-induced inclusions (Fig. 6). Luminal exudate includes mucus,
reactivation of latent infections, thus exposing other proteinaceous fluid, heterophils, macrophages, red
susceptible birds. Mechanical transmission of virus via blood cells, sloughed syncytia of epithelial cells
fomites also is possible. The disease spreads horizontally bearing intranuclear herpesvirus inclusions (Fig. 7).
via the respiratory tract after it has been introduced. The lamina propria is generally inflamed, congested
However, spread is often less rapid than with other viral and sometimes focally hemorrhagic.
respiratory diseases of chickens. There is no evidence of
vertical transmission. DIAGNOSIS
The signs and lesions of the pathogenic type of ILT are
distinctive enough to incite suspicion of ILT. However, there
CLINICAL SIGNS
may be few signs and lesions with ILT of low pathogenicity.
Signs of markedly pathogenic ILT ILT can usually be confirmed by one or more of the following
5. There is marked dyspnea (Fig. 1), often with loud steps:
gasping sounds and coughing. Severely affected
chickens often raise and extend their head and neck 1. Demonstration of the characteristic multinucleated
during inspiration (Fig. 2) and make loud wheezing epithelial syncytial cells bearing eosinophilic
sounds. intranuclear herpesvirus inclusions in tissues including
6. Expectoration of bloody mucus may occur as a conjunctiva, nasal turbinates, larynx and trachea
consequence of coughing and head shaking. Beaks, histologically during early stages of the disease.
faces, or feathers of occasional birds may be bloody. 2. Demonstration of viral antigen or DNA in clinical
7. High morbidity and considerable mortality are common. samples, usually tracheal epithelium, by the use of
Morbidity as high as 50-70% has been reported but the fluorescent antibody, immunoperoxidase, electron
mortality usually is in the 10-20% range. There is also microscopy, DNA hybridization techniques, antigen
lowered egg production. The disease often persists for capture ELISA and PCR.
as long as 2-4 weeks in the flock, a course longer than 3. Growth of the virus on the chorioallantoic membrane
that of most viral respiratory diseases of chickens. of embryonating chicken eggs. Typical plaques are
produced and inclusion bodies can be demonstrated
Signs of ILT of low pathogenicity in them by histologic means and by the fluorescent
1. Signs often include hemorrhagic conjunctivitis with antibody technique.
watery eyes, lacrimation, persistent nasal discharge,
swollen infraorbital sinuses, generalized unthriftiness 4. Exposure of known-immune and known-susceptible
and lowered egg production. chickens to virus.
CONTROL
1. Avoid adding vaccinated, recovered, or exposed birds
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to a susceptible flock because these birds may include

recovered carrier birds with latent infections. Better
yet, raise susceptible flocks in strict quarantine and
never add birds of any kind.
2. Premises contaminated with laryngotracheitis virus
should be depopulated, cleaned, disinfected, and left
vacant for 4-6 weeks before being used again. Due to
the heat-labile nature of the virus, virus destruction is
enhanced by heating the contaminated poultry house
(38°C for 72 hours).
3. In areas where ILT is endemic, vaccination of layers is
frequently practiced and is quite effective. Attenuated
vaccines are available and can be administered by Fig. 1
eyedrop, in the drinking water, or by aerosol spray. Broiler chicken with marked dyspnea.
Drinking water vaccination may not be reliable
because it depends upon the vaccine contacting nasal
epithelium with high virus titers. Birds vaccinated prior
to 10 weeks of age should be revaccinated at 10 weeks
of age or older to confer lifelong immunity. Vaccination
of broilers, when indicated, should be done before 4
weeks of age to minimize losses from severe vaccine
reaction. Do not mix ILT vaccines with other vaccines.
4. Rarely, clinical ILT, indistinguishable from the natural
disease, may occur 1-4 weeks after vaccination. These
vaccine-related episodes are usually characterized by
low morbidity and mortality.
5. ILT is a reportable disease in some states and
provinces.
TREATMENT
There is no effective treatment. However, vaccination of
unaffected birds and those in other houses on an infected
Fig. 2
farm may provide protection and stop the outbreak. Severely affected chicken raising and extending its head
and neck during inspiration.
ZOONOTIC POTENTIAL
None reported.
Fig. 3
Chicken with swollen eyelids.
VIRAL DISEASES 61
INFECTIOUS LARYNGOTRACHEITIS
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Fig. 4
Hemorrhagic tracheal mucosa with fibrinonecrotic exudate.
Fig. 5
Formation of tracheal casts that resulted in tracheal occlusion and
death from suffocation.
Fig. 7
Fig. 6 Micrograph of the tracheal lumen debris from a case of
Trachea with formation of multinucleated syncytial cells containing laryngotracheitis. Note the numerous intranuclear inclusion bodies
the characteristic eosinophilic intranuclear herpesvirus inclusions. in sloughed epithelial cells and synctia formation (40X).
NEWCASTLE DISEASE a. Lentogenic—these are mildly pathogenic

(examples: B-1, F, LaSota).
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DEFINITION b. Mesogenic—these are moderately pathogenic.

Newcastle disease (ND) is a viral disease of many kinds c. Velogenic—these are markedly pathogenic
of poultry, wild and cage birds characterized by marked (examples: Milano, Herts, Texas GB).
variation in morbidity, mortality, signs and lesions. For the
purposes of policies, control measures and international Most enzootic APMV-1 strains are lentogenic or mesogenic.
trade, ND is currently defined as: “an infection of birds Vaccines prepared from lentogenic strains tend to produce
caused by a virus of avian paramyxovirus 1 (APMV-1) that immunity that is weak and of short duration so that
meets one of the following criteria for virulence: frequent revaccination is necessary to maintain immunity.
Conversely, more pathogenic (mesogenic) strains used for
a. The virus has an intracerebral pathogenicity index vaccine tend to produce longer, stronger immunity but may
(ICPI) in day-old chicks (Gallus gallus) of 0.7 or produce mortality in unthrifty chickens and are not used
greater, or in the United States. All velogenic strains are classified as
select agents in the US.
b. Multiple basic amino acids have been
demonstrated in the virus at the C-terminus of
the F2 protein and phenylalanine at residue 117, EPIZOOTIOLOGY
which is the N-terminus of the F1 protein.” 1. Virus-containing excretions from infected birds,
including aerosols and feces, can contaminate feed,
OCCURRENCE water, footwear, clothing, tools, equipment, and the
The disease usually occurs in chickens or (less often) in environment. Exposure of susceptible birds to any
turkeys, although most poultry and many wild and cage of these sources of virus can result in transmission
birds are susceptible. All age groups are susceptible. The via inhalation or ingestion. Also, infected poultry may
disease occurs in all poultry-raising countries. Natural or spread the virus if their tissues are used without proper
experimental infection has been demonstrated in at least processing in rendered products.
241 bird species. 2. Eggs laid by infected hens may contain virus. Such
eggs seldom hatch and few are laid due to cessation
HISTORICAL INFORMATION of production caused by NDV infection. If they are
1. ND first appeared in Java, Indonesia and Newcastle- accidentally broken in the hatcher, the entire hatch
upon-Tyne, England in 1926. Within 10 years it had of chicks may be exposed. The exposed, apparently
spread to many countries throughout the world. The normal chicks may then be divided into small lots of
disease persists in many countries and in its velogenic birds and widely disseminated before the disease
form is one of the most devastating diseases of poultry, becomes apparent.
with mortality up to 100% in chickens. 3. Live-virus vaccines may constitute a reservoir of
2. APMV-1 strains of low to moderate virulence have APMV-1. Chickens often shed the vaccine virus.
been present in the United States since about 1940. There is no evidence that attenuated viruses regain
In chickens these forms are well controlled by often- their virulence through passage.
repeated vaccinations. These forms have seldom 4. At various times APMV-1 has been isolated from
been a major problem except in chickens. sparrows, pigeons, doves, crows, owls, and waterfowl.
3. Velogenic ND, the most pathogenic type, occurred in Recent experience suggests these birds do not play a
the United States in 1941, 1946, and 1951 but was significant role in the spread of ND.
quickly eradicated. Extensive outbreaks began in
California (and other locations) in 1971 and 2002 and CLINICAL SIGNS
were eradicated at great expense ($52M and $170M, Based on clinical signs in infected chickens strains of
respectively). APMV-1 have been grouped into five pathotypes:
4. It has become apparent that velogenic ND is usually 1. Asymptomatic enteric: subclinical enteric infection;
introduced by imported cage birds or fighting cocks, in
many instances by illegally introduced birds. 2. Lentogenic or respiratory: mild respiratory infection;
3. Mesogenic: respiratory signs and occasional nervous
ETIOLOGY signs with low mortality;
The causative agent of ND is APMV-1, a single-stranded
RNA virus belonging to the genus Avulavirus of the family 4. Neurotropic velogenic: respiratory and nervous signs
Paramyxoviridae. The many known strains of APMV-1 with high mortality;
vary greatly in pathogenicity and are often referred to as: 5. Viscerotropic velogenic: hemorrhagic intestinal lesions
are frequently seen with high mortality.
VIRAL DISEASES 63
Adult chickens - Lentogenic APMV-1 infection Young chicks - Velogenic APMV-1 infection
A. May not produce any clinical signs at all, or may A. Signs are similar to those induced with mesogenic
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produce mild respiratory signs and decreased strains in young birds but mortality is very high
egg production in laying flocks. A few eggs may (50-100%) and the course is more acute.
be soft-shelled, roughened, or deformed. B. In wild and cage birds, APMV-1 infection often is
Adult chickens - Mesogenic APMV-1 infection inapparent. Signs, when apparent, are variable
but often include gasping respiration, diarrhea,
A. Sudden onset with mild depression and anorexia.
and later signs of CNS involvement. Sudden
Respiratory signs usually occur but may be in a
deaths are often the first indication of ND.
mild or inapparent form. Mortality is low or absent.
B. Signs suggestive of CNS disease may occur in a LESIONS
few birds but often do not appear. Lentogenic and mesogenic APMV-1 infection
C. In layers, production almost completely ceases A. Usually gross lesions are minimal in young or old
within a few days. Eggs laid are of low quality birds although there may be mild conjunctivitis,
and may be soft-shelled, roughened, or deformed rhinitis, tracheitis (Fig. 3) and airsacculitis that
(Fig. 1). Production is resumed slowly, or not at can be complicated with secondary bacterial
all, depending on the stage of lay at the time of infections such as Escherichia coli resulting in
infection. colisepticemia, pneumonia and airsacculitis. With
mesogenic strains, a drop in egg production may
Adult chickens - Velogenic APMV-1 infection be reported.
A. Signs vary according to tropism of the virus.
Dyspnea often is marked. There is violent B. Microscopically, there is deciliation, necrosis,
diarrhea, conjunctivitis, paralysis, and death in 2-3 attenuation of the respiratory epithelium with
days in many chickens. There may be swelling infiltration of the lamina propria by a mixture of
and darkening of tissues about the eyes with mononuclear cells with fewer heterophils. Luminal
sticky ocular and nasal discharge. Some birds exudate is composed of exfoliating epithelial cells,
that survive a few days may exhibit signs of CNS some mucus and a mixture of inflammatory cells,
involvement (e.g., tremors, twisting of the head Velogenic APMV-1 infection
and neck, circling, paresis, paralysis, terminal A. Ocular and respiratory lesions include conjunctival
clonic spasms). Morbidity and mortality are high— hemorrhage (Fig. 4), edema, hemorrhage,
up to 100%. congestion and necrosis of the tracheal epithelium
Young chicks - Lentogenic APMV-1 infection (Fig. 5) with paratracheal edema most often
A. Broilers may show sudden onset of respiratory observed near the thoracic inlet and inflammation
signs including gasping (Fig. 2), sneezing, of the air sacs, with catarrhal or fibrinoheterophilic
coughing, rales, and nasal and lacrimal discharge. exudates if complicated with a secondary bacterial
Some birds may have swollen heads. Even mild infection such as E. coli.
B1 strain vaccines may cause these signs in B. Facial edema (Fig. 6) with hemorrhage and
broilers with low immunity. epidermal necrosis and congestion and petechial
hemorrhage of the comb and wattles has been
Young chicks - Mesogenic APMV-1 infection described.
A. Sudden onset with marked depression and
C. Focal to locally extensive hemorrhage and/or
prostration. Marked respiratory signs that include
necrosis in the oral-pharyngeal and esophageal
gasping, coughing, hoarse chirping, and nasal
mucosa can be prominent (Fig. 7).
discharge.
D. Hemorrhages occasionally occur in the mucosal
B. Signs of CNS disease may accompany or closely
surface of the proventriculus (Fig. 8) or in the
follow the onset of respiratory signs. Abnormal
gizzard, Peyer’s patches, of the small (Fig. 9) and
positions of the head and neck (“star gazers”) are
large intestine and the cecal tonsils (Fig. 10). There
common. Usually only a modest number (0-25%)
can be focal necrosis of the spleen. Mature birds
show CNS signs.
in production can have egg yolk in the abdominal
C. Eventually there is paralysis, prostration, trampling cavity and ovarian follicles are regressing with
by pen-mates, and death. Mortality can be very hemorrhagic stigmata.
high (up to 50%) regardless of whether CNS signs
E. With peracute mortality, gross lesions can be
occur.
minimal.
F. Microscopic lesions in the CNS include
nonsuppurative encephalomyelitis with
neuronal degeneration, perivascular cuffing with ZOONOTIC POTENTIAL

lymphocytic cells, multifocal gliosis and endothelial Humans who come in close contact with APMV-1 may
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hypertrophy. Vascular lesions include medial develop a temporary, localized eye infection (conjunctivitis).
degeneration, microvascular hyalinization and There were suggestions that a more generalized infection
thrombosis, endothelial necrosis with widespread resulting in chills, headaches and fever may sometimes
congestion, hemorrhage and edema. Primary occur, with or without conjunctivitis. Human-to-human
and secondary lymphoid organs show marked spread has not been described.
lymphocyte necrosis sometimes associated with
hemorrhage. In the respiratory system, there is
widespread decilation of the tracheal epithelium
with mucosal congestion, edema and hemorrhage
and marked lymphohistiocytic cellular infiltrates in
the lamina propria. Multifocal lymphoid infiltrates
in the pancreas has been reported.
DIAGNOSIS
Clinical diagnosis based on history, signs, and lesions may
establish a strong index of suspicion once ND has been
positively identified in an area, but laboratory confirmation
should always be pursued in order to identify the strain.
Laboratory diagnosis typically includes:
1. Virus isolation and subsequent pathogenicity testing,

2. RT-PCR – demonstration of viral RNA and subsequent
typing,
3. Serology - demonstration of increasing titer of
Newcastle antibody in the flock from onset to
convalescence by ELISA or HI.
APMV-1 hemagglutinates the erythrocytes of many
species, including those of many birds. Hemagglutination
and hemagglutination inhibition tests are helpful in virus
identification.
CONTROL
1. Chickens and turkeys can be immunized against
ND by proper vaccination. The method of vaccine
administration has considerable influence on the
immune response. Low-virulence live-virus vaccines
are administered by a variety of routes and schedules
from hatching through grow-out. Killed-virus oil-
emulsion vaccines are administered parentally as
a final vaccine prior to the onset of egg production.
Although proper vaccination protects the birds from
serious clinical disease it does not prevent virus
replication and shed, which could be a source of
infection to other flocks.
2. Stringent laws are in effect pertaining to the importation
of poultry, poultry products, and cage birds. However,
enforcement is often a difficult and nebulous problem.
3. ND is a reportable disease. All suspected outbreaks
of ND must be reported to animal health authorities
immediately.
TREATMENT
No treatment available.
VIRAL DISEASES 65
NEWCASTLE DISEASE
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Fig. 1
Soft-shelled, roughened and deformed eggs. Fig. 2
Severe dyspnea and gasping in a young broiler
chicken affected with Newcastle disease.
Fig. 3
Severe tracheitis in a broiler
chicken affected with lentogenic
Newcastle disease. Note the Fig. 4
tracheal cast in the lumen. Conjunctival hemorrhage.
Fig. 5 Fig. 6
Diphteritic laryngotracheitis. Facial edema in a young broiler.
NEWCASTLE DISEASE
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Fig. 7
Diphtheritic oro-pharyngo-esophagitis. Fig. 8
Proventricular hemorrhages.
Fig. 9
Small intestine hemorrhage. Fig. 10
Cecal tonsil necrosis.
VIRAL DISEASES 67
VIRAL ARTHRITIS is swelling and discoloration of the skin over the site of
tendon rupture (Fig. 3).
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DEFINITION LESIONS
Avian reoviruses have been associated with several 1. In chickens, in the acute phase of the disease there
poultry disease conditions including enteric and respiratory is typically bilateral swelling and inflammation of the
syndromes, hepatitis and so-called stunting/malabsorption tendons and tendon sheaths just above the hock and
syndrome. However, a direct link between the virus and a along the posterior aspect of the shanks. The tendon
disease has only been demonstrated for viral arthritis. sheaths are edematous and the hock joints may
contain small amounts of yellow coloured or blood
Viral arthritis is a reovirus infection primarily of meat-type tinged exudates (Fig. 4). The articular cartilages of the
chickens characterized by arthritis and tenosynovitis hock may be eroded and the synovial membranes of
(primarily of the tarsus and metatarsus) and, occasionally, the hock and tendons are thickened, edematous and
by rupture of the gastrocnemius tendon(s). may contain hemorrhages (Fig. 5).
2. Chickens that cannot extend the hock often have
OCCURRENCE rupture of the gastrocnemius tendon, usually just
Viral arthritis occurs primarily in meat-type chickens with above or over the hock joint with green discolouration
rare reports of the disease in egg-type chickens and of the skin and subcutaneous tissues as a result of the
turkeys. hemorrhage. This is especially true of older, heavier
birds.
HISTORICAL INFORMATION 3. In chronic cases there is usually less inflammatory
Viral arthritis was first reported in 1957. Since then there exudate and more fibrosis of affected tendons and
have been numerous reports on the disease and much tendon sheaths with fusion.
has been learned about it and the virus that causes it.
Viral arthritis is of special importance to the broiler industry 4. Turkeys with viral arthritis show lameness, swollen
because broilers frequently are infected. hock joints and ruptured tendon.
5. Microscopically, in experimental infections during the
Numerous turkey flocks in North Central United States acute phase, there is thickening of the tendon sheaths,
have been experiencing turkey viral arthritis since 2009. with synoviocyte proliferation, infiltration of lymphocytes
and macrophages. The synovial spaces contain
heterophils, macrophages, exfoliating synoviocytes
ETIOLOGY
and there is periostitis. In the chronic phase, there is
Avian reoviruses are double-stranded RNA viruses
synovial villous hyperplasia, formation of subsynovial
belonging to the genus Orthoreovirus of the family
lymphoid nodules, increase in fibrous connective tissue
Reoviridae. The reovirus is quite resistant to many
and marked infiltration of lymphocytes, macrophages
environmental factors.
and plasma cells with fibrosis of tendons and tendon
sheaths leading to eventual fusion (Fig. 6). Myocardial
EPIZOOTIOLOGY lesions include multifocal infiltrates of heterophils,
Reovirus is discharged in the feces of infected chickens sometimes with populations of mononuclear cells
and may contaminate eggshells. It is transmitted laterally between myofibres.
to susceptible chickens. Egg transmission has been
demonstrated. Reovirus is known to persist in infected DIAGNOSIS
birds for at least 289 days. Age-associated resistance has 1. A tentative diagnosis often can be made on the basis
been described. of history and bilateral enlargement of the tendon
sheaths of the shanks and histological confirmation of
the inflammation of the tendon sheaths and tendons
CLINICAL SIGNS
and myocardial infiltration of heterophils sometimes
1. Lameness and swelling of the tendon sheaths of the
accompanied by mononuclear cells.
shanks and of the gastrocnemius tendon above the
hock are early signs (Fig. 1). The shanks of affected 2. The presence of the virus can be confirmed by
chickens are enlarged. Many infected birds are in good isolation of the virus in chicken liver and kidney cell
condition but some are unthrifty and stunted. Mortality cultures or chicken embryos, by RT-PCR and by direct
usually is quite low. fluorescent antibody test.
2. If the gastrocnemius tendon has been ruptured, the 3. If acute and convalescent sera can be obtained it may
affected foot cannot be extended and the bird cannot be possible to demonstrate seroconversion reovirus
bear weight on the affected leg. If both tendons are using the agar-gel precipitin test or ELISA. Antibody
ruptured, the bird is immobilized (Fig. 2). There usually may disappear as early as 4 weeks post-infection in
some birds but it persists in birds with joint involvement.
4. It is essential to exclude other causes of lameness poultry-raising areas, and the resistance of the virus
including mycoplasmosis (especially infectious to inactivation, prevention of this disease should be
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synovitis), staphylococcal and other bacterial directed at preventing early infection.

arthritides such as salmonellosis, and pasteurellosis
and bone deformities, and certain nutritional diseases. TREATMENT
It should be remembered that dual infections can exist. No treatment is available.
CONTROL ZOONOTIC POTENTIAL

1. Vaccination of breeder flocks with live and inactivated None reported.
vaccines results in protection of 1- day-old chicks.
2. Due to the age-associated resistance to disease after
2 weeks, the ubiquitous distribution of the virus in
VIRAL DISEASES 69
VIRAL ARTHRITIS
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Fig. 1 Fig. 2
The tendon sheaths of the shank and above the hock are markedly Chickens with clinical signs of viral arthritis
swollen. “tendinitis”/”tenosynovitis” tend to sit and are reluctant to move.
Fig. 3
Fig. 4
Swelling and discoloration of the skin over the site of tendon
Ruptured gastrocnemius
rupture.
tendon with hemorrhage.
Fig. 6
On the right; infected tendon sheaths from the digital flexor tendons
of the shank of a chicken with viral arthritis showing thickened
Fig. 5 synovium due to hyperplasia of synovial cells and connective tissue
Starting at about 42 days post-infection, erosions with extensive accumulation of lymphocytes, plasma cells and
appear in the cartilage of the posterior and distal tibia. heterophils in the synovial cavity. Normal tendon sheath on the left
(H&E, 30X).
TURKEY CORONAVIRUS ENTERITIS 3. Good husbandry and supplemental heat tend to

suppress mortality. Mortality varies with the age of the
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DEFINITION birds affected and can range from 5 to 50% in natural

Enteritis caused by a turkey coronavirus (TCV) is an acute, infections.
highly infectious disease of turkeys, especially poults, 4. The course of the disease in a flock is around 2 weeks.
characterized by anorexia, diarrhea, dehydration, and Recovery may be prolonged, particularly in males, and
variable mortality. the flock may become uneven in size.
LESIONS
OCCURRENCE 1. Marked dehydration and emaciation may be seen.
The disease occurs throughout the year in turkeys of all
ages, but is seen more frequently in young turkeys. It is 2. The small intestine is thin-walled and distended with
recognized in the United States, Canada, Australia, Brazil, foamy yellow fluid content (Fig. 1).
Italy and United Kingdom. 3. The bursa of Fabricius is often small.
4. Histologically, within the small intestine, there is
HISTORICAL INFORMATION prominent villus atrophy and sloughing of intestinal
Coronavirus enteritis was first reported in 1951 in villi with cryptal hyperplasia and moderate lymphoid
Washington and shortly thereafter in Minnesota. Historically and heterophilic infiltration of the superficial and deep
it was also called “blue comb” and “mud fever”. lamina propria.
5. There is necrosis of the superficial bursal epithelium
ETIOLOGY with heterophils within and beneath the epithelium and
1. Turkey coronavirus belongs to family Coronaviridae. moderate depletion of lymphoid follicles.
Viral particles are enveloped, pleomorphic but often
spherical and 80-160 nm in diameter. Genetic material DIAGNOSIS
of the virus is a single-stranded positive sense RNA. 1. The history, signs, and lesions are suggestive of the
diagnosis.
2. Under experimental conditions the virus is readily
destroyed in batteries and cages. Destruction of the 2. The virus can be isolated in embryonating eggs and
virus is more difficult under natural conditions because can be identified by electron microscopy (EM). EM
it survives well in frozen feces. can also be used to detect virus particles in intestinal
contents. Immunohistochemistry can detect TCV
3. A number of other enteric viruses including rotavirus, antigens (Fig. 2).
reovirus, astrovirus, enterovirus, and calicivirus have
been identified from turkey feces. Their role in enteritis 3. RT-PCR has been described as a sensitive and
is still not fully understood. specific diagnostic test for detection of viral nucleic
acid.
EPIZOOTIOLOGY 4. ELISAs have been used to detect antibodies against
The virus spreads by contact of susceptible birds with TCV.
infected birds or their feces. Once introduced into a flock,
the disease spreads rapidly among susceptible birds. The 5. In differential diagnosis one should consider the
virus is shed in the feces of recovered birds for several following diseases:
weeks. Further, the virus persists in frozen feces for several Young Poults Growing and Mature Turkeys
months. There is no evidence that the virus is transmitted (Less than 7 weeks)
vertically. Salmonellosis Erysipelas
Hexamitiasis Trichomoniasis
Starve outs Hemorrhagic enteritis
CLINICAL SIGNS
(very young birds only)
1. In young poults the signs appear suddenly after an
Coccidiosis
incubation period of 1-5 days. Signs include anorexia,
depression, frothy diarrhea, subnormal temperatures,
darkening of the head and skin, and loss of weight. CONTROL
Birds tend to huddle around heat sources. Spread is 1. No licensed vaccine is available for immunization;
rapid and morbidity is close to 100%. therefore prevention is the preferred method of control.
2. The signs seen in young poults may also be observed in 2. Turkeys should be reared under the all-in, all-out
laying turkeys but usually are less marked. Moreover, system. Use quarantine and a high standard of
there is a sudden decrease in egg production and sanitation to prevent introduction of the virus.
some eggshells are chalky. 3. If the disease has been present in prior broods,
thoroughly clean and disinfect the premises after
VIRAL DISEASES 71
complete depopulation. Leave the premises empty

for at least a month, perhaps longer during the winter
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season.
TREATMENT
No treatment is available.
ZOONOTIC POTENTIAL
None reported.
Fig. 1 Fig. 2
The small intestine is thin-walled and distended with fluid content. Immunohistochemistry of the intestines.
TURKEY VIRAL HEPATITIS usually more evident later in the course of the disease
and on the dorsal side of the pancreas.
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DEFINITION 3. Microscopically, inclusion bodies have not been

Turkey viral hepatitis is a contagious, often subclinical identified. The lesions observed grossly are found
disease of turkey poults characterized by lesions in the to be focal areas of necrosis, which subsequently
liver and pancreas. become infiltrated with mixed inflammatory cells in
which lymphocytes and reticular cells predominate;
heterophils are present but not in high numbers.
OCCURRENCE
Syncytial cells arising from hepatocytes can often be
The clinical disease is seen only in turkey poults less than
found along lesion margins.
5 weeks old. Other birds and mammals appear not to be
affected. The disease has been observed in most turkey- DIAGNOSIS
producing areas of the world. 1. Typical lesions in both liver and pancreas are
diagnostic. If turkey viral hepatitis is suspected,
HISTORICAL INFORMATION both liver and pancreas need to be submitted for
Turkey viral hepatitis was first reported in 1959. histopathologic examination even if there are no visible
Subsequently, the disease has been reported in a number lesions in the latter; often microscopic lesions can be
of states and countries but has seldom been associated found in the pancreas in the absence of gross lesions.
with severe mortality. Incidence and distribution is difficult If lesions are present only in the liver, they will have to
to evaluate due to the subclinical nature of the disease. be differentiated from those of blackhead and systemic
bacterial infections.
ETIOLOGY 2. Isolation and identification of the virus can be used for
The etiologic agent is a virus that has been suggested to confirmation. An agar-gel precipitin test using rabbit
be a picornavirus based on its molecular, immunologic and antisera to the virus has been developed but is not in
morphologic features. It can be grown in the yolk sac of general use.
5-7-day-old chicken or turkey embryos. Embryo mortality
occurs in 4-10 days. The virus rarely achieves high titers CONTROL
despite repeated embryo passages. Young turkey poults 1. A high standard of sanitation along with proper nutrition
can be infected following parenteral inoculation of infective and good husbandry should minimize the effects of the
tissue suspensions. disease. There is no vaccine for prevention. Treatment
of concurrent diseases is important.
2. Eggs from infected flocks should not be used
EPIZOOTIOLOGY
for hatching because there may be transovarian
Up to 28 days after infection, the virus can be isolated
transmission of virus.
consistently from feces and liver of infected poults.
Transmission readily occurs by direct or indirect contact of TREATMENT
susceptible poults. There is clinical evidence suggestive of There is no proven effective treatment. Fortunately, most
egg transmission of virus. well cared for flocks recover in a few weeks.
CLINICAL SIGNS
The disease is usually subclinical. It may be that signs are
apparent only if there are other concurrent diseases or
stresses on the poults. Infected flocks in the early stages of
the disease show variable depression with sporadic deaths
of well-fleshed birds. Morbidity varies greatly. Mortality is
usually very low (>5%) but has been as high as 25% during
a 7-10 day period in occasional flocks.
LESIONS
1. In the liver, there are focal gray areas 1 mm or more
in diameter that may coalesce (Fig. 1). Lesions are
often slightly depressed and can be concealed by
congestion and focal hemorrhages. Bile staining may
be apparent.
2. In the pancreas, lesions are less consistent and
appear as focal gray to pink areas (Fig. 2). They are
VIRAL DISEASES 73
TURKEY VIRAL HEPATITIS

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Fig. 1 Fig. 2
Focal gray areas 1 mm or more in diameter in the liver. In the pancreas, focal gray to pink areas of necrosis.
BACTERIAL DISEASES 4. During the last decade Chlamydophila psittaci

outbreaks have occurred relatively infrequently among
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Revised by Richard M. Fulton, new sections on Campylo- birds and humans. However, in 1974-1975 there
bacter and E. cecorum by Martine Boulianne were at least 11 outbreaks in turkey flocks, mostly
in Texas. People were infected in at least seven of
the outbreaks. More recently, outbreaks in ducks
AVIAN CHLAMYDOPHILOSIS/ have been described. These outbreaks again have
focused attention on the public health aspects of avian
AVIAN CHLAMYDIOSIS chlamydiosis.
(Psittacosis; Ornithosis)
5. During the past few years chlamydiosis has been
recognized as a common and major problem in
DEFINITION
imported and domestic exotic birds.
Avian chlamydophilosis is a reportable, acute or chronic
infectious disease of poultry, many caged birds and wild ETIOLOGY
and migratory birds. In clinically ill birds, the disease is 1. In birds the etiologic agent is Chlamydophila psittaci
characterized by systemic, pulmonary, or enteric signs (Chlamydia psittaci). Chlamydia is closely related to
and lesions. The latent, inapparent chlamydial infection rickettsia.
has long been recognized as the predominant and most
important state in the zoonotic relationship between 2. C. psittaci can be grown in chicken embryos, cell
chlamydial agent, birds and humans. culture, mice, and guinea pigs. Chlamydia form
intracytoplasmic inclusion bodies in many kinds of
In the Psittacidae (parrots, parakeets, cockatoos, macaws, cells, including epithelial and macrophages, and
etc.) and humans, avian chlamydiosis is called psittacosis. inclusions can be demonstrated in stained smears
Historically, avian chlamydiosis has been called ornithosis (Fig. 1) and histologic sections. All chlamydia are
in other avian species. highly susceptible to tetracyclines. They are obligate
intracellular gram negative bacteria and cannot be
grown in artificial media.
OCCURRENCE
Chlamydophilosis occurs in many kinds and ages of 3. Isolates of C. psittaci vary greatly in pathogenicity.
birds. Most acute outbreaks are in young birds. Parrots, Concurrent infection, especially with Salmonella,
parakeets, cockatiels, and pigeons frequently are infected. sometimes enhances the pathogenicity of C. psittaci.
In poultry, occasional outbreaks occur in turkeys. Chickens Younger birds are more susceptible. Crowding or
seldom are affected. Severe outbreaks occasionally have otherwise unfavorable environmental conditions and
been reported in shorebirds and migratory birds. Important stress from shipping, racing, and handling contribute
outbreaks of psittacosis occasionally occur in humans, to the severity of the disease.
usually following exposure in poultry processing plants. 4. A common group-specific antigen is present in
The presence of wild pigeons in some cities in North all chlamydia. Antibody to that antigen can be
America, Europe, and Asia poses a major problem in demonstrated in the sera of exposed or sick birds after
efforts to control human chlamydiosis. an appropriate interval of time has elapsed.
EPIDEMIOLOGY
HISTORICAL INFORMATION 1. It is believed that wild birds that are carriers (and
1. Psittacosis is a significant public health concern. The cage birds) transmit chlamydia to their nestlings and
incidence in humans in the US appears to be on the some surviving nestlings in turn become carriers. A
decline since between 1987 through 1996 831 cases of delicate host-parasite relationship is established so
psittacosis were reported to the United States Center that stressed carriers intermittently shed chlamydia
for Disease Control while there has been fewer than in their secretions and excretions thus exposing other
50 cases reported per year since 1996. In the United susceptible birds.
States most human cases were related to exposure of
people to infected cage birds, especially parrots, or to 2. Chlamydiosis may become epizootic when large
sick turkeys in processing plants. numbers of birds, including disseminating carriers,
are in close contact. Transmission is primarily by
2. Some of the first recognized outbreaks of avian inhalation of chlamydia in fecal dust but also can result
chlamydiosis were in pigeons. Important outbreaks from ingestion of C. psittaci.
soon were recognized in turkeys and ducks.
3. It is suspected that wild birds may transmit chlamydia
3. Interest in chlamydiosis waned somewhat with the to poultry. Pigeons are strongly suspected of being
introduction of antibiotics that control mortality in important disseminators. Wild migratory birds such
people with the infection. as gulls, egrets, and ducks are known to excrete
chlamydia under certain conditions. Little is known of
BACTERIAL DISEASES 75
possible transmission of chlamydia between infected in demonstrating chlamydia. A definitive diagnosis

mammals and poultry but the chlamydia found in is usually obtained by isolation and identification of
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mammals are believed to be distinct from those in chlamydia organisms, genetic detection or by a fourfold
birds. rise in antibody titer to chlamydial group antigen.
CLINICAL SIGNS 2. Every precaution should be taken to avoid self-infection.

1. Mild outbreaks of avian chlamydophilosis result in few Psittacosis is highly contagious and many laboratory
signs and may go unrecognized. Alternatively, mild workers have been infected while handling infected
respiratory signs or diarrhea may be noted. birds or their tissues. Dead birds should be completely
immersed in effective disinfectant solutions because
2. In more pathogenic outbreaks in turkeys there is the highly infectious nasal and fecal secretions dried
depression, weakness, inappetence, and loss of weight on feathers can give rise to infectious aerosols.
and there may be nasal discharge and respiratory
distress. Frequently there is marked, yellowish-green 3. Chlamydophilosis in turkeys must be differentiated
carefully from Mycoplasma gallisepticum infection,
diarrhea. Similar signs occur in many other kinds of
influenza, aspergillosis, septicemic colibacillosis and
birds such as ducks, geese, and pigeons and may
cholera. Lesions in turkeys closely resemble those
reflect systemic, pulmonary, or enteric involvement. A
of M. gallisepticum infection. In general, diagnostic
watery diarrhea is noted in ducks, geese, and pigeons.
specimens from birds for chlamydia diagnosis should
An unbalanced gait has been reported in ducks,
geese, and pigeons. also be cultured for species of Salmonella, Pasteurella,
Mycoplasma, and other bacteria as well as viruses.
3. In pigeons, conjunctivitis often occurs and should
lead the diagnostician to suspect chlamydiosis. Other 4. Spleen, liver, lung, fibrinous exudate, air sacs, nasal
signs include depression, anorexia, diarrhea, or rales. washings and mucosa, fecal samples, or intestinal
The latter signs resemble those seen in many cage loops should be used for microbiologic or pathologic
birds with psittacosis. evaluation.
LESIONS CONTROL
1. Because there is no effective vaccine against
1. The basic lesions in chlamydophilosis are
chlamydophilosis, prevention of the disease in poultry
characterized by fibrinous response grossly with
depends upon avoidance of exposure. Facilities should
pleocellular infiltrate and necrosis histologically.
be cleaned and disinfected prior to use. Flocks should
These basic tissue responses may lead to pneumonia,
be started and raised as units and no birds should be
airsacculitis, hepatitis, myo- and epicarditis, nephritis,
added to a started flock.
peritonitis, and splenitis.
2. Poultry should not be exposed to other birds, especially
2. In turkeys the severity of lesions is in proportion to the
wild birds, animals, or their excreta. A preventive level of
pathogenicity of the strain of C. psittaci. In turkeys
tetracycline can be added to poultry rations if exposure
that succumb, there is wasting, vascular congestion,
of the flock is suspected or anticipated. Poultry farm
fibrinous pericarditis (Fig. 2), fibrinous airsacculitis,
workers should not own any pet birds or poultry.
and perhaps fibrinous perihepatitis. The lungs are
congested and often there is a fibrinous pneumonia. 3. Federal law specifies how commercial birds imported
The spleen is enlarged and congested, and may be for resale, research, breeding, or public display
the only lesion. must be handled. During the quarantine period, all
exotic birds of the psittacine family are treated with
3. In pigeons there is conjunctivitis with encrusted, swollen
chlortetracycline as a precautionary measure against
eyelids. There may be hepatomegaly, airsacculitis and
psittacosis. The quarantine period, designed to prevent
enteritis.
the introduction of velogenic Newcastle disease, is 30
4. In cage birds that succumb, the spleen frequently days and an effective treatment for chlamydophilosis
is enlarged and contains white foci. Often there is requires 45 days.
hepatomegaly with focal necrosis and yellowish
discoloration, airsacculitis, pericarditis, and congestion TREATMENT
of the intestinal tract. Avian chlamydophilosis is a reportable disease in most
states and must be reported to the state veterinarian or
DIAGNOSIS other designated officials. Flocks should be treated only
1. A tentative diagnosis can be made on history, signs, under supervision. Infected turkey flocks often have been
and lesions and the demonstration of intracytoplasmic treated with chlortetracyclines and slaughtered under
inclusions on impression smears (Fig. 3) made from supervision without human infection.
fresh exudates (monocytic cells) from the surface
of the air sac (epithelial cells), spleen, liver, lung,
serous surface, and pericardium. Where available,
the fluorescent antibody technique may be useful
AVIAN CHLAMYDIOSIS
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Fig. 1 Fig. 2
Inclusions can be demonstrated in stained smears (Giemsa stain Fibrinous pericarditis in a turkey.
elementary bodies).
Fig. 3
Giemsa stain elementary bodies in smear.
AVIAN TUBERCULOSIS acid-fast bacilli. Their demonstration permits a strong

(Avian TB; TB) presumptive diagnosis of tuberculosis.
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EPIDEMIOLOGY
DEFINITION 1. In chickens (and many other birds) small round to oval
Avian tuberculosis is a slow-spreading, usually chronic, nodules (tubercles) develop as diverticuli along the
granulomatous infection of semimature or mature birds, intestine. These tubercles discharge viable tubercle
characterized by progressive weight loss and, ultimately, bacilli into the intestine. Infectious feces and other
by emaciation and death. excretions contaminate feed, water, litter, and soil
and survive in the environment for months to years.
OCCURRENCE Transmission of the organism is predominantly through
Avian tuberculosis occurs in many kinds of birds, including ingestion of contaminated feed, water, litter, and soil.
poultry, game birds, cage birds, wild birds, and zoo birds. 2. During intermittent periods of bacteremia, tubercle
Most outbreaks are encountered in old backyard chickens. bacilli spread from the intestine to most other organs
Avian tuberculosis also occurs in mammals, including and tissues. If bacteremic or dead infected poultry
swine, sheep, mink, cattle, and, rarely, humans. Among are cannibalized or consumed by other susceptible
mammals, swine are more frequently infected. Avian poultry or mammals (e.g., swine) the bacillus can be
tuberculosis is worldwide in distribution. transmitted.
3. Other sources of dissemination of the bacilli include
HISTORICAL INFORMATION offal from infected chickens, excretions from wild birds
1. Tuberculosis in chickens was first recognized as a (pigeons, sparrows, starlings, etc.), contaminated
separate disease about 1884. Once identified, it soon shoes or equipment, and the feces of infected
was recognized in many countries. Avian tuberculosis mammals, especially swine.
eventually was found to be transmissible to certain
4. With the increased popularity of exotic birds as
other birds and mammals, especially swine, and was
pets, M. avium has become increasingly important
shown to sensitize cattle to tuberculin and johnin.
as a potential zoonotic agent. Although M. avium of
2. In the United States there once were many farm flocks human origin and M. avium of avian origin differ in
of chickens and a farm flock often was kept for years. their genetic makeup, there is concern that M. avium
In old flocks avian tuberculosis was a very common can cause disseminated disease in humans with
disease. Later, farm flocks largely were replaced by immunosuppressive disease conditions (e.g., AIDS).
large commercial flocks, which are sold after one
laying cycle, a practice that greatly restricts the spread CLINICAL SIGNS
of avian tuberculosis. 1. In chickens there is progressive wasting leading
to emaciation, although the appetite is usually
3. Avian tuberculosis is seldom seen today in poultry
maintained. Diarrhea is common and there may be
species. However, there is a tendency toward the
lameness in occasional birds. The skin of the face,
reestablishment of small farm flocks, which probably
wattles, and comb often appears pale.
will be kept long enough for tuberculosis to develop.
2. The course in the individual bird and in the flock is
4. Avian tuberculosis commonly infects swine, interferes
prolonged. Total morbidity and total mortality are
with the eradication of bovine tuberculosis, and
high, although both are spread over a period of many
sometimes infects humans. However, there presently
months and hence are misleading unless records are
is no formal eradication program for this disease.
kept.
ETIOLOGY
1. The etiologic agent is Mycobacterium avium
LESIONS
1. A bird with advanced tuberculosis is very light in weight
subspecies avium (referred herein as M. avium), a
and there is marked emaciation. Few other diseases
highly resistant, acid-fast bacillus. It resists heat, cold,
result in such extreme emaciation. These features are
water, dryness, pH changes, and many disinfectants
unique enough that they should alert the prosector to
and survives in soil for years.
the possibility of avian tuberculosis.
2. Destruction by disinfection is impractical on most poultry
2. In chickens, gray to yellow nodules (tubercles) often
farms. M. avium is distinct from the bacilli that cause
are attached to and scattered along the periphery of
human and bovine types of tuberculosis, although all
the intestine (Fig. 1). Smaller, discrete granulomas
three types share many similar characteristics.
usually are present in parenchymatous organs,
3. M. avium is present in large numbers in avian tubercles. especially the liver and spleen (Fig. 2). In advanced
Stained impression smears or histologic sections cases few organs are spared and tubercles often can
made from the centers of tubercles readily reveal the be demonstrated in the bone marrow of the femur. The
lung often has few or no gross lesions.
DIAGNOSIS infected birds that might be disseminators. Thoroughly

1. A history of a chronic disease and persistent clean and disinfect buildings between flocks. Maintain
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mortality in an old flock is suggestive of tuberculosis. a high standard of sanitation at all times.
Diagnosis often can be confirmed by the postmortem 2. Young birds should be raised away from old birds on
demonstration of typical gross lesions and the clean premises. Insofar as is possible, raise them in
demonstration of acid-fast bacilli in impression smears quarantine, thus avoiding exposure to all possible
or sections of tubercles (Fig. 3 and 4). The tubercle carriers including wild birds.
bacillus should be cultured and identified.
3. The use of tuberculin testing or ELISA serology
2. Tuberculin testing was once utilized as a flock test and monitoring may be of value in aviaries to identify and
is still available but has fallen into disuse. Chickens remove infected birds before widespread dissemination
are tested by inoculating avian tuberculin into one of the disease occurs.
wattle. The other wattle is used as a control. Turkeys
are tested by wing web inoculation. Skin tests are TREATMENT
read in 48 hours. The tuberculin test has been used in Avian tuberculosis is a reportable disease in some states
other avian species with some success. and appropriate authorities should be notified. Treatment
3. An enzyme-linked immunosorbent assay (ELISA) has of avian tuberculosis is not recommended because of the
been developed for the detection of mycobacterial zoonotic potential. Furthermore, M. avium is resistant
antibodies in serum and this test has greater promise to many of the drugs used in treating other types of
in the detection of avian tuberculosis in individual tuberculosis.
exotic birds and aviaries.
CONTROL
1. All poultry should be maintained in single-age groups.
This will help control the disease by eliminating
AVIAN TUBERCULOSIS
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Fig. 1 Fig. 2
Nodules (tubercles) are attached to and scattered along the Smaller, discrete granulomas in parenchymatous organs,
periphery of the intestine of a chicken. especially the liver and spleen.
Fig. 3 Fig. 4
Demonstration of acid-fast bacilli in section of a tubercle. Acid-fast bacilli in liver of a finch.
BORDETELLOSIS 2. Strains vary greatly in virulence but virulence does not

(Turkey Coryza; Bordetella avium) appear to be related to the presence or absence of
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plasmids.
DEFINITION 3. B. avium produces hemagglutinin, heat-stable and
Bordetellosis is an acute, persistent, contagious upper heat-labile toxins, a dermonecrotic toxin, a tracheal
respiratory disease of turkeys characterized by ocular cytotoxin, and an osteotoxin.
exudation and rhinitis in young turkeys and tracheitis in 4. Presence of other infectious agents, notably
older turkeys caused by Bordetella avium. Newcastle virus, other paramyxoviruses, Mycoplasma
gallisepticum, Pasteurella and Escherichia coli
OCCURRENCE increases the severity of bordetellosis.
1. Bordetellosis occurs most commonly in turkeys 1-6
weeks of age. All ages of turkeys are susceptible,
EPIDEMIOLOGY
1. B. avium is susceptible to most disinfectants and
including breeders.
environmental conditions, especially drying.
2. Outbreaks of the disease occur in most turkey-
2. Although carrier state has not been confirmed, older
producing areas of the United States. Similar diseases
flocks are thought to serve as carriers and the most
have been reported from Canada, Australia, Germany,
important source of infection for younger susceptible
France, England, Italy, Israel, and South Africa.
flocks on multiage farms. Transmission between
3. Farms with continuous confinement production and flocks occurs as a result of human activity. There is no
multiage flocks have the greatest problems with evidence of egg transmission.
bordetellosis. Bordetellosis occurs most commonly in
3. Litter and contaminated water have been shown to be
the summer and fall.
sources of infection. The organism has been found to
4. B. avium has been recovered from chickens and persist for at least 6 months in moist litter but not dry
occasionally other avian species. Presence of B. litter. Contaminated water can remain in water lines
avium has been associated with increased severity of and be a source of infection for new flocks.
respiratory disease in broilers, especially when flocks
4. Infection of flocks less than 10 days of age strongly
are concurrently infected with infectious bronchitis
suggests the environment as the source of the
virus, but its role as a primary pathogen in chickens is
organism. Infection between 2 and 4 weeks may result
less obvious than in turkeys.
either from the environment if poults had substantial
HISTORICAL INFORMATION maternal immunity or introduction from an outside
1. The term turkey coryza (TC) was first used in source. Outbreaks in flocks over 4 weeks of age result
Canada in 1967 to describe a clinically distinct, acute from introduction of B. avium.
respiratory disease of turkeys. TC was recognized
in Iowa in 1971. Following greater awareness of TC,
CLINICAL SIGNS
1. Onset is abrupt 4-7 days after exposure, with high
others recalled similar disease outbreaks that occurred
morbidity and low mortality. Growth rate is decreased.
in turkey- producing areas for at least the last three
decades. As the number of turkeys being reared in 2. In young turkeys, initial clinical signs are clear,
confinement has increased, TC has been identified mucoid, nasal discharge and frothy ocular exudate
as an increasingly important respiratory disease and accompanied by sneezing, “snicking”, and flicking of
cause of economic loss. the head. Activity is reduced and heat sources are
sought out.
2. The terms alcaligenes rhinotracheitis and turkey
bordetellosis were introduced following preliminary 3. Exudates become progressively thicker with pasting
identification of the causative agent as Alcaligenes of nostrils and matting of eyelids. The palpebral
faecalis or Bordetella bronchiseptica-like, respectively. opening often assumes an almond shape. There are
voice changes or loss in more severely affected birds,
ETIOLOGY accompanied by tracheal rales. Birds show mouth
1. B. avium has been identified as the cause of breathing. The intermandibular tissue tends to balloon
bordetellosis. B. avium can be distinguished from giving the profile a baggy appearance (Fig. 1). Poults
other species of Bordetella and nonfermenting, gram- may scratch at matted eyes causing trauma to eyelids.
negative bacteria. Hemagglutination of guinea pig Dried exudate is commonly found on the upper wings
erythrocytes is associated with pathogenicity and is and lower neck where the bird wipes off nasal-ocular
useful in distinguishing B. avium from B. hinzii (formally exudates. Swollen infraorbital nasal sinuses are not
B. avium-like). More recently, some strains of B. hinzii typical of bordetellosis but are occasionally seen in a
have been shown to cause clinical signs and lesions of few birds.
bordetellosis in turkeys but not chickens.
4. Tracheal rales persist for several weeks after apparent developed to detect antibodies to B. avium. The
recovery. Turkeys have been found to be culturally microagglutination and ELISA tests are commonly
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positive for at least 4 months after infection. used for diagnostic purposes.
5. In uncomplicated outbreaks, mortality remains low. CONTROL
In bordetellosis outbreaks complicated by other 1. Clean and disinfect the brooder house and all
respiratory disease agents mortality usually begins 10- equipment between flocks. Make sure house and
14 days after onset of clinical signs and may be high equipment are thoroughly dry. Depopulate problem
(10-60%). Escherichia coli is the most common cause farms.
of mortality. Flocks in poor environments, especially if
ammonia levels are high, have higher mortality and 2. Flush water lines with disinfectant between flocks. Use
greater production losses. halogens or similar substances to treat drinking water.
6. In older turkeys, nasal and ocular exudation does not 3. Control traffic patterns. Traffic should always move
occur. Typically the only sign observed in these birds from younger to older flocks without backtracking.
is tracheal rales. Ideally only one person who has no other contact
with poultry should care for a single brooder house
LESIONS (isolation brooding).
1. Epiphora, serous to catarrhal rhinitis, sinusitis, and 4. Prevent contact between wild birds and young turkeys.
tracheitis with hyperemia of the trachea are the only
consistent lesions. In severely affected birds, there is 5. An oil-emulsion bacterin is available for use in breeder
distortion of tracheal rings in proximal segments of the hens. This will provide poults with maternal immunity
trachea, which leads to narrowing of the tracheal lumen for up to 4 weeks, the interval when infection generally
and retraction of the larynx. Cross sections through an results in a more severe disease.
affected segment will reveal the characteristic flattening 6. A live vaccine prepared from a temperature-sensitive
or dorsal infolding of the trachea (Fig. 2). Death occurs mutant of B. avium is available for use in poults. Two
by suffocation from an obstructed trachea. doses are recommended, the first given via spray
2. A variety of other lesions can be found in complicated cabinet in the hatchery with a booster administered
outbreaks, depending upon the etiologic agents through the drinking water at 2-3 weeks of age.
present.
TREATMENT
3. B. avium attaches readily to ciliated epithelial cells Although B. avium is susceptible to most antibiotics on
of the upper respiratory tract (Fig. 3). This leads to sensitivity tests, treatment with antibiotics is generally
deciliation, altered mucus production, impairment ineffective. This is thought to be due to failure of the
of mucociliary clearance, and mucus accumulation. antibiotic to reach effective levels in the trachea where
Inflammatory changes are not pronounced but are the organism is located. Aerosol administration of
chronic, which leads to distortion of tracheal rings and oxytetracycline is effective in reducing clinical signs during
hyperplastic bronchial-associated lymphoid tissue. the treatment period but has little long-term benefit. The
4. Infection with B. avium has been shown to interfere best management for an infected flock is to move the birds
with vaccination for fowl cholera but the mechanism to range if possible. If not, increase ventilation, increase
is unknown. house temperature, and frequently stimulate the flock to
move thus encouraging them to eat and drink. Higher
DIAGNOSIS density “stress” rations and use of vitamins and electrolytes
1. The bacterium is readily isolated from the trachea. in water are useful adjuncts to general support of sick birds.
Typical nonfermenter colonies occur on MacConkey
agar in 48-72 hours.
2. If high populations of fermenting organisms are present
on the plate, B. avium may be inhibited. This situation
often occurs when the disease has been going on for
several weeks. Early in the outbreak, almost pure,
dense growths of B. avium are readily obtained.
3. B. avium should be looked for in any respiratory
disease of turkeys even if another cause is identified
because it is a significant predisposing factor to severe
respiratory disease outbreaks.
4. A variety of serological tests including rapid plate
agglutination, microagglutination, and enzyme-linked
immunosorbent assay (ELISA) tests have been
BORDETELLOSIS
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Fig. 2
Fig. 1 Cross-section of the trachea, normal on left and characteristic
Young turkey showing mouth breathing, frothy ocular exudate and flattening or dorsal infolding of the trachea (on the right).
the intermandibular edema (bottlejaw).
Fig. 3
Partial deciliation of the tracheal epithelium. B. avium attaches
readily to ciliated epithelial cells of the upper respiratory tract.
BOTULISM recover within 24 hours. Pseudobotulism is now

(Limberneck; Western Duck Sickness) considered to be a transient manifestation of Marek’s
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disease.
DEFINITION EPIDEMIOLOGY
Botulism is an intoxication caused by ingestion of the toxins 1. C. botulinum is ubiquitous in nature and commonly
of Clostridium botulinum. present in feeds. When ideal conditions for growth
occur, large amounts of exotoxin may be formed. If
OCCURRENCE adequate toxin is consumed, botulism will develop.
1. In birds, botulism occurs frequently in wild waterfowl, Improperly sterilized canned fruits and vegetables,
captive pheasants and occasionally in chickens. spoiled animal feeds, decaying poultry carcasses and
Except for vultures, most birds are susceptible. Most the insects that feed on them can contain enough
outbreaks in poultry occur in semimature or mature exotoxin to be lethal, even when taken in small
chicken flocks. Many mammals, including humans, amounts.
are susceptible. 2. It is speculated that wild waterfowl contract botulism in
2. In waterfowl (especially wild ducks) occurrence is the following ways:
related to shallow water conditions in lakes and ponds A. The toxin may be consumed in decaying
with much decaying vegetation and alkaline water. vegetation in shallow, alkaline lakes as they dry
3. In some intense broiler rearing areas there is a recurring up or are created by irrigation during the summer.
form of botulism on certain premises. Outbreaks Alternatively, it may be that the toxin is in larvae
occur in almost every new flock with a seasonal high or crustaceans in the vegetation. Invertebrates
incidence in the warmer months. killed by anaerobic conditions contain toxin from
growth of C. botulinum within them and may be
HISTORICAL INFORMATION consumed by some waterfowl. This condition may
1. The first report of botulism in chickens was made in also occur in small ponds via water temperature
the United States in 1917. Within 25 years the disease inversion following summer storms.
had been reported frequently in chickens and in B. Ducks that die from various causes may allow
turkeys and waterfowl. toxin production and dissemination after death by
2. During the first half of the 1900s, humans and chickens C. botulinum normally present in their intestine.
sometimes died from eating improperly canned foods Toxins are formed in the cadavers. Ducks that
containing the toxins of C. botulinum. Small farm flocks feed on the cadavers or on maggots from the
and home canning are now out of vogue and botulism cadavers may be poisoned.
is seldom seen in farm flocks or humans. However, 3. A growing body of evidence suggests that C. botulinum
botulism is still an important disease of wild waterfowl, type C can produce toxin within the intestinal tract of
especially ducks. Botulism seldom occurs in well- the live broiler chicken. This type of botulism has been
managed commercially raised poultry. termed toxico-infectious botulism.
ETIOLOGY CLINICAL SIGNS
1. Botulism is caused by ingestion of the preformed toxins Signs appear within a few hours to days. Clinical signs
of C. botulinum in feeds, foods, dead poultry, or toxin- include drowsiness, weakness, and progressive loss of
containing maggots (Fig. 1). Although C. botulinum or control and flaccid paralysis of the legs, wings, neck, hence
its spores are not pathogenic and are commonly found the term ‘limberneck’ (Fig. 2 and 3) and eyelids. Paresis
in the environment and in the intestinal tract, under soon progresses to paralysis and the recumbent bird closes
ill-defined circumstances it colonizes the intestines, its eyes and appears to be in a deep coma. Fine tremors
produces toxin and causes botulism. of muscles and feathers occur in some birds. Death may
2. The toxin of C. botulinum is extremely potent. The occur shortly or may be delayed for a few hours. Most
minimum lethal dose (MLD) for guinea pigs is 0.00012 visibly affected birds die.
mg/kg subcutaneously (The MLD for cobra venom is
0.002 mg/kg). The toxin is relatively heat stable.
LESIONS
3. Based on specific conditions, there are eight types Most birds with botulism are free of gross lesions. Rarely,
of toxins produced by C. botulinum. Type C is most in birds that have lived for some time, there may be mild
common in poultry outbreaks although other types enteritis. The upper digestive tract (especially the crop)
have occurred. may contain putrid ingesta or maggots but is usually empty.
4. Botulism should not be confused with pseudobotulism
of chickens. Pseudobotulism closely resembles
botulism except that affected birds almost invariably
DIAGNOSIS .
1. In chickens and turkeys diagnosis is based largely on
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history, signs, the presence of putrid feed or maggots

in the digestive tract, looseness of feathers (chickens
only), and the absence of lesions. Finding a decaying
cadaver upon which birds have been feeding may
assist in diagnosis.
2. Saline gizzard or intestinal washings or blood serum
from an affected bird can be tested for toxicity. Either
can be injected into mice that have been inoculated
with protective antiserum and into mice without
antiserum. Results should clarify diagnosis. Culture is
meaningless.
3. A group of affected birds can be treated with polyvalent Fig. 1
antitoxin. Recovery in a high percent of the birds tends Decaying waterfowl carcass with toxin-containing maggots.
to confirm a diagnosis of botulism. Unfortunately,
commercial availability of antitoxins may be a problem.
CONTROL
1. The disease can be avoided by preventing access
of poultry to any source of toxin. Sick and dead birds
should be picked up regularly and frequently because
they are a common source of toxin.
2. Type C toxoid can be used to immunize birds, although
this is seldom done.
3. Wild ducks can be baited or frightened away from
shallow lakes. Water sometimes can be pumped into
shallow lakes to raise the water level and botulism
may not occur.
4. On broiler farms where botulism is enzootic, the
prophylactic use of selenium and antibiotics has been
effective. They also aid in treatment of affected flocks.
TREATMENT Fig. 2
1. Antitoxin can be given to valuable affected birds. Flaccid paralysis of the legs, wings, neck in a chicken.
Results often are good although this will depend
on the specificity of the antisera. Type C antitoxin is
usually given. Polyvalent antisera (especially types A
and C) are preferred but often difficult to obtain. It is
important that the treated birds have access to fresh,
clean, nonalkaline water.
2. Because toxico-infectious botulism has not been
experimentally induced, treatment of this condition
is based solely on the apparent response to therapy
during field outbreaks of this condition. Treatment of
flocks with sodium selenite and vitamins A, D, and
E has been reported to reduce mortality. Treatments
with bacitracin, streptomycin, chlortetracycline, and
penicillin have also been reported to be efficacious.
Fig. 3
Flaccid paralysis of the legs, wings, neck in ducks (limberneck).
CAMPYLOBACTER common human pathogens in the occurrence of bacterial

gastro-enteritis
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DEFINITION
Campylobacteriosis is a disease caused by the bacteria ETIOLOGY
Campylobacter sp. It occurred as a disease of egg-laying Thermophilic Campylobacter species C. jejuni and C.
chickens in the 1950’s and 60’s and was known at that time coli can be isolated from the intestines of poultry. It is a
as vibrionic hepatitis. The disease in chickens has since microaerophilic, small curved or spiral Gram-negative
disappeared. Campylobacteriosis more recently has been rod with a rapidly darting motility under a phase-contrast
recognized as a leading cause of human foodborne illness microscope.
and is even more common than Salmonellosis. There
are many sources of campylobacteriosis in humans, but Unlike Salmonella, Campylobacter does not tolerate
poultry is often considered as a major source. exposure to oxygen or drying, and does not multiply on
food left at room temperature. Indeed, since the optimal
This bacteria does not cause disease in poultry but since growth temperature of thermotolerant Campylobacter lies
the handling and consumption of raw or undercooked between 37 and 42oC (very close to the chicken body
poultry is the most frequently identified source of sporadic temperature), they are not able to grow below 30oC i.e., at
campylobacteriosis in humans, it is important to understand room temperature.
this bacteria to better implement control and preventative
measures.
EPIDEMIOLOGY
Campylobacter is a commensal organism in avian hosts.
OCCURRENCE Colonization is mostly with C. jejuni with a much lower
Campylobacter is a common cause of diarrhea in the proportion of C. coli strains. It occurs mostly in the ceca,
developing world, particularly in the under five year of more specifically in the intestinal mucous layer covering
age group. Most developed countries, with surveillance the intestinal crypts. Large percentages of poultry lots at
systems, have reported an increase in the number of slaughter can be found to be Campylobacter positive, but
cases over the last 25 years. In European countries, the since sampling methodology varies greatly from one study
overall incidence of human campylobacteriosis ranged to another, comparison is almost impossible. In Canada
from 50 to 90 cases per 100,000 people in 2005, while the and Europe, prevalence estimates range from 18% to 82%
United States reported a 12.7 per 100,000 the same year. in broiler chicken carcasses.
Australia had a similar level to that of Europe while New
Zealand was the highest of all industrialized countries with Broilers are typically shown to be free of Campylobacter
396 per 100,000 in 2003. It is now agreed that the most at a day of age and detection in a flock is usually possible
common source for campylobacteriosis is the handling or at 2 to 3 weeks of age. Maternal immunity is thought to
consumption of raw or undercooked poultry products. play a protective role in delaying Campylobacter infection.
Interestingly, experimental studies have demonstrated
HISTORICAL INFORMATION that day-old chicks are susceptible to colonization and
In poultry, in the 1950s, a possible association was Campylobacter has also been isolated from the ovaries
established between sporadic cases of vibrionic hepatitis and semen of broiler breeders as well as from paper pad
in laying hens and vibrio-like organisms now known as liners in hatching box. Vertical transmission is still being
Campylobacter jejuni. Layers during these episodes debated.
showed a drop in egg production with increased mortality.
Lesions were found in the liver and appeared stellate, The organism can rapidly spread horizontally in chickens,
asterisk-shaped, or cauliflower-like. This condition presumably through fecal contact, a common water source
mysteriously disappeared in the late 1960s but since then, or with flies as vectors. The latter might partly explain the
cases have occasionally been reported in the literature. seasonality of campylobacteriosis in poultry flocks with an
observed higher prevalence in summertime. Indeed, recent
Awareness of the public health implications of trials using insect screens on chicken houses found that
campylobacteriosis in humans has evolved over the past this sole preventative mean reduced flock prevalence by
century. In 1886 Escherich observed organisms similar up to 70%. Once infection has entered the broiler house,
to Campylobacter in fecal samples from children with its spreads rapidly; within 10-14 days post-infection, more
diarrhea while Campylobacter was isolated as Vibrio than 90% of the birds in a flock will be positive.
fetus in 1909 from spontaneous abortions in livestock.
The development of selective growth media in the 1970’s When Campylobacter positive chickens enter the
allowed easier culture of Campylobacter from human slaughterhouse with large numbers of Campylobacter in
feces. Soon Campylobacter species were established as the intestines, as well as on the feathers and skin, this
inevitably leads to a cross-contamination of the equipment,
environment and other processed birds.
CLINICAL SIGNS
Chickens are carriers of Campylobacter and typically do
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not exhibit clinical signs or lesions. Egg drop and increased

mortality in egg-laying chickens was observed with vibrionic
hepatitis.
LESIONS
No lesions are observed in carrier birds. Hepatitic necrosis
consisting of small stellate whitish foci to fairly large diffuse
areas has been described in egg-laying chickens with
vibrionic hepatitis (Fig. 1).
DIAGNOSIS
1. Culture of the causative organism from egg-laying
hens with lesions.
Fig. 1
2. Bile is a better source of organism than liver. Hepatic necrosis.
3. Samples are best kept at 4oC.
CONTROL
Biosecurity, including rodent and insect control.
TREATMENT
No treatment is currently used.
CONCLUSIONS
Campylobacteriosis is currently only a public health
concern and not a poultry health concern. It is important
that a thorough knowledge of transmission of and infection
with Campylobacter be developed in order to provide
effective and economical means of controlling its incidence
in poultry.
COLIBACILLOSIS followed by penetration. Chicks may hatch with a

(Escherichia coli Infections) latent infection; however, active infection will typically
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only occur if some environmental stress or lesions

initiates the disease process.
DEFINITION
Avian colibacillosis is an infectious disease of birds CLINICAL SIGNS AND LESIONS
in which Escherichia coli is the primary or secondary A variety of lesions from which E. coli has been isolated
pathogen. Infections include airsacculitis, cellulitis, include:
omphalitis, peritonitis, salpingitis, synovitis, septicemia and
coligranuloma. 1. Airsacculitis
Respiratory signs occur and vary in severity. This pathology
OCCURRENCE may be associated with poor environmental conditions
Colibacillosis occurs in all types and age groups of poultry such as dusty litter, poor ventilation, high ammonia
as well as in other birds and many kinds of mammals. levels, sudden variation in the barn temperatures, but
Most reported outbreaks in poultry have been in chickens, also with concomitant respiratory (infectious bronchitis
turkeys, and ducks. Many outbreaks occur in poultry raised virus, Newcastle disease virus, laryngotracheitis virus,
under a low standard of sanitation, poor environmental mycoplasmas) or immunosuppressive (infectious bursal
conditions, or after a respiratory or immunosuppressive disease, chicken anemia virus) diseases. In these cases,
disease. Infection is more frequent in young than mature E. coli is a secondary pathogen and will cause the
birds. Colibacillosis is common throughout the world. airsacculitis lesions. Air sacs are normally thin, glistening
and transparent (Fig. 1) but bacterial infection will cause
the air sacs to become thickened, number of blood
HISTORICAL INFORMATION vessels within the air sac walls increases and exudate
Colibacillosis was first described in chickens in 1894. Since will accumulate within the cavity of the air sac. An acute
then, there have been numerous reports on colibacillosis inflammation will be characterized by the presence of
in poultry and considerable research on the disease has mucous exudate (Fig. 2) which will eventually become
been completed. Many investigators doubt that E. coli is fibrinous (Fig. 3). Thickened air sacs and caseous exudate
a primary pathogen. Others are convinced that certain in the air sac will be present (Fig. 4) in more severe and
serotypes are primary pathogens and their opinion seems chronic cases. There often is an accompanying adhesive
to prevail. Most investigators agree that E. coli frequently pericarditis, fibrinous perihepatitis and peritonitis (hence a
can be isolated from a variety of well-defined syndromes polyserositis). Airsacculitis occurs chiefly in 3-7-week-old
in poultry. broilers, probably peaking at 5-6 weeks.
ETIOLOGY 2. Pericarditis
The etiologic agent is Escherichia coli (E. coli). The O Most serotypes of E. coli, after a septicemia, cause a
(somatic) antigen serotypes most commonly associated pericarditis (Fig. 5). Opaqueness and thickening of the
with disease outbreaks are O1, O2, O35, O36, and O78. pericardial sac, an edematous epicardium along with
The K (capsular) antigens most commonly associated myocarditis typically occurs. Pericarditis can also be
with virulence are K1 and K80. In the intestinal tract of caused by other bacteria including Chlamydophila sp.
normal poultry, nonpathogenic serotypes far outnumber
pathogenic serotypes, with 10% to 15% of intestinal 3. Omphalitis and yolk sac infection
coliforms being potential pathogens. E. coli is often isolated in pure culture from organs or the
yolk sac of recently hatched birds having depression,
septicemia, and variable mortality. With omphalitis the
EPIDEMIOLOGY
navel is swollen and inflamed (Fig. 6) and the bird feels
1. E. coli is present in the intestine of birds and
wet. Abnormal yolk material and peritonitis is typically seen
mammals and is disseminated widely in feces. Birds
on necropsy of birds with an E. coli infection of the yolk sac
are continuously exposed through contaminated
(Fig. 7).
feces, water, dust, and environment. Any time a
bird’s resistance to disease is impaired, pathogenic
A great variety of other organisms such as species of
or facultative pathogenic strains may infect the bird.
Aerobacter, Proteus, Klebsiella, Pseudomonas, Salmonella,
Sequestered E. coli in such sites as the intestine,
Bacillus, Staphylococcus, enteric Streptococcus, and
nasal passages, air sacs, or reproductive tract may
Clostridia are frequently isolated from yolk sacs of embryos
be a latent source of infection. Certain pathogenic
and navels of chicks, most likely as mixed infections.
serotypes may have the ability to infect a normal bird.
2. E. coli has been isolated from the eggs of normal hens. 4. Coliform septicemia of ducks (duck septicemia)
Its presence has been attributed to ovarian infection, E. coli, Salmonella, and Riemerella (Pasteurella)
oviduct infection, and to eggshell contamination anatipestifer produce respiratory signs, airsacculitis,
pericarditis, perihepatitis, and peritonitis. In outbreaks of R. include dehydration and emaciation. Synovitis-arthritis may
anatipestifer, involvement of the air sacs and a dry, thin also be caused by reovirus, or species of Mycoplasma,
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transparent covering over visceral organs are present. In Staphylococci, and Salmonella.
coliform septicemia (E. coli) usually a moist, granular to
coagulative exudate of varying thickness is present on 10. Panophthalmitis and meningitis
abdominal and thoracic viscera and surfaces of air sacs. Occasional birds have a hypopyon and/or hyphema,
The spleen and liver are swollen and dark with bile staining usually in one eye, which is blind. Likewise, meningitis is a
of the liver. rare sequelae to E. coli septicemia.
5. Acute septicemia 11. Cellulitis (Infectious process)

An acute septicemic disease caused by E. coli resembles This is one of the most common causes of condemnation
fowl typhoid and fowl cholera. Birds are in good flesh at slaughter in broiler chickens in the United States,
and have full crops suggesting acuteness of the disease. some European countries, and Canada. It is recognized
This can occur in young or mature birds. There are primarily at post-mortem inspection, with no abnormality
sudden deaths, and variable morbidity and mortality. having been noted in live birds. The USDA Food Safety
Parenchymatous organs are swollen with congested and Inspection Service designates cellulitis as “infectious
pectoral muscles. Livers are green in color and may have process” or “IP”. Gross lesions include variable yellowing
small necrotic foci. There may be petechial hemorrhages, and thickening of the skin lateral to the vent (Fig. 11) and
pericarditis, or peritonitis. Acute systemic disease may extending in severe cases over the ventrocaudal aspect of
also be caused by various Pasteurella, Salmonella, the breast. On incising the skin a yellow caseous plaque of
Streptococci, and other organisms. variable size (Fig. 12) is noted in the subcutis. Histologically
there is cellulitis involving both dermis and subcutis. The
6. Enteritis inflammatory reaction includes edema and heterophil
Enteritis caused by E. coli is considered rare but pathogenic infiltration in active areas, whereas there is accumulation
attaching effacing E. coli have been reported. Diarrhea and of a walled-off causative sheet of exudate surrounded by
dehydration are noted on clinical examination. At necropsy a zone of giant cells in more chronic areas of involvement.
there is enteritis, often with excessive fluid in the intestines. Coccobacillary bacteria can be seen in microcolonies within
E. coli may be isolated from parenchymatous organs. the exudate and E. coli is recovered quite consistently on
culture. This condition may affect up to 8% of entire flocks
7. Salpingitis at slaughter resulting in extensive trim-out, downgrading,
This lesion may occur following entry of coliform bacteria or whole-carcass condemnation. Cellulitis is caused by the
from the vagina in laying hens. It is also likely to develop secondary infection of skin wounds. Risk factors such as
when the left greater abdominal air sac becomes infected certain broiler breeds, poor feathering, sex (males more
by E. coli, causing a chronic salpingitis. Affected birds susceptible), skin scratches, increased stocking density
usually die during first 6 months postinfection and never and litter type have been associated with this condition.
lay. The oviduct is distended with exudate (Fig. 8) that
may be caseous and has a foul odor. No specific signs are DIAGNOSIS
noted but there may be an upright (penguin) posture. Diagnosis of primary colibacillosis is based on the
isolation and typing of a coliform into one of the serotypes
8. Coligranuloma (Hjärre’s disease) recognized as pathogens. Diagnosis based merely on the
Signs vary in this uncommon disease of chickens and
isolation of E. coli is of questionable validity. The possibility
turkeys. Nodules (granulomas) occur along the intestinal
of other infections (viruses, bacteria, fungi, Chlamydophila,
tract, and mesentery, and in the liver (Fig. 9). The spleen is
and mycoplasmas) should have been eliminated through
not involved. The lesions resemble those of tuberculosis. culture or other means. When E. coli is isolated secondary
The agent is a mucoid coliform, possibly not E. coli. to some other primary disease, it should be diagnosed as
Granulomas of the liver have many causes, some of which secondary colibacillosis.
would include the anaerobic genera Eubacterium and
Bacteroides.
CONTROL
9. Synovitis and osteoarthritis 1. Measures should be taken to minimize eggshell
Affected birds are lame or recumbent. There is swelling of contamination of newly laid hatching eggs. Eggs
one or more tendon sheaths or joints (Fig. 10). Synovitis should be disinfected on the farm prior to storage and
and/or osteoarthritis are frequently a sequel to a systemic should be stored under ideal conditions. Scrupulous
infection. With synovitis many birds will recover in about 1 hatchery sanitation, disinfection, and/or fumigation
week. Osteoarthritis is a more severe and chronic condition procedures should be practiced.
where the joint is inflamed and the associated bone has 2. A vigorous sanitation program should be followed in
osteomyelitis. These severe chronic infections make birds raising poultry.
unwilling or unable to walk and necropsy findings often
3. Diseases, parasitism, and other stresses on a flock

should be minimized as much as possible. Dust should
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be controlled.
4. Only feeds free of fecal contaminations should be fed
to poultry. Pelleted feeds are more likely to be free of
contamination.
5. Treatment of water with halogens and related
compounds as well as conversion to nipple drinkers
has greatly decreased the incidence of septicemic
forms of colibacillosis.
TREATMENT
Numerous antimicrobials have been utilized for treatment.
These have included tetracyclines, neomycin, sulfa drugs
and others but E. coli has developed resistance to many of
these commonly used antimicrobials. Antibiotic sensitivity
testing is therefore strongly suggested as well as record
keeping of treatment history by farm.
COLIBACILLOSIS
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Fig. 1 Fig. 2
Air sacs are normally thin, glistening and transparent. An acute inflammation will be characterized by the presence of
mucous exudate in the air sacs.
Fig. 4
Fig. 3 Chronic airsacculitis: caseous exudate and thickened
Fibrinous exudate and neovascularization of the air sacs. air sacs.
Fig. 5
Pericarditis and
Fig. 6
perihepatitis.
Swollen and inflamed navel in a case of omphalitis.
COLIBACILLOSIS
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Fig. 7 Fig. 8
E. coli infection of the yolk Oviduct is distended with caseous
sac. Note the periombilical exudate.
neovascularization.
Fig. 9 Fig. 10
Nodules (granulomas) along Arthritis and synovitis.
the intestinal tract, and
mesentery, and in the liver.
Fig. 12
Fig. 11 Subcutaneous caseous exudate in the right
Cellulitis: yellow discoloration of the skin in inguinal area of a broiler chicken carcass at
the right inguinal area of a broiler chicken slaughter.
carcass at slaughter.
ENTEROCOCCUS CECORUM Sagittal section of the vertebral column will show abscess
formation (Fig. 2), necrosis of the bone resulting in the
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DEFINITION dorsal displacement and compression of the overlying

Recently, Enterococcus cecorum has been recognized as spinal cord (Fig. 3).
an emerging avian pathogen, associated with spondylitis,
femoral head necrosis, and osteomyelitis in broiler chicken Histopathology reveals heterophilic to granulomatous
and broiler breeder flocks in Europe and North America. inflammation of the synovium and tendon sheath of the
E. cecorum can cause significant economic losses, due to affected joints, focal osteomylitis of the affected bones,
mortality and culling, poor feed conversion and increased with Gram-positive coccoid bacteria visible in the lesions.
condemnations.
DIAGNOSIS
OCCURRENCE Lesions and isolation of E. cecorum are diagnostic.
E. cecorum arthritis and osteomyelitis have been reported
in Europe, United States and Canada in broiler chickens Vertebral osteomyelitis should be differentiated from other
and broiler breeders. causes of spinal cord compression e.g. spondylolisthesis.
HISTORICAL INFORMATION CONTROL

Enterococcus cecorum joint and bone infections in broilers Clean, disinfect and fumigate the premises.
were first described in 2002.
Water sanitation has been reported to reduce the incidence.
ETIOLOGY The pattern of recurrent disease at the flock level might

Enterococcus spp. are facultative anaerobic, Gram- be stopped with amoxicillin and/or tylosin administered in
positive, catalase-negative cocci. Members of this genus prevention starting at a day of age.
are widespread and normal inhabitants of the intestinal
tract of mammals and birds.
EPIDEMIOLOGY
Broiler chickens, mostly males, start presenting clinical
signs at the age of 7 – 14 days and the morbidity will
increase in the following weeks. Mortality at the end of the
growing period will reach 2 to 7%. The problem seems to
be recurring in the same barn.
The condition can be observed in broiler breeders as

early as 3 weeks of age with males being predominantly
affected.
The pathogenesis is not well understood, but since E.

cecorum is a normal inhabitant of the gastrointestinal flora,
increase in numbers and invasion into systemic circulation
could occur.
CLINICAL SIGNS
Affected birds are lame and reluctant to walk. Some may
sit back on their hocks (Fig. 1) and tails with their feet and
shanks raised.
LESIONS
The disease appears to have a shorter clinical course in
broiler chickens, with macroscopic inflammatory lesions in
hock and stifle joints and corresponding tendon sheaths,
as well as osteomyelitis of the femur and tibiotarsus, or the
thoracic vertebra. In broiler breeders, typical cases present
arthritis lesions and osteomyelitis of the fourth thoracic
vertebra.
ENTEROCOCCUS CECORUM
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Fig. 1 Fig. 2
Chicken sitting on its hocks. Abscess in the vertebral column of a male broiler chicken.
Fig. 3
Necrosis of the bone resulting in the dorsal displacement and
compression of the overlying spinal cord.
ERYSIPELAS EPIDEMIOLOGY
1. The organism is shed in the feces of some recovered
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DEFINITION turkeys for up to 41 days. It also is shed in the feces

Erysipelas is an acute septicemic disease occurring most of infected swine and lambs. Because turkeys can
commonly in older male turkeys, characterized by serosal, be infected experimentally by the oral route, it is
cutaneous, and muscular hemorrhages and splenomegaly. believed that oral exposure is a common route of
Chronic erysipelas (polyarthritis, endocarditis) occurs natural infection. Infection may occur after ingestion
occasionally, usually after acute outbreaks. of contaminated soil, water, fish meal, meat meal, or
following cannibalism of infectious live or dead birds.
OCCURRENCE 2. The organism can also infect turkeys through breaks

Erysipelas is of primary importance in turkeys although in the skin or mucous membranes. Cutaneous wounds
outbreaks sometimes occur in geese, ducks, pheasants, commonly occur in tom turkeys, which are inclined to
other game birds, wild birds, and (rarely) in chickens. fight as they reach puberty. A typical maneuver during
Sporadic cases have been reported in many wild birds. fighting is to grab the snood of the opponent and shake
Erysipelas also occurs in swine, sheep, sea mammals, him violently causing considerable trauma to this skin
fish, and many wild animals. In humans, erysipelas is appendage. The snood is considered to be a prime
caused by streptococci, whereas Erysipelothrix typically site of infection with Erysipelothrix for this reason.
causes a localized inflammation designated erysipeloid 3. Stress often precedes outbreaks of erysipelas. A
but may cause septicemia and death. In turkeys erysipelas major outbreak of erysipelas occurred in a large goose
usually occurs in toms approaching market weight; it flock after the birds were plucked. Other stressors
seldom occurs in turkeys less than 10 weeks old, although include such things as poor sanitation, bad weather,
no age or sex resistance has been found experimentally. vaccinations, changes in the ration, etc. The role of
The peak incidence in tom turkeys roughly coincides with vectors, if any, is unknown.
puberty and the disease occurs occasionally in hen turkeys 4. Important outbreaks of erysipelas have been reported
following artificial insemination. Because the bacterium is in hen turkeys following artificial insemination.
ubiquitous in nature, erysipelas probably affects poultry Presumably, infectious semen comes from carriers
and birds throughout the world. that shed the organism in their semen.
5. Injecting numerous birds in a flock with the same
HISTORICAL INFORMATION needle may spread the organism if septicemic birds
The economic significance of erysipelas in turkeys was are present.
pointed out in 1939 and the disease was soon recognized
as a major disease of turkeys. In the United States, 6. Erysipelothrix can persist for years in the soil.
recognition of erysipelas in turkeys as an important Outbreaks occur most commonly during the late fall
disease roughly paralleled the recognition of erysipelas and winter following periods of cold, wet weather.
as an important disease of swine. The disease, while still Repeated reoccurrence on a farm is common even
occurring, is not common today because most turkeys with flocks in confinement.
are raised in confinement, thus reducing exposure to the 7. Feeding dead turkeys to swine has resulted in
organism. outbreaks of erysipelas in the pigs. There is clinical
evidence indicating that people who move between
ETIOLOGY swine herds and turkey flocks can spread the organism
The etiologic agent is Erysipelothrix rhusiopathiae. It is a from the pigs to turkeys.
Gram-positive, slender, slightly bent, pleomorphoric rod. CLINICAL SIGNS
Filamentous, beaded forms that tend to decolonize easily 1. The onset of erysipelas in turkeys is usually sudden
are often seen in cultures. It grows well on enriched media with a few birds being found dead. At that time
especially when incubated in a 5-10% carbon dioxide careful examinations of the flock often reveals other
atmosphere (candle jar). Colonies tend to be quite small turkeys that squat on the floor, and appear sleepy
and grow slowly, making them easily overgrown by faster and depressed. They can be aroused but have an
growing bacteria. Selective and enrichment media assist unsteady gait when forced to move. Occasional birds
in recovering the organism. Production of hydrogen sulfide may exhibit respiratory signs or have yellow-green
in iron-containing media is a useful characteristic for diarrhea.
presumptive identification of isolates. The organism is quite
resistant to many environmental factors and disinfectants 2. Within a few days morbidity increases markedly. The
and remains viable in favorable (alkaline) soils for months course of the disease in affected turkeys is short, often
to years. only a few hours or overnight and most visibly sick
birds die.
3. Occasionally, infected turkeys have a swollen snood CONTROL

or irregular, dark red skin, and demarcated lesions 1. Poultry should be raised separately from older turkeys,
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on their dewlap, face, or head (Fig. 1). In recently which may be carriers. Poults should be started and
inseminated, infected hens there may be perineal raised as a flock and no birds should be added. Contact
congestion and hemorrhage. should be prevented between the turkeys and animal
4. Crippled birds with swollen joints are seen in chronic carriers, especially sheep and swine. Raise turkeys
infections. These often occur after an acute outbreak. in houses that were cleaned and disinfected and on
ranges without a history of outbreaks of erysipelas.
LESIONS 2. If erysipelas is enzootic in the area, turkeys should
1. The lesions are those of a septicemia. The carcass is be vaccinated with bacterin when 8-12 weeks old.
congested and parenchymatous organs (liver, kidney, Immunity is enhanced if bacterin inoculation is repeated
spleen) are swollen. Splenomegaly is often marked at least once. Breeders should be revaccinated prior to
(Fig. 2). onset of egg production. A live oral erysipelas vaccine
2. Petechial or suffusive hemorrhages often occur is also available for water vaccination.
in heavy muscle masses, in pericardial fat, on the 3. Semen for artificial insemination should come from
epicardium, under serous membranes, and in mucous tom turkeys with no history of erysipelas infection.
membranes. Hemorrhages vary greatly.
4. Formerly, desnooding of males was a common
3. There usually is a marked catarrhal enteritis, often hatchery practice. This practice is declining because
more apparent in the duodenum, with excess mucus outbreaks of erysipelas are not as common and oral
in the gut. infection with acute systemic disease now appears to
4. Skin lesions occur occasionally and are more apparent be more common than skin infection.
on the face, head, and neck. Inseminated hens may 5. Selection for genetic resistance may be possible.
have peritonitis, perineal congestion, and hemorrhage. Strains of turkeys selected for rapid growth have been
5. Purulent arthritis, often in more than one joint, and found to be more susceptible to naturally occurring
vegetative valvular endocarditis are seen in chronic erysipelas than unselected lines or lines selected for
cases. high egg production.
6. In all organs the dominant histopathologic finding TREATMENT
is vascular damage as evidenced by generalized 1. Penicillin and erysipelas bacterin often are inoculated
congestion, edema, focal hemorrhages, disseminated simultaneously into all birds of an infected flock. Sick
fibrin thrombi and numerous Gram-positive bacterial birds should be inoculated with a fast-acting form of
aggregates either within fibrin thrombi or engulfed by penicillin. It may be necessary to repeat the inoculation.
reticuloendothelial cells (Fig. 3). A longer acting form of penicillin can be used in birds
DIAGNOSIS not obviously sick.
1. History, signs, and lesions may suggest erysipelas but 2. Water-soluble penicillin used at a rate of 1,5 million
the etiologic agent should be isolated and identified units/gal is effective, but the disease often resumes
for confirmation. Erysipelas must be differentiated after treatment is stopped. Depending on market
from fowl cholera. Helpful necropsy findings are the conditions the cost of treatment may be greater than
markedly enlarged spleen seen in erysipelas but not the value of the commercial birds.
fowl cholera, and the pneumonia that often occurs
in fowl cholera but not erysipelas. Erysipelas also PUBLIC HEALTH
should be differentiated from acute colisepticemia, Slaughter plant management should be notified prior to
salmonellosis, streptococcosis, chlamydiosis, and the affected flock being slaughtered since these birds
virulent Newcastle disease. Erysipelas can occur could serve as a source of infection for the slaughter plant
concurrently with other diseases including fowl cholera, employees.
chlamydiosis, and internal parasitism.
2. Gram-stained impression smears from the cut surface
of liver, spleen, and bone marrow will reveal Gram-
positive, slightly bent, thin bacilli. Stained smears may
be valuable differentiating erysipelas from cholera
and colisepticemia. If available, fluorescent antibody
technique can be used to identify the organism in
smears or tissue sections.
ERYSIPELAS
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Fig. 2
Fig. 1
Splenomegaly.
Turkey with a markedly swollen
snood and dewlap.
Fig. 3
Numerous Gram-positive bacterial aggregates in the liver of a 22
week-old pheasant. Gram stain.
FOWL CHOLERA 3. P. multocida is easily destroyed by many disinfectants

(Cholera; Pasteurellosis) and by sunlight, heat, and drying. However, the
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organism persists for months in decaying carcasses

and moist soil.
DEFINITION
Fowl cholera is an infectious disease of poultry, waterfowl, EPIDEMIOLOGY
and many other birds, usually appearing in poultry as an 1. Poultry flocks that have recovered from an outbreak
acute septicemic disease with high morbidity and mortality. of fowl cholera will remain carriers of P. multocida
A chronic, localized form, most common form in chickens, and spread the disease to susceptible flocks. These
occurs in poultry and may follow the acute form, or may carriers harbor the organism in the choanal cleft and
occur independently. contaminate feed, water, and the environment with
oral fluids. Likewise, wild birds may carry the organism
OCCURRENCE and introduce it into the poultry flock if appropriate
Fowl cholera is a disease of many species of birds, including biosecurity practices are not followed.
chickens, turkeys, geese, ducks, quail, canaries, and 2. Several mammalian species are carriers of P.
many wild and zoo birds. Perhaps all birds are susceptible multocida and may introduce the organism to poultry
under appropriate conditions. In poultry, most outbreaks flocks. Swine, cats and raccoons have been shown
occur in semimature or mature birds, although there to be carriers of P. multocida and those isolated have
are exceptions. The disease occurs more frequently in been shown to be pathogenic in poultry.
turkeys than in chickens. The disease occurs frequently in
3. Birds that die of septicemic cholera have the agent
domesticated waterfowl and often causes extensive losses
in most of their tissues. Cannibalism of sick or dead
among wild waterfowl. Geese are highly susceptible. Fowl
birds is an important method of dissemination of the
cholera is more likely to occur in birds that are stressed
disease.
by such things as poor sanitation, parasitism, malnutrition,
and other diseases. Fowl cholera occurs worldwide and 4. Resistance to cholera is correlated to humoral immunity.
is a relatively common disease. There is no relationship Immunosuppression increases susceptibility.
between cholera in humans (caused by Vibrio cholerae) 5. P. multocida is resistant enough to be readily spread
and fowl cholera. on contaminated crates, feed bags, shoes, equipment,
etc.
Fowl cholera has been recognized as a disease of poultry CLINICAL SIGNS
for more than 200 years. About 100 years ago, Pasteur 1. With acute cholera, sudden unexpected deaths occur
isolated the organism and used it in one of the first vaccines. in the flock. Mortality often increases rapidly. Laying
In the United States, Dr. Salmon studied the disease as chickens may be found dead on the nest. Geese have
early as 1880. Fowl cholera was one of four major livestock been reported to just drop dead while walking across
diseases that stimulated formation of the Veterinary a barnyard. Poisoning is often initially suspected in
Division of the United States Department of Agriculture. outbreaks of acute cholera.
Although fowl cholera has been recognized and studied 2. Sick birds show anorexia, depression, cyanosis, rales,
for almost 200 years, it still remains an important disease nasal and oral discharge of mucus, and white watery
of poultry. or green mucoid diarrhea. The course of illness is
short and often followed by death. Affected chickens
often conceal themselves under equipment.
ETIOLOGY
1. The etiologic agent is Pasteurella multocida, a Gram- 3. Chronic fowl cholera is most common in chickens.
negative, bipolar-staining rod that grows readily on Often there is swelling of a joint, wattle (Fig. 1), foot
blood agar but not on MacConkey agar. Virulence pad, or tendon sheath. Exudate, often caseous, may
among isolates is highly variable. Encapsulated strains accumulate in a conjunctival sac or infraorbital sinus.
are usually highly virulent; unencapsulated isolates There may be torticollis in a few birds (Fig. 2).
are typically of low virulence. 4. Abscesses of the infraorbital sinuses and middle ear
2. The organism varies greatly in its antigenic makeup, infection resulting in torticollis, often occur in turkeys
a characteristic responsible for difficulties in producing with chronic cholera.
effective bacterins and vaccines. The gel diffusion 5. In turkey breeders there is a drop in egg production and
precipitin test has been used to describe 16 P. increased mortality following handling of hens during
multocida serotypes, all of which have been isolated insemination. Affected toms produce thin, watery, poor
from avian hosts. Serotypes 1, 3, and 3X4 are most quality semen.
commonly isolated from poultry outbreaks.
LESIONS 6. Several serological tests have been developed.

1. Lesions may be absent if the disease is very Currently an enzyme-linked immunosorbent assay
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acute. Usually there are petechial and ecchymotic (ELISA) is commercially available and widely used.
hemorrhages at a few sites, for example, on the heart, Serology is used primarily to evaluate efficacy of
under serous membranes, in mucous membranes, vaccination rather than for diagnosis of a disease
on the gizzard, or in abdominal fat. There is often outbreak.
a generalized hyperemia of the upper intestine.
Acute lesions develop as a result of disseminated CONTROL
intravascular coagulation. In layers and breeder hens, 1. P. multocida is not transmitted through the egg. Obtain
free yolk in the peritoneal cavity, acute oophoritis with clean birds and raise them in quarantine on disease-
regressing follicles, and acute diffuse peritonitis are free premises and away from all birds and mammals
frequently seen. These lesions can accompany many that might be carriers. Never add birds to the flock
other acute diseases. as they may be carriers. Avoid stresses, insofar as is
possible, and practice a high standard of sanitation.
2. In acute cases of cholera, as with other septicemias,
there often is hepatomegaly. If the birds live a few 2. Pick up and destroy all sick or dead birds before
days, there may be a few or many small necrotic foci they can be cannibalized. Birds with cholera are
in the liver (Fig. 3). Consolidation of lungs is a common teeming with P. multocida and are important in the
finding in affected turkeys (Fig. 4 and 5). With time, transmission of the agent. Dispose of carcasses by
these lesions become sequestered as necrotic areas burying or burning to prevent them from being fed on
in the lungs and these lung lesions often are extensive. by scavengers (including dogs and cats).
3. In chronic cases there may be localized inflammatory 3. Although bacterins are not always effective, in many
lesions. These often involve a joint, tendon sheath instances they do a good job of immunizing birds,
(Fig. 6), wattle, conjunctival sac, infraorbital sinus, the especially if they can be repeated at least once. They
nasal turbinates, the middle ear, or cranial bones at often are given when birds are about 8 and 12 weeks
the base of the skull. Caseous exudate in a localized old. Bacterins do not provide good cross-protection
lesion (Fig. 7) should arouse suspicion of cholera. between serotypes. Oil-emulsion bacterins are used
to immunize breeders prior to production. They can
DIAGNOSIS cause serious drops in egg production if given to
1. At necropsy, Gram-stained impression smears of laying birds. Bacterins should contain the serotype of
liver, spleen or heart blood from septicemic cases P. multocida that causes the disease at that premise.
often reveal bipolar-stained, Gram-negative rods 4. Live vaccines are given via wing web inoculation to
suggestive of P. multocida (Fig. 8). Use of blood stains chickens and via drinking water or wing web inoculation
or methylene blue readily demonstrates the bipolar to turkeys. In the United States live vaccines are
morphology of the organism. based on the Clemson University (CU) strain of P.
2. Although the history, signs, and lesions may strongly multocida. This is a naturally occurring low-virulent
suggest fowl cholera, P. multocida should be isolated organism. Since its introduction as a commercial
and identified for confirmation. Isolates should be tested product, two milder mutants of the original CU strain
for antibiotic susceptibility because of widespread have been produced: PM-1 and M-9 strains. They
resistance and should be serotyped, especially if frequently are given to turkeys at 2-6- week intervals
routine treatment and vaccination procedures appear beginning at 6-7 weeks of age in the drinking water.
ineffective or if vaccination for future prevention is Some turkey breeders are vaccinated via the wing
desired. web. Layers and breeders are inoculated by wing web
stick at 10-11 weeks of age, and revaccinated in 6-8
3. Cholera must be differentiated carefully from erysipelas
weeks. Fowl pox vaccine may be given concurrently in
and acute colibacillosis in turkeys and other birds that
the opposite wing. The live vaccines have been shown
are susceptible to both diseases. Erysipelas is caused
to be safe but vaccine reaction problems can occur in
by a Gram-positive rod. Cholera can be differentiated
the field, presumably because of immunosuppression,
readily from most septicemic and viremic diseases of
concurrent diseases, breed sensitivity, late vaccination,
poultry by the isolation of P. multocida.
or management stress such as intentional feed
4. Cholera always should be suspected if there are restriction. Parenteral administration may result in
epizootic losses in domesticated or wild waterfowl. a localized lesion, or, more seriously, arthritis. Live
5. Related organisms can cause cholera like diseases or vaccines confer better resistance than killed bacterins
complicate other diseases. These include Pasteurella and offer a broad spectrum of protection against most
gallinarum, P. haemolytica, R. anatipestifer, Moraxella serotypes.
osloensis, and Yersinia pseudotuberculosis. 5. Following an outbreak, depopulation should be
considered because many surviving birds become
carriers and transmit P. multocida. Following

depopulation, the premises and equipment should be
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thoroughly cleaned and disinfected and, if possible,

kept free of poultry for a few weeks.
6. Continuous medication programs have been used but
are generally more costly than a vaccination program.
7. Reduce rodents, scavengers, and predators in the
farm environment and limit their contact with flocks.
8. Differing susceptibilities among genetic lines of turkeys
have been shown, suggesting that selection for
resistance to fowl cholera may be possible.
TREATMENT
1. Many sulfa drugs and antibiotics will lower the mortality
from cholera but mortality may resume when treatment Fig. 2
is discontinued. Most medications are given in the Head tilt (torticolis) due to otitis in a broiler breeder.
feed or water. Sulfaquinoxaline is one of the better
treatments but will depress egg production in layers
and may throw them completely out of production.
Care should be taken to use only those products
approved by the Food and Drug Administration for the
class of poultry being treated. Drugs and antibiotics in
common use include:
Sulfadimethoxine Tetracyclines
Sulfadimethoxine + ormetoprim Erythromycin
Sulfaquinoxaline Streptomycin
Sulfamethazine Penicillin
2. Moving an infected flock to clean premises or markedly

improving sanitation during an outbreak may slow the
course of cholera. Use of live vaccine during the early
course of an outbreak may be effective.
3. If cholera cannot be controlled, it may be necessary to
Fig. 3
market the flock early. Be sure to adhere to regulations White foci of necrosis in the liver of a chicken with
relating to withdrawal of medication. acute fowl cholera.
Fig. 1
Chronic fowl cholera in a broiler breeder. Severe swelling of the Fig. 4
wattles. Subacute to chronic pneumonia in a turkey. Notice the unilateral
involvement of the lung.
FOWL CHOLERA
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Fig. 6
Subacute to chronic fowl cholera in a broiler breeder with severe
Fig. 5 synovitis, cellulitis and tendonitis.
Histopathology of the lung with acute fowl cholera.
Fibrinosuppurative exudate in the parabronchi extending into the
adjacent parenchyma.
Fig. 7
Fig. 8
Facial cellulitis in a turkey with acute fowl cholera.
Gram-stained impression smear of liver with bipolar-stained, Gram-
negative rods suggestive of P. multocida. Wright’s stain.
GANGRENOUS DERMATITIS LESIONS

(Necrotic Dermatitis) 1. There are scattered patches of darkened, gangrenous
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skin (Fig. 1), often with cutaneous sloughing or feather

loss in affected areas. Marked emphysematous or
DEFINITION
serosanguineous cellulitis (Fig. 2) underlies some skin
Gangrenous dermatitis is typically a disease of young
lesions, especially with clostridial infections.
growing chickens characterized by necrotic areas of the
skin and by a severe, underlying, infectious cellulitis. 2. Swelling and infarction may be apparent in
parenchymatous organs with necrotic foci in the liver.
OCCURRENCE 3. Severe atrophy of the bursa of Fabricius and possibly
Most outbreaks have occurred in chickens 4-20 weeks old. thymus is usually present.
Young birds of this age group may be poorly feathered.
Outbreaks often occur in excessively warm, humid houses. DIAGNOSIS
Gangrenous dermatitis also occurs in turkeys and has A tentative diagnosis often can be made on the basis of
recently been a problem for turkey producers. history and gross lesions. For confirmation, smears or
histologic sections of affected tissues will reveal bacteria.
Bacteria can be cultured from the area of cellulitis.
Gangrenous dermatitis was reported first in 1930 although
most outbreaks have been reported since 1963. Some CONTROL
of the more recent reports have suggested that affected 1. The cause of skin trauma should be found and
flocks may be immunologically deficient. eliminated. If cannibalism is a cause, it may be
necessary to trim the beaks or improve the quality
of previous beak trimming. Mechanical feeders and
ETIOLOGY equipment should be examined carefully as a source
Skin lesions develop because of trauma and growth of possible trauma.
of Clostridium septicum, C. perfringens type A, and
2. Vaccinate the breeder flock for infectious bursal
Staphylococcus aureus either singly or in combination.
disease and chicken anemia virus to prevent or reduce
possible immunosuppression in the progeny.
EPIZOOTIOLOGY
3. As much as possible, eliminate all stresses on the
1. Cutaneous wounds probably occur initially as a result
birds (e.g., parasitism, malnutrition, coccidiosis, etc.).
of cannibalism, mechanical trauma (from mechanical
feeders, etc.), or other trauma. Bacteria either invade 4. Improve sanitation in the house, particularly that of the
or multiply within traumatized skin and underlying feeders, waterers, and litter. A thorough cleaning and
tissue and their toxins or metabolites cause cellulitis. disinfection of the house may be helpful. If litter in the
Septicemia and toxemia follow, leading to death. house stays wet, improve moisture control. Repeat
problem houses may benefit from salting the floor at
2. Increased susceptibility of affected flocks to
clean out. Cheap grade feed salt is used on the soil at
infection is an important factor in the pathogenesis.
a rate of 60-100 lb/1,000 ft2.
This increased susceptibility is commonly related
to immunosuppression secondary to infectious 5. Broad-spectrum antibiotics (e.g., penicillin,
bursal disease or chicken infectious anemia virus. erythromycin, and tetracyclines) can be added to the
Reticuloendotheliosis virus and adenovirus have also ration of the flock and will reduce mortality.
been implicated.
TREATMENT
3. Other factors that may enhance susceptibility include In addition to adding broad-spectrum antibiotics to the
aflatoxicosis, nutritional insufficiency or imbalance, or ration, valuable birds can be treated individually with
poor poultry house management and sanitation. penicillin, tetracyclines, or other fast-acting antibiotics.
CLINICAL SIGNS
A sudden, sharp increase in mortality is often the first
indication of onset. When sick birds are observed, they are
depressed, and sometimes prostrate or lame. Skin lesions
often, moist and crepitant, are apparent in live or dead
birds. The course of the illness is often less than 24 hours.
Mortality varies but can be quite high.
GANGRENOUS DERMATITIS
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Fig. 1 Fig. 2
Darkened, gangrenous skin of a broiler Emphysematous and
chicken with gangrenous dermatitis. serosanguineous cellulitis in
a chicken with gangrenous
dermatitis.
INFECTIOUS CORYZA 4. There are several strain classification schemes. The

(Coryza) Page scheme recognizes three antigenic types (A,
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B, C) of A. paragallinarum, although all types share

certain antigens. Hemagglutinins produced by the
DEFINITION organism appear to be important antigens capable
An acute or subacute disease of chickens, pheasants,
of inducing protection against infectious coryza.
and guinea fowl characterized by conjunctivitis, oculonasal
Bacterins are available that allow limited protection to
discharge, swelling of infraorbital sinuses, edema of the
laying chickens.
face, sneezing, and sometimes by infection of the lower
respiratory tract. Prolonged outbreaks are now believed EPIDEMIOLOGY
to be outbreaks complicated by other diseases, especially Chronically ill or apparently healthy carrier birds are the
Mycoplasma gallisepticum infection (chronic respiratory major reservoirs of infection and readily transmit the agent
disease). to susceptible chickens. Transmission probably occurs
by inhalation of infectious aerosol coughed into the air
OCCURRENCE or through ingestion of contaminated feed or water. The
Chickens are primarily affected, although the disease has etiologic agent can be transmitted by fomites, although it
been reported in pheasants and guinea fowl. All ages of soon perishes outside of the host. Recovered birds are
chickens are susceptible although most natural outbreaks frequently carriers.
occur in chickens that are half grown or older. The
disease is seen more frequently on chicken farms where CLINICAL SIGNS
facilities are never emptied of chickens. The disease has 1. Usually there is a rapid onset and morbidity is high in
a worldwide distribution. Infectious coryza does not occur the flock. Feed consumption, egg production or growth
in turkeys and should not be confused with turkey coryza are reduced noticeably.
caused by Bordetella avium.
2. There is oculonasal discharge, conjunctivitis with
some adherence of eyelids, edema of the face (Fig. 1)
HISTORICAL INFORMATION (occasionally of the wattles) (Fig. 2), respiratory noises,
Infectious coryza was believed to be a separate disease and, perhaps, diarrhea. Later, some of the birds may
of chickens as early as 1920 but this was not confirmed have swollen infraorbital sinuses and/or exudate in the
until 10-15 years later. The incidence of coryza has varied conjunctival sac. There is considerable variation in the
markedly. Presently coryza is a disease of considerable severity and length of course in flock outbreaks.
importance, especially on multiage egg production
3. Respiratory signs usually persist for only a few weeks.
complexes.
Persistence of signs occurs when complicated by fowl
pox, M. gallisepticum, infectious bronchitis, Pasteurella
ETIOLOGY sp., or infectious laryngotracheitis and unthrifty birds
1. The etiologic agent, Avibacterium paragallinarum will become apparent. Persistence of signs was once
(formerly Hemophilus paragallinarum and H. attributed entirely to strains of A. paragallinarum of low
gallinarum) is a Gram-negative, bipolar-staining, virulence.
nonmotile rod with a tendency toward filament
formation. A. paragallinarum requires V-factor GROSS LESIONS
(nicotinamide adenine dinucleotide), which is available 1. There is catarrhal inflammation of nasal passages
in certain enriched medium (i.e., chocolate agar). It and sinuses and nasal discharge often is apparent
grows on blood agar (with a Staphylococcus aureus (Fig. 3). One or both infraorbital sinuses may be
nurse colony) as dewdrop-like satellite colonies in a distended with exudate (similar distension can occur
microaerophilic environment. V-factor independent with localized fowl cholera, pox, vitamin A deficiency,
isolates have been described from South Africa and and staphylococcal infection).
Mexico. 2. There is conjunctivitis, frequently with adherence of
2. A. paragallinarum is not a very resistant organism the eyelids or with accumulation of cheesy exudate in
and will persist outside of the host for only a few the conjunctival sac.
days. It is easily destroyed by many disinfectants 3. There often is edema of the face and, occasionally,
and by environmental factors. The organism is of the wattles. In complicated cases there may be
susceptible in vitro to many chemicals and antibiotics, tracheitis, pneumonia, or airsacculitis.
including spectinomycin, neomycin, novobiocin, and
tetracycline. DIAGNOSIS
3. A. paragallinarum is present in sinus exudate and is 1. Typical history, signs, and lesions are suggestive
easily demonstrated in stained smears. of coryza, although other respiratory diseases of
chickens must be ruled out.
2. A smear of sinus exudate should be made and Gram

stained. It should reveal Gram-negative, bipolar-
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staining rods with a tendency toward filament formation

and pleomorphism.
3. Aseptically collect sinus exudate and swab it on blood
agar. On the same plate then make an S-shaped streak
of S. aureus (use a strain that excretes V-factor), which
will serve as a feeder colony. Incubate the culture in a
candle jar. Tiny dewdrop satellite colonies (Fig. 4) of A.
paragallinarum will grow adjacent to the feeder colony.
The organism can be further identified by biochemical
means or by a PCR test specific for A. paragallinarum.
4. A nonpathogenic species, Avibacterium avium,
(Hemophilus avium) may be cultured from the
sinus, either alone or with A. paragallinarum.
A. paragallinarum is catalase negative and the
nonpathogenic species is catalase positive.
5. Put a small amount of sinus exudate in the infraorbital
sinus of a few young susceptible chickens. Typical
signs and lesions develop in 3-5 days (rarely less).
6. Hemagglutination inhibition and immunodiffusion tests
can be used to detect A. paragallinarum antibodies in
serum. Both tests are serotype specific.
CONTROL
1. Depopulate, if necessary, to eliminate all carrier birds.
Leave the premises vacant for two to three weeks after
thorough cleaning and disinfection before restocking
with 1-day-old or other coryza-free chickens. As much
as possible, raise them in quarantine.
2. Commercial bacterins can be used to immunize
chickens and protect only for the serotype included
in the vaccine. All pullets to be housed on multiage
infected farms should receive two injections of the
bacterin at 4-week intervals prior to 20 weeks of age.
The first vaccination should be given after the birds
reach 10 weeks of age.
TREATMENT
Various sulfonamides and antibiotics have been used to
alleviate the severity, usually in feed or drinking water.
Birds usually respond to treatment but relapses may
occur when treatment is discontinued. Erythromycin and
oxytetracycline are commonly used in layer operations.
INFECTIOUS CORYZA
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Fig. 1 Fig. 2
Facial edema in a White Leghorn pullet. Male broiler breeder with edema of both face and wattles.
Fig. 3 Fig.4
White Leghorn pullet with slight facial edema and showing nasal 48-hr culture of A. paragallinarum on Casman blood agar showing
discharge. satellite growth of S. epidermidis streak.
MYCOPLASMOSIS been shown to cause periorbital swelling, conjunctivitis and

mortality.
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PREFACE
Mycoplasmas belong to the Order Mycoplasmatales, HISTORICAL INFORMATION
are the smallest prokaryotic organism (DNA content) In the United States the disease was first described in
cultivatable on artificial medium and are completely devoid turkeys in 1905, then in chickens in 1935. MG became
of a cell wall. The absence of a cell wall accounts for their of major importance as the poultry industry expanded
pleomorphic shape, fried-egg colony appearance and their over the last 25 years. The first of a series of national
resistance to penicillin-like antibiotics. Over twenty-five conferences on mycoplasmosis in poultry was held in
species have been identified from avian hosts although 1962 and recognized the importance of MG. Considerable
several isolates are unidentifiable. Generally, mycoplasmas progress has been made in the control and eradication of
have a narrow host range. Four mycoplasma species are MG, especially in turkeys, but the disease is still of major
considered pathogenic to commercial poultry; Mycoplasma importance.
gallisepticum, M. synoviae, M. meleagridis and M. iowae.
Pathogenic species generally infect the respiratory system MG is one of the more costly poultry diseases, sharing that
but other systems may be involved. Transmission is distinction in the United States with Marek’s disease and
generally by direct contact although egg transmission, Newcastle disease. A few years ago the annual loss from
carrier birds and fomites are of importance. The cultivation MG was estimated at 125 million dollars.
of Mycoplasma sp. is somewhat demanding and requires
specialized media containing 10 – 15% serum, yeast-
ETIOLOGY
derived components and unique factors for certain species.
1. M. gallisepticum is the etiologic agent. In poultry flocks,
Colony morphology is variable but is characterized by a
other infecting organisms complicate or increase the
“fried-egg” appearance. In general, colony morphology,
pathogenicity of MG infections. Typical complicating
cultural characteristics or carbohydrate fermentation are
organisms include: infectious bronchitis virus,
not useful for speciation. Identification to the species level
Newcastle disease virus, Escherichia coli, Pasteurella
is usually based on immunologic tests utilizing species-
multocida, and Avibacterium paragallinarum.
specific antisera or amplified DNA type tests. Inoculation of
5-7 day-old embryos is an alternative isolation procedure 2. M. gallisepticum seldom survives for more than a few
utilized when artificial media is unrewarding. Alternatively, days outside of the host. Carrier birds are essential for
clinical material can be inoculated into young chickens or its survival.
turkeys and a comparison of pre-inoculated sera with 3-5 3. In chickens the organism may be present and cause
week post-inoculated sera by the immunologic tests may no disease until triggered by stress, such as changes
provide clues as to which Mycoplasma sp. is involved. in housing, management, nutrition, or weather;
vaccination against or infection with infectious
I. MYCOPLASMA GALLISEPTICUM bronchitis or Newcastle disease; or increased levels of
dust or ammonia in the environment.
INFECTION
4. M. gallisepticum strain variability exists and accounts
(MG; Chronic Respiratory Disease (CRD); for the variability of host susceptibility, clinical
Infectious Sinusitis of Turkeys) presentation and immunologic response.
(See Table on Page 116)
EPIDEMIOLOGY
DEFINITION M. gallisepticum is transmitted in some of the eggs
A mycoplasma infection characterized by respiratory signs (transovarian transmission) laid by inapparent carriers.
and lesions, a prolonged course in the flock and primarily Infected progeny then transmit the agent horizontally,
affecting chickens and turkeys. In turkeys the disease probably through infectious aerosols coughed into the
is frequently manifested by swelling of the infraorbital air and through contamination of feed, water, and the
sinus(es) and called infectious sinusitis. environment. The agent probably can be transmitted by
other species of birds, domestic or wild. In addition the
agent can be transmitted mechanically on shoes, feed
OCCURRENCE sacks, crates, etc.
Mycoplasma gallisepticum (MG) occurs primarily in
chickens and turkeys but also has been reported in
partridge, pheasants, peafowl, quail, guinea fowl, ducks, CLINICAL SIGNS
geese, and pigeons. All ages of chickens and turkeys can Signs usually develop slowly in the flock. They vary
have the disease although the very young are seldom in severity depending on strain of organism, and may
submitted for the disease. Since 1994, a serious M. persist for weeks or months. Signs are the same as those
gallisepticum infection of free-ranging house finches has observed with many other avian respiratory diseases.
They include coughing, sneezing, snicks, rales, ocular and
nasal discharge, and, in turkeys, swelling of the infraorbital MG ELISA test. Cross-reactions usually do not occur
sinus(es) in occasional birds. Additional signs are listed when the HI or ELISA test is used. Flocks recently
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below. vaccinated with oil-based vaccines may also produce

false-positive agglutination tests.
1. Adult layers- Drop in feed consumption and egg 3. A commercial PCR test specific for M. gallisepticum is
production. Egg production continues at a lower level. available. Tracheal swabs from a number of birds can
Mortality is low but there may be many unthrifty birds. be tested.
2. Broilers (4-8 weeks old) - Signs are more pronounced 4. Isolation and identification of M. gallisepticum can be
than in adult birds and the disease is more severe. cultured from exudate, trachea, sinuses, air sacs, or
Feed intake and growth rate are reduced. Mortality is lungs on artificial media (Fig. 8) or in chick embryos.
variable but may be high, particularly if poor husbandry, MG identified isolates can be compared by molecular
exposure, or other stress factors are present. techniques for epidemiologic purposes.
3. Turkeys- In addition to swelling of one or both 5. In many instances it will be necessary to differentiate
infraorbital sinuses (Fig. 1), infected turkeys may have MG from other respiratory diseases of poultry, usually
nasal exudate wiped on their wings. Alternatively, if by culture or serologic tests. Pulmonary and air sac
the air sacs and lungs are primarily involved, mortality lesions may be confused with colibacillosis and
from pneumonia and airsacculitis may be very high aspergillosis. In turkeys, fowl cholera is a frequent and
although few birds have swollen sinuses. important complication and may be accompanied by
LESIONS a fibrinous pneumonia. Sinusitis in turkeys can also
1. Poor physical condition and loss of weight are usually be caused by avian influenza, M. synoviae infection,
apparent and suggest the presence of a chronic cryptosporidiosis, and avian metapneumovirus.
disease. CONTROL
2. There is marked catarrhal inflammation of the nasal 1. Depopulation of infected premises should precede
passages, sinuses, trachea, and bronchi and air sacs establishment of a “clean” flock. Thoroughly clean and
(Fig. 2). Air sacs often are thickened (Fig. 3) and opaque disinfect the houses and leave them vacant for a few
and may contain hyperplastic lymphoid follicles in their weeks.
wall (Fig. 4). Recent vaccination against Newcastle 2. Prevention is based largely on obtaining chicks or
disease or infectious bronchitis may enhance opacity poults hatched from eggs from MG-free breeder flocks.
of air sacs. Air sacs often contain mucoid or caseous The MG-free progeny are then raised in quarantine.
exudate. MG-free breeder flocks have been established for both
3. The following classic triad of lesions is often the chickens and turkeys as part of the National Poultry
basis of extensive condemnation of infected birds at Improvement Plan. They are monitored by serologic
slaughter: airsacculitis, fibrinous perihepatitis, and testing to assure that they and their eggs are free of M.
adhesive pericarditis (Fig. 5). These lesions are not gallisepticum. Quarantine measures must be strictly
pathognomonic and may occur with chlamydiosis or enforced and good management and sanitation must
septicemia. be practiced to keep a flock free of infection.
4. In infectious sinusitis of turkeys, lesions may be 3. The vaccination of replacement pullets scheduled
restricted to swelling of the infraorbital sinuses. to enter MG positive layer complexes is practiced in
Conversely, sinusitis may be absent although rhinitis, most states. Three live commercial vaccines (F-strain,
tracheitis, and airsacculitis occur and there may TS 11 and 6/85) are available and are administered
be a fibrinous pneumonia. Occasional turkeys and via fine spray or eye-drop to birds during the growing
chickens may have the oviduct distended with exudate period to protect them from clinical disease during
(salpingitis). the laying period. The live F-strain MG vaccine is
pathogenic in turkeys. An oil-emulsion- based bacterin
DIAGNOSIS is also available for use in replacement pullets destined
1. A history of chronic respiratory disease accompanied for multiage egg production complexes where MG is
by lowered feed consumption, poor weight gains, or established in older hens.
lowered egg production is suggestive of MG. Typical
4. Many MG-free breeder flocks were established initially
gross lesions are very suggestive.
by identifying small flocks that were not infected and
2. Positive serum plate (Fig. 6) or tube agglutination using that flock as a nucleus. In addition egg dipping
tests for MG on sera from a few birds in the flock (in antibiotic solutions), heat sterilization, and antibiotic
strengthen the diagnosis. Because sera from birds treatment of hatching eggs have all been used in
with Mycoplasma synoviae may cross-react, it is a attempts to obtain disease-free progeny from infected
good plan to confirm some of the agglutination tests breeder flocks. All of the latter three methods reduce
with the hemagglutination inhibition (HI) test (Fig. 7) or the number of infected progeny that hatch from eggs
from infected flocks. No antibiotic or drug given to cause of condemnation at slaughter. MM infection was
infected breeders will prevent them from laying some found to be the cause.
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infected eggs. 3. M. meleagridis has been eliminated from the major

primary turkey breeders. Infection in commercial flocks
TREATMENT
is not uncommon.
1. Marketing an infected flock with a low incidence of
the disease may be more economical than treatment 4. Skeletal abnormalities have been referred to as
because treatment is very expensive and doesn’t clear TS-65 (Turkey Syndrome 65) and crooked necks
the infection. Consider this possibility initially. abnormalities have been referred to as wryneck.
2. Improve the management, husbandry, or nutrition if ETIOLOGY
possible. In particular, try to reduce the dust to which 1. The etiologic agent is M. meleagridis. The organism is
the birds are exposed if dust is excessive. Remove fastidious in its growth requirements and, presumably,
accumulated manure and improve ventilation if easily destroyed by environmental factors and most
ammonia levels are excessive. Eliminate all possible disinfectants.
sources of stress.
2. Concurrent infection with other mycoplasmas can
3. Many broad-spectrum antibiotics have been used occur and increases the severity of lesions.
for treatment and will suppress losses. However,
relapses often occur when treatment is discontinued. EPIDEMIOLOGY
Most antibiotics are given in feed or water, preferably 1. Infected breeder hens lay some eggs containing M.
in water. Tylosin and tetracyclines have been used meleagridis, transmitting mycoplasma to some of their
extensively for treatment. Injectable antibiotics may be progeny. Organisms are spread horizontally to many
more effective if the disease is advanced and if the hatchmates via aerosols from the respiratory tract or
flock is small enough to be treated individually. Be sure to the vent on contaminated hands during vent-sexing.
to follow recommended antibiotic withdrawal times to
2. In some progeny, the organism later spreads to and
prevent residues in meat.
localizes in the reproductive tract. In male turkeys
II. MYCOPLASMA MELEAGRIDIS localization is often in the cloaca and/or phallus and
their semen may contain the agent.
INFECTION
3. Artificial insemination of turkey hens with pooled
(MM Infection) infected semen is an important method of MM spread.
(See Table on Page 116) 4. Most tom and hen turkeys overcome MM infection
DEFINITION after one breeding season. By then the infection has
An egg-transmitted mycoplasmosis of turkeys already been transmitted to many of their progeny.
characterized by inapparent venereal infection in breeder 5. MM has a distinct predilection for the bursa of Fabricius
turkeys, airsacculitis in recently hatched poults and late and can cause immunosuppression, which may
embryo mortality. explain why infected turkeys are more susceptible to
other infections, especially colibacillosis.
OCCURRENCE CLINICAL SIGNS
Mycoplasma meleagridis (MM) infection is confined to Most of the following signs are mild or inapparent on casual
turkeys and occurs in all age groups. The disease is examination and go unobserved.
usually inapparent except in nonhatching turkey embryos
or recently hatched poults in which it causes airsacculitis. 1. Often there is impaired hatchability, due to late term
Most large turkey breeder flocks are now free of MM embryo death, in eggs from infected flocks. Embryo
infection. mortality is highest after eggs are transferred to the
hatcher and at pipping.
HISTORICAL INFORMATION 2. Poults hatched from infected lots of eggs may have
1. Airsacculitis in newly hatched poults was first noted in a high incidence of starve outs and may make poor
1958 but was not considered a major cause of loss weight gains.
because the lesions usually regressed. Airsacculitis
at time of slaughter was usually attributed to infection 3. Young growing poults may show mild respiratory signs
with Mycoplasma gallisepticum (MG) or Mycoplasma and occasional poults may have sinusitis.
synoviae (MS). 4. Small numbers of poults may have skeletal
2. After MG and MS infections were brought under abnormalities associated with a deforming
control, airsacculitis still remained as a significant osteomyelitis in cervical vertebrae (crooked neck) or
leg deformities.
5. Adult breeders usually show no signs (Fig. 1) of 4. Repeated serologic testing alone has not been
venereal or respiratory infection. successful in establishing clean flocks. However, both
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egg dipping and testing programs have value.

LESIONS
1. Infected, pipped, unhatched embryos and recently 5. Poults are often injected with an antibiotic during
hatched poults have a variable degree of airsacculitis servicing in the hatchery, which probably aids in
(Fig. 2) manifested by thickening of air sac membranes reducing MM infections.
and possibly by the presence of small amounts of 6. Treatment of semen with antibiotics results in an
yellow exudate in the air sacs (Fig. 3). In uncomplicated unacceptable decrease in sperm viability.
MM, lesions regress and disappear in most turkeys by
marketing time. TREATMENT
Because MM is sensitive to tylosin and tetracyclines,
2. Poults with wryneck may have a cervical airsacculitis they may be of value in controlling airsacculitis in infected
and osteomyelitis of adjacent vertebrae that can be turkeys. It is unlikely they would be effective in controlling
demonstrated microscopically. venereal infection. Use of lincomycin/spectinomycin in the
3. Adult breeders are free of gross lesions of the drinking water (2 g/gal) for the first 5-10 days of life reduced
genitalia. However, outbreaks of airsacculitis, the incidence of airsacculitis and improved weight gains.
synovitis, and sinusitis have been observed in mature
and semimature turkeys from which only MM could be
isolated.
III. MYCOPLASMA
SYNOVIAE INFECTION
4. MM can also cause a generalized skeletal disorder
historically known as turkey syndrome 65 (TS 65) (MS, Infectious Synovitis; Tenovaginitis)
characterized by chondrodystrophy, or unilateral or (See Table on Page 116)
bilateral varus deformities (Fig. 4) and perosis.
DEFINITION
DIAGNOSIS Predominately a subclinical upper respiratory infection of
1. Monitor pipped embryos and weak, cull poults for the chickens and turkeys. Systemic infection results in an acute
presence of air sac lesions. or chronic condition of chickens and turkeys characterized
2. Diagnosis can be made by the isolation and by inflammation of synovial membranes and, usually, by
identification of MM from infected tissues or exudates. exudate in the joints and tendon sheaths of many infected
The organism is fastidious and requires special media. birds. Synovial involvement is referred to as infectious
Isolates must be differentiated from MG, MS, and other synovitis.
mycoplasmas by serologic methods or fluorescent
antibody techniques. OCCURRENCE
3. Turkeys infected with MM develop antibodies in 3-5 Respiratory M. synoviae infections are common in multi-age
weeks. These antibodies can be demonstrated by commercial layer flocks and are predominately subclinical.
plate and tube agglutination tests. Positive reactors The Infectious Synovitis form occurs in chickens, especially
can be confirmed by hemagglutination inhibition tests. in broilers, but the disease also occurs in turkeys. The
These tests alone are not adequate for eradication disease is usually seen in young (4-12-week-old) chickens
of infection but can indicate infection in a flock. Test or young (10-12-week-old) turkeys. It has been seen
antigens are commercially available. in adult layers and in chicks as young as 6 days of age.
Synovitis occurs throughout the year but is more severe
CONTROL during the cold, damp seasons or whenever the litter is
1. Poults should be obtained from MM-free breeder wet. The disease is probably worldwide in distribution.
flocks. The incidence of clinical disease has greatly decreased in
2. A breeder flock free of MM infection can be established recent years in the United States.
by inoculating all of the turkey eggs for hatching with
0.6 mg of gentamicin sulfate and 2.4 mg of tylosin in a HISTORICAL INFORMATION
0.2-ml volume. The newly hatched flock is monitored Infectious synovitis was first described in chickens in
by culturing pipped (unhatched) eggs and 1-day-old 1954 and in turkeys in 1955. Although the disease was
cull poults and by using the plate agglutination test on uncommon initially, it is now well established. It is said to
sera from the flock. be less commonly encountered today than a decade ago.
3. Dipping the eggs from infected breeder flocks into
solutions of tylosin or gentamicin will substantially ETIOLOGY
reduce the incidence of infection in the progeny. 1. The etiologic agent is M. synoviae (MS), a fastidious
Dipping is often combined with temperature- or organism that requires nicotinamide adenine
pressure-differential techniques. dinucleotide for growth. There appears to be only one
serotype of the organism, although isolates vary in orange or yellow. Breast blisters often are present
pathogenicity. secondary to trauma from resting on the floor.
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2. M. synoviae is a fastidious organism. It can usually be 3. Respiratory lesions may be absent or consist of
grown in 5-7-day-old embryonating chicken eggs or in a mild mucoid tracheitis, airsacculitis (Fig. 3), or
special mycoplasma media. A commercially available sinusitis, lesions that are usually associated with M.
PCR test can rapidly identify a MS positive flock. gallisepticum infection (chronic respiratory disease).
3. Convalescent sera from birds with M. synoviae will Such birds may not have the usual lesions of synovitis
agglutinate commercially available M. synoviae plate described above.
antigen. During the early stages of synovitis the sera DIAGNOSIS
may also agglutinate Mycoplasma gallisepticum plate 1. Typical signs and gross lesions, especially epizootic
antigen. Cross-reactions usually do not occur when lameness and characteristic exudate in swollen joints
hemagglutination inhibition (HI) or ELISA tests are or tendon sheaths, are suggestive of synovitis. The
used to separate M. synoviae from M. gallisepticum diagnosis can be strengthened by obtaining positive
infection. plate agglutination tests for synovitis on sera from birds
EPIDEMIOLOGY in the flock (Fig. 4). Three to 5 weeks are required for
1. Transovarian transmission is an important means of antibody formation to have occurred.
spread of the infectious agent. Only a small number 2. M. synoviae can be isolated on special media or in
of eggs from reactor birds carry M. synoviae and most 5-7-day embryonating chicken eggs. Trachea (Fig. 5),
of them are laid during the earlier stages of infection. sinuses, air sacs or synovial exudate are preferable
2. Infection also spreads horizontally via the respiratory for culture. The isolated Mycoplasma can be identified
tract. Such spread is slow and only part of the infected by direct fluorescent antibody techniques applied to
birds develop joint lesions. colony imprints (Fig. 6). Alternatively, exudate may be
inoculated into the foot pad of chickens and turkeys
3. The organism has a predilection to localize in synovial- to reproduce typical lesions. Later, their preinoculation
lined structures such as joints, tendon sheaths and and convalescent sera may be tested against M.
bursas (breast blisters). It also localizes in the ovary synoviae antigen and M. gallisepticum antigen. The HI
and, occasionally, in the air sacs or sinuses. test can be used to confirm agglutination test results.
CLINICAL SIGNS 3. A commercial PCR test specific for M. synoviae is
1. Lameness in many birds and a tendency of affected available. Tracheal swabs from a number of birds can
birds to rest on the floor are prominent early signs. be tested.
Many affected birds have pale head parts and swollen 4. Synovitis must be differentiated from arthritis caused
hocks or foot pads. The feces of acutely affected birds by Staphylococci, fowl typhoid, pullorum disease,
often are green. Eventually, affected birds become and viral arthritis. Agents of the first three are easily
dehydrated and thin because of failure to eat and drink cultured. Viral arthritis should infect experimentally
regularly. inoculated chickens but not turkeys.
2. Morbidity is usually low to moderate but may be high
if there is damp, cold weather or the litter is wet. CONTROL
Mortality is usually less than 10% unless there are 1. In most areas it is now possible to get chicks or poults
other diseases present or the husbandry is poor. that were hatched from eggs from MS-free flocks. If
possible, start with such chicks or poults.
3. A slight, transient egg production drop maybe observed
in acutely infected layer flocks. 2. As far as possible, raise the birds in quarantine under
the all-in, all-out system.
4. Respiratory tract infections are usually asymptomatic.
3. Synovitis can usually be prevented by continuously
LESIONS giving the birds a low-level antibiotic in the feed. This
1. In the early phase of synovitis most synovial-lined is an expensive procedure. Many antibiotics used for
structures (joints, tendon sheaths) contain a sticky, treatment can be used for prevention but are fed at a
viscid, grey to yellow exudate (Fig. 1). This is usually lower level.
more voluminous in swollen hock or wing joints or 4. Commercial M. synoviae vaccine is available and
under swollen foot pads (Fig. 2). maybe beneficial in certain management situations.
2. In later stages of the disease the birds may be
emaciated or thin and there may be no lesions in TREATMENT
internal organs. Exudate in joints and tendon sheaths Treatment of lame birds with well-established synovitis
may be inspissated or joint surfaces may be stained is usually not very satisfactory. Relatively high levels of
antibiotics are required and may be given in feed or water.
Tetracyclines have been widely used. Streptomycin has
been used intramuscularly in small groups of birds where any cause disease. The only other mycoplasma of note that
they could be handled individually. occasionally causes clinical disease in commercial poultry
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flocks is M. iowae. M. iowae, like M. meleagridis, is spread

venereally and typically causes reduced hatchability and
IV. OTHER MYCOPLASMA INFECTIONS late term embryo mortality in turkeys.
Many other species of mycoplasmas are isolated from
poultry, especially hobbyist and household flocks. Few if
MYCOPLASMA GALLISEPTICUM
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Fig. 2
Fig. 1 Acute MG airsacculitis in the abdominal air sac of a broiler chicken.
Swollen sinuses in a MG infected turkey.
Fig. 4
Lymphoid nodules are prominent in this air sac. Increased air
Fig. 3
sac thickness is due also to a diffuse infiltration of lymphocytes,
Thickened posterior thoracic air sac in a chicken.
macrophages and plasma cells.
Fig. 5
Classic triad of lesions; adhesive pericarditis, fibrinous perihepatitis Fig. 6
and airsacculitis. Serum-plate-agglutination test with MG antigen. The serum sample
on the right is positive, and the sample on the left is negative.
MYCOPLASMA GALLISEPTICUM
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Fig. 7 Fig. 8
HI test with 3 negative and 3 positive sera. Sera are diluted from Typical MG colonies as observed by microscopic examination of
top-to bottom, beginning at 1:10. Sera in rows 2, 3, and 4 are from agar medium at 35X.
negative control birds (the top well is a serum control). Sera in rows
5, 6, and 7 are from MG-infected chickens. Their titers are 1:640,
1:320 and 1:80 respectively. Rows 8 and 9 are antigen controls and
rows 10 and 11 are cell controls. Rows 1 and 12 are empty.
MYCOPLASMA MELEAGRIDIS
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Fig. 1 Fig. 2
Flock of MM positive turkey hens with no clinical signs of infection. Mild airsacculitis.
Fig. 3
Fig. 4
MM-caused airsacculitis in a 4 week-old poult; the lesion has
Bowing of the tarsometatarsal bones of a 3-week-old
progressed from the thoracic air sacs to the abdominal air sacs by
poult infected during embryonic development with the
this age. If the disease is uncomplicated, the lesions will regress
pathogenic RY-39 strain of MM.
within 16 weeks.
MYCOPLASMA SYNOVIAE INFECTION

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Fig. 2
Fig. 1
Enlarged footpads typical of MS infectious synovitis.
Incised swollen hock joint of chicken with MS synovitis.
Fig. 4
Fig. 3 Rapid serum-plate test to detect for the presence of antibodies for
Chronic airsacculitis: thickening of the air sac membrane with large MS in the sera of infected chickens or turkeys. Agglutination of the
masses of caseous exudate. rose-bengal-stained antigen is noted by aggregates or clumps of MS
organism by specific antibodies produced by the infected birds.
Fig. 6
Fig. 5 Greenish glow of colonies MS positive in the fluorescent-antibody
Chicken with its tongue pulled aside to position the larynx (FA) test.
for insertion of a cotton swab to obtain tracheal exudate for
culture of most avian mycoplasma, including MS. Tracheal
infection tends to persist for several weeks to months.
THE MYCOPLASMOSESA
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Name(s) of the Disease Etiologic Agent Nature of the Disease Major Lesions
Mycoplasma Mycoplasma A respiratory disease. Airsacculitis, adhesive pericarditis,

gallisepticum gallisepticum fibrinous perihepatitis. Occasionally
infection; chronic causes synovitis or salpingitis.
respiratory disease
Infectious sinusitis Mycoplasma Unilateral or bilateral Swollen infraorbital sinus(es) may or

gallisepticum sinusitis. May may not be followed by airsacculitis,
spread to or occur pericarditis, and perihepatitis.
initially in the lower
respiratory system.
Infectious synovitis Mycoplasma Involves synovial Swollen joints and tendon sheaths.
synoviae lining of joints, tendon Feet, shanks, hocks more obviously
sheaths. Results in affected. Occasionally causes
lameness, debility. airsacculitis in broilers and turkeys.
Mycoplasma meleagridis Mycoplasma A venereal infection Airsacculitis in nonhatching or

infection; MM infection meleagridis of turkeys, usually newly hatched poults. May spread
transmitted by horizontally to other young poults
infected semen. as an airsacculitis. May lead to
Produces airsacculitis airsacculitis in market birds.
in many progeny.
Mycoplasma Mycoplasma Associated with Infected turkey embryos die

iowae infection iowae reduced hatchability from about 18 days of incubation
and embryo mortality with lesions of stunning and
in turkeys. May congestion with hepatitis,
spread venereally. edema and splenomegaly.
A
More than 20 serotypes of Mycoplasma have been identified in chickens, turkeys, and ducks. These are the most
significant pathogens.
NECROTIC ENTERITIS GROSS LESIONS

1. Lesions are usually found in the mid-small intestines,
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DEFINITION which are distended and friable.

Necrotic enteritis is an acute bacterial infection primarily of 2. The intestine is typically distended, the mucosa is
chickens and turkeys, although other avian species can be covered by a brownish diphtheritic membrane (Fig. 1)
affected. The disease is characterized by sudden death, and contents consist of foul-smelling brown fluid (Fig.
distended intestines with necrosis of the intestinal mucosal. 2).
3. Severe dehydration with darkening of the breast
OCCURRENCE muscle and swelling and congestion of the liver may
Chickens 2-10 weeks of age raised on litter are most also be present (Fig. 3, normal and congested livers).
frequently involved. Turkeys that are 7-12 weeks of
age are also affected. Both species usually have some DIAGNOSIS
predisposing enteric condition. 1. Intestinal mucosal appearance and typical history of
acute and dramatic increase in mortality is strongly
suggestive of necrotic enteritis.
Necrotic enteritis was first reported in 1961 and has been 2. Histologically, there is heavy clostridial colonization
reported to occur where ever poultry are produced. of the villous epithelium accompanied by coagulative
necrosis of the mucosa (Fig. 4).
ETIOLOGY 3. Identification of a predisposing factor is necessary for

1. Clostridium perfringens (mostly type A but also C) successful treatment and prevention.
and their toxins are the cause of necrotic enteritis.
CONTROL
These bacteria are anaerobic Gram-positive rods
1. Good management practices of cleaning and
and produce double-zoned hemolysis on blood-agar
disinfection of poultry houses prior to bird placement
plates.
are essential. Repeat problem houses may benefit
2. Alpha toxin is produced by C. perfringens type A and from salting the floor at cleanout. Cheap grade feed
C and beta toxin is produced by C. perfringens type C salt is used on the soil at a rate of 60-63 lb/1,000 ft2.
and is responsible for the mucosal necrosis.
2. All predisposing factors must be controlled and the
3. Recent research on the pathogenesis of necrotic coccidia prevention program verified.
enteritis has focused on a gene known as NetB which
3. Administration of appropriate feed medication may be
is responsible for producing a pore forming compound.
warranted.
4. C. perfringens are ubiquitous and are normal
inhabitants of the intestinal tract. TREATMENT
Determination of predisposing condition will dictate specific
5. Slower peristaltism or intestinal mucosal damage
medication. The clostridial component of this disease
is necessary for the Clostridia to attach, proliferate
usually responds well to the same antibiotics specified
and produce sufficient toxin. Coccidiosis, ascarid
for ulcerative enteritis (i.e., bacitracin, penicillin, and
migration, hemorrhagic enteritis in turkeys, and severe
lincomycin).
salmonella infection are predisposing conditions for
mucosal damage.
EPIDEMIOLOGY
Necrotic enteritis often develops as an acute terminal
complication of other primary intestinal diseases or in
situations where the intestinal microflora is disturbed or the
host is severely immunosuppressed. A disturbed intestinal
microflora can result from sudden changes in feed
formulation such as addition of high levels of fish meal or
wheat. Immunosuppression from infectious bursal disease
or hemorrhagic enteritis frequently precedes necrotic
enteritis.
CLINICAL SIGNS
The acute onset of depressed, ruffled birds occurs; these
birds rapidly progress to death. There is a rapid increase
in mortality.
NECROTIC ENTERITIS
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Fig. 1 Fig. 2
In a case of necrotic enteritis, the intestine are typically distended NE in a broiler chicken: Intestinal contents consist of foul-
with the mucosa covered by a brownish diphtheritic membrane. smelling brown fluid.
Fig. 3 Fig. 4
Severe dehydration with darkening of the breast muscle and Histologically, there is heavy clostridial colonization of the
swelling and congestion of the liver may also be present (chicken villous epithelium accompanied by coagulative necrosis of the
dead with necrotic enteritis on the right, normal chicken on the mucosa.
left).
ORNITHOBACTERIUM 2. In most disease situations, other primary respiratory

agents can be demonstrated (Bordetella avium,
RHINOTRACHEALE INFECTION
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Mycoplasma sp., Pasteurella sp., Escherichia coli,

(OR, ORT) paramyxovirus, and infectious bronchitis virus).
DEFINITION CLINICAL SIGNS

Ornithobacterium rhinotracheale (OR) is a recently Mild respiratory signs are most frequently observed
encountered bacterium which has been associated with with only a slight increase in mortality. Older birds may
respiratory disease in poultry. Certain bacteriologic and experience more severe respiratory signs with gasping,
pathologic aspects of the organism and disease have only marked respiratory effort and an increase in mortality.
recently been investigated.
LESIONS
OCCURRENCE Mild sinusitis, tracheitis, or unilateral or bilateral lung
O. rhinotracheale has recently been found with an increasing consolidation may be observed. Turkeys frequently
frequency in broiler and turkey operations experiencing have blood-stained mucous in the mouth. Serofibrinous
respiratory problems. OR is frequently isolated with other pleuropneumonia (Fig. 2) and inflammation of the air
respiratory agents (i.e., Escherichia coli, Bordetella avium, sacs (Fig. 3 and 4) are noted macroscopically and
Mycoplasma sp. and respiratory viruses). Broiler and meat histopathologically (Fig. 5 and 6).
turkey operations see primarily birds with respiratory signs,
with no consistent mortality. Condemnation and decreased DIAGNOSIS
feed efficiency have been reported. Egg production can Bacterial culture is required to demonstrate O.
be decreased in layer or breeder flocks. Mortality appears rhinotracheale’s involvement in respiratory disease. Care
more severe in turkey breeder operations. must be taken to prevent its overgrowth by other bacteria.
In turkeys, differentiation from Pasteurella multocida,
HISTORICAL INFORMATION Riemerella anatipestifer and/or Escherichia coli requires
O. rhinotracheale was first isolated in 1981 in Germany bacterial culture.
and in 1986 in the United States. In 1994, the bacterial
organism was named by Vandamme. CONTROL
Little is known on the prevention of O. rhinotracheale. It
ETIOLOGY is frequently present in consecutive flocks on the same
1. O. rhinotracheale is a pleomorphic Gram negative rod ranch. Currently, there is no commercial vaccine available
(Fig. 1) which grows well (but slowly) on blood agar but autogenous bacterins have been used with some
plates. After 24 hours of incubation at 37 C in 7.5% apparent benefit.
CO2, OR colonies are pinpoint in size and show no
hemolysis. No growth is observed on MacConkey TREATMENT
agar plates. Treatments with tetracycline and amoxicillin have been
2. Key biochemical tests include the Gram’s stain reaction reported in Europe. Limited success has been reported
and morphology (short plump rods, club shaped rods, with enrofloxacin and trimethoprim/sulfa. Most isolates in
or long filamentous rods), positive oxidase test, positive the United States have been reported as being susceptible
b-galactosidase (ONPG) test, and negative catalase to ampicillin, erythromycin, penicillin, spectinomycin
test. No reaction is observed in most carbohydrates. and tylosin but sensitivity testing of the isolate is often
necessary.
3. The api-ZYM system (Biomerieux, France) is most
useful. This system gives fourteen positive reactions
and five negative reactions (lipase, b-glucuronidase,
b-glucosidase, a-mannosidase, and a-fucosidase).
EPIDEMIOLOGY
1. O. rhinotracheale has been isolated from broiler and
layer chickens, turkey and chicken breeders, meat
turkeys, duck, goose, gull, guinea fowl, pigeons, ostrich,
quail, pheasants, partridges, and chukers. Isolates are
most frequently obtained from respiratory sites such
as the trachea, sinuses, and lungs. Occasionally,
systemic involvement is indicated by isolations from
the heart, spleen, liver, bone, and joint.
ORNITHOBACTERIUM RHINOTRACHEALE INFECTION

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Fig. 1 Fig. 2
Ornithobacterium rhinotracheale is a pleomorphic Gram negative Serofibrinous pleuropneumonia in a turkey.
rod.
Fig. 3 Fig. 4
Airsacculitis in a 28-day-old broiler chicken caused by ORT. Airsacculitis in a 35 day-old broiler chicken caused by ORT
infection.
Fig. 5 Fig. 6
Pneumonia and pleuritis in a 55 week-old turkey breeder hen. Severe fibrinoheterophilic inflammation of lung associated with
Ornithobacterium rhinotracheale infection in a 55-week-old
turkey breeder hen.
PSEUDOMONAS INFECTION LESIONS

Gross lesions due to Pseudomonas are not specific and
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DEFINITION may include yolk sacs which may have watery yellow or
Pseudomonas can cause localized or generalized disease caseous exudate, swollen joints with fibrinous exudate,
in chickens and turkeys of all ages. In poultry Pseudomonas edema and fibrin in the subcutis, fibrinous exudate in
is most commonly associated with hatchery and incubation the anterior chamber of the eyes, pericardium, air sac,
problems and yolk sac infections. Pseudomonas can also and capsule of the liver; necrotic foci in the liver, spleen,
cause infection in other species of birds, such as ducks, kidneys and occasionally in the brain. Nasal gland
geese, pheasants, ostriches, pet and captive birds. adenitis associated with Pseudomonas aeruginosa has
been reported in ducks. Histologically, the lesions of a
Pseudomonas infection generally consist of mild to severe
OCCURRENCE fibrinosuppurative or fibrinoheterophilic inflammation
Young birds as well as birds stressed and immunodeficient mixed with large numbers of rod-shaped Gram-negative
are very susceptible to Pseudomonas. Severe outbreaks bacteria.
have also occurred due to the use of contaminated
vaccines and antibiotics as a result of poor hygienic
conditions during mixing and handling of these products. DIAGNOSIS
Tentative diagnosis of Pseudomonas infections can
be made based on careful analysis of the history in
ETIOLOGY combination with clinical signs, gross and microscopic
Pseudomonas aeruginosa is the most common species that lesions. Demonstration of Gram-negative rods in the
causes infections in poultry and other birds. Pseudomonas smears from lesions can provide a tentative and quick
is a motile, Gram-negative, non-spore forming aerobic rod- diagnosis. Definitive diagnosis can be made by isolation
shaped bacteria. Other species such as P. fluorescence on suitable media and identification of the organisms.
has been associated with death of turkey embryos and P. Pseudomonas sp. can be isolated from various lesions
stutzeri has been isolated from chickens with respiratory such as yolk sac, pericardium, air sacs, joints, liver, lungs,
disease. Pseudomonas (Burkholderia) pseudomallei skin and other organs.
infections have been reported from Australia in psittacines
that had septicemic lesions.
CONTROL AND TREATMENT
Steps should be taken to identify and eliminate the source of
EPIDEMIOLOGY Pseudomonas. Cleaning and disinfection of the incubators,
Pseudomonas organisms are ubiquitous in nature and hatchers, equipment and the environment are fundamental
are most commonly found in contaminated water and soil. to the control and prevention of Pseudomonas.
Pseudomonas is generally considered an opportunistic
bacterium that can cause various clinical signs and Due to the antimicrobial resistance of Pseudomonas spp.
pathology. Other factors such as concurrent infections with sensitivity tests should be performed frequently. Some
viruses and bacteria can influence infection. Pseudomonas of the antibiotics that may be helpful in reducing losses
is one of several bacteria that are commonly isolated from include gentamicin, streptomycin, amikacin, enrofloxacin.
dead embryos, newly hatched chicks, poults, ducklings
and others. Contact with infected birds, continuous
intense management of broilers and turkeys with different
ages and without periodic change of litter and cleaning
and disinfection influences the spread of bacteria.
Pseudomonas aeruginosa has also been isolated from the
surface of eggs and skin of processed broiler chickens.
CLINICAL SIGNS
Clinical signs due to Pseudomonas in poultry depend on
whether the disease is localized or systemic. These include
ruffled feathers, anorexia, stunting, depression, weakness,
respiratory signs, swelling of the head, swollen joints or
foot pads, lameness, opisthotonus, diarrhea, corneal
opacity and swollen conjunctiva. Sudden death without
any apparent clinical signs is also common. Morbidity and
mortality can vary from 2 -10 % but can be much higher
depending upon management factors and concurrent
diseases.
SALMONELLOSIS I. PULLORUM DISEASE

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PREFACE DEFINITION
Bacteria of the genus Salmonella have long presented Pullorum disease is an infectious, egg-transmitted disease
serious challenges to the poultry and other food animal of poultry, especially chicks and turkey poults, often
industries and are responsible for significant health characterized by white diarrhea and high mortality in young
problems. In this section salmonella infections are birds and by asymptomatic adult carriers.
presented in four parts covering pullorum disease, fowl
typhoid, arizonosis, and paratyphoid. The essential OCCURRENCE
background information on each disease is provided Pullorum disease occurs primarily in young chicks
within these parts. It is noteworthy that although the host- and turkey poults. Many other species can be infected
specific salmonellae (Salmonella pullorum and Salmonella naturally but they usually play an insignificant role in the
gallinarum) literally prevented intensive large-scale poultry epidemiology of this disease. Pullorum disease occurs in
production prior to the evolution of practical testing and all age groups of chickens and turkeys but causes greatest
eradication programs in breeders, it is now the paratyphoid loss in those less than 4 weeks old and is worldwide in
infections that threaten public acceptance of poultry distribution.
products by virtue of concern for food-borne infection.
Paratyphoid salmonella infections are relatively common
1. The bacillus that causes pullorum disease was
in poultry and all reasonable steps should be taken to
first described in 1899. Within a few years pullorum
minimize contamination of the finished product. The
disease was recognized as a common, worldwide,
poultry industry is justifiably proud of its efficient production
egg-borne disease of chickens. A tube agglutination
systems which provide a wide spectrum of economical
test that would detect carriers was developed in 1913
and appealing products. It is our duty as professionals to
and a whole blood test was developed in 1931. These
make every effort to protect the industry from either implied
tests permitted development of eradication programs.
unwholesomeness or true food safety problems.
2. Losses from pullorum disease were once so severe
With the advent of molecular technology, molecular that they impaired expansion of the poultry industry.
bacteriologists have re-examined old bacterial classification Pullorum disease sometimes was spread through
and naming schemes to make them more scientifically hatchery-infected chicks. Extensive losses from
accurate. For instance, paratyphoid salmonella (motile, not pullorum disease and fowl typhoid were partly
host adapted to the avian species in contrast to the non- responsible for stimulating the development of the
motile host adapted S. pullorum and S. gallinarum) have National Poultry Improvement Plan; the plan contains
been subdivided biochemically into 5 distinct subgenera. measures for the control of hatchery-disseminated
Further subdivision based on genetic analysis has yielded diseases.
only 2 species. One, namely S. enterica, contains more 3. Through the application of control measures now
than 2,500 previously named, motile, non-host adapted detailed in the voluntary National Poultry Improvement
salmonella. This species contains S. enterica subspecies Plan, pullorum disease has been eliminated from
enterica serovar Enteritidis more commonly referred to as commercial poultry in the United States. The disease
S. Enteritidis and S. enterica subspecies enterica serovar still persists in small backyard flocks. It probably could
Typhimurium also referred to as S. Typhimurium. In addition, be eradicated if proven control measures could be
the bacterium previously named S. pullorum, the agent enforced for all poultry and exotic birds.
of pullorum disease and S. gallinarum, the agent of fowl
4. Pullorum disease still causes catastrophic losses when
typhoid have been reclassified and renamed S. enterica
no effort is made to control it. This occurs repeatedly
subspecies enterica serovar Pullorum and S. enterica
in developing countries trying to establish a poultry
subspecies enterica serovar Gallinarum. As is evident, this
industry.
development has led to a longer naming schema and a
potential for miscommunication and misunderstanding for ETIOLOGY
the scientist and the student. For the purposes of discussion 1. The etiologic agent is S. Pullorum, a nonmotile, Gram-
in this section, the shortened naming scheme provides negative bacillus adapted to poultry. This organism,
more concise and more easily understood nomenclature like many other Salmonella spp., tends to infect young
and will be used. Thus, salmonella such as S. enterica birds more frequently than older individuals and to
subspecies enterica serovar Pullorum, and others, will be establish a bacteremia. S. Pullorum closely resembles
referred to in their shortened form such as S. Pullorum. S. Gallinarum, the cause of fowl typhoid. They share
certain antigens and usually cross-agglutinate on
serologic tests.
2. The organism is rather resistant under moderate LESIONS

climatic conditions and can survive for months.
Adults
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However, it can be destroyed by thorough cleaning

Often there are no lesions. Occasionally there is a nodular
followed by disinfection. The organism can be killed by
myocarditis, pericarditis, or abnormal gonads. An abnormal
formaldehyde gas, which may be used in fumigation of
ovary may have hemorrhagic, atrophic, or discolored
fertile eggs and hatchers.
follicles (Fig. 1). Less frequently there is oviduct impaction,
EPIDEMIOLOGY peritonitis (Fig. 2), or ascites. Affected testes may have
1. S. Pullorum is primarily spread vertically through white foci or nodules.
occasional infected eggs laid by infected carrier hens.
Many of the infected chicks hatch and then transmit Young chicks and poults
the organism horizontally to other birds in the hatch 1. There may be few or no lesions in very young birds
through the digestive and respiratory systems. Sale of that die after a short septicemic course. Occasional
exposed but apparently healthy birds to many different dead birds feel wet. Many birds have pasted white
purchasers can result in widespread dissemination of feces in the vent area.
the etiologic agent.
2. Classically there are nodules in one or more of the
2. Adult carriers also shed the organism in their feces. following sites: lungs, liver, gizzard wall, heart (Fig.
Slow horizontal spread to other adults is possible 3), intestinal or cecal wall, spleen, and peritoneum.
through contamination of feed, water, and the Frequently there are petechial hemorrhages or foci of
environment. Also, contamination of nests and eggs necrosis in the liver. Later there may be swollen joints
therein can result in eggshell penetration and infection in occasional birds.
of chicks that hatch from those eggs.
3. When the intestine is opened, white plaques may be
3. Cannibalism of infected bacteremic birds can result in found in the intestinal mucosa and cheesy cores of
transmission. debris may be found in the intestine or ceca. Plaques
and cecal cores (Fig. 4) occur more frequently in birds
CLINICAL SIGNS that die later in the course of the outbreak.
Adults
4. The spleen frequently is enlarged (Fig. 4 and 5). (This
Usually there are no signs. The infected adult may or may lesion, along with mucosal plaques and cecal cores,
not appear unthrifty. An infected hen may or may not be a also occurs frequently in Salmonella infections other
productive layer. than pullorum disease.) The ureters frequently are
distended with urates.
Young chicks and poults
1. In a setting of fertile eggs with a few infected embryos, DIAGNOSIS
there may be reduced hatchability. A few of the newly 1. In young chicks and poults, typical history, signs,
hatched birds appear weak or soon die. In others and lesions may suggest pullorum disease. Positive
that develop bacteremia sudden death may occur. agglutination tests, either plate or tube (Fig. 6),
Mortality may be low during the first few days if only a using sera from convalescent surviving birds may
few of the eggs contained the organism. strengthen the diagnosis. Chicks hatched by small,
noncommercial operators are more likely to be positive
2. Morbidity and mortality begin to increase around the for S. Pullorum.
4th or 5th day. Sick birds appear sleepy and weak.
There is anorexia, white adherent diarrhea with pasting 2. For a definitive diagnosis, S. Pullorum must be isolated
of the vent area, huddling near heat sources and shrill and identified. The organism should be typed at a
chirping. A few days later there may be respiratory typing center to aid in epidemiologic investigation. Due
signs in birds that inhaled the organism in the hatcher. to state animal health laws, legal complications may
Losses usually peak during the 2nd or 3rd week and occur so identification should be confirmed.
then diminish. Survivors often are irregular in size and 3. The National Poultry Improvement Plan provides
some are unthrifty, stunted, or poorly feathered. Many details for confirming infection in adult reactor birds.
remain carriers and disseminators of the etiologic Specified organs are pooled and cultured for S.
agent. Pullorum.
3. Mortality varies greatly but often is very high and can 4. Diseases that must be differentiated from pullorum
approach 100%. Mortality is increased by shipping, disease in young birds include:
chilling, or poor husbandry. Conversely, mortality
A. Chilling. Chilling is often associated with white
may be surprisingly low and the disease may go
diarrhea.
unrecognized.
B. Omphalitis (navel infection). Omphalitis occurs in
this age group, often with diarrhea.
C. Typhoid, paratyphoid, arizonosis, and colibacillosis. OCCURRENCE

It will be necessary to isolate and identify the Most outbreaks occur in chickens or turkeys but the
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etiologic agent to rule out these infections. disease occasionally occurs in other poultry, game birds,
and wild birds. In chickens and turkeys most outbreaks
CONTROL occur in recently hatched, young birds, but unlike pullorum
1. Prevention is based on establishment and disease, the disease often continues for months. Many
maintenance of pullorum-free breeder and multiplier outbreaks occur in semimature flocks with no history of an
flocks by serologic testing and other measures. The earlier onset.
following tests are used:
A. The stained antigen, rapid whole blood test is HISTORICAL INFORMATION
typically performed in flocks in the field. This same A disease that probably was fowl typhoid was recognized
antigen can be used for the rapid serum test in the in 1888. By the early 1900s many outbreaks, both in the
laboratory. United States and abroad, had been reported. Between
B. Tube agglutination test is performed on sera and 1939 and 1946 there was a marked increase in outbreaks
is primarily used to confirm plate test reactions. in the United States and fowl typhoid was a major disease
C. An enzyme-linked immunosorbent assay (ELISA) of poultry. Application of testing and control measures (now
has also been developed for the serologic detailed in the National Poultry Improvement Plan) greatly
diagnosis of pullorum disease. reduced the incidence of both fowl typhoid and pullorum
disease. Fowl typhoid is seldom encountered today in
2. Noninfected eggs from tested clean flocks should be the United States but persists as a challenging disease
hatched in a properly disinfected hatcher and raised on problem in several countries.
pullorum-free premises, preferably under quarantine.
3. Detailed regulations for control of pullorum disease ETIOLOGY
are given in the National Poultry Improvement Plan. The etiologic agent is Salmonella Gallinarum. This
A copy of the plan can be obtained from The National organism shares many antigens with Salmonella Pullorum,
Poultry Improvement Plan, USDA-APHIS-VS, Suite the agent that causes pullorum disease, and the two
300, 1506 Klondike Road, Conyers, GA 30094 organisms usually cross-agglutinate. As a consequence,
or consulted on the website of the federal register birds exposed to or infected with either disease can be
of the United States: http://69.175.53.20/federal_ identified by the same agglutination test.
register/2011/mar/22/2011-6539.pdf.
4. The poultry producer can avoid pullorum disease by
EPIDEMIOLOGY
purchasing chicks only from those hatcheries that
The epizootiology of fowl typhoid is similar to that of
participate in the National Poultry Improvement Plan
pullorum disease. Relatively speaking, transmission
or a similar eradication program. Exposure of the flock
of infection through eggshell contamination may be of
to carriers or a contaminated environment must be
somewhat greater importance than with pullorum disease.
avoided.
Also, S. Gallinarum is more frequently transmitted among
TREATMENT growing or mature flocks and the incidence and mortality in
Insofar as chemotherapy perpetuates the carrier state, older birds is usually higher.
treatment of pullorum-infected birds is indefensible and
should not be recommended under any circumstance. CLINICAL SIGNS
Signs of fowl typhoid and pullorum disease are similar in
birds less than approximately 1 month old. Semimature
II. FOWL TYPHOID and mature birds with fowl typhoid often have pale head
DEFINITION parts (comb, wattles, face), shrunken combs and wattles,
Fowl typhoid is an infectious disease, primarily of chickens and diarrhea. Mortality can be substantial. In one extensive
and turkeys, with many of the clinical and epidemiologic experiment, many broods of birds were hatched from eggs
features and lesions that occur with pullorum disease. from a typhoid-infected flock of hens. Approximately one
third of all hatched birds died with typhoid.
In the following material only the differences between fowl
typhoid and pullorum disease are emphasized. Most of the LESIONS
facts concerning pullorum disease (see Pullorum Disease) 1. Lesions of fowl typhoid and pullorum disease are
are applicable to fowl typhoid. similar in chicks and young poults (see pullorum
disease).
2. Lesions of acute fowl typhoid in older birds include:
A. A bile-stained (“bronzed”) enlarged liver with or ETIOLOGY

without small necrotic foci (Fig. 1). 1. The etiologic agent is Salmonella arizonae (syn.
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B. Enlargement of the spleen and kidneys. Arizona arizonae and Arizona hinshawii). It is a non-
spore forming, Gram-negative, motile bacterium in the
C. Pallor throughout the cadaver and thin watery family Enterobacteriaceae.
blood.
2. S. arizonae ferments lactose slowly, usually requiring
D. Enteritis in the anterior small intestine, often with a few days. Slow-fermenting S. arizonae may be
ulceration. mistaken for other Salmonella species unless the
3. In older birds, chronic fowl typhoid lesions resemble fermentation tubes are held for a sufficient period.
those seen in pullorum disease (see pullorum disease).
EPIZOOTIOLOGY
DIAGNOSIS 1. S. arizonae often localizes in the ovary of carrier birds.
S. Gallinarum should be isolated and identified for When this happens, the organism is included within
diagnosis. It should be carefully differentiated from other eggs, infects the developing embryo, and results in
salmonella and paracolon organisms. infected progeny.
2. Infected adult birds are frequently intestinal carriers and
CONTROL intermittent shedders of S. arizonae. Contamination
Control is as for pullorum disease. Fortunately, control of of eggshell surfaces with feces leads to eggshell
both pullorum disease and fowl typhoid is accomplished by penetration and infection of progeny.
the same program encompassed in the National Poultry 3. Infected progeny that hatch from infected eggs transmit
Improvement Plan. the organism horizontally to uninfected birds in the
hatch and later may become carriers and shedders of
III. ARIZONOSIS the organism.
4. Exposure to the agent can also occur via reptiles,
DEFINITION rats, mice, and many other mammals, contaminated
Arizonosis is an egg-transmitted infection, seen primarily hatchers, or fomites. Transmission frequently is via
in young turkey poults, characterized by variable signs and fecal contamination of feed, water, or environment. The
lesions related to septicemia or to localization of infection in organism can persist in a contaminated environment
the intestine, peritoneal cavity, eye(s), brain, or other sites. for months.
5. As with many salmonellae, S. arizonae has few, if any,
OCCURRENCE species barriers. Interspecies transmission occurs
Most outbreaks occur in turkeys. Although all ages are readily and there are many carriers.
susceptible, the disease is most common in poults less
than 3 weeks old. Chicks, ducklings, canaries, psittacines, CLINICAL SIGNS
and other birds occasionally have been found to be In young poults there may be listlessness, diarrhea,
infected. Infection frequently occurs in reptiles, which can pasting of feces in the vent area, huddling near heat
serve as reservoirs. Infection in humans has occurred sources, ataxia, trembling, torticollis (Fig. 1), excessive
but is not common. The disease probably is worldwide in mortality (3-5% is most common, although losses up to
distribution. 50% have been reported), and poor growth. Cloudiness
(turbidity) and enlargement of the eye(s) causing blindness
HISTORICAL INFORMATION may occur in infected poults. Central nervous system
1. Arizonosis in chicks was reported in 1936, although signs occur in birds with brain lesions. Signs in young birds
it was not clearly differentiated from paratyphoid closely resemble those seen with paratyphoid. Moderate to
infection. In 1939 the etiologic agent of arizonosis was marked uneven growth in the flock is seen even after the
definitively characterized and found to cause a fatal clinical disease has ended. Affected eyes undergo atrophy
septicemia in reptiles in Arizona. and are useful in identifying previously infected flocks.
Adult carriers usually show no signs.
2. In the 1940s to 1960s arizonosis was recognized as
an important and widely distributed disease of many
turkey flocks. LESIONS
1. Typically, lesions of septicemia are observed, including
3. Historically the etiologic agent of arizonosis was an enlarged, mottled, yellow liver, a retained yolk sac
considered to be in the genus Arizona. Since 1982 the and peritonitis. Occasionally there are cheesy plugs
etiologic agent of arizonosis has been characterized in the intestine or cecum and infected yolk sacs
as a subspecies of the genus Salmonella based on develop into abscesses in poults that survive the initial
DNA relatedness to this genus. septicemia.
2. A small but significant number of poults have opacity IV. PARATYPHOID INFECTION
or turbidity of the eye(s) (ophthalmitis) (Fig. 2). This
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useful lesion is not pathognomonic because it can also (Salmonellosis; Paratyphoid)

occur with paratyphoid, aspergillosis, or colibacillosis.
However, it occurs more frequently with arizonosis.
DEFINITION
Paratyphoid is an acute or chronic disease of poultry, many
3. Purulent exudate in the meninges, lateral ventricles of other birds, and mammals caused by any one of a large
the brain, or in the middle and inner ear is seen in birds group of salmonellae that are not host specific.
with central nervous system signs (Fig. 3).
DIAGNOSIS OCCURRENCE
The etiologic agent must be isolated and identified. Signs Paratyphoid infection occurs in many kinds of birds and
and lesions are inadequate for separating arizonosis mammals; it occurs frequently in poultry. It also occurs in
from other infection salmonella infections. S. arizonae rats, mice, and other rodents, in many reptiles, and in some
can usually be recovered from liver, spleen, heart blood, insects. It is a frequent disease of humans. In most animals
unabsorbed yolk, intestine, or other organs. It is readily the young are more frequently and severely affected. Adults
recovered from infected eyes, ears, and brains. S. arizonae tend to be more resistant but can be infected, especially
persists for several weeks in atrophied eyes, from which if stressed prior to exposure. Paratyphoid infection is
the organism can be easily recovered. Also, it may be worldwide in distribution.
cultured from nonhatching embryos, eggshells, or organs
from infected breeder birds and environmental samples. These bacterial infections are of much more importance
Enrichment procedures used to isolate other salmonellae for public health impact than for economic losses in the
are equally effective for detecting S. arizonae. affected animals. Poultry products have been repeatedly
implicated in human outbreaks of salmonellosis and all
health management personnel in the poultry industry
CONTROL need to be sensitive to this legitimate consumer concern.
1. If infected breeder flocks can be identified, they
Although detailed epidemiology is outside the scope of this
should not be used as a source of fertile eggs.
book, the technical details in this chapter should provide
Unfortunately, there is no readily available serologic
essential background on the control of avian salmonella
test for identification of infected flocks or individual
infections. The National Poultry Improvement Plan and
birds. Such flocks often are identified by culturing
more recently the Food and Drug Administration are
the agent from their eggs or progeny. Primary turkey
involved in the regulatory aspects of Salmonella Enteritidis
breeder companies in the United States are now free
(SE) infection while NPIP has programming in place to
of S. arizonae infection, but commercial breeder flocks
allow poultry breeder farms to attain Salmonella monitored
are still occasionally affected.
status and FDA a monitoring and control program for SE in
2. One-day-old poults are usually inoculated at the egg laying chickens.
hatchery with antibiotics to control mortality from
arizonosis. Gentamicin is most commonly used.
ETIOLOGY
Strains resistant to gentamicin have been found and
1. Paratyphoid salmonella have consisted of salmonella
have caused high losses in poults. In these cases,
that are motile and not host adapted in contrast with S.
the use of injectable tetracyclines or ceftiofur may be
Pullorum and S. Gallinarum, which are nonmotile and
helpful.
highly host adapted.
3. Most of the measures used for prevention of
2. There are more than 2,500 serovars of S. enterica
paratyphoid are applicable for control of arizonosis
but only 10% of these have been isolated from
(see under paratyphoid).
poultry. Distribution of serovars varies geographically
TREATMENT and overtime. Frequent isolates in the United States
Useful antibiotics and drugs include gentamicin, include:
tetracyclines, and sulfonamides. Treatment does not S. Enteritidis S. Typhimurium
prevent birds from becoming carriers and shedders of S. Heidelberg S. Kentucky
the organism. Experimentally, use of a bacterin in turkey S. Braenderup S. Hadar
breeder hens has been found to be helpful in reducing S. Muenster S. Senftenberg
shedding and coupled with good management procedures,
eventually eliminating the disease from breeder flocks. 3. M
ost paratyphoid organisms contain endotoxin, which
is responsible for their pathogenic effects.
4. Paratyphoid organisms are moderately resistant in
their natural environment but are susceptible to most
disinfectants and to fumigation with formaldehyde gas.
EPIDEMIOLOGY a few days or longer. These strongly suggest the

1. Paratyphoid organisms often localize in the intestine presence of salmonellosis but are not pathognomonic
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or gallbladder of carriers. They are intermittently shed for any one species of Salmonella.
in the feces and thus contaminate eggshells, feed 4. 4. Inflammation of the oviduct and ovaries, with
and water. Poultry, other birds, reptiles, insects, and pericarditis, perihepatitis and/ or peritonitis, has been
various mammals including humans can disseminate observed in flocks naturally infected with S. Enteritidis
salmonella. (Fig. 1).
2. Infection of young chicks occurs primarily by fecal
contamination of eggshells with paratyphoid organisms DIAGNOSIS
and subsequent penetration into the eggs. Some The etiologic agent should be isolated from multiple organs
chicks are infected at the time of hatch and infection and positively identified. Using polyvalent salmonella
spreads horizontally. antiserum, most labs can identify any isolate as Salmonella.
Some, namely S. Enteritidis and S. Typhimurium, have
3. Localization of paratyphoid organisms in the ovary rapid antigen detection kits as well as PCR tests making
with subsequent vertical transmission occurs in rapid and accurate diagnosis easier. Typing centers can
some instances (e.g. S. Enteritidis). The frequency of provide the service of complete species and genetic typing
this method of spread is unknown but thought to be and should be utilized for this specialized work. Selective
transitory or intermittent. media often are utilized in isolating Salmonella from the
4. Contaminated animal proteins (tankage, meat scraps, gut.
etc.) can transmit the agents. These products often
are contaminated after processing. Heated, pelleted CONTROL
products seldom contain living salmonella. 1. Breeder flocks should be monitored bacteriologically
5. Interspecies transmission of paratyphoid organisms for Salmonella infection in conjunction with efforts to
does occur, often through environmental contamination. minimize flock exposure.
Rodents are an important reservoir for paratyphoid 2. If possible, all birds should be sold after one lay season
organisms. Paratyphoid is an important public health thus eliminating carriers. While the premise is vacated,
problem and this aspect of the disease is by far the it should be thoroughly cleaned and disinfected.
greatest challenge to the poultry industry. Eliminating rodents by trapping them, is an essential
step in the eradication of Salmonella from a farm.
CLINICAL SIGNS
1. Signs usually are seen only in young birds (less than 4 3. In flocks provided with nests the nests should be kept
weeks of age). There is somnolence, profuse diarrhea clean. Replace nesting material frequently as needed.
followed by dehydration, pasting or wetting of the vent Maintain a high standard of sanitation in all operations.
area, drooping wings, shivering, and huddling near 4. Gather eggs frequently and store them in a cool place.
heat sources. Separate dirty eggs from clean eggs at the time of
2. There usually is high morbidity and mortality (especially gathering. Egg sanitation may be necessary at the
during the first 2 weeks of brooding), although these poultry farm during the storage that precedes storage
are variable. The course often is short in individual and incubation at the hatchery.
birds. 5. Fumigate hatching eggs as recommended during
3. Increased mortality can be observed in layers naturally incubation (done routinely). Practice scrupulous
infected with S. Enteritidis at the onset of lay. hatchery sanitation.
6. Raise new broods of birds in the all-in, all-out system.
LESIONS
Add no new birds to the started brood. Do not permit
1. There may be a few or no lesions in birds that die
contact with wild birds, mammals, rodents, or reptiles.
after a short septicemic course, perhaps only a few
Control insect populations.
petechial hemorrhages.
7. Provide uncontaminated feed ingredients in the ration.
2. There usually is dehydration and marked enteritis,
Pelleted feeds are more likely to be free of salmonella
often with focal necrotic lesions in the mucosa of the
as long as there is no cross contamination after the
small intestine. Occasionally there are necrotic foci
pelleting process.
in the liver. In young birds there often is unabsorbed
yolk material in the yolk sac and overt omphalitis. Less 8. If necessary, specific antigens may be prepared and
frequent lesions include blindness, joint infections, used in an agglutination test for elimination of carriers.
or swollen eyelids, the latter two being common in This has been done for S. Typhimurium but not for
pigeons. most other paratyphoid organisms. Once developed,
these test antigens can be used on a regular basis at
3. Raised plaques in the intestinal mucosa and cheesy
the time of the annual pullorum-fowl typhoid test.
cecal cores are often seen in birds that survive for
9. One-day-old chicks and poults are often inoculated

at the hatchery with antibiotics to control mortality
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from paratyphoid and other bacterial infections. This

practice may help control early mortality but the same
positive result can be accomplished by the good
breeder flock and hatchery management practices
enumerated above.
10. Many commercial vaccines, both live and killed, are
available for vaccination of commercial egg layers
and broiler breeders, against S. Enteritidis and S.
Typhimurium. Unfortunately, they do not prevent
infection but do reduce shedding.
TREATMENT
Treatment with antibiotics does not eliminate Salmonella
infections and has very minimal value. Use of antimicrobials
to eliminate Salmonella colonization may imperil their
medical usefulness by promoting resistance.
PULLORUM DISEASE
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Fig. 2
Fig. 1 Severe fibrinosuppurative peritonitis in a hen.
Abnormal ovary with atrophic and discolored follicles.
Fig. 3
Misshapened heart in a 6-week-old chicken due to the presence of Fig. 4
numerous yellow nodules in the myocardium. Note the thickened Splenomegaly and hepatomegaly in a 18-day-old chick. Notice the
pericardium and discolored, mottled liver due to chronic passive white cast in the cecum.
congestion.
Fig. 5
Enlarged and mottled white spleen in an adult chicken. Fig. 6
Tube agglutination test showing Pullorum positive and negative
tests. Note floccules in the positive tube.
FOWL TYPHOID
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Fig. 1
Bile-stained (“bronzed”) enlarged liver with small necrotic foci in a
FP positive adult chicken.
ARIZONOSIS
Fig. 1 Fig. 2
Torticollis in a young poult affected with S. arizonae. Poult with opacity of the eye (ophthalmitis).
Fig. 3
Encephalitis in a young poult.
PARATYPHOID INFECTION
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Fig. 1
Pericarditis, perihepatitis and
peritonitis in a naturally SE infected
layer.
SPIROCHETOSIS birds are weak, squat on the ground, and later may become
paralyzed. Morbidity and mortality vary greatly depending
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DEFINITION on the virulence of the B. anserina strain. Morbidity and

Spirochetosis or nonrelapsing borreliosis is a septicemic mortality may approach 100% in highly susceptible flocks.
disease of most poultry and many other birds. Acute cases
are characterized by depression, cyanosis, diarrhea, and LESIONS
leg weakness progressing to paralysis and death. 1. There usually is marked enlargement of the spleen,
which is mottled by ecchymotic hemorrhages.
OCCURRENCE 2. The liver frequently is enlarged and may contain
Spirochetosis occurs naturally in chickens, turkeys, geese, small hemorrhages, infarcts, or foci of necrosis. The
ducks, pheasants, grouse, and canaries. Many other birds kidneys may be enlarged and pale. There usually is
can be infected experimentally. In the United States the bile-stained mucoid enteritis. The histopathology has
disease usually has occurred in turkeys, chickens, and been well described but microscopic lesions are not
pheasants. All age groups are susceptible if not previously diagnostic for the disease.
exposed. The disease is widely distributed in tropical
and temperate regions. In the United States it has been DIAGNOSIS
recognized in California, New Mexico, Texas, and Arizona. 1. Spirochetosis should be suspected if the tick A.
persicus is found on typical sick birds. However,
nymphs and adult ticks live in the house and feed
HISTORICAL INFORMATION mostly at night.
1. Spirochetosis, one of the major scourges of poultry,
was first reported in 1891. Spirochetosis has occurred 2. The spirochetes can be identified in Giemsa-stained
only a few times in the Southwestern United States. blood smears (Fig. 1) or by dark-field or phase-contrast
It has been reported in California in 1946 and 1993 microscopy of blood and other fluids. Spirochetes
as well as in Arizona in 1961. The disease is of major can be concentrated in the buffy coat of centrifuged
importance in those countries where it is enzootic. blood. This may facilitate identifying birds with low
spirochetemia. Spirochetes may not be observed
2. There is potential for spread of spirochetosis in the during late stages of the disease.
southwestern states because the presence of the tick
vector, Argas persicus. 3. In doubtful cases, the spirochete can be demonstrated
by isolating it in six chick embryos inoculated
ETIOLOGY with defibrinated blood from a typical early case.
1. The etiologic agent is Borrelia anserina, a spirochete Alternatively, young chicks or poults can be inoculated
with 5-8 spirals that is up to 30 microns long. with serum or tissue suspensions and their blood
can be examined daily for spirochetes, which usually
2. The organism is not very resistant outside the host and
appear in 3-5 days.
must be maintained in some vector between hosts.
4. The spirochete can be identified in specially stained
EPIDEMIOLOGY tissue sections. Also, the fluorescent antibody test
1. B. anserina can be transmitted through infectious can be used to identify it in tissues or blood. Agar-gel
droppings but usually is transmitted by blood sucking precipitin tests have been used to detect spirochete
arthropods. Argas persicus is the usual vector and antibodies and antigens.
mosquitoes of the genus Culex may serve as vectors.
Mites may serve as mechanical carriers. CONTROL
1. Spirochetosis can be prevented by controlling or
2. A. persicus remains infective for up to 430 days after
eradicating all the vectors and transmitters of B.
feeding on an infected host. Further, the tick passes
anserina. It may be difficult to eradicate the fowl tick
the spirochete to its progeny.
without destroying infested wooden buildings and
3. Infectious vectors and mites transmit the spirochetes all the birds in infected flocks. Isolating the roost by
to susceptible birds when they feed upon them. suspending it from wires or placing the supports of the
Recovered birds clear the infection completely and do roost in pans filled with oil is helpful in reducing tick
not become carriers. feeding.
4. Transmission can also occur through ingestion of 2. A wide variety of bacterins and vaccines has been
infected ticks, cannibalism of moribund birds, or prepared abroad but are not available in the United
scavenging of infected carcasses. States. They appear to be reasonably effective
although they produce a shorter, weaker immunity
CLINICAL SIGNS than is desirable unless revaccination is practiced.
Infected birds are depressed, cyanotic, thirsty, and often Immunity is serotype specific and my not protect
have a diarrhea that includes excessive white urates. The against others.
TREATMENT
In countries where spirochetosis is enzootic, numerous
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drugs and antibiotics, including penicillin, streptomycin,

tylosin and tetracyclines have been used successfully for
treatment.
Fig. 1
Spirochetes in Giemsa-stained blood smears.
STAPHYLOCOCCOSIS 2. Gangrenous dermatitis

Affected areas of the skin are dark red, moist, thickened,
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DEFINITION and clearly demarcated from adjacent normal skin.

Staphylococcosis is a systemic disease of birds Usually traumatic lesions such as punctures or scratches
characterized most frequently by purulent arthritis and are present. The serosanguinous fluid seen in clostridial
tenosynovitis. infections is minimal or absent. Staphylococcal gangrenous
dermatitis is typically secondary to immunosuppression
caused by infectious bursal disease or chicken infectious
OCCURRENCE anemia virus.
Staphylococcal infections of poultry occur worldwide and
affect all classes of birds. Outbreaks are most important 3. Cellulitis
in turkeys and broilers. The organisms are common in A purulent inflammation is present in subcutaneous
the environment and are especially associated with the tissues. Traumatic lesions may or may not be present. The
skin. Most diseases produced by Staphylococcus sp. are overlying skin tends to be dry and discolored.
associated with a break in the skin or beak (trauma, beak
trimming, toe trimming, foot pad burns etc.). Avian infections 4. Abscesses
tend to be caused by types occurring in birds rather than There are localized purulent lesions in the skin. The
human strains. Isolates pathogenic for one class of poultry plantar surface of the foot is a common site and results in
are usually pathogenic for other classes of birds. Toxigenic bumblefoot. Abscesses result from puncture wounds.
strains capable of causing food poisoning can contaminate
the skin of processed poultry. The source of these strains at 5. Septicemia
present is in debate. Biotyping indicates processing plant There is an acute increase in mortality with congestion
worker origin while plasmid profile indicates poultry origin. of the internal organs. It is usually associated with a
processing event of the bird such as beak trimming or
HISTORICAL INFORMATION some other trauma to the skin.
Staphylococci were first discovered to be a cause of
arthritis in geese in 1892. Since that time they have been 6. Arthritis/periarthritis/synovitis
identified as the cause of a variety of localized and systemic Any joint, tendon sheath, or synovial bursa can be
diseases in many different avian species and in most areas affected. Arthritis/periarthritis/synovitis is seen clinically as
of the world. The disease was more common in turkeys swollen (Fig. 1), hot joints, especially hock joints. It occurs
when they were raised on range than it is now. as a sequel to septicemia and can be experimentally
reproduced by intravenous injection of pathogenic strains.
Initially, affected tissues are acutely inflamed and contain
ETIOLOGY white to yellow soft fibrinopurulent exudate. Later, the
1. Most staphylococci isolates have been identified as exudate becomes caseous. Fibrosis of affected tissues
Staphylococcus aureus, a Gram-positive coccus occurs late. Affected birds often have bile stasis of the liver.
occurring in clusters. Pathogenic isolates are usually High numbers of large mononuclear cells are seen in blood
coagulase positive. smears.
2. Biotyping and phage-typing is frequently used to
distinguish strains. Isolates from different geographic 7. Discospondylitis (spondylitis)
areas tend to be different phage types. Particular The joints of articulating thoracolumbar vertebrae are
phage types are often endemic on a particular farm affected. The process spreads to affect adjacent vertebrae.
and tend to reappear in successive flocks. Lesions may become so extensive that pressure on the
3. Organisms are moderately resistant to common spinal cord will develop causing paresis and paralysis.
disinfectants. Chlorine-containing disinfectants are
efficacious in the absence of organic material. 8. Osteomyelitis
This is a sequel to septicemia. Organisms localize in
4. Toxins produced by staphylococci can increase both metaphyseal vessels invading the cartilage of the growth
the virulence and pathogenicity of a particular strain. plate of actively growing bones. Initially, pale yellow, friable
bone is seen in affected areas adjacent to the growth plate,
LESIONS especially in the proximal tibia and metatarsus. Necrotic
Diseases produced by staphylococcus infections include:
areas, abscesses, and sequestra are seen later (Fig. 2).
1. Omphalitis
9. Endocarditis
Although infections of the yolk sac occur, they are less
This is an uncommon sequel to septicemia. There are
common than omphalitis caused by other bacteria.
vegetations on the mitral and/or aortic valves. Emboli from
Sources of the bacterium include the breeder flock,
valve lesions cause infarcts in the brain, liver, and spleen.
hatchery environment, and hatchery workers.
10. Green liver-osteomyelitis complex in turkey

This is a condition observed at slaughter. Normal-appearing
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processed turkey carcasses present green discoloration

of the liver (Fig. 3) and associated arthritis/synovitis, soft-
tissue abscesses, and osteomyelitis of the proximal tibia
(Fig. 4). Staphylococcus aureus is most commonly isolated
from these lesions but other opportunistic bacteria such as
Escherichia coli have also been isolated.
DIAGNOSIS
1. Gross lesions are suggestive. A rapid, presumptive
diagnosis can be made by identifying the typical cocci
in smears from lesions.
2. Organisms can be readily cultured and identified from
lesions and often from the livers of affected birds.
CONTROL
1. Because staphylococci are ubiquitous in the
environment their presence cannot be prevented.
When an outbreak is associated with a particular
environment, the source should be sought and
eliminated.
2. Protect broilers from infectious bursal disease with an
appropriate vaccination program.
3. Take measures to reduce the occurrence of traumatic
skin lesions and foot pad burns, as well as any enteric
disease which would damage the integrity of the
intestinal mucosa.
4. The respiratory tract has also been identified as an
important portal of entry for pathogenic staphylococci
in turkeys. Exposing chickens or turkeys to a live
avirulent vaccine, namely strain 115 of Staphylococcus
epidermidis, by aerosol at 10 days and again at
4-6 weeks substantially reduced the incidence of
staphylococcosis and improves overall flock livability.
5. Avoid overly severe feed restriction in breeder
replacements which has been associated with an
increased incidence of staphylococcosis.
TREATMENT
1. High levels of antibiotics effective against staphylococci
may be helpful if given early in the course of the
disease.
2. Resistance to antibiotics is common and isolates
should be tested for sensitivity.
3. U
sually treatment is not cost effective and preventive
programs should be relied on.
STAPHYLOCOCCOSIS
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Fig. 2
Fig. 1 Necrotic foci and abscesses in the proximal tibia.
Swollen and distended metatarsal joint in a broiler chicken.
Fig. 3 Fig. 4
Green liver discoloration observed at slaughter in a turkey Osteomyelitis of proximal tibiotarsus of a turkey.
carcass.
ULCERATIVE ENTERITIS CLINICAL SIGNS

(Quail Disease) 1. In most species signs are similar to those seen with
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coccidiosis in chickens. These include listlessness,

humped appearance, retracted neck, drooping wings,
DEFINITION
partially closed eyes, ruffled feathers, diarrhea,
Ulcerative enteritis is an acute bacterial infection of
anemia, and perhaps bloody feces. In quail, white
upland game birds, turkey poults, and young chickens
watery droppings are rather distinctive. In chicken
characterized by ulcerations of the intestinal tract and by
flocks a course of 2 or 3 weeks is common and then
focal and/or diffuse hepatic necrosis.
the chickens recover slowly.
2. Sudden death may occur without signs being apparent,
OCCURRENCE especially during onset. Birds that die suddenly may
Ulcerative enteritis occurs frequently in young, captive,
be well muscled and fat, especially in quail. Birds with
upland game birds and with increasing frequency in
prolonged illness are often emaciated.
turkey poults and young chickens. Quail are the most
susceptible host species. Young birds are affected more 3. Mortality may be very high with quail, up to 100% within
frequently than adults although the disease occurs a few days. Mortality in chickens seldom exceeds 10%.
frequently in adult quail. The disease is widespread in the Game birds other than quail usually have a higher
United States and is known to occur in Europe and Asia. mortality than chickens but less than occurs in quail.
In chickens it frequently occurs in association with other
diseases, including coccidiosis, chicken infectious anemia, LESIONS
and infectious bursal disease. Recently, the etiology 1. Lesions are similar in most birds. Most cases
of ulcerative enteritis is thought to be the cause of focal presented for necropsy have deep ulcers scattered
duodenal necrosis (FDN) in egg laying chickens. throughout the intestine, including the ceca, and the
ulcers may be numerous enough to coalesce. Ulcers
(Fig. 1) may be round or lenticular, the latter shape
HISTORICAL INFORMATION being more common in the upper intestine. Deep
Ulcerative enteritis was reported in the United States in ulcers often can be detected through the serosa of
1907 and had been observed prior to that time in Great the unopened intestine (Fig. 2) and may penetrate it
Britain. It was first referred to as quail disease, a name to induce peritonitis. The intestine may contain blood,
retained for many years despite recognition of the disease thus mimicking coccidiosis. Acute cases have severe
in many other birds. The disease was recognized in enteritis of the small intestine.
chickens by 1934 and in domestic turkeys by 1944. The
2. The affected liver usually contains large, yellow or
disease has increased in incidence and is now a well-
tan areas or focal yellow lesions, or both. The lesions
recognized disease. At one time the agent was mistakenly
tend to be colorful and distinctive. The spleen is often
believed to be Clostridium perfringens.
enlarged and may be hemorrhagic.
ETIOLOGY DIAGNOSIS
The etiologic agent is Clostridium colinum, a Gram- 1. Typical intestinal ulcerations and the distinctive colorful
positive, anaerobic, spore-forming bacillus. The organism lesions in the liver strongly suggest ulcerative enteritis.
is very resistant. It withstands boiling for 3 minutes or 70 Stained impression smears made from the cut surface
C for 10 minutes. Boiling suspected material is useful of the liver may reveal the rod-shaped bacillus with its
in killing other contaminating bacteria during isolation subterminal spore.
attempts. C. colinum can best be isolated from the typically 2. For confirmation the etiologic agent should be isolated
affected fresh liver. The preferred medium is tryptose- and identified. The organism must be differentiated
phosphate-glucose agar with 8% horse plasma. Cultures carefully from Clostridium difficile and C. perfringens.
are incubated anaerobically.
3. Care should be taken to differentiate the disease in
chickens from coccidiosis. Coccidiosis often is present
EPIDEMIOLOGY in the same bird and assessing the relative importance
1. The etiologic agent is spread primarily through the of the two diseases may be difficult. Both diseases
droppings of acutely affected or recovered carrier birds may be contributing to mortality.
and spores persist in the soil for years. Interspecies
transmission can occur among susceptible birds. CONTROL
2. Infection can be spread by flies that feed on infectious 1. Raise the flock in facilities and on ground where the
droppings. The disease is highly contagious, especially disease has never occurred. Do not add birds. Prevent
among quail. contact with all other species of birds. Raising birds on
wire is of value if feasible.
2. Keep old birds and young birds separated. If possible,

do not have both age groups on the same premises.
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Practice careful sanitation including frequent cleaning

and disinfection. Promptly remove and destroy all sick
birds.
3. Streptomycin, bacitracin, penicillin, lincomycin, and
tetracyclines have all been used intermittently in feed
or drinking water for prevention of the disease. Rotating
the use of these different antibiotics and chemicals will
help prevent the emergence of C. colinum isolates
which are resistant to antimicrobials.
TREATMENT
Most of the antibiotics and chemicals used in feed and
water for prevention can be used at higher levels for
treatment. These treatments should be administered in the
drinking water.
Fig. 1
Deep and coalescing ulcers scattered throughout the intestine.
Fig. 2
Deep ulcers detected through the serosa of the unopened intestine.
YERSINIOSIS LESIONS
Gross lesions due to Yersiniosis primarily involve liver
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DEFINITION and spleen. These organs can be enlarged with either a

Yersiniosis is a septicemic disease affecting various few pale foci of necrosis or yellow granulomas scattered
species of birds caused by the bacterium Yersinia throughout. Similar foci can also be found in the lungs,
pseudotuberculosis. The disease has been reported in heart, kidneys, skeletal muscles and swollen joints. In
turkeys, chickens, ducks, and in Passeriformes (canaries addition catarrhal enteritis, osteomyelitis and myopathy
and finches), Psittaciformes (parrots, parakeets), have been described in turkeys.
Columbiformes (pigeons and doves), Piciformes (toucans),
Cuciliformes (turacos), raptors and other captive and Histologically acute lesions generally consist of mild to
free flying birds. Mammals including humans are also severe necrosis of the parenchyma accompanied by
susceptible to Yersinia pseudotuberculosis. fibrinosuppurative or fibrinoheterophilic inflammation
usually associated with numerous colonies of Gram-
negative bacteria of bacilli morphology. In chronic infections
OCCURRENCE these necrotic foci and inflammation will be surrounded by
Among poultry, sporadic outbreaks have occurred in multinucleated giant cells.
commercial turkeys.
DIAGNOSIS
ETIOLOGY A presumptive diagnosis can be made based on clinical
The etiology of Yersiniosis is Yersinia pseudotuberculosis. signs, gross and microscopic lesions. Gram stain of
Other species of Yersinia such as Y. pestis, Y. smears from lesions can provide a tentative and quick
enterocolitica, Y. frederiksenii, Y. intermedia and others diagnosis. Gross lesions in liver and spleen and other
have not been associated with disease in birds. Yersinia organs have to be differentiated from other bacterial
are Gram-negative rod-shaped bacteria than can be motile diseases, such as, mycobacteriosis, salmonellosis, etc...
or non motile, depending on the incubation temperature. Y. pseudotuberculosis can be isolated readily from most
Pathogenic Y. pseudotuberculosis carries a virulent lesions such as liver, spleen, bone, joints, lungs, intestine
plasmid of which six serovars have been identified and and other organs.
serovar 1 is most commonly isolated from birds.

EPIDEMIOLOGY Y. pseudotuberculosis is ubiquitous in the environment
Yersinia spp. are ubiquitous in the environment and are and water; steps should be taken to reduce their numbers.
worldwide in distribution. It has been isolated from many Biosecurity implementation, total confinement of birds, bird
vertebrates and water. It multiplies at low temperatures; and rodent proofing the houses and aviaries are essential
therefore, infections are common in the winter and spring. for preventing Yersiniosis. Treating chronic infections
Rodents (rats, mice), hares and rabbits and some wild can be extremely difficult. Prompt diagnosis and use of
birds serve as reservoirs. Transmission is probably through tetracyclines have been beneficial in reducing mortality in
contaminated water, feed and environment. Factors such outbreaks of Yersiniosis in turkeys and ducks.
as cold weather, chilling and concurrent diseases can
predispose the birds for Yersiniosis. Antimicrobial testing of isolates of Y. pseudotuberculosis
has shown that antibiotics such as ampicillin, penicillin,
CLINICAL SIGNS enrofloxacin, spectinomycin, tetracyclines, sulfonamides,
Clinical signs due to Yersiniosis depend on whether the neomycin, ormetoprim/sulfa, and gentamicin can be
disease is acute or chronic; the chronic form being more effective in treatment. However, sensitivity tests should be
common. In general clinical signs include lethargy, diarrhea, performed on each isolate before antibiotics can be used.
dyspnea and dehydration. In chronic infections symptoms
include loss of weight, swollen joints, and paresis.
In one outbreak of 9 and 12 week–old turkeys, anorexia,

watery yellow-green droppings, depression and acute
lameness were observed with morbidity ranging from 2-15
% with increased mortality due to cannibalism. In acute
infections of some species of birds such as wood peckers,
toucans and turacos there may not be any clinical signs but
birds are found dead.
FUNGAL DISEASES 5. Infections in the brain, posterior chamber of the eye

or other visceral tissues result from systemic invasion
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Revised by Dr. H.L. Shivaprasad from the respiratory tract.

6. The difference between localized and disseminated
lesions due to aspergillosis has been attributed to the
ASPERGILLOSIS genetic differences between species of Aspergillus
(Brooder Pneumonia; Mycotic strains and their ability to produce elastase.
Pneumonia; Pneumomycosis)
CLINICAL SIGNS
DEFINITION 1. Dyspnea, gasping, cyanosis and accelerated, labored
Aspergillosis is an acute or chronic disease, primarily breathing (Fig. 1) frequently are observed. Rales do
affecting the respiratory system. Peritoneal, visceral and not usually accompany these respiratory diseases.
systemic infections especially involving brain and eyes Other signs include diarrhea, anorexia, somnolence,
can also occur. The most common etiology is Aspergillus progressive emaciation, dehydration and increased
fumigatus but A. flavus can be involved. Aspergillosis thirst.
occurs frequently in turkeys, chickens, and game birds. 2. Morbidity is variable. Mortality is high in clinically
This condition has also been reported in penguins, raptors, affected birds. Increased mortality will be noted in
migratory waterfowl, psittacines and zoologic specimens, affected flocks during loadout, hauling and following
such as flamingos. All species of birds probably are insemination. Affected birds often die during or just
susceptible. Aspergillosis was first described in a wild duck after handling especially if held by their legs.
in 1833 and in turkeys as early as 1898. There are some 3. Signs of central nervous system disturbance may occur
other species and genera of fungi that may cause similar in a small percentage of the birds if there has been
disease syndromes. spread to the brain. Signs often include ataxia, falling,
pushing over backwards, opisthotonos, paralysis, etc.
EPIDEMIOLOGY 4. A gray-white opacity may develop in one or both eyes
1. Embryos. Aspergillus fumigatus can penetrate egg when there is eye infection. Ocular discharge occurs
shells under ideal growth conditions and thus infect when the conjunctiva is infected and there can be
the embryos. Such eggs will often appear green when corneal ulceration. A large mass of exudate typically
candled (the embryo will be dead). Infected embryos accumulates in the medial canthus under the third
may hatch with well developed lesions. eyelid.
2. Chicks and poults. If infected eggs break in the
hatchery, large numbers of spores are released which LESIONS
contaminate the hatchery environment and air systems 1. Mycelial growth with sporulation may be apparent as
can lead to severe outbreaks in very young birds fuzzy gray, blue, green or black material (sporulating
(less than 3 weeks of age). Eggs punctured for in ovo fungus) or pale yellow plaques on air sac, pleura,
injection are particularly susceptible to contamination. pericardium, peritoneum or in the syrinx and main
Even low-level contamination of hatchers or air bronchi of the lungs.
systems can result in mortalities of 50% or greater 2. Pale yellow or gray circumscribed nodules or plaques
when in ovo injection is used. Navel infections can also in the lungs (Fig. 2), air sacs bronchi or trachea (Fig.
occur. 3) (usually the syrinx); less often in the brain, eyes,
3. Adults. Infection usually follows inhalation of large heart, kidneys, liver, or at other sites. In mature birds
numbers of spores from heavily contaminated feed, two patterns of air sac infection are found: disc-like
litter or environment. Conjunctival infections may occur plaques in the recurrent bronchi of the caudal thoracic
from heavy exposure to airborne spores following and/or abdominal air sacs or markedly distended air
traumatic injuries. It is believed that healthy birds resist sacs containing copious fluid and soft fibrinopurulent
infection but that resistance can be overwhelmed by exudate.
massive exposure combined with depressed host
DIAGNOSIS
defenses. Debilitated and overcrowded birds are
1. The signs and gross lesions of aspergillosis are very
most susceptible. Market age tom turkeys and turkey
suggestive of the diagnosis which can be confirmed
breeders are commonly affected.
by microscopic demonstration of fungus in fresh
4. Aspergillus fumigatus and A. flavus are normally preparations made from the lesions or in histologic
present in litter and feed. Enormous numbers of spores sections.
can be produced under ideal conditions. Sporulating
2. Microscopic examination reveals septate, branching
colonies of Aspergillus fumigatus are blue-green and
hyphae within lesions. Hyphae can be seen in fresh
can often be observed grossly.
preparations cleared with 10% KOH or stained with
FUNGAL DISEASES 141
lactophenol cotton blue. If fungus is grossly visible TREATMENT

in the lesions, the typical fruiting bodies (Fig. 4) and 1. If aspergillosis is diagnosed in a flock, cull clinically
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spores can be easily found. In histologic sections, affected birds and remove any contaminated feed and
special stains (methenamine-silver, PAS, Gridley) are litter. Clean and disinfect the house and then spray it
useful for demonstrating fungi in tissues. Nodules in with 1:2000 copper sulfate solutions or other fungicide
the lungs usually appear as granulomas containing and allow it to dry.
fungal hyphae.
2. Valuable captive birds can be treated with Nystatin
3. Using sterile technique, the fungus can be cultured or Amphotericin-B or other anti-mycotic agents.
by tearing a nodule or plaque open and putting it on Often antibiotics are given simultaneously to prevent
fungus media. Aspergillus will usually grow on blood secondary bacterial infection. Intravenous fluids may
agar in 24-48 hours. Sabouraud’s dextrose agar (Fig. also be required. Ketaconizole, Miconozole and related
5) is a more selective medium. Since aspergillus drugs have been found effective for treating individual
spores are common laboratory contaminants, growth birds but are too expensive for commercial flocks.
of only a few colonies may not be sufficient for a
definitive diagnosis. For confirmation, tissue invasion
should then be demonstrated.
4. Typical lesions of aspergillosis are unlike those of
other avian respiratory diseases except pulmonary
granulomas associated with complicated Mycoplasma
gallisepticum infection. Grossly aspergillus lesions
especially in the lungs can resemble lesions
caused by Staphylococcus aureus in turkey poults.
Histopathologic differentiation is usually easy.
5. Another fungus, Ochroconis (previously Dactylaria)
gallopava, can cause lesions in the lungs or brain of
young chickens and turkey poults. Signs and lesions
resemble those caused by aspergillosis. The two fungi
can be differentiated by culture. Numerous giant cells
are characteristic of microscopic brain lesions caused
by O. Gallopava. On histopathology, pigmented fungus
can be readily recognized but culturing is necessary
for positive identification.
CONTROL
1. Collect clean eggs. Disinfect or fumigate eggs before
setting. Do not set cracked eggs or eggs with poor
shell quality.
2. Thoroughly clean, disinfect and fumigate incubators
and hatchers. Inspect air systems and change air filters
regularly in hatcheries. Monitor hatchery environment
for mold contamination.
3. Use only dry, clean litter and freshly-ground, mold-free
feeds. Store feeds and litters properly so as to inhibit
growth of mold. Make sure feed bins and feed lines
are kept clean, dry and free of mold growth. Do not
permit feed to cake in feeders. Avoid wet litter under or
around the waterers or feeders. Mold inhibitors may
be added to feed to control fungus growth and prevent
infection; however, this will add expense.
4. Optimize the ventilation and humidity in the poultry
house to reduce air-borne spores. Humidity should
be kept in the mid-range, neither too low nor too
high. Alternating wet and dry conditions are an ideal
situation for Aspergillus. The fungus multiplies during
the wet period producing abundant spores which then
become aerosolized when conditions become dry.
ASPERGILLOSIS
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Fig. 2
Fig. 1 Bird with yellow to white mycotic nodules in the lung.
Gasping chicks.
Fig. 3 Fig. 4
Mycotic nodule in the trachea. Aspergillus fruiting body.
Fig. 5
Aspergillus fumigatus on Sab Dex
media.
FUNGAL DISEASES 143
CANDIDIASIS DIAGNOSIS
(Thrush; moniliasis, crop mycosis, sour 1. Characteristic gross lesions are generally adequate for
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diagnosis. Histopathologic examination of the affected

crop, muguet, soor, levurosis)
mucosa usually will confirm invasion of the tissue by
the septate fungal hyphae.
DEFINITION
Candidiasis is a disease of the digestive tract caused by 2. Candida albicans grows readily on Sabouraud’s
the yeast-like fungus Candida albicans and probably other dextrose agar. However, since Candida is commonly
species of Candida. The disease generally involves the present in normal birds, only the demonstration of
upper digestive tract and usually occurs as a secondary massive numbers of colonies is of significance.
infection.
CONTROL
1. Practice a high standard of sanitation in the poultry
EPIDEMIOLOGY operation. Phenolic disinfectants or iodine preparations
Candida albicans is a common yeast-like fungus that has should be used to sanitize equipment.
been recognized as a commensal organism in poultry
2. Prevent other diseases or management practices that
and mammals for many years. Candidiasis has been
might debilitate the birds.
reported from a variety of avian species, such as, chickens,
turkeys, pigeons, game birds, waterfowl, and geese. In 3. Avoid over treatment of birds with antibiotics, drugs,
poultry it seldom has been considered a disease of major coccidiostats, growth stimulants and other agents that
importance. Young birds tend to be more susceptible than might affect the bacterial flora of the digestive tract.
adult birds although all ages can be affected. When birds
become debilitated or the normal digestive tract flora is TREAMENT
altered, the ingestion of fungus in the feed and water can 1. Copper sulfate at a 1:2000 dilution in drinking water is
result in mucosal invasion. The production of a soluble commonly used both for prevention and treatment but
endotoxin may also contribute to pathogenicity. Common its value is controversial. Nystatin in feed or water has
predisposing causes include lack of good sanitation, shown efficacy against candidiasis in turkeys.
prolonged treatment with antibiotics, heavy parasitism, 2. Routine addition of antifungal drugs to rations probably
vitamin deficiency, high carbohydrate diets, and immune is a waste of money since elimination of contributing
suppressing or debilitating infectious diseases. factors or other diseases usually will prevent
candidiasis. However, if sanitation is at fault and cannot
be improved, antifungal drugs may be advisable.
CLINICAL SIGNS
Signs are non-specific and include, listlessness,
inappetence, retarded growth, and ruffled feathers. In
advanced cases diarrhea may occur. The signs may
be masked by the clinical signs of a primary disease.
In advanced cases, the crop may not empty and may
become fluid filled. The bird may regurgitate fluid with a
sour, fermentative odor, i.e. the name “sour crop”.
LESIONS
1. Lesions vary greatly in severity. They are more
common in the crop, mouth, pharynx and esophagus,
but may involve the proventriculus and, less often, the
intestine. Lesions involving the crop are one of the
most findings in turkey poults.
2. The affected mucosa is often diffusely or focally
thickened (Fig. 1), raised, corrugated and white,
looking like terry cloth (Fig. 2). Lesions may also appear
as proliferative white to gray pseudomembranous or
diphtheritic patches and as shallow ulcers. Necrotic
epithelium may slough into the lumen as masses of
soft cheesy material.
3. Lesions of a primary predisposing disease may also be
present and should be investigated. In particular one
should search for evidence of coccidiosis, parasitism
or malnutrition especially vitamin A deficiency.
CANDIDIASIS
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Fig. 1 Fig. 2
Crop mycosis. Severe crop mycosis.
FUNGAL DISEASES 145
OCHROCONOSIS
(Previously known as DACTYLARIOSIS)
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DEFINITION
A neurotropic, mycotic disease of turkey poults and young
chickens with many of the clinical and pathologic features
of aspergillosis. Ochroconis gallopava is a dematiaceous
(Phaeohyphomycosis) pigmented septate fungus that has
distinctive reddish brown in its walls. It occurs in the soil,
saw dust, other litter, decaying vegetation and thermal
springs. It is most common as an incidental finding in the
granulomas of lungs of turkey poults. Signs of Ochroconosis
(incoordination, tremors, torticollis, circling, recumbency)
are related to mycotic lesions in the brain (Fig. 1). Lesions
also occur with less frequency in the air sacs, liver and
eyes (globes). The etiologic agent, Ochroconis (Dactylaria)
gallopava, grows naturally in old sawdust which often is
used as poultry litter. Fig. 1
Mycotic encephalitis.
FAVUS
(Avian ringworm, Avian dermatophytosis)
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DEFINITION
Favus is a mycotic infection found primarily in gallinaceous
birds. Favus is rare in commercial poultry today, but is
occasionally reported in backyard flocks, especially exotic
and game chickens. Characteristic lesions include white
crusting or powder-like material on the comb and wattles
(Fig. 1) that can extend to the feathered portion of the
skin to form scutula around the bases of feather follicles.
The fungus has predilection for the keratin layer of the
epidermis and feather follicles causing hyperkeratosis,
hence powder-like material seen grossly. Microsporum
gallinae is the agent most often isolated, although M.
gypseum and Trichophyton simii have also been isolated.
Topical treatment with nystatin has been efficacious on
individual birds.
Fig. 1
White crusting of comb (chicken on the right).
FUNGAL DISEASES 147
MYCOTOXICOSIS 5. Zeolytes, a class of silica-containing compounds used

as anticaking agents in feed formulation, and as aids
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DEFINITION in the improvement of eggshell quality, show promise

Mycotoxicosis is a disease caused by a toxic fungal as a practical and economical method of reducing the
metabolite. Mycotoxicoses may affect both humans and effects of certain mycotoxins. Hydrated sodium calcium
animals. Poultry mycotoxicoses are usually caused by aluminosilicate has been shown to bind aflatoxin B1,
fungi that colonize and invade grains and feeds, but other possibly by sequestration in the digestive tract, and
environmental aspects may be involved. reduce its toxicity to chickens.
TREATMENT
OCCURRENCE 1. Remove the toxic feed and replace it with unadulterated
1. Grains and forages used as foodstuffs support the feed.
growth of certain fungi when environmental conditions 2. Treat concurrent diseases (parasitic, bacterial)
of temperature and humidity are suitable. Some of these identified in the diagnostic evaluation.
fungi produce metabolites that are toxic to humans
and animals and cause disease (mycotoxicosis) by 3. Substandard management practices should be
either ingestion or cutaneous exposure. immediately corrected as they have increased
detrimental effects in a flock stressed by mycotoxins.
2. Mycotoxicoses occur throughout animal-rearing
regions of the world. Although specific mycotoxins 4. Vitamins, trace minerals (selenium), and protein
form more frequently in certain geographic locations, requirements are increased by some mycotoxins
interstate and international shipment of grains may and can be compensated for by feed formulation and
result in widespread distribution of a mycotoxin water-based treatment.
problem.
I. AFLATOXICOSIS
DIAGNOSIS
1. A definitive diagnosis of mycotoxicosis should involve
1. During the 1950s, a disease in dogs called hepatitis
the isolation, identification, and quantitation of the
X occurred in the southeastern United States and
specific toxin(s). This is usually difficult to accomplish
was tied to the consumption of moldy dog food. It
in the modern poultry industry because of the rapid
was later reasoned to have been caused by the same
and voluminous use of feed and ingredients.
mycotoxin responsible for high mortality in turkeys
CONTROL due to hepatic toxicity (turkey X disease) in England
1. Prevention of mycotoxicoses requires the detection in 1960. Peanut meal imported to England from Brazil
and control of mycotoxin contamination in feed was highly contaminated with fungi of the Aspergillus
ingredients and the application of feed manufacturing flavus-Aspergillus parasiticus group, which produced
and management practices that prevent mold growth aflatoxins.
and mycotoxin formation. 2. The aflatoxin story was historically important because
2. Feeds and grains can now be screened for several unlike ergotism and alimentary toxic aleukia, which
mycotoxins (aflatoxin, T-2 toxin, ochratoxin, were sporadic and relatively localized phenomena,
zearalenone) using monoclonal antibody detection aflatoxicosis attracted global attention concerning the
kits. Many poultry companies already routinely test potential problems of mycotoxins in the food chain,
grain for aflatoxin contamination by a chromatographic and the ease by which these problems could be widely
procedure (minicolumn technique). distributed.
3. Mycotoxins can form in decayed, crusted, built-up ETIOLOGY
feed in feeders, feed mills, and storage bins. This can 1. Mycotoxins of the aflatoxin group (B1, B2, G1, G2)
be prevented by inspection of bins between flocks to are the cause of aflatoxicosis. Aflatoxin B1 is the most
certify absence of feed residue and by cleaning bins common in grains and is highly toxic. Aflatoxin forms
and feeders when necessary. Use of tandem feed bins in peanuts, corn, and cottonseed, and their products,
on farms allows cleaning between successive feed in other grains, and in poultry litter. A. flavus is the
deliveries. primary producer of aflatoxin in grains, but not all
4. Antifungal agents added to feeds to prevent fungal strains of the fungus are toxigenic.
growth have no effect on toxin already formed, but 2. Like other mycotoxins, aflatoxin is produced only
may be cost-effective management in conjunction when substrate, temperature, and humidity are
with other feed management practices. Several ideal. Favorable conditions for toxin formation may
commercial products, most of which contain proprionic be localized within a volume of stored or transported
acid, should be applied according to manufacturers’ grain creating toxic “hot spots”. Once formed, the toxin
instructions. is stable.
3. Grains damaged by insects and drought stress, and III. ERGOTISM

broken pieces of grain (screenings) are more likely to
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support fungal growth and toxin formation. HISTORICAL INFORMATION

4. Aflatoxin B1 is a potent, naturally occurring carcinogen 1. Ergotism was recognized in central Europe in the
and thus has special public health considerations. Middle Ages and is the oldest known mycotoxicosis.
Humans with ergotism (St. Anthony’s fire) experienced
CLINICAL SIGNS an initial cold sensation in the hands and feet followed
Aflatoxicosis in poultry is primarily a disease of the liver by an intense burning sensation. Gangrene of the
(Fig. 1) with important ramifications for other body systems, extremities developed in both humans and afflicted
which may ultimately cause production problems and animals. The disease occurred where bread was
mortality. Affected birds have reductions in growth, carcass made from rye and other grains parasitized by
pigmentation, egg production, and immune function, and toxigenic strains of the fungus Claviceps purpurea.
have increased nutrient requirements for protein, trace The mold colonizes and replaces kernels of grain to
elements (selenium), and vitamins. The disease may be form a hard, dark purple or black mass called an ergot
fatal. or sclerotium.
2. Although the pharmaceutical properties of the ergot
LESIONS were recognized in China 5,000 years ago, it was not
At necropsy, lesions are minimal with either transient until 1875 that alkaloids present in the sclerotium were
exposure or exposure to a low concentration of toxin. recognized as the cause of ergotism.
Jaundice, generalized edema and hemorrhages, tan (Fig.
2) or yellow discoloration of the liver, and swelling of the ETIOLOGY
kidneys (Fig. 3) are seen with more severe intoxication. 1. The ergot alkaloids are a large family of compounds,
Microscopic changes in the liver occur as necrosis of and may cause constriction of blood vessels
hepatocytes, lipid accumulation in hepatocytes, bile duct (vasoconstriction) which results in their pharmacologic
proliferation, and fibrosis. These are common reactions and toxicologic effects.
of this organ to toxic insult and although they may be 2. Claviceps spp. that colonizes wheat, rye, and triticale
suggestive of aflatoxicosis, are not pathognomonic. are the most common causes of ergotism of humans
and animals.
II. CITRININ MYCOTOXICOSIS CLINICAL SIGNS
In chickens, ergotism causes reductions in growth and egg
ETIOLOGY production, and nervous incoordination.
Citrinin is a mycotoxin that was first isolated from Penicillium
citrinum but is also produced by other species of Penicillium
and by a few species of Aspergillus. Citrinin may be a factor LESIONS
in renal disease in food animals in Denmark, but no other Lesions include abnormal feather development, necrosis
documented case studies involving poultry are known. of the beak, comb, and toes, and enteritis.
CLINICAL SIGNS IV. OCHRATOXICOSIS

Experimental citrinin mycotoxicosis in the chicken, turkey,
and duckling has shown that chickens are relatively HISTORICAL INFORMATION
resistant, but all develop clinical illness of marked watery 1. Ochratoxin has been detected in kidneys of chickens
fecal droppings related to increases in water consumption with renal lesions in a processing plant in Denmark.
and urine output. Metabolic alterations of electrolytes 2. Three disease outbreaks in the United States involving
and acid-base balance occur. Young birds have reduced 360,000 turkeys were associated with ochratoxin
weight gain. concentrations of up to 16 ppm.
ETIOLOGY
LESIONS Ochratoxins A, B, and C are usually produced by toxigenic
Citrinin produces marked functional changes in kidneys,
strains of P. viridicatum but may be produced by other
however, gross lesions may be slight or overlooked. Swelling
species of Penicillium and by Aspergillus ochraceus.
of kidneys and microscopic lesions of nephrosis may
Ochratoxin A is the most toxic and is the greatest threat to
occur following severe exposure. In these circumstances,
poultry production.
lymphoid tissues may be depleted and necrosis occurs in
the liver.
CLINICAL SIGNS
1. Reductions in feed intake and increases in mortality.
2. Weight loss.
FUNGAL DISEASES 149
3. Drops in egg production have been reported from ETIOLOGY

Ochratoxin A. More than 40 trichothecene mycotoxins are known to exist.
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T-2 toxin is one of the most toxic to poultry.

LESIONS
1. Gross and microscopic lesions in the kidneys and liver.
CLINICAL SIGNS
2. Experimental ochratoxicosis in chickens causes a 1. Chickens with fusariotoxicosis (trichothecene
dose-related reduction in weight gain, and gross and mycotoxicosis) have had reduced growth, abnormal
microscopic lesions occur in the target organs, liver feathering (Fig. 1), severe depression, and bloody
and kidney. Visceral gout and reductions in plasma diarrhea.
carotenoids, immune function, and certain blood
coagulation factors also occur. 2. In chickens, pigeons, ducks, and geese, the caustic
properties of the trichothecenes have been manifested
V. OOSPOREIN MYCOTOXICOSIS as feed refusal, extensive necrosis of the oral mucosa
and areas of the skin in contact with the mold, and
ETIOLOGY symptoms of acute gastrointestinal disease.
Oosporein is a toxic pigment produced by Chaetomium sp.
3. Experimental fusariotoxicosis, reproduced in chickens
and other fungi and is a contaminant of cereal grains and
with pure T-2 toxin closely resembled the spontaneous
feedstuff.
disease but lacked the extensive hemorrhages.
CLINICAL SIGNS LESIONS

Oosporein mycotoxicosis, studied in chickens and turkeys, 1. Trichothecene mycotoxicosis may cause necrosis of
causes a dose-related decrease in growth and an increase the oral mucosa (Fig. 2), reddening of the mucosa of
in water consumption. Chickens are more susceptible than the remainder of the gastrointestinal tract, mottling of
turkeys. the liver, distention of the gallbladder, atrophy of the
spleen, and visceral hemorrhages.
LESIONS VII. ZEARALENONE MYCOTOXICOSIS
Visceral and articular gout as a result of nephrotoxicity.
In experimental studies, chickens have shown relative
VI. TRICHOTHECENE MYCOTOXICOSIS insensitivity to the effects of zearalenone. Zearalenone
(Fusariotoxicosis) mycotoxicosis has been recognized since 1927 as the
cause of a syndrome resembling estrogen stimulation in
HISTORICAL INFORMATION pigs and cattle in the United States and elsewhere.
1. A disease called alimentary toxic aleukia occurred
in the Russian people in the early 20th century, the ETIOLOGY
1930s, and especially during the Second World War. Zearalenone is a mycotoxin produced by Fusarium roseum
Labor shortages during the war necessitated the (Gibberella zeae) and other Fusarium spp. A period of
overwintering of grains (wheat, rye, and millet) in the warm temperature and high humidity followed by low
fields and harvesting was delayed until spring. Bread temperature is most conducive to toxin formation on grains
made from the new grain caused acute gastroenteritis,
followed by the formation of ulcers of the face and
oral membranes, facial edema and lymph node CLINICAL SIGNS
enlargement, and in the later stages, bone marrow 1. Zearalenone-contaminated feed has been associated
disorders, anemia, and uncontrolled hemorrhages. with high mortality (40%) in a flock of 24,000 broiler
Morbidity and mortality greater than 50% occurred in breeder chickens. Affected birds had cyanotic combs
some villages. Similar problems occurred in livestock and wattles and had difficulty walking.
and poultry in the region. 2. Turkeys may develop swelling of the cloaca and
2. The disease is now recognized as a mycotoxicosis reduced fertility.
caused by colonization of grains by toxigenic species 3. Male geese may have reductions in sperm quantity
of Fusarium. These fungi produce mycotoxins of the and viability.
trichothecene group, many of which cause caustic
injury to mucous membranes and skin, the basis of the LESIONS
facial, oral, and gastrointestinal features of the disease. 1. Affected chickens have had ascites and cysts both
They also affect rapidly dividing cells (radiomimetic inside and outside of the oviduct. The oviducts were
effect) manifested by disorders of the bone marrow swollen and inflamed, and were obstructed with
(anemia, hemorrhagic disorders) and by abortions. fibrinous fluid. Some oviducts had ruptured.
AFLATOXICOSIS
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Fig. 1 Fig. 2
Tan liver (3ppm aflatoxin in feed) vs. normal liver. (on the right) Tan liver (3ppm aflatoxin in feed).
Fig. 3
Swollen kidneys (3ppm aflatoxin in feed) vs. normal kidneys. (on
the right)
TRICHOTHECENE MYCOTOXICOSIS
Fig. 1
Fig. 2
Abnormal feathering.
Oral ulceration & necrosis.
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Summary Table of Most Common Mycotoxicosis in Poultry
Aflatoxins Fumonisins Oosporein Tricothecene Ochratoxins Citrinin Ergotism Zearalenone
Names B1, B2, G1 and T2, DAS, DON Ochratoxins Ergot alkaloids
G2 are natural A, B & C (ergotamine,
contaminants more than 100 ergocristine)
fungal metabolites
Major Aspergillus mostly Fusarium Chaetomium Primarily isolated Produced by Penicillium Claviceps Fusarium
producers Aspergillus flavus moniliforme trilaterale from Fusarium spp. A. ochraceus, citrinum purpurea or other graminearum
and A. parasiticus Penicillium Claviceps species
Type A (more toxic viridicatum and Fusarium
to chickens) other species roseum
of Penicillium
14 PEB
Ochratoxin A –the
most common
toxic mycotoxin
for poultry and
the most toxic
Toxic Target organ: Liver Disruption of Primary Primary inhibition Target organ: the Reversible Arterial and Potent
action sphingolipid renal tubular of protein kidney interferes renal damage venous estrogenic
*potent synthesis damage synthesis followed with DNA, RNA & vasoconstriction properties
hepatocarcinogen by secondary protein synthesis
in humans Very low toxicity disruption of DNA Necrosis of Low toxicity
for poultry & RNA synthesis Affects renal peripheral tissues for poultry
carbohydrate
Affect rapidly metabolism Decreased blood
dividing cells such (gluconeogenesis) flow to extremities
as those lining the = damage to the
GI tract, the skin, epithelium of Possible
and lymphoid and renal proximal endothelial
erythroid cells convoluted tubules damage
Extensive necrosis Decreased

of mucous electrolyte
membranes and absorption
skin in contact
with the toxin Increased water
excretion
Acute effects on
digestive tract and
bone narrow
FUNGAL DISEASES
Immunosuppressive
151
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152
Clinical Decreased Decreased Dose-related Decreased Decreased feed Marked watery Reduced growth Reduced
signs feed intake body weight decrease feed intake intake, weight loss fecal droppings fertility
in growth Decreased egg
Decreased Reduced growth Increased Increased water production
body weight Increased mortality consumption
water Severe depression Increased Nervous signs
Poor skin consumption Increased water diuresis (incoordination)
Abnormal feathering consumption
Decreased egg Reduced
production Bloody diarrhea Humid litter weight gain
Avian Disease Manual
(young birds)
Decreased Decreased egg
immunity production Humid litter
Lesions Jaundice Increased Dehydration Circumscribed Pale and swollen Swollen kidneys Gangrenous- Oviduct
liver weight proliferative yellow kidneys like lesions hypertrophy
Generalized Swollen and caseous plaques Degeneration
edema and Increased pale kidneys in oral mucosa Secondary and necrosis Necrosis of the Cloacal
hemorrhages, kidney weight secondary visceral gout of tubular beak, comb, toes swelling
tan or yellow Reddening of
visceral and epithelial (turkeys)
discoloration GI mucosa
Liver hepatic articular gout Pale and cells of both Enteritis
of the liver necrosis Mottling of the liver enlarged liver proximal and Reduction
Liver: Periportal with biliary distal tubules. in sperm
hyperplasia Gallbladder quantity
necrosis with bile Regression and
distention and viability
duct proliferation cellular depletion
and fibrosis Splenic atrophy of lymphoid (geese)
organs.
Depletion of Visceral
lymphoid organs hemorrhages
Sources Peanuts, corn, Corn and corn Cereal grains Fusarium spp. are Widespread Often coexists Open Corn, corn
cottonseed, and based feed feedstuff important pathogens natural in cereals with inflorescence of products, rice
their products, to plant producing contaminant of ochratoxin A graminaceous
cereal grains, (corn, cereal grains (corn, wheat, plants (rye,
In other grains wheat, barley, (barley, oats, barley, oats, wheat, triticale
and in poultry litter oats, rice, rye….) rye, maize) rye and rice) barley, oats,
sorghum, corn,
rice) and several
grass species.
Treatments None Vitamin C

supplementation
might reduce
some adverse
effects.
PARASITIC DISEASES 153
PARASITIC DISEASES CONTROL

Pesticides treatments are highly regulated chemicals
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Revised by Dr. Steve H. Fitz-Coy and all have hazardous potential for animal and human
health tissue residues, and environmental contamination.
A current listing of approved pesticides should be obtained
EXTERNAL PARASITES from local agricultural authorities or university specialists.
Examples of classes of products approved by the EPA
I. LICE for control of mites and lice include: organophosphates,
carbamates, pyrethrins, and pyrethroids. Treatment is
DEFINITION simplified by the fact that the louse is only found on the
Lice are insect ectoparasites. Lice are generally species bird and not in the environment. In general, the efficacy
specific, meaning for each species of bird or mammal, of the treatment is dependent on the application of the
there are particular species of lice. chemical. The agent must penetrate to the skin in order
to kill the lice. Also the entire bird must be treated as the
ETIOLOGY lice are very mobile and will move away from the treated
In domestic fowl, more than 40 species of lice have been areas. Lice eggs are not affected by insecticide treatment,
reported. Some of the most important chicken lice include therefore a minimum of two treatments are required.
the Body Louse (Menacanthus stramineus), Head Louse Treatment should be performed on 7 to 10 day intervals.
(Culclotogaster heterographa), Shaft Louse (Menopon Egg-laden feathers should be removed from the premises.
gallinae), Wing Louse (Lipeurus caponis), Fluff Louse Routine examination for infestation should be performed
(Gonicocotes gallinae) and the Brown Chicken Louse for resident flocks on a bi-weekly or monthly basis.
(Goniodes dissimilis). Also important are the Large Turkey
Louse (Chelopistes meleagridis), and the Slender Pigeon
Louse (Columbicola columabae). Birds may be parasitized
simultaneously by more than one species.
EPIDEMIOLOGY
As is evident from the common names, certain lice prefer
different regions of the bird. They feed on scales of the
skin and feathers. The life cycle is approximately 3 weeks.
The entire life cycle is on the host. Lice will die in 5 to 6
days if separated from their host. Spread from bird to bird
is dependent on close contact. Lice problems tend to be
worse in the autumn and winter months.
CLINICAL SIGNS
Lice probably are not highly pathogenic for adult birds
but the discomfort caused by the biting louse can have
Fig. 1
tremendous effects on flock performance. Heavy infestation Clumps of louse eggs attached to
of young birds is especially harmful due to the disruption of feathers.
sleep.
LESIONS
Careful examination of the vent area, the underside of
the wings, the head (crest and beard) and legs will reveal
these pests. Most bird lice are straw-colored and vary in
size from 1-6 mm, but some may reach 10 mm. Louse
eggs often can be found attached to feathers in clumps
called “nits” (Fig. 1).
DIAGNOSIS
Diagnosis is based on gross observation of skin and
feathers.
II. MITES mites are difficult to treat as the feather shaft protects them
from chemical agents. Isolate affected birds. Treat as for
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DEFINITION Dermanyssus gallinae (red mites).

Mites are very small, barely discernible without
magnification. They are not host specific and will infest any D. SCALY LEG MITE. (Knemidokoptes mutans)
avian species. Mites feed on blood, feathers, skin or scales. This mite represents a group of closely related mites that
Some mites do not spend their entire life on the bird; only live primarily within unfeathered skin, often on the shanks
visiting to feed, therefore, the bird and the environment and feet. It cannot be seen without magnification. The
must be treated to affect control. The most common mites affected skin becomes thickened and hyperkeratotic with
of poultry species are listed below. white, powdery, exfoliating crusts (Fig. 2). Some mites in
this group attack the beak of birds. Without treatment, the
A. CHICKEN MITE –RED MITE affected bird will eventually become crippled. Long term
(Dermanyssus gallinae) treatment of individual birds is necessary for recovery.
Common red mites are up to 0.7 mm long x 0.4 mm and Spread through a flock is usually slow.
appear black or gray or red if engorged with blood. Red
mites feed mostly at night and may not be found on the hosts CONTROL
during the day. Inspection at night is usually necessary Treatment must be tailored to the species of mite affecting
to confirm infestation. Their life cycle can be completed the bird, i.e., accurate identification is important. In many
in as few as 7 days. During the day, they may be found cases, the bird and the environment must be treated
in colonies in the cracks or joints of roosts or nests. They simultaneously. Insecticides for mites can be applied
can survive for over 30 weeks without food. This makes as powders, dusts or sprays. It is important that the
treatment of the facility imperative in control of this pest. insecticide penetrates to the skin. For mites that live off the
Anemia and mortality can result from heavy infestations, host (e.g. Dermanyssus gallinae), facilities can be treated
especially in young birds. They have been reported to by spraying a wet-able powder or liquid spray that will
transmit the agents of fowl cholera and spirochetosis. They penetrate small cracks and crevices. Floors and bedding
frequently parasitize caged layers. Treat both birds and should also be treated. Pesticides are highly regulated
facilities. Repeat treatment in one week. chemicals and have hazardous potential for animal and
human health and environmental contamination. A current
B. NORTHERN FOWL MITE listing of approved pesticides should be obtained from local
(Ornithonyssus sylviarum) agricultural authorities or university specialists. A notable
These mites are common bloodsuckers of a wide variety of exception is the Scaly leg mite (Knemidocoptes mutans)
poultry and other birds. They are known to or suspected of which can only be treated by direct application of an oil
harboring agents that cause fowl pox, Newcastle disease, based product, such as petroleum jelly or cooking oil and
ornithosis and certain encephalitides. These mites stay kerosene (50:50) on a daily basis for at least 2 weeks or
on the birds continuously looking like moving red to black until the appearance of the legs returns to normal. Gentle
specks. Heavy infestations appear as blackened feathers, washing of affected areas with soapy water to loosen and
often near the vent with scabbed and cracked skin (Fig. mildly hyperkeratinized areas is also helpful.
1). Mite egg sacs are in white or off-white clusters located
under the wings, above and below the vent, in the beard
and crest and on the feathers of the proximal thigh. After
handling or at necropsy they may transfer to the hands and
arms of the handler or diagnostician. Northern fowl mites
parasitize caged layers, especially during the wintertime,
and often are seen crawling on eggs. All birds in the flock
should be treated twice in a 5-7 day interval.
C. DEPLUMING MITES (Knemidokoptes gallinae)

A variety of feather mites live on the feathers or in the
quills of domestic and wild birds. Feather mites tend to be
somewhat host specific. They cause breakage or complete
loss of feathers. The depluming mite of chickens, pheasants
and pigeons (Knemidokoptes gallinae) burrows into the
basal shafts of the feathers producing intense irritation that
will cause the host to pull out its body feathers. Loss of
feathers can lead to inability to control body temperature
and may increase susceptibility to other diseases. These
MITES
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Fig. 1 Fig. 2
Northern fowl mites infestation. Severe hyperkeratosis of the feet of a silkie chicken.
III. MISCELLANEOUS PESTS of viral diseases such as Pox and Equine Encephalitis.
Generally a blood meal is necessary for egg production
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A. BEDUGS (Cimex lectularius) by the female mosquito. They also transmit protozoa that
Bedbugs attack mammals and birds, including poultry and cause avian malaria-like syndromes. Mosquitos’ bites
pigeons. Adult parasites are up to 5.0 mm long and have cause irritation which may affect performance.
8 abdominal segments. Bedbugs usually feed at night
and may be observed on parasitized birds. Bedbugs can H. FOWL TICKS (Argas persicus)
survive in houses for a year in the absence of poultry. Birds Soft ticks including the “fowl tick” parasitize a wide range
parasitized by bedbugs soon become unthrifty and anemic. of poultry, wild birds and, occasionally, mammals. Some
of the ticks not only cause anemia, skin blemishes or tick
B. CHIGGERS (Neoschongastia americana) paralysis but also transmit Borrelia anserina, the agent that
Larval mites of Neoschongastia americana are a serious causes spirochetosis. Fowl ticks occur more frequently
pest of turkeys and birds in southern states. In turkeys the in the southwestern states, including California. The ticks
larvae attach to the skin and cause localized skin lesions spend relatively little time on their hosts and are easily
that lead to market downgrading. The lesions resemble overlooked.
pimples and may be very numerous.
C. DARKLING BEETLE AND LESSER

MEALWORM. (Alphatobius diaperinus)
This beetle (Fig. 1 and 2) and its larvae (Fig. 3) often are
present in poultry house litter. They may act as disease
vectors for Marek’s disease virus and Infectious Bursal
disease virus. Botulism toxin has been found in these
beetles. They probably serve as vectors for tapeworms.
Their primary importance to the commercial poultry industry
is economic due to the severe damage they can cause to
the insulation and wall materials of modern poultry houses.
D. STICKTIGHT FLEAS
(Echidnophaga gallinaceae)
In poultry these parasites usually are tightly attached in
clusters to the skin of the head. They irritate the skin, cause
anemia, lower egg production and may kill young birds.
The adult fleas are about 1.5 mm long and reddish brown.
E. PIGEON FLIES (Pseudolynchia canariensis)

Dark brown, bloodsucking flies, about 6.0 mm long, that
often parasitize pigeons, especially nestlings. The flies
cause anemia and dermatitis. These flies also transmit
Hemoproteus columbae, the cause of a malaria-like
disease of pigeons.
F. BLACKFLIES (Simuliidae)
Grey-black, thick, humpbacked insects up to 5.0 mm
long. Swarms of the flies attack mammals and birds,
including poultry. Blackflies are the vectors for protozoan
(leukocytozoonosis) and filarial worms (Ornithofilaria
fallisensis) in ducks. These biting insects require a blood
meal for the maturation of eggs. The blood sucking
blackflies can produce severe anemia and may kill young
birds.
G. MOSQUITOS
Multiple genera and species of mosquitoes feed on birds,
including poultry. Mosquitos are most important as vectors
MISCELLANEOUS PESTS
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Fig. 1 Fig. 2
Darkling beetles. Darkling beetles.
Fig. 3
Darkling beetles larvae.
INTERNAL PARASITES The life cycle is direct, adult worms are embedded in the
lining of the intestine. Eggs (Fig. 3) are laid and passed in
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the droppings, embryonation occur in six to eight days.

I. NEMATODES, CESTODES AND
TREMATODES (“WORMS” AND FLUKES)
D. TAPEWORMS
DEFINITION Tapeworms or cestodes are flattened, ribbon-shaped
The most important internal parasites of poultry belong worms composed of numerous segments or division (Fig.
to the taxonomic group Nematodes. They have spindle 1). Tapeworms vary in size from very small to several
shaped bodies with tapered ends and are also known inches in length. Several species of tapeworms affect birds
as roundworms. Eggs are shed in the host droppings. but the most commonly found in poultry are Raillietina
Infection is established when a bird ingests an cesticillus (Fig. 2) and Choanotenia infundibulum.
embryonated egg from the environment (direct life-cycle)
or when a bird consumes an intermediate invertebrate host Tapeworms use intermediate hosts for their lifecycles, birds
that is infected with the parasite (indirect life-cycle). Other become infected by eating the intermediate hosts. These
internal parasites of diagnostic significance are Cestodes hosts include snails, slugs, beetles, ants, grasshoppers,
(tapeworms) and Trematodes (flukes). earthworms, houseflies and others. The intermediate host
becomes infected by eating the eggs (Fig. 3) of tapeworms
that are passed in the bird feces.
A. ASCARIDS (Large Intestinal Roundworms)
One of the most common parasitic roundworms of poultry
The pathology or damage tapeworms produce in poultry is
(Ascaridia galli) occurs in chickens and turkeys. Adult
questionable; however, it is believed that occlusion of the
worms are about one and a half to three inches long and
intestines is a fairly common finding.
about the size of an ordinary pencil lead (Fig. 1). Heavily
parasitized birds may be droopy, emaciated and show
signs of diarrhea. Feed efficiency is usually impaired in EPIDEMIOLOGY
severe cases. Animals in modern commercial poultry systems have
a lower incidence and worm burden by the less access
The life cycle of this worm is simple with no intermediate to many parasites and intermediate hosts; however, the
host, females lay thick heavy-shelled eggs in the incidence in backyard and free range flocks can be higher
intestine that pass in the feces. Over two to three weeks with a significant worm burden. Also, clinical disease in
embryo develops into the infective stage in the egg; the all-in-all-out production systems for commercial broilers
embryonated eggs may stay viable for long periods. Birds and turkeys is rare. The short life span of the commercial
become infected by eating eggs that have reached the broiler or turkey also circumvents severe parasitism. In
infective stage. Normal cleaning and disinfecting agents meat birds, ascaridiasis is the most common parasitism
do not kill the eggs. observed. Commercial caged layers rarely have parasites
without intermediate hosts (e.g.tapeworms) because of
their lack of contact with the soil. Commercial turkeys and
B. CECAL WORMS broilers reared on built-up litter, breeder flocks, non-caged
These worms (Heterakis gallinae) are found in the ceca
commercial laying hen flocks, backyard flocks, game birds
of chickens, turkeys and other birds (Fig. 1 and 2). The
and pet or zoo animals are likely to exhibit higher rates of
worms themselves are not considered a major threat, but
parasitism.
they are highly considered a major carrier/vector for the
agent that causes blackhead (Histomonas meleagridis).
CONTROL
The life cycle is similar to that of the large roundworm. Eggs Control measures that interrupt the life-cycle are effective
(Fig. 3) are produced in the ceca and pass in the feces and for most nematodes with direct cycles of infection. For
become infective in approximately two to three weeks. parasites with indirect life-cycles (some nematodes,
cestodes and trematodes), control is often aimed at
elimination of the intermediate host such as beetles or
C. CAPILLARIA (Capillary or Thread Worms) other insects, snails or slugs, or preventing access of
There are many Capillaria species that affect birds; but
poultry to the intermediate host.
in commercial poultry the commonly encountered are
Capillaria annulata and Capillaria contorta (Fig. 1). These
Piperazine is the only FDA approved treatment for internal
occur in the crop and esophagus of the hosts (Fig. 2).
parasites in meat and egg producing fowl. It is effective
These may cause thickening and inflammation of the
against ascarids in areas where resistance has not
mucosa, and occasionally severe losses are sustained in
developed. It is applied in the drinking water. FDA regulations
turkeys and game birds. Severe infestation may lead to
now allow the off-label use of drugs approved for other food
mortality.
animals for treatment of poultry. Fenbendazole has been
used as a feed or water additive has been successfully B. HAEMOPROTEUS

used against Capillaria, and Heterakis infections.
DESCRIPTION
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Thiabendazole, mebendazole, cambendazole, levamisole

Haemoproteus belongs to the family Plasmodiidae and
and tetramisole have been used against Syngamus and
shares similarities with Plasmodium and Leucocytozoon.
other nematodes such as Trichostrongylus. Pyrantel
Over 120 species have been reported from birds, mostly
tartrate and citarin have also been effective against some
in wild waterfowl, raptors, passerines, and others. Infection
nematode infections. Butynorate is approved for treatment
is host-specific. Species occurring in domestic poultry and
of some cestodes of chickens.
pet birds include Haemoproteus meleagridis which has
SEE TABLE OF COMMON WORMS been diagnosed in domestic and wild turkeys, H. columbae
AND FLUKES ON PAGE 177 and H. saccharovi in pigeons and doves and H. nettionis
in waterfowl.
II. BLOOD-BORNE
PROTOZOAL PARASITES EPIZOOTIOLOGY
Biting flies and midges act as vectors. Sporogony occurs in
INTRODUCTION the insect host and enters the avian host through fly bites.
Avian species act as host for a number of blood-borne Schizonts (meronts) commonly infect pulmonary vascular
protozoal parasites. Although these infections are for the endothelium or other visceral endothelial cells. Merozoites
most part inapparent and undiagnosed, they can offer a invade erythrocytes and mature. In some Haemoproteus
diagnostic challenge to the uninformed. Diagnosis is species a second cycle of schizogony occurs involving the
generally by microscopic evaluation of blood smears or development of megaloschizonts in cardiac and skeletal
histologic sections. The parasites can be differentiated by muscles before merozoites invade red blood cells.
their tissue distribution, size and physical characteristics.
CLINICAL SIGNS, LESIONS & DIAGNOSIS
PREVENTION AND TREATMENT Most infections are inapparent and remain undiagnosed.
These diseases are rarely treated. Few effective treatments Clinical signs have been reported in quail, turkeys, pigeons,
are known. Clopidol (Coyden) has been administered in and some psittacines. Generally, only a small proportion
the feed to turkeys for treatment of Leukocytozoonosis of birds infected exhibit clinical symptoms. Turkeys
at 0.0125 to 0.025% for 14-16 weeks with apparent experimentally infected with H. meleagridis have developed
success. Prevention is attempted by vector control. In severe lameness, diarrhea, depression, emaciation and
enzootic areas, screening of housed flocks and programs anorexia. Anemia and hepatomegaly have also been
to control the black flies and midges have failed to control reported. Myopathy associated with megaloschizonts
the disease. Most avoid raising poultry where conditions has been reported in wild turkeys where skeletal muscles
are ideal for propagation of vector species. Elimination of contained fusiform cysts oriented parallel to the muscle
carriers by yearly disposal of old poultry may be helpful if fibers. Enlarged gizzards have been rarely reported in
contact with local, wild birds that are carriers is avoided. pigeons. Lameness, dyspnea, sudden death associated
with edematous lungs and visceral organ enlargement
has been rarely reported in Muscovy ducks infected with
A. ATOXOPLASMA H. nettionis. Gametocytes and pigment granules can be
A coccidial protozoan that primarily parasitize captive and
visualized adjacent to the nuclei of red blood cells in blood
possibly wild passerine birds; these organisms have had
smears stained with Giemsa or Wright’s stain (Fig. 1).
a controversial taxonomic association for many years with
Schizonts can be seen in vascular endothelial cells of the
other known members of the suborder Eimeriorina such
lung and visceral organs.
as Toxoplasma, Lankesterella, or Isospora. The parasite
is spread by fecal-oral route; the lifecycle consists of an
intestinal and an extraintestinal forms. The oocysts are C. LEUKOCYTOZOA
shed in the droppings. Differentiation of the oocysts DESCRIPTION
from Isospora based on microscopic evaluations may Leucocytozoonosis is an acute or chronic protozoal
be challenging; both organisms, the sporulated oocysts disease of birds, including turkeys, ducks, geese, guinea
have two sporocysts and four sporozoites. Acute deaths fowl and chickens. The disease was first observed in wild
may occur in young birds, older birds may be chronically bird species and reported in turkeys in 1895. Relatively
infected and show no signs. Hepatosplenomegaly is few reports of acute outbreaks of leucocytozoonosis in
common. Tumor-like lesions may be present in the liver and domestic poultry have been made during the last decade.
spleen of chronically infected birds. The parasite can be The disease is generally clinically inapparent. Most acute
visualized microscopically as a clear notch in the nucleus outbreaks are in young poultry whereas the chronic form
of mononuclear cells and sometimes in erythrocytes. of the disease usually occurs in older birds (breeding
Cytology may be useful for the extraintestinal stages and stock). Black flies (Simuliidae) and culicoid midges serve
histopathology for the intestinal forms.
as intermediate hosts. The disease is most common in

poultry housed near slow streams, shallow lakes or near
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marshy areas. Most outbreaks occur during the warmer

seasons of the year when black flies are numerous. In the
United States leucocytozoonosis occurs more frequently in
southeastern states and in the upper Midwest.
EPIDEMIOLOGY
Birds appear to be the only hosts of most Leucocytozoons.
The etiologic agents are Leucocytozoons but their
classification may be inaccurate. Commonly applied
names include: L. smithi (turkeys), L. simondi (ducks), L.
neavei (guinea fowl) and L. andrewsi (chickens). Wild or
domestic birds that survive the disease are inapparent
carriers of leucocytozoons during the winter. During
the warm seasons black flies (Simuliidae) and midges
(Culicoides) feed on the carriers and become infected by
the leucocytozoons. The parasites undergo sporogeny
in the insects and pass to glands in their oral cavity. The
insects then act as vectors and transmit leucocytozoons
to young susceptible birds on which they feed. Birds that
survive the disease become carriers in turn.
CLINICAL SIGNS, LESIONS & DIAGNOSIS

There is usually a sudden onset and numerous birds soon
show signs. There is depression, anorexia, thirst, loss of
equilibrium, weakness, and anemia. There may be rapid
labored breathing. The course often is short and affected
birds die or improve within a few days. Mortality varies
but often is high. In birds that live a few days there may
be splenomegaly (Fig. 1), hepatomegaly and evidence
of anemia. The most pronounced lesion often is splenic
enlargement. Microscopically, gametes usually are seen
within enlarged, distorted erythrocytes, leucocytes or
both types of cells on blood smears stained with Wright
or Giemsa stains (Fig. 2 and 3). Histologic sections of the
liver and brain often reveal megaloschizonts or schizonts.
D. PLASMODIUM
Plasmodium infections have been rarely reported in
domestic pigeons, canaries, turkeys, penguins, falcons,
bald eagles and cliff swallows. Plasmodia species are often
not host-specific. The parasite causes a disease similar
to malaria in man and is spread through the injection of
infected blood by mosquito vectors. Parasites are found in
red blood cells (Fig. 1).
E. TRYPANOSOMES
Motile protozoa found in the plasma of numerous species
of wild and domestic birds. Pathogenic significance in
domestic poultry appears to be minimal or nil. A wide range
of insect vectors includes mosquitoes, Culicoides (midges),
Hippoboscids (black flies), mites and Simulids.
NEMATODES, CESTODES AND TREMATODES (“WORMS” AND FLUKES)

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ASCARIDS
Fig. 1
Ascaridia.
CECAL WORMS
Fig. 1
Heterakis worms.
Fig. 2 Fig. 3
Heterakis in caecum. Heterakis egg.
NEMATODES, CESTODES AND TREMATODES (“WORMS” AND FLUKES)

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CAPILLARIA
Fig. 1
Capillaria worms.
Fig. 2 Fig. 3
Capillaria in crop. Capillaria egg.
TAPE WORMS
Fig. 1
Severe tapeworm infestation.
Fig. 2 Fig. 3
Adult tapeworm Raillietina, 12-13 cm. Tapeworm egg (Raillietina spp).
BLOOD-BORNE PROTOZOAL PARASITES

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HAEMOPROTEUS
Fig. 1
Haemoproteus: Gametocytes and pigment granules
adjacent to the nuclei of erythrocytes.
LEUKOCYTOZOA
Fig. 2
Fig. 1
Numerous leucocytozoons in blood smear.
Splenomegaly.
PLASMODIUM
Fig. 3 Fig. 1
Leucocytozoon (gamete) in distorted, elongated leucocyte. Plasmodium in erythrocytes.
III. PROTOZOAL INFECTIONS region of the gut parasitized, the nature of lesions
produced, pre-patent periods, sporulation times, etc.
OF THE DIGESTIVE TRACT
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Identification frequently can be made with reasonable

A. COCCIDIOSIS accuracy by using several of these features by
someone skilled at the art. Recently, molecular tools
DEFINITION have developed and demonstrated to be effective in
Avian coccidiosis is a common protozoal disease of poultry the identification of several Eimeria species. Precise
and many other birds characterized by diarrhea and identification is of some value in selecting the most
enteritis. Coccidiosis in poultry affects the intestinal tract, effective anticoccidial(s) for control.
except for renal coccidiosis in geese.
5. With controlled exposure via the use of live coccidia
vaccines, the birds develop long term immunity, often
OCCURRENCE without clinical signs of infection. Current vaccines
Coccidiosis is found in all segments of the poultry are given either at pre-hatch or post-hatch; immunity
industry and has a world-wide distribution. depends upon self exposure to selected Eimeria for
The development of intensive confinement production the stimulation and development of immunity. Poultry
systems has increased the economic significance of this maintain their immunity to a species of coccidia by
disease. Subclinical disease has been recognized as having repeated re-exposure. The host remains susceptible
important impact on performance in commercial meat-bird to coccidial species not yet encountered. Birds may be
production and negative impacts on flock uniformity of infected simultaneously with more than one species.
layer and breeder pullets. The development of effective
anticoccidial drugs and vaccines has made prevention of 6. Oocysts are maintained in the litter of the poultry
clinical disease and negative effects on performance more house or can be easily transported to poultry farms on
manageable. Uncontrolled coccidiosis may cause of loss boots, shoes, clothing, crates, vehicle wheels, by other
of production and even mortality. Coccidiosis can be one animals and insects. People are important vectors of
of the predisposing factor for necrotic enteritis caused by coccidia. Wet litter and warm temperatures facilitate
Clostridia perfringens. In gamebird production, coccidia sporulation and precipitate outbreaks of coccidiosis.
control is important in preventing outbreaks of ulcerative
enteritis or “quail disease”, caused by Clostridia colinum.
ETIOLOGY
1. Coccidiosis in chickens and turkeys is caused by the
protozoal species of Eimeria. There are nine described
species of Eimeria in chickens and seven in turkeys,
but not all are severe pathogens. Coccidia are host
specific; hence do not pass among the various classes
of poultry, with the exception of E. dispersa that affect
turkeys, quail and other gallinaceous birds.
2. Coccidia have a direct but complex life cycle. Infection
is by the fecal-oral route. Ingestion of infected feed,
water, litter and soil results in infection. Sporulated
(infective) coccidial oocyst is ingested, sporozoites
are released to initiate a series of asexual replications
followed by a sexual cycle that lead to development
of thousands of new oocysts in the intestine or ceca.
Unsporulated oocysts are shed in the feces. These
oocysts sporulate within 24 hr and then are infectious
for other chickens or turkeys. A single oocyst may give
rise to more than 100,000 progeny.
3. Coccidia produce lesions in the gut by destruction
of the epithelial cells in which they develop and
multiply, and by trauma to the intestinal mucosa and
submucosa. Intestinal damage is directly proportional
to the number of sporulated oocysts and the species
ingested by a susceptible host.
4. Speciation of coccidia by microscopic features of
oocysts (size, shape, color, length and width), the
COCCIDIA OF CHICKENS bright red (Fig. 6). Intestinal content may be bloody. Very
large oocysts (30.5 x 20.7 microns), often with a golden
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Nine species of Eimeria have been described in chickens: color and large gamonts are diagnostic for this species.
E. acervulina, E. necatrix, E. maxima, E. brunetti, E. tenella. Subclinical infections may impede absorption and result in
E. mitis, E. mivati, E. praecox and E. hagani. Clinical disease poor skin pigmentation. This species is very prevalent in
is determined by the species of the infecting coccidia. Less commercial poultry operations.
pathogenic species produce few or no lesions. The more
pathogenic species often cause diarrhea which may be D. Eimeria brunetti.
mucoid or bloody. Dehydration often accompanies the Eimeria brunetti causes enteritis in the lower small
diarrhea. Diarrhea and dehydration are soon followed by intestine, rectum and proximal cecum. In severe cases, a
ruffled feathers, anemia, listlessness, weakness, retraction fibrinous or fibrinonecrotic mass of debris may cover the
of the head and neck and somnolence. Growth rate is often affected mucosa or produce caseous cores in the ileum
adversely affected. In laying hens coccidiosis is usually and rectum (Fig. 7). These oocysts are fairly large (24.6
manifested by a drop in egg production. Depigmentation x 18.8 microns), each with a polar granule. E. brunetti is a
of the skin may be apparent in well established cases. moderately severe pathogen that can produce moderate
Morbidity and mortality within a flock may vary greatly, but mortality, loss of weight gain, and poor feed conversion.
both can be very high.
E. Eimeria tenella.
A. Eimeria acervulina. Eimeria tenella is highly pathogenic, causes a marked
E. acervulina is a moderately severe pathogen causing typhlitis (Fig. 8) with occasional involvement of the adjacent
enteritis in the anterior one third of the intestinal tract areas of the intestine. Blood is often apparent in the ceca
(Fig. 1). The enteritis can be mild to severe and cause (Fig. 9) and feces in the early stages of the infections;
thickening of the mucosa. May affect skin pigmentation later, cheesy cecal cores may be found. Large clusters
due to malabsorption of carotenoids and reduce feed of schizonts may be seen in microscopic scrapings of the
conversion. Transverse white to gray striations are visible ceca. E. tenella can cause high morbidity, mortality and
in the mucosa (Fig. 2). Oocysts in mucosal scrapings are reduced weight gain in commercial broilers or layer pullets.
moderate in size and egg shaped (18.3 x 14.6 microns). This species is commonly found in commercial poultry.
This type of coccidiosis occurs rather frequently in older
birds. This location is also favored by other less pathogenic F. E. mitis.
species i.e. frequently multiple species will be present, There are no clinical lesions with this species, the lower
obscuring the diagnosis. This species is one of the most small intestine which may appear pale and flaccid.
prevalent in commercial poultry operations. Pathogenic effects on weight gain and a cessation in egg
production of Single Comb White Leghorn hens have been
B. Eimeria necatrix. demonstrated.
Eimeria necatrix causes severe enteritis characterized
by congestion, hemorrhage, necrosis and blood in the G. E. mivati.
middle small intestine with bloody feces (Fig. 3). The Causes reduced weight gain and mortality. This species
intestine often is markedly dilated, inflamed and thickened. is moderately pathogenic causing bloody mucoid enteritis,
White to yellow foci and petechial hemorrhages may be in severe cases lesions may extend throughout the
seen through the serosa of the unopened gut (Fig. 4); entire small intestine (Fig. 10). White spots may be seen
these lesions are the development of the large schizonts scattered throughout the serosa and are visible in the
predominantly in the mid small intestines (Fig. 5). This mucosa. Oocysts in mucosal scrapings are relatively
species is often mistaken or confused with E. maxima; the small and broadly ovoid in shape (15.6 x 13.4 microns).
lesions with E. necatrix have the appearance of salt ands This location is also favored by other species such as E.
pepper (dark red). Oocysts develop only in the ceca, and acervulina, thereby obscuring the diagnosis.
the oocysts may not be numerous; moreover, mortality
may precede the appearance of oocysts in the feces. Often H. E. praecox.
causes high mortality. Often causes disease in commercial Causes watery intestinal contents with mucus and mucoid
broiler breeders or layer pullets. casts in the duodenum. There may be reduced weight
gain, loss of pigmentation, dehydration and poor feed
C. Eimeria maxima. conversion.
Eimeria maxima is moderately pathogenic and may cause
moderately high mortality. It causes mild to severe enteritis I. E. hagani.
sometimes with thickening of the intestinal wall and Reportedly causes watery intestinal contents and catarrhal
marked dilatation of the the middle small intestine, these inflammation. This species is relatively rare in commercial
resemble E. necatrix, but the lesions of E. maxima are broiler chickens.
COCCIDIA OF TURKEYS hardened mucosal debris appearing as loose whitish

cecal cores (Fig. 12). Lesions are principally located in the
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Seven species of Eimeria have been described in turkeys in ceca but generally extend to the lower small intestine and
the USA. The four pathogenic species of Eimeria in turkeys cloaca. Oocysts are ellipsoidal and very elongated (25.6 x
are: E. adenoeides, E. meleagrimitis, E. gallapovonis, and 16.6 microns). This species is one of the most pathogenic
E. dispersa. Nonpathogenic species include: E. innocua, of the turkey coccidia. Infections in young poults may
E. meleagridis, and E. subrotunda. Coccidiosis in turkeys produce high mortality and infection in older turkeys can
resembles the disease in chickens; the diarrhea may be cause considerable weight loss. E. meleagridis may also
watery, mucoid and bloody and mortality may occur. be found in this area. This species is relatively common in
litter samples from commercial operations.
A. Eimeria meleagrimitis.
Eimeria meleagrimitis causes spotty congestion and DIAGNOSIS
petechiae from duodenum to ileum, dilation of jejunum, 1. Gross necropsy should be performed on fresh (<
and mucosal casts (Fig. 11) in the anterior two thirds of the 1 hour) dead birds typical of the flock. Post mortem
intestine. Lesions are most severe in the jejunum and from changes can quickly obscure gross lesions.
there extend anteriorly and posteriorly. Oocysts in mucosal 2. Diagnosis is made primarily on the basis of clinical
scrapings are small in size (19.2 x 16.3 microns) and signs and the appearance and location of gross
ovoid. This species is considered a moderate pathogen. intestinal lesions. Large numbers of oocysts may be
Mortality, morbidity, weight loss, dehydration and general present in mucosal scrapings from affected birds.
unthriftiness may occur in young poults as a result of Fresh mount wet smears and or histologic examination
infection. Non-pathogens E. innocua and E. subrotunda of the intestine can confirm the presence of asexual
may also be found in this region. This species is one of the or sexual stages of coccidia (sporozoites, merozoites,
commonly found Eimeria in litter from commercial turkey schizonts). A history indicating recent flock exposure to
facilities. This species is fairly prevalent in commercial a large source of sporulated oocysts may be helpful.
turkey operations.
3. Subclinical infection is common. The presence of a
few oocysts in the feces does not justify a diagnosis of
B. Eimeria dispersa. clinical disease.
Eimeria dispersa produces a cream-colored serosal
surface, dilation of intestine and yellowish mucoid feces in 4. Coccidiosis frequently occurs in association with
the middle one third of the intestine. Lesions are principally other avian diseases, such as necrotic enteritis,
located in the midgut region, but some infection may extend ulcerative enteritis, salmonellosis and histomoniasis.
from the duodenum to the cecal necks. Oocysts are large Immunosuppressive diseases may increase the
(26.1 x 21.0 microns) and broadly ovoid. The oocyst wall is severity and incidence of clinical disease.
distinctively contoured and lacks the double wall common
CONTROL
to other species. The prepatent period is the longest of
1. Anticoccidial compounds in feeds are the most
the turkey coccidia, 120 hours. This species is considered
common method of control. However, coccidia may
mildly pathogenic but can cause reduction of weight gain
become resistant to the anticoccidials, therefore
and diarrhea in young poults. This species also parasitized
rotation of types of products may be used to prolong
other avian hosts (quail and other phesants). This species
efficacy. No anticoccidial is highly effective against
is fairly prevalent in commercial turkey operations.
all species of coccidia although some are effective
against multiple species. Several anticoccidials are
C. Eimeria gallapovonis. approved for prevention of coccidiosis, although not
Eimeria gallapovonis causes edema, ulceration of mucosal all are commercially available such as Amprolium,
ileum, yellow exudate, and flecks of blood in feces. Monensin, Clopidol, Nicarbazin, Robenidine,
Lesions are principally located in the posterior one third of Decoquinate, Lasalocid, Halofuginone, Narasin,
the intestine (ileum and large intestine) and ceca. Oocysts Diclazuril and Semduramycin. Not all products might
are relatively large (27.1 x 17.2 microns), elongated and be able to be used for all poultry species; turkeys are
ellipsoidal. The prepatent period is 105 hours. This extremely sensitive to Salinomycin and Narasin. Care
species can cause high mortality in young poults; however, should be taken in choosing the product to be used.
the prevalence is low. 2. Immunization. Commercial coccidiosis vaccines are
available. Planned exposures of young chicks or
D. Eimeria adenoides. poults to small numbers of oocysts by coarse spray at
Eimeria adenoides affects the posterior one third of the the hatchery or in feed, water or gel blocks or in ovo at
intestine and is responsible for liquid feces with mucus 18 to 19 days incubation have been used successfully.
and flecks of blood. There is edema and swelling of the The number of oocysts of each Eimeria species
cecal and/or intestinal wall. Cecal contents often contain provided in the vaccine is critical to initiating immunity
without causing clinical disease. Some vaccines 3. When consecutive broods of poults are raised in
contain drug-sensitive strains of Eimeria, facilitating the same facilities, especially if sanitation is poor,
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the establishment of drug-sensitive populations and there appears to be an increase in the number of
extending the usefulness of anticoccidials. Some Spironucleus in each brood and a corresponding
vaccines may contain attenuated and or precocious increase in signs of the disease in the later broods.
lines of Eimeria. 4. The disease has been reported in many different
3. Natural Exposure. If chickens are exposed to modest countries and states. It usually occurs during the
numbers of oocysts in their environment, they develop warmer months of the year and on facilities that
immunity to the species of coccidia represented. maintain a poor standard of sanitation. Heximitiasis is
Exposure must be moderate or clinical signs will currently rare in commercial production, but may be
appear. Exposure can be limited if dry litter conditions seen in backyard or ornamental flocks.
are maintained. Wet litter (including wet areas around
waterers) is especially to be avoided. This practice is CLINICAL SIGNS
rarely used in large commercial operations. 1. Initially the affected birds are nervous and very active.
They chirp excessively, shiver, crowd around any heat
TREATMENT source and have subnormal temperatures. There
Prevention is emphasized. However, chemical is watery or foamy diarrhea and the birds dehydrate
agents widely used for treatment include amprolium, rapidly.
sulfadimethoxine, sulfaquinoxaline, sulfamethazine. Sulfas 2. Later the birds are more depressed, stand with their
should not be used in layers. Required withdrawal times heads retracted, feathers ruffled and wings drooping.
are usually required prior to marketing. Increasing vitamins Terminally the birds go into a coma, struggle and die.
A and K in feed or water may reduce mortality and hasten Terminal signs appear to be related to hypoglycemia.
recovery, respectively.
3. Morbidity is high. Mortality varies with age and the
quality of husbandry provided. Mortality may be very
B. HEXAMITIASIS/SPIRONUCLEOSIS high (75-90%) in young birds that are poorly housed
and which receive no treatment.
DEFINITION
Hexamitiasis is a protozoal disease characterized by DIAGNOSIS & LESIONS
catarrhal enteritis and by foamy or watery diarrhea. 1. The cadaver is dehydrated. The intestine is flabby,
may have areas of bulbous dilatation and contains
The etiologic agent in turkey poults and most other excessive mucus and gas. The proximal one-half of the
susceptible birds is Spironucleus meleagridis (previously intestine is inflamed. Cecal tonsils may be congested.
known as Hexamita meleagridis). The etiologic agent in
2. Spironucleus meleagridis is found in the crypts of
pigeons is Spironucleus columbae.
Lieberkuhn, especially in the duodenum and upper
jejunum of infected birds, including older carriers. The
HISTORICAL INFORMATION protozoan is roughly 3 by 9 microns, has 8 flagella and
1. For many years hexamitiasis was confused with two nuclei that resemble eyes. It moves with a rapid,
trichomoniasis. In 1938 Hinshaw and others first clearly darting motion.
identified hexamitiasis and its etiologic agent. Rather
3. Duodenal scrapings should be examined from a
extensive losses were attributed to hexamitiasis during
freshly killed, infected bird using reduced light or
the early development of the turkey industry, in range
phase contrast microscopy. Many S. meleagridis in the
flocks.
upper intestine suggest hexamitiasis. If only recently
EPIDEMIOLOGY dead birds are available, warm saline added to the
1. In turkeys, Hexamitiasis usually is seen in 1 to 9-week- scrapings may revive enough of the Spironucleus
old poults. Hexamitiasis also occurs in gamebirds for identification. Dead S. meleagridis are difficult
(pheasants, quail, chukar partridge, etc.), peafowl to identify so it is preferable to submit live birds for
and ducks. Pigeons have their own distinct form of necropsy.
hexamitiasis. 4. The history, signs and lesions are suggestive of the
2. The parasite is shed in feces which contaminate feed, disease but must be differentiated from coronaviral
water and range. Recovered birds are often inapparent enteritis, paratyphoid infection, trichomoniasis and
carriers. Susceptible birds get the organism by blackhead.
ingestion. Interspecies transmission, e.g., from game
birds to turkey poults, occurs readily. This method of
CONTROL
1. Hexamitiasis seldom is reported now, or may be
transmission is more likely in poults on range.
undiagnosed. Improved sanitary practices and
management on turkey farms may have reduced
the incidence or antihistomonal chemicals routinely among other galliformes including peafowl, pheasant
given for blackhead control may also be controlling and quail.
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hexamitiasis. 3. Recently, blackhead has become a big concern for

2. Short periods of depopulation combined with thorough commercial pullet flocks and many of these outbreaks
cleaning and disinfection of buildings will greatly are reoccurring.
reduce the population of S. meleagridis.
ETIOLOGY
3. Clean and disinfect feeders and waterers and keep 1. The etiologic agent is the protozoan Histomonas
them on large wire platforms so concentrations of meleagridis, assisted by secondary bacteria. In the
droppings are not available to the birds. experimental absence of bacteria, the histomonad
4. Do not hold possible carriers from old flocks. Raise appears not to be pathogenic. H. meleagridis is a
only birds of the same age group together. flagellate in the lumen of the cecum but assumes an
5. Prevent contact of poults with captive or wild ameboid form in tissue.
gamebirds. Avoid using gamebird ranges for poults. 2. A larger histomonad distinguished by its 4 flagella,
H. wenrichi, also occurs in the cecum but is not
TREATMENT pathogenic.
No current medication is approved for food animals in the
United States. Antiprotozoal drugs such as Metronidazole EPIDEMIOLOGY
may be considered in non-food animals. Supportive Transmission of H. meleagridis to susceptible birds is
treatment such as increasing the brooding house possible via three routes:
temperature to a point where the birds appear comfortable
may be beneficial for young birds. 1. Ingestion of fresh feces. This route probably is relatively
unimportant except for spread within a flock.
C. HISTOMONIASIS 2. Ingestion of embryonated cecal worm ova containing
(Blackhead; Enterohepatitis) the protozoan. Within these resistant ova the
histomonad can survive for years. H. meleagridis is
DEFINITION liberated in the intestine when ingested ova hatch and
Histomoniasis is a protozoal disease caused by then invades the cecal wall and initiates the disease.
Histomonas meleagridis affecting a wide range of birds 3. Ingestion of earthworms containing cecal worm larvae
including turkeys, chickens, peafowl, grouse, quail, other within their tissues. Earthworms serve as transport
gallinaceous birds and ducks. The disease is characterized hosts for the cecal worm and the cecal worm acts as a
by necrotizing lesions involving the ceca and liver. transport host for the histomonad. Infection results after
the cecal worm larvae are liberated during digestion.
OCCURRENCE
Histomoniasis occurs in commercial and non-commercial DIAGNOSIS
turkeys, especially young turkeys and if left untreated, most 1. Diagnosis can be made on the basis of clinical signs
may die. Blackhead also occurs in chickens, but to occur and characteristic lesion. Typical well-developed
at a lower prevalence and severity. Young birds are more lesions are pathognomonic and consist of typhlitis and
frequently and severely affected. characteristic hepatic lesions (Fig. 1).
2. In turkeys histomoniasis appears 7-12 days after
exposure. Initially there is listlessness, moderate
anorexia, drooping wings and yellow (“sulfur colored”)
1. Histomoniasis once limited the expansion of the turkey
feces. Head parts may be cyanotic (“blackhead”)
industry. Prior to development of safe antihistomonal
although they often are not. In chickens with
drugs, it could be controlled only by cumbersome and
histomoniasis there may be some blood in the feces.
relatively ineffective measures designed to prevent
exposure of turkeys to the embryonated ova of cecal 3. Later the affected turkey is depressed and stands with
worms (Heterakis gallinarum). its wings drooping, eyes closed, head drawn close
to the body. Emaciation is common in chronic cases,
2. Significant growth of the turkey industry occurred
usually in older birds. In young turkeys morbidity and
after safe antihistomonal drugs were developed. The
mortality are high, up to 100%. Older birds tend to be
disease is now uncommon and these drugs are no
more resistant.
longer used routinely. It occurs sporadically when
turkeys are raised where chickens were previously 4. Gross lesions. There is a bilateral enlargement of the
located. The disease is still common in chickens but ceca with thickening of the cecal walls (Fig. 2). The
its effect on production is mild and rarely recognized. mucosa usually is ulcerated. The ceca often contain
Histomoniasis remains an important cause of death caseous cores which are yellow, gray or green and
may be laminated. In chronic cases the cores may
have been expelled. Peritonitis occurs when the cecal or keep them outside of the lot but accessible
wall becomes perforated. through a wire fence.
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5. Liver contains irregularly-round, depressed, target- TREATMENT

like lesions that vary in (Fig. 3). They often are yellow
There is currently no approved medication for treatment of
to gray but may be green or red. They vary greatly in
histomoniasis in food animals. Small groups of birds not
diameter but often are 1-2 cm and may coalesce to
being raised for consumption can be effectively treated
produce larger lesions.
individually with metronidazole at a dose of 30 mg/kg orally
6. Lesions may not be entirely typical in birds under SID for 5 days. Antihelmintic treatment may help suppress
treatment, less susceptible avian species or young the population of cecal worms.
turkeys in the early stages of the disease. In most
infected flocks typical lesions usually can be found if
an adequate number of birds are examined. In quail,
D. TRICHOMONIASIS
cecal lesions may not occur even though mortality is (Canker in pigeons and doves;
high. Frounce in falcons)
7. Microscopically, histomonads can be found in the
DEFINITION
inflamed cecal walls and necrotic foci which develop in
Trichomoniasis is caused by Trichomonas gallinae, a
the liver (Fig. 4). In birds killed for necropsy the agent
flagellated protozoan. Pathogenicity varies greatly by
sometimes can be identified in smears from the ceca
strain. The disease is characterized by raised caseous
or in scrapings from the margin of hepatic lesions.
lesions in the upper digestive tract, but may extend to other
CONTROL tissues. Pigeons, doves, turkeys, chickens and raptors are
1. Histomoniasis usually can be prevented by adding commonly affected.
antihistomonal drugs to the ration in proper dosage.
No current preventive medication is approved in the HISTORICAL INFORMATION
U.S. Histostat (nitarsone) is still used in poultry outside Trichomoniasis was once recognized as an important
the U.S. In quail, a cholinesterase inhibiting carbamate disease of turkeys and chickens, especially of ranged
(Sevin) increases susceptibility to histomoniasis. turkeys, but is seldom reported now. Conversely,
2. Control by the use of antihistomonal drugs may fail trichomoniasis in pigeons and doves continues to be a
unless reasonably good sanitation is practiced. common and significant disease. Trichomoniasis may
have played a role in the extinction of the carrier pigeon.
3. Control by the use of attenuated H. meleagridis Trichomoniasis can be a consequential disease in raptors.
organisms; recently experimental demonstrations
showed good promise of immunizing poults against
severe challenges. EPIDEMIOLOGY
1. The organism is fragile in the environment and
4. Other measures that assist in control follow:
transmission occurs only through contact with infected
A. Do not keep chickens and turkeys (or other oral secretions or through water contaminated by oral
susceptible birds) on the same farm. secretions of carriers. Pigeons are believed to be the
B. Do not use chicken ranges for turkeys or other natural hosts and primary carriers. The prevalence of
susceptible birds unless those ranges have been the infection is near 100% for adult pigeons. Carrier
free of chickens for at least 4 years. birds show no signs or lesions.
C. H. meleagridis is quickly destroyed by 2. Pigeons and doves transmit trichomonads to their
disinfectants and drying unless protected within young during feeding of regurgitated partially digested
earthworms or within the cecal worm ova. Avoid crop content (pigeon milk). Transmission in raptors
exposure to vectors. If possible, raise susceptible (hawks, owls, eagles, etc.) and their young, is through
birds on sandy, dry, loose soil. Prevent access ingestion of infected prey. Turkeys and chickens
to earthworms after rains. In range birds, rotate probably contract the disease after consuming stagnant
ranges periodically if possible. Some operators surface water containing T. gallinae. Other disease
with small lots replace the top few inches of soil may predispose turkeys to clinical trichomoniasis.
every few years using power equipment or plow 3. In established flocks or lofts, trichomoniasis may only
the lots to reduce the number of cecal worm ova be noted as a clinical disease after introduction of
and other pathogens. a more virulent strain of T. gallinae by new birds or
D. Reduce access of birds to their own droppings or exposure to wildlife carriers.
to feed and water contaminated with droppings.
Place feeders and waterers on large wire platforms
DIAGNOSIS
1. Typical signs and lesions are very suggestive of the
diagnosis. In pigeons, doves and raptors, yellow
plaques or raised cheesy masses involve the upper IV. OTHER PROTOZOAL INFECTIONS
digestive tract. Masses often are large and conical
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or pyramidal and can be surprisingly invasive in soft A. CRYPTOSPORIDIOSIS

tissue (Fig. 1). Lesions are usually most extensive in
the mouth, pharynx or esophagus (Fig. 2) but may DEFINITION
occur at other sites including the crop, proventriculus Cryptosporidiosis is a protozoal disease, characterized
or sinuses. In raptors, lesions may also occur in the in avians by acute or chronic disease of the respiratory
liver and are accompanied by peritonitis. or digestive tracts. Two avian species of Cryptosporidium
are recognized, based upon tissue (site) specificity and
2. Infected squab (baby pigeons) become depressed
organism morphology. Cryptosporidium meleagridis infects
and die at 7-10 days of age. Lesions of the oral cavity
only the small intestine, while Cryptosporidium baileyi
are most common but may also occur in the nasal
infects the digestive tract (especially the bursa of Fabricius
turbinates and brain. The infection may become
and cloaca) and can also infect the respiratory tract. The
systemic, with lesions in the liver and other visceral
organism has a coccidian life cycle that is completed
organs.
in an intracellular, but extracytoplasmic location on the
3. Adults pigeons, doves and raptors often have difficulty microvillous border of epithelial cells.
in closing their mouth because of lesions in the oral
cavity. They drool and make repeated swallowing
movements. Watery eyes may be apparent in HISTORICAL INFORMATION
occasional birds with lesions in the sinuses or periorbital 1. Dr. Earnest Tyzzer first described infections by
area. Rare cases with penetrating cranial lesions may Cryptosporidium muris (gastric mucosa) and C.
show signs of central nervous disturbances, including parvum (small intestine) in laboratory mice (1907).
loss of balance. 2. Tyzzer also was the first to describe and report
4. Lesions are similar in turkeys but frequently are (1929) infections by Cryptosporidium in the cecum
found only in the crop and upper or lower esophagus. of chickens, but no signs of disease were noted. The
Occasionally the proventriculus contains lesions. first report of avian morbidity and mortality caused
Infected turkeys often have a gaunt appearance by Cryptosporidium (1955) involved the distal small
with a hollowed area over the crop. Swallowing intestine of turkeys. The first report of respiratory
movements often are apparent and infected birds may cryptosporidiosis in any species also involved turkeys
have an unpleasant odor (“sour crop”). Morbidity and (1978).
mortality in affected birds varies but can be quite high. 3. Cryptosporidiosis was recognized in humans in 1976,
Demonstration of trichomonads in the oral fluids may and was soon identified as a life-threatening enteric
not be significant in the absence of lesions since many disease associated with acquired immune deficiency
normal birds have some trichomonads. Small plaques syndrome (AIDS) and other immunosuppressive
in the mucosa should not be confused with pox or disorders.
candidiasis.
EPIDEMIOLOGY
CONTROL The disease is spread through ingestion or inhalation of
1. Eliminate any known infected birds and all suspected oocysts shed in feces or in respiratory secretions. Oocyst
carriers. If possible, depopulate at regular intervals will remain viable in the environment for long periods.
and thoroughly clean and disinfect the premises. Add Infections by C. meleagridis and C. baileyi have been
no birds to an established flock since they may be reported in chickens, turkeys, quail, pheasants, peafowl,
carriers of a more virulent strain. Permit no contact psittacines, finches, and waterfowl. Avian species of
among pigeons, doves and susceptible poultry. Cryptosporidium spp. do not appear to infect mammals,
2. Provide a source of clean, fresh water, preferably including man, i.e. no known public health threat exists.
running water being replaced constantly. Eliminate Other species of Cryptosporidia have documented zoonotic
all sources of stagnant water. Disinfect watering potential, passing between man and other mammalian
containers and water lines regularly (e.g. chlorine). species, reptiles, amphibians, and fish. Cryptosporidiosis
can be a severe and life-threatening disease in an
3. Avoid feeding infected pigeons and doves to captive immunosuppressed host, but immunosuppression is not a
raptors. requirement for either infection or disease. Some infections
are asymptomatic.
TREATMENT
There is currently no approved medication for treatment
of trichomoniasis in food animals. Birds not being raised CLINICAL SIGNS
for food can be effectively treated individually with 1. Clinical signs of cryptosporidiosis are not specific
metronidazole (Flagyl) at a dose of 30 mg/kg orally SID for for the disease and other pathogens are frequently
5 days, or with Enheptin. involved. Involvement of the small intestine causes
diarrhea that may be fatal in young turkeys, quail, salmonellosis, candidiasis, turkey viral hepatitis,
and psittacines. Mortality in young quail may exceed intestinal reovirus infections, and other parasites.
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95%. Digestive tract infections in broilers may cause

reduced carcass pigmentation. CONTROL
1. Reduction or elimination of oocysts from the
2. Respiratory cryptosporidiosis produces signs related
environment is the primary means of controlling the
to the site of infection: naso-ocular discharges, spread of Cryptosporidium.
swollen sinuses, coughing, sneezing, dyspnea, and
rales. Fatalities may occur with deep lung and air sac 2. Stringent cleaning followed by disinfection with either
infections. Concurrent infections by other respiratory steam or autoclaving is necessary for oocyst destruction
pathogens are the rule rather than the exception. to break the cycle of infection. Most disinfectants will
not inactivate oocysts. Either formol saline (10%) or
LESIONS 5% ammonia will inactivate oocysts after a minimum
1. The small intestine becomes dilated with fluid. of 18 hours contact. Undiluted commercial bleach is
Ceca may be distended with foamy, fluid contents. also effective.
Histopathology includes shortening of villi with
necrosis and loss of enterocytes from the villous tips, TREATMENT
and the presence of numerous organisms in the brush 1. Drugs used for coccidiosis and other protozoan
border of the mucosal epithelium (Fig. 1). Organisms diseases have been ineffective for cryptosporidiosis
may also be found in the cecal tonsil mucosa, and in in animals. Therapeutic agents are minimally effective
the mucosa of the bursa of Fabricius and cloaca. The for reducing the severity of clinical disease and for
bursal mucosal epithelium may be hyperplastic with interfering with replication of the organism.
heterophilic infiltration. 2. Supportive therapy for individual animals is a
2. Respiratory cryptosporidiosis causes gray or white consideration, but with multiple animals, continued
mucoid exudate on the mucosal surface infected: shedding of infective organisms may infect others
conjunctiva, sinuses or nasal turbinates, trachea, in a flock, cage, or aviary. Treatment and control of
bronchi, or air sacs. Marked enlargement of the concurrent or secondary infections reduces mortality.
infraorbital sinuses may occur in turkeys. Infected
lungs may appear gray and firm. B. SARCOSPORIDIA
DIAGNOSIS DEFINITION
1. Most cases of cryptosporidiosis are recognized during A parasitic infection caused by species of the genus
histologic examination of either biopsy specimens Sarcocystis first described by Lankester in 1882.
or tissues collected at necropsy. The organisms Sarcocystis has a world-wide distribution but is rarely
are basophilic with H&E stain, are 2 to 4 microns in reported in domestic fowl. The incidence is high in wild
diameter, and are intimately associated with mucosal waterfowl and some passerines, such as grackles. Not
brush borders. an economically important disease in domestic poultry,
but does occur extensively in wild ducks and game birds.
2. Cytology can be used to confirm the diagnosis. Touch Although not a public health hazard, the parasite is killed by
impressions of mucosal surfaces can be examined cooking or freezing. Most affected carcasses are discarded
by phase-contrast or interference phase-contrast for esthetic reasons.
microscopy. They can also be air dried and stained with
red carbon fuschin or with Giemsa stain. Differentiation
from yeasts may be necessary with Giemsa stain. ETIOLOGY
1. At least five species of Sarcocystis have been
3. Flotation techniques for oocyst identification from feces identified. S. horwathi is regarded as the etiologic
include Sheather’s sucrose solution, zinc sulfate (33% agent in chickens (also call S. gallinarum). S. anatina
to saturated), and sodium chloride (36% to saturated). and S. rileyi (Balbiani rileyi) are found in ducks.
Oocysts are 4 microns in diameter, with a thick cell
wall, prominent residual body, smaller globular dense 2. All species of Sarcocystis have similar developmental
bodies, and curved sporozoites. stages and an obligatory two host life cycle. Sarcocysts
in cardiac, smooth, or skeletal muscle tissues are
4. Concurrent respiratory tract pathogens identified eaten by a definitive host, releasing cystozoites
with respiratory cryptosporidiosis include Escherichia which penetrate the intestinal wall and develop in the
coli, Pasteurella multocida, Newcastle disease virus, subepithelial tissue. Oocysts are produced and shed
adenovirus, infectious bronchitis virus, and reovirus. in the feces fully sporulated. When sporocysts are
5. Most broiler chickens with bursal cryptosporidiosis ingested by the intermediate host they go through a
have had infectious bursal disease, but it is not a series of asexual reproductive cycles in endothelial
pathogenic requirement. Among other avian hosts, cells of various organs. Merozoites are eventually
diseases that occur with cryptosporidiosis include released, invade muscle tissue and eventually develop
into the macroscopically visible sarcocysts (1.0-6.5

x 0.48-1.0 mm), each containing numerous banana-
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shaped cystozoites (bradyzoites ;2-3 x 8-15 microns).
DIAGNOSIS
Usually based on gross lesions, i.e. the presence of large,
pale sarcocysts in the muscle tissue (Fig. 1), arranged in
parallel with the muscle fibers. Diagnosis can be confirmed
histologically.
COCCIDIA OF CHICKENS
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Fig. 1 Fig. 2
Eimeria acervulina. Eimeria acervulina; transverse white to gray striations are visible in
the mucosa of the jejunum.
Fig. 4
Fig. 3 Eimeria necatrix: ballooning and distention of the intestines.
Severe E. necatrix infection. Infections are usually
midintestinal and characterized by hemorrhage and
ballooning.
Fig. 6
Moderate E. maxima infection. Serosal surface are speckled with
Fig. 5 numerous red petechiae and intestine contains orange mucus.
Eimeria necatrix: presence of large schizonts predominantly in the
mid small intestines.
COCCIDIA OF CHICKENS
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Fig. 7
E. brunetti.
Fig. 8
Eimeria tenella: blood can be seen through the cecal wall.
Fig. 9
Severe E. tenella infection. The cecal wall is distended with blood.
Fig. 10
Eimeria mivati.
COCCIDIA OF TURKEYS
Fig. 12
Fig. 11
Eimeria adenoides.
Eimeria meleagrimitis.
HISTOMONIASIS
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Fig. 1 Fig. 2
Hepatitis and typhlitis. Cecal cores.
Fig. 4
Fig. 3
Histomonads in liver at histology.
Hepatitis: typical irregularly-round, depressed, target-like
lesions.
TRICHOMONIASIS
Fig. 2
Extensive lesions in the mouth, pharynx, esophagus and crop.
Fig. 1
Large masses invading the soft tissues of the upper digestive tract.
CRYPTOSPORIDIOSIS
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Fig. 1
Presence of numerous organisms in the brush border of the
mucosal epithelium at histology.
SARCOSPORIDIA
Fig. 1
Presence of large, pale sarcocysts in the muscle tissue.
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COMMON INTERNAL PARASITES OF POULTRY

Parasite Common name Description Lifecycle Site of Infection Lesions/Clinical signs Comments
Oxyspirura sp. Eyeworm Nematode up to 2.0 cm Indirect or direct. Conjunctival sac, often Conjunctivitis, Occurs in all types of
Cockroaches are beneath the nictating opthalmitits, protrusion poultry and wild birds
intermediate hosts membrane, or in of nictitating membrane,
for some species. nasolacrimal duct adherence of eyelids
Syngamus Gapeworms Red nematodes Indirect or direct Trachea and possibly Gasping, gaping, dyspnea Occurs in all
trachea up to 2.0cm long, earthworms, slugs, large bronchi. and head shaking species of poultry.
forked appearance, snails are intermediate Generally difficult to
male and female in hosts for many species treat. Cyathostoma
permanent copulation bronchialis may
cause gasping in
domestic geese.
Capillaria sp. Cropworms Thin, threadlike Direct Crop or crop and Infected tissues Occurs in all species
nematodes up to esophagus become thickened of poultry. Best
C. annulata 60 mm long and inflamed. Causes identified in mucosal
malnutrition, emaciation scrapings, difficult
C. contorta and severe anemia to see grossly
or
Gongylonema
ingluvicola
Ascaridia galli Roundworms Large, thick, yellow- Direct Lumen of small intestine Weight loss, potential Affects chicken,
white nematodes intestinal blockage turkey, dove, duck
Eggs ingested by insects and blood loss and goose. Fowl > 3
remain infective mo. develop immune
resistance. Similar
to A. dissimilis
reported in turkeys
and A. columbae
in doves, pigeons
Capillaria sp. Intestinal worms Hairlike nematodes Direct or indirect Mucosa of small Huddling, emaciation, Occur in many
with earthworm intestine and ceca diarrhea, hemorrhagic poultry species
6 to 25 mm long intermediate host enteritis, or death.
Thickened upper intestine
PARASITIC DISEASES
with catarrhal exudate

177
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Parasite Common name Description Lifecycle Site of Infection Lesions/Clinical signs Comments
178
Dispharynx sp. Proventricular Grossly visible, 3 to 18 Indirect. Grasshoppers, Mucosa and glands Diarrhea, emaciation Occur in poultry
worms mm long nematodes cockroaches, sowbugs of proventriculus and anemia. Mucosal and other birds
Tetrameres sp. and pillbugs are ulceration, necrosis,
intermediate hosts hemorrhage and swelling
Cyrnea sp.
Cheilospirura Gizzard worms Small, broad nematodes Indirect. Grasshoppers, Under the gizzard lining Muscular wall of gizzard Numerous poultry
sp. up to 25 mm long beetles, weevils and may be sacculated species.
sandhoppers are or ruptured. Mucosa
Amidostomum intermediate hosts ulcerated, necrotic
sp. or sloughed.
Heterakis Cecal worms Small white nematode Direct. Eggs may be Most numerous in Marked inflammation Affects numerous
gallinarum up to 15 mm long ingested by earthworms the tips of the ceca and thickening, nodules poultry species.
where they hatch in cecal walls. May see Acts as carrier
and live for months hepatic granulomas for Histomonas
meleagridis
(blackhead)
Cestodes Tapeworms Flattened, ribbon- Indirect. Many Intestine Small lesions at Usually infect a
shaped, segmented. invertebrate intermediate point of attachment. definitive host, but
Raillietina sp. Usually grossly visible hosts; flies, snails, Enteritis proportional are not host specific.
beetles, earthworms, to degree of infection
Choantaenia crustaceans
sp., Davainea
sp.,
Hymenolepis
sp.
Amoebotaenia
sp.
Trematodes Skin flukes Hemispherical, Requires a molluscan Skin, usually near vent Forms cutaneous Not host specific.
flattened shape, up intermediate host and cysts, usually with 2 Affect poultry
to 5.5 mm long may use a second flukes in vent area and wild birds.
intermediate host Other flukes may
invade oviduct,
digestive organs,
kidney, circulatory
organs and eye
NUTRITIONAL DISEASES 179
NUTRITIONAL DISEASES VITAMIN DEFICIENCIES

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Revised by Dr. H.L. Shivaprasad Chickens are particularly susceptible to vitamin deficiencies
because they get little or no benefit from microbial
Introduction: synthesis of vitamins in their digestive tract. These birds
Nutrients including amino acids, carbohydrates, fats, also have a fast growth rate and are raised in modern
vitamins, inorganic chemical elements, energy, water and management conditions hence submitted to various
oxygen are essential for normal growth and development, stresses. Their feed can be shipped or stored for various
livability, work and reproduction. These nutrients should periods of time, at different temperatures, submitted to
be in proper concentration and balance to be effective. oxidative stress, these accounting for possible potency
Nutrient requirements have been well established for loss. For the above reasons, increased dietary vitamin
growing chicks and poults, as well as for laying –type hens levels are required in commercial diets in order to optimize
and for broiler and turkey breeders. growth and performances, when compared to the minimal
requirements of the NRC established to prevent clinical
Various factors can influence nutritional diseases in birds signs in ideal conditions.
in general. It is important to understand these factors as
they are necessary for taking corrective steps. These If birds received vitamins below requirement levels for any
include human errors such as omission of an ingredient or length of time, classical deficiency pathologies will develop
two or groups of vitamins (water soluble and fat soluble), at various speeds, depending on the age, the quantity of
improper mixing, improper storage, miscomputations in vitamin passed on from the breeder hen, and the vitamin
feed formulations and misfeeding to wrong species or storage level. For example, clinical signs will appear rapidly
sex or age of the birds. Other important factors that can in young chicks, with the young embryo being the most
influence nutritional diseases include poor nutritive value of sensitive model. Problems with water soluble vitamins
an ingredient, nutrient and mineral interactions, poor shelf such as B are soon observed because they are not stored
life and insufficient feed availability. Poor health of the birds to any extent, even excreted via the urine if in excess, while
due to bacteria, viruses, parasites and other causes can fat soluble vitamin deficiencies can take longer to develop
result in anorexia, dysphagia, maldigestion, malabsorption, because of adipose tissue and liver storage in older birds.
decreased storage or utilization, increased excretion or
secretion and increased requirements that can also cause Since it is today a common practice to include vitamins and
malnutrition. minerals in feed composite premixes, we are less likely to
observe individual classical vitamin deficiencies, such as
Malnutrition in poultry can result in a generalized or a specific the ones described below, unless one has been omitted
disease. Specific conditions such as encephalomalacia or from a premix. It is therefore not unusual to see a situation
rickets are easy to diagnose and treat. But generalized where the entire premix has been inadvertently excluded
or subclinical disease or signs such as loss of weight or with as a consequence, the development of a complex
failure to thrive due to marginal deficiencies of nutrients are array of clinical signs.
very difficult to diagnose and treat. The latter are probably
more common in the field than realized. Malnutrition can
also suppress immune system, decrease reproductive
performance, decrease weight gain, cause feather
problems and decrease response to therapeutic agents.
Diagnosis of malnutrition in poultry can generally be based

on history such as recent feed change, clinical signs, gross
and microscopic lesions, analysis of feed if available, liver
and serum, serum chemistry, radiography for the birds
and estimating peroxide levels in the feed which indicates
rancidity. Feeding trials with suspected feed can also be
performed but are time consuming, expensive and often
disappointing. Treatment is another option to diagnosing
diseases; for example, curled-toe paralysis due to riboflavin
(vitamin B2) deficiency where the birds will respond to
supplementation of riboflavin or multiple B vitamins if the
condition is diagnosed and treated promptly.
BIOTIN DEFICIENCY
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DEFINITION
Biotin is common in poultry feedstuffs, yet recent evidence
concludes some of this biotin may be biologically
unavailable. Turkeys seem more sensitive to biotin
deficiency than chickens.
ASSOCIATED DISORDERS
Biotin acts as a coenzyme in carboxylases which are
involved in lipid and carbohydrate metabolism. First signs
of biotin deficiency are related to reduced cell proliferation.
1. Dermatitis. Biotin deficiency causes an exudative Fig. 1

dermatitis around the mouth and eyes (Fig. 1) and on Exudative dermatitis around the mouth.
the feet and legs (Fig. 2), which must be differentiated
from pantothenic acid deficiency. In turkeys dermatitis
and cracking of foot pads occurs (foot pad dermatitis),
soon followed by chondrodystrophy.
2. Chondrodystrophy (old name = perosis). A growth-
plate disorder, where long bones are shorter than
normal, is a sign of biotin deficiency in growing chickens
and turkeys. Biotin may also play a role in varus leg
deformities because it affects bone remodeling.
3. Fatty liver and kidney. Fatty liver and kidney syndrome
in broiler chickens is a biotin-responsive disease.
Chicks exhibit depressed growth, hypoglycemia,
increased plasma-free fatty acids, and increased ratio
of C 16:1 to C 18:0 fatty acids, in liver and adipose
tissue. Necropsy reveals pale liver and kidney with
Fig. 2
accumulation of fat. It has been suggested that biotin Exudative dermatitis on feet.
deficiency may impair gluconeogenesis by decreasing
the biotin-containing enzyme pyruvic carboxylase and,
therefore, increasing the conversion of pyruvate to
fatty acids.
4. Fatty liver syndrome. Biotin may also be a complicating
factor in fatty liver syndrome in laying hens.
5. Embryonic abnormalities and reduced hatchability.
Biotin is essential for embryonic development.
Embryos from deficient hens display parrot beak,
chondrodystrophy, micromelia and syndactyly. Two
peaks of embryonic mortality occur: one during the 1st
week and another during the last 3 days of incubation.
TREATMENT
Water-soluble vitamins are readily available and may be
administered as needed. To avoid problems, most starter
and grower rations are supplemented with 0.1 to 0.3 mg/
kg of biotin.
RIBOFLAVIN DEFICIENCY occurs at 4 days. Embryos with moderate inadequacies die

(Vitamin B2 Deficiency; Curled Toe Paralysis) at 14 days incubation, with the appearance of shortened
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limbs, mandible malformations, possible edema, and

defective down. But one study failed to reproduce typical
DEFINITION ‘clubbed down’ condition experimentally in the progeny of
Riboflavin supplementation is generally required in rations
broiler breeders fed riboflavin deficient diet. Clubbed down
for growing chicks, poults, and ducklings because few
is caused by the failure of the down feathers to rupture the
poultry feedstuffs contain large quantities.
sheaths and may be seen in the neck and vent areas of late-
stage embryos or hatched chicks. In marginal deficiencies
CLINICAL SIGNS mortality will be delayed until pipping with dwarfism and
Riboflavin is essential for growth and tissue repair in all clubbed down the major signs.
animals. Many tissues may then be affected by riboflavin
deficiency, the most severely being the epithelium and
LESIONS
myelin sheaths of various nerves.
In young poultry, riboflavin deficiency produces specific
changes in the main peripheral nerve trunks. There may be
Chicks marked swelling and softening of sciatic and brachial nerves
The characteristic clinical sign is “curled toe” paralysis and loss of cross striations (Fig. 3). Myelin degeneration,
caused by lesions to the sciatic nerve; however, if the Schwann cell proliferation, and axis cylinder fragmentation
deficiency is absolute or very severe, the chick will die have been observed (Fig. 4). Congestion and premature
before curled toe paralysis develops. In mild cases, chicks atrophy of the thymic lobes may also be observed.
tend to rest on their hocks and the toes are only slightly
curled (Fig. 1) or not at all. In moderate cases, there is TREATMENT
marked weakness of the legs and a distinct curling of the Marked and dramatic improvement and alleviation of
toes on one or both feet. In severe cases, the toes are clinical signs can be expected if treatment occurs early
completely curled inward or under (Fig. 2), the legs are in the course of the disease. Water-soluble vitamins are
extremely weak, and birds walk on their hocks with the readily available and can be administered in the water if
aid of their wings (“wing-walking”). At rest, the wings may needed. Irreversible damage will occur over time.
droop. Leg muscles are atrophied and the skin is dry and
harsh. Other signs include stunting, diarrhea after 8-10
days, and high mortality at about 3 weeks. Feather growth
in chicks is not generally impaired.
Poults
A dermatitis resulting in encrustations on eyelids and
corners of the mouth will develop in approximately 8 days.
The vent becomes encrusted, inflamed, and excoriated.
Other clinical signs are similar to the chick. Growth is
retarded or completely ceases by about day 17. Mortality
occurs at about day 21.
Ducklings
Ducklings and goslings usually have diarrhea, stunting, and
a bowing of the legs in conjunction with chondrodysplasia.
Laying hens
Riboflavin deficiency will cause decreased egg production
and decreased hatchability that is roughly proportional to
the degree of deficiency, with an increase in hepatic size
and fat content.
Embryos
Embryonic mortality peaks at 4, 14, and 20 days of
incubation are typical of riboflavin deficiency, with peaks
more prominent early as deficiency becomes severe. In
severe cases, embryonic death due to circulatory failure
RIBOFLAVIN DEFICIENCY
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Fig. 1 Fig. 2
Curled toes in a riboflavin deficient poult. Severe case of riboflavin deficiency.
Fig. 3
Swollen sciatic nerve with loss of cross striations. Fig. 4
Myelin degeneration, Schwann cell proliferation, and axis cylinder
fragmentation in sciatic nerve.
VITAMIN A DEFICIENCY production, decreased hatchability and embryonic

mortality are observed.
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OCCURRENCE 2. Scattered birds in the flock have inflammation of the

Most outbreaks of vitamin A deficiency occur in young birds, eyes or sinuses and the eyes and sinuses may be
usually 1-7 week-old chicks or poults. Other outbreaks swollen. Mucoid or caseous exudate accumulates in
occur in pullets or hens. Because rations compounded the conjunctival sac and may be voluminous. There is
by owners of small, backyard flocks are more likely to be nasal and ocular discharge. Owners often report “the
deficient, most outbreaks are seen in those flocks. But birds have a cold”.
vitamin A deficiency can also occur in commercially raised
flocks. LESIONS
1. In young birds the eyelids are inflamed, often adhered,
by sticky exudate. There may be excessive urates in
ETIOLOGY the ureters, in collecting tubules of the kidneys, and in
1. Most poultry rations contain some alfalfa meal or new the bursa of Fabricius.
yellow corn, both excellent sources of provitamin A
carotenoids which are easily converted into vitamin 2. In layers, 1-3-mm white pustule-like lesions are present
A by enzymes in the intestinal mucosa. If rations do in the mucosa of the mouth, pharynx, esophagus (Fig.
not contain alfalfa meal and if stored (depleted) corn 2), and sometimes in the crop (Fig. 3). Mucoid exudate
is utilized, the ration may be low in vitamin A unless a often is present in nasal passages. Conjunctival sacs
vitamin A supplement is added. Vitamin A is naturally or sinuses contain mucoid or caseous exudate and
derived from fish oils. may be greatly distended. There may be a delicate
pseudomembrane lining the trachea.
2. Birds hatched from layers low in vitamin A have very
low vitamin A reserves. If they are placed on deficient 3. Microscopically the original epithelium is replaced
rations after hatching, they soon will be deficient in by a keratinizing epithelium. There is squamous cell
vitamin A. metaplasia of the secretory and glandular epithelium
(Fig. 4) of the upper respiratory and digestive tracts,
3. Birrds raised on range get large amounts of vitamin A which blocks the mucous gland ducts resulting in
from green plants. During confinement, this source of glands becoming distended with necrotic material.
vitamin A is not available and deficiency may develop
unless the formulated ration includes other sources. DIAGNOSIS
4. Since vitamin A is a fat soluble vitamin and if the fat 1. A careful study of the formula used in compounding the
used in the diet is rancid, there can be a deleterious ration may reveal the likelihood of deficiency of vitamin
effect on its availability. A. One should consider not only the ingredients used
but the quality of those ingredients. Analysis of the
CLINICAL SIGNS ration is expensive and time consuming and may be
Vitamin A is involved in numerous processes: it plays misleading unless the sample is truly representative.
a role in vision, maintains mucous membrane integrity 2. Signs and lesions often are suggestive of vitamin A
and cerebrospinal fluid pressure, is required for normal deficiency. Microscopic demonstration of squamous
growth and reproduction. It acts as an antioxidant, is cell metaplasia is nasal passages may assist in
photoprotective and an anticarcinogen. diagnosis.
Recently hatched birds (chicks and poults) 3. Low vitamin A levels in the liver are indicative of vitamin
A deficiency.
1. Signs appear in 1-7 weeks according to the amount of 4. Swollen infraorbital sinuses and exudate in the
vitamin A stored in the egg and present in the feed. First conjunctival sacs occur with other diseases of poultry.
there is anorexia, growth retardation, then drowsiness, Differential diagnosis should consider infectious coryza
mild ataxia and increased mortality. of chickens, chronic fowl cholera, infectious sinusitis of
2. Birds usually die before the development of eye turkeys, and influenza of turkeys, ducks, geese, and
lesions. However, in birds surviving over 1 week, quail.
eyelids become inflamed and perhaps adhered with a
CONTROL
cheesy like material present in nostrils and eyes (Fig.
1. Prevention is easily accomplished by feeding a ration
1).
with adequate vitamin A (broiler chickens and turkeys:
Adult birds 7 000 to 12 500 U.I/kg, with the highest recommended
1. Depending on liver storage levels, severe deficiency levels in breeders: 10 000 to 14 000 U.I./kg).
of vitamin A over a period of 2-5 months is necessary 2. Avoid long storage of prepared feeds or ingredients
before signs develop. Unthriftiness, decreased egg for those feeds. Buy or prepare feeds only in relatively
small quantities.
3. Add chemical antioxidants to feeds at the time of normal levels for about 2 weeks. Then feed a balanced
preparation to protect vitamin A content or add stable ration at normal levels.
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forms of vitamin A.
TREATMENT
Treat affected flocks by adding a water-dispersible vitamin
A supplement to the drinking water. Alternatively, add a
stabilized vitamin A supplement to the ration at 2-4 times
Fig. 2
Distended, impacted mucosal glands resembling pustules in the
oesophagus.
Fig. 1
Caseous exudate present under the eyelids.
Fig. 4
Fig. 3 Squamous metaplasia.
Distended and impacted mucous glands forming small white
nodules in crop.
VITAMIN E DEFICIENCY Encephalomalacia

Signs are those associated with lesions of the central
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DEFINITION nervous system and include ataxia, loss of balance,

Three distinct disorders (syndromes) related to or caused falling over backwards while flapping the wings, sudden
by vitamin E deficiency have been recognized in poultry. prostration on the side with legs outstretched, toes flexed,
Each disorder usually occurs alone, although there are and head retracted (Fig. 1). Birds that show clinical signs
occasional overlaps. The three disorders are: often continue to eat. The deficiency usually occurs
between the 15th and 30th day of life; however, it may
1. Encephalomalacia (crazy chick disease). occur as early as the 7th and as late as the 56th day.
2. Exudative diathesis.
Exudative diathesis
3. Muscular dystrophy.
There is a severe edema caused by increased capillary
Although each of these syndromes is associated to some permeability. This edema is located along the ventrum
degree with vitamin E deficiency, each can be prevented of the thorax, the abdomen, and perhaps under the
by dietary changes unrelated to the vitamin E content mandible. Birds with extensive edema may have difficulty
of the ration. There is some interaction with synthetic in walking and may stand with their legs far apart because
antioxidants, selenium and sulfur-containing amino acids, of accumulation of subcutaneous fluid ventral to the
especially in preventing exudative diathesis and muscular abdomen.
dystrophy.
Muscular dystrophy
OCCURRENCE Signs are usually inapparent but there may be locomotor
Vitamin E deficiencies usually are seen in young chicks problems.
or turkey poults but also occur in ducklings and, perhaps,
in other poultry. Deficiencies usually occur in birds raised LESIONS
in confinement i.e., birds compelled to eat only what is
Encephalomalacia
offered to them. Most outbreaks occur in birds fed rations
that are high in polyunsaturated fats (e.g., cod liver oil, soy The swollen cerebellum often contains yellow or congested,
bean oil), that oxidize and become rancid. Vitamin E is very hemorrhagic, or necrotic areas visible on the surface
unstable with oxidative destruction enhanced by minerals (Fig. 2). Swollen and hemorrhagic cerebella are quite
and polyunsaturated fats in diet. striking in turkey poults suffering from encephalomalacia.
Lesions occur less frequently on the cerebrum. Lesions
are accentuated by formalin fixation for a few hours. In
ETIOLOGY turkeys, poliomalacia of the lumbar spinal cord can be
1. Vitamin E and the selenium-containing enzyme found microscopically.
glutathione peroxidase prevent cell membrane
destruction caused by peroxides and other powerful
Exudative diathesis
oxidants produced as metabolic by-products.
There is green-blue blood-stained viscous edema in
2. There is evidence that vitamin E, selenium, and sulfur- the skin and subcutis of the ventrum (Fig. 3). Muscular
containing amino acids perform separate functions but dystrophy occasionally is apparent in breast or leg muscles
still act together to prevent the accumulation of harmful of the same birds. Distention of the pericardium with fluid
peroxides in tissue. Peroxides are derived, in part, has been the cause of sudden deaths in birds (Fig. 4).
from polyunsaturated acids in feeds.
3. 3. The following facts are of interest in considering Muscular dystrophy
etiology: In chicks white to yellow degenerative muscle fibers give a
A. Encephalomalacia can be prevented by adding streaked appearance to skeletal muscles of the breast or
synthetic antioxidants to the feed. legs (Fig. 5). In poults the musculature of the gizzard may
B. Exudative diathesis can be prevented by adding contain gray areas of muscle degeneration (Fig. 6).
selenium to the feed.
C. Muscular dystrophy can be prevented by adding DIAGNOSIS
cysteine, a sulfur-containing amino acid, to the 1. The diagnosis can usually be made on the basis of
feed. typical signs and gross lesions.
2. Examination and analysis of the ration may indicate
CLINICAL SIGNS rancidity or likelihood of deficiency of vitamin E and/or
Vitamin E is involved in several metabolic functions but selenium. Feed analysis for vitamin E activity can be
mostly play a role of natural antioxidant. time-consuming and expensive, therefore care should
be taken to submit truly representative samples. Liver

can also be analyzed for vitamin E and selenium.
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Storage temperature and duration are very important

in evaluating the quality of the vitamin E ingredient.
3. Gross and microscopic examination of typical lesions
is of considerable value in confirming suspected
vitamin E deficiency, especially with encephalomalacia
or muscular dystrophy.
CONTROL
1. Mix new batches of feed at frequent intervals. Use only
high quality ingredients. Avoid storage of mixed feeds
for periods longer than 4 weeks. If prolonged storage
is necessary, add chemical antioxidants.
2. Use only stabilized fats in the feed.
3. Store feeds in a cool, dry place to reduce vitamin and
other quality losses.
4. Avoid improperly compounded do-it-yourself -type
rations. Most well-known, commercially prepared
feeds are superior in quality to unplanned, self-mixed
feeds.
TREATMENT
1. Recommended vitamin E levels are 30 to 150 mg/kg
in the diet. Be sure an antioxidant (0,25kg of BHT or
santoquin per 1000kg of feed) is in the feed if storage is
long or environmental temperatures high. However the
newest forms of vitamins are enveloped hence more
resistant to heat treatments, humidity and storage. A
dose of 0.3 ppm of selenium is recommended in the
broiler chicken and turkey diets. Zero to 3 week-old
chicks and 0 to 6 week-old turkeys should receive
half of this selenium in an organic form which is more
readily available to the bird.
2. Oral administration of a single 300 IU of vitamin E per
bird will often cure exudative diathesis or muscular
dystrophy. Birds with encephalomalacia do not usually
respond well to treatment.
VITAMIN E DEFICIENCY
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Fig. 1 Fig. 2
Chicks with paresis/paralysis. Hemorrhagic cerebellum.
Fig. 3 Fig. 4
Exudative diathesis: edema of subcutaneous tissues. Pericardium distended with fluid.
Fig. 5
Nutritional myopathy with degeneration of the muscle fibers. Fig. 6
Gizzard muscle degeneration.
Other nutritional diseases 2. Egg layers can experience increased number of

thin-shelled and soft-shelled eggs followed soon by
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decreased egg production.

RICKETS 3. Laying hens suffering from cage layer fatigue lie on
their side, with their legs extended or they crouch in
DEFINITION the corner of their cage.
In poultry a deficiency of vitamin D3, phosphorus or a wide
imbalance in the calcium:phosphorus ratio of the diet can LESIONS
cause rickets. The term osteomalacia has been used to 1. In young birds bones, beaks and claws are soft and
denote similar condition in laying chickens. rubbery and the epiphyses of long bones often are
enlarged. There is a characteristic beading of the
ribs, most noticeable at their junction with the spinal
OCCURRENCE column. Ribs are thickened and tend to bend so that
Deficiencies of vitamin D3 and phosphorus are encountered the thorax is flattened laterally. The beak becomes soft
most frequently in young chicks or poults a few weeks old. and rubbery and can be bent or flexed easily (Fig. 1).
Calcium deficiencies usually affect birds of the same age Parathyroids often are markedly enlarged.
or adult layers. Rickets occurs more frequently in small
flocks of poultry raised on carelessly formulated rations. 2. Feathering is usually poor and an abnormal black
Most commercial feeds are carefully compounded and banding of feathers has been observed in colored
are adequate in required nutrients. The incidence of breeds such as red or buff chickens.
rickets is increased in chickens with infectious stunting or 3. In laying hens bones are soft and easily broken, ribs
malabsorption syndrome. may become beaded (Fig. 2) and parathyroids are
enlarged (Fig. 3).
ETIOLOGY DIAGNOSIS
1. There are numerous forms of vitamin D, however only
1. In young birds, their age, signs, and lesions are all
cholecalciferol or vitamin D3 acts as the nutritional
useful in diagnosis. Softening of the beak and beading
precursor of 1,25 dihydroxycholecalciferol, the
of the ribs are almost pathognomonic.
hormone that stimulates active transport of calcium
and phosphorus across the intestinal epithelium, bone 2. Careful calculation of the calcium:phosphorus ratio,
and shell formation. Because of this role in calcium and vitamin D3 levels of the ration may reveal that it is
transport, as the ratio of calcium to phosphorus deficient or imbalanced. Chemical analysis of the ration
becomes wider or narrower, vitamin D3 requirements for minerals and D3 can be done but is expensive and
increase. time consuming. A single sample may not be typical of
the ration. Extensive sampling may be advisable for
2. Although rickets can occur because of phosphorus
forensic reasons.
deficiency, most outbreaks are the result of inadequate
vitamin D3. Sometimes vitamin D2 is erroneously fed CONTROL
to poultry instead of D3. 1. Feed a balanced ration with adequate calcium,
3. Young, rapidly growing chickens or turkeys phosphorus, and vitamin D3 levels. Rations should
experiencing malabsorption or any intestinal condition be carefully compounded to fit the age, purpose, and
impairing nutrient absorption, may develop rickets production of the flock. Note that poultry requires
even with adequate dietary levels of phosphorus and vitamin D3 a form differing from vitamin D2, which often
vitamin D3. Failure to absorb and/or utilize nutrients is fed to other types of livestock. Rovimix Hy-D, a
in the ration is considered to be secondary to other commercial form of 1,25 dihydroxycholecalciferol can
causes. also be given to the birds alone or in combination with
vitamin D3.
4. Calcium deficient laying hens may suffer from cage
layer fatigue (up to 30 weeks of age) or bone breakage 2. The following calcium:phosphorus ratios are
(old hens). recommended:
Broiler chickens: 1,35 to 1,5 :1,
CLINICAL SIGNS Turkeys (0 to 6 weeks): 1,5 :1
1. In young growing flocks, affected birds develop a
Turkeys (end of growth): 1,35 to 1,5 :1
lame, stiff-legged gait. There is retardation of growth.
Commercial layer: 5,8 to 7:1 (varies according the egg
There may be enlargement of the ends of long bones,
production period)
especially noticeable in the hocks. Birds often rest in
Breeders: 4,5 to 5,5 :1
a squatting position.
TREATMENT daily for a few days. If the affected layers are caged
1. Adjust the ration to fit the age and production level of layers, they should be removed from their cage and
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the flock. If the ration has been deficient in vitamin D3 confined on the floor until fully recovered.
give three times the usual amount for a period of 2-3 3. If housed birds are deficient in vitamin D3, it may be
weeks. Then go back to a balanced ration with the useful to turn them out on range or otherwise expose
usual recommended level. Liquid vitamin D3 will also them to sunlight.
treat the birds.
4. Removing hens affected with cage layer fatigue from
2. Calcium-deficient, paralyzed, or down layers can be cages during the early stages of lameness may result
given 1g of calcium carbonate in a gelatin capsule in recovery.
Fig. 2
Fig. 1 Beaded ribs.
Rubbery beak.
Fig. 3
Enlarged parathyroids (arrows).
FATTY LIVER-HEMORRHAGIC (recent) or green to brown (older). Large amounts of fat

are present within the abdominal cavity and surrounding
SYNDROME
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the viscera.
(FLHS; Fatty Liver Syndrome)
TREATMENT
OCCURRENCE There has been no clear elucidation of dietary causes
Fatty liver-hemorrhagic syndrome (FLHS) is a sporadic
of FLHS other than excessive caloric intake. Reducing
disease with worldwide distribution that occurs primarily
obesity of laying hens is the only successful preventive
in caged layers. Outbreaks are most common in high-
measure to date. However, further loss of production may
producing flocks during hot weather.
result from diet changes during the laying cycle. Lipotropic
agents such as vitamin E, vitamin B12, biotin, methionine
HISTORICAL INFORMATION and choline have been widely used with variable results.
Fatty liver syndrome was first reported in 1956 and was soon Management practices that reduce heat stress and
observed by many other diagnosticians. The appearance minimize mold growth in feed may also be helpful. Results
of the syndrome coincided with the practice of confining of feeding particular nutrients or formulations of nutrients to
layers to cages. There has been much speculation as to treat FLHS are inconsistent.
the cause of the syndrome. In 1972, the syndrome was
reproduced experimentally by force-feeding hens. The
lesions closely resembled those of the natural disease.
This appears to be a multifactorial problem.
ETIOLOGY
1. Excessive consumption of high-energy diets combined
with restricted activity is believed to result in excessive
fat deposition in the liver.
2. Contributing factors may include a genetic component.
3. The syndrome may be caused by a deficiency of
lipotrophic agents, which are necessary for mobilization
of fat from the liver.
4. Aflatoxin in laying hen diets has been shown to
increase fat content (dry weight basis) approximately
20% over controls and may play a contributing role.
5. FLHS and caged layer fatigue are often diagnosed Fig. 1
simultaneously. Subcapsular hepatic
hemorrhage with rupture of the
CLINICAL SIGNS parenchyma.
Outbreaks of FLHS are often associated with a sudden
drop in egg production (from 78-85% to 45-55%). The
flock overall may be obese (body weights 25-30% above
normal). Some birds may have pale combs and wattles
covered with flaking epidermis. Mortality increases
moderately with occasional hens in full production dying
suddenly and unexpectedly. Often hens are found dead
with pale heads. Mortality rarely exceeds 5%.
LESIONS
Dead birds have large blood clots in the abdomen, often
enveloping the liver, as a result of subcapsular hepatic
hemorrhage and rupture of the parenchyma (Fig. 1).
Subcapsular hematocysts or hematomas may be visible
within the parenchyma (Fig. 2). Liver is generally enlarged,
pale, yellow and friable. Fat content in livers generally
exceeds 40% dry weight and may reach 70%, hence the
Fig. 2
yellow coloration. Clinically healthy birds in the same flock Enlarged, pale, yellow liver with subcapsular
may also have hematomas in the liver, either dark red hematocyst.
MISCELLANEOUS DISEASES 191
MISCELLANEOUS DISEASES CLINICAL SIGNS

Clinically affected broiler chickens are smaller than normal
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Revised by Dr. H.L. Shivaprasad and depressed with ruffled feathers. Severely affected
birds show abdominal distension with reluctance to move,
respiratory distress, and cyanosis (Fig. 1).
CARDIOVASCULAR
DISEASES OF CHICKENS LESIONS
1. Hypertrophy and dilation of the right ventricle (Fig.
I. ASCITES OR PULMONARY 2) with or without accumulation of straw-colored
HYPERTENSION SYNDROME ascitic fluid in the peritoneal cavities, (Fig. 3), and a
generalized passive congestion are characteristic of
DEFINITION ascites secondary to PHS (Fig. 4).
Ascites secondary to pulmonary hypertension syndrome 2. Hydropericardium, protein clots in the ascitic fluid, and
(PHS) is one of the most important causes of mortality in a fibrotic liver (Fig. 5) may be present in chickens with
broiler chicken flocks. It is associated with rapid growth and chronic PHS.
a high metabolic rate.
3. Microscopic lesions show generalized passive
congestion.
OCCURRENCE
Ascites occurs worldwide in rapidly growing broiler chicken DIAGNOSIS
flocks. Macroscopic lesions are diagnostic.
If mortality in a flock is abnormally high, look for causes

HISTORICAL INFORMATION decreasing oxygen availability to the broiler chicken
Ascites was first reported in 1968 in broiler chickens raised
(poor ventilation, high altitude, concomitant respiratory
at a high altitude. However, the incidence of ascites caused
pathology, etc.), or increasing oxygen needs (rapid growth,
by PHS, where broilers are grown at a low altitude, has
cold rearing temperature stimulating the metabolic rate).
increased over the past several years and coincides with
genetic and nutritional improvements that resulted in better
Other pathological mechanisms can be involved in the
growth rate and feed conversion.
development of ascites, and toxicities due to sodium,
phenolic compounds, coal-tar derivatives, and dioxin,
ETIOPATHOGENESIS among others, might also be considered.
Four pathophysiological mechanisms are recognized to
cause ascites: increased hydrostatic vascular pressure,
CONTROL
decreased oncotic pressure, increased capillary
Lowering the oxygen requirement by slowing the metabolic
permeability, and impaired lymphatic drainage. Although
rate will reduce, and if severe enough, prevent ascites. A
numerous chemical toxicities have been reported to
variety of feed restriction and light programs have been
cause ascites in broiler chickens through one of these
used or recommended. The goal is to find a program that
mechanisms, the most common form of ascites in fast-
will maintain feed efficiency while reducing metabolic rate
growing broiler chickens is caused by increased hydrostatic
without increasing days to market.
vascular pressure.
Rapid growth, elevated metabolic rate, and therefore a TREATMENT

high oxygen demand impose an increased workload on There is no treatment.
the heart. This, combined with the insufficient pulmonary
capillary capacity of the modern broiler chicken, aggravates II. SUDDEN DEATH SYNDROME
the pulmonary hypertension and further precipitates right
ventricular hypertrophy. OF CHICKENS
DEFINITION
Hypertrophy is soon followed by dilation, right ventricular
Apparently healthy fast-growing broiler chickens, mainly
failure, passive congestion, and then ascites. This
males, die suddenly after a short terminal wing-beating
process is accelerated in birds because of an anatomical
convulsion. Dead birds are found lying on their back (Fig.
particularity. The right atrioventricular valve is a muscular
1). This is a common cause of “normal mortality” in a flock.
flap, an extension of the right ventricular wall. Any
hypertrophy of the latter affects the valve and its apposition
against the septum, facilitating venous regurgitation, OCCURRENCE
passive congestion, and ascites. This condition occurs from 1- 8 weeks of age in most
intensive broiler-growing areas of the world. The incidence
in a flock varies from 0.5% to more than 4% in some cases.

Sixty to 80% of the affected birds are males.
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This syndrome has been recognized for 30 years and has
been described as acute death syndrome, heart attack,
flip-over, dead in good body condition, and lung edema.
ETIOLOGY
The cause is unknown but this condition affects highly
performing broiler chickens. It is suggested that death is
the result of ventricular fibrillation secondary to a possible
imbalance of metabolites or electrolytes. It is classified
as a metabolic disease and the incidence appears to be
affected by genetic, environmental, and nutritional factors.
CLINICAL SIGNS
There are no premonitory signs. Large healthy broiler
chickens will start to convulse and wing flap, and rapidly
die lying on their back.
LESIONS
Birds are in good body condition with a full digestive tract
(Fig. 2). There is red and white mottling of the breast muscle
(Fig. 3), the ventricles of the heart are contracted, and the
auricles dilated with blood. Lungs might be congested
secondary to postmortem blood pooling. There are no
specific histopathologic lesions.
DIAGNOSIS
Dead birds appear healthy and there are no lesions except
the findings described above.
CONTROL
Various feed and light regimens have been tried with little
success in decreasing the incidence of sudden death
without decreasing feed conversion.
TREATMENT
There is no treatment.
III. ROUND HEART DISEASE

OF CHICKENS
This myocardial degeneration used to affect mature
chickens (> 4 months of age) but has not been
diagnosed in commercial poultry flocks for years. Birds
die with a bilateral ventricular hypertrophy and dilation.
Histopathology reveals myocardial fatty infiltration. The
etiology is unknown.
ASCITES OR PULMONARY HYPERTENSION SYNDROME

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Fig. 1 Fig. 2
Broiler that died of ascites following right ventricular failure. Note Cross-section of fixed hearts showing marked right ventricular
the cyanosis and enlarged abdomen. hypertrophy and dilation and hypertrophy of the right AV valve (V).
Fig. 4
Fig. 3 Broiler carcasses showing generalized passive congestion, enlarged
Accumulation of straw-colored ascitic fluid in the peritoneal heart and large quantity of yellow clotted protein (fibrin) and fluid
cavities. that can accumulate in the peritoneal cavities.
Fig. 5
Hydropericardium, protein clots in the ascitic fluid, and a fibrotic
liver may be present in chickens with chronic PHS.
ASCITES OR PULMONARY HYPERTENSION SYNDROME

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Fig. 1 Fig. 2
Dead broiler lying on its back, a regular finding in a broiler barn. Chicken carcasses in good body condition with a full digestive tract
(arrows). The ventricles of the heart are contracted, and the auricles
dilated with blood.
Fig. 3
Broiler chicken showing a full crop and red and
white mottling of the breast muscle.
CARDIOVASCULAR similarities to human dilated cardiomyopathy, turkey is

being used as an animal model.
DISEASES OF TURKEYS
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I. AORTIC RUPTURE OR III. SUDDEN DEATH SYNDROME OF

DISSECTING ANEURYSM TURKEYS (PERIRENAL HEMORRHAGE)
Aortic rupture is an occasional cause of mortality DEFINITION
in 12-16-week-old heavy turkeys, characterized by Sudden death syndrome of turkeys (SDS) or perirenal
massive internal hemorrhage from a ruptured lower or, hemorrhage syndrome causes death in heavy- turkey
less commonly, upper aorta. The cause is unknown flocks, particularly during grow-out period. Turkeys in good
but some contributing factors such as the relatively high body condition, mainly males, die suddenly with postmortem
blood pressure of turkeys, their natural susceptibility to lesions of acute generalized passive congestion.
atherosclerosis, and the absence of an intramural vasa
vasorum (intrinsic vascularization of the artery) in the lower
OCCURRENCE
aorta, might all play a role in the pathogenesis. Copper and
SDS is the main cause of mortality in fast-growing turkeys
zinc levels of the liver are normal in affected birds. Genetics
8-15 weeks of age, but has been reported in turkeys older
might play a role in the incidence as the progeny of certain
than 20 weeks of age. This syndrome is uncommon in
breeder lines seem to have a higher incidence. The carcass
female turkeys.
is typically in good body condition but pale. Blood may be
seen in the mouth or nostrils. A large amount of clotted
blood is found in the body cavity, surrounding the kidneys HISTORICAL INFORMATION
or filling the entire body cavity (Fig. 1) if rupture occurs in The condition was first reported in 1973 under the
the lower aorta, or surrounding the heart if it occurs in the name sporadic renal hemorrhage. The disease has also
upper aorta. Careful examination will reveal a longitudinal been named perirenal hemorrhage syndrome, acute
tear in the wall of the aorta (Fig. 2). Microscopically there hypertensive angiopathy, or sudden death with perirenal
is subintimal fibrosis and decreased elastic tissue in the hemorrhage. These confusing terms that describe lesions
tunica media. Management procedures to decrease the but give no indication of etiology and pathogenesis likely
incidence of this condition consist of avoiding excitement refer to the same condition.
in the birds.
ETIOLOGY
Similar to aortic rupture, coronary artery aneurysm and Through intense genetic selection and high-energy diets,
rupture can also occur in rapidly growing male turkeys. the industry has developed a rapidly growing, heavily
Necropsy of such birds reveals hemopericardium and muscled turkey. SDS of turkey occurs during a period
hemorrhage in the coronary groove. The cause and of fast growth and often follows exposure to stress or
pathogenesis of this condition is unknown but is probably increased activity level in the flock.
similar to aortic rupture
Experimental studies have demonstrated the inability of
II. DILATED CARDIOMYOPATHY OF the cardiovascular system of the domestic turkey to meet
metabolic needs generated by exercise; within minutes,
TURKEYS (ROUND HEART DISEASE) turkeys develop hypotension combined with severe
This condition causes mortality in turkey poults most lactic acidosis. Turkeys dying of SDS also show greater
commonly between 1 and 4 weeks of age and is a ventricular weights and cardiac changes described as
common occasional finding in commercial turkey flock. concentric left ventricular hypertrophy.
Affected poults are found dead with a severe bilateral
dilated cardiomyopathy (Fig. 1 and 2) often accompanied It has been hypothesized that a certain percentage of the
by secondary ascites and hydropericardium (Fig. 3), and turkey population has concentric left ventricular hypertrophy
congestion of other organs. If the poult survives with this which reduces myocardial blood flow and impairs coronary
cardiac disorder, growth will stop and the bird will soon vascular reserve. Exercise or stress could therefore
show ruffled feathers, unwillingness to move, respiratory prompt acute myocardial ischemia triggering ventricular
distress, and death. Livers will often show chronic passive arrhythmias and terminal ventricular fibrillation. Ventricular
congestion and centrolobular hepatocyte degeneration arrhythmias could also be precipitated by the severe lactic
with cytoplasmic vacuolation of hepatocytes. Microscopic acidosis developing during exercise subsequent to tissue
changes in the myocardium are usually nonspecific. The hypoxia. Thus, an inadequate cardiovascular response of
etiology is unknown, but several factors such as genetic the turkey to stress or exercise may create hemodynamic
factors, early viral myocarditis and hypoxic conditions instability leading to sudden death.
during incubation have been suggested. Because of its
CLINICAL SIGNS
There are no clinical signs, except violent agonal wing
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flapping preceding death.
LESIONS
Turkeys dying of SDS are in good body condition with
the digestive tract filled with ingesta, demonstrating the
suddenness of death. Lesions are indicative of an acute
generalized passive congestion with subcutaneous
varicoses, pulmonary congestion and edema, perirenal
hemorrhage (Fig. 1), a swollen severely congested spleen,
and congestion of other organs.
Perirenal hemorrhage has been reported to occur in other

conditions and is not pathognomonic of the so-called SDS
of turkeys. Birds possess a renal portal system with a
superficial peritubular capillary plexus at the periphery of
the renal lobule. Local passive congestion would therefore
result in pooling of blood in the perirenal area and possible
diapedesis, explaining the hemorrhages observed at the
surface of the kidneys.
DIAGNOSIS
Lesions are diagnostic. Aortic aneurysm affects the same-
age turkey, but in aortic aneurysm, birds are pale and free
blood is present in the body cavity of the turkey.
CONTROL
Avoid excitement in the flock.
TREATMENT
There is no treatment.
AORTIC RUPTURE
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Fig. 1
Fig. 2
Aortic rupture: massive internal hemorrhage.
Ruptured aorta.
DILATED CARDIOMYOPATHY OF TURKEYS
Fig. 1
Severe bilateral dilated cardiomyopathy: cross-section of the heart. Fig. 2
Various degrees of dilated cardiomyopathies (Normal heart on
the right).
Fig. 3
Severe bilateral dilated cardiomyopathy with hydropericardium and
secondary ascites.
SUDDEN DEATH SYNDROME OF TURKEYS

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Fig. 1
Perirenal hemorrhage.
DIGESTIVE DISORDERS
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I. PENDULOUS CROP
Pendulous crop is a condition sporadically observed in
broiler chicken and turkey flocks. Birds have a greatly
distended crop (Fig. 1) filled with feed and malodorant
material. Crop mucosa can be ulcerated or infected by
Candida albicans. Affected birds keep eating but since
feed transit is affected, they soon lose weight, eventually
become emaciated and die. Affected carcasses reaching
market age are condemned at slaughter. Increased water
intake during sudden hot weather has been proposed as a
possible cause since birds will over drink and eat at night
when the temperature cools down. This appears to “over
stretch” the muscular wall of crop and even sometimes the
proventriculus, leading to permanent distention. Hereditary Fig. 1
predisposition has also been suggested in turkeys. Broiler chicken with a greatly distended crop.
II. PROVENTRICULAR DILATION

Proventricular dilation has been reported in birds fed a
finely ground diet. The gizzard of birds fed such a diet
does not need to contract much, hence its poor muscular
development with secondary proventricular dilation. The
proventriculus is enlarged with thin walls and no clear
demarcation between the gizzard and proventriculus
(Fig. 1). Excessive histamine amounts will also cause
proventricular dilation and flaccidity along with gizzard
erosions.
Fig. 1
Enlarged proventriculus.
DIGESTIVE DISORDERS II. POLYCYSTIC ENTERITIS OF BROILER

OF CHICKENS CHICKENS or RUNTING-STUNTING
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SYNDROME OF BROILER CHICKENS

I. DYSBACTERIOSIS
DEFINITION
DEFINITION Polycystic enteritis (PE) is most common in the
Terminology used in Europe to describe an intestinal Southeastern United States but is seen sporadically on the
microflora imbalance and overgrowth characterized by West coast as well as other parts of the United States. It is
enteritis and mild diarrhea. a disease of economic concern in other parts of the world
most notably in Australia and Europe. It is characterized by
OCCURRENCE large numbers of chicks with marked growth depression,
Dysbacteriosis is commonly observed after 21 days of age watery diarrhea, and cystic enteritis. The condition is
in European commercial broiler chicken flocks but can named after the characteristic severe microscopic cystic
occur as early as 15 days of age. dilation of intestinal crypts.
HISTORICAL INFORMATION OCCURRENCE

There has been an increase in the number of broiler PE may appear in chicks as early as 6-7 days of age, but
chicken flocks affected with dysbacteriosis with the ban of the usual peak of the problem occurs at around 10-12 days
growth promoters in Europe in 1999. of age, mostly during winter and spring. Farms that have
short downtimes between flocks appear to be at higher risk
for the disease. Turkeys are not known to be affected.
ETIOLOGY
Overgrowth of an abnormal bacterial duodenal
population has been demonstrated in birds affected HISTORICAL INFORMATION
with dysbacteriosis. Clostridium spp. has been shown to Runting Stunting Syndrome (RSS) has been recognized
contribute to this overgrowth. The absence of antimicrobial in chickens since the late 1970s. This condition occurs
growth promotors, animal protein and animal fat appear to sporadically, usually with increasing severity over a year
predispose birds to the disease. Other predisposing factors period within a given farm, then declines afterwards. During
may include non-specific stress, mycotoxins and systemic 2003-2005 a new clinical and pathological presentation
disease. appeared and caused economically significant problems
in the Southeastern United States, and some countries in
Asia, Middle East, and Latin America. In contrast to RSS,
CLINICAL SIGNS persistent problems with PE have been noted on specific
Dysbacteriosis is characterized by normal water
“problem” farms as successive flocks are affected. Many
consumption, humid litter, poorly formed and wet feces and
research institutions are actively studying this condition,
a reduction in feed intake.
further characterizing enteric viruses, developing diagnostic
tests and searching for potential vaccine candidates.
LESIONS
Thinning and ballooning of the small intestines accompanied
ETIOLOGY
by viscous or watery intestinal contents (Fig. 1).
The disease has been reproduced by placing broiler
chicks on contaminated litter obtained from previously
DIAGNOSIS affected farms, and by gavaging birds with intestinal
History of diarrhea, wet droppings. Elimination of any other contents from affected chickens. These resulted in severe
causes of diarrhea and wet litter. Empirical therapeutic weight depression. Multiple viruses have been identified
response to antimicrobial effective against Clostridium from chicks with PE including rotavirus, reoviruses and
perfringens or other enteric pathogens might be a diagnostic astroviruses. Bacteria do not appear to be involved in
indicator for both necrotic enteritis and dysbacteriosis. the disease as primary agents. Vertical transmission is
considered a possibility and is being investigated.
Monitoring litter quality with a litter box and an underlying CLINICAL SIGNS
absorbent paper might help in assessing any changes in Affected flocks show large numbers of depressed chicks
fecal water content and alert to early signs of diarrhea. huddling around feeders and drinkers within hours
Antibiotics might be required if there is associated mortality after placement. Litter quickly becomes damp. Feed
or subsequent necrotic enteritis. Competitive exclusion consumption decreases, there is loss of flock uniformity
products might help. and many chicks will show severe growth depression
(5 up to 20%) (Fig. 1). If allowed to remain in the flock,
stunted chickens do not recover. This will translate in
increased need for culling, reduced livability, increased CLINICAL SIGNS

feed conversion, and days to market. Affected birds are pale and significantly smaller than
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uninfected flock mates. They show poor growth rate,

LESIONS increased feed conversion, and the passage of undigested
At necropsy, affected chicks have small livers with enlarged or poorly digested feed in the feces.
gallbladder, pale, dilated thin-walled intestines with watery
contents and undigested food (Fig. 2 and 3). Histologically, LESIONS
intestinal lesions consist of numerous large cysts involving At necropsy affected broilers show proventricular
intestinal crypts with degenerating or necrotic cells and enlargement, especially the isthmus between the
mucin inside the lumen of these cysts (Fig. 4). As the proventriculus and ventriculus (Fig. 1), with mottled
condition progresses, intestinal villi become shortened and thickened, firm walls. Attenuation of mucosal papilla where
clubbed. ducts from the glands open into the lumen may be seen.
The mucosa appears roughened. Dilated, cystic glands
DIAGNOSIS are not indicative of TVP since this is a postmortem
History, clinical signs, and microscopic intestinal lesions change occurring rapidly following death. Four lesions
are suggestive of the disease. characterize the microscopic changes in the proventriculi
(Fig. 2): 1) necrosis of the glandular epithelium, 2)
CONTROL lymphocytic infiltration in the interstitium of proventricular
Built-up litter and short downtime may contribute to glands and mucosa, 3) hyperplasia of ductal epithelium,
PE. Proper brooding temperature minimizes early poor and 4) replacement of lost glandular epithelium by ductal
uniformity and delayed growth. Heat treatment of affected epithelium. Epithelial cell nuclei are swollen, pale, and
houses during downtime is likely to mitigate the condition. often have prominent nucleoli. Lesions do not occur in
other tissues.
TREATMENT
There is no specific treatment. Good husbandry and DIAGNOSIS
symptomatic support of an affected flock will lessen TVP is difficult to identify on the basis of gross lesions. In
economic losses. Severely stunted chicks will not recover contrast, microscopic lesions are sufficiently characteristic
and should be culled. to provide a diagnosis. Confirmation requires demonstration
of the novel Birnavirus by PCR. Correlation between
histopathology and virus presence is very high.
III. TRANSMISSIBLE VIRAL
PROVENTRICULITIS CONTROL, PREVENTION AND TREATMENT
DEFINITION There are no specific treatment, prevention, or control
Transmissible viral proventriculitis (TVP) is a transmissible measures for TVP other than biosecurity measures
proventricular inflammation of viral etiology found in effective against infectious agents.
commercially raised broiler chickens and associated with
increased proventricular fragility, impaired feed digestion, IV. Focal Duodenal Necrosis
poor growth performances, and increased contamination Focal Duodenal Necrosis (FDN) is a pathology that has
and decreased efficiency at processing. been observed in laying hens in United States since 1996.
This condition is characterized by lower egg production
HISTORICAL INFORMATION goals, and/or lower egg weight standards. Lesions are
Within the past few years, commercial broiler chickens located in the duodenal loop where single to multiple dark
from Southeastern United States, the West coast and grey focal areas can be seen through the serosa (Fig. 1).
probably others regions of the States have sporadically These areas correspond to areas of necrosis or ulceration
been affected with this disease. of the intestinal epithelium (Fig. 2). Histologically, focal
necrosis of the duodenal epithelium, with numerous gram-
ETIOLOGY positive bacteria covering the villi tips, is observed (Fig. 3).
TVP has experimentally been reproduced with
homogenates from proventricular tissue of affected birds Although the presence of Clostridium colinum has been
and a virus that is consistent with a novel Birnavirus identified by molecular methods, other bacteria have also
(different from Infectious Bursal Disease Virus). Presence been found, no causes and effects have been established
of the virus in proventricular lesions, in natural and and there remains much uncertainty about the cause,
experimentally infected birds, indicates it is the cause of nature and risk factors for the condition. FDN can be
the disease. Chicks can be experimentally infected by treated and prevented with the addition of antimicrobials
oral or intracoelomic inoculation, but the natural route of commonly used to prevent necrotic enteritis in broiler
infection is unknown. chickens, such as zinc bacitracin, in the feed.
DYSBACTERIOSIS
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Fig. 1
Thinning of the small intestines accompanied by mucoid intestinal
contents.
POLYCYSTIC ENTERITIS OF BROILER CHICKENS
Fig. 1 Fig. 2
Loss of flock uniformity with many chicks affected with At necropsy, affected chicks have small livers with enlarged
severe growth depression (in the middle). gallbladder, pale, dilated thin-walled intestines with watery
contents and undigested food.
Fig. 4
At microscopy, numerous large cysts involving intestinal crypts with
Fig. 3 degenerating or necrotic cells and mucin inside the lumen of these
Chick showing pale, dilated thin- cysts are observed.
walled intestines.
TRANSMISSIBLE VIRAL PROVENTRICULITIS

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Fig. 1 Fig. 2
28 day-old broiler with At microscopy of the proventriculus there is necrosis
proventricular enlargement of the glandular epithelium, lymphocytic infiltration in
(especially the isthmus between the interstitium of proventricular glands and mucosa,
the proventriculus and gizzard). hyperplasia of ductal epithelium, and replacement of lost
glandular epithelium by ductal epithelium.
Focal Duodenal Necrosis
Fig. 1 Fig. 2
Multiple grey areas can be seen through the serosal surface Numerous circular to coalescing areas of necrosis, at various stages
of the duodenal loop. of inflammation, can be observed on the duodenal mucosa.
Fig. 3
Focal necrosis of the duodenal epithelium, with
numerous Gram-positive bacteria covering the villi
tips.
DIGESTIVE DISORDERS OF TURKEYS mycotoxins have also been implicated in increasing the
severity of the disease.
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I. POULT ENTERITIS COMPLEX

(PEC) C. POULT ENTERITIS MORTALITY
Poult enteritis complex is a terminology used to describe
SYNDROME (PEMS)
various infectious intestinal diseases of young turkeys. It DEFINITION
includes numerous conditions such as turkey coronavirus Two clinical forms of PEMS have been identified; an acute
(TCV), poult malabsorption or runting-stunting syndrome, form with a sharp peak of mortality (mortality is greater
and poult enteritis mortality syndrome (PEMS). These or equal to 9% between 7 and 28 days of age, and daily
diseases all have the following common features: mortality on three consecutive days is greater than 1%),
less than six-week-old turkeys develop diarrhea, soon and a less severe form (mortality exceeds 2% between 7
followed by growth retardation and secondary nutritional and 28 days but daily mortality does not reach 1% during
deficiencies. However, while TCV is well characterized, three consecutive days), which has been referred to as
poult malabsorption or runting-stunting syndrome and Excess Mortality of Turkeys (EMT).
PEMS remain poorly defined in terms of etiology. Basic
pathogenesis involves intestinal mucosal injury by one Sick poults show diarrhea, dehydration, anorexia, growth
or more viruses, and possible secondary opportunistic depression, immunosuppression, and mortality, but also
infection by bacteria. a variety of physiological abnormalities, including reduced
body temperature, reduced energy metabolism and
A. TURKEY CORONAVIRUS hypothyroidism.
(TCV). See page 70.
OCCURRENCE
B. POULT MALABSORPTION / The disease occurs only in turkeys, when they are 7 to 28
RUNTING-STUNTING SYNDROME days of age. There appears to be an age susceptibility; the
younger the flock, the more severe the clinical expression.
DEFINITION In the field, hens economically are more affected than
Poult malabsorption / runting-stunting syndrome is an toms. The acute form of PEMS has mostly been observed
intestinal disease condition of young turkeys (Fig. 1 and 2) in the southeastern United States and presents a seasonal
characterized by malabsorption/maldigestion of nutrients pattern i.e., from late spring to early fall. While this form
that may result in stunting, secondary nutritional diseases was prevalent in the late 90’s, it is now an uncommon
such as rickets or encephalomalacia, and secondary occurrence. However, EMT is still regularly reported.
infections such as cryptosporidia or bacterial enteritis.
ETIOLOGY
OCCURRENCE The etiology of PEMS is still unknown. The disease can be
Poult malabsorption / runting-stunting syndrome generally experimentally reproduced by either contact exposure or
occurs in turkeys between 7 and 28 days of age. Nutrient oral inoculation of healthy poults with intestinal contents of
absorption and/or digestion are inhibited, causing infected poults, and it is believed that transmission is strictly
decreased growth rate, stunting, poor feathering, skeletal horizontal. Several agents, including turkey coronavirus,
problems, and an uneven flock. Lack of uniformity and rotavirus, astrovirus, reovirus, Group 1 aviadenovirus,
skeletal lesions may persist throughout the grow-out torovirus and unidentified small round viruses, have been
period. isolated or identified from PEMS cases. However, most
have been found capable of reproducing the disease alone
ETIOLOGY or has been consistently associated with the disease. In
Poult malabsorption/runting-stunting syndrome is a addition to viruses, certain atypical Escherichia coli strains
multifactorial disease of unclear etiology. Viruses regularly including attaching and effacing E. coli as well as other
isolated from intestinal tracts of affected poults include bacteria, and various protozoa have also been associated
astrovirus, enterovirus, parvovirus and rotavirus. However, with PEMS.
the detection of a viral agent from a diseased host does
not in itself constitute a cause and effect relationship for CLINICAL SIGNS
that disease. In addition, Cryptosporidia, Cochlosoma, and Affected poults are initially hyperactive and vocal but within
coccidia have been identified and will increase severity twenty-four hours they become depressed, anorexic,
and disease duration. Salmonella species and Gram- and huddle together near heat sources. Feed and water
positive filamentous bacteria are also commonly isolated consumption drop, while diarrhea develops. Litter quality
from affected birds. Dietary factors such as high protein rapidly deteriorates from abundant and watery droppings.
levels in starter feeds, poor quality fats and fish meal, and Marked lack of uniformity can be observed few days after
the onset of the disease (Fig. 1). Clinical signs will wane
within seven to ten days, but unevenness will worsen and
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remain for the duration of the life of the flock (Fig. 2).
LESIONS
Lesions are characteristics of an acute severe diarrheal
disease. Carcasses are dirty and exhibit signs of
dehydration (Fig. 3) and emaciation. The digestive tract can
be empty with occasional presence of some litter material
in the gizzard while small intestines are thin-walled and
dilated with fluid and gas (Fig. 4 and 5). Ceca can also be
distended (Fig. 6) with frothy contents. Lymphoid organs
are atrophied in more severely affected birds (Fig. 7 and 8).
DIAGNOSIS
Diagnosis of PEC requires flock records comparison for
analysis of growth and brooding performance, clinical
evaluation, collection of diagnostic samples such as sera,
fecal droppings, water and feed samples, necropsy, and
isolation and identification of enteric pathogens.
CONTROL
Biosecurity is of primary importance to control PEC.
Biosecurity procedures include management of dead
bird disposal, litter management, movement of used
litter, controlling traffic patterns of people and vehicles,
rodent control and water sanitation. Affected farms should
be placed under quarantine and premises should be
thoroughly cleaned, disinfected and fumigated. All-in/all-
out production or separate brooding and finishing units are
helpful. No vaccines are available.
TREATMENT
Supportive care for affected flocks includes raising house
temperatures slowly until poults appear comfortable.
Water-soluble vitamins and/or electrolytes should be
added to the drinking water. Vitamin E added to the feed
at twice the recommended level has been shown to be
helpful. Antibiotics have been used with mixed success.
They should be directed toward Gram-positive bacteria
since those with Gram-negative activity may further upset
normal intestinal flora.
Any action that will increase feed intake, such as walking

frequently through the flock, remixing feed, top dressing
feed with rolled oats, whole grains, etc., should have a
positive effect of PEC. On farms considered at high risk
of experiencing PEC, it is recommended to avoid placing
birds from young breeders because their progeny is smaller
and would be more susceptible to the disease.
POULT MALABSORPTION / RUNTING-STUNTING SYNDROME

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Fig. 2
Fig. 1 Dilated and thinned-walled intestines with gaseous and watery
Dilated and thinned-walled intestines contents.
with gaseous and watery contents.
POULT ENTERITIS MORTALITY SYNDROME

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Fig. 1 Fig. 2
Marked lack of uniformity can be observed few days after the onset Uneven turkey flock.
of the disease.
Fig. 4
Fig. 3 Poults with small intestines that are thin-walled and dilated with
Dehydrated poult (on the fluid and gas.
left) vs a normal poult (on the
right). Note the darker shank
characteristic of dehydration
and the vent soiled with
diarrhea of the PEMS affected
poult (left).
Fig. 5 Fig. 6
Small intestines are thin-walled and filled with fluid, gas and/or Distended ceca.
poorly digested, liquid intestinal content.
POULT ENTERITIS MORTALITY SYNDROME (PEMS)

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Fig. 7 Fig. 8
Normal thymus in a poult. Note the thymic lobes running alongside Atrophied thymus in a PEMS affected poult.
the jugular vein.
MUSCULOSKELETAL DISORDERS IV. DEEP PECTORAL MYOPATHY

This condition, also named green muscle disease, is an
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It is generally agreed that skeletal disorders are a major exertional myopathy involving the supracoracoideus (deep
source of economic loss in poultry. The specific cause of pectoral) muscle (Fig. 1 and 2) of heavy meat-type birds.
most leg problems is difficult to determine; they are often Vigorous wing beating increases subfascial pressure in
considered to have a genetic basis but may be influenced this muscle and results in ischemic necrosis. The lesion
by or due to environmental or nutritional factors. With the is unilateral or bilateral and the macroscopic appearance
advance of nutrition and the use of computer-generated varies according to the age of the condition. Earlier lesions
diets, deficiencies responsible for arthroskeletal conditions consist of edema followed by hemorrhage and necrosis. In
are quite uncommon. However, most of the actual problems chronic cases, the necrotic muscle has contracted due to
are associated with rapid growth and the incidence can be fibrosis and is uniformly green. The defect is then visibly
reduced by restricting growth rate. apparent at the abattoir as a depression in the breast over
the affected muscle and causes downgrading. Turkey
I. ANGULAR BONE DEFORMITY leg edema is another condition occurring secondary to
exertional myopathy, for example during transportation to
(Valgus-Varus Deformity of the Intertarsal Joint)
slaughter.
Angular bone deformity or valgus and varus deformity of
the intertarsal joint is the most common form of long bone
distortion found in broiler chickens and turkeys. There is V. FEMORAL HEAD NECROSIS
lateral (Fig. 1) or medial (Fig. 2) angulation of the shaft of (FHN)
the distal tibiotarsal bone resulting in deviation of the lower Femoral head necrosis (FHN) is a poorly defined and often
part of the leg and frequent bending of the proximal shaft inappropriately used term for numerous lesions of meat-
of the tarsometatarsus. Flattening of the tibial condyles and type birds. It has been used for and/or confused with the
displacement of the gastrocnemius tendon may also occur. following conditions (VI, VII, and VIII).
With severe angulation, the birds will walk on the hock joint
with bruising of the area, ulceration of the overlying skin,
and sometimes secondary infection. This condition results
VI. IATROGENIC TRAUMA TO
in significant trimming at processing. THE FEMORAL HEAD
During growth the femoral head is cartilaginous, and
separation of the proximal femoral epiphysis from the femur
II. CHONDRODYSTROPHY on disarticulation of the coxofemoral joint is common during
Chondrodystrophy is a generalized disorder of the routine necropsy. The teres ligament and joint capsule
growth plate of long bones that impairs growth, while frequently pull the articular cartilage and, occasionally, the
mineralization and appositional growth remain normal. It femoral epiphysis detaches from the femoral shaft and
occurs in young growing poultry. In the past this condition remains in the acetabulum. This epiphyseal separation
was often described as perosis. Any condition, whether exposes dark, rough and pitted physes. This is not a lesion
of genetic, nutritional, or environmental origin, resulting but an artifact. Epiphyseal separation may also occur
in a failure of physeal chondrocytes to proliferate can be spontaneously in live birds during rough handling and has
called a chondrodystrophy. Chondrodystrophy results in been referred to as traumatic epiphyseolysis.
shortened long bones, enlargement of hock joints, and
often secondary valgus or varus deformity (Fig. 1) and
subluxation of the gastrocnemius tendon. VII. OSTEOPOROSIS
With this condition, long bones are fragile and the growth
plate is irregular; thus the femur is more susceptible to
III. CONTACT DERMATITIS OF FOOT PADS breakage during necropsy. No necrosis in the femoral
(PODODERMATITIS OR BUMBLEFOOT) head is present. Otherwise, any condition causing
This condition is characterized by a local injury to integument increased bone fragility, such as rickets, or the so-called
of the avian foot, usually the digital or plantar metatarsal malabsorption maldigestion syndrome, might result in
pads, which lead to scab formation and inflammation of the shattering of fragile femoral necks during necropsy.
subcutaneous tissues (Fig. 1). Common sequelae include
tendonitis, septic arthritis, and osteomyelitis. Trauma, poor VIII. OSTEOMYELITIS
litter condition, increased ammonia and devitalization The physis of the proximal femur affected by bacterial
of the weight-bearing plantar structures are generally osteomyelitis is fragile and disarticulation during routine
suggested to initiate the disease. Severe foot lesions result necropsy may break the femoral neck. Small foci of
in lameness, reluctance to move, body weight depression osteomyelitis (Fig. 1) will be observed in the physes and
and might lead to sternal bursitis (breast burn or breast metaphyses.
blister), and a cause of carcass downgrading at slaughter.
IX. OSTEOMYELITIS / SYNOVITIS young birds and occurs more frequently in heavier birds.
Osteomyelitis is usually one manifestation of a systemic Marked malposition of one or both legs is observed from
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disease. It occurs when, following a bacteremic episode, the hock(s) distally. In early cases, the hock is flattened,
there is formation of an infective focus in the bone (see widened, and slightly enlarged. In advanced cases, the
previous figure). Escherichia coli and Staphylococcus leg from the hock distally deviates sharply from its normal
aureus are most commonly isolated; less commonly, position, usually laterally. Dissection usually reveals that
Salmonella, Yersinia, Streptococcus, Pasteurella, and the gastrocnemius tendon at the hock has slipped from its
Arizona are cultured from these lesions. More recently, trochlea.
an increased incidence of osteomyelitis of the thoracic
vertebrae associated with Enterococcus cecorum has XII. RICKETS
been observed in broiler chickens and broiler breeders. The
See section on Nutritional Diseases
epiphyses of long bones, vertebral bodies, and associated
joints are usually affected. Lesions in long bones consist XIII. SHAKY LEG
of focal yellow areas of caseous exudate or lytic areas. This is a severe lameness of 8-18-week-old turkeys.
Spondylitis can result in pressure on the spinal cord and The etiology is unknown and specific lesions are absent.
paresis. Affected joints are swollen and filled with purulent Affected birds spend most time sitting and if stimulated will
exudates (Fig. 1). Treatment is rarely effective. Prevention walk with great difficulty, on “shaky legs”. It is believed that
is based on adequate treatment of septicemic diseases. lameness is triggered by soft tissue (muscle or tendon)
pain. Most turkeys recover as growth slows, but other
X. OSTEOPOROSIS lesions, such as breast blister, might have developed
(Cage Layer Fatigue) secondary to the prolonged sitting. Shaky-leg as a flock
problem secondary to inactivity caused by pododermatitis
Osteoporosis refers to a decrease in bone volume but no from wet litter has been reported.
loss in density and affects laying hens reared in cages and
is most common at the end of a laying cycle. Clinical signs
are variable and include posterior paralysis (Fig. 1) or acute XIV. SPLAY LEG
death with or without changes in egg production. Paralyzed This condition occurs in young birds from hatching to 2
hens are initially alert and may be laying on their sides (Fig. weeks of age. There is lateral deviation of the leg (Fig. 1),
2). On postmortem examination birds have brittle, fragile usually at the knee but occasionally at the hip. Splay leg
bones, thin cortices (Fig. 3), and sometimes fractures. may be unilateral or bilateral. The condition results from
Sternae are often deformed and there is a characteristic birds being on slippery surfaces. A high incidence has
infolding of the ribs at the costochondral junctions (Fig. 4). been seen in poults brooded on brown paper.
Parathyroid glands can be prominent or severely enlarged
(Fig. 5). In the acute death form, an egg is present in the XV. SPONDYLOLISTHESIS
shell gland, with the shell partially or totally calcified and no Spondylolisthesis affects broiler chickens and is
macroscopic lesion. It is hypothesized that this acute form characterized by posterior paresis and paralysis due
is due to acute hypocalcemia. Osteoporosis can be caused to deformation and displacement of the fourth thoracic
by a vitamin D3, calcium, or phosphorus deficiency, or an vertebra resulting in a pinched spinal cord (Fig. 1). It is
imbalance in the calcium and phosphorus ratio. Adding considered to be a developmental problem influenced by
extra vitamin D and calcium to the diet may be of some conformation and growth rate. Affected birds are ataxic or
benefit. Lack of activity, strain of birds, and type of housing may assume a hock-sitting posture with their feet slightly
are considered to be important risk factors. Cage layer raised off the ground, and use their wings to move (Fig. 2).
fatigue can be a problem in a flock, but bone breakage at Severely affected birds often become laterally recumbent
processing due to osteoporosis may be a more significant and die from dehydration if not culled. This condition has
problem in terms of economic losses and in respect to been referred to in the past as “kinky back”. Osteomyelitis
animal welfare. of the thoracic vertebrae will cause similar clinical signs.
XI. PEROSIS XVI. TENDON AVULSION AND RUPTURE

(Slipped Tendon) Normal or excessive physical stress on the intertarsal
The term perosis describes the subluxated or slipped joint of growing heavy meat-type birds frequently can
gastrocnemius tendon, which is secondary to long bone causes rupture of the gastrocnemius or peroneus tendons.
shortening or enlarged condyles of the hock joint caused Swelling and red to green discoloration can be noted in the
by growth plate damage (chondrodystrophy). Nutritional affected region (Fig. 1). It has been suggested that viral-
deficiencies affect the development of the growth plate, the induced tenosynovitis may predispose birds to a ruptured
classical example being manganese deficiency, but, less gastrocnemius but this condition has been observed
frequently, choline, biotin, folic acid, niacin, or pyridoxine without any evidence of prior tenosynovitis.
may be involved. The deformity involves the hocks of
XVII. TIBIAL DYSCHONDROPLASIA

Dyschondroplasia is a very common growth-plate cartilage
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abnormality of fast-growing meat-type birds (broilers and

turkeys) characterized by persistence of the cartilage
with failure of removal of avascular prehypertrophying
chondrocytes. The cause is multifactorial, but rapid growth
and electrolyte imbalance leading to metabolic acidosis
are considered primary risk factors. Common dietary
causes of dyschondroplasia include excessive chloride
and excessive phosphorus with respect to calcium levels.
Certain Fusarium spp. mycotoxins also produce this
lesion. The pathogenesis is poorly understood, but three
mechanisms have been suggested: rapidly produced
prehypertrophying chondrocytes do not hypertrophy
as quickly as they are produced to allow penetration by
metaphyseal vessels, an inadequate vascular invasion of
the cartilage cannot initiate hypertrophy, or chondrolysis is
defective. Without hypertrophy and vascular penetration,
degeneration and calcification do not occur and a mass
of prehypertrophying cartilage remains in the metaphysis.
The lesion is characterized by an abnormal mass of
cartilage below the growth plate (Fig. 1). If the mass is
small, the condition will be subclinical. However, lameness
will be observed if the mass of remaining cartilage is
very large, the weakened bone may eventually bow or
fracture (Fig. 2). The lesion is most commonly observed
in the proximal tibiotarsus, probably because this bone is
routinely sectioned during necropsy.
XVIII. TIBIAL ROTATION

(Twisted Leg)
This condition affects young broiler chickens and turkeys.
There is lateral rotation of the distal tibia on its long axis,
which results in lateral deviation of the lower leg (Fig. 1
and 2). Rotation is usually unilateral and can approach 90
degrees (Fig. 3). Morbidity is low (less than 1% in broiler
chickens, but occasionally up to 5% in turkeys), and the
cause is unknown. Tibial rotation must be differentiated
from slipped tendon, because the tendon remains in place
in tibial rotation.
XIX. TWISTED TOES

Twisted toes are common in heavier breeds. Most digits
or a single digit may be bent laterally or medially (Fig. 1).
There is no known economic significance, but abnormal
weight bearing on the toes may cause ulceration followed
by pododermatitis. This is different from the ventral
curling of toe due to paralysis and secondary to riboflavin
deficiency.
ANGULAR BONE DEFORMITY

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Fig. 2
Varus deformity in a turkey.
Fig. 1
Valgus deformity in a young broiler.
CHONDRODYSTROPHY
Fig. 1
Young turkeys with chondrodystrophy resulting in shortened long
bones, enlargement of hock joints, and secondary valgus or varus
deformity.
CONTACT DERMATITIS OF FOOT PADS
Fig. 1
Pododermatitis in a broiler breeder hen.
DEEP PECTORAL MYOPATHY

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Fig. 1 Fig. 2
Deep pectoral myopathy. Deep pectoral myopathy.
OSTEOMYELITIS
Fig. 1
Foci of osteomyelitis in the femoral head.
OSTEOMYELITIS / SYNOVITIS
Fig. 1
Affected joint is swollen and filled with purulent exudate.
OSTEOPOROSIS
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Fig. 2
Acute paralysis; paralyzed hens are initially alert and may be laying
Fig. 1 on their sides.
Leghorn hen affected with cage layer fatigue demonstrating
posterior paralysis.
Fig. 4
Characteristic infolding of the ribs at the costochondral junctions.
Fig. 3
Histological longitudinal section of the femur of a
normal (top) and a laying hen with osteoporosis
(bottom).
Fig. 5
Parathyroid glands can be prominent or severely enlarged (arrows).
SPLAY LEG
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Fig. 1
Splay leg in a broiler chicken.
SPONDYLOLISTHESIS
Fig. 1 Fig. 2
Deformation and displacement of the fourth thoracic vertebra Affected birds are ataxic and assume a hock-sitting posture with
resulting in a pinched spinal cord. their feet slightly raised off the ground, using their wings to move.
TENDON AVULSION AND RUPTURE
Fig. 1
Ruptured gastrocnemius tendon in a broiler chicken carcass at
slaughter.
TIBIAL DYSCHONDROPLASIA
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Fig. 1
Tibial dyschondroplasia is characterized by an abnormal mass of
cartilage below the growth plate observed at sagittal section of the Fig. 2
proximal tibia. If the mass of remaining cartilage is very large, the weakened bone
may eventually bow or fracture.
TIBIAL ROTATION
Fig. 2
Fig. 1 Lateral rotation of the distal tibia on its long axis, which results in
Broiler chicken with rotated tibia. lateral deviation of the lower leg.
Fig. 3
Rotation is usually unilateral and can approach 90 degrees.
TWISTED TOES
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Fig. 1
Twisted toes in a 8 week-old broiler chicken.
REPRODUCTIVE DISORDERS 2. Neoplasms of the oviduct per se are rare or are rarely
recognized. Adenocarcinomas of the oviduct arise
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I. OVARIAN LESIONS predominantly in the upper magnum and tend to be

1. Atrophy and inactivity of the ovary is perhaps the most highly invasive, frequently resulting in widespread
disturbing lesion in a hen of productive age. In the peritoneal implantation. The much more common tumor
absence of other diseases, this finding is indicative occurs in the mesosalpinx arising from smooth muscle
of severe stress such as lack of feed and water and in the center of the ligament. These leiomyomas are
is often accompanied by neck or body molt and always firm and encapsulated and vary in size from
other evidence of difficulties including emaciation, barely detectable to several centimeters in diameter.
dehydration, and so on. Large leiomyomas may occasionally interfere with
oviduct function.
2. Neoplasms affecting the ovary are fairly frequent and
include involvement by Marek’s disease, lymphoid 3. Salpingitis is usually seen as a sporadic individual
leukosis, and myelocytomatosis. Adenocarcinomas, bird problem, although, in flocks with Mycoplasma
granulosa cell tumors, and arrhenoblastomas are infection, Salmonella infections, and some outbreaks
also seen in hens. Adenocarcinomas are particularly of pasteurellosis and colibacillosis, this lesion may
common and are striking in their presentation because occur with substantial incidence. Infections affecting
of numerous trancoelomic implants on the surfaces of the left greater abdominal air sac or the peritoneal
abdominal organs. Ovarian neoplasms are generally cavity have the potential for extension into the oviduct
readily identified by histopathological evaluation. as a descending inflammatory process in this tubular
organ. In many cases, however, oviductal infections
3. Oophoritis or follicular regression is associated with appear to originate in the distal extremity, suggesting
a variety of infectious diseases. The normally turgid that infection ascends from the cloacal orifice. In the
yellow ovules become wrinkled, hemorrhagic, or early stages of salpingitis the only apparent changes
discolored (green, gray-yellow, beige, etc.) (Fig. 1 and may be irregularities in the mucosal surfaces including
2) and many times there is evidence of premature erosions or small ulcerations, edema of the mucosal
rupture with spillage of yolk material into the abdominal folds, and accumulation of adherent fibrinopurulent
cavity. Follicular regression and rupture with abdominal exudate. As the lesion progresses the amount of
yolk material is also a frequent finding in extreme exudate in the lumen increases rapidly and, ultimately,
dehydration. Among the infectious diseases notorious the oviduct becomes an irregular thin-walled sac filled
for this ovarian effect are velogenic Newcastle disease, with laminated masses of yellow cheesy exudate (Fig.
avian influenza, fowl cholera, pullorum disease, fowl 1). The oviduct becomes nonfunctional early in the
typhoid, and some strains of Salmonella Enteritidis infection and the ovaries of affected hens are usually
and Escherichia coli. atrophied. It is however possible, that some of the
4. Ovarian cysts are occasionally encountered in laying oviductal content in salpingitis represents impacted
hens, sometimes in active functional ovaries. Usually egg components (Fig. 2). Apart from specific bacterial
these cysts are very thin walled and contain clear infections noted above, which might be present in
fluids. It is frequently difficult histologically to identify the early stages of salpingitis, the luminal exudate in
the origin of ovarian cysts but it is presumed that most terminal stages may yield a wide array of bacteria and
are of follicular origin. even fungi.
4. Impacted or egg-bound oviducts are seen sporadically
II. OVIDUCT LESIONS in cull hens. This condition may be more prevalent
1. Atresia, hypoplasia, and atrophy of the oviduct have
in pullets that were brought into production too early
been documented in hens of laying age. Simple
(prior to full body development) or hens that are
atrophy associated with severe stress, chronic
extremely obese. Whether oviduct obstruction results
infection, certain intoxications, etc., is most common.
from a lodged egg or an intermingled mass of broken
Hypoplasia as a result of early infectious bronchitis
shells, shell membranes, or aggregates of coagulated
in sexually immature pullets may lead to “false layer”
albumin and yolk, the result is the same. When
status in hens with fully developed ovaries and
impaction occurs in the uterus or vagina (which is
partially developed oviducts. Many of these have the
usually the case) eggs enclosed by shell membranes
external appearance of active layers but yolk material
may be found in the abdominal cavity. This indicates
is deposited in the abdominal cavity leading to the
that eggs continued to form but were refluxed back into
classical “yolk peritonitis”. Hereditary atresia of the
the peritoneal cavity. Hens with numerous abdominal
oviduct has been reported and the condition may
eggs may assume a penguinlike posture.
affect segments or the entire oviduct. Again yolks and
any surrounding albumin deposits cannot pass and 5. Cystic oviducts are seldom clinically significant
are refluxed back into the abdominal cavity. but cystic remnants of the right oviduct are very
prevalent. In the chicken only the left components of
a paired embryonal reproductive system develop after
hatching. Segments of the right oviduct may develop

to varying degrees. These segments are closed (no
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anterior or posterior drainage) and, if the wall contains

significant glandular tissue, a fluid secretion will
accumulate resulting in production of cysts. These
cysts usually occur on the right side adjacent to the
cloaca and range from barely perceptible in size to
massive cysts occupying most of the abdominal cavity.
Affected hens appear to have ascites (water belly) but
if the abdomen is opened carefully the fluid is found
to be contained within a cyst. Cysts have also been
described in the left oviduct but they are much less
common. Left oviductal cysts may form in segments
of the oviduct proper, in the wall of the oviduct or in
the mesosalpinx adjacent to the oviduct. Oviductal
cysts may be intriguing postmortem findings but they
rarely, if ever, have any significant impact on flock
performance.
6. Prolapse or eversion of the terminal oviduct can
occur with alarming prevalence in some layer
flocks and ranges from barely perceptible everted
vaginal mucosa protruding from the vent to elongate
exteriorized segments of prolapsed oviduct (Fig. 3).
Circumstances in which this problem is most severe
include young poorly developed pullets just coming into
egg production, flocks with higher than recommended
cage densities, increased levels of cannibalism
associated with hyperactive flocks (hysteria) or flocks
exposed to a sudden surge of increased light intensity
(as in open houses in the first bright days of spring),
increasing levels of obesity, and flocks that were poorly
beak trimmed with substantial regrowth of beak tips.
When oviposition occurs there is a normal eversion of
the uterus or vaginal mucosa surrounding the egg as
it is delivered. In poorly developed or obese birds this
everted mucosa may be slow to retract afterwards. If
there is any increased tendency toward cannibalism in
the flock, cage- or pen-mates will peck at the everted
mucosa causing trauma and edema, which will further
slow or prevent retraction. Continuing irritation of the
exposed mucosa may promote straining and overt
prolapse of the oviduct. An association has also
been observed between a tendency for eversion and
prolapse and an increased incidence of salpingitis.
Also losses from cannibalism and culling are
increased in flocks with a high rate of uterine/vaginal
prolapse. Control of this condition can be achieved to
some degree by allowing full development of pullets
before bringing them into lay, maintaining proper
stocking density of cage or floor houses, careful
control of lighting intensity, proper beak trimming, and
maintaining feed formulations and consumption levels
to avoid obesity, especially in older hens.
OVARIAN LESIONS
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Fig. 1
Atretic ovary and oviduct. Fig. 2
Atretic ovary and oviduct.
OVIDUCT LESIONS
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Fig. 2
Salpingitis: compacted egg components and caseous exudate in
Fig. 1 oviduct.
Salpingitis: fibrinopurulent exudate present in the
lumen of the oviduct with peritonitis.
Fig. 3
Laying hen dead from prolapsed
oviduct.
URINARY DISORDERS Although usually unilateral, both ureters may be involved.

One or more lobes of the kidney drained by the obstructed
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UROLITHIASIS ureter often are severely atrophied (Fig. 1). The opposite
functional kidney may be hypertrophied. Many affected
(Nephrosis, Renal Gout, Caged Layer Nephritis) hens will have white chalky material (urate deposits) on
DEFINITION serosal membranes of various visceral organs.
Urolithiasis is an etiologically undefined condition seen
particularly in caged laying hens and characterized by DIAGNOSIS
blockage of one or both ureters by urate concretions Diagnosis is based on classical ureteral and renal lesions in
with attendant atrophy of one or more lobes of the kidney most of dead birds necropsied. Observation of urolithiasis in
drained by the obstructed ureter. an occasional dead bird is indicative of a sporadic individual
bird problem and is of little consequence. Confirmation of
OCCURRENCE etiologic factors noted above is usually difficult unless feed
This condition has been recognized for years as a samples have been retained for analysis.
sporadic individual bird problem in laying flocks. More
recently urolithiasis has been described as a flock problem CONTROL
accounting for substantial mortality in caged layers in Until etiologic factors are better defined, it is difficult to
England, the United States, and other countries throughout make specific recommendations. It is advisable to respect
the world. limits of calcium and available phosphorus in rations during
grow-out and to avoid electrolyte imbalance, mycotoxins
ETIOLOGY and water deprivation.
A number of causative factors have been implicated in
precipitating urate deposits in kidneys, joints, or on serosal
surfaces throughout the body. These include dehydration,
excessive dietary protein (30-40%), dietary calcium excess
(3% or greater), sodium bicarbonate toxicity, mycotoxins
(oosporin, ochratoxin), vitamin A deficiency, and
nephrotropic strains of infectious bronchitis virus. However,
the recently described urolithiasis in caged layers appears
to be associated with feeding relatively high calcium levels
(3% or greater) during the pullet grow-out period. Available
phosphorus in the grower ration appears to be contributory
in that urolithiasis is enhanced when levels are below
0.6%. Many clinicians feel that infectious bronchitis viruses,
or even ‘hot’ vaccine strains might be involved in the
process and there also is evidence that dietary electrolyte
imbalances (low sodium and potassium, high chlorides)
may play a role. Finally, many diagnosticians consider
all current etiologic explanations of this condition to be
unsubstantiated, or at best, poorly supported hypotheses.
CLINICAL SIGNS
In many cases of urolithiasis there is no consistent
clinical sign other than increased mortality. Among signs
associated with the condition are depression, weight loss,
and an inclination of affected birds to hide. Roughened or
thin eggshells may increase slightly in affected flocks and
total egg production will decrease in parallel to increasing
mortality. Mortality may be gradual and persistent (2-4% Fig. 1
per month) throughout the productive lifetime of the hens or Nephrotropic Infectious bronchitis strain; Renal
it may be more precipitous. Total mortality has approached hypertrophy with atrophy of some lobes.
50% in severely affected flocks.
LESIONS
The affected ureter is usually markedly distended by
cylindrical concretions surrounded by thick mucus.
INTEGUMENT DISORDERS
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I. KERATOCONJUNCTIVITIS
(Ammonia Burn)
Keratoconjunctivitis is an inflammation caused by
excessive levels of ammonia in poorly ventilated poultry
houses. Chickens appears to be more susceptible to
ammonia toxicity than turkeys. Lesions include keratitis,
conjunctivitis, and a corneal opacity with a possible
ulceration (Fig. 1). Birds may become blind, but recovery
is possible depending on the severity of damage to the
cornea. Because ammonia is produced by the degradation
of uric acid by bacteria in the litter, control of litter moisture
and proper ventilation will prevent this problem.
Fig. 1
Broiler breeder male with corneal opacity and
ulceration following exposure to high environmental
ammonia levels.
II. SCABBY HIP SYNDROME

Scabby hip syndrome is a lesion observed at the slaughter
plant in broiler chickens and is characterized by superficial
ulceration and scabbing of skin on the thighs (Fig. 1). This
is a multifactorial problem; poor feathering, high stocking
density, and poor litter conditions have been incriminated.
Affected carcasses are downgraded. In recent years,
improvements in litter management and use of nipple
drinkers have contributed to the reduction in incidence of
this condition.
Fig. 1
Scabby hip in a broiler chicken carcass at slaughter.
III. STERNAL BURSITIS

BREAST BLISTER or BREAST
BURN or BREAST BUTTON
Sternal bursitis is a fluid-filled lesion located on the ventral
aspect of the keel bone of poultry (Fig. 1). Chickens and
turkeys have a synovial bursa, the sternal bursa, which
under repeated trauma increases in size and may become
secondarily infected. This lesion is closely associated with
locomotor problems in heavy birds and increased contact
time with litter. Such blisters, if not too large, are trimmed
from the carcass at processing resulting in downgrading.
The terms breast blister, breast button, breast burn are
also used for this condition.
Fig.1
Sternal bursitis: fluid-filled lesion located on the ventral aspect of the
keel bone of a broiler breeder following prolonged ventral decubitus.
IV. XANTHOMATOSIS
Xanthomatosis is an unusual condition characterized by
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the abnormal subcutaneous intracellular accumulation of

cholesterol clefts mixed with multinucleated giant cells and
macrophages, in chickens. Skin lesions are initially soft
with fluctuating honey-colored fluid, and later become firm
with marked thickening and irregularity of the surface (Fig.
1). This condition is rare and in the past was probably due
to contamination of feed fat with hydrocarbons.
But xanthomatosis probably representing fat necrosis and

granuloma formation can occur in various parts of the body
in various species of birds including poultry.
Fig. 1
Xanthomatosis characterized by an irregular
surface and thickened skin.
BEHAVIOR DISORDERS
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I. CANNIBALISM
This vice can cause severe losses in some poultry flocks.
Many forms are described, the most common ones being
feather pulling, and vent, head (Fig. 1), and toe picking.
Feather pulling occurs in any age of bird. In severe cases
birds will die of hemorrhage and carcasses will be picked
and eaten by pen-mates. Vent picking in cage-reared
laying hens is most common in overweight birds. There is
a normal eversion and prolapse of the vagina at lay. If the
hen is obese, the vaginal mucosa will be exposed for a
prolonged time and cage-mates will be attracted by this
shiny red mucosa. The assaulted hen will bleed to death
and dried blood will be present on the feathers of the
pericloacal area and on the back of the legs. A pecking
order has often to be established in a poultry flock and
head lesions are common in turkeys, even though birds Fig. 1
have trimmed beaks. Toe picking occurs in young chicks Head pecking in a broiler breeder hen.
started on paper or in batteries, and is often initiated
by hunger. Several predisposing factors such as light
intensity, dense stocking, reduced animal protein feed
content, lack of vitamins, amino acids, or salt in feed,
sodium imbalance due to heat stress, being without feed
for too long, and irritation from external parasites have
all been mentioned. Recent work has shown that feather
pecking may be related to low levels of insoluble fiber in
the diet. Once a bird develops this habit, it will continue.
Outbreaks can be sometimes controlled by using red light
or reducing light intensity. In laying stock and commercial
turkey flocks, trimming a third of the upper beak with laser
or electrocautery is a widely used preventive measure.
II. HYSTERIA
Sporadic cases of broiler chicken and replacement pullet
flocks with extremely high activity levels have been reported.
The cause is unknown but tryptophan supplementation
appears to alleviate the problem.
MANAGEMENT-RELATED DISORDERS TREATMENT AND CONTROL

Check temperature, luminosity and bird’s distribution in the
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I. DEHYDRATION/STARVATION brooding area as well as water and feed availability. Cold

birds will huddle together while hot birds will be panting
OF CHICKS/POULTS and lying on their belly, often too weak to be interested in
Losses due to so-called “normal mortality” should not be finding the water.
more than 1% in the first 10 days of the growout period.
Any mortality higher than this should be investigated
II. HYPOGLYCEMIA-SPIKING
MORTALITY SYNDROME IN
DEFINITION
Dehydration and starvation are the most common causes BROILER CHICKENS
of mortality in chicks and poults during their first week DEFINITION
of life. Young birds which cannot find water nor feed will Hypoglycemia-spiking mortality syndrome (HSMS) is
eventually die of starvation and inanition, once the yolk has characterized by a sudden increase in mortality (>0.5%) for
been absorbed i.e., before the fifth day. But dehydration at least 3 consecutive days, in a previously healthy, normal
and starvation can also occur at any age and in various appearing broiler chicken flock aged between 7 and 21
species of birds. days of age. Two clinical forms have been described; type
A more severe but of short duration and type B, a milder
ETIOLOGY form occurring over a longer period.
Failure to eat and/or drink can be related to farm
management conditions. Since recently hatched ETIOLOGY
chicks/poults are poikilothermic, optimal environmental Although the disease has been reproduced with tissue
temperatures are a must for the brooding period. A comfort homogenates and viral particles have been identified in
zone i.e., an area where environmental temperature is affected birds, the etiology is still unknown and the causal
ideal for the chick/poult must be established inside the agent remains to be identified. Clinical signs and death
barn. Check temperature charts since this temperature are caused by hypoglycemia. Hypoglycemia could either
varies according to age and species. Feed and water must be explained by a virus blocking pancreatic glucagon
be located in the bird’s comfort zone in a brightly lit area production or hypothetically related to melatonin deficiency
(60 to 100 lux), in order for the young bird to access them. and associated glycogenolysis. Melatonin deficiency could
be caused by a lack of a long dark period. Stress and/or
Severe diarrhea and high environmental temperatures can acute fasting could trigger HSMS in either situation.
also cause dehydration.
CLINICAL SIGNS
CLINICAL SIGNS Flock experiences a rapid, unexplained increase in
Birds that die of dehydration or starvation do not usually mortality, which will decrease as quickly in a matter of a few
show other signs of illness than weakness before death. days. Live chicks are found recumbent and uncoordinated
Bear in mind that uncomfortable chicks/poults will be noisy (Fig. 1), frequently lying on their breasts with legs
before becoming depressed. Affected individuals are also extended. Evidence of blindness and hyperexcitability can
smaller. be seen. Death occurs rapidly, often within a few hours.
Blood glucose levels are lower than <150mg/dL. Birds with
LESIONS very low levels from undetectable to less than 60 mg/dL
Dehydrated carcasses are light with darker feet and beak. frequently occur.
Legs appear thinner with a prominent metatarsal vein.
The skin adheres tightly to dark pectoral muscles. Upon LESIONS
opening the coelomic cavity, white chalky material (urates There are no specific gross or microscopic lesions.
deposits) can be observed on various serosal surfaces Birds appear normal and typically have food in the crop.
(Fig. 1, 2 and 3) including joints (Fig. 4). Kidneys are often Infrequently sinusoidal congestion or small hemorrhages
pale and enlarged with increased urates and ureters are are seen in the liver (Fig. 2).
often dilated with urates (Fig. 5). There is none or very little
feed in the gizzard.
DIAGNOSIS
Mortality pattern (a high spike in a mortality curve at 7-21
DIAGNOSIS days of age) and low blood glucose levels in clinically
Based on history and lesions. affected birds are diagnostic. If a chemical analyzer is not
easily accessible, glucose test strips and hand held monitor
can measure fairly accurately blood glucose levels in the
field. TheraSense FreeStyle glucose meter (Abbott Labs) retardation and loss of flock uniformity. At necropsy there
works with avian blood (Note: other glucometers also may will be serous to caseous exudates in the upper respiratory
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work, but have not been tried or reported). tract with airsacculitis in the case of secondary bacterial
infection.
Although it is important to give a 24 hour period of full light DIAGNOSIS
to day-old chicks, a progressively decreasing day length Diagnosis is based on poor environmental conditions,
resulting in a long daily dark period will usually prevent this clinical signs and lesions. ELISA antibody titers to infectious
problem. bronchitis are within normal.
III. HEAT STRESS and HYPERTHERMIA Treatment and prevention

Chicks must be provided with optimal environmental
High temperatures are stressful for poultry and frequently
temperature and rearing conditions. Antibiotics can be
cause death from hyperthermia. Millions of birds die
administered if there is secondary bacterial infection.
each year from hyperthermia usually because of high
environmental temperature, but also because of electric
power failure in closed buildings. Birds do not have sweat
glands and thermoregulate via non-evaporative cooling
(radiation, conduction and convection). Effect of ambient
temperature on body temperature varies with body heat
production which is directly related to body mass and feed
intake (metabolism). If panting fails to prevent increase
in body temperature birds will become depressed,
then comatose, and soon die. Lethal internal high body
temperature is 116oF for chicks and 117oF for adult birds.
Dead birds are usually found on their breast, in good
body condition. Breast muscles may have a cooked, pale
appearance. Prevention of hyperthermia is based mainly
on proper building insulation, optimal ventilation and
evaporation techniques, feed removal early in the day to
reduce metabolic heat production and adequate drinking
water availability.
Panting and increased respiratory rates affect acid-base

balance and cause respiratory acidosis. Higher blood
pH will reduce plasma ionized calcium, which is needed
for eggshell formation, hence the risk for increased thin-
shelled eggs in summertime laying flocks.
IV. VACCINE REACTION

(ROLLING REACTION)
DEFINITION
A normal respiratory (Newcastle disease or infectious
bronchitis) vaccine reaction occurs within the week after
hatchery vaccination. However, if environmental conditions
are poor, or the flock is infected with vertically transmitted
Mycoplasma spp., this reaction might aggravate with
possible secondary Escherichia coli or Mycoplasma spp.
infection.
Clinical signs and lesions

Affected chicks will show head shaking, wet eyes with nasal
discharge and mild coughing or sneezing (Fig. 1). Chicks
will appear depressed and will huddle together or under
a heat source. There will be increased mortality, growth
DEHYDRATION/STARVATION OF CHICKS/POULTS
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Fig. 1 Fig. 2
Dehydrated chick: white chalky material (urates deposits) present on Urate deposits on pericardium.
various serosal surfaces. Note the pale kidneys and dilated ureters.
Fig. 3 Fig. 4
Urate deposits on muscle surfaces. Presence of urate deposits in the joint.
Fig. 5
Pale and enlarged kidneys with bilateral ureter dilation.
HYPOGLYCEMIA-SPIKING MORTALITY SYNDROME IN BROILER CHICKENS

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Fig. 1 Fig. 2
Hypoglycemia in live chicks. Small hemorrhages in the liver.
VACCINE REACTION
Fig. 1
Young chicken with ocular discharge.
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230
Etiology Susceptibility Clinical signs and lesions Comments

Disease(s)
Aspergillosis Usually Aspergillus Young birds are more Various CNS signs. Respiratory Yellow mycotic nodules often
fumigatus. susceptible than adults signs usually precede CNS signs grossly visible in brain. Lesions
and predominate. A minority of aspergillosis in lungs or air
develop CNS involvement. sacs, perhaps in conjunctival
sac or globes of eyes.
Avian botulism Ingestion of toxin Most species of birds Paralytic, often fatal disease, Important environmental
produced by the characterized by ascending factors contribute to the
(limberneck) bacterium Clostridium paresis and paralysis. initiation of avian botulism,
botulinum outbreaks then perpetuated

No gross lesions by the bird-maggot cycle.
Avian influenza Orthomyxovirus Turkeys, ducks, Highly variable. In mild form: Enzootic forms in U.S. usually
(strains vary greatly pheasants, quail, many often swollen sinuses, ocular or mild to moderate in severity
(AI) in pathogenicity). wild birds, other poultry. nasal discharge. In severe form: and involve respiratory system.
hemorrhages, exudation, focal Egg production declines and
Not a significant pathogen of necrosis in respiratory, digestive, shell abnormalities common in
ducks. Ducks are believed urogenital, cardiovascular, turkeys. Most outbreaks of AI in
to be a major reservoir for or multiple systems. U.S. are in turkeys and ducks.
avian influenza virus.
Hong Kong 2003, first report of
H5N1 Hong Kong (2002) HPAI H5N1 causing deaths in
lethal for wild waterfowl. resident and migratory water-
fowl. 460 geese died from H5N1
in Xinjiang, China (2005). Now
also in Europe and Africa.
Avian Paramyxovirus 1 Presumably all ages but Drop in egg production, birds Rarely diagnosed in ducks. No
DISEASES OF THE DUCK
Paramyxovirus and other APMV’s not recognized clinically go into moult. Essex ‘70 outbreak reported in ducks during
Written by Peter R. Woolcock and Martine Boulianne
1 (Newcastle (4, 6, 8, 9) other than in laying ducks. strain will kill experimentally whole of Essex ‘70 UK epidemic.
Disease) and other infected ducklings. In geese Exotic NDV in US (Oct 2002-
APMV’s (4, 6, 8, 9) VVND seen in VVND pathology and 2003, no reports in ducks).
geese in China. high mortality (China).
Avian tuberculosis Mycobacterium avium All avian species Round nodules (granulomas) Usually seen in older birds. Can
attached to serosa of gut. Focal be a problem is established in
granulomas in many other captive flocks. Causative bacilli
organs. Extreme emaciation readily demonstrated in acid-
in advanced cases. fast-stained smears of lesions.
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Name of
Disease(s)
Chlamydophilosis/ Chlamydophila psittaci Turkeys, pigeons, ducks, Can be acute, subacute This is a zoonosis and a
Chlamydiosis cage and wild birds. or inapparent. Pericarditis, public health concern.
(psittacosis, often adhesive. Also with
ornithosis) airsacculitis, fibrinous
perihepatitis, splenomegaly,
and hepatomegaly.
Colibacillosis Escherichia coli Turkeys, chickens, Pericarditis, often adhesive. Often with airsacculitis,
septicemia. commercial ducks. fibrinous perihepatitis.
Duck viral hepatitis Picornavirus Ducklings, typically less Signs: acute onset, short Typical lesions in young ducklings
type I (DHV-1) Genus: Avihepatovirus than 4 weeks old. course, high morbidity and almost pathognomonic.
mortality. Liver swollen and
Now renamed with many hemorrhages. Worldwide incidence.
DHAV-1, DHAV- Economically important disease
2 and DHAV-3 for commercial duck industry.
identified in
China, South
Korea & Taiwan
Duck viral Astrovirus Ducklings up to 6 weeks. Liver hemorrhages, As DHV type I, deaths
hepatitis type II Complicated by DHV swollen kidneys. may be slightly slower.
type I and septicemia.
Adults not susceptible. Only reported in UK. May see
extensive biliary hyperplasia in
liver sections, cf. aflatoxicosis.
Also reported in China.
Duck viral Astrovirus Ducklings up to 3-5 wks. Liver hemorrhages As DHV type I, lower
hepatitis type III Complicated by DHV mortality, higher morbidity.
type I and septicemia.
Adults not susceptible. Only reported in USA.
Duck virus enteritis Herpesvirus Mostly adult ducks but also Lesions of vascular damage on Epizootic losses in waterfowl
(duck plague) from 2 wks of age. (Also mucosa of GIT, lymphoid organs are suggestive. Typical
in geese and swans). & parenchymatous organs: lesions and inclusion bodies
Widespread hemorrhages, helpful in diagnosis. An
severe enteritis. Perhaps exotic, reportable disease.
elevated plaques in esophagus,
ceca, cloaca or bursa.
Hemorrhage and/or necrosis in

lymphoid rings or discs of gut.
231
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232

Disease(s)
Eastern equine Alphaviruses Pheasants, partridges, Circling or staggering followed Microscopic lesions only.
encephalomyelitis turkeys, Pekin ducks, quail. by paralysis. Perhaps blindness Transmitted by mosquitoes.
in recovered birds. Often high
morbidity and mortality.
Fowl cholera Pasteurella multocida Water birds, domestic Sick birds appear lethargic or Acute infections are common
poultry, game birds. drowsy. Abnormal positions and may result in rapid
(Avian cholera of head and neck. Ataxia, death and ‘explosive‘die-offs.
or avian loss of equilibrium. Chronic infections with lower
pasteurellosis) mortality can also occur.

Lesions of septicemia
(hemorrhages and petechiation
on serosal surfaces) and multiple
foci of necrosis in liver. Birds are
often in good body condition.
Goose Parvovirus Parvovirus In geese & Muscovy ducks < 1 wk - anorexia, prostration In China since 1956. E Europe &
(GPV) Other only. 0-4 wk. Younger & rapid death. France in 1960’s. Not thought to
names:Derzsy’s birds more susceptible. be present in USA - considered
Disease, Goose High mortality in young Older - anorexia, polydipsia a foreign animal disease.
influenza, Goose goslings (1-10 days). Adults and weakness. Nasal and
plague, not susceptible, but do ocular discharge, head
respond immunologically. shaking. Eyelids red and
swollen, profuse white diarrhea.
Survivors may be stunted.
Pale myocardium, congested,

swollen liver, spleen & pancreas.
Leukocytozoonosis Leukocytozoon sp. Turkeys, ducks, geese, Pallor, splenomegaly, liver Outbreaks correspond with hot
guinea fowl, chickens. degeneration and hypertrophy months when simulid flies and
in some birds. Leukocytozoons culicoid midges are numerous;
visible in blood smears. Schizonts these flies breed in and along
often in liver, spleen, brain. water courses. Surviving
birds (wild or domesticated)
often act as carriers. Signs
in birds related to anemia.
Muscovy duck Parvovirus Young Muscovy Similar to Goose parvovirus, First in W France 1989. Also in
parvovirus ducklings only but skeletal muscle maybe Japan and Europe. USA 1998. As
pale and more affected. yet no vaccines available in USA
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Name of
Disease(s)
Renal coccidiosis Eimeria are Chickens, turkeys, Infected birds may be emaciated Part of the parasite life cycle
species-specific ducks, geese, perhaps and have a prominent keel. In occurs in the kidney.
and many cause in most birds. severe infections, kidneys may
renal coccidiosis . become enlarged and pale, Young birds and those that
containing multiple spots or have been stressed by various
Duck: E. boschadi, foci of infection that coalesce conditions are most likely to have
E. somatarie into a mottled pattern. clinical cases of renal coccidiosis.
Geese: E. truncata Most reports of renal coccidiosis Mortality has occurred in

are of asymptomatic birds free-ranging wild geese,
Swan: E. christianseni or birds that show minor eider ducklings, and double-
physiological or pathological crested cormorants.
changes due to the parasite.
Disease in domestic geese
is usually acute, lasts only
2–3 days, and can kill large
segments of the flock.
Riemerella Riemerella anatipestifer Ducks of any age and Ocular and nasal discharges, Worldwide, probably the most
anatipestifer turkeys. Other waterfowl, mild sneezing, tremors of the economically important infectious
chickens and pheasants head and neck, ataxia and coma. disease of farm ducks.
New duck disease, may also be affected. Lesions of septicemia, mostly
duck septicemia fibrinous exudate on serosal Prevention with good biosecurity,
2-7 week-old ducks are surfaces. Mortality may vary husbandry and hygiene, control
most susceptible from 2 to 75% in young ducks. with depopulation and disinfection
of the infected premises.
Various antibiotics have been
shown to be effective. Vaccines
available in some countries.
Sarcocystis Sarcocystis rileyi Macroscopic form observed No a cause of mortality but heavy Common parasitic infection
in dabbling ducks, less infection may cause muscle of some species of waterfowl
frequent in other species of loss and be quite debilitating. in North America.
ducks, geese and swans.
Most often adult birds. Multiple cream-colored, Sarcocystis is destroyed by
cylindrical cysts resembling rice cooking. Affected carcasses
grains run parallel to the muscle should therefore be discarded not
fibers of various muscles. only because of the unaesthetic
appearance of the muscles but

because very little is known about
the health hazard to humans.
233
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234

Disease(s)
West Nile virus Flavivirus Ducks, geese Death in wild birds. Brain Reported in New York 1999,
hemorrhages, splenitis, Israel and Romania. Commercial
splenomegaly, nephritis. geese in Canada 2002, ~25%
mortality in goslings. Bird to bird
transmission reported but mostly
transmitted by mosquitoes.
Wet pox Poxvirus Most birds, including poultry. 1-5 mm yellow-gray plaques Skin lesions often on face,
in mucosa of mouth, pharynx, wattles, eyelids, comb, feet, legs,
or esophagus. Less often in ear lobes, caruncle, snood.

sinuses or conjunctiva.
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Name of
Disease(s)
Aspergillosis Usually Aspergillus Young birds are more Respiratory signs usually Yellow mycotic nodules may be
(Brooder fumigatus susceptible than adults precede CNS signs and observed in the lungs, airsacs,
Pneumonia) predominate. A minority tracheal bifurcation, sinuses, and
develop CNS involvement. occasionally in the brain or eyes.
Avian botulism Ingestion of toxin Most species of birds Paralytic, often fatal disease, Important environmental factors
produced by the characterized by ascending (failure to pick up dead birds
(Limberneck) bacterium Clostridium paresis and paralysis. in the flight pens) contribute to
botulinum the initiation of avian botulism
No gross lesions outbreaks then perpetuated
by the bird-maggot cycle.
Avian tuberculosis Mycobacterium avium All avian species Round nodules (granulomas) Usually seen in older birds. Can
attached to serosa of gut. be a problem is established in
Focal granulomas in many captive flocks. Causative bacilli
other organs. Extreme readily demonstrated in acid-
emaciation in advanced cases. fast-stained smears of lesions.
Capillaria annulata Capillaria annulata Pheasants, partridges, Severe ingluvitis seen in Earthworms also serve
quail, turkeys, grouse, oesophagus and crop. as intermediate hosts.
(Crop threadworm) guinea fowl Drooling and weight loss. Scrapings from crop mucosa
examined microscopically
Can also cause mortality. show characteristic ova.
Colibacillosis Escherichia coli All avian species Highly variable mortality A common disease secondary
are susceptible. and morbidity may be to stress, poor environmental
present. Septicemia and conditions and previous exposure
Written by Eva Wallner-Pendleton
polyserositis are common. to other infectious diseases of

the respiratory and GI tract.
Blackhead Histomonas Turkeys, chickens, Yellow diarrhea and Frequent worming to prevent
DISEASES OF THE GAMEBIRDS
meleagridis pheasants, chukar biliverdiurea, weight loss. heavy cecal worm infections.
partridges, quail Severe necrotic typhilitis Histostat can also be used
and peafowl and hepatitis seen. preventatively in the feed.
Eastern equine Alphaviruses Pheasants, partridges, Circling or staggering followed Microscopic lesions only.
encephalomyelitis turkeys, Pekin ducks, quail. by paralysis. Perhaps blindness Transmitted by mosquitoes.
in recovered birds. Often high
morbidity and mortality.
235
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236

Disease(s)
Fowl cholera Pasteurella multocida Water birds, domestic Sick birds appear lethargic or Acute infections are common and
(Avian cholera poultry, game birds. drowsy. Abnormal positions may result in rapid death and high
or avian of head and neck. Ataxia, mortality. Chronic infections with
pasteurellosis) loss of equilibrium. lower mortality can also occur.
Lesions of septicemia
(hemorrhages and petechiation
on serosal surfaces) and
multiple foci of necrosis in liver.
Birds are often in good body

condition at time of death.
Leukocytozoonosis Leukocytozoon sp. Turkeys, ducks, geese, Pallor, splenomegaly, Outbreaks correspond with hot
guinea fowl, chickens. liver degeneration and months when simulid flies and
hypertrophy in some birds. culicoid midges are numerous;
Leukocytozoons visible in these flies breed in and along water
blood smears. Schizonts courses. Surviving birds (wild or
often in liver, spleen, brain. domesticated) often act as carriers.
Signs in birds related to anemia.
Marble Spleen Siadenovirus (Type Pheasants, can be Sudden death in older No commercial vaccines for
Disease II adenovirus) propagated in turkey birds, usually 12 weeks of pheasants are available.
poults, guinea fowl age to adult. Depression,
acute pulmonary congestion
and edema, enlarged,
mottled spleens.
Mycoplasma Mycoplasma Chickens, turkeys, Sinusitis, upper and lower Common in situations where
gallisepticum (MG) gallisepticum gamebirds respiratory disease observed. gamebirds are raised in close
proximity to infected poultry.
Infectious sinusitis However, the significance of
other mycoplasmas found in
gamebirds is poorly understood.
Pox Infections Avipox virus Most birds, including Skin lesions observed on Quailpox virus vaccine available
game birds the featherless regions of for quail and sometimes
the head, neck, and feet. used in other poultry.
1-5 mm yellow-gray plaques

in mucosa of mouth, pharynx,
trachea or esophagus.
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Name of
Disease(s)
Quail Bronchitis Fowl adenovirus-1 Bobwhite quail, Acute respiratory illness Secondary bacterial infections with
(Serotype I Japanese quail (“snicking”, conjunctivitis, E. coli common. Older birds may
adenovirus) coughing, sinusitis). High be carriers. No treatment available,
mortality seen in 1-3 week but maternal antibodies from
old quail. Less severe recovered breeders may reduce
illness in older birds. severity of infection in progeny.
Increased mucus and
thickened tracheal mucosa.
Pneumonia, airsacculitis,
hepatomegaly, splenomegaly.
Syngamus trachea Syngamus trachea Pheasants, turkey poults Coughing, gasping, Found in birds raised outdoors
infections and young chickens are weight loss are seen. when access to infected
the most susceptible intermediate hosts (such as
(gapeworms) Characteristic red worms are earthworms) is available,
seen in the tracheal lumen. especially after heavy rains
bring them to the surface.
West Nile virus Flavivirus Observed in grouse and Morbidity and mortality Reported in New York in 1999,
ornamental pheasants, variable. Brain hemorrhages, Israel and Romania. Bird to bird
splenitis, splenomegaly, transmission reported but mostly
Corvidae and birds of prey. enteritis, nephritis. transmitted by mosquitoes.
237
APPENDIX
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Revised by Drs Linnea J. Newman and Jean E. Sander
DISEASES OF CHICKENS AND TURKEYS CORRELATED WITH AGE
By knowing the species affected, salient clinical feature, and age of the flock, it is often possible to make a list of
potential differential diagnoses. In the following table, some of the more common diseases are presented by age and
clinical problem. Of course, this will not be absolute but can be used as a guide.
BROILERS, PULLETS, LAYERS
Typical losses to 7 weeks of age are 4-5%. Losses in the first 2 weeks account for 30-50% of total mortality.
A. BROODING PERIOD (0-2 weeks)
2. Mortality/ Poor Growth
A. Improper incubation conditions - small, weak hatchlings or increased susceptibility to infection

B. Navel and yolk sac infection (Salmonella, Escherichia coli, Staphylococcus, Proteus, etc.)
C. Polycystic Enteritis or Runting and Stunting Syndrome (Malabsorption Syndrome)
D. Starveout/dehydration — floor temperature, water management
E. Vaccine contamination
F. Baby chick nephropathy
2. Respiratory Disease
A. Aspergillosis (Brooder Pneumonia)

B. Vaccine Problems —Respiratory reaction
3. Musculoskeletal Disease
A. Rickets
B. Splay Leg
4. CNS Disease
A. Avian Encephalomyelitis
B. Encephalomalacia (Vitamin E Deficiency)
C. Hypoglycemia (Spiking Mortality)
D. Poor vaccine placement (in ovo Pox, MDV)
5. Eye Disease
A. Keratoconjunctivitis (Ammonia Burn)

B. Mycotic Keratoconjunctivitis
B. GROWING PERIOD (2-8 weeks)
1. Mortality
A. Ascites
B. Aspergillosis
C. Chicken Infectious Anemia
D. Classic Infectious Bursal Disease
E. Coccidiosis
F. Gangrenous Dermatitis
G. Histomoniasis (Blackhead)
H. Inclusion Body Hepatitis
I. Marek's Disease
J. Necrotic Enteritis
K. Ulcerative Enteritis
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A. Avian Influenza
B. Avian Metapneumovirus (Swollen Head Syndrome)
C. Colibacillosis
D. Infectious Bronchitis
E. Infectious Laryngotracheitis
F. Mycoplasmosis
G. Newcastle Disease
3. Muskoloskeletal Disease
A. Angular Bone Deformity (Valgus-Varus Deformities)

B. Infectious Synovitis
C. Marek’s Disease
D. Osteomyelitis (e.g. Staphylococcosis, Enterococcus cecorum)
E. Pododermatitis
F. Rickets
G. Septic arthritides (e.g. Staphylococcosis, Escherichia coli, Enterococcus cecorum)
H. Spondylitis (Enterococcus cecorum)
I. Spondylolisthesis (Kinky Back)
J. Tibial Dyschondroplasia
K. Toxicity (Ionophore/3-Nitro, Botulism)
L. Viral Arthritis
4. CNS Disease
A. Arbovirus infections (Eastern equine encephalitis virus)

B. Avian Encephalomyelitis
C. Encephalomalacia (Vitamin E deficiency)
D. Marek’s Disease
E. Newcastle Disease
5. Skin Disease
A. Exudative Diathesis (Vitamin E deficiency)

B. Fowl Pox
C. Gangrenous Dermatitis
D. Marek’s Disease (Skin Leukosis)
6. Other
A. Candidiasis (Crop Mycosis)

B. Cellulitis
C. Immunosuppression - IBD, CIA
D. Intestinal Parasites (Capillaria, Roundworms, Tapeworms, etc.)
E. Mycotoxin
C. PULLET PERIOD (8-20 weeks)
A. Avian Influenza
B. Infectious Bronchitis
C. Infectious Coryza
D. Infectious Laryngotracheitis
E. Mycoplasmosis
F. Newcastle Disease

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2. Neoplastic Disease
A. Lymphoid Leukosis
B. Marek's Disease
3. Systemic Diseases
A. Fowl Cholera (Pasteurellosis)

B. Colibacillosis
4. Intestinal Disease
A. Coccidiosis
B. Necrotic Enteritis
D. LAYERS (>20 weeks)
A. Avian Influenza
B. Infectious Bronchitis
C. Infectious Coryza
D. Infectious Laryngotracheitis
E. Mycoplasmosis
2. Egg Production Drop
A. Avian Encephalomyelitis
B. Avian Influenza
C. Hepatitis E Virus
D. Infectious Bronchitis
E. Infectious Coryza
F. Mismanagement (lights, water, nutrition, etc.)
G. Mycoplasmosis (M. gallisepticum)
H. Newcastle Disease
3. Neoplastic Disease
A. Lymphoid Leukosis
B. Marek’s Disease
C. Various other tumors (Carcinoma, Sarcoma)
4. CNS Disease
A. Fowl Cholera (Pasteurellosis)

B. Newcastle Disease
5. Cage Layer Fatigue
6. Cannibalism
7. Fatty Liver Hemorrhagic Syndrome
8. Fowl Mites
9. Hysteria
10. Parasitism (Capillariasis, Heterakis, Roundworms, etc.)
11. Salpingitis/Peritonitis
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12. Uterovaginal Prolapse
E. SPORADIC DISEASES
1. Arbovirus Infections
2. Avian Tuberculosis
3. Botulism
4. Other Parasitic Diseases
5. Salmonellosis (Pullorum,Typhoid)
6. Streptococcosis
TURKEYS
A. EARLY BROODING PERIOD (0-3 weeks)
1. Mortality/Poor Growth
A. Candidiasis
B. Cannibalism
C. Coccidiosis
D. Cryptosporidiosis
E. Omphalitis (Salmonella, S. arizonae, E. coli, Proteus, etc.)
F. Mismanagement (Starveout, dehydration, poor beak trimming)
G. Poult Enteritis andMortality Syndrome
H. Poult malabsorption / runting-stunting syndrome
I. Turkey Viral Hepatitis
A. Aspergillosis (Brooder Pneumonia)

B. Turkey Coryza (Bordetellosis)
A. Rickets
B. Splay Leg
C. Staphylococcosis
D. Tibial Rotation
4. CNS Disease
A. Arizonosis
B. Avian Encephalomyelitis
C. Encephalomalacia (Vitamin E Deficiency)
D. Mycotic Encephalitis (Aspergillus, Ochroconis)
5. Eye Disease
A. Ammonia Burns
B. Arizonosis
C. Injuries
D. Mycotic Keratoconjunctivitis (Aspergillus)

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B. LATE BROODING/EARLY GROWING PERIOD (3-12 weeks)
1. Mortality
A. Aortic Rupture (Dissecting Aneurysm)

B. Hemorrhagic Enteritis
C. Histomoniasis (Blackhead)
D. Sudden Death Syndrome of turkeys / Perirenal Hemorrhage Syndrome
E. Leucocytozoonosis
F. Necrotic Enteritis
G. Round Heart Disease (Dilated Cardiomyopathy)
H. Ulcerative Enteritis
A. Avian Influenza
B. Bordetellosis (Turkey Coryza)
C. Colibacillosis
D. Fowl Cholera (Pasteurellosis)
E. Mycoplasmosis (MM, MS, MG)
G. Avian Metapneumovirus infection (Turkey rhinotracheitis)
A. Bacterial Arthritides (Staphylococcus, Escherichia coli)

B. Contact dermatitis of foot pads
C. Spondylolisthesis ("Kinky Back")
4. Other
A. Mycotoxins
B. Roundworms
C. FINISHING PERIOD (>12 weeks-market)
1. Mortality
A. Aortic Rupture (Dissecting Aneurysm)

B. Cannibalism
C. Erysipelas
2. Respiratory Diseases
A. Aspergillosis
B. Avian Influenza
C. Chlamydiosis
D. Fowl Cholera (Pasteurellosis)
E. Newcastle Disease
F. Ornithobacterium infection (ORT)
A. Angular Bone Deformity (Valgus-Varus Deformities)

B. Bacterial Arthritides (Staphylococcus, E. coli, Erysipelas, Pasteurella multocida)
C. Osteomyelitis
D. Scoliosis
E. Tibial Dyschondroplasia
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4. Other
A. Breast Buttons/Blisters
B. External Parasites (Mites, Lice)
C. Internal Parasites (Round Worms, Cecal Worms)
D. Pendulous Crop
E. Turkey Pox
D. BREEDERS (>30 weeks). Diseases of the finishing period can also occur during the laying period.
1. Mortality
A. Aspergillosis
B. Fowl Cholera (Pasteurellosis)
C. Salpingitis/Peritonitis
2. Neoplasia
A. Lymphoproliferative Disease
B. Reticuloendotheliosis
3. Egg Production Drop
A. Arbovirus infections (EEEV, WEEV, HJV)

B. Avian Influenza
C. Avian Metapneumovirus infection
D. Mismanagement (lights, water, nutrition, etc.)
E. Mycoplasmosis
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DISEASES WITH LESIONS IN THE CARDIOVASCULAR SYSTEMS
Name of Disease(s) Etiology Species Affected Lesions Comments
Ascites Metabolic; related to Young, fast- growing Enlarged heart. Ascites. Enlarged or Exacerbated by low oxygen conditions at hatch
rapid growth rate and chickens (males > cirrhotic liver. Fibrin exudation in severe or brooding, high altitude, heavy dust, lung
high yield in broiler females). cases. pathology. Controlled via lighting programs to
chickens. slow growth.
Chlamydiosis Chlamydophila psittaci Turkeys, pigeons, ducks, Pericarditis, often adhesive. Often with airsacculitis, fibrinous perihepatitis,
cage and wild birds. splenomegaly, and hepatomegaly.
Colibacillosis Escherichia coli Turkeys, chickens, Pericarditis, often adhesive. Often with airsacculitis, fibrinous perihepatitis.
septicemia. commercial ducks.
Dissecting aneurysm Unknown. Non- Turkeys. Occasionally, Ruptured artery, usually abdominal aorta. Sudden deaths in rapidly growing, highly
(aortic rupture) infectious. A strong chickens. Rarely, aortic arch. Extensive internal conditioned birds. Losses can be extensive.
nutritional influence, hemorrhage. Usually in males.
especially copper
metabolism.
Endocarditis Various bacteria: Chickens and turkeys. Yellow, irregular masses on the heart Low incidence.
Erysipelas, Pasteurella, valves.
Staphylococcus,
Streptococcus.
Marek’s disease Herpesvirus Chickens Focal or multifocal tumors in the May be associated with tumors in other organ
myocardium. systems.
Mycoplasma M. gallisepticum Turkeys, chickens, other Pericarditis, often adhesive. Often with airsacculitis, fibrinous perihepatitis.
gallisepticum infection poultry, birds.
Pullorum disease, fowl Salmonella Pullorum, Chickens, turkeys, and Nodules in myocardium. Adhesive Oophoritis or orchitis may occur in some adult
typhoid, possibly S. Gallinarum, geese. pericarditis. birds. Enteric or septicemic diseases with
paratyphoid other salmonellae. diarrhea in young birds.
Round heart disease Possibly toxic agents in Chickens and turkeys. A greatly enlarged, round heart. Ascites. Uncommon in chickens. Most outbreaks
turkeys (antitrypsin and Fibrin exudation in severe cases. associated with built-up litter. Variable
furazolidone implicated). mortality. Potentiated by furazolidone treatment
in turkeys.
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DISEASES WITH SIGNS SUGGESTIVE OF CNS DISEASEA
Aspergillosis Usually Aspergillus Usually young chicks Various CNS signs. Respiratory signs Yellow mycotic nodules often grossly visible in
fumigatus. and poults or captive usually precede CNS signs and brain. Lesions of aspergillosis in lungs or air
game birds. predominate. A minority develop CNS sacs, perhaps in conjunctival sac or globes of
involvement. eyes.
Avian Hepatovirus Chicks, young poults, Tremors of head and neck and legs. Microscopic lesions in the CNS. Survivors often
encephalomyelitis (Picornaviridae) and pheasants. Paresis progressing to paralysis and develop cataracts. Invert the birds to accent the
(epidemic tremor) prostration. tremors for diagnosis.
Bacterial encephalitis Salmonella, S. arizonae, Turkey poults, chicks. Various CNS signs. Ophthalmitis and Exudate grossly visible in meninges and
paratyphoid species, omphalitis often present in some of the ventricles. Confirm by culture.
Escherichia coli. poults.
Botulism Preformed toxin of Usually chickens Paresis progressing to paralysis of legs, No gross or microscopic lesions of value.
Clostridium botulinum. neck, wings, nictitating membrane. Loose Perhaps putrid feed or maggots in crop.
feathers.
Encephalomalacia, Vitamin E deficiency Chicks (usually less Ataxia, falling and flying over backwards, Hemorrhage and malacia of cerebellum often
(Crazy chick disease) than 8 weeks old), loss of balance; prostration with legs grossly visible. Confirm by microscopy.
turkeys (usually 2-4 outstretched, toes flexed, and head and Perhaps exudative diathesis along ventrum or
weeks old). neck back. muscle necrosis.
Enterococcus cecorum Enterococcus cecorum Chickens Incoordination, abnormal gait Associated with spondylitis, femoral head
necrosis, and osteomyelitis in broiler chicken
and broiler breeder flocks.
Equine Alphaviruses Pheasants, partridges, Circling or staggering followed by Microscopic lesions only. Transmitted by
Encephalomyelitis turkeys, Pekin ducks, paralysis. Perhaps blindness in recovered mosquitoes.
Virus quails, chickens. birds. Often high morbidity and
mortality.
Fowl cholera Pasteurella multocida Turkeys, chickens, Abnormal positions of head and neck. A localized form of chronic fowl cholera.
perhaps other species. Ataxia, loss of equilibrium. May/may not accompany acute outbreak.
Lesions may be present in cranial bones or
inner ear.
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DISEASES WITH SIGNS SUGGESTIVE OF CNS DISEASEA
Hypoglycemia-spiking Unknown. Arenavirus, Young chicks and Ataxia and death. Dead often found Sudden, high mortality that may last 1- 2 days.
mortality syndrome rotavirus, poults (< 3 weeks). ventrally recumbent with head and neck Often associated with a stress event such as
(HSMS) thiamine deficiency, outstretched. movement from brood chamber to whole
mycotoxins have been house. Capsular or parenchymal liver
implicated. hemorrhage may be present. Blood sugar levels
are very low in affected compared to normal

birds.
Marek’s disease Alpha herpesvirus Chickens usually 6•20 Paresis progressing to paralysis of a leg or Microscopically there are infiltrating neoplastic
weeks old. wing. Often one leg is held forward and cells in affected nerve trunks and the CNS.
one leg is held backward in the Grossly, lesions may be visible in affected nerve
recumbent bird. trunks.
Newcastle disease Paramyxovirus Usually chickens but In chicks CNS signs, usually proceeded Microscopic lesions are present and helpful in
most birds susceptible. by respiratory signs. Progressive paresis diagnosis. Only a small part of birds with
followed by paralysis and death. respiratory signs have CNS signs.
Ochroconosis Ochroconis gallopava Turkey poults, chicks. Incoordination, tremors, torticollis, Focal gross brain lesions, often pulmonary
(Previously known as (fungus) (previously paralysis, perhaps ocular opacities. nodules or airsacculitis. Fungus often in
Dactylariosis) known as Dactylaria sawdust litter.
gallopava)
Pox vaccination Fowl pox vaccine Chickens < 2 weeks. Ataxia, mild extensor rigidity. Head In ovo administration of pox vaccine; errors in
reaction Low incidence for 5•7 drawn back, wings drawn up, tiptoe gait. subcutaneous injection. May relate to vaccine
days. titer.
A
Signs suggestive of CNS disease in birds include ataxia, paralysis, circling, trembling, twisting of the head and neck, falling over backward, and loss of
balance. Any combination of CNS signs may occur.
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DISEASE WITH LESIONS IN THE MOUTH, PHARYNX, ESOPHAGUS, CROP, PROVENTRICULUS, GIZZARD
Candidiasis Candida albicans Poultry, game birds, Gray, thin, pseudomembranous patches Often secondary to parasitism, malnutrition,
(crop mycosis) perhaps other birds. on the mucosa. Little inflammation. poor sanitation, impaction, antibiotic usage,
other disease. Affects any or all organs listed in
title.
Capillariasis Capillaria contorta, Chickens, turkeys, Worms sewn into inflamed, thickened In the esophagus and crop. Common in game
C. annulata game birds. mucosa. birds. Scrapings usually necessary for
identification.
Duck plague Herpesvirus Ducks, geese, swans. Hemorrhage and necrosis of the Intranuclear inclusions produced in infected
(Duck virus enteritis) esophageal and cloacal tissue. Liver has tissue.
petechial hemorrhages.
Mycotoxicosis Trichothecenes All poultry Oral ulcerations Produced by Fusarium species of mold.
Pendulous crop If epizootic, influenced Turkeys, chickens, Crop and esophagus enlarged, perhaps Secondary mycosis often present in atonic crop
by coarse roughage; or perhaps others. impacted. or esophagus. Sporadic cases sometimes from
by genetics in turkeys. vagal paralysis.
Trichomoniasis Trichomonas gallinae Raptors, doves, Raised conical masses in mucosa of Many trichomonads in oral fluids. Lesions
(canker in pigeons; pigeons, turkeys, mouth, pharynx, esophagus, crop. sometimes in proventriculus. Also in the liver
frounce in falcons) chickens. of pigeons and some raptors. Lesions often
invasive.
Vitamin A deficiency Inadequate Chickens, turkeys. Pustule-like lesions in esophagus, Sticky eyelids and ataxia often the only gross
vitamin A perhaps mouth and pharynx. Variable lesions and signs in young birds. Squamous
rhinitis, sinusitis, conjunctivitis. Perhaps metaplasia of columnar epithelium in
excessive urates in urinary tract or cloaca. esophageal mucous glands and nasal
epithelium.
Wet pox Avipoxvirus Most birds, including 1•5 mm yellow-gray plaques in mucosa Skin lesions often on face, wattles, eyelids,
poultry. of mouth, pharynx, or esophagus. Less comb, feet, legs, ear lobes, caruncle, snood.
often in sinuses or conjunctiva.
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DISEASES WITH LESIONS IN THE INTESTINE
Arizonosis Salmonella arizona Poults, chicks. Enteritis, unabsorbed yolk. Large mottled Poults often unthrifty and with excessive
liver, perhaps peritonitis or intraocular mortality. Perhaps diarrhea.
turbidity.
Avian Tuberculosis Mycobacterium avium Chickens, most other Round nodules (granulomas) attached to Usually seen in old chickens kept beyond one
poultry and birds. serosa of gut. Focal granulomas in many laying season. Causative bacilli readily
other organs. Extreme emaciation in demonstrated in acid- fast-stained smears of
advanced cases. lesions.
Coccidiosis Many species of Eimeria Chickens, turkeys, Enteritis of variable severity and location. Five major pathogens for chickens are listed.
ducks, geese, perhaps in E. acervulina – upper small intestine. E. For details see text. Coccidiosis often occurs
most birds. necatrix and E. maxima ••mid-small concurrently with other diseases. Uncommon
intestine. E. tenella ••ceca. E. brunetti – in ducks, geese.
posterior gut.
Colibacillosis Escherichia coli Chickens, turkeys. Enteritis, omphalitis, salpingitis, Many syndromes identified. Seen in very young
peritonitis, arthritis, and and in adults. Three serotypes of the agent
panophthalmitis are frequent lesions. In account for most outbreaks. Often a secondary
respiratory disease often associated with infection.
pericarditis, perihepatitis, and
airsacculitis. See notes.
Coligranuloma A mucoid coliform Chickens, turkeys. Granulomas along cecum, duodenum, in Resembles avian tuberculosis but no acid-fast
mesentery and liver. bacteria in lesions. Must be differentiated from
avian tuberculosis. An uncommon disease.
Duck virus enteritis Herpesvirus Wild or domestic Widespread hemorrhages, severe Epizootic losses in waterfowl are suggestive.
(Duck plague) ducks, geese, swans. enteritis. Perhaps elevated plaques in Typical lesions and inclusion bodies helpful in
esophagus, ceca, cloaca or bursa. diagnosis. An exotic, reportable disease.
lymphoid rings or discs of gut.
Fowl typhoid Salmonella gallinarum Chickens, turkeys, In recently hatched, same as pullorum Closely resembles pullorum in recently hatched
occasionally other (below). In older birds, pale cadaver, chicks and poults but mortality persists into
poultry. marked enteritis, splenomegaly, gray foci adulthood. Diarrhea and anemia in older birds.
in liver, bile-stained (bronze) liver.
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Hemorrhagic enteritis Adenovirus Turkeys often 6-12 Severe enteritis in small intestine with Bloody feces often noted. Mortality may be
of turkeys (HE) (Siadenovirus) weeks old. much blood in the gut. Spleen enlarged high. A similar virus causes marble spleen
and mottled early in the course. disease in pheasants. Subclinical HE may be
associated with immunosuppression and
secondary Escherichia coli infection.
Hexamitiasis (new Spironucleus meleagridis. Turkey, poults, game Catarrhal enteritis in upper half of small Escherichia coli infection birds have watery
name Spironucleosis) In pigeons S. columbae. birds, pigeons. intestine. Local bulbous dilations in diarrhea. They often die in convulsions. Closely
affected gut. Spironucleus in crypts of resembles paratyphoid or transmissible
Lieberkuhn. enteritis.
Histomoniasis Histomonas meleagridis Turkey poults, game Ceca swollen and usually with cecal Typical lesions in ceca and liver are
(blackhead) birds, chickens, cores. Circular or oval recessed lesions in pathognomonic.
replacement pullets. liver.
Infectious bursal Avibirnavirus Chickens typically 3•6 Marked inflammation of the bursa of Diarrhea, incoordination, dehydration, vent
disease weeks old. Fabricius, which is swollen early but picking are usual signs. Course is about 1 week.
atrophied later. Enlarged spleen. Immune system damaged. May be followed by
Hemorrhages common in heavy muscles. secondary infection such as inclusion body
hepatitis, gangrenous dermatitis, ulcerative or
necrotic enteritis, etc…
Internal parasitism Ascarid Many birds, including Parasites usually visible in appropriate Microscopic exam of scrapings necessary to
tapeworms, poultry. location. Variable degree of enteritis. identify Capillaria.
cecal worms, Emaciation may be marked.
Capillaria spp.
Marek’s disease Alpha herpesvirus Chickens. Diffuse neoplasia involving an area of Focal of diffuse neoplasia usually apparent in
gut. other visceral organs, e.g., liver, spleen, gonads,
kidneys, lungs.
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Necrotic Enteritis Clostridium perfringens Chickens. Focal or diffuse necrosis of intestinal Most common in flocks raised without
mucosa, particularly the ileum. antibiotics, in the presence of coccidiosis,
intestinal irritants such as non-starch
polysaccharides (wheat, barley, rye diet),
biogenic amines.
Nonspecific enteritis Many infectious agents. Poultry and other birds. Enteritis accompanies many infectious Other diseases that may have enteritis include:
diseases that have lesions of greater cholera, erysipelas, salmonellosis, vibrionic
diagnostic value in other systems. hepatitis, spirochetosis, botulism, aflatoxicosis,
influenza, candidiasis, and others.
Paratyphoid Salmonella sp. (about 20 Poults, chicks, other Severe enteritis. Often mucosal plaques Usually in birds less than 8 weeks old but
major species). young birds. Sometimes and/or cheesy cecal cores. Occasionally occasionally in older birds. Occurs frequently in
in adult poultry. the other lesions described for pullorum young turkey poults. Interspecies transmission
disease may occur. possible.
Pullorum disease Salmonella Pullorum Chickens, turkeys, Enteritis, dehydration, unabsorbed yolk. Typically epizootic in birds up to 4 weeks old.
occasionally other Nodules in lungs, heart, or gizzard. Begins shortly after hatching. White adherent
poultry. Perhaps mucosal plaques, cecal cores, diarrhea common. Persists in some adults as
and focal necrotic hepatitis. May present oophoritis, orchitis, or myocarditis.
as synovitis in broilers.
Turkey coronavirus Coronavirus Turkeys, especially Marked mucoid enteritis, dehydration. Diarrhea present. Mortality may be very high
enteritis poults. with young poults. Less severe in older turkeys.
Ulcerative enteritis Clostridium colinum Captive game birds, Acute enteritis early. Usually many deep A common disease of game birds. Resembles
(quail disease) turkeys, chickens. ulcers along the intestine. Enlarged coccidiosis in chickens. Often secondary in
spleen. Focal and/or diffuse yellow areas chickens.
in liver.
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DISEASES WITH LESIONS IN LIVERA
Aflatoxicosis Toxin usually from Poults, pheasants, Liver pale and mottled and with bile duct Toxin in feeds, especially peanut meal; in
(mycotoxicosis) Aspergillus flavus. chicks, ducklings. hyperplasia. Catarrhal enteritis. spilled feed in litter; in litter alone. Signs often
include ataxia, convulsions, opisthotonos. The
only signs may be unthriftiness, poor weight
gain, low production.
Avian Tuberculosis Mycobacterium avium Usually in chickens. Focal granulomas in the liver. Lesions Usually encountered in older chickens – those
Also, other poultry and often are numerous. Nodules over 1 year. Extreme emaciation is the
wild birds. (granulomas) along the periphery of the hallmark of tuberculosis.
gut. Lesions in most organs and marrow
in advanced cases. Emaciation.
Duck Hepatitis Virus type Picornavirus Ducklings, typically less Liver swollen and with many Signs: acute onset, short course, high morbidity
I (DHV-1) than 4 weeks old. hemorrhages and mortality. Typical lesions in young
ducklings almost pathognomonic.
Duck Hepatitis Virus type Astrovirus Ducklings up to 5 Liver swollen and with many Death within 1 to 2 hours after onset of clinical
3 (DHV-3) weeks of age hemorrhages signs. Convulsions, opisthotonos. Mortality
rarely > 30% but high morbidity.
Fowl cholera Pasteurella multocida Poultry, wild birds, Diffuse streaking of the liver in acute Focal hepatic lesions closely resemble those of
especially waterfowl. cases. Later there may be 1-3-mm focal salmonellosis, tuberculosis, and listeriosis. Fowl
areas of hepatic necrosis. cholera often septicemic.
Histomoniasis Histomonas Turkeys, game birds, Recessed round to oval focal hepatic Classical hepatic and cecal lesions together are
(Blackhead) meleagridis chickens. lesions up to 2.0 cm. Typhlitis pathognomonic. Frequently occurs in turkeys
with/without cecal cores. raised with or after chickens. Agent transmitted
in ova of cecal worms and in earthworms.
Inclusion body hepatitis Adenovirus Chickens typically 5-8 Yellow-tan hepatic areas with Often follows infectious bursal disease, which
weeks old. hemorrhages. Intranuclear inclusions. damages immune system.
Perhaps icterus. Hemorrhages at many
sites (skin, muscles, subserosa).
A
This table contains only diseases that are more frequently encountered, are more significant economically, or have hepatic lesions clearly of diagnostic
value. Many other avian diseases may have hepatic lesions, e.g., psittacosis, Arizona (paracolon) infection, turkey viral hepatitis, synovitis, Riemerella
anatipestifer infection, staphylococcosis, and listeriosis.
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DISEASES WITH LESIONS IN LIVERA
Leukosis complex Retroviruses Chickens, perhaps Focal or diffuse neoplastic lesions in the If epizootic in chickens less than 5 months old
other species. liver. Other organs frequently affected the disease may be Marek’s disease. In older
with focal or diffuse neoplastic lesions. birds, probably lymphoid leukosis. See section
on viral tumors.
Salmonellosis, Salmonella Pullorum, Chickens and turkeys. Sometimes 1-3 mm focal areas of hepatic Salmonella infections predominate in the
Pullorum disease, S. Gallinarum, Many kinds of poultry, necrosis. Often splenomegaly. Enteritis, young. Many are transmitted through the egg.
fowl typhoid, paratyphoid other Salmonella. birds, and mammals sometimes with raised plaques in the Interspecies transmission possible with
have paratyphoid. mucosa and with cheesy plugs in the gut paratyphoid. Salmonella infections often are
or cecum. May be septicemic with few septicemic.
lesions, especially in the very young.
Ulcerative enteritis Clostridium colinum Captive game birds, Focal and/or diffuse yellow areas in the A common disease of captive game birds.
turkeys, chickens. liver. Deep ulcers scattered throughout Increasing in poults and chickens.
the intestine.
Vibrionic hepatitis Campylobacter fetus Chickens, usually well Asterisk or cauliflowerlike foci of hepatic Only about 10% of affected birds have hepatic
spp. jejuni started or adults. necrosis. Sometimes hemorrhages, lesions. Campylobacter often cultured from bile.
subcapsular hematocyst, ascites, or
hydropericardium.
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DISEASES WITH LESIONS IN HEMOPOIETIC SYSTEM
Chicken infectious anemia Gyrovirus Chickens (2-4 weeks Anemia, thymic atrophy. Pale pink to Often associated with gangrenous dermatitis.
(CIA) (Circoviridae) old). yellow bone marrow. Particularly on wings (blue wing disease).
Course is usually about 1 week. Affected
broilers can be traced to a CIA-shedding
breeder flock.
Duck virus enteritis (Duck Herpesvirus Wild or domestic Widespread hemorrhages. Severe Epizootic losses in waterfowl are suggestive.
plague) ducks, geese, swans. enteritis. Perhaps elevated plaques in Typical lesions and inclusion bodies helpful in
esophagus, ceca, rectum, cloaca, or bursa. diagnosis. An important reportable disease.
lymphoid rings (discs) of gut.
Infectious bursal disease Avibirnavirus Chickens typically 3-6 Marked inflammation of the bursa of Diarrhea, incoordination, dehydration, vent
weeks old. Fabricius, which is swollen early but picking are usual signs. Course is about 1 week.
atrophied later. Enlarged spleen. Immune system damaged. May be followed by
Hemorrhages common in heavy muscles. inclusion body hepatitis or gangrenous
dermatitis.
Leukocytozoonosis Leukocytozoon sp. Turkeys, ducks, geese, Pallor, splenomegaly, liver degeneration Outbreaks correspond with hot months when
guinea fowl, chickens. and hypertrophy in some birds. simulid flies and culicoid midges are numerous;
Leukocytozoons visible in blood smears. these flies breed in and along water courses.
Schizonts often in liver, spleen, brain. Surviving birds (wild or domesticated) often
act as carriers. Signs in birds related to anemia.
Lymphoid leukosis Retroviruses Chickens, perhaps Internal neoplasms. Neoplastic May resemble Marek’s disease. Usually
other species. lymphoblastic cells in bursa of Fabricius observed in chickens over 4 months old.
and many other organs. Neoplasia frequently in liver, spleen, kidneys;
nodular tumors in bursa of Fabricius.
Marek’s disease Alpha herpesvirus Chickens, perhaps Internal neoplasms. Neoplastic Often epizootic in chickens 6-20 weeks old.
other species. pleomorphic lymphoid cells infiltrate, Persists in older birds. May closely resemble
CNS, spleen, liver, kidney, nerve trunks, lymphoid leukosis. Bursa of Fabricius seldom
iris, ovary, and many other organs. neoplastic.
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DISEASES WITH LESIONS IN THE MUSCULOSKELETAL SYSTEM
Biotin deficiency Biotin deficiency Turkey poults. Large twisted hocks and bowed shanks. Lesions include hyperkeratotic skin at corners
Hyperkeratosis of skin on soles of feet of mouth and on eyelids.
and toes.
Cage layer fatigue Controversial etiology. Chickens (caged layers). Bones that easily break and splinter. Leg weakness or inability to stand. May recover
(osteoporosis, adult Possibly low Fractures, sometimes vertebral. if promptly removed and kept on floor.
rickets) phosphorus, low Depletion of bone mineral.
calcium, or imbalance.
Caging a factor.
Contact dermatitis of Trauma with secondary Chickens, turkeys, Swollen foot or toepads often with open Usually sporadic. Concrete floors without litter
foot pads bacterial infection of falcons, other birds. lesions. May involve joints or toes or feet. may result in many cases. In falcons related to
(Pododermatitis or feet. small, hard perches.
Bumblefoot)
Crooked (twisted) toes Unknown Chickens, turkeys. Affected toes deviated laterally or Incidental finding. Don’t identify as cause of
medially. lameness or confuse with riboflavin deficiency.
Deep pectoral Ischemia following Chickens, turkeys. Unilateral or bilateral green areas of An aseptic necrosis of muscle that follows stress
myopathy (green exertion. necrosis in deep pectoral muscles. leading to muscle swelling.
muscle disease)
Enterococcus Cecorum Enterococcus Cecorum Chickens Incoordination, abnormal gait Associated with spondylitis, femoral head
necrosis, and osteomyelitis in broiler chicken
and broiler breeder flocks.
Gout (articular gout) A metabolic disease with Chickens, turkeys, White to gray semisolid tophi deposited Similar uric acid crystals may be deposited on
deposition of uric acid possibly other birds. in and around joints. Affected joints viscera, especially the pericardium and capsule
crystals. enlarged and distorted. Most obvious on of liver. Perhaps in the ureters.
feet and legs. Emaciation.
Infectious synovitis Mycoplasma synoviae Chickens, turkeys. Joints and tendon sheaths swollen, most Many birds are lame and squat on floor. Breast
apparent on hocks, shanks, feet. Sticky blisters a common sequel. Other mycoplasmas
synovial exudate. Sometimes the liver is may produce similar lesions
green.
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DISEASES WITH LESIONS IN THE MUSCULOSKELETAL SYSTEM
Nutritional myopathy Deficiency of vitamin E, Chickens, turkeys, In chickens and ducks necrotic muscle In chicks muscle lesions may be accompanied
selenium, and sulfur- ducks. fibers in breast muscles or legs appear as by encephalomalacia or exudative diathesis.
containing amino acids. white streaks or masses. In turkeys gray-
white patches in gizzard musculature.
Osteomyelitis Various bacteria Poultry and other birds. Osteomyelitis at various sites. Commonly Sporadic. Nonspecific.
metastasize to marrow. in femur, tibia, or vertebra.
Osteopetrosis Associated with Chickens. Shanks and other long bones thickened, Higher incidence in roosters. Bone lesions non-
retrovirus infections. heavy, dense and with small marrow neoplastic.
cavity.
Chondrodystrophy Usually manganese or Poultry and game birds Gastrocnemius tendon often slips off May be unilateral or bilateral. A disease of
(perosis or slipped choline deficiency. in captivity. trochlea at hock and leg deviated (usually rapidly growing, young birds. Often in flocks
tendon) Sometimes niacin, laterally) at hock. Bizarre position of leg fed mostly corn.
biotin. distal to hock.
Rickets Imbalance or deficiency Poultry and other birds In young birds - soft beaks and bones, Usually seen in birds a few weeks old;
of Ca/P/vitamin D3. raised in captivity. beaded ribs, crooked keels, enlarged deficiency of vitamin D3 frequently the cause.
epiphyses, and enlarged paratyphoids.
Splay leg
Slippery surface under Young chickens, Lateral deviation of legs at hips. High incidence in flocks brooded on slippery
birds. turkeys. paper.
Staphylococcal arthritis Staphylococcus aureus Turkeys, chickens. Affected joints swollen, painful, usually Affected birds often severely crippled. Arthritis
infection with with exudate. Lesions may be generalized often preceded by septicemia. Common disease
localization in various but usually involve hocks and feet. May in turkeys.
joints. involve thoracolumbar junction.
Tibial dyschondroplasia Possibly influenced by Broiler chicks, young Anterolateral bowing of tibias. Abnormal Squatting, reluctance to move, abnormal
genotype. May be related turkeys. mass of cartilage in proximal tibia and/or posture and gait. Retarded growth. Similar
to excess phosphorus or metatsus. Perhaps fracture at site. syndrome in ducks.
other dietary factors. Normal parathyroids. Osteomyelitis
often occurs concurrently.
Viral arthritis (reovirus Reovirus Chickens (meat type), Swelling of tendons and tendon sheaths, Sometimes leads to rupture of gastrocnemius
infection) turkeys. mostly near hocks. tendon(s).
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DISEASES WITH LESIONS IN THE REPRODUCTIVE TRACT
Egg yolk peritonitis Yolk ovulated into Layers. Yolk material among abdominal organs. Rarely associated with abnormal ovary or
peritoneal cavity. Peritonitis of variable severity. oviduct. Occasionally accompanies many acute
Exact cause unknown. diseases.
Internal laying Eggs regurgitated into Layers. Hard- or soft-shelled eggs in peritoneal Perhaps some cases are a sequel to oviduct
peritoneal cavity. cavity. Peritonitis. damage from infectious bronchitis.
Cause unknown.
Lymphoid leukosis Retrovirus Chickens, perhaps Neoplasia of ovary. Focal or nodular Accompanied by many other neoplastic lesions.
other species. neoplasia of the bursa of Fabricius. Usually in sexually mature birds. See notes on
lymphoid leukosis (Avian leukosis
(ALV)/sarcoma viruses).
Marek’s disease Alpha herpesvirus Chickens, perhaps Neoplasia of ovary. Atrophy of bursa of Often accompanied by other neoplastic lesions.
other species. Fabricius. Usually in sexually immature birds. See notes
on Marek’s disease.
Prolapse of oviduct Unknown. Often Layers. Oviduct prolapsed and often Occurs frequently in young, fat pullets
accompanies obesity. cannibalized. beginning to lay.
Pullorum disease Salmonella Pullorum, Adult chickens and Oophoritis with bloody, cheesy or Sometimes accompanied by focal myocarditis
fowl typhoid, S. Gallinarum, turkeys. atrophic follicles. Orchitis. and pericarditis.
paratyphoid Salmonella sp.
Salpingitis May accompany Layers. Salpingitis of variable extent. Oviduct A common cause of routine daily mortality in
mycoplasmosis or may be dilated with exudate. laying hens. May be an incidental finding in
follow infectious broilers with a history of airsacculitis.
bronchitis. Usually
nonspecific. E. coli
commonly cultured.
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DISEASES WITH LESIONS IN THE RESPIRATORY TRACTA
Name of Disease(s) Etiology Species Affected LesionsB Comments
Aspergillosis Aspergillus fumigatus Most poultry and birds Mycotic granulomas usually in lungs, Usually transmitted via moldy feed, litter, or
susceptible. Commonly perhaps along airways. Mycotic plaques hatchery contamination. Ochroconis gallopava
in chickens, turkeys, or fuzzy mycelium often in air sacs. and other fungi may produce similar signs and
waterfowl, penguins, Lesions may transplant or metastasize to lesions.
captive game birds. internal organs, brain, globes of eyes.
Rarely in conjunctival sac.
Avian chlamydiosis Chlamydophila psittaci Occasionally turkeys, Variable, but often airsacculitis, Among poultry, most often seen in turkeys.
ducks. More often in pericarditis, fibrinous perihepatitis. May infect humans processing infected poultry,
wild exotic birds. Splenomegaly may be the only lesion in resulting in flu-like symptoms.
chronic cases.
Avian influenza Orthomyxovirus (strains Turkeys, ducks, Highly variable. In mild form: often Enzootic forms in U.S. usually mild to
(AI) vary greatly in pheasants, quail, many swollen sinuses, ocular or nasal moderate in severity and involve respiratory
pathogenicity). wild birds, other discharge. In severe form: hemorrhages, system. Egg production declines and shell
poultry. exudation, focal necrosis in respiratory, abnormalities common in turkeys. Most
digestive, urogenital, cardiovascular, or outbreaks of AI in U.S. are in turkeys and
multiple systems. See AI section. ducks.
Avian Metapneumovirus Chickens and turkeys of Upper respiratory signs with nasal and Variations in clinical presentation dependent
Metapneumovirus any age, pheasants, ocular exudate, swollen heads and on secondary infections. Egg production drops.
infections guineas sinuses.
Bordetellosis (Turkey Bordetella avium Turkeys, chickens. Nasal, ocular, and sinus exudation. Causes deciliation of trachea leading to
coryza) Tracheitis. Perhaps flattened trachea. increased susceptibility to other respiratory
Pneumonia uncommon in diseases.
uncomplicated cases.
A
Respiratory signs include one or more of the following: snicks, sneezes, dyspnea, gasping, rapid breathing, rales, ocular or nasal discharge, swollen
sinuses. Signs in broilers may be severe, even with the milder strains. Secondary Escherichia coli infection is common.
B
Unless stated otherwise lesions are those seen in turkeys or chickens.
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DISEASES WITH LESIONS IN THE RESPIRATORY TRACTA
Name of Disease(s) Etiology Species Affected LesionsB Comments
Infectious bronchitis Coronavirus Chickens. Mild to moderate inflammation of Signs predominantly respiratory. Little
(IB) respiratory tract. Occasional mortality unless complicated and mostly in
nephropathic outbreaks. When chicks less than 10 weeks old. In layers, egg
complicated by mycoplasmosis, severe production may drop as much as 50%. May
airsacculitis, pericarditis, fibrinous result in the production of wrinkled egg shells
perihepatitis. and/or cystic salpingitis.
Infectious Iltovirus (Herpesviridae) Chickens. Occasionally Usually severe hemorrhagic Usually in semimature or mature chickens.
laryngotracheitis pheasants. laryngotracheitis with bloody exudate Spreads more slowly than other viral diseases.
and possibly fibrinous casts or cheesy May cause high mortality. Severe dyspnea with
plugs. Occasionally only mild loud gasping and expectoration of bloody
laryngotracheitis with conjunctivitis. exudate. Mild form has few signs and lesions.
Mycoplasma M. gallisepticum Primarily chickens, Airsacculitis of variable severity. Usually Often secondary to other diseases and
gallisepticum infection turkeys, but also in pericarditis and, perhaps, fibrinous vaccinations (especially Newcastle and
(MG) many other perihepatitis. infectious bronchitis) and stresses. Usually a
poultry/birds. chronic respiratory disease.
Newcastle disease Paramyxovirus (strains Most poultry and birds Highly variable with various viral strains. Enzootic ND in U.S. usually manifested as a
(ND) vary greatly in susceptible. Usually Enzootic ND produces few/no gross respiratory disease but a modest number of
pathogenicity). seen in chickens. lesions. Exotic ND produces many but young birds may show concurrent or closely
variable lesions: swelling around eyes and following CNS signs. Exotic ND rarely in the
on neck, hemorrhages at many sites U.S. In layers with ND egg productions drops
including intestinal mucosa, severe drastically or ceases.
tracheitis. See ND section.
A
Respiratory signs include one or more of the following: snicks, sneezes, dyspnea, gasping, rapid breathing, rales, ocular or nasal discharge, swollen
sinuses. Signs in broilers may be severe, even with the milder strains. Secondary Escherichia coli infection is common.
B
Unless stated otherwise lesions are those seen in turkeys or chickens.
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DISEASES WITH LESIONS IN SKIN
Biotin deficiency Biotin deficiency Chicks, turkey poults. Dermatitis on feet and shanks. Crusty, In turkeys enlarged hocks and bowing of the
scab like lesions at the commissures of metatarsus usually are more obvious and may
the mouth, perhaps of the eyelids. precede or accompany cutaneous lesions.
Sometimes implicated in perosis, especially in
poults.
Cellulitis Escherichia coli Young chickens. Yellow, thickened skin in the ventral area Bacterial infection secondary to skin scratches.
with subcutaneous exudates that may be
edematous to caseous.
Erysipelas Erysipelothrix Turkeys, usually older Acute septic disease with serosal, The bacteria reside in the soil and enter skin
rhusiopathiae males cutaneous, and muscular hemorrhages wounds created when males fight. Most
and splenomegaly. common in toms housed outside.
External Parasites Mites, lice, etc. All poultry types. Ectoparasites move fast but may be Ectoparasites may cause discomfort adversely
visible around the vent. Feces and/or affecting performance.
eggs may be seen on the skin or feather
shafts.
Fowl pox , Poxvirus Perhaps all birds. Yellow pustules or dark brownish-red Yellow or gray plaques may occur in oral cavity,
pigeon pox, scabs on any unfeathered skin (face, pharynx, conjunctiva, sinuses. Can be
canary pox, wattles, eyelids of chickens; caruncle, transmitted by mosquitoes. Intracytoplasmic
turkey pox snood of turkeys; feet and legs of cage inclusion bodies in epithelium of lesions.
and wild birds).
Gangrenous dermatitis Skin wounds with Chickens. Traumatized skin with an underlying Severe losses have occurred in 4-16 week-old
secondary cellulitis. chickens and turkeys. Some outbreaks follow
Staphylococcus, infectious bursal disease or adenoviral
Clostridia, etc. infection.
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DISEASES WITH LESIONS IN THE SKIN
Pantothenic acid Deficiency of Chicks, perhaps other Dermatitis on feet and shanks. Crusty Ataxia followed by inability to stand. Myelin
deficiency in chicks pantothenic acid. poultry. scab like lesions at the commissures of degeneration in much of cord.
the mouth, perhaps of the eyelids.
Riboflavin deficiency Riboflavin deficiency Turkey poults and Poults: Dermatitis on feet, shanks. Poults and chicks may walk on hocks or sprawl
chicks. Crusts at corners of mouth, on eyelids, with toes curled. A common deficiency.
vent. Chicks: drooping wings. Both:
hypertrophy and myelin degeneration of
nerve trunks.
Vesicular dermatitis Photosensitizing seeds, Chickens, perhaps Vesicles or scabs on unfeathered skin Affected skin wrinkled, ulcerated, and shrunken
(photosensitization) plants, feeds other birds. (comb wattles, face, legs caruncle, feet). after vesicles rupture.
with/without fungus;
phenothiazine. Sunlight
required on skin.
Xanthomatosis Uncertain etiology. Chickens. Thickened, roughened yellow areas of Skin lesions are permanent. Affected birds
Possibly toxic materials skin. Swelling of the wattle(s) of condemned at slaughter. Cholesterol crystals
in animal fats. intermandibular area and large foamy macrophages in affected skin.
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DIFFERENTIAL DIAGNOSIS OF COMMON RESPIRATORY DISEASE OF CHICKENSA
Diagnostic Aid Mesogenic Newcastle Infectious Bronchitis Infectious Mycoplasma Infectious

Disease Laryngotracheitis gallisepticum infection Coryza
Speed of spread Rapid Rapid Moderate Slow; persistent Rapid

in the flock
Duration of flock 2 weeks 2 weeks 2-4 weeks Weeks to months Weeks to months
signs
Egg production Nearly complete Up to 50% 1-20% 1-20% 1-20%

drop cessation of lay.
Mortality in 25-90% 5-60% Rarely occurs in 5-40% (seldom occurs in Seldom occur in chicks.
chicks less than 3 chicks. chicks)
weeks old
Mortality in 0-5% (very high with Usually 0 Up to 50% Low; many culls Low; many culls.
adults exotic Newcastle).
Egg-borne No No No Yes No
transmission
Etiology Paramyxovirus Coronavirus Iltovirus Mycoplasma gallisepticum Avibacterium

(Herpesvirus) paragallinarum
Vaccines Yes Yes Yes Yes Yes

available
A
Aspergillosis, avian influenza, and chlamydiosis have been omitted from this table although they may be classified as respiratory diseases. Occasional
respiratory noises may be heard with certain other diseases if the bird is sick enough that mucus secretion accumulates in the respiratory tract.
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POULTRY DRUG USE GUIDE
Diagnostic Aid Mesogenic Newcastle Infectious Bronchitis Infectious Mycoplasma Infectious

Disease Laryngotracheitis gallisepticum infection Coryza
Natural carrier Rarely Yes - up to 2 weeks Yes – probably lifelong Yes Yes
chickens (vaccinates also). (vaccinates also).
Clinical diagnosis Adults cease lay within Acute epornitic Severe dyspnea with Chronic respiratory signs Respiratory signs with
3 days. In chicks, acute respiratory disease bloody mucus from influenced by weather facial edema ocular and
respiratory disease without CNS signs but the nares and high and season. nasal discharge. Exudate
with CNS signs in with sharp drop in egg mortality in adult has foul odor.
some and high production and shell birds.
mortality. quality.
Unique features Produces hemorrhagic Curling, stunting of Pocks on CAM, Growth in special broth; Tiny dewdrop colonies on
of agent skin and death in embryos with passaging. intranuclear in- but not on blood agar blood agar in candle jar
chick embryos. Does not clusions in CAM and initially. (needs Staph nurse
Hemagglutinates. hemagglutinate. tracheal epithelium. Hemagglutinates. colony). Pleomorphic,
Gram negative.
Serologic tests HI test of value after 5 VN test of value. ELISA test available. Plate and tube No test.
days; VN test of value ELISA test available. Seroconversion is agglutination tests. HI
after 10-21 days. slow. test. ELISA test available.
ELISA test available. Seroconversion is slow.
PCR Yes (RT-PCR) Yes (RT-PCR) Yes (PCR/RFLP) Yes (commercial kits Yes (ERIC-PCR)
available)
Often none. Possibly Possibly none. Often Bloody mucus on face, Marked airsacculitis. Facial edema. Eyelids
Gross lesions mild airsacculitis and airsacculitis and beak. Severe tracheitis Fibrinous perihepatitis, adhered. Mucoid ocular
airway inflammation. tracheitis. with cheesy plugs in adhesive pericarditis. and nasal discharge.
dead bird.
POULTRY DRUG USE GUIDE 263
POULTRY DRUG USE GUIDE

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Revised by Drs Linnea J. Newman and Jean E. Sander
The following listing of approved poultry drugs for United States use is intended to provide a general guide of dose and
preslaughter withdrawal time. When calculating withdrawal time, each day is a full 24 hours long, starting with the hour
the bird last received the drug. The listing is neither inclusive nor exclusive and may change. Many of the listed drugs
are approved for use in combination with other drugs. Drug approval does not indicate cross-clearance. For information
regarding approved combinations and specific indications of use, the reader should consult one of the references listed
at the end of this section. Italicized compounds are not for use in laying hens.
When the decision is reached to use antimicrobials for therapy, veterinarians should strive to optimize
therapeutic efficacy and minimize resistance to antimicrobials to protect public and animal health.
CHICKEN DRUG LIST

Active Ingredients Route Withdrawal Time (days) Dose
Amprolium Water 0 0.006 - 0.024%
AmproliumA Feed 0 36.3 – 227 g/ton

Bacitracin methylene
Water 0 27.5 – 158 mg/L
disalicyclate
Feed 0 4-200 g/ton
disalicyclateB
Bacitracin zinc Water 0 100-400 mg/gal
Bacitracin zincB Feed 0 4 - 50 g/ton
Bambermycins Feed 0 1-2 g/ton
Ceftiofur sodiumC SQ 0 0.08-0.20 mg/chick
Chlortetracycline Water 1 100-1,000 mg/gal
Chlortetracycline Feed 1 10-500 g/ton
Clopidol Feed 5 113.5 – 227 g/ton
CyromazineD Feed 3 0.01 lb/ton
Decoquinate Feed 0 27.2 g/ton
Diclazuril Feed 0 0.91 g/ton
Erythromycin Water 1 0.500 g/gal
Gentamicin sulfate Inject 35 0.2 mg
A
36.3 - 113.5 g/ton for laying hens.
B
10-25 g/ton for laying hens.
C
For use in day-old chicks only. Extralabel use of cephalosporins in chickens is prohibited by the FDA.
D
For US in layers or breeders only.

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Halofuginone
Feed 4 2.72 g/ton
Hydrobromide
Lasalocid Feed 0 68-113 g/ton
Lincomycin Feed 0 2 – 4 g/ton
Lincomycin HCl Water 0 16 mg/L

Lincomycin/
833 mg antibacterial
Water 3
action/L
Spectinomycin E
Monensin Feed 0 90-110 g/ton
Narasin Feed 0 54-72 g/ton

54 - 90 g/ton of
Narasin/nicarbazin Feed 5
combination
Neomycin/Oxytetracycline Feed 3 10 – 50 g/ton
Nicarbazin Feed 4 113.5 g/ton
Nitarsone Feed 5 170.1 g/ton

Oxytetracycline
Water 0 200 - 800 mg/gal
hydrochloride
Oxytetracycline Feed 0-3 10-500 g/ton
Penicillin (from
Feed 0 2.4 – 50 g/ton
procaine penicillin)
Piperazine Water 14 50 – 100 mg/bird
Robenidine hydrochloride Feed 5 30 g/ton
Roxarsone Water 5 5 ml / gal
Roxarsone Feed 5 22.7-45.4 g/ton
Salinomycin Feed 0 40-60 g/ton
E
Use only up to 7 days of age.

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Semduramicin Feed 0 22.7 g/ton

Spectinomycin
Water 5 0.5 – 2 g/ gal
dihydrochloride
Spectinomycin
Inject 0 2.5 mg/bird
dihydrochlorideC
Steptomycin Sulfate Water 4 0.5-1.5 g/ gal
Sulfadimethoxine Water 5 1.875 g/gal

Sulfadimethoxine/ 113.5 g/ton/
Feed 5
ormetoprim 68.1 g/ton
Sulfamethazine sodium Water 10 61-89 mg/lb BW/day
0.025-0.04%
Sulfaquinoxaline Water 10
10 – 45 mg/lb/day
Tetracycline hydrochloride Water 5 89 mg/L
Tylosin tartrate Water 1 100 - 500 mg/L
TylosinF Feed 0-5 4 - 1000 g/ton
Virginiamycin Feed 0 5-20 g/ton
Zoalene Feed 0 36.3 – 113.5 g/ton
F
For layers use 20-50 g/ton dose. Highest dose level (1,000 g/ton) requires 5-day withdrawal.
TURKEY DRUG LIST

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Amprolium Water 0 4-16fl oz/50 gal
Amprolium Feed 0 113.5 – 227 g/ton
Water 0 400 mg/gal
disalicyclate
Feed 0 4-200 g/ton
disalicyclate
Bacitracin zinc Feed 0 4-50 g/ton
Bambermycins Feed 0 1-2 g/ton
Ceftiofur sodium A
SQ 0 0.17 – 0.5 mg/poult
Chlortetracycline Water 1 100-400 mg/gal
Chlortetracycline Feed 1 10-400 g/ton
Clopidol Feed 5 113.5 – 227 g/ton
DiclazurilB Feed 0 0.91 g/ton
Erythromycin Water 1 57.8 – 115.6 mg/L
FenbendazoleB Feed 0 14.5 g/ton

Gentamicin Inject 63 1 mg/bird
Halofuginone
Feed 7 1.36 – 2.72 g/ton
Hydrobromide
LasalocidB Feed 0 68-113 g/ton
Monensin Feed 0 54-90 g/ton
Neomycin/
Feed 5 10 – 200 g/ton
Oxytetracycline
Neomycin sulfate Water 0 10 mg/lb BW/day
Nitrasone Feed 5 170.1 g/ton
Oxytetracycline
Water 5 200 - 400 mg/gal
hydrochloride
Oxytetracycline Feed 0 10-200 g/ton
Penicillin
Water 1 1.5 Million units/gal
(G potassium)
Penicillin (from
Feed 0 2.4 - 50 g/ton
procaine penicillin)
Piperazine sulfate Water 14 100-200 mg/bird
Ractopamine
Feed 0 4.6-11.8 g/ton
Hydrochloride
Roxarsone Feed 5 22.7-45.4 g/ton
Roxarsone Water 5 5 ml /gal

Spectinomycin
Inject 0 1.0-5 mg/bird
dihydrochloride
Sulfadimethoxine Water 5 0.938g/gal

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Sulfadimethoxine/ 56.7 g/ton/

Feed 5
Ormetoprim 34.05 g/ton
53-130 mg/lb
Sulfamethazine sodium Water 10
BW/day
0.025 – 0.04%
Sulfaquinoxaline Water 10
3.5 – 55 mg/lb/day
Triple Sulfa
(sulfamethazine,
Water 14 0.025% solution
sulfamerazine,
sulfaquinoxaline)
Tylosin tartrate Water 3 500 mg/L
Virginiamycin Feed 0 10-20 g/ton
ZoaleneB Feed 0 113.5 – 170.3 g/ton
A
For use in day-old poults only. Extralabel use of cephalosporins in turkeys is prohibited by the FDA.
B
Do not use in breeding turkeys.
REFERENCES
1. Arriuja-Dechert, A. (ed) 1999. Compendium of Veterinary Products, 5th ed. Adrian J. Bayley, Pub., Port Huron,
MI.
2. FDA Website: www.accessdata.fda.gov/scripts/animaldrugsatfda/index.cfm?gb=1&showtype=adv

(last consulted July 20th, 2012).
3. Lundeen, T. (ed.) 1999. 2011. Feed additive Compendium, The Miller Publishing Co., Minnetonka, MN
NECROPSY OF THE FOWL If alive, the fowl may be killed by any of three methods.
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Written by Drs Richard J. Julian and Martine Boulianne A. Administration of CO2 gas in an appropriate
closed container.
History B. Disarticulate the head at the atlantooccipital joint
As with disease investigation in other species, a good (Fig. 1).
history will often provide clues that will help solve the
C. Intravenous injection of barbiturate (Fig. 2).
problem. Obtain information on the type of bird, age,
feed and water source and consumption rate, growth, Moisten the feathers with water containing detergent. If
production, morbidity and mortality, the owner’s description psittacosis is suspected, the bird should be soaked in 5%
of the case, vaccination program, drugs being used etc… Lysol solution and a laminar flow hood should be used for
the necropsy.
In any poultry operation, many of the problems can
relate to management, environmental factors, and stress If swabs are desired for culturing, use sterile instruments to
rather than to infection so if you are on the premises, cut the infraorbital sinus, a joint, or to remove any organs.
examine carefully the housing conditions. Is the ventilation All unnecessary manipulations and delays prior to culture
adequate? Are ammonia fumes a problem? Is it too hot or increase the probability of contamination. Take intestinal
too cold? Is the litter wet or is it too dry and dusty? Is the cultures last.
room too light? Are there sufficient hours of light for best
production? Is the nest area darkened? Are the roosts too
high? Do the birds appear comfortable? Chickens can talk Necropsy
and the sounds they make can indicate comfort, hunger, 1. Examine the head, including the eyes, ears, nostrils,
pain, panic, or disease. comb, wattles, mouth, and beak (Fig. 3).
Infected eyes and conjunctivitis are often seen in
case of a respiratory disease such as infectious
Examination of Live Specimens
sinusitis (Mycoplasma gallisepticum infection),
Check the general appearance of the individual or group
infectious coryza, infectious laryngotracheitis (ILT),
and try to determine which organ or system is involved
infectious bronchitis (IBV), and Newcastle Disease
in the illness. Note any signs or lesions that might point
(ND). Keratoconjunctivitis with central corneal ulcers
to a diagnosis. If the birds show lameness or paralysis, is
suggests ammonia burn.
the lesion in the nervous system, bones, joints, muscles
or skin? Some conditions, particularly those affecting
Swollen sinuses are seen in infectious coryza in
locomotion, are easier to diagnose in live birds. Botulism
chickens, infectious sinusitis, Cryptosporidium and
which produces neck paralysis in chickens (leg and
Bordetella infection in turkeys and pheasants. They
wing paralysis are more obvious in turkeys, ducks, and
may also be seen as the result of other infections such
pheasants) is an example.
as avian influenza (AI).
Examine the skin of the head, body, and legs for lice and
Chronic fowl cholera causes swollen wattles in adult
mites, injury (particularly cannibalism), molting, swellings,
chickens. Fowl pox causes scabs on the comb, eyelid,
cyanosis, or staphylococcal or clostridial dermatitis. Listen
and wattle, but must be differentiated from injury. Pox
for unusual breathing sounds (snicking, gurgling) and look
also occurs in turkeys, pigeons, doves, canaries and
for gasping or head-shaking that might indicate respiratory
other avian species. A frozen comb or wattles is usually
distress. Mouth-breathing (panting) is normal in chickens
mottled red and white before becoming gangrenous.
in hot weather. Exudate from nostrils and eyes and dirty
feathers also suggest respiratory infection. Examine the
If the bird has had its beak trimmed, check for proper
droppings for evidence of diarrhea and the presence of
healing, overgrowth of the lower beak or over-trimming
blood.
(cut too short).
If a post-mortem examination is to be carried out, birds
Injury on the head, neck, or breast or back may
that are representative of the problem in the flock must be
indicate predators. Dermatitis and scabby or crusty
selected. If there has been mortality, both sick and dead
lesions around the mouth and eyes suggest vitamin
birds should be opened. A couple of cull birds will not
B deficiency.
provide the answer. If the problem is a drop in production,
try to find birds that look like they have recently stopped
2. Cut across the upper beak (Fig. 4) and examine
laying. It is important to do both an external and an internal
the sinuses (Fig. 5). Then insert one blade of a
examination and to follow a specific pattern to avoid
sterile scissors into the infraorbital sinus. Make a
missing important lesions.
longitudinal lateral incision through the wall of each
NECROPSY OF THE FOWL 269
sinus and examine them (Fig. 6). Cut through one Muscular degeneration due to vitamin E-selenium
lateral commissure of the mouth (Fig. 7) and down deficiency can cause lameness, particularly in ducks.
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the esophagus into the crop (Fig. 8). Examine the oral Sarcosporidial cysts produce small, white lesions in
cavity, note the content and odor of the esophagus the muscle of waterfowl.
and crop.
White plaques in the mouth, esophagus, or crop Gangrenous dermatitis is caused either by
may be caused by capillaria worms, yeast infection Staphylococcus or Clostridium septicum infection.
(candidiasis), or possibly trichomoniasis or vitamin A The clostridial infection shows fairly typical lesions
deficiency, but most frequently by fowl pox (wet form). of emphysematous or serosanguineous cellulitis
Single white plaques in the mouth are common in hens in affected areas. Scabby hip syndrome can be
and turkey breeders and occur where salivary ducts observed on the thighs and is usually associated
open into the mouth. Tricothecene mycotoxicosis may with overcrowding, poor litter conditions, or poor
produce similar lesion in young chickens and turkeys. feathering. Cellulitis is characterized by the presence
of a subcutaneous caseous plaque on the side of the
If the crop is enlarged and full, it may be an impacted lower abdomen, often near the vent.
or a sour crop (pendulous crop). The problem may be
caused by excess water intake, defects in the crop Skin leukosis is Marek’s disease virus causing viral
itself, partial blockage of the proventriculus or gizzard dermatitis in the feather follicles. At processing this
or Marek’s disease. Necrosis of the crop in sparrows can be confused with scabby hip or other causes of
and other songbirds feeding around bird feeders is dermatitis.
caused by Salmonella infection.
5. Examine the feet, their plantar surfaces, then bones
3. Examine the soft palate and larynx and cut down the and joints of the lower limbs for abnormality and
trachea (Fig. 9). deformity. Break the metatarsal bone to verify for
strength (Fig. 14). Using a sharp knife or scalpel,
Wet fowl pox lesions are seen on the roof of the mouth open each tibiotarsal joint and examine the joint fluid
and on the larynx. for signs of exudate (Fig. 15). Make a longitudinal cut
through the anterio-medial aspect of the tibial head to
Granulation, congestion, and mucus in the trachea expose the growth plate of immature birds (Fig. 16).
are seen in IBV, Escherichia coli infection, infectious With an osteotome split one femur longitudinally and
coryza and bordetellosis. Hemorrhage and blood examine the bone marrow.
clots occur in ILT and occasionally in ND or infectious
coryza and may cause severe gasping. Angular bone (valgus-varus) deformity of the intertarsal
joint is caused by lateral or medial bending of the tibio-
Gapeworms in pheasants, quail, and other birds tarsal and metatarsal bones and is a common problem
are caused by Syngamus and cause gasping. in meat-type chickens. It has a variety of possible
Cyanthastoma cause similar infection in waterfowl causes (nutritional, genetic, management, etc.).
and tracheal flukes may be found in waterfowl in the Slowing growth in young broilers will help prevent leg
tropics. deformity.
4. Check under the wings (Fig. 10) and on the abdomen Other types of hock and stifle lameness are frequent
for lice and mites, and the vent for injury. in heavy roasters and turkeys and may be mainly due
to injury as the result of heavy weight and fast growth.
Incise the loose skin between the medial surface of
each thigh and the abdomen (Fig. 11), reflect the legs Check for poor bone-breaking strength (osteoporosis
laterally and dislocate the hip joints (Fig. 12). Connect or cage layer fatigue) or, in young birds, for rubbery
the lateral skin incisions with a transverse skin incision bones, soft beaks, and beaded ribs (rickets) which
across the middle of the abdomen and reflect the skin may indicate calcium, phosphorus or vitamin D3
of the breast anteriorly (Fig. 13). Tightly adhering skin imbalance. While cage layer fatigue maybe due to
and dark tissues indicate dehydration. Examine the nutritional factors, it is also associated with continuous
skin, integument, and muscles. high production.
Emaciation, along with small organs, suggests Curled-toes in young birds may indicate a riboflavin
malnutrition, beak injury (poor trimming), peck order deficiency, but in older birds and turkeys it may be
(behavioral) problems, chronic disease (coccidiosis), due to genetic factors or a lack of roosts. Cracked feet
bumblefoot or other lameness, or chronic poisoning and foot dermatitis may be pantothenic acid or biotin
(lead, insecticide, etc.). deficiency, but scaly leg in cage birds is likely parasitic
(mites). Toe injury in young birds may be cannibalism In young birds, examine the lungs and air sacs for
or mechanical injury. yellow-white foci or plaques caused Aspergillosis
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(brooder pneumonia). Gasping in young birds is a sign

Swelling of the feet, hocks or other joints suggests of tracheal or bronchial injury, obstruction, irritating
articular gout, infectious synovitis (Mycoplasma fumes or an infectious agent.
synoviae) or other localized bacterial infection. These
bacterial infections often extend into osteomyelitis. In baby chicks, look for yolk sac infection (omphalitis),
Infection in the wing joints in pigeons is usually due to peritonitis or pericarditis in which the abdomen can
Salmonella. In broilers, roasters and broiler breeders be swollen, wet, and discolored. The yolk sac may
viral arthritis may cause lameness or ruptured tendons. be infected with E. coli, Salmonella, Staphylococcus,
If growing birds are lame and there is no evidence Pseudomonas, etc…
of infection or rickets, split some bones and look for
necrosis due to osteomyelitis or dyschondroplasis. Baby birds also die because they did not learn how to
Lameness may require splitting the spine at T4 to look eat (starve-outs) or drink (dehydration). Deaths occur
for spondylolisthesis. Also, consider Marek’s disease mainly between 4 and 6 days of age once the yolk sac
and examine the sciatic nerve (Fig. 17) by separation has been absorbed.
or section of the adductor muscles.
Broiler chickens that die suddenly from flip-over
6. At this point, remove the breast carefully by cutting (sudden death syndrome, heart attack), heat stroke,
through the pectoral muscles on each side of the or suffocation (piling-up) have congested, edematous
keel and over the costrochondral junctions (Fig. 18). lungs, a full digestive tract and congested mottled
Examine the organs, paying particular attention to the breast muscle.
air sacs (Fig. 19), lungs, and liver. Carefully push the liver
and gizzard to the left, incise the peritoneum (Fig. 20) Turkeys (6-18 wks old) die suddenly of unknown
and cut the esophagus cranially to the proventriculus cause and have perirenal hemorrhage, swollen spleen
(Fig. 21) to exteriorize the whole gastrointestinal tract and congested liver and lungs. Turkeys with aortic
and remove it after transecting the rectum. rupture will have a large blood clot in the abdomen
If there is fibrin on the liver and/or in the pericardial and chickens or turkeys with hepatic lipidosis may also
sac, suspect secondary E. coli infection. These have hemorrhage and hematoma of the liver. .
lesions in turkeys and cage birds might also be due to
Chlamydophila psittaci, or in ducks due to Riemerella Birds that die from anemia are pale and the blood
anatipestifer infection. is watery. Birds may have bled to death (pick-outs,
ruptured fatty liver, acute cecal coccidiosis, ruptured
Peritonitis in layers is usually “egg peritonitis” frequently aorta, hemorrhagic enteritis in turkeys, etc…) and are
with secondary E. coli infection, although acute fowl pale.
cholera may also causes peritonitis.
To identify anemia due to parasites in the red blood
White crystals on the heart sac, liver, and other tissues cells (Leukocytozoon for duck, Plasmodium for
and organs are uric acid crystals (visceral gout) and canary), a blood smear needs to be collected from a
are secondary to hyperuricemia from nephritis or live, sick bird and examined by Wright’s stain or Diff
water deprivation. Quick.
Tumors in or on the organs may be due to Marek’s Sulfa poisoning also produces anemia with widespread
disease, lymphoid leukosis, or other tumors. Multiple hemorrhage in the tissues. Chicken infectious anemia
small tumors on organs and peritoneum in adult hens virus (CIA) produces similar lesion.
are frequently metastasis from a carcinoma of the
oviduct or pancreas. This may result in ascites. 7. Remove and examine the heart (Fig. 22) and its
pericardial sac. Open the heart to visualize the valves.
Ascites may also result from heart or liver disease or Right ventricular dilation and hypertrophy can
from ingestion of some toxic material. sometimes be observed in broiler chickens whereas a
bilateral dilated cardiomyopathy can be seen in turkey
Focal white lesions on organs may be due to poults, both often accompanied by secondary ascites.
tuberculosis (Mycobacterium avium) or other bacterial
septicemia. Histomoniasis causes large irregular Pericarditis and endocarditis will be sometimes
circumscribed lesions on the liver in turkeys, pheasants observed as lesions of septicemia.
and peacocks but less so in chickens.
8. Examine the lymphoid system; the spleen (located at A yellow or hemorrhagic liver particularly with focal
the junction of the proventriculus and gizzard, (Fig. 23), necrosis may be viral hepatitis which is seen in
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bursa (dorsally to the cloaca, (Fig. 24) and lymphoid broiler chickens, pigeons, ducks, raptors, owls and
tissue of the neck (thymus). Lymphoid tissues of the psittacines.
intestines (peyers’s patches and cecal tonsils) will be
examined upon opening the gut. 10. Examine the testicles in males (Fig. 28) or the single
Infectious bursal disease (IBDV) will affect the bursa left ovary in females (Fig. 29) and cut the oviduct
of Fabricius and initially cause bursal edema (4-5 days longitudinally in adult females.
post-infection) before atrophy (7 days post-infection). The development of the ova helps to identify length of
This disease causes immunosuppression and illness. Shrinking ova indicate illness of several days’
increases the susceptibility to secondary infections. duration or one from which the bird may be recovering.
Small, sac-like ova indicate that the bird has been out
Swelling, congestion and hemorrhage with or without of lay for a week or more and may be in a molt.
focal necrosis in the spleen, liver and lymphoid tissue
suggest septicemia (fowl cholera, fowl typhoid, Semi-solid (cooked) ova indicate bacterial infection.
streptococcosis, colisepticemia or erysipelas) or
viremia (ND and highly pathogenic AI). An impacted oviduct may be secondary to vent-
picking, egg material left in the oviduct, or the bird may
Marek’s disease and lymphoid leukosis produce be egg-bound. Infection (Mycoplasma, IBV, E. coli)
tumors in lymphoid tissue except for the bursa which can cause salpingitis as well.
is only affected by lymphoid leukosis (occasional
Marek’s lesions may occur in the stroma of the bursa). A large or small fluid-filled cyst in the right abdomen
beside the cloaca is the cystic remnant of the right
9. With a scissor or an enterotome, make a longitudinal oviduct.
incision through the proventriculus (Fig. 25). Open
the proventriculus, gizzard (Fig. 26), small (Fig. 27) A drop in production may be related to systemic
and large intestines to the cloaca. Check the cloaca disease (IBV, MG, avian encephalomyelitis, influenza-
carefully for evidence of picking injury. like, ND, etc...) or management failure (lack of light,
If hens are not properly beak-trimmed or are too temperature change, lack of water) or nutritional
fat, mortality from “pick-out” is common. The whole problems etc.
intestine may be picked out through the cloaca.
Prolapse of the vagina (and cloaca) may occur from Deformed shells suggest IBV, and soft shells (higher
straining, secondary to injury or inflammation. than 1-2%) may indicate calcium or vitamin D
deficiency.
Examine the digestive tract for lesions and the
various kinds of enteritis (hemorrhagic, necrotic, A normal-appearing dead bird with an egg in the shell
ulcerative, etc...), parasites (roundworms, capillary gland or a recently laid egg may have died from acute
worms, tapeworms, cecal worms, and coccidia), and hypocalcemia. These birds often have fragile bones.
gastrointestinal accidents. A large proventriculus in
broilers may be from lack of fibre in the diet resulting in Hard (fibrotic) or swollen testes indicate bacterial
poor development of the gizzard. infection (Paratyphoid).
Green staining of the digestive tract is just bile and 11. Examine the kidneys and ureters (Fig. 30).
indicates that the bird is not eating. The liver and spleen Ureters plugged with urates or hard stony material
may be small (if the bird is thin) and the gallbladder full. (urolithiasis) and swollen pale kidneys indicate
hyperuricemia and nephrosis. This may be due to lack
Check the ceca, intestine and liver for lesions of of water, or a Calcium/Phosphorus imbalance.
histomoniasis, avian tuberculosis, coccidiosis or
tumor, the liver for other varieties of bacterial, viral or Swollen kidneys and nephritis may be due to IBV
protozoal hepatitis, cholangiohepatitis etc., and the (nephrotrophic strain) or E. coli infection and usually
pancreas for tumors. cause death from uricemia as well.
A large, yellow liver may be normal fat storage in a 12. Examine the lungs by reflecting them medially from
laying bird (estrogen stimulation) but layers can die their attachment to the rib cage (Fig. 31 and 32).
from a ruptured fatty liver. Pneumonia in turkeys is caused by a Pasteurella
multocida infection (fowl cholera) and the lungs may
be quite solid. ND, AI and E. coli infection can also

cause pneumonia.
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13. Disturbances of the nervous system may cause

incoordination, staggering, paralysis, walking
backwards (with wings flapping for balance), tremors,
stargazing, and other odd behaviors. In case of
lameness, paresis, paralysis, or incoordination,
examine the brachial plexus, intrapelvic portion of the
sciatic nerves that you can expose by removal of the
overlying portion of the kidneys, spinal cord, and brain.
To examine the brain, disarticulate the head and skin
it. Remove the calvarium with strong scissors using
the same technique as for mammals (Fig. 33).
When Marek’s disease affects the peripheral and/
or central nervous system it causes lameness,
incoordination and paralysis. Avian encephalomyelitis
(AE) (epidemic tremor) affects birds up to 3-4 weeks
old from non-immune parents.
ND may produce CNS disturbances in pigeons as

well as respiratory, intestinal and reproductive lesions
in chickens, pheasants, turkeys, and wild and cage
birds of all ages. Bacterial infection (Pasteurella,
Salmonella, Staph. etc.) and fungi (Aspergillus, etc.)
also cause meningoencephalitis, occasionally in
outbreak proportions.
Vitamin E deficiency (avian encephalomalacia) causes

lesions in the cerebellum (soft, dark areas) which may
be visible grossly.
Arsanilic acid and other feed additives and toxins

may cause CNS disturbances, while others like the
ionophores and coffee weed seeds (Cassia) cause
muscle damage that mimics paralysis.
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Fig. 1 Fig. 2
Dislocation of the atlantooccipital joint. Intravenous injection of barbiturate.
Fig. 3 Fig. 4
Examination of the head. Cut across the upper beak .
Fig. 5 Fig. 6
Sinus and turbinates exposed. Infraorbital sinus exposed.
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Fig. 7 Fig. 8
Scissors at commissure of the beak. Oesophagus being exposed.
Fig. 9 Fig. 10
Trachea being cut opened. Check the feathers and skin under the wings and on the abdomen.
Fig. 11 Fig. 12
Incision of the loose skin between the medial surface of each thigh Hip joint dislocation.
and the abdomen.
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Fig. 13 Fig. 14
Removal of the skin of the breast anteriorly. Breaking the metatarsal bone to verify for strength.
Fig. 15 Fig. 16
Opening of the tibiotarsal joint and examination of the joint fluid. Longitudinal cut through the anterio-medial aspect of the tibial
head to expose the growth plate.
Fig. 17 Fig. 18
Examination of the sciatic nerve . Removal of the breast.
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Fig. 19 Fig. 20
Examination of the air sacs. Carefully pushing the liver and gizzard to the left to incise the
peritoneum.
Fig. 21 Fig. 22
Cutting the esophagus cranially to the proventriculus. Removal of the heart.
Fig. 23
Fig. 24
Examination of the spleen located at the junction of the
Examination of the bursa located dorsally to the cloaca.
proventriculus and gizzard.
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Fig. 25 Fig. 26
Longitudinal incision through the proventriculus. Proventriculus and gizzard opened.
Fig. 27
Opening the duodenum.
Fig. 28
Testicles.
Fig. 30
Kidneys and ureters (scissors tip).
Fig. 29
Single left ovary in an immature female chicken.
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Fig. 31 Fig. 32
Taking the lung out. Lung being exposed.
Fig. 33
Cerebrum and cerebellum being exposed.
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DISEASE TEXT FIGURES SUBJECT CREDIT/AUTHOR PAGE
VIRAL DISEASES
ARBOVIRUS INFECTIONS
Eastern equine encephalitis Figure 1a Perivascular cuffing in the brain; HP ML Brash; AHL; University of Guelph 8
Photo Index
Figure 2a Meningoencephalitis in a pheasant; HP ML Brash; AHL; University of Guelph 8

Figure 3a Meningoencephalitis in a pheasant; HP ML Brash; AHL; University of Guelph 8
Figure 4a Myocardial necrosis; HP ML Brash; AHL; University of Guelph 8
Figure 5a Immunohistochemistry (brain) ML Brash; AHL; University of Guelph 8
West Nile Virus Figure 1b General weakness in a WNV affected duck Alex Weisz, Guelph Poultry Veterinary Services 9
Figure 2b Flaccid heart with pale striking Alex Weisz, Guelph Poultry Veterinary Services 9
Figure 3b Myocarditis; HP MJ Stalker; AHL; University of Guelph 9
Figure 4b Immunohistochemistry (myocardium) MJ Stalker; AHL; University of Guelph 9
Figure 5b Immunohistochemistry (brain) MJ Stalker; AHL; University of Guelph 9
AVIAN ADENOVIRAL INFECTIONS

I. INCLUSION BODY HEPATITIS Figure 1 Jaundiced chicken JA Fricke; Poultry Health Services; Alberta; Canada 16
Figure 2 Swollen liver JA Fricke; Poultry Health Services; Alberta; Canada 16
Figure 3 Swollen kidneys JA Fricke; Poultry Health Services; Alberta; Canada 16
Figure 4 Necrotic hepatitis; HP HL Shivaprasad; CAHFS, UC Davis 16
Figure 5 Liver intranuclear inclusion bodies; HP HL Shivaprasad; CAHFS, UC Davis 16
II. HEMORRHAGIC ENTERITIS Figure 1 Hemorrhagic enteritis Cornell University 17

OF TURKEYS Figure 2 Intestinal & Spleenic Hemorrhage HJ Barnes; NCSU 17
Figure 3 Spleen intranuclear inclusion bodies; HP ML Brash; AHL; University of Guelph 17
III. EGG DROP SYNDROME-1976
IV. QUAIL BRONCHITIS Figure 1 Tracheitis Cornell University 17
AVIAN ENCEPHALOMYELITIS Figure 1 Chick with CNS signs Cornell University 19

Figure 2 Opacity of the eye in a turkey HL Shivaprasad; CAHFS, UC Davis 19
Figure 3 Cataract Cornell University 20
Figure 4 Whitish areas in musculature of the gizzard HL Shivaprasad; CAHFS, UC Davis 20
Figure 5 Perivascular cuffing in the brain; HP HL Shivaprasad; CAHFS, UC Davis 20
Figure 6 Brain, Central Chromatolysis; HP HJ Barnes; NCSU 20
Figure 7 Lymphoid aggregates in proventriculus ;HP HL Shivaprasad; CAHFS, UC Davis 20
AVIAN INFLUENZA Figure 1 LPAI; sinusitis in a turkey HL Shivaprasad; CAHFS, UC Davis 24

Figure 2 LPAI; fibrinopurulent sinusitis HL Shivaprasad; CAHFS, UC Davis 24
Figure 3 LPAI; airsacculitis HL Shivaprasad; CAHFS, UC Davis 24
Figure 4 LPAI; atretic ovarian follicles HL Shivaprasad; CAHFS, UC Davis 24
Figure 5 LPAI; egg yolk peritonitis HL Shivaprasad; CAHFS, UC Davis 24
Photo Index
Figure 6 LPAI; bronchopneumonia in a turkey HL Shivaprasad; CAHFS, UC Davis 24

Figure 7 HPAI; edema of the head J Copps; National Centre for Foreign Animal Disease, Canada 25
Figure 8 HPAI; edema of the head J Copps; National Centre for Foreign Animal Disease, Canada 25
Figure 9 HPAI; shank hemorrhages J Copps; National Centre for Foreign Animal Disease, Canada 25
279
Figure 10 HPAI; proventricular hemorrhages R Crespo; CAHFS, UC Davis 25

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280
AVIAN PNEUMOVIRUS INFECTION Figure 1 Turkey poult with nasal discharge KV Nagaraja; U of Minnesota 28
Figure 2 Sinusitis in a turkey KV Nagaraja; U of Minnesota 28
Figure 3 Submandibular edema in a dyspneic turkey KV Nagaraja; U of Minnesota 28
Figure 4 Swollen head syndrome in a chicken T Aziz; NCVDL; NCDA&CS 28
Figure 5 Immunohistochemistry in the nasal turbinates KV Nagaraja; U of Minnesota 28
AVIAN NEPHRITIS VIRUS Figure 1 Swollen kidneys in a chicken HL Shivaprasad; CAHFS, UC Davis 29
AVIAN VIRAL TUMORS Figure 1 Typical paresis HJ Barnes; NCSU 35

I. MAREK’S DISEASE Figure 2 Infiltration of iris HL Shivaprasad; CAHFS, UC Davis 35
Figure 3 Sciatic plexus enlargement HL Shivaprasad; CAHFS, UC Davis 35
Figure 4 Nerve enlargement & loss of striations HJ Barnes; NCSU 35
Figure 5 Discoloration of iris HJ Barnes; NCSU 35

Figure 6 Infiltration of feather follicles Cornell University 35
Figure 7 Visceral tumors HL Shivaprasad; CAHFS, UC Davis 36
Figure 8 Liver tumors HL Shivaprasad; CAHFS, UC Davis 36
Figure 9 Heart tumors HL Shivaprasad; CAHFS, UC Davis 36
Figure 10 Kidney tumors HL Shivaprasad; CAHFS, UC Davis 36
Figure 11 Proventricular tumor HJ Barnes; NCSU 36
Figure 12 Nerve infiltration; HP HL Shivaprasad; CAHFS, UC Davis 36
II. AVIAN LEUKOSIS/ Figure 1 Osteopetrosis Cornell University 37

SARCOMA VIRUS Figure 2 Visceral tumors in liver, heart and spleen Cornell University 37
Figure 3 Visceral tumors in bursa, kidneys and ovary Cornell University 37
Figure 4 Myelocytomatosis HL Shivaprasad; CAHFS; UC Davis 37
Figure 5 Hemangioma M Boulianne, University of Montreal 37
Figure 6 Transformed LL bursal follicle (bottom); HP AAAP Slide set #3 37
III. RETICULOENDOTHELIOSIS Figure 1 Liver tumor HL Shivaprasad; CAHFS, UC Davis 38
IV. LYMPHOPROLIFERATIVE
DISEASE
CHICKEN INFECTIOUS ANEMIA Figure 1 Hematocrit tubes AAAP Slide Set #20 40
Figure 2 Normal and atrophied thymus AAAP Slide Set #20 40
Figure 3 Normal and fatty bone marrow AAAP Slide Set #20 40
Figure 4 Petechiaes and hemorrhages in muscles AAAP Slide Set #20 40
Figure 5 Chick with dermatitis AAAP Slide Set #20 40
Figure 6 Normal and atrophied thymus; HP AAAP Slide Set #20 40
Figure 7 Normal and fatty bone marrow; HP AAAP Slide Set #20 41
Figure 8 Normal and atrophied Bursa of Fabricius; HP AAAP Slide Set #20 41
DUCK VIRAL HEPATITIS Figure 1 Opisthotonos in a duck HL Shivaprasad; CAHFS, UC Davis 45

Figure 2 Swollen liver with hemorrhages HL Shivaprasad; CAHFS, UC Davis 45
Figure 3 Hepatic necrosis and hemorrhages; HP HL Shivaprasad; CAHFS, UC Davis 45
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FOWL POX Figure 1 Pox scab HL Shivaprasad; CAHFS, UC Davis 48

Figure 2 Skin pox HL Shivaprasad; CAHFS, UC Davis 48
Figure 3 Skin pox AAAP Slide Set #16 48
Figure 4 Wet pox HJ Barnes; NCSU 48
Figure 5 Wet pox AAAP Slide Set #16 48
Figure 6 Turkey pox HL Shivaprasad; CAHFS, UC Davis 48
Figure 7 Tracheal epithelial hyperplasia; HP HL Shivaprasad; CAHFS, UC Davis 49
Figure 8 Cytoplasmic inclusion bodies; HP HL Shivaprasad; CAHFS, UC Davis 49
HEPATITIS E VIRUS Figure 1 Enlarged and hemorrhagic liver HL Shivaprasad; CAHFS, UC Davis 51
Figure 2 Enlarged and mottled spleens HL Shivaprasad; CAHFS, UC Davis 51
Figure 3 Hepatic hemorrhages; HP HL Shivaprasad; CAHFS, UC Davis 51
Figure 4 Amyloidosis in liver; HP HL Shivaprasad; CAHFS, UC Davis 51
Figure 5 Amyloidosis in liver; HP HL Shivaprasad; CAHFS, UC Davis 51
INFECTIOUS BRONCHITIS Figure 1 Chick with ocular discharge M Boulianne; University of Montreal 53
Figure 2 Misshapened eggs M Boulianne; University of Montreal 54
Figure 3 Urolithiasis HL Shivaprasad; CAHFS; UC Davis 54
Figure 4 Tracheitis HL Shivaprasad; CAHFS; UC Davis 54
Figure 5 Airsacculitis M Boulianne; University of Montreal 54
Figure 6 Tracheitis; HP HL Shivaprasad; CAHFS; UC Davis 54
Figure 7 Nephritis; HP HL Shivaprasad; CAHFS; UC Davis 54
INFECTIOUS BURSAL DISEASE Figure 1 Depressed chicken AAAP Slide Set # 14 57

Figure 2 Edematous bursa Cornell University 57
Figure 3 Hemorrhagic bursa HL Shivaprasad; CAHFS; UC Davis 57
Figure 4 Caseous exudate in bursa ML Gaucher; University of Montreal 57
Figure 5 Atrophied bursas AAAP Slide Set # 14 57
Figure 6 Muscle petechiation HL Shivaprasad; CAHFS; UC Davis 57
Figure 7 Lymphoid necrosis in bursa and normal; HP HL Shivaprasad; CAHFS; UC Davis 58
Figure 8 Atrophied bursa; HP HL Shivaprasad; CAHFS; UC Davis 58
INFECTIOUS
LARYNGOTRACHEITIS Figure 1 Chicken with dyspnea JA Fricke; Poultry Health Services; Alberta; Canada 60
Figure 2 Extended neck in a chicken M Boulianne; University of Montreal 60
Figure 3 Swollen eyelids JA Fricke; Poultry Health Services; Alberta; Canada 60
Figure 4 Hemorrhagic tracheitis HL Shivaprasad; CAHFS; UC Davis 61
Figure 5 Tracheal casts HL Shivaprasad; CAHFS; UC Davis 61
Figure 6 Intranuclear inclusion bodies; HP HL Shivaprasad; CAHFS; UC Davis 61
Figure 7 Intranuclear inclusion bodies; HP HL Shivaprasad; CAHFS; UC Davis 61
Photo Index
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282
NEWCASTLE DISEASE Figure 1 Misshapened eggs M Boulianne; University of Montreal 65

Figure 2 Chicken with dyspnea M Boulianne; University of Montreal 65
Figure 3 Tracheitis M Boulianne; University of Montreal 65
Figure 4 Conjunctival hemorrhage R Crespo; CAHFS, UC Davis 65
Figure 5 Diphtheritic laryngotracheitis R Crespo; CAHFS, UC Davis 65
Figure 6 Facial edema AAAP Slide set #4 65
Figure 7 Diphtheritic oro-pharyngo-esophagitis R Crespo; CAHFS, UC Davis 66
Figure 8 Proventricular hemorrhages R Crespo; CAHFS, UC Davis 66
Figure 9 Small intestine hemorrhage R Crespo; CAHFS, UC Davis 66
Figure 10 Cecal tonsil necrosis R Crespo; CAHFS, UC Davis 66
VIRAL ARTHRITIS Figure 1 Swollen hocks AAAP Slide Set # 1 69

Figure 2 Bird sitting on hocks AAAP Slide Set # 1 69
Figure 3 Ruptured gastrocnemius tendon L Munger; RADDL; NC Dept of Ag 69
Figure 4 Ruptured gastrocnemius tendon HL Shivaprasad; CAHFS; UC Davis 69
Figure 5 Eroded cartilage AAAP Slide Set # 1 69
Figure 6 Tendinitis/synovitis vs normal; HP AAAP Slide Set # 1 69
TURKEY CORONAVIRUS ENTERITIS Figure 1 Enteritis Cornell University 71

Figure 2 Immunohistochemistry of the intestines JS Guy; NCSU 71
TURKEY VIRAL HEPATITIS Figure 1 Hepatic necrosis HJ Barnes; NCSU 73

Figure 2 Pancreatic necrosis HJ Barnes; NCSU 73
BACTERIAL DISEASES
AVIAN CHLAMYDOPHILOSIS Figure 1 Giemsa stain elementary bodies Cornell University 76
Figure 2 Pericarditis Cornell University 76
Figure 3 Giemsa stain elementary bodies Cornell University 76
AVIAN TUBERCULOSIS Figure 1 Multifocal tubercles in intestines JA Fricke; Poultry Health Services; Alberta; Canada 79
Figure 2 Granulomas in liver and spleen HL Shivaprasad; CAHFS; UC Davis 79
Figure 3 Acid-fast bacilli in a tubercle; HP HL Shivaprasad; CAHFS; UC Davis 79
Figure 4 Acid-fast bacilli in liver; HP T Aziz; NCVDL; NCDA&CS 79
BORDETELLOSIS Figure 1 Conjunctivitis and bottle jaw HJ Barnes; NCSU 82

Figure 2 Collapsed trachea HL Shivaprasad; CAHFS, UC Davis 82
Figure 3 Trachea; HP HL Shivaprasad; CAHFS, UC Davis 82
BOTULISM Figure 1 Decaying carcass with maggots TK Bollinger; University of Saskatchewan 84

Figure 2 Limberneck in a chicken Cornell University 84
Figure 3 Limberneck in ducks TK Bollinger; University of Saskatchewan 84
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CAMPYLOBACTER Figure 1 Hepatic necrosis Y Robinson; Canadian Food Inspection Agency 86

COLIBACILLOSIS Figure 1 Normal airsac JA Fricke; Poultry Health Services; Alberta; Canada 90
Figure 2 Acute airsacculitis JA Fricke; Poultry Health Services; Alberta; Canada 90
Figure 3 Fibrinous airsacculitis JA Fricke; Poultry Health Services; Alberta; Canada 90
Figure 4 Chronic airsacculitis BR Charlton; CAHFS, UC Davis 90
Figure 5 Pericarditis & perihepatitis BR Charlton; CAHFS, UC Davis 90
Figure 6 Omphalitis HJ Barnes; NCSU 90
Figure 7 Omphalitis JA Fricke; Poultry Health Services; Alberta; Canada 91
Figure 8 Salpingitis BR Charlton; CAHFS, UC Davis 91
Figure 9 Coligranulomas Cornell University 91
Figure 10 Arthritis and synovitis JA Fricke; Poultry Health Services; Alberta; Canada 91
Figure 11 Cellulitis; skin lesions Y Robinson; Canadian Food Inspection Agency 91
Figure 12 Cellulitis; subcutaneous lesions Y Robinson; Canadian Food Inspection Agency 91
ENTEROCOCCUS CECORUM Figure 1 Chicken sitting on its hocks JA Fricke; Poultry Health Services; Alberta; Canada 93
Figure 2 Abscess in the vertebral column JA Fricke; Poultry Health Services; Alberta; Canada 93
Figure 3 Necrosis in the vertebral column ML Brash; AHL; University of Guelph 93
ERYSIPELAS Figure 1 Swollen & necrotic snood & wattle HJ Barnes; NCSU 96
Figure 2 Splenomegaly RM Fulton; DCPAH; Michigan State University 96
Figure 3 Liver, Gram stain; HP T. Aziz; NCVDL; NCDA&CS 96
FOWL CHOLERA Figure 1 Swollen wattles AAAP Slide Set # 19 99

Figure 2 Torticollis AAAP Slide Set # 19 99
Figure 3 Hepatic necrosis AAAP Slide Set # 19 99
Figure 4 Fibrinous pneumonia AAAP Slide Set # 19 99
Figure 5 Fibrinous pneumonia (HP) AAAP Slide Set # 19 100
Figure 6 Synovitis AAAP Slide Set # 19 100
Figure 7 Facial cellulitis AAAP Slide Set # 19 100
Figure 8 Gram-stained impression smear of liver AAAP Slide Set # 19 100
GANGRENOUS DERMATITIS Figure 1 Gangrenous skin JA Fricke; Poultry Health Services; Alberta; Canada 102
Figure 2 Emphysematous cellulitis JA Fricke; Poultry Health Services; Alberta; Canada 102
INFECTIOUS CORYZA Figure 1 Swollen sinus AAAP Slide Set # 10 105

Figure 2 Swollen wattles AAAP Slide Set # 10 105
Figure 3 Nasal exudate AAAP Slide Set # 10 105
Figure 4 Culture of A. paragallinarum AAAP Slide Set # 10 105
Photo Index
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MYCOPLASMOSIS
I. MYCOPLASMA Figure 1 Swollen infraorbital sinuses AAAP Slide Set # 11 112
GALLISEPTICUM INFECTION Figure 2 Acute airsacculitis AAAP Slide Set # 11 112
Figure 3 Airsacculitis AAAP Slide Set # 11 112
Figure 4 Airsacculitis; HP AAAP Slide Set # 11 112
Figure 5 Pericarditis, perihepatitis, airsacculitis AAAP Slide Set # 11 112
Figure 6 Rapid serum-plate-agglutination test AAAP Slide Set # 11 112
Figure 7 Hemagglutination inhibition (HI) test AAAP Slide Set # 11 113
Figure 8 Typical MG colonies AAAP Slide Set # 11 113
II. MYCOPLASMA
MELEAGRIDIS INFECTION Figure 1 Healthy appearing MM infected breeder flock AAAP Slide Set #13 114
Figure 2 Mild airsacculitis AAAP Slide Set #13 114

Figure 3 Airsacculitis HJ Barnes; NCSU 114
Figure 4 Bilateral varus deformity AAAP Slide Set #13 114
III. MYCOPLASMA
SYNOVIAE INFECTION Figure 1 Synovial exudate AAAP Slide Set # 12 115
Figure 2 Swollen footpads AAAP Slide Set # 12 115
Figure 3 Airsacculitis AAAP Slide Set # 12 115
Figure 4 Rapid serum-plate-agglutination test AAAP Slide Set # 12 115
Figure 5 Swabbing a chicken AAAP Slide Set # 12 115
Fluorescent-antibody (FA) test
Figure 6 AAAP Slide Set # 12 115
NECROTIC ENTERITIS Figure 1 Necrotic enteritis M Boulianne; University of Montreal 118

Figure 2 Diarrhea M Boulianne; University of Montreal 118
Figure 3 Dehydrated carcass M Boulianne; University of Montreal 118
Figure 4 Necrotic enteritis; HP T Aziz; NCVDL; NCDA&CS 118
ORNITHOBACTERIUM
RHINOTRACHEALE INFECTION Figure 1 Gram stain PC Van Empel; Intervet International 120
Figure 2 Pleuropneumonia T. Aziz; NCVDL; NCDA&CS 120
Figure 3 Airsacculitis PC Van Empel; Intervet International 120
Figure 4 Airsacculitis M Salem; Lohman Animal Health 120
Figure 5 Pleuropneumonia; HP T Aziz; NCVDL; NCDA&CS 120
Figure 6 Pneumonia; HP T Aziz; NCVDL; NCDA&CS 120
SALMONELLOSIS
I. PULLORUM DISEASE Figure 1 Atretic ovarian follicles F. Williams, III; Cornell University 129
Figure 2 Peritonitis AAAP Slide Set # 22 129
Figure 3 Nodular myocarditis AAAP Slide Set # 22 129
Figure 4 Cecal cores AAAP Slide Set # 22 129
Figure 5 Splenomegaly AAAP Slide Set # 22 129
Figure 6 Tube agglutination test AAAP Slide Set # 22 129
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II. FOWL TYPHOID Figure 1 Bile-stained ("bronzed") liver AAAP Slide Set # 22 130
with necrotic foci
III. ARIZONOSIS Figure 1 Torticollis HJ Barnes; NCSU 130

Figure 2 Cloudy eye HJ Barnes; NCSU 130
Figure 3 Encephalitis HJ Barnes; NCSU 130
IV. PARATYPHOID INFECTION Figure 1 Peritonitis, pericarditis, perihepatitis HL Shivaprasad; CAHFS; UC Davis 131
SPIROCHETOSIS Figure 1 Blood smear showing spirochetes Cornell University 133
STAPHYLOCOCCOSIS Figure 1 Swollen joint RM Fulton; DCPAH; Michigan State University 136
Figure 2 Osteomyelitis RM Fulton; DCPAH; Michigan State University 136
Figure 3 Green liver T Aziz; NCVDL; NCDA&CS 136
Figure 4 Osteomyelitis T Aziz; NCVDL; NCDA&CS 136
136
ULCERATIVE ENTERITIS Figure 1 Intestinal ulcers HJ Barnes; NCSU 138

Figure 2 Intestinal ulcers HL Shivaprasad; CAHFS, UC Davis 138
FUNGAL DISEASE
ASPERGILLOSIS Figure 1 Gasping chicks AAAP Slide Set #9 142
Figure 2 Lung nodules AAAP Slide Set #9 142
Figure 3 Tracheal plug HL Shivaprasad; CAHFS, UC Davis 142
Figure 4 Aspergillus fruiting body AAAP Slide Set #9 142
Figure 5 Aspergillus fumigatus on Sab Dex media AAAP Slide Set #9 142
CANDIDIASIS Figure 1 Crop mycosis HL Shivaprasad; CAHFS, UC Davis 144

Figure 2 Severe crop mycosis HL Shivaprasad; CAHFS, UC Davis 144
OCHRONOSIS Figure 1 Mycotic encephalitis HJ Barnes; NCSU 145
FAVUS Figure 1 White crusting of comb Cornell University 146
MYCOTOXICOSIS Figure 1 Tan liver vs. normal liver A Bermudez; VMDL, University of Missouri 150
Photo Index
I. AFLATOXICOSIS Figure 2 Tan liver A Bermudez; VMDL, University of Missouri 150

Figure 3 Swollen kidneys vs. normal A Bermudez; VMDL, University of Missouri 150
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II. CITRININ MYCOTOXICOSIS

III. ERGOTISM
IV. OCRATOXICOSIS
V. OOSPOREIN MYCOTOXICOSIS
VI. TRICHOTHECENE
MYCOTOXICOSIS Figure 1 Abnormal feathering F Hoerr; Auburn University 150
Figure 2 Oral ulceration & necrosis F Hoerr; Auburn University 150
VII. ZEARALENONE
MYCOTOXICOSIS
PARASITIC DISEASES
PARASITES AND PESTS
LICE Figure 1 Lice eggs on feathers Cornell University 153
MITES Figure 1 Northern fowl mites HL Shivaprasad; CAHFS, UC Davis 155

Figure 1 Scaly leg mites M Boulianne; University of Montreal 155
MISCELLANEOUS PESTS Figure 1 Darkling beetles ML Gaucher; University of Montreal 157

Figure 2 Darkling beetles ML Gaucher; University of Montreal 157
Figure 3 Darkling beetle larvae ML Gaucher; University of Montreal 157
I. NEMATODES, CESTODES AND

TREMATODES
ASCARIDS Figure 1 Intestinal ascarids HJ Barnes; NCSU 161
CECAL WORMS Figure 1 Heterakis worms Elanco 161

Figure 2 Heterakis in caecum Elanco 161
Figure 3 Heterakis egg Elanco 161
CAPILLARIA Figure 1 Capillaria worms Elanco 162

Figure 2 Capillaria in crop HL Shivaprasad; CAHFS, UC Davis 162
Figure 3 Capillaria egg Elanco 162
TAPEWORMS Figure 1 Tapeworm infestation HL Shivaprasad; CAHFS, UC Davis 162

Figure 2 Adult tapeworm Raillietina Elanco 162
Figure 3 Tapeworm egg (Raillietina spp) Elanco 162
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II. BLOOD-BORNE PROTOZOAL

PARASITES
HAEMOPROTEUS Figure 1 Haemoproteus R Nallar; University of Saskatchewan 163
LEUCOCYTOZOA Figure 1 Splenomegaly HL Shivaprasad; CAHFS, UC Davis 163

Figure 2 Leucocytozoons in blood smear C Dubé; University of Montreal 163
Figure 3 Leucocytozoon in leucocyte G Fitzgerald; University of Montreal 163
PLASMODIUM Figure 1 Plasmodium in erythrocytes G Fitzgerald; University of Montreal 163
III. PROTOZOAL INFECTIONS OF

THE DIGESTIVE TRACT
COCCIDIOSIS
Figure 1 E. acervulina HJ Barnes; NCSU 173
Figure 2 E. acervulina M Boulianne; University of Montreal 173
Figure 3 E. necatrix AAAP Slide Set #7 173
Figure 4 E. necatrix HJ Barnes; NCSU 173
Figure 5 E. necatrix; HP HL Shivaprasad; CAHFS; UC Davis 173
Figure 6 E. maxima AAAP Slide Set #7 173
Figure 7 E. brunetti SH Fitz-Coy, Merck 174
Figure 8 E. tenella M Boulianne; University of Montreal 174
Figure 9 E. tenella AAAP Slide Set #7 174
Figure 10 E. mivati SH Fitz-Coy, Merck 174
Figure 11 E. meleagrimitis HJ Barnes; NCSU 174
Figure 12 E. adenoides HJ Barnes; NCSU 174
HISTOMONIASIS Figure 1 Hepatitis & cecal cores HJ Barnes; NCSU 175

Figure 2 Cecal cores HL Shivaprasad; CAHFS, UC Davis 175
Figure 3 Hepatitis HL Shivaprasad; CAHFS, UC Davis 175
Figure 4 Histomonads in liver; HP HL Shivaprasad; CAHFS, UC Davis 175
TRICHOMONIASIS Figure 1 Lesions in the upper digestive tract HL Shivaprasad; CAHFS, UC Davis 175
Figure 2 Lesions in the upper digestive tract HL Shivaprasad; CAHFS, UC Davis 175
IV. OTHER PROTOZOAL

INFECTIONS
Photo Index
CRYPTOSPORIDIOSIS Figure 1 Cryptosporidia; HP HL Shivaprasad; CAHFS, UC Davis 176
SARCOSPORIDIA Figure 1 Sarcocysts in muscle Cornell University 176

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NUTRITIONAL DISEASES
BIOTIN DEFICIENCY Figure 1 Exudative dermatitis HJ Barnes; NCSU 180
Figure 2 Exudative dermatitis HJ Barnes; NCSU 180
RIBOFLAVIN DEFICIENCY Figure 1 Curled toe paralysis HL Shivaprasad; CAHFS, UC Davis 182
Figure 2 Severe curled toe paralysis HL Shivaprasad; CAHFS, UC Davis 182
Figure 3 Swollen sciatic nerve HL Shivaprasad; CAHFS, UC Davis 182
Figure 4 Myelin degeneration; HP HL Shivaprasad; CAHFS, UC Davis 182
VITAMIN A DEFICIENCY Figure 1 Caseous exudate under eyelid HL Shivaprasad; CAHFS, UC Davis 184
Figure 2 Distended mucosal glands in oesophagus HL Shivaprasad; CAHFS, UC Davis 184
Figure 3 Distended mucosal glands in crop HL Shivaprasad; CAHFS, UC Davis 184
Figure 4 Squamous metaplasia; HP HL Shivaprasad; CAHFS, UC Davis 184
VITAMIN E DEFICIENCY Figure 1 Chicks with paresis/paralysis HJ Barnes; NCSU 187

Figure 2 Hemorrhagic cerebellum HJ Barnes; NCSU 187
Figure 3 Exudative diathesis HL Shivaprasad; CAHFS, UC Davis 187
Figure 4 Pericardium distended with fluid HL Shivaprasad; CAHFS, UC Davis 187
Figure 5 Myopathy HL Shivaprasad; CAHFS, UC Davis 187
Figure 6 Gizzard muscle degeneration HJ Barnes; NCSU 187
RICKETS Figure 1 Rubbery beak Cornell University 189

Figure 2 Beaded ribs HJ Barnes; NCSU 189
Figure 3 Enlarged parathyroids HL Shivaprasad; CAHFS, UC Davis 189
FATTY LIVER-HEMORRHAGIC Figure 1 Subcapsular hepatic hemorrhage HL Shivaprasad; CAHFS, UC Davis 190
SYNDROME Figure 2 Liver with subcapsular hematocyst HL Shivaprasad; CAHFS, UC Davis 190
MISCELLANOUS DISEASES
CARDIOVASCULAR DISEASES OF
CHICKENS
I. ASCITES OR PULMONARY
HYPERTENSION SYNDROME Figure 1 Cyanotic chicken carcass AAAP #23 193
Figure 2 Ventricular hypertrophy and dilation HJ Barnes; NCSU 193
Figure 3 Ascites AAAP #23 193
Figure 4 Enlarged hearts and ascites AAAP #23 193
Figure 5 Fibrotic liver AAAP #23 193
II. SUDDEN DEATH SYNDROME Figure 1 Dead bird on its back M Boulianne; University of Montreal 194
Figure 2 Full digestive tract RJ Julian, University of Guelph 194
Figure 3 Mottled muscles, full crop M Boulianne; University of Montreal 194
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CARDIOVASCULAR DISEASES OF
CARDIOVASCULAR
TURKEYS DISEASES OF
TURKEYS
I. AORTIC RUPTURE OR Figure 1 Internal hemorrhage HJ Barnes; NCSU 197
I. AORTIC RUPTURE
DISSECTING OR
ANEURYSM Figure 12 Internal
Rupturedhemorrhage
aorta HJ
HLBarnes;
Shivaprasad;
NCSUCAHFS, UC Davis 197
DISSECTING ANEURYSM Figure 2 Ruptured aorta HL Shivaprasad; CAHFS, UC Davis 197
II. DILATED CARDIOMYOPATHY Figure 1 Dilated cardiomyopathy HJ Barnes; NCSU 197

II. DILATED CARDIOMYOPATHY
OF TURKEYS Figure 12 Dilated cardiomyopathy HJ
HLBarnes;
Shivaprasad;
NCSUCAHFS; UCDavis 197
OF TURKEYS Figure 23 Dilated cardiomyopathy
Hydropericardium and ascites HL Shivaprasad;
HJ Barnes; NCSUCAHFS; UCDavis 197
Figure 3 Hydropericardium and ascites HJ Barnes; NCSU 197
III. SUDDEN DEATH SYNDROME

III. SUDDEN DEATH
OF TURKEYS SYNDROME
(PERIRENAL
OF TURKEYS (PERIRENAL
HEMORRHAGE) Figure 1 Perirenal hemorrhage HJ Barnes; NCSU 198
HEMORRHAGE) Figure 1 Perirenal hemorrhage HJ Barnes; NCSU 198
DIGESTIVE DISORDERS
DIGESTIVE DISORDERS
I. PENDULOUS CROP Figure 1 Pendulous crop M Boulianne; University of Montreal 199
I. PENDULOUS CROP Figure 1 Pendulous crop M Boulianne; University of Montreal 199
II. PROVENTRICULAR DILATION Figure 1 Enlarged proventriculus HL Shivaprasad; CAHFS; UCDavis 199
II. PROVENTRICULAR DILATION Figure 1 Enlarged proventriculus HL Shivaprasad; CAHFS; UCDavis 199
DIGESTIVE DISORDERS OF
DIGESTIVE
CHICKENS DISORDERS OF
CHICKENS
I. DYSBACTERIOSIS Figure 1 Dysbacteriosis Elanco 202

I. DYSBACTERIOSIS Figure 1 Dysbacteriosis Elanco 202
II. POLYCYSTIC ENTERITIS Figure 1 Loss of flock uniformity J Smith; Fieldale Farms 202
II. POLYCYSTIC ENTERITIS Figure 12 Loss of flock
Dilated uniformity
thin-walled intestines J Smith; Fieldale Farms 202
Figure 23 Dilated thin-walled intestines J Smith; Fieldale Farms 202
Figure 34 Dilated thin-walled
Polycystic intestines
enteritis; HP Smith;
JHL Fieldale Farms
Shivaprasad; CAHFS; UCDavis 202
Figure 4 Polycystic enteritis; HP HL Shivaprasad; CAHFS; UCDavis 202
III. TRANSMISSIBLE VIRAL Figure 1 Proventricular enlargement JS Guy; NCSU 203

III. TRANSMISSIBLE VIRAL
PROVENTRICULITIS Figure 12 Proventricular
Proventriculitis;enlargement
HP JS
T Aziz;
Guy; NCVDL;
NCSU NCDA&CS 203
PROVENTRICULITIS Figure 2 Proventriculitis; HP T Aziz; NCVDL; NCDA&CS 203
IV. FOCAL DUODENAL NECROSIS Figure 1 Necrotic areas in the duodenum E. Gingerich; Diamond V 203
IV. FOCAL DUODENAL NECROSIS Figure 12 Necrotic areas
foci ininthe duodenum
theduodenum E. Gingerich; Diamond V 203
Figure 23 Necrotic
Duodenalfoci
necrosis; duodenum
in the HP E. Gingerich;
P.A. Diamond
Dunn; Penn V
State University 203
Figure 3 Duodenal necrosis; HP P.A. Dunn; Penn State University 203
DIGESTIVE DISORDERS OF TURKEYS
DIGESTIVE DISORDERS OF TURKEYS
Photo Index

B. POULT MALABSORPTION / Figure 1 Dilated thin-walled intestines HL Shivaprasad; CAHFS; UCDavis 206
B. POULT MALABSORPTION
RUNTING-STUNTING /
SYNDROME Figure 12 Dilated thin-walled intestines HL Shivaprasad; CAHFS; UCDavis 206
289
RUNTING-STUNTING SYNDROME Figure 2 Dilated thin-walled intestines HL Shivaprasad; CAHFS; UCDavis 206
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C. POULT ENTERITIS MORTALITY Figure 1 Lack of uniformity HJ Barnes; NCSU 207

SYNDROME Figure 2 Uneven turkey flock HJ Barnes; NCSU 207
Figure 3 Dehydrated poult HJ Barnes; NCSU 207
Figure 4 Thin-walled and dilated small intestines JS Guy; NCSU 207
Figure 5 Poorly digested intestinal content HJ Barnes; NCSU 207
Figure 6 Distended ceca HJ Barnes; NCSU 207
Figure 7 Normal thymus in a poult HJ Barnes; NCSU 208
Figure 8 Atrophied thymus HJ Barnes; NCSU 208
MUSCULOSKELETAL DISORDERS
I. ANGULAR BONE DEFORMITY Figure 1 Valgus RJ Julian; University of Guelph 212

Figure 2 Varus RJ Julian; University of Guelph 212
II. CHONDRODYSTROPHY Figure 1 Chondrodystrophy RJ Julian; University of Guelph 212
III. CONTACT DERMATITIS OF Figure 1 Pododermatitis M Boulianne; University of Montreal 212

FOOT PADS
IV. DEEP PECTORAL MYOPATHY Figure 1 Deep pectoral myopathy HL Shivaprasad; CAHFS, UC Davis 213
Figure 2 Deep pectoral myopathy HJ Barnes; NCSU
VIII. OSTEOMYELITIS Figure 1 Femoral osteomyelitis HJ Barnes; NCSU 213
IX. OSTEOMYELITIS / SYNOVITIS Figure 1 Synovitis M Boulianne; University of Montreal 213
X. OSTEOPOROSIS Figure 1 Posterior paralysis AAAP Slide Set #8 214

Figure 2 Acute paralysis AAAP Slide Set #8 214
Figure 3 Osteoporosis; HP AAAP Slide Set #8 214
Figure 4 Infolding of the ribs AAAP Slide Set #8 214
Figure 5 Enlarged parathyroid glands AAAP Slide Set #8 214
XIV. SPLAY LEG Figure 1 Splay leg M Boulianne; University of Montreal 215
XV. SPONDYLOLISTHESIS Figure 1 Spondylolisthesis HJ Barnes; NCSU 215

Figure 2 Hock-sitting posture AAAP Slide Set #8 215
XVI. TENDON AVULSION AND Figure 1 Ruptured gastrocnemius tendon AAAP Slide Set #8 215
RUPTURE
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XVII. TIBIAL DYSCHONDROPLASIA Figure 1 Tibial dyschondroplasia HJ Barnes; NCSU 216

Figure 2 Tibial dyschondroplasia HL Shivaprasad; CAHFS, UC Davis 216
XVIII. TIBIAL ROTATION Figure 1 Tibial rotation AAAP Slide Set #8 216
Figure 2 Tibial rotation HJ Barnes; NCSU 216
Figure 3 Tibial rotation HJ Barnes; NCSU 216
XIX. TWISTED TOES Figure 1 Twisted toes AAAP Slide Set #8 217
REPRODUCTIVE DISORDERS
I. OVARIAN LESIONS Figure 1 Atretic ovary and oviduct M Boulianne; University of Montreal 220
Figure 2 Atretic ovary and oviduct M Boulianne; University of Montreal 220
II. OVIDUCT LESIONS Figure 1 Salpingitis RJ Julian; University of Guelph 221

Figure 2 Salpingitis RJ Julian; University of Guelph 221
Figure 3 Prolapsed oviduct RJ Julian; University of Guelph 221
URINARY DISORDERS
UROLITHIASIS Figure 1 Urolithiasis HL Shivaprasad; CAHFS, UC Davis 222
INTEGUMENT DISORDERS
I. KERATOCONJUNCTIVITIS Figure 1 Keratoconjunctivitis M Boulianne; University of Montreal 223
II. SCABBY HIP SYNDROME Figure 1 Scabby hip syndrome Y Robinson; Canadian Food Inspection Agency 223
III. STERNAL BURSITIS Figure 1 Sternal bursitis M Boulianne; University of Montreal 223
IV. XANTHOMATOSIS Figure 1 Xanthomatosis Cornell University 224
BEHAVIOR DISORDERS
CANNIBALISM Figure 1 Head pecking M Boulianne; University of Montreal 225
Photo Index
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MANAGEMENT-RELATED
DISORDERS
I. DEHYDRATION/STARVATION Figure 1 Dehydrated chick M Boulianne; University of Montreal 228
Figure 2 Urate deposits on pericardium JA Fricke; Poultry Health Services; Alberta; Canada 228
Figure 3 Urate deposits on muscles JA Fricke; Poultry Health Services; Alberta; Canada 228
Figure 4 Urate deposits in the joint JA Fricke; Poultry Health Services; Alberta; Canada 228
Figure 5 Bilateral ureter dilation JA Fricke; Poultry Health Services; Alberta; Canada 228
II. HYPOGLYCEMIA-SPIKING Figure 1 Hypoglycemia in live chicks JA Fricke; Poultry Health Services; Alberta; Canada 229
MORTALITY SYNDROME Figure 2 Small hemorrhages in the liver JA Fricke; Poultry Health Services; Alberta; Canada 229
IV. VACCINE REACTION Figure 1 Young chicken with ocular discharge M Boulianne; University of Montreal 229
APPENDIX
NECROPSY OF THE FOWL Figure 1 Cervical dislocation M Boulianne; University of Montreal 273
Figure 2 Intravenous injection of barbiturate M Boulianne; University of Montreal 273
Figure 3 Examination of the head M Boulianne; University of Montreal 273
Figure 4 Cut across the upper beak M Boulianne; University of Montreal 273
Figure 5 Sinus and turbinates exposed M Boulianne; University of Montreal 273
Figure 6 Infraorbital sinus exposed M Boulianne; University of Montreal 273
Figure 7 Scissors at commissure of the beak M Boulianne; University of Montreal 274
Figure 8 Esophagus being exposed M Boulianne; University of Montreal 274
Figure 9 Trachea being opened M Boulianne; University of Montreal 274
Figure 10 Check the feathers and skin M Boulianne; University of Montreal 274
Figure 11 Incision of skin between thigh & abdomen M Boulianne; University of Montreal 274
Figure 12 Hip joint dislocation M Boulianne; University of Montreal 274
Figure 13 Removal of the skin of the breast M Boulianne; University of Montreal 275
Figure 14 Breaking the metatarsal bone M Boulianne; University of Montreal 275
Figure 15 Opening of the tibiotarsal joint M Boulianne; University of Montreal 275
Figure 16 Cut through the tibial head M Boulianne; University of Montreal 275
Figure 17 Examination of the sciatic nerve M Boulianne; University of Montreal 275
Figure 18 Removal of the breast M Boulianne; University of Montreal 275
Figure 19 Examination of the air sacs M Boulianne; University of Montreal 276
Figure 20 Incision of the peritoneum M Boulianne; University of Montreal 276
Figure 21 Cutting the esophagus M Boulianne; University of Montreal 276
Figure 22 Removal of the heart M Boulianne; University of Montreal 276
Figure 23 Examination of the spleen M Boulianne; University of Montreal 276
Figure 24 Examination of the bursa M Boulianne; University of Montreal 276
Figure 25 Incision of the proventriculus M Boulianne; University of Montreal 277
Figure 26 Proventriculus and gizzard opened M Boulianne; University of Montreal 277
Figure 27 Opening the duodenum M Boulianne; University of Montreal 277
Figure 28 Immature testicles M Boulianne; University of Montreal 277
Figure 29 Single left immature ovary M Boulianne; University of Montreal 277
Figure 30 Kidneys and ureters M Boulianne; University of Montreal 277
Figure 31 Taking the lung out M Boulianne; University of Montreal 278
Figure 32 Lung being exposed M Boulianne; University of Montreal 278
Figure 33 Cerebrum and cerebellum being exposed M Boulianne; University of Montreal 278
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Index
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A Avipoxvirus, 46, 247

Adenoviruses, 10-11
Aflatoxicosis, 101, 147-148, 150, B
231, 250-251, 285 Bedbugs, 156
Aortic rupture (Dissecting aneurysm), 195, Biotin deficiency, 180, 254, 259, 288
197, 209, 212, 239, 242, 244, 289-290 Birnaviridae, 55
APMV-1, 62-64 Blackflies, 156
Arbovirus, 6, 239, 241, 243, 279 Bordetella avium, 80, 103, 119, 257
Ascaridia galli, 158, 177 Bordetellosis (Turkey coryza, TC),
Ascarids, 158, 161, 286 80-82, 103, 241-242, 257, 269, 282
Ascites (pulmonary hypertension), 1, Borrelia anserina, 132, 156
123, 149, 191, 193-195, 197, 219, Botulism (Limberneck, Western Duck
238, 244, 252, 270, 288-289 Sickness), 83-84, 156, 230, 235,
Aspergillosis (Brooder pneumonia, Mycotic 239, 241, 245, 250, 268, 282
pneumonia, pneumomycosis), 75,
107, 126, 140-142, 145, 230, 235, C
238, 241-243, 245, 257, 270, 285
Cage layer fatigue, 188-189, 210,
Aspergillus flavus, 151, 251 214, 240, 254, 269
Aspergillus fumigatus, 140, 142, 257, 285 Campylobacter, 85-86, 252, 283
Astrovirus, 29, 44, 70, 204, 231, 251 Candida albicans, 143, 199, 247
Atadenovirus, 10 Candidiasis (Thrush, moniliasis, crop
Atoxoplasma, 159 mycosis), 143-144, 170-171,
Aviadenovirus, 10, 204 239, 241, 247, 250, 269, 285
Avian chlamydiosis (Psittacosis, Ornithosis), Cannibalism, 1, 6, 46-47, 94, 97, 101, 123,
74-76, 154, 231, 253, 257, 268, 282 132, 139, 219, 225, 240-242, 268, 270, 291
Avian encephalomyelitis (AE, Epidemic Capillaria (Thread worm), 158-159, 162,

tremor), 18-20, 238-241, 245, 271-272, 279 177, 235, 239, 247, 249, 269, 286
Avian influenza (AI), 21-25, 42-43, 45, Cecal worms, 158, 161, 169, 178,
53, 107, 218, 230, 239-240, 242-243, 243, 249, 251, 271, 286
257, 262, 268, 271-272, 279 Cellulitis, 87-88, 91, 100-102,
Avian leukosis/sarcoma virus 134, 239, 259, 269, 283
(ALV), 30-33, 37, 256, 280 Chicken infectious anemia (CIA, Chicken
Avian metapneumovirus infection Anemia Virus, Chicken Anemia Agent,
(aMPV), 26-28, 242-243 Blue Wing Disease), 11, 33, 39-41, 87,
101, 137, 238-239, 253, 270, 280
Avian nephritis virus (ANV), 29, 280
Chicken mite, 154
Avian tuberculosis (TB, avian TB),
77-79, 230, 235, 241, 248, 251, 271 Chiggers, 156
Avian viral tumors, 30, 280 Chlamydophila psittaci (Chlamydia

psittaci), 74, 231, 244, 257, 270
Avibacterium paragallinarum (Hemophilus
paragallinarum), 103, 106 Chondrodystrophy, 109, 180,209-
210, 212, 255, 290
Avibirnavirus, 55, 249, 253
Circoviridae, 39, 253 Enterovirus, 44, 70, 204

Citrinin, 148, 151-152, 286 Ergotism, 147-148, 151-152, 286
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Clostridium botulinum, 83, 245 Erysipelas, 13, 70, 94-96, 98, 242,
Clostridium colinum, 137, 201, 250, 252 244, 250, 259, 271, 283
Clostridium perfringens, 117, 137, 250 Erysipelothrix rhusiopathiae, 94
Clostridium septicum, 101, 269 Escherichia coli, 13, 26, 52, 63, 80-81,
87, 106, 119, 135, 204, 210, 218,
Coccidiosis, 13, 43, 55-56, 70, 101, 117,
227, 231, 235, 238-239, 242,
137, 143, 164-167, 171, 233, 238,
244-245, 248-249, 258-259, 269
240-241, 248, 250, 269-271, 287
Excess mortality of turkeys (EMT), 204
Colibacillosis, 12, 75, 87-91, 98,
107-108, 124, 126, 218, 231, 235,
239-240, 242, 244, 248, 283 F
Contact dermatitis of foot pads (podo- Fatty liver-hemorrhagic syndrome (FLHS,
dermatitis, bumblefoot), 134, Fatty liver syndrome), 50, 180, 190
209-212, 239, 242, 254, 269, 290 Favus (Avian ringworm, Avian der-
Coronavirus, 52, 70, 204, 250, 258, 261, 282 matophytosis), 146, 285
Cryptosporidiosis, 107, 170-171, 176, 241, 287 Femoral head necrosis, 92, 209, 245, 254
Cryptosporidium, 170-171, 268 Focal Duodenal Necrosis 137, 201, 203, 289
Cystic oviducts, 218 Fowl Cholera (Cholera, Pasteurellosis),
13, 22, 43, 68, 75, 81, 88, 95, 97-100,
D 103, 107, 154, 183, 218, 232, 236, 240,
242-243, 245, 250-251, 268, 270-271, 283
Darkling beetle, 156, 286
Fowl pox (Pox, Avian pox), 19, 33, 46-49, 98,
Deep pectoral myopathy (Exertional myopathy, 103, 154, 156, 170, 234, 236, 238-239,
green muscle disease), 209, 213, 290 243, 246-247, 259, 268-269, 281
Dehydration/starvation of chicks/poults, 228 Fowl ticks, 156
Depluming mites, 154 Fowl typhoid, 88, 110, 122, 124-125,
Dermanyssus gallinae, 154 127, 130, 248, 252, 256, 271, 285
Digestive disorders, 199-200, 204, 289 Fusarium, 149, 151-152, 211, 247
Dilated cardiomyopathy of turkeys, 197
Duck hepatitis (DH, DHV, Duck viral hepatitis), G
29, 42-45, 231, 247-248, 251, 253, 280 Gangrenous dermatitis (Necrotic der-
Duck virus enteritis (DVE, Duck plague), matitis), 39, 56, 101-102, 134,
42-43, 231, 247-248, 253 238-239, 249, 253, 259, 269, 283
Dysbacteriosis, 200, 202, 289 Gapeworms, 177, 237

Gyrovirus, 39, 253
E
Eastern equine encephalitis virus H
(EEEV), 6-8, 239, 243 Haemoproteus, 159, 163, 287
Egg drop syndrome, 10, 13, 279 Heat stress and hyperthermia, 227
Eimeria, 1, 164-167, 173-174, 233, 248 Hemorrhagic enteritis of turkeys
Enterococcus cecorum, 92-93, (HEV), 10, 13, 17, 50-51
210, 239, 245, 254, 283
Index 295
Hepatitis E virus (HEV, Hepatitis-Splenomegaly Lesser mealworm, 156

syndrome in chickens), 50-51, 240, 281 Leukocytozoa, 159, 163
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Hepatovirus, 18, 245 Lice, 153, 243, 259, 268-269, 286

Herpesviridae, 59, 258 Lymphoid leukosis (LL), 31-34, 37, 240,
Herpesvirus, 30-31, 42, 59, 61, 231, 252-253, 256, 270-271, 280
244, 246-249, 253, 256, 261 Lymphoproliferative disease of turkeys
Heterakis gallinae, 158 (LPD), 30, 33-34, 243, 280
Hexamitiasis, 70, 167-168, 249
Highlands J virus (HJV), 6-7, 243 M
Histomonas meleagridis, 158, 168, 178, 249 Mareks’ Disease (MD), 19, 30-36, 39, 83,
106, 156, 218, 238-240, 244, 246, 249,
Histomoniasis (Blackhead, Enterohepatitis),
252-253, 256, 269-272, 280, 293
72, 158, 166-169, 175, 178, 235,
238, 242, 249, 251, 270-271, 287 Microsporum gallinae, 146
Hypoglycemia-spiking mortality syndrome in Mites, 132, 153-156, 160, 240,
broiler, 167, 180, 226, 229, 238, 246, 292 243, 259, 268-270, 286
Hysteria, 219, 225, 240 Mosquitos, 6, 17, 33, 46, 132, 156,
160, 234, 235, 237, 245, 259
I mycobacterium avium, 77, 230,
235, 248, 251, 270
Iatrogenic trauma, 209
Mycoplasma gallisepticum (MG, Chronic
Iltovirus, 59, 258, 261
Respiratory Disease, CRD, infectious
Inclusion body hepatitis (IBH), 10-11, 16, Sinusitis of turkeys), 75, 80, 83, 103,
55-56, 238, 249, 251, 253, 279 106-110, 112-113, 141, 169-170, 180, 186,
Infectious bronchitis (IB, IBV), 52-54, 226, 236, 242, 258, 261, 263-268, 271, 284
80, 87, 103, 106-107, 119, 171, Mycoplasma iowae, 106, 111
218, 222, 227, 239-240, 256, 258,
Mycoplasma meleagridis (MM), 72-73,
261-262, 268-269, 271, 281
108-109, 114, 116, 153-154, 156,
Infectious bursal disease (IBD, IBDV, 172, 177-178, 183, 234, 236,
Gumboro disease), 11, 33, 39, 55-58, 242, 247, 251-252, 284
101, 117, 134-135, 137, 156, 171, 201,
Mycoplasma synoviae (MS, Infectious
238-239, 251, 253, 259, 271, 281
Synovitis, Tenovaginitis), 107-110,
Infectious coryza (Coryza), 80, 103-105, 183, 115-116, 239, 242, 254, 270, 284
239-242, 257, 261-262, 268-269, 283
Mycoplasmosis, 22, 68, 106, 108,
Infectious laryngotracheitis (ILT), 59-61, 239-240, 242-243, 256, 258, 284
103, 239-240, 268-269, 281
Mycotoxicosis, 147-151, 247,
251, 269, 285-286
K Myelocytomatosis, 31-32, 37, 218, 280
Keratoconjunctivitis (ammonia burn),
223, 238, 241, 268, 291
N
Knemidokoptes gallinae, 154
Necrotis enteritis (NE), 117-118, 164, 166-167,
Knemidokoptes mutans, 154 200-201, 238, 240, 242, 249-250, 284
Nematodes, 158-159, 161-162, 177-178, 286
L Newcastle disease (ND), 19, 22, 42-43,
Large intestinal roundworms, 158 45, 62-66, 75, 87, 95, 106, 154,
171, 218, 227, 239-240, 242-243, Poxviridae, 46

246, 258, 268-269, 271-272, 282 Poxvirus, 46-47, 234, 259
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Northern fowl mite, 154 Proventricular dilation, 199, 289

Pullorum disease, 110, 122-125, 129,
O 218, 244, 250, 252, 256, 284
Ochratoxicosis (ochratoxin),
147-149, 151-152, 222 Q
Ochroconis gallopava (Dactylaria Quail bronchitis, 10, 14, 17, 237, 279
gallopava), 145, 246, 257
Ochroconosis (Dactylariosis), 145, 246 R
Oophoritis, 98, 218, 244, 250, 256 Red mite, 154
Oosporein, 149, 151-152, 286 Reovirus infections, 171
Ornithobacterium rhinotracheale Reticuloendotheliosis (RE), 30-34,
(ORT, OR), 119-120, 242, 284 38, 101, 243, 280
Ornithonyssus sylviarum, 154 Retrovirus, 30, 33, 256
Orthomyxovirus, 230, 257 Riboflavin deficiency (Vitamin B2 de-
Osteomyelitis, 88, 92, 108-109, 134-136, ficiency, Curled toe paralysis),
139, 209-210, 213, 239, 242, 181-182, 211, 254, 260, 288
245, 254-255, 270, 285, 290 Rickets, 179, 188, 204, 209-210, 238-239,
Osteoporosis, 209-210, 214, 254, 269, 290 241, 254-255, 269-270, 288
Ovarian cysts, 218 Round heart disease of chickens, 192
Oviducts, 13, 53, 149, 218
S
P Salmonella gallinarum, 124, 248
Paramyxovirus, 22, 27, 62, 119, Salmonella pullorum, 122, 124,
230, 246, 258, 261 244, 250, 252, 256
Pasteurella multocida, 97, 119, 171, Salmonellosis (Paratyphoid infection), 13,
232, 236, 242, 245, 251, 271 68, 70, 85, 95, 122, 126-127, 131, 139,
Pendulous crop, 199, 243, 247, 269, 289 166-168, 171, 241, 250-252, 284
Perosis (slipped tendon), 109, Salpingitis, 87-88, 107, 116, 218-219, 221,
180, 209-211, 255, 259 240, 243, 248, 256, 258, 271, 283, 291
Picornaviridae, 18, 44, 245 Scabby hip syndrome, 223, 269, 291
Picornavirus, 72, 231, 251 Scaly leg mite, 154
Pigeon flies, 156 Shaky leg, 210
Plasmodium, 159-160, 163, 270, 287 Siadenovirus, 10, 236, 249
Polycystic enteritis of broiler chickens Spirochetosis, 132-133, 154, 156, 250, 285
(Runting-Stunting Syndrome of Spironucleus, 167-168, 249
broiler chickens), 200, 202 Splay leg, 210, 215, 238, 241, 255, 290
Poult enteritis mortality syndrome Spondylolisthesis, 92, 210, 215,
(PEMS), 204, 207-208 239, 242, 270, 290
Poult malabsorption/runting- Staphylococcosis, 134-136, 239, 241, 253, 285
stunting syndrome, 204
Poultry enteritis complex (PEC), 204-205, 289
Index 297
Staphylococcus aureus, 101, Vitamin E deficiency, 185-187,

103, 134-135, 141, 255 238-239, 241, 245, 272, 288
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Sternal bursitis (breast blister, breast button, West Nile virus (WNV), 6-7, 9, 234, 237, 279
breast burn), 209-210, 223, 291 Western equine encephali-
Sticktight fleas, 156 tis virus (WEEV), 6-7, 243
Sudden death syndrome of turkeys (perirenal Xanthomatosis, 224, 260, 291
hemorrhage), 195-196, 198, 242, 270, 289 Yersinia pseudotuberculosis, 98, 139
Syngamus trachea, 237 Yersiniosis, 139
Synovitis, 68, 87-88, 91, 100, 109-110, Zearalenone, 147, 149, 151-152, 286
115-116, 134-135, 210, 213, 239,
250, 253-254, 270, 282-283, 290
Tapeworms, 156, 158, 178, 239, 249, 271, 286
Tendon avulsion, 210, 215, 290
Tendon rupture, 67
Tibial dyschondroplasia, 211,
216, 239, 242, 255, 291
Tibial rotation (twisted leg), 211, 216, 241, 291
Transmissible viral proventricu-
litis (TVP), 201, 203
Trichomonas gallinae, 169, 247
Trichomoniasis (Canker, Frounce), 70,
167-170, 175, 247, 269, 287
Trichothecene (Fusariotoxicosis), 149-150, 286
Trypanosomes, 160
Turkey coronavirus enteritis (tcv), 70, 204, 282
Turkey rhinotracheitis, 26, 242
Turkey viral hepatitis, 72-73,
171, 241, 253, 282
Twisted toes, 211, 217, 291
Ulcerative enteritis (Quail disease), 117, 137,
164, 166-167, 238, 242, 250, 252, 285
Urolithiasis (nephrosis, gout, renal gout,
Caged layer nephritis), 29, 52, 148-149,
152, 222, 254, 270-271, 281, 291
Vaccine reaction (rolling reaction),
60, 98, 227, 229, 292
Valgus, 209, 212, 239, 242, 269, 290
Varus, 109, 180, 209, 212, 239,
242, 269, 284, 290
Viral arthritis, 67, 69, 110, 239, 255, 270, 282
Vitamin A deficiency, 103, 143,
183, 222, 247, 288
Acknowledgements
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We gratefully acknowledge the contributions of the following resources:
American Association of Avian Pathologists (AAAP), Avian Diseases, 12627 San Jose Blvd, Suite 202, Jacksonville,
Florida 32223-8638
American Association of Avian Pathologists (AAAP), Slide Study Sets 1 – 25, 12627 San Jose Blvd, Suite 202,
Jacksonville, Florida 32223-8638
Saif, YM. (ed). 2008. Diseases of Poultry, 12th ed. Iowa State University Press, Ames, IA
Davis, JW, RC Anderson, L Karstad, and DO Trainer (ed). 1971. Infectious and Parasitic Diseases of Wild Birds. The
Iowa State University Press, Ames, IA
Jordan, FTW. (ed). 2001. Poultry Diseases, 5th ed. W. B. Saunders, London; New York
Macwhirter, P. 1987. Everybird. A Guide to Bird Health, Inkata Press, Sydney, Australia.
Kahn, CM. 2005. The Merck Veterinary Manual, 9th ed. Merck and Co., Inc., Whitehouse Station, NJ.
Rosskopf, WJ and RW Woerpel (ed). 1996. Diseases of Cage and Aviary Birds, 3rd ed. Williams & Wilkins, Baltimore,
MD.
Proceedings of the Western Poultry Disease Conference, 1973-2012. Cooperative Extension, University of California,
Davis, CA
Dufour-Zavala, L, DE Swayne, JR Glisson, MW Jackwood, JE Pearson and WM Reed (eds). 2008. A Laboratory Manual
for the Isolation and Identification of Avian Pathogens, 5th ed. AAAP, 12627 San Jose Blvd, Suite 202, Jacksonville,
Florida 32223-8638
Randall, CJ. 1991. Color Atlas of Diseases and Disorders of the Domestic Fowl and Turkey, 2nd ed. Iowa State University
Press, Ames, IA
Fletcher, OJ, T Abdul-Aziz. Avian Histopathology. 2008, 3rd ed. AAAP, 12627 San Jose Blvd, Suite 202, Jacksonville,
Florida 32223-8638
Ritchie BW, GJ Harrison, and LR Harrison. 1994. Avian Medicine: Principles and Application, Wingers Publishing, Inc.,
Lake Worth, FL
Shane, SM. (ed.) 1995. Biosecurity in the Poultry Industry, AAAP, 12627 San Jose Blvd, Suite 202, Jacksonville, Florida
32223-8638
Steiner, CV and RB Davis. 1981. Caged Bird Medicine, Iowa State University Press, Ames, IA
Wobeser, GA. 1997. Diseases of Wild Waterfowl, Plenum Press, New York, NY
World Veterinary Poultry Association. Avian Pathology, Taylor & Francis Ltd., London
CONTRIBUTING AUTHORS 299
CONTRIBUTING AUTHORS
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Martine Boulianne Davor Ojkic

Faculté de médecine vétérinaire Animal Health Laboratory
Université de Montréal University of Guelph
PO Box 5000 PO Box 3612
St Hyacinthe, QC Canada J2S 7C6 Guelph, ON Canada N1H 6R8
Marina L. Brash Linnea J. Newman

Animal Health Laboratory Merck Animal Health
University of Guelph 17 Pine Street
PO Box 3612 North Creek, NY 12853
Guelph, ON Canada N1H 6R8
Jean E. Sander
Bruce R. Charlton Ohio State University-CVM
CAHFS Turlock Branch 6828 Spruce Pine Drive
University of California – Davis Columbus, OH 43235
3327 Chicharra Way
Coulterville, California 95311 H. L. Shivaprasad
CAHFS-Tulare Branch
Steve Fitz-Coy 999 E. Edgemont Drive
Merck Fresno, CA 93720
PO Box 2074
Salisbury, MD 21802 United States Eva Wallner-Pendleton
Pennsylvania Animal Diagnostic Laboratory
Richard M. Fulton System/PennState University
Diagnostic Center for Population 149 Centennial Hills Road
and Animal Health Port Matilda, PA 16870
Michigan State University
PO Box 30076 Peter R. Woolcock
Lansing, Michigan, 48909 CAHFS - University of California – Davis
West Health Sciences Drive
Mark W. Jackwood Davis, California 95616
Department of Population Health
College of Veterinary Medicine
The University of Gerogia
953 College Station road
Athen, Georgia 30602-4875
Richard J. Julian
Ontario Veterinary College
Dept of Pathobiology
Guelph, ON Canada N1G 2W1
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AVIAN DISEASE MANUAL

American Association of Avian Pathologists

Seventh Edition Published by the

Copyright © 1979, 1983, 1989, 1996, 2000, 2006, 2012 by

Library of Congress Control Number (LCCN)

International Standard Book Number (ISBN)

Cover photo by Marco Langlois

Copies available from:

Preface to the 7th Edition

Martine Boulianne, Editor

Preface to the 7th edition....................................................................................................................................................... iii

How do we investigate a sick poultry flock?.......................................................................................................................... 1

Fungal diseases................................................................................................................................................................. 140

Parasitic diseases............................................................................................................................................................... 153

Nutritional diseases............................................................................................................................................................ 179

Miscellaneous diseases..................................................................................................................................................... 191

Diseases of the duck (table)............................................................................................................................................... 230

Diseases of the game birds (table).................................................................................................................................... 235

Poultry drug use guide....................................................................................................................................................... 263

Necropsy of the fowl........................................................................................................................................................... 268

Photos index....................................................................................................................................................................... 279

Contributing Authors........................................................................................................................................................... 299

How do we investigate a sick flock? Flock visit

Written by Martine Boulianne

Table 1. Expected mortality rates according to the bird type

on the birds’ health. Poultry barns should provide clean

the tibiotarsal vein is a good option for turkeys and ducks.

and chlorine levels can be estimated with specific color

If ventilation is suboptimal during the visit, ammonia,

The visit report

VIRAL DISEASES CLINICAL SIGNS

ARBOVIRUS INFECTIONS WEEV – associated with neurologic disease in turkeys

Multifocal hepatic necrosis and splenic, thymic and CONTROL

mosquitoes do not thrive, or by the use of screens,

West Nile Virus

Eastern Equine Encephalitis

West Nile Virus

DEFINITION attributed to adenoviral causation should be scrutinized

EPIZOOTIOLOGY HISTORICAL INFORMATION

2. Historically, IBH occurred in immunologically deficient LESIONS

CONTROL CLINICAL SIGNS

DIAGNOSIS HISTORICAL INFORMATION

free embryonated duck or goose eggs or cell culture of CLINICAL SIGNS

signs including tracheal rales, coughing, and sneezing.

old specific-pathogen-free embryonating eggs or cell TREATMENT

CONTROL ZOONOTIC POTENTIAL

INCLUSION BODY HEPATITIS

HEMORRHAGIC ENTERITIS OF TURKEYS

AVIAN ENCEPHALOMYELITIS EPIDEMIOLOGY

a period up to 1 month, some layers shed virus in some

AVIAN INFLUENZA inhibition tests. Cross-protection does not occur between

CLINICAL SIGNS DIAGNOSIS

6. Different states and industries take different approaches

they have recovered from infection is common in