Poultry Pathology Salman Lateef

POULTRY PATHOLOGY
UAF sub campus T T Singh
2012
M.Arslan CS
M.Arslan CS | Confidential
2 POULTRY PATHOLOGY
CLASS LECTURES
Course NO: patho-505
Course Title: Poultry Pathology
DELIEVERED BY: DR. SALMAN LATIF BUTT
SEMESTR: 7TH
Prepared by: M.Arslan CS (2009-ag-2062)
Recommended books:
1. Diseases of poultry by Y.M. Saif

2. Poultry Diseases by F.T.W. Jordan
M.Arslan CS
3 POULTRY PATHOLOGY
Sr. No Disease Page#
1. Introduction 4
2. ND 5
3. IB 10
4. ILT 12
5. APV 14
6. AI 16
7. IBD 19
8. CIA 21
9. HPS 24
10. IBH 26
11. Pox 27
12. MD 29
13. AE 32
14. Bacterial Diseases 34
15. Protozoal Diseases 57
16. Mycotoxicosis 59
17. Nutritional Deficiencies 61
18. Appendix 63
19. Tables 70
20. Poultry Serology 89
21. Terms 105
M.Arslan CS
4 POULTRY PATHOLOGY
Introduction
The
Poultry industry facing continuously disease challenges. The prevention
of disease is better than cure & the best preventive practice is biosecurity
at all levels.
There are 5 sections of poultry diseases
I. Viral
II. Bacterial
III. Protozoal
IV. Fungal
i. Mycosis (fungus involves directly i.e in Candidiasis)
ii. Mycotoxicosis (toxins of fungus are involved in disease)
V. Heavy metal toxicity
Viral diseases are more important. Viruses are of 2 types

i. DNA
ii. RNA
RNA viruses are more virulent than DNA viruses. The genome of DNA viruses is non-
segmented but it may be segmented in RNA virus, so having greater chance of mutation.
The positive sense virus is more virulent than negative sensed virus.
Bacteria is may be
 Gram positive or Gram negative

 Acid fast positive or Acid fast negative
 Motile or non-motile
 May be intracellular i.e Mycobacterium
Heavy metal toxicity causes damage to Liver and kidney. The heavy metal toxicity is due to bio
accumulation of toxins i.e. Arsenic, Cadmium, Copper, Cobalt, Lead etc.
M.Arslan CS
5 POULTRY PATHOLOGY
ND (Newcastle Disease)
History
 1st time is originated in New castle in England & at the same time in Ranikhet in India.
 It was 1st observed in chicken
Etiology
 Causative agent is Paramyxovirus type 1

 Enveloped virus covered by 2 layers of Glycoproteins
 Having 2 epitopes , Haemagglutinins for attachment of RBCs and Neuraminidaze for
detachment
 RNA virus having non-segmented genome
 High concentration of Formalin/ Phenol can deactivate the virus
Types
 Neurotropic (develop at latter stage of disease)

- Hit CNS & PNS
 Viscerotropic (hit viscera, develop in earlier stages of disease)
- Lesions will be in digestive system
- Respiratory system
- Lymphatic/immune system (ceacal tonsils, spleen)
Strains of ND
Strain Virulence Examples

Lentogenic Low Lasota (vaccinal strain)
Mesogenic Mild Muktisvar F1
Velogenic Very virulent Asiatic, Melano, Texas,
- Neurotrophic Hertz, GB
-Viscerotrophic
M.Arslan CS
6 POULTRY PATHOLOGY
Disease Duration
 5-15 days
Incubation period
 5-15 days
Host
 Hit all poultry birds all the times except Guinea fowl. But heavy virus load can also cause
disease in Guinea fowl.
Distribution
 Pandemic
Mortality
 0-25%
 May be 100% with concurrent infection i.e A.I, Cocci
etc
Transmission True vertical= pathogen is

transmitted from parent to
 Horizontal
offspring
 False Vertical (cause death of embryo of 13-15 day)
False vertical= the pathogen
Clinical Signs transmitted to egg is cause
Clinical signs depend upon system which is affected by death of embryo
PMV.
 Digestive System
 Greenish whitish diarrhea
 Dehydrated bird (ruffled feather)
 Less feed intake
 More water intake
M.Arslan CS
7 POULTRY PATHOLOGY
 Respiratory System
 Sneezing, Gasping, Coughing
 Serous & mucoid nasal discharge
 Ocular discharge
 Nervous System
 Paralysis of wings & legs (Unilateral & bilateral)
 Stargazing
 Torticulus
 Blindness
Post-mortem Lesions
 Digestive system
 Pin point hemorrhages in proventriculus
 Button like/ Lenticular ulcer in duodenal loop & in Jejunum
 Hemorrhages in ceacal tonsils
 Spleenomegaly & hepatomegaly is may observed
 Tracheitis
 Congestion/inflammation of trachea & ulcer may be present in severe cases
 Oedematous lungs (due to secondary viral infection)
 Nervous System
 Congested brain
 Serosa of brain will be red
 Encephalomalacia
Microscopic Lesions
 Villi will be absent at Ulcer

 Destroy different compartments of brain(Glial cells) (due to which bird loose grip, face
Torticulus, show stargazing)
M.Arslan CS
8 POULTRY PATHOLOGY
Differential Diagnosis
The Lesions of ND may be comparable with
i. AI
ii. IB
iii. ILT
A1
 Hit all system of body

 Hemorrhages on shank are present in AI & not in ND
 No proventriculus hemorrhages in proventriculus
 No Lenticular ulcer in AI
 Diarrhea color is whitish in AI & Greenish whitish in case of ND
 Body temperature is very high in AI as compared to ND
IB
 Lesions in kidney (Urate deposition)
 Watery albumin
 IB affected mostly young ones while ND hit birds of all ages
 Hit only respiratory system
ILT
 Mucoid hemorrhages (paint brush) in Trachea
Treatment
There is no proper treatment for ND. But the following may be effective to lesser the infection
 Vaccine (1st live then killed during infection)(Days;3-5, 21, 33 then after every month in
layer )
 Selmore, ceva, intervet, isovac, ICI, Murush/Merial
 Lasota or muktisver is normally used
 Vaccine the bird by changing strain which was vaccine before infection
 Don’t vaccine the bird in immunosuppressive diseases i.e CIA, IBD, COCCI,
MD, LL
M.Arslan CS
9 POULTRY PATHOLOGY
Combinations of ND vaccine
 Live vaccine
i. ND(Lasota) + IB(H1120) (Isovac)
 Killed vaccine
Many combinations i.e
I. ND+EDS+IB+TRT (OVO4)
 Immunobooster
 Skim milk 5g/liter
 Yoghurt
 Sale the flock when mortality in flock is more than 1000 birds/ day in ECH.
Multimedia
 Tricad of ND
1) Proventricular hemorrhages
2) Lenticular Ulcer
3) Hemorrhages in ceacal tonsils
 Increased & fluffy bursa with hemorrhages =ND+IBD
 ND destroy Lachrymal gland
 Putrefied embryo due to ND infection
 Oophritis =ND+AI
M.Arslan CS
10 POULTRY PATHOLOGY
IB (Infectious Bronchitis)
Infectious disease of upper respiratory tract spread with very small incubation period, affected
young ones more severely than adult birds.
Etiology
 Causative agent is Corona virus, its name is due to its crown like shape
 Small, enveloped, RNA virus
 Some strains of IB can multiply in embryonated eggs
 Strains of IB are categorized into:
i. Nephrotrophic (destroy nephron)
Mass (massachusets), Ark, Conn, M-52, D-275, D-278, H 4/91
ii. Respiratory
H120, H 4/95
Incubation period
 18-36 hours
Host
 Only chicken
 Signs are different in layers and in broilers
 Chicken of 2 weeks are more susceptible
 Only hit adult layers not adult broilers
Mortality
 25%
 Depends upon concurrent infection
Horizontal Transmission
 Mostly through aerosol
Clinical signs
IB hits 2 systems of body
M.Arslan CS
I. Respiratory
II. Urinary
 Coughing, Gasping
 No Nasal discharge in Broilers. But there will be a nasal discharge in Layers
 Cyanotic membranes (AI&IB)
 Ruffled feathers
 Cause watery albumin in eggs in adult layers
 Urinary System
 Shrill cry (due to kidney pain)
Gross lesions
 Tracheitis
 Tracheal plugs
 Excessive deposition of urtaes in Kidney & ureter (due to less water, water-soluble uric
acid converted into non-soluble crystals of uric acid. The sharp edges of crystals destroy
the parenchyma of kidney, which leads to kidney failure)
Microscopic lesions Pychnotic Nuclei= condensed nuclei
 Extension of collecting ducts Karyolysis= absence of nucleus
 Glomerulonephritis Karyo hexis= division of nucleus

 Urate inside tubules into parts
 Pychnotic nuclei
Egg Quality deterioration
Treatment
EDS, ND =external
 Vaccination (along with ND at 3-4 days)
IB = internal
 Respiratory soothers
 Bromaxhain
 Eucalyptus
-Menthol, Mercobeth (1cc/3liter & 1cc/ 8 liter for spray)
M.Arslan CS
ILT (AVIAN DIPHTHERIA)

Viral contagious disease of URT of chicken primarily, characterized by squawking, gasping,
coughing, expectoration of bloody exudates through nostrils & oral cavity.
 It is a disease of hilly areas & prevalent in winter & autumn season but high temperature
can increase severity of disease.
 Birds of 3-8 month of age are most susceptible to ILT.
Etiology
 Causative agent is Herpes virus, Tapeia avium
 Enveloped, DNA virus of 150-250 nm diameter
 Virus can stay in house for 30-50 days at 25-370C
 Dissolved by lipid absorbent
Incubation period
 5-12 days
Host
 Primarily chicken
 Turkey & pheasants are accidental host of ILT
Mortality
 Mortality is up to
i. 5% in sub-acute form
ii. 50% in acute
iii. 90-100% in per acute
Clinical signs
 SUB-ACUTE FORM
 Loss of appetite
 Conjunctivitis (watery eyes due to secondary bacterial infection may lead to blindness)
 Coughing
 Sneezing
M.Arslan CS
Virus=obligatory
 ACUTE FORM intracellular organism
 Signs of sub-acute form+
 Gasping Tracheal epithelium=
 Squawking ciliated columnar epithelium
 Sitting & shed their feathers
 Sleepy condition
 Per-ACUTE FORM
 Sign of sub-acute & acute form +
 Expectoration of bloody mixed exudate
Gross lesions
 Hemorrhages in Lacrimal gland
 Tracheitis
 Blood clots in Trachea
 Respiratory plugs (sometimes)
 Ulcer in Trachea
 Sub-coetaneous inflammatory exudate in head region (wheat straw color)
 Inflammation of intra orbital sinuous
 Necrosis material in Trachea (which cause Asphyxial death to bird)
Microscopic lesions
 Start of disease
 Oedema of epithelium
 Congestion
 Middle of disease
 Intranucleur inclusion bodies (appear only at middle stage of disease but not at end stage
b/c membrane sloughed out from Trachea)
Treatment
 No specific treatment
 Vaccination at age of 2-3 months of age
 Eucalyptus & Bromaxhain are used as supported treatment (Menthol, Mercobeth,
Eukaneth)
M.Arslan CS
APV (TRT, SHS, PNEUMONITIS)

History
 1st studied in 1956
Etiology
 Causative agent is Avian Paramyxo Virus Type 2 & 3(APV-II & APV-III) & these types
are interconvertalbe
 APV belongs to family paramyxoviridae & this virus is non-Haemagglutinating
 Cause more damage to broiler than layer
Incubation period
 3-4 days
Natural Host
 Turkey & Broiler breeder for TRT
 SHS hit only broilers (16-32 days)
Mortality
 50-100 %
Morbidity
 Upto 50%
Transmission
 Wild birds are source of APV infection
Clinical signs
 Swollen head (SHS)
 Head shaking
 Opisthotonus appearance (Bulging of eyes from eye socket)
 Nasal discharge (Only in TRT)
 Decrease egg production
 Sneezing, coughing & gasping
 Puffy appearance of comb
M.Arslan CS
Gross lesions
 Thick yellow exudate on cutting the comb
 Cheesy material in Sinuses (Asphyxia) TRT= Turkey Rhino Tracheitis
 Congestion in Trachea(if trachea is involved)
SHS=Swollen head syndrome
Microscopic lesions
 Loss of cilia in tracheal membrane
Diagnosis
 Gold standard is “ISOLATION & IDENTIFICATION”
Differential diagnosis
 It may confused with ND & AI
 Yellow material from comb is also observed in case of AI
 Nasal discharge is observed in in ND & also in TRT
Control
 Only killed vaccines are used (for long immunity)
 Restrict the entry of wild birds
 Vaccination is practiced only in Turkey & in Broiler breeder
 Live vaccines are may be administrated at 12-13 weeks of age & killed at 21 weeks of
age
M.Arslan CS
Avian Influenza
 Fowl plague, Avian plague, Fowl pest, Avian pest, Avian syndrome, orthomyxo infection
Viral disease caused by Influenza virus-A, both in acute & in sub acute from & it is
characterized by rattles, rales, severe lacrimation, Oedema of head, Sneezing, Diarrhea, &
sudden decrease in egg production (even upto 0%) with mortality ranging from 90-100%.
Etiology
 Causative agent is Influenza virus type A(Influenza patho/proto virus type A) of family
Orthomyxoviridae
 Enveloped, RNA, single stranded, Negative sense virus
 Segmented genome (having 8 segments), so more chances of mutation
 Having 8 segments of genome but produce 10 proteins(structural + non-structural)
 80-100 nm size
 Virus is mostly present in organic matter
 Type A, B & C is only pathogenic types. Only type A affects chicken & type B & C
affects humans & pigs
 Ordinary disinfectants can kill these viruses, 5% sod. Hypochloride, β-propiolactam, sod.
Dodisyl Sulphate (SDS), Formaldehyde, Phenolics & 10% NaOH sol. Also effective.
Never use disinfectant alone but in combination.
Incubation period
 5-12 days
Host
 Chicken & Turkey
 Geese, sparrows, ducks, crows, pheasents, sea gulls, wild & migratory bird are careers of
of AI virus.
Distribution
 World wide
Mortality
 90-100 %
Transmission
 Only Horizontal
 Frequent visitors of bird show can be a big source of infection.
M.Arslan CS
Types of Disease
i. HPAI
ii. MPAI or LPAI
Systems involved
 Respiratory, Integumentary, urinary, reproductive
Clinical signs
LPAI
Respiratory System
 Rattles, Rales, Coughing, Sneezing, Depression (ruffled feather + lower the wings),
Huddling, Sleepy condition
Digestive System
 Mild type diarrhea, Vent pasting
Reproductive System
 Decrease in egg production, misshapen ova/eggs
HPAI
 Bloody discharge from nares

 Severe coughing & sneezing
 Severe diarrheic condition
 Chalky white to simple watery diarrhea
 S/C hemorrhages all over the body which are prominent in shank region
 Egg production reduced to 0%
 Bluish comb & wattles (Cyanosis)
 Birds in sleepy condition
 Complete cessation of feed & water intake
 Hemorrhages on surface of shanks
 Misshapen ova & weak shelled eggs
Post-mortem lesions
Respiratory System
 Rhinitis (Inflammation of nasal mucosa)

 Tracheitis
 Hemorrhages on internal mucosa of trachea
 Congestion of lungs
 Blackish discoloration of lungs along with pus in lungs (due to sec bacterial infection)
M.Arslan CS
Digestive system
 Paint brush hemorrhages in all intestine

 Thick intestinal mucosa Amentadine
 Destruction of Payer’s patches which leads Its cost is very high which is 1.5
to ulcer in intestine laakh/dose/30,000 birds
Cardiovascular System There are more chances of drug
resistance. So it cannot be used
 Echynotic hemorrhages on heart
twice in a flock.
Urinary system
 Pale yellow kidney

 Nephritis
 Bulging of kidney from bony socket
Reproductive System
 Oophritis
 Dissolved ova Heart Hemorrhages
 Egg yolk peritonitis
1. AI
 Regressed & discolored ova (dark yellow)
2. CIA
 Oedematous oviduct (isthmus)
3. Fowl cholera
4. Gentamycin toxicity
Control
 Control the source of infection
 Multivalent killed vaccine may effective (H5,
H7, H9)
 Check titer against AI before vaccination of ND
Bony socket
 Vaccine the broiler against AI at 14th day with
killed vaccine It is deeper in broiler, so observation
 Don’t vaccine the bird during production of swelling is difficult but in layer it is
not so deeper and come out from
Treatment
bony socket on swelling.
 Cylovir
 Amentadine
M.Arslan CS
IBD (Avian Nephrosis, Gumboro)

It is an accute contageous disease of chicken & turkey having lymphoid organs as a primary
target producing prolong & persistent immunosuppression (for 4-10 weeks)
History
 Ist observed in 1962 in Delaware state of Gumboro in USA
Etiology -Viridae=family
-virinae= sub-family
 Causitive agent is Birna virus of Birnaviridae family belongs to
genus Avibirna
 Genome consists of 2 strands of Double stranded RNA (dsRNA)
 Remains in poultry shed even for years depend upon
environmental conditions. Organic matter save the virus from disinfectant
 This virus survives for 8 months at 370C
Incubation period
 2-3 days
Host
 Chicken & Turkey
 But no clinical sign & gross lesions are observed in Turkey
Mortality
 0% in case of only IBD
 20-30% with concurrent infection
Morbidity
 Upto 100%
Pathygnomonic lesion=Characteristic lesion
Transmission
 Horizontal Transmission
M.Arslan CS
Clinical signs
 Severe & sudden viremia produces high temperature of body
 Ruffled feathers  Whitish diarrhea
 Dehydrated bird  Vent pasting
 Sleepy condition of bird
 Solemness
 Outbreak of cannibalism (bird picking own feathers on vent due to irritation)
 Constant huddling
Gross lesions
 Muscoskeletal system
 Deep intramuscular hemorrhages in pectoral & thigh muscle
 Digestive system
 Pin point hemorrhages at junction of Proventriculus & Gizzard (also in CIA)
 Edematous condition in duodenum loop & in whole intestine
 Thick intestinal mucosa
 Lymphatic system
 Destroy Payer’s Patches which may leads to Ulcer & sometimes bleeding at Payer’s
Patches
 Inflamed & hemorrhagic bursa
Microscopic lesions
 On Bursa slide, Lymphoid follicles are replaced by fibrinous tissues
Treatment
 Se + Vit. E is used as supportive therapy
Vaccine Day
1st 7-10
2nd 19-20
3rd 30
4th 10 wks
th
5 16 wks
 Vaccination is not perfromed at 1st day b/c of presence of MDA (remains for 10 days)
M.Arslan CS
CIA (Cytolytic Disease)

Immunosuppressive disease of chicken & Japanese quail, caused by severe anemic condition
with secondary bacterial & fungal infection
History
 1st identified in Japan in 1979 by Yuasa
Target Organs
 Spleen, Bone marrow, Thymus & some extent to bursa
Etiology
 Causative agent is Gyro virus / Circovirus of Circoviridae(having nucleic acid in circular
fashion) family
 SS, -ve sense, DNA virus having 2.3 kpb genomic structure
 Gyro virus has different strains in different areas. CUX1 strain is found in central & far
Asian countries
Incubation period
 8 days
3 TYPES OF VIRUS PROTEINS
Host
i. VP-1
 Chicken & Japanese quail ii. VP-2
iii. VP-3
 Susceptible age is 2-4 weeks
VP-3 is most dangerous & also
Distribution called apoptin initiater & disease
is also called Cytolytic disaes.
 Pandemic
Mortality
 Up to 30% & may reach to 70% with concurrent infection
Morbidity
 20-40%
 It depends upon concurrent infection i.e MD, IBD, sec0 bacterial infection, fungal
infection etc
M.Arslan CS
Transmission
 Horizontal & Vertical
 May cause Economic losses up to 18%
Clinical signs
 Anemia—pale comb & wattles
 Depressed bird
 Bluish area under wing
 S/C hemorrhages
 Increased blood clotting time
Hematology
Parameter Normal CIA
PCV 27% 12
Hb 12g/dL 2
 Anisocytosis (immature RBC,s in circulation due to insufficient Hb level)
Gross lesions
 Hemorrhages on heart
 Pin point hemorrhages at junction of Proventriculus & Gizzard
 Deep intramuscular hemorrhages in Thigh & chest region
 Subcutaneous hemorrhages in chest & thigh region
 Ongoing bleeding from different regions of body & prolonged at wing web
 Thymic atrophy
 Pale yellow bone marrow
 Hemorrhages in thigh region & sometimes bleeding is also observed in Thymus
Pathogenesis
The virus destroys the bone, Thymus & spleen. The bone marrow has progenitor cells. The
progeny of RBC’s & Thrombocytes is Hemcytoblast & Thromboblast respectively. By
destruction of these progenitor cells ,bird have reduced number of RBC’s & Platelets, which
leads to severe anemic condition & hemorrhages due to failure of blood clotting. The destruction
of Thrombocytes leads to continues bleeding in different regions of body
M.Arslan CS
Diagnosis
 Clinical signs
 Isolation & Identification
 PCR
 ELISA
Cell Lines
- MDCC
- MSB-1
- BHK-1
Treatment
 Vaccination of disease is at 14 weeks of age
NOTE
 Recovery of disease is after 28 days
HOW INCUBATION PERIOD IS MEASURED??
The virus is injected in peritoneum and observed its shedding in

feces. This interval is considered as incubation period.
Types of bone marrow
i. Red
ii. Pale
M.Arslan CS
HPS (Angara Disease)

It is vertically transmitted viral disease of heavy breeds (but sometimes light breeds also affected
i.e pigeon, quail) producing less morbidity and high mortality.
History
 This disease was 1st time observed in Angara goath in Karachi by Kernel Ashraf
Etiology
 Causative agent is Adeno virus type-IV
 DNA virus
Incubation period
 48-78 hours
Host
 Chicken & Turkey are natural host of HPS
 Accidental hosts include Pigeon, Sparrows, and Pheasants etc.
Mortality & Morbidity

 Causes high mortality even up to 100%
 Morbidity is low
Transmission
 Vertical
 Horizontal
 Vertical transmission depends upon some circumstances i.e if parent flock is
immuned to this virus then chances of
transmission are less.
Clinical signs The dead birds with

 No clinical sign in acute form dorsal recumbence is
 Signs are observed in sub-acute from due to HPS and a
 Gasping nervous sign due to
 High mucous contents in feaces
anoxic condition in brain
M.Arslan CS
 White diarrhea
 Sudden cardiac death (birds are death with dorsal recumbency
Gross lesions Anoxia
Absence of O2
 Swollen liver
 Sersangous fluid 10-11 ml in pericardium
 Pulmonary edema
 More mucoid digesta
Pathogenesis
Liver has many vital functions. One of the vital functions is to make water carrying protein,
Albumin protein. The adenovirus-IV will destroy hepatocytes & there is no production of
Albumin protein. As a result, the water goes in dependent parts (most dependent is heart),
accumulate in heart. The pumping of heart is stopped due to this accumulation which leads to
anoxic condition of brain. Due to stop of heart pumping, Vasodilatation of veins in lungs will
lead to water accumulation in lungs which is termed as PULMONARY EDEMA.
Microscopic lesions
 Basophilic intranuclear inclusion bodies in Hepatocytes
 Necrosis of hepatocytes
 Edema of pneumocytes
Control
 Killed vaccine at 17 days , 6th week, 10th week
Differential diagnosis Toxin Binder

 IBH, Slat poisoning  Ultrasorp
 Tonymyconil
Treatment
 Mycofix
 Addition of Toxin binder in feed approx. 100g/bag  Toxiban
 Dilution of feed  Mycodox
 Liver homogenate (50% chance of recovery)
 Vit. E + Se
M.Arslan CS
IBH (Inclusion Body Hepatitis)

It is a HPS like disease with same target organs with some different lesions. It is caused
by Adeno virus type 3. The IBH has differentiating features from HPS. IBH is vertically
transmitted.
 Depression
 Inappetance
 Pallor of comb and wattles
HPS IBH
Swollen liver with less hemorrhages Swollen liver with severe hemorrhages like
blood streaks
10-13 ml fluid in pericardium Negligible
Vaccine: HPS killed vaccine is used for control of IBH
Mycotoxin + HPS= Liver like IBH
Techniques for Toxin identification
 LCG=Liquid chromatography
 CCA=Column clearance assay
 HPLC=High Pressure Liquid chromatography
 UHPLC=Ultra HPLC
 GC=Gas chromatography
Enrofloxacin
In broiler at 30 days can cause
Lameness to bird which results
in less feed intake.
M.Arslan CS
Pox
Synonymous: Small pox, fowl pox diphtheric pox, fibroprolifertine syndrome, variala, chicken
pox, pigeon pox (according to species)
Viral slowly spreading disease characterized by proliferative nodules lesions on unfeathered

areas in form of cutaneous form (dry form) & in wet form. It is characterized by diphtheria
membranes on mucosal surface of respiratory system particularly in avian species
It prevalent in 2 forms
1. Cutaneous form (dry form)

2. Diphtheria form (wet form)
Pox disease causes death in 7-10 days if come in general circulation. Most dangerous form is wet
form of pox in peacock. Dry form appears first and then lesions of wet pox will appear.
Etiology
 Causative agent is pox virus
 Largest virus of poxviridiae family (300 nm)
 Virus remains inside shed & get entry on injury
Host
 Avian species
 Natural host is chicken & turkey
 Accidental host sparrow, mynah, pheasant, starling, alala are carrier of disease

 Slowly spreading disease with less morbidity & mortality
Transmission
 Horizontal only
 2 things are required for pox
1. Season (harvesting season, when more production of
mosquito)
2. Injury (mechanical injury, may due to mosquito mites,
cages)
M.Arslan CS
Pathogenesis
Erythema (red areas) Popules Vesicles Postules Nodules
Clinical signs
 Grayish-black nodules on unfeathered areas
 Decrease in egg production
 Decrease in feed & water intake
 Rubbing of head region by birds
 Bright red ulcers on pallet covered with yellow Camel Pox
diphtheria membrane
It is disease of camel which
Gross lesions causes mortality within 4-5
days in diphtheria form.
 Diphtheric membrane in pallet region & in tracheal
region
Microscopic lesions
 Bossel bodies in cells
 Oval shaped ulcers in poultry (star shaped in human & half moon like in large animals)
Diagnosis
 Isolation and identification
 Clinical signs
 Molecular diagnostic tests i.e VNT
Control
 By managemental conditions
 Stop mosquito entry inside the shed
 Separate and cull diseased birds b/c scar of nodules can spread disease to healthy birds
Treatment
 Give OTC, Remove scar and apply pyodine or polyfax or cenmynthine
 This Treatment is only for desi birds
M.Arslan CS
Mareck’s Disease
Highly contagious viral disease of chicken characterized by intensive proliferation
of mononuclear cells (monocytes), throughout nervous system particularly
Peripheral Nervous System.
In proliferative from, virus will
Etiology multiply in almost every organ.
Virus not multiply itself, it hit DNA
 Caused by Herpes virus group B
on lymphocyte & occupies
Incubation period lymphocyte control, hence
lymphocyte transformed. The
 4-5 weeks cytoplasm of lymphocytes
becomes bluish & immature cells
Host in circulation were observed.
 Natural host is chicken while Turkey, Goose, Japanese quail are accidental host
Distribution
 Pandemic
Transmission
 Horizontal i.e Air borne transmission of epithelial cells of skin(dandruff, feathers)
 Infectious form of virus is in Feather follicles
 Disease can be transmit within flock or between flock
3-Forms of Disease
1. Acute / Visceral form
2. Classical form / Latent form/ Locomotory paralysis
3. Proliferative form
Clinical signs
 Acute form
 Depression
 Mild ataxia
 Solemness/sleepy condition
 Paralysis (sometimes)
M.Arslan CS
 Swollen feather follicles

 Classical form /Latent form / Locomotory Paralysis
 Bicycle ridden birds (one leg forward & 2nd backward)
 Leg paralysis (unilateral/ bilateral)
 Head down
 Wing paralysis (damage of schiatic nerve )
 Impaction (due to damage of vaugal nerve)
 Blindness (damage of optic nerve)
 Choaking (retention of digesta inside GIT)
 Diarrheic condition may present (if intestine controlling nerves are destroyed)
 Proliferative from
 Tetragonal, elliptical corona of eyes
Gross lesions
 Acute form
 Tiny nodules on every organ especially on muscles (Chest & Thigh)
 Dark grey to white Diffused proliferative granular tumors in liver, lungs, heart,
kidney, spleen, bursa, ovarian tissue (red color in Fowl cholera)
 Hardness of Proventriculus indicate outcome of disease
 Chronic form
 Lameness
 Loss of cross striations in schiatic nerves (AE, LL, MD)
Diagnosis
 Clinical signs, PM lesions
 Isolation & identification
 PCR
 Proteomics
Treatment & Control

 No treatment
 Control with the help of vaccine
 Cull the flock if mortality is more than 25 birds in 1000 birds.
 Vaccination
- At day first
- Vaccine is cell associated, preserved at -1960C
M.Arslan CS
3 serotypes of vaccine
i. Rispon strain of HV-B

ii. HVT ( Herpes virus of turkey)
iii.
Routes of Vaccine
1. S/C
2. I/P (intraperitonium, in abdominal wall)
Neoplastic Diseases of Chicken

 Mareck’s Disease
 Lymphoid Leucosis
 MD could not come before 4-5

weeks of age
MD vs LL
LL
 No lameness of schaitic nerve

 No deshaping of eyes
M.Arslan CS
A.E (Avian Encephalomyelitis )

Contagious viral disease of young chicken characterized by less mortality and morbility
Etiology
Enterovirus of picornaviridae family
Host
Chicken, Turkey, Pheasant and Quail
I.P
2 weeks
Transmission
15-30 % vertically transmitted. More chances of horizontally transmission between the flock and
within the flock
Mortality
2-3 % Maximum mortality rate
Susceptible Age
Up to 10 days old chicken to 4 weeks of age
Susceptibility factor
Age; young chicks for clinical disease more susceptible as compare to older
Season; Dec ----- Jan
Clinical Sign;
 Neurological disorder
 Depression
 Ataxia
 Staggering gate, Incordination

M.Arslan CS
 Lateral recombancy
 Tremoring of head
 Sometime stargazing appearance
 Swirling movements
P.M lesion
No P.M lesion
Microscopic lesions
 Sever gliosis in spinal cord ( Increase number of glial cell )
 Nucleus is absent in the neurons.
Immunization
Live & killed vaccine
Disease chances 8-10 day == 4-6 week
Don’t vaccine during production & before 10 weeks
Vaccination
 After 10 weeks of age & before production
 Beta- Propiolactane based vaccine immunized the birds for 4 month
Control
 By immunizing the parent flock
 By nerve tonics
M.Arslan CS
POULTRY PATHOLOGY
Poultry Pathology
M.Arslan CS
UAF sub campus T T Singh

1/1/2012
M.Arslan CS
Bacterial Diseases
Sr# Disease Page #
1. Salmonellosis 3
2. Fowl typhoid 6
3. Colibacillosis 8
4. Infectious coryza 10
5. Mycoplasmosis 13
6. Fowl cholera 15
7. Necrotic enteritis 19
8. Spirochetosis 21
M.Arslan CS
Enterobacter
Enterobacter are normal bacteria which are normally present in intestine. The Enterobacteriaceae is a
large family of Gram-negative bacteria of small and large intestine. These bacteria includes
 E.coli
 Salmonella
 Shigella
 Klebsiella
 Proteus
Salmonella and E.coli are responsible for disease production. These are opportunistic bacteria. These
bacteria cause disease only in septicemic condition. Some bacteria produce toxins (endo/exo) i.e E.coli
produce endotoxin.
Main route of bacterial diseases is feacal contamination. Bacterial toxins produce septicemic condition in
bird which is lethal for bird. This is why the lesions of Enterobacter produce all over the body.
There are different strains of E.coli, some are pathogenic while other are non-pathogenic. The 0157 strain
of E.coli is pathogenic strain of E.coli.
Salmonella also have a group of strains.
Salmonellosis
It is a group of diseases caused by Enterobacter that are gram negative & non-lactose fermenter.
Prominent disorders of salmonella are
 Pullorm
 Fowl typhoid
Pullorm
Bacterial disease of young chicks, characterized by high early chick mortality, weakness, prostration
(middle stage of paralysis) & vent pasting with chalky white diarrhea (Sulpher color in fowl typhoid).
Etiology
 Caused by Salmonella pullorm
 Gram negative, non-motile, non-lactose fermenter, bacillus, exist as individual bacilli
M.Arslan CS
Isolation & Identification

 Isolation can be done on Nutrient agar, Mackonky agar, TSI agar, SS agar, Selenit broth
 Mackonky agar is best
 S.pullorm produces white color colonies on Mackonky agar (pink in case of E.coli)
Incubation period
 5-7 days
Host
 Chicken is natural host while accidental hosts include Turkey, pheasant & Goose.
Mortality
 Mortality upto 20 % , morbidity is 50%
Transmission
 Horizontal and vertical transmission
 Musca domestica & Tubaneous fly (horse fly) are mechanical vectors of pullorm disease
 Contaminated material is excellent source of horizontal transmission
Zoonosis
 Yes E.coli Salmonella
Clinical signs Lactose Non-lactose
fermenter fermenter
 Weak birds Produce pink White
 Somnolence/sleepy condition colonies on
 Wetty appearance Mackonky
 Birds sitting on their hocks agar
 Swollen joints
 Chalky white diarrhea with vent pasting
 Shrill cry
 Chirping voiding diarrhea
 blindness
Gross lesions
M.Arslan CS
 White foci on Liver surface

 White color nodules on surface of heart, lungs, spleen
& on serosal surface of small intestine
Causes of high ECM
 Dark congested liver (before foci formation)
 Amber color fluid in hock joints  Salmonella
 Swollen kidney  Mycoplasma

 White foci on kidney (sometime)  Mycoplasma is
 White foci on Iris, leads to blindeness (also a clinical haemagglutinating bacteria
sign)
 Enteritis like condition / severe enteritis Disinfection
 Perforation of intestine (hole in intestine)
 Before chick arrival
Diagnosis  Before nest installation

 70% chances of mycoplasma
 Clinical signs during nest installation
 Molecular diagnostic techniques i.e PCR Biosecurity
Control 1. Conceptual
2. Structural
 Control is important than treatment 3. Operational
 With the use of antibiotics disease suppressed but not
eliminated. After 15-30 days of administration, disease
will again reappears
 Screening tests should be performed on regular basis AMP cell protects Enterobacter from
immune system
Treatment
 Antibiotics are used
 Nitrofuran especially Furaltadone & Furazolidone
 Usually furaltdone is administered after arrival of disease while Furazolidone is provided
through feed continuosly
 Florfenicol have excellent results but should not be recommended due to adverse effects.
Its half life is 7 months, so its residues in meat can affect human health adversly
M.Arslan CS
Fowl Typhoid
Etiology
Etiologic agent is Salmonella gallinarum, a non-motile, Gram negative and bacillus bacteria
which cannot produce true toxins. While the S.pullorm produce toxins.
Disease exist in 2 Forms
i. Acute
ii. Chronic
Incubation period
 7 days
 Spread period is 3 days
Susceptible Host
 Chicken, Turkey & pheasant
Transmission
 No true vertical transmission is reported while adult birds are carriers of this bacteria
 70-80% eggs are carrying the bacteria which come from Fowl Typhoid infected flock
Public Importance
 This disease have zoonotic importance (by consumption of eggs from infected flock)
Clinical signs
 High rise in body temperature along with vent pasting which is due to Greenish or bright
Sulfer color diarrhea (Sulfer color is due to high level of Stercobilinogen which is formed
from lyses of hemoglobbin)
 2 peaks of temperature 107 & 1100F
 Anemia (comb & wattles)
 Brownish Discoloration of All  Increased thirst
membranes  Gasping (only in acute form)
M.Arslan CS
Effect on Hematology
 Thin watery blood with PCV 16-22% (normal 27%)
Gross lesions
 Nodules on wall of intestine
 Multifocal ulcers in small intestine
 Bronze color liver (Bile stained)
 Friable Liver and Brittle Spleen
 Nodules in myocardium
 Nodules in lungs (at start of disease)
 Nodules on heart (at start of disease)
Diagnosis
 Isolation & Identification (Mackonky agar, SSagar, Nutrient agar, Selenite broth)
 PM lesions
 Molecular tests i.e PCR
Treatment
 Floramphenicol (Neflor)
 Furazolidone is not specific against S.gallinarum
 Broth is used for transportation while agar is not

 Enterobacter give round colonies and Mycobacterium give colonies like fried egg.
High Number of
1. Hetrophills in bacterial diseases (6-7 2. Lymphocyte against virus
times more) 3. Eosinophills against fungus
Feaces
1. Ceacal 2 times/day 2. Intestinal 12-14 times/day

Salmonella Pullorm vs S.gallinarum
S.pullorm is toxin producing bacteria (endo + exo), which destroy circulatory system during
early ages. While S.gallinarum cannot produce true toxins, so not cause damage to young ones.
M.Arslan CS
Colibacillosis
Colibacillosis is a disease of multiple systems in body characterized by fibrinous inflammatory
condition.
Etiology
 Caused by Escherichia coli of Enterobactericae family
 Gram negative Lactose fermenter bacteria having bacilli shape
 These are the normal micro flora of gut but can cause disease when bird is
immunosuppressed
 0157 is pathogenic strain of E.coli
 E.coli produce endo & exo toxins which are absorbed by general circulation, then the
body reacts against these toxins by producing an inflammatory condition which may
leads to death
Host
 Chicken are turkey hit primarily but Quail is accidental host
Transmission
 No true vertical transmission
 Horizontal transmission is may occur within and between flocks
Clinical signs
 Chalky white diarrhea  Swollen joints
 Depression  Difficult breathing
 Sleepy condition  Decrease in feed and water intake
Gross lesions
 Fibrinous peri-hepatitis
 Fibrinous pericarditis
 Fibrinous air sacculitis
M.Arslan CS
 Severe enteritis
 Dark black color digesta in small intestine especially in duodenum
 Thinning of wall of intestine
 paint brush hemorrhages in on surface of intestine
 Fibrinous spleenomegaly
 Wheat straw color fluid is present in joints (some time jelly like structure)
 S/C bluish discoloration of shanks
 Spill yoghurt like appearance in body
Diagnosis
 Isolation & identification (Mackonky, SS(Shigella & Salmonella), nutrient agar &
Selenite broth)
 PCR, ELISA
Treatment
 Amoxicillin + Colistin have synergistic effect
 Use those antibiotic which stay longer in intestine
 Over dosing of colistin can cause unrecoverable toxicity (i.e nervous signs like ND)
 Normal dosage for colistin 1cc/8 liter.
Treatment Recommendation Depends upon:

ITO CELLS
1. Weight
2. Age These cells are Produce fiber.
3. Season
When number increased, then high
number of fibers will produce which
leads to fibrinous appearance
Atropine is a universal antidote drug which can be
use against any toxicity.
Infectious Coryza
Bacterial respiratory disease characterized by catarrhal inflammation of URT (sinuses & trachea)
& LRT (including air sacs & some time lungs)
M.Arslan CS
Etiology
 Etiologic agent is Haemophillus gallinarum ( or paragallinarum)
 G-ve, nonmotile bacteria.
 Sometimes show bipolar staining
 Very fragile bacteria which may die within 13 hours at normal temperature
 Bacteria resides in infraorbital sinuses
 Growth Requirement
2 factors are required for growth of this bacterium,
a. X factor
b. V factor
Paragallinarum required both factor while gallinarum required X-factor for growth.
Incubation period
 1-2 days
Host
 Chicken is primary host
 Susceptible host includes Pigeon, pheasant,

Turkey & Peacock(More susceptible)
Respiratory Diseases of Major Concern
Distribution
1. ILT
 Sporadic (only in winter) 2. Mycoplasmosis
3. Infectious Coryza
Mortality & Morbidity 4. Pasturllosis
 More morbidity & less mortality
 Depend upon concurrent infection
Transmission
 B/W & W/I flocks
M.Arslan CS
 Carriers includes Musca domestica, crews, rodents etc
 Transmitted w/I flock by contaminated water, sneezing, aerosolic etc
Clinical signs
 Severe coughing, severe sneezing
 Gangling sound
 Mouth breathing
 Catarrhal Conjunctivitis, sticky eyelids, closure of eyes (unilateral or bilateral)
 Sudden decrease in egg production
 Swollen head, S/C edema of head region PUS
 Loss of feed & water intake Avian Mammals

On ripening liquid
Gross lesions become solid
 Catarrhal air sacculitis (Pathgnomonic)
 Partial blackening of lungs
 Catarrhal sinusitis
 Blockage of sinuses
 Presence of caseous material sinuses (caseous plug like that of ILT)
Diagnosis
 Clinical signs
 Isolation & Identification(need a medium which contain X & V factor)
 Molecular Techniques
 Mycoplasmosis  Pasturllosis  ILT, IB, ND

 IC attacks only I winter in sporadic form
M.Arslan CS
 ILT is disease of hilly areas
 Pasturllosis is found more in game birds. Long comb & wattles are clear signs.
 Incubation period of mycoplasosis is of 2 weeks while 1-2 days for infectious coryza
Treatment
 Sulpha drugs  Erythromycin
 Streptomycin  Trimithoprim (TPM)
Treatment for Peacock Abscess
o Give time of about 15 days to ripening the abscess
o Apply anesthesia before operation (Ketamin HCL 0.5 ml I/M)
o Then make a surgery/ operate the abscess
o Disinfect the demarked area with Pyodine
o Give stab concision with help of scalpel blade without causing damage to eye
o Remove debris material with the help of groove detector
o Soak a cotton bandage and fill the area with bandage
o Stitching the cut area
o Keep it for 24 hours & then remove cotton swab & stitching
o Inject Tribrissen injection 0.5 ml I/M & 0.5 ml Amivicon orally
M.Arslan CS
Mycoplasmosis
The set of diseases which are caused by mycoplasma species is termed as mycoplasosis.
Mycoplasma is smallest bacteria which lack cell wall. Its size is equal to pox virus which is
largest virus (300 nm).
Mycoplasma Synoviae
Sub-clinical & non-contagious , mild type of respiratory disease characterized by swollen joints
& accordingly blisters on chest muscle along with decrease in egg production & sometimes bird
become immunocompromised.
Etiology
 Caused by Mycoplasma synoviae
Incubation period
 10-15 days
 High morbidity and low mortality
Transmission
 Rare reports are present on vertical transmission
Clinical signs
 Swollen joint  Blisters, bruises on chest muscle
 Gangrenous dermatitis (as wound on chest lead to secondary bacterial infection of

clostridia spp. Which produce toxins & results in destruction of epithelium )
Gross lesions
 Caseous cheesy material is present in synovial cavities particularly in hock joints
 Putrid smell on opening the bird
M.Arslan CS
Mycoplasma Gallisepticum
Respiratory disease caused by Mycoplasma gallisepticum, characterized by sudden & severe
respiratory signs e.g swollen head, severe conjunctivitis, severe ocular discharge, mucoid nasal
discharge along with sneezing, coughing & decrease in egg production in layers.
Etiology
 Etiologic agent is Mycoplasma gallisepticum
 Smallest bacteria of about 300 nm size and devoid cell wall
Incubation period
 10-15 days
Host
 Chicken & Turkey are natural host
 Accidental hosts are pigeon, peafowl & pheasant. Wild birds are carriers of MG.
 Mortality up to 15%
 It depends upon age & concurrent infection. (mortality is very high at early age)
 Morbidity may upto 100%
Transmission
 Horizontal and Vertical
 Horizontal transmission may be within flock (aerosol, contaminated utensils) or b/w

flocks
 Routes of Vertical Transmission
1. Air Sac route (abdominal air sac have direct contact with ovary)
2. Feacal oral route 3. Through semen
4. Through oviduct
M.Arslan CS
Clinical signs
 Sneezing, coughing, swollen head, watery discharge from eyes & conjunctivitis
 Decrease in egg production up to 50%
 Swollen joint (MS)
Gross lesions
 Mild mucous production in trachea  Prominent keel bone (important in

Layer breeder)
 Sinusitis
 Misshapen ova, Dissolved ova
 Air sacculitis
 Soapy appearance of air sacs
 Blackening of ova
 Fibrinous Pericarditis
Diagnosis
 Isolation and Identification (Freys Medium, contain horse serum & high level of
Nicotine(NAD, which is reducing agent)
 ELISA
 PCR [RT-PCR (Reverse transcription PCR ) & R-T-PCR (Real Time PCR)]
ND, IB, IC, AI & Pasturllosis
Treatment
 Use only Liophilic antibiotics
 Doxycycline + Tylocin have synergistic effects
 Erythromycin (if H.paragalinarum is present)
M.Arslan CS
Fowl Cholera (Hog cholera, Pasturllosis)

Highly infectious bacterial disease of adult bird & characterized by acute & sub-acute
inflammatory conditions in visceral organs & sub-cutaneous hemorrhages in chicken, turkey,
ducks but clinical signs are very severe in Water fowl.
Etiology
 Caused by pasturela multocida(vibrio multocida)
 G-ve, non-motile, encapsulated, comma shaped, usually present in pairs
 Very virulent in producing endotoxins
 Usually present in URT but this bacteria can localize in bones & air sacs
 Pasturela gallinarum P.hemolyticum produce diseases in species other than chicken
Incubation period
 3-7 days
Host
 Almost every species affected by pasturrela
 More susceptible is Water fowl >duck > turkey > chicken(quite resistent)
Susceptible Age
 Bird of 8 weeks are most susceptible
Mortality
 Upto 15%
 May reach to 70% in stress, immunosuppression or concurrent infection
Transmission
 Horizontal
 Rats & mice are serve as biological vectors for pasturllosis
M.Arslan CS
Clinical signs
Reproductive, Digestive, Respiratory (URT) & integumentary systems are affected by pasturrela
3-forms of Disease
1) Per-acute
2) Acute
3) Chronic
 Swollen wattles & comb (chronic)
 Mucoid exudates from nares
 Generalized arthritis
 Conjunctivitis (Uni or bi lateral)
 Loss of body weight
Gross lesions
 Small necrotic foci on Liver surface
 Swollen liver
 Hemorrhages in lungs
 Hemorrhages in coronary fatty tissues on heart (Pathgnomonic)
 White nodules on lungs (in chronic form)
 Sever necrotic dead debris in lungs parenchyma
 Blackening of lungs
 Necrotic areas on lungs
 Misshapen ova
M.Arslan CS
 Caseous/cheesy material in long bones (especially in humerous)
 Wheat straw color fluid in comb & wattles
 Severe hemorrhages in duodenum loop
Diagnosis
 Clinical signs Liver Imprints
 PM lesions  Take a piece of Liver

 Keep on slide and press
 Isolation and identification  Stain it and check bacteria
under microscope
 Liver Imprints  P.multocida are present in
pairs & may look like distant
 PCR, ELISA
birds in paintings.
Control
 Adopt proper Biosecurity
Treatment
 Sulpha drugs (feed)
 Chlortetracycline (feed)
 Chloramphenicol (Inj., feed, water)
 Streptomycin (injection)
 Streptomycine is most prferrable
 Chlortetracycline is also beneficial
 Sulfa drugs are antimicrobial, which only inhibit the production of bacteria and hence make
a bird carrier which can transmit disease to healthy ones.
M.Arslan CS
Necrotic Enteritis
It is a group a bacterial disease or group of diseases caused in chicken & turkey by bacteria.
(Clostridium perfringens type C). It is G+ve bacteria, charatcterized by severe enteritis of small
intestine and usually followed by Coccidiosis.
Etiology
 Etiologic agent is Clstridium perfringens type C
 G+ve, anaerobic bacteria which normally remains in ceaca but produce toxins when
come in small intestine
Host
 Chicken, Turkey, & Quail are Natural host
Distribution/Pattern of Disease
 Sporadic
Mortality
 Up to 25%
Transmission
 Horizontal
 Bacteria is present in spore form(non-vegetative form)
 Also transmit through dust
Clinical signs
 Anorexia/ inappetance
 Severe depression
 Black color feaces
 Undigested feed material remains in the crop
 Bluish discoloration of comb
M.Arslan CS
Gross lesions
 Congested chest muscle (anemic if followed by cocci)
 Severe congested liver
 Inflammation of serosa of small intestine
 Blood clots in duodenal loop (pathgnomonic)
 Bleeding in small intestine
 Sloughing of mucosa 
 Ceacal core 1. After Coccidiosis,

Necrotic Enteritis is
 Ulcers in small intestine (sometime)
occur
 Turkey towel like appearance of small intestine 2. Limited areas which
 Velvety appearance of small intestine confined the debris
material in ceaca is
 Edematous mesentery
called Ceacal core & its
Diagnosis shape is like of onion.
 Clinical signs, PM lesions 
 Impression smear
Control
 Use chlorinated water (last option)
 Disinfect with Glutraldehyde (Glutex) to protect next flock
Treatment
 Lincomycin (Feed or water)
 Preferred through feed
M.Arslan CS
Spirochetosis
It is named as Spirochetosis b/c it is caused by spirochete bacteria which is elongated spring like
in shape.
It is bacterial disease of layer bird characterized by high body temperature, anemia, jaundice
along with locomotory dysfunction or incoordination.
Etiology
 Caused by a spirochete Borrelia anserine
 largest , spring like bacteria of 0.3µm/300 nm
 stain by Wright’s stain
Incubation period
Immature RBC’s
 3-5 days
 Misshapen
Host  Larger size
 Lighter stain
 Chicken (Layer)
Course of Disease
 Up to 1 week with intermittent fever
Mortality
 Up to 60%
Transmission
 Vector borne disease
 Only transmitted within flock by “blue tick” named as Argus persicus (soft shell tick)
 All the 3 stages of this tick (Nymph, Larva, Adult) are infectious for bird
 Mechanical vectors are required to transmit disease between flock i.e crews, rodents etc
Clinical signs
 High body temperature up to 1100F (IBD, Fowl Typhoid..but less than Spirochetosis)
 Listlessness (uneasy feeling)  Greenish diarrhea

 Ruffled feathers  Swollen joints
M.Arslan CS
 Increased thirst  Anemia

 Jaundice like appearance (paler appearance of membranes)
Gross lesions
 Spleenomegaly
 Mottled spleen (abnormal appearance i.e spots on spleen)
 Hepatomegaly
 Fibrinous pericarditis
 Cooked appearance of chest muscle
 Hematological Changes
 High rise of immature RBC’s
 High rise in leukocytes
 Presence of swishing bodies (springs are present on blood smear against Wright’s stain)
Pathogenesis
 Body gives more immune response to antigens which are more proteinacious. As Borrelia
anserine have ore protein , so chicken body gives a great immune response to this
bacteria & high body temperature is caused.
Diagnosis
Difference between RBC of Chicken
 Clincal signs, PM lesions, Blood profile & Mammal
Control Chicken Mammal
 Disinfection Oval Biconcave Disc
shaped
 Ectoparasites
i. Eccofleece (cypermetherine), 10% --
1ml/Liter……………..100% 0.1 ml/Liter
ii. Naguvan 3g/100 ml
Treatment
 Penicillin
 OTC
 Streptomycin
M.Arslan CS
Protozoal Diseases
Protozoa are of 2 types. 1). Sporulative 2). Budding
Sporulative protozoa are more dangerous for poultry in production of disease. B/C in sporulating
protozoa, 8 cells are produced from single cell while only 2 cells are produced in budding protozoa.
Eimeria spp. Are mmore important in poultry & these are very much selective to produce infection.
Coccidiosis
Infectious protozoal litter borne disease of chicken characterized by severe hemorrhages throughout the
gut (from duodenal loop to ceacal tonsils).
In intestinal cocci, duodenum is rarely affected & more affected part is jejunum. Intestinal cooci is more
prevalent in layer birds but ceacal cocci in broilers.
Etiology
 Caused by Eimeria spp.
 There are 16 types of Eimeria spp. But only 9 are pathogenic to poultry
 Important spp. In Pak. are, E.necatrix, E.tannela. E.intestinalis, E.maxima, E.burnetti,
E.negani(less important)
 Necatrix & tannela produce ceacal cocci
 Maxima & intestinalis produce intestinal cocci
Course of Disease
 4-5 days
Host
 Chicken is natural host & carriers are Turkey & Geese

 Depend on concurrent infection with clostridia spp. (linked disease which produce
favorable environment for each)
Transmission
M.Arslan CS
 Horizontal through feacal oral route or infected litter route
Clinical signs
 Anemia
 Poor FCR
 Irregular body weight
 Bloody diarrhea (color is chocolate in N.E but fresh in cocci)
 Pale comb & wattles
Gross lesions
 Pale liver
 Round pin point hemorrhages in small intestine (also in round worms & lead toxicity but
irregular & less in number in round worm infestation. While Bigger, bluish & having a
point at centre in lead toxicity) in circular manner.
 Severe hemorrhages in enteric mucosa (intestinal cocci)
 Severe bleeding in ceacum (ceacal cocci)
 Swollen kidney
Diagnosis
 PM lesions
 Microscopic oocysts or oocyte (double walled structure in which sporozytes are present)
Treatment
 Toltrazuril
 Amprolium
 Clopidol
Treatment schedule
2 day on 1 day off 2 day on 1 day off 2 day on
M.Arslan CS
Mycotoxicosis
Mycotoxins are side products of fungus. Fungus is sometime beneficial & sometime harmful.
Mycotoxicosis is condition in which Mycotoxins produce pathogenic effects on Liver, intestine
& spleen.
 Mycotoxins are genotoxins….produce aduct…break clump of DNA…cell become unable

to produce toxin…affected genes effects are appears
 These toxins affect both meat & egg type birds
 Mostly poultry is affected by Aspergillus flavus, Aspergillus ochraceus & Aspergillus
parasiticus
Mycelia spread spores mostly on shaking or any disturbance. Mycotoxins are not even kill durin
feed formulation process. (i.e. Pelleting at 85-900C).
 Main source of aflatoxin is Rice & maize is main source of ochratoxin. Ochratoxin is less
toxic than aflatoxin
Mycotoxins
i. Aflatoxin
ii. Ochratoxin
iii. Deoxynevalinol (DON)
iv. Trichothesis
v. Fumonisin
vi. T2-toxin
Susceptibility Grade
Most susceptible poultry bird to Mycotoxins is duck & least susceptible is chicken. So chicken is
gold standard for Mycotoxins. It means that the toxin which affect chicken, then it can affect
every poultry spp.
Host
Congestion= pooling of blood W/I cavity
 Chicken, turkey, duck, pheasent
Hematoma= blood coagulation over
surface
 Depend on concurrent infection
Hemorrhage = bleeding W/O flow
M.Arslan CS
Transmission
 Through Grain, formulated feed & dust
Clinical signs
 Anemia
 Poor FCR
 Irregular growth pattern Aflatoxin= Hepatotoxin
 Paler discoloration of comb & Ochratoxin= Nephrotoxin
wattles
 Hemorrhages(mostly S/C)
 Severe bleeding (vit. K)
 Deformed embryo (teratogenic effect)
Gross lesions
 Paler Liver along with bloody  Ascites
streaks  Rupturing of liver (sometimes)
 Severe enteritis  Hematoma formation
 Hydro pericardium (w/o enlargement  Nephritis (ochratoxin)
of Liver)

Microscopic lesions
 Severe vascular degeneration of  Perivascular cuffing
hepatocytes  Presence of Giant cells (mess of
 Darkly stained pychnotic nuclei macrophages)
 Glomerulonephritis
Diagnosis
 Typical analytical tools i.e. HPLC, GC, chromatography
 Serum antibodies
Control
 Check quality of grains
 Add toxin binder
i. Mineral based i.e. HSCAS (hydrated calcium alluminium silicates)
ii. Yeast based i.e. Sacchromyces cerevicae
Maximum tolerate level of aflatoxin

 20 ppm
M.Arslan CS
Nutritional Deficiencies
Vitamin Deficiencies
Vitamins are of 2 types 1) Water soluble 2) fat soluble
FAT SOLUBLE
A = Retinol D = Ergocalciferol
E = Tocopherol K = Phyloquinone
WATER SOLUBLE
B1 = B2 = B3 = Niacine B5 = B6 =
Thiamine Riboflavin Pantothenic Pyridoxine
acid
B12= C = Ascorbic H= Biotin Folic acid
Cyanocobal acid
amine
Fat soluble vitamins are more important than water soluble vitamins b/c their deficiency or
excessiveness cause more severe changes. The excessiveness of ADEK can cause toxicity to bird.
 Vitamin A & D are particularly important in Breeder

 Vitamin E is more important in Layer
 Vitamin K for all birds especially broilers
Vitamin A
 Epithelilization of body epitheliums (esp. vascular system)
 Normal growth of body
 Vision
 Feather growth
o Xeropthalmia
o Blood spots on surface of yolk
o Stunted growth
o Opacity of eyes
o Ruffled feathers
o White spots on Liver
M.Arslan CS
Vitamin E
Vitamin E is natural antioxidant. It is oxidant scavenging vitamin which save the body from free radicals.
Vitamin E has synergistic effect with Se.
o Natural anti oxidant

o Exudative diathesis
o Dermatitis
o Decrease egg production
Vitamin D
 Active from is D3 (cholecalciferol)
 Bone mineralization
o Rickets
o Osteoporosis
 There are 2 hormones for calcium balance in the blood 1) Calcitonin 2) PTH
Calcitonin that works to reduce the calcium level in the blood stream& deposit it on bone. While PTH
resorb calcium from bones , when deficient in circulation.
M.Arslan CS
M.Arslan CS
1. Etiology
ND
 Causative agent is Paramyxovirus

 Enveloped virus covered by 2 layers of Glycoproteins
 Having 2 epitopes , Haemagglutinins for attachment of RBCs and Neuraminidaze for detachment
 RNA virus having non-segmented genome
 High concentration of Formalin/ Phenol can deactivate the virus
IB
 Causative agent is Corona virus, its name is due to its coron like shape
 Small, enveloped, RNA virus
 Single stranded, +ve sense
 Some strains of IB can multiply in embryonated eggs
 Strains of IB are categorized into:
iii. Nephrotrophic (destroy nephron)
Mass, Ark. Conn, M-52, D-275, D-278, H 4/91
iv. Respiratory
H120, H 4/95
ILT
 Causative agent is Herpes virus, Tapeia avium

 Enveloped, DNA virus of 150-250 nm diameter
 Virus can stay in house for 30-50 days at 25-370C
 Dissolved by lipid absorbent
AI
 Causative agent is Influenza virus type A(Influenza patho/proto virus type A) of family Orthomyxoviridae
 Enveloped, RNA, single stranded, Negative sense virus
 Segmented genome (having 8 segments), so more chances of mutation
 Having 8 segments of genome but produce 10 proteins(structural + non-structural)
 80-100 nm size
 Virus is mostly present in organic matter
 Type A, B & C is only pathogenic types. Only type A affects chicken & type B & C affects humans & pigs
 Ordinary disinfectants can kill these viruses, 5% sod. Hypochloride, β-propiolactam, sod. Dodisyl Sulphate (SDS), Formaldehyde,
Phenolics & 10% NaOH sol. Also effective.
Never use disinfectant alone but in combination.
IBD
 Causitive agent is Birna virus of Birnaviridae family belongs to genus Avibirna

 Genome consists of 2 strands of Double stranded RNA (dsRNA)
 Remains in poultry shed even for years depend upon environmental conditions. Organic matter save the virus from disinfectant
 This virus survives for 8 months at 370C
CIA
 Causative agent is Gyro virus / Circovirus of Circoviridae(having nucleic acid in circular fashion) family
 SS, -ve sense, DNA virus having 2.3 kpb genomic structure
 Gyro virus has different strains in different areas. CUX1 strain is found in central & far Asian countries
HPS/IBH
 Causative agent is Adeno virus type-IV/ type-3
 DNA virus
Pox
M.Arslan CS
 Causative agent is pox virus  Largest virus of poxviridiae family (300 nm)
 Virus remains inside shed & get entry on injury
MD A.E
 Caused by Herpes virus group B  Enterovirus of picornaviridae family
Pullorm
 Caused by Salmonella pullorm
 Gram negative, non-motile, non-lactose fermenter, bacillus, exist as individual bacilli
Colibacillosis
 Caused by Escherichia coli of Enterobactericae family  These are the normal micro flora of gut but can cause
disease when bird is immunosuppressed
 Gram negative bacteria having bacilli shape
 0157 is pathogenic strain of E.coli
 E.coli produce endo & exo toxins which are absorbed by general circulation, then the body reacts against these toxins by producing
an inflammatory condition which may leads to death
Infectious Coryza
 Etiologic agent is Haemophillus gallinarum ( or  Very fragile bacteria which may die within 13 hours at
paragallinarum) normal temperature
 G-ve, nonmotile bacteria.  Bacteria resides in infraorbital sinuses
 Sometimes show bipolar staining
 Growth Requirement
2 factors are required for growth of this bacterium, d. V factor
c. X factor Paragallinarum required both factor while gallinarum required X-

factor for growth.
MG
 Etiologic agent is Mycoplasma gallisepticum  Smallest bacteria of about 300 nm size and devoid cell
wall
Cholera
 Caused by pasturela multocida(vibrio multocida)  Usually present in URT but this bacteria can localize in
bones & air sacs
 G-ve, non-motile, ecapsulated, comma shaped, usually
present in pairs  Pasturela gallinarum P.hemolyticum produce diseases
in species other than chicken
 Very virulent in producing endotoxins
N.E
 Etiologic agent is Clstridium perfringens type C  Bacteria normally remains in ceaca but produce toxins
when migrate into small intestine
 G+ve, anaerobic bacteria which remains in ceaca &
produce toxins when come in small intestine
Spirochetosis
M.Arslan CS
 Caused by spirochete Borrelia anserine
 largest , spring like bacteria of 0.3µm/300 nm
 stain by Wright’s stain
2. Mechanism of Disease Transmission

 Transovarial route  Direct transmission  Mechanical vectors
 Transmission on egg  Indirect transmission  Feed
shell  Dissemination by  Vaccines
 Horizontal wind
Transmission  Biological vectors
3.
4. Diseases of Brooding
 Omphalitis  Reoviridae
 AE  Pullorm
 IB  Aspergillosis
 CIA
5. Diseases of breeder
 EDS  AI  Necrotic Enteritis
 ND  Mycoplasmosis  MS
 IBD  Fowl typhoid  Mycotoxicosis
 CIA  Pullorm  Roundworms
6. Diseases Which deteriorate egg quality
 EDS  IB
 ND  Salmonellosis
 AI
7. Immunosuppressive Diseases
 IBD  LL  Coccidiosis
 MD  CIA
8. Diseases of High mortality & Low morbidity
 HPS  APV
 ILT (per acute)  AI
 Spirochetosis
M.Arslan CS
9. Diseases with high morbidity & less mortality
 IBD  Pullorm
 AE  Mycoplasmosis
10. Disease with less mortality & Less morbidity
 CIA  Pox
 Fowl cholera
11. Antihelmitic
 Cypermetherne (Eccofleece)  Coopex
 Naguvan  Albendazol
 Saguvan
12. Vectors
A vector is an invertebrate that transmit disease to vertebrate.
1. Biological vector 2. Mechanical vector

Biological Vectors
A vector in which multiplication of a pathogen can occur.
 Wild birds are reservoirs of avian influenza and Pasteurella spp.

 Rodents carry a wide range of diseases including pasteurellosis and salmonellosis.
 Insects are responsible for transmission of various d Biological Vectors
 Insects are responsible for transmission of various diseases. Pox, West Nile and Highland
 J arbovirus may be transmitted by mosquitoes
 Spirochetosis by Argas persicus ticks.
 Litter beetles ( Alphitobius diaperinus) are reservoirs of a wide range of infections including
Marek’s disease, IBD, salmonellosis, pasteurellosis and coccidiosis.
 The poultry red mite, D. gallinae could act as a biological vector of S. enteritidis and natural
carriage of these bacteria by the mite on poultry premises has also been reported. It was also
found that D. gallinae carried other pathogens such as E. coli, Shigella sp., and Staphylococcus,
thus increasing the list of pathogenic agents potentially transmitted by the mite.
Mechanical Vectors
 The housefly, Musca domestica, as a possible mechanical vector of Newcastle disease virus in the
laboratory and field.
 House flies transmit campylobacteriosis.
M.Arslan CS
Vector Disease
Musca domestica Compylobacter, ND
Argas persicus Spirochetosis
Mosquito Pox, LL,
Beetle MD, IBD, Salmonella, Cocci
D.gallinae(rat) AI, Pasturella, S.enteritidis,
E.coli, Shigella, Staphylococcus
References
1. ASA Handbook on Poultry Diseases by American Soybean Association (Simon M.Shane)
2. Handbook of Poultry Diseases by Rakesh Kumar Shukla
3. http://www.healthybirds.umd.edu/Disease/index.cfm
4. http://www.ncbi.nlm.nih.gov/pubmed/20377736
5. Zoonosis
 Zoon= animal  Osis= anything
Zoonotic Disease
Any disease come from animals & affected human beings
Types of Zoonosis
1. Direct Zoonosis 3. Meta zoomosis

2. Cyclozoonosis 4. Saprozoonosis
I. Direct Zoonosis
Direct transmission of pathogen from infected animal to susceptible human.
 Rabies from dog  ND from poultry
 Glanders from Horse
II. Cyclozoonosis:
Transmission of disease from vertebrate to vertebrate.
 Strangles and Glanders from Horse to human
 Equine Influenza from Horse to human
 Taenia solium from pig/poultry via feaces
 Taenia saginta from pig/poultry via feaces
III. Metazoonosis (meta=different)
Type of Zoonosis in which 2 types of hosts (vertebrate & invertebrate) are involved in
transmission of disease.
 Arbo virus from animal to human via insects
 Crimian congo hemorrhagic fever from Bovine to Man via ticks
M.Arslan CS
IV. Saprozoonosis (sapro=soil, dung)

Type of Zoonosis which requires non-living for transmission
 Anthrax  Giardiasis  Aspergillosis
 Tetanus  Colibacillosis
Food borne Zoonotic infections
Pathogen Signs in Human Temp. of growth Ph
Bacillus creus Diarrhea & emesits 10-480C 4-9
Comylobacter jejuni Gastroenteritis in babies 30-47 6-7
Clostridium botulinum Flaccid paralysis(botulism) 10-40 More than 4
C.perfringens type-D Pulpy kidney disease in 15-50 More than 7
animals
E.coli 0157 Nervous signs, Hemorrhagic 10-40 4-9
enteritis, hemorrhagic
enterocolitis,
Listeria monocytogenes (raw Nervous signs, may lead to 2-44 5-7
milk. Under-cooked food) death
Salmonella 5-46 1-14
Staph aures Enteritis or enterotoxemea 6-46 9
Yersinia enterocolitica 2-45 4-9
Tapeworms of Poultry
 Tricanela spirallus
 Taenia saginata
 Taenia solium
 Toxoplasma gondii
 Balentedium colii
M.Arslan CS
Swab method
 Take sterile cotton swab and rub on carcass esp. on neck and gut
 Cut swab and dip into broth directly
 Incubate at 370C for 24 hours
 Bacteria is judged on colony bases
1. Bacterial Diseases
Disease Etiology Incubation Mort.. Morb, Pathgnomonic lesion Treatment
period
Pullorm S.pullorm, G-ve, non-motile, 5-7 d 20 50 Round Necrotic foci on Nitrofuran (furaltadon
non-lactose fermenter Liver or furazolidon)
Fowl Typhoid S.gallinarum, g-ve, 7 Bile stained, friable Floramphenicol (Neflor)
liver
Colibacillosis E.coli,G-ve, Lactose Coligranuloma all over Colistin + Amoxicillin
fermentor, bacilli shaped, the body
0157
I.C H.gallinarum, G-ve, non- 1-2 d Catarrhal air sacculitis Erythromycin,
motile, resise in infra-orbital Streptomycin
sinuses, X & Y factor required
for growth
MS M.synoviae 2 weeks Cheesy material joints Doxycycline + tylocin,
MG M.gallinarum, no cell wall, 15 100 Soapy air sacs erythromycin
intracellular,
Fowl cholera P.multocida, g-ve, non motile, 15,, 70 Hemorrhages on Streptomycin,
cooma shaped coronary fatty tissues Chlortetracyclin
on heart
N.E C.perfringens A Blood clots in duodenal Lincomycin
M.Arslan CS Page 70
loop
Spirochetosis B.anserina Hepatomaegaly & Penicillin, OTC,
mottled liver Streptomycin
2. Viral diseases
Disease Causative agent Incubation Etiology Mortality Pathgnomonic signs and
period lesions
ND Paramyxo virus 5-15 d Paramyxo, enveloped, 0-25% Torticulus, Nervous signs
non-segmented RNA, SS, 0-100 Tricad= Hemorrhages in
-ve sense proventriculus, Ceacal
tonsils & lenticular ulcer
in intestine
IB Corona virus 18-36 h Corona, SS, Enveloped, 25%
+ve sense RNA
ILT Tapeia avium (harpes 5-12 d Taepea avium, enveloped, 0-5 Asphyxial death,
virus) DNA, 0-50 Respiratory plugs in
90-100 Trachea
APV APV-II & APV-III 3-4 days ND 50-100
AI Influenza virus A 5-12 days Influenza virus-A, 8 90-100% Hemmorhages all over
segments, SS , –ve sense the body
RNA virs,
IBD Birna virus 2-3 days RNA, ds, -ve sense 0, 20-30% Inflammed bursa
enveloped
CIA Gyro virus 8d DNA, ss, -ve sense 30%, 70% Thymic atrophy
HPS Adeno virus-IV 48-78 hours DNA 100% Serosangal fluid in
pericardium
IBH Adeno virus -3 DNA Swollen liver with blood
M.Arslan CS Page 71
streaks
Pox Pox virus 5-7 days DNA Greyish black nodules on
unfeathered area
MD 4-5 weeks DNA Proliferative granular
tumors in Liver, Lungs,
heart, Kidney, spleen,
bursa,ovarian tissue
AE 2weeks DNA 2-3
3. Postmortem Lesions & Clinical Signs of Viral Diseases
Clinical signs PM Lesions

ND
 Digestive System  Digestive system
 Greenish whitish diarrhea  Pin point hemorrhages in proventriculus
 Dehydrated bird (ruffled feather)  Button like/ Lenticular ulcer in duodenal
 Less feed intake loop & in Jejunum
 More water intake  Hemorrhages in ceacal tonsils
 Respiratory System  Spleenomegaly & hepatomegaly is may
 Sneezing, Gasping, Coughing observed
 Serous & mucoid nasal discharge  Respiratory System
 Ocular discharge  Tracheitis
 Nervous System  Congestion/inflammation of trachea &
 Paralysis of wings & legs ulcer may be present in severe cases
(Unilateral & bilateral)  Oedematous lungs (due to secondary viral
 Stargazing infection)
 Torticulus  Nervous System
 Blindness  Congested brain
 Serosa of brain will be red
 Osteomlacia
IB
 Tracheitis
 Respiratory System  Tracheal plugs
 Coughing, Gasping  Excessive deposition of urtaes in Kidney & ureter (due to less
 No Nasal discharge in Broilers. But there will be a nasal water, water-soluble uric acid converted into non-soluble
discharge in Layers crystals of uric acid. The sharp edges of crystals destroy the
 Cyanotic membranes (AI&IB) parenchyma of kidney, which leads to kidney failure)
 Cause watery albumin in eggs in adult layers
 Urinary System
 Shrill cry (due to kidney pain)
ILT
 SUB-ACUTE FORM  Hemorrhages in Lacrimal gland
 Loss of appetite  Tracheitis
 Conjunctivitis (watery eyes due to secondary bacterial  Blood clots in Trachea
infection may lead to blindness)  Respiratory plugs (sometimes)
 Coughing  Ulcer in Trachea
 Sneezing  Sub-coetaneous inflammatory exudate in head region (wheat
 ACUTE FORM straw color)
M.Arslan CS Page 72
 Signs of sub-acute form+  Inflammation of intra orbital sinuous
 Gasping  Necrosis material in Trachea (which cause Asphyxial death to
 Squawking bird)
 Sitting & shed their feathers
 Sleepy condition
 Per-ACUTE FORM
 Sign of sub-acute & acute form +
 Expectoration of bloody mixed exudate
APV
 Swollen head (SHS)  Thick yellow exudate on cutting the comb
 Head shaking  Cheesy material in Sinuses (Asphyxia)
 Opisthotonus appearance  Congestion in Trachea(if trachea is involved)
 Nasal discharge (Only in TRT)
 Decrease egg production
 Sneezing, coughing & gasping
 Puffy appearance of comb
AI
Respiratory System
LPAI  Rhinitis (Inflammation of nasal mucosa)
Respiratory System  Tracheitis
 Rattles, Rales, Coughing, Sneezing, Depression (ruffled  Hemorrhages on internal mucosa of trachea
feather + lower the wings), Huddling, Sleepy, condition  Congestion of lungs
Digestive System  Blackish discoloration of lungs along with pus in lungs (due to
 Mild type diarrhea, Vent pasting sec bacterial infection)
Respiratory System Digestive system
 Decrease in egg production, misshapen ova/eggs  Paint brush hemorrhages in all intestine
HPAI  Thick intestinal mucosa
 Bloody discharge from nares  Destruction of Payer’s patches which leads to ulcer in intestine
 Severe coughing & sneezing Cardiovascular System
 Severe diarrheic condition  Echynotic hemorrhages on heart
 Chalky white to simple watery diarrhea Urinary system
 S/C hemorrhages all over the body which are  Pale yellow kidney
prominent in shank region  Nephritis
 Egg production reduced to 0%  Bulging of kidney from bony socket
 Bluish comb & wattles (Cyanosis) Reproductive System
 Birds in sleepy condition  Oophritis
 Complete cessation of feed & water intake  Dissolved ova
 Hemorrhages on surface of shanks  Egg yolk peritonitis
Misshapen ova & weak shelled eggs  Regressed & discolored ova (dark yellow)
 Oedematous oviduct (isthmus)
IBD
 Severe & sudden viremia produces high temperature  Muscoskeletal system
of body  Deep intramuscular hemorrhages in pectoral & thigh muscle
 Ruffled feathers  Digestive system
 Dehydrated bird  Pin point hemorrhages at junction of Proventriculus & Gizzard
 Whitish diarrhea (also in CIA)
 Vent pasting  Edematous condition in duodenum loop & in whole intestine
 Sleepy condition of bird  Thick intestinal mucosa
 Solemness  Lymphatic system
 Outbreak of cannibalism (bird picking own feathers on  Destroy Payer’s Patches which may leads to Ulcer & sometimes
vent due to irritation) bleeding at Payer’s Patches
 Constant huddling  Inflamed & hemorrhagic bursa
CIA
 Anemia—pale comb & wattles  Hemorrhages on heart
 Depressed bird  Pin point hemorrhages at junction of Proventriculus & Gizzard
 Bluish area under wing  Deep intramuscular hemorrhages in Thigh & chest region
 S/C hemorrhages  Subcutaneous hemorrhages in chest & thigh region
 Increased blood clotting time  Ongoing bleeding from different regions of body & prolonged
Hematology at wing web
M.Arslan CS Page 73
Parameter Normal  Thymic CIA
atrophy
PCV 27%  Pale yellow
12 bone marrow
Hb 12g/dL  Hemorrhages
2 in thigh region & sometimes bleeding is also
 Anisocytosis (immature RBC,s in circulation due to observed in Thymus
insufficient Hb level)
HPS
 No clinical sign in acute form  Swollen & necrosed liver
 Signs are observed in sub-acute from  Sersangous fluid 10-11 ml in pericardium
 Gasping  Pulmonary edema
 High mucous contents in feaces  More mucoid digesta
 White diarrhea
 Sudden cardiac death (birds are death with dorsal
recombancy)
IBH
HPS IBH
Swollen liver with less hemorrhages Swollen liver with severe hemorrhages like blood streaks
Dark brown Liver Pale discoloration
10-13 ml fluid in pericardium Negligible
Fowl Pox
 Grayish-black nodules on unfeathered areas  Diphtheric membrane in pallet region & in tracheal region
 Decrease in feed & water intake
 Rubbing of head region by birds
 Bright red ulcers on pallet covered with yellow
diphtheria membrane
MD
 Acute form  Acute form
 Depression  Tiny nodules on every organ especially on muscles
 Mild ataxia (Chest & Thigh)
 Solemness/sleepy condition  Dark grey to white Diffused proliferative granular
 Paralysis (sometimes) tumors in liver, lungs, heart, kidney, spleen, bursa,
 Swollen feather follicles ovarian tissue (red color in Fowl cholera)
 Classical form /Latent form / Locomotory Paralysis  Hardness of Proventriculus indicate outcome of
 Bicycle ridden birds (one leg forward & 2nd disease
backward)  Chronic form
 Leg paralysis (unilateral/ bilateral)  Lameness
 Head down  Loss of cross striations in schiatic nerves (AE, LL,
 Wing paralysis (damage of schiatic nerve ) MD)
 Impaction (due to damage of vaugal nerve)
 Blindness (damage of optic nerve)
 Choaking (retention of digesta inside GIT)
 Diarrheic condition may present (if
intestine controlling nerves are destroyed)
 Proliferative from
 Tetragonal, elliptical corona of eyes
AE
 Neurological disorder NO
 Depression
 Ataxia
 Staggering gate, Incordination
 Lateral recombancy
 Tremoring of head
 Sometime stargazing appearance
 Swirling movements
M.Arslan CS Page 74
4. Postmortem Lesions & Clinical Signs of Viral Diseases
Clinical Signs PM Lesions

Pullorm
 Weak birds  White foci on Liver surface
 Somnolence/sleepy condition  White color nodules on surface of heart, lungs, spleen &
 Wetty appearance on serosal surface of small intestine
 Birds sitting on their hocks  Dark congested liver (before foci formation)
 Swollen joints  Amber color fluid in hock joints
 Chalky white diarrhea with vent pasting  Swollen kidney
 Shrill cry  White foci on kidney (sometime)
 Chirping voiding diarrhea  White foci on Iris, leads to blindeness (also a clinical sign)
 Enteritis like condition / severe enteritis
 Perforation of intestine (hole in intestine)
Fowl Typhoid
 High rise in body temperature along with vent pasting  Nodules on wall of intestine
which is due to Greenish or bright Sulfer color diarrhea  Multifocal ulcers in small intestine
(Sulfer color is due to high level of Stercobilinogen which is  Bronze color liver (Bile stained)
formed from lyses of hemoglobbin)  Friable Liver and Brittle Spleen
0
 2 peaks of temperature 107 & 110 F  Nodules in myocardium
 Anemia (comb & wattles)  Nodules in lungs (at start of disease)
 Brownish Discoloration of All membranes  Nodules on heart (at start of disease)
 Increased thirst
 Gasping (only in acute form)
Effect on Hematology
 Thin watery blood with PCV 16-22% (normal 27%)
Colibacillosis
 Chalky white diarrhea  Fibrinous peri-hepatitis
 Depression  Fibrinous pericarditis
 Sleepy condition  Fibrinous air sacculitis
 Swollen joints  Severe enteritis
 Difficult breathing  Dark black color digesta in small intestine especially in
 Decrease in feed and water intake duodenum
 Thinning of wall of intestine
 paint brush hemorrhages in on surface of intestine
 Fibrinous spleenomegaly
 Wheat straw color fluid is present in joints (some time jelly
like structure)
 S/C bluish discoloration of shanks
 Spill yoghurt like appearance in body
Infectious Coryza
 Severe coughing, severe sneezing  Catarrhal air sacculitis (Pathgnomonic)
 Gangling sound  Partial blackening of lungs
 Mouth breathing  Catarrhal sinusitis
 Catarrhal Conjunctivitis, sticky eyelids, closure of eyes  Blockage of sinuses
M.Arslan CS Page 75
(unilateral or bilateral)  Presence of caseous material sinuses (caseous plug like
 Sudden decrease in egg production that of ILT)
 Swollen head, S/C edema of head region
 Loss of feed & water intake
MG
 Sneezing, coughing, swollen head, watery discharge from  Mild mucous production in trachea
eyes & conjunctivitis  Sinusitis
 Decrease in egg production up to 50%  Air sacculitis
 Swollen joint (MS)  Soapy appearance of air sacs
 Fibrinous Pericarditis
 Prominent keel bone (important in Layer breeder)
 Misshapen ova, Dissolved ova
 Blackening of ova
MS
 Swollen joint  Caseous cheesy material is present in synovial cavities
 Blisters, bruises on chest muscle particularly in hock joints
 Gangrenous dermatitis (as wound on chest lead to  Putrid smell on opening the bird
secondary bacterial infection of clostridia spp. Which
produce toxins & results in destruction of epithelium )
Fowl cholera
 Swollen wattles & comb (chronic)  Small necrotic foci on Liver surface
 Mucoid exudates from nares  Swollen liver
 Generalized arthritis  Hemorrhages in lungs
 Conjunctivitis (Uni or bi lateral)  Hemorrhages in coronary fatty tissues on heart
 Decrease in egg production (Pathgnomonic)
 Loss of body weight  White nodules on lungs (in chronic form)
 Sever necrotic dead debris in lungs parenchyma
 Blackening of lungs
 Necrotic areas on lungs
 Misshapen ova
 Caseous/cheesy material in long bones (especially in
humerous)
 Wheat straw color fluid in comb & wattles
 Severe hemorrhages in duodenum loop
Necrotic Enteritis
 Anorexia/ inappetance  Congested chest muscle (anemic if followed by cocci)
 Severe depression  Severe congested liver
 Black color feaces  Inflammation of serosa of small intestine
 Undigested feed material remains in the crop  Blood clots in duodenal loop (pathgnomonic)
 Bluish discoloration of comb  Bleeding in small intestine
 Sloughing of mucosa
 Ceacal core
 Ulcers in small intestine (sometime)
 Turkey towel like appearance of small intestine
 Velvety appearance of small intestine
 Edematous mesentery
Spirochetosis
M.Arslan CS Page 76
 High body temperature  Spleenomegaly
 Listlessness  Mottled spleen (abnormal appearance i.e spots on spleen)
 Ruffled feathers  Hepatomegaly
 Greenish diarrhea  Fibrinous pericarditis
 Swollen joints  Cooked appearance of chest muscle
 Increased thirst
 Anemia
 Jaundice like condition
5. DISEASES AFFECTING LIVER
HPS Swollen liver

IBH Swollen liver with severe hemorrhages like blood streaks, pale discoloration
MD Proliferative granular tumors in liver
Pullorm Dark congested Liver, white foci on Liver
Fowl typhoid Friable, Bronze color
Colibacillosis Fibrinous perihepatitis
Necrotic Enteritis Severely congested
Fowl cholera Swollen, necrotic foci
Colbacillosis Fibrinous perihepatitis
N.enteritis Congested
Sprochetosis Hepatomegaly
Coccidisois Paler
Mycotoxicosis Paler color liver along with bloody streaks
6. Diseases affecting Kidney
IB Excessive deposition of urate in kidney & ureter

AI Buldging of kidney from bony sock, paler kidbey
Pullorm Swollen kidney, white foci
IBD Nephrosis
MD Proliferative granular tumors
7. Diseases affecting Lungs
M.Arslan CS Page 77
ND Edematous lungs
AI Congested lungs, blackish lungs alongwith pus in lungs
HPS Pulmonary oedma
MD Proliferative granular tumors on spleen
Pullorm Whit color nodules on lungs
Fowl typhoid Nodules on lungs
I.Coryza Partial blackening of lungs
F.Cholera Hemorrhages, white nodules, blackening
8. Diseases affecting Heart
AI Hemorrhages on heart
CIA Hemorrhages on heart
HPS Serosangous fluid in pericardium (10-13 ml)
MD Proliferative granular tumors on heart
Pullorm White nodules on heart
FT Nodules on heart
Colibacillosis Fibrinous carditis
Mycoplasmosis Fibrinous pericarditis
F.cholera Hemorrhages on coronary fatty tissues on heart
9. Routes of Disease Transmission
Route Disease
Egg transmission Mycoplasma, Salmonella, Reovirus, adenovirus
Egg shell transmission E.coli, Salmonella, Omphalitis
Direct transmission Coryza, Mycoplasma, salmonella, ILT, Pasturella
Indirect transmission IBD, Salmonella
Wind transmission VvND, ILT
Feed Salmonella, IBD
Vaccine Adeno virus, Reovirus
10. Inflammation
Ear Otitis Lungs Pneumonitis

Liver Hepatitis Uterus Hystritis
Throat Pharyngitis Penis Balonitis
M.Arslan CS Page 78
Colon Colitis Urethra Urethritis
Brain Encephalitis Ova Oophritis
Stomach Gastritis vagina Vaginitis
Mouth Stomatitis Tongue Glossitis
Hips Bursitis Testes Orchitis
11. Susceptible Age Groups of Disease
Disease Common age Groups

IBD 0-6 weeks
IB Less than 10 weeks (kidney form), all age groups (respiratory)
ILT 3-8 months
MD 12-24 weeks
LL More than 14 weeks
EDS More than 17 weeks
Reovirus infection (A.E) 1-4 weeks
CIA Less than 3 weeks
IBH 4-9 weeks
HPS 3-5 weeks
Colisepticemia Less than 8 weeks
Infectious coryza More than 8 weeks
Pullorm 0-4 weeks
Omphalitis 0-2 weeks
Fowl Cholera 8 weeks
12. Digestive system
Organ or tissue involved Key symptoms Possible Condition Associated symptoms; diagnostic aids
Crop Sour crop; cheesy ulceration; “yellow Trichomaniasis Lesions also present in liver; disease most
buttons” of necrosis common in pigeons and wild doves;
microscopic examination of lesions
Dropped crop Genetic, Hot weather
M.Arslan CS Page 79
Preventriculus Swollen Fish meal contaminated Usually associated with heavy feeding of
poor quality fish meal
Pin point Hemorrhages ND Lenticular ulcer, hemorrhages in ceaca,
nervous signs
Harder MD Tumors,
Pin point hemorrhages at junction of IBD, CIA Thymic atrophy in CIA, inflamed bursa with
provetntriculus & Gizzard hemorrhages in IBD
Gizzard Erosion Impaction; Vitamin deficiency Loss of weight
or decomposed feed
Easily removable cuticle & white colonies Mycotoxicosis
under it
Duodenum Thickened wall; white streaks on outer Intestinal coccidiosis Some diarrhea; emaciation if condition of
surface (E. acervulina) long duration; seen in older birds
Inflammation; gut filled with mucus Capillaria; Round-worms; Presence of worms in intestine; diarrhea;
tapeworms unthriftiness; microscopic examination for
capillaria suggested.
Bleeding in duodenal loop Necrotic enteritis Turkey towel like appearance of intestine
Pancreas Swollen; white areas of necrosis Avian Monocytosis (Nonspecific Hits pullets in early production; usually
Infectious Enteritis; Bluecomb) follows hot weather spells; head parts turn
blue’ kidneys and ureters filled with urates
Jejunum and ileum Swelling of middle third of intestine; Intestinal coccidiosis Loss of appetite; chronic diarrhea;
mucus spotted with blood (E.necatrix) emaciation; mortality may be high
Lower half of intestine swollen; lumen Intestinal coccidiosis(E. Blood-spotted diarrhea; loss of appetite;
filled with pink-tinged mucus maxima) emaciation; disease runs short course
Rectum and ceca inflamed Intestinal Coccidiosis (E. Diarrhea; emaciation; some deaths
brunetti)
Ceca Swollen; yellow core; cheesy exudates; Pullorum High mortality in chicks 1 to 3 weeks of
ulceration age, marked depression; diarrhea; chicks
huddle for warmth; nodules may be
present in liver, heart and gizzard; white
plaques on outside of intestine
Paratyphoid Symptoms similar to pullorum; mortality
may be high at 4 days or 10 to 12 days; no
other lesions may be evident
Blackhead (Enterohepatitis) Liver lesions also present; sulfur-colored
droppings; darkened head parts
Hexamitiasis Watery, foamy stool; stiff, awkward gait;
disease affects turkeys only
Swollen; filled with blood or blood clots; Cecal Coccidiosis Bloody droppings; loss of appetite; ruffled,
cheesy, blood-tinged exudates unkempt appearance; high mortality,
unless checked
Miscellaneous Fluid in abdominal cavity (ascites) Lymphoid Leukosis Liver enlarged with tumors
Marek’s Disease Nerve involvement
Gas leak brooders Edema and Ascites
Heart disease Heart is enlarged or the heat sac is filled
with caseous material; round heart
Hemorrhagic intestine, lymphoid areas Velogenic Newcastle disease These lesions usually associated with other
findings and symptoms of respiratory
distress
Thickened membranes over heart See alsoMycoplasma
(pericarditis); abdominal cavity gallisepticum
(peritonitis); and air sacs (airssacculitis)
Enteritis; diarrhea Blackhead Predominant cecal and liver lesions; sulfur-
colored diarrhea
Hexamitiasis Affects young poults; foamy, watery
diarrhea; birds may die in convulsions
Typhoid Swollen liver and spleen; sudden deaths
Erysipelas (turkeys) Hemorrhages in muscles and other tissues;
snood and caruncle swollen in toms;
septicemia in hens
Cholera Liver swollen. Light-colored, has necrotic
spots, breaks apart easily when handled;
M.Arslan CS Page 80
high mortality rate
Avian Monocytosis Chalky white, pasty urates in kidneys;
ureters, and other serous surfaces; affects
young pullets about to start to lay
Overdose of laxatives or History of faulty use of drugs
chemicals
Tuberculosis Deep ulcers filled with caseous material in
intestinal tract; hard nodules (tubercles) in
other organs of body
Hemorrhagic Disease Bloody droppings; hemorrhagic areas in
muscles of legs, breast and heart
Internal Parasites Diarrhea; unthriftiness; presence of
parasites I intestine
Necrotic enteritis Swollen intestine with necrotic lining
(coninious lesion, mostly of posterior
intestine)
Ulcerative enteritis Inflammation of middle to lower intestine
with ulcers (discrete lesions); may be
yellow areas on liver
Liver Yellow color; small gray-white areas of Pullorum High mortality in chicks 1 to 3 weeks of
necrosis; presence of small nodules age; marked depression; diarrhea; nodules
also may be present in lung, heart and
gizzard
Slightly swollen, light-colored, “cooked” Fowl Cholera Many birds die without warning; high
appearance; small gray-white sports of mortality rate
dead tissues (necrosis)
Swollen; light gray to white nodules Lymphoid Leukosis or Marek’s Spleen, kidneys and other organs also may
(tumors with soft centers) Disease be involved
Swollen; large hard nodules Tuberculosis Bird emaciated; “razor” breasted; deep
ulcers filled with cheesy exudate found in
intestine; acid-fast stain, test entire flock
within avian tuberculin
Greatly enlarged, friable (breaks apart Fowl Typhoid Swollen spleen; comb and wattles pale;
easily); greenish-bronze color; gray- sudden deaths, birds may react to
white sports of necrosis pullorum stained-antigen test
Round depressions or ulcers Blackhead (Enterohepatitis) Cecal walls thickened and ulcerated;
yellow-green exudates; dry, cheesy core;
sulfur-colored droppings
Enlarged; small areas of necrosis (gray- Ornithosis (Psittacosis) Air sac involvement; enlarged spleen;
white sports of dead tissue); membrane lesions quite often missed; laboratory
over the liver testing of blood samples recommended
Enlarged; greenish-rose in color Synovitis (M. synoviae) Swollen spleen; presence of pus in
inflamed joints and extending along
tendons
Swollen; yellow color; small areas of Pullet Disease Disease usually affects birds first starting
necrosis to lay; “hot weather” disease; white,
chalky deposits in pancreas, kidneys and
ureters
Staphylococcosis Swollen, inflamed joints; acute form of
disease characterized by sudden deaths
and no apparent symptoms; isolation of
causative organisms in laboratory will
confirm diagnosis
Enlarged; hemorrhagic areas pinpoint in Hepatitis (inclusion-body) Affects young birds and pullets in
size and larger; areas turn yellow in color production; low mortality; marked drop in
egg production
Enlarged; covered with hemorrhagic Duck Viral Hepatitis Sudden onset; high mortality (90%) in
areas ducklings under 4 weeks of age; kidneys
appear mottled
M.Arslan CS Page 81
Swollen liver New Duck syndrome Respiratory symptoms; nervous symptoms
(incoordination); thickened membranes
over heart (pericarditis); air sac
involvement
Spleen Swollen, dark-mahogany colored, often Vibrionic Hepatitis, Acute Spleen also swollen; bone marrow usually
with fine gray-colored streaks in a netlike Lymphoid Leukosis or Marek’s gray colored or dark red and watery
arrangement Disease
Swollen Pullorum High mortality in chicks 1 to 3 weeks of

age; nodules or necrotic areas in liver,
heart and gizzard; white plaques on
outside of lower intestine
Typhoid Primarily a disease of older birds; liver

enlarged; bronze-mahogany color; many
sudden deaths, high mortality
Synovitis Liver swollen; greenish-rose color; pus in

swollen joints and extending along
tendons
Ornithosis (Psittacosis) Liver enlarged; necrotic areas in liver; air

sac involvement
Swollen; hemorrhagic Erysipelas (turkeys) Hemorrhages found in other tissues; snood

and caruncle swollen; deaths may be
sudden with no apparent symptoms,
higher incidence of infection in toms
Swollen; presence of hard nodules with Tuberculosis Similar lesions present in other organs;
gritty centers bird emaciated; ulcers filled with cheesy
exudate found in intestine; flock should be
tested with avian tuberculin
Swollen; presence of tumor-like masses Lymphoid Leukosis or Marek’s Liver and other organs infiltrated with
with soft centers Disease similar lesions; fluid in abdominal cavity
(ascites)
Swollen New Duck Syndrome Respiratory symptoms; nervous symptoms

(incoordination); thickened membranes
over heart (pericarditis); air sac
involvement
M.Arslan CS Page 82
Swollen, dark-mahogany colored Acute Lymphoid Leukosis or Liver also swollen; bone marrow usually
Marek’s Disease gray colored or of a dark-red consistency
Swollen; spotted Spirochetosis (turkeys, chickens Liver swollen

and ducks)
Any septicemic disease
13. Respiratory System
Organ or tissue involved Key symptoms Possible Condition Associated symptoms; diagnostic aids
Nostrils, Sinus cavities Nasal discharge IB – Infectious Bronchitis Sudden onset; rapid spread; rattling cough;
no nervous symptoms
“Wet Pox” Black, wart-like nodules on head parts;
suffocation
Nasal discharge, swelling of the facial Infectious Coryza Sudden onset; rapid spread; air sacs may
tissues and/or sinuses be involved; isolation ofHaemophilus
gallinarum
Mycoplasma gallisepticuminfection Swollen sinuses in turkeys
CRD (chronic respiratory disease) in
chickens; low mortality; thickening air sacs;
mild sinusitis
Fowl cholera (chronic) Cheesy exudates in wattles; disease may
flare up in acute form when birds are
subjected to “stress”; isolation
ofPasteurella multocida
Nutritional Roup (Vitamin A Egg production and hatchability reduced;
deficiency) yellow-white pustules in mouth and
esophagus; chalky deposits in cloaca, vent,
heart, kidneys
Pharynx, Larynx, Bronchi and Cheesy patches on lining of larynx and “Wet Pox” Black, wart-like nodules on head parts;
Trachea trachea suffocation
Mild tracheal involvement with clear IB – Infectious bronchitis Sudden onset; rapid spread; rattling cough;
exudates egg production may fall 50%; no nervous
symptoms
Trachea and Bronchi filled with mucus or Laryngotracheitis Distressed breathing; neck extended on
blood-tinged plugs inspiration; mortality as high as 50%;
deaths due to suffocation
Nasal and tracheal lesions vary with Newcastle Disease Sudden onset; rapid spread of respiratory
virulence of virus from mild exudative symptoms; nervous symptoms also present
change to frank blood (particularly in chicks); egg production
drops to zero
Swelling Infectious Coryza Marked nasal discharge; swelling of facial
tissues; isolation of H. gallinarum
Mycoplasma gallisepticuminfection Slow spread and persistence of symptoms;
marked involvement of air sacs; large
number of culls.
Presence of red worms in trachea and Gapeworms High mortality in chicks; of primary
lungs importance in pheasant and turkey
operations.
Lungs Grayish nodules in lungs Pullorum Diseases High mortality in newly hatched chicks;
nodules also may be seen in heart and
M.Arslan CS Page 83
gizzard; raised plaques on inside of lower
intestines; unabsorbed yolk sac
White nodules in lungs Mycoplasma gallisepticuminfection Slow spread and persistence of symptoms;
marked involvement of air sacs; large
number of culls
Yellow nodules in air sacs and lungs Aspergillosis History of moldy litter or feed; mortality
may run high in young chicks and poults;
lesions may have fur-like down with
yellow-green tint
Congestion Smothering Heavy losses at night; chicks piled up in
corners; no other lesions; eliminate
possibility of pullorum disease in all cases
Grayish areas of consolidation Complicated infection, E.coli, etc Marked air sac involvement; history of slow
(pneumonia) spread; persistence of symptoms; fibrin
covering heart and liver
Air Sacs Thickened; covered with yellow exudates IB – Infectious bronchitis Sudden onset; rapid spread of respiratory
symptoms; no nervous symptoms; egg
production drops to 50%
Mycoplasma gallisepticum plus Slow spread; persistence of respiratory
secondary infections in chickens symptoms; low mortality; high percentage
of culls
Mycoplasma meleagridis Circumscribed caseous lesions
Newcastle Disease Sudden onset; rapid spread of respiratory

symptoms; some nervous symptoms; egg
production drops to zero
Aspergillosis Exposed to moldy litter and feed; high
mortality in young chicks and poults;
lesions may be covered with fur-like down
with yellow-green tint
Infectious Coryza Marked nasal discharge; swelling of facial

tissues; isolation of H. gallinarum
Ornithosis (Psittacosis) Enlarged spleen and liver; small areas of

necrosis (gray-white sports); thickened
membrane over heart and liver, mainly in
turkeys and pigeons.
New Duck Syndrome Respiratory symptoms; nervous symptoms

(incoordination); liver and spleen swollen;
thickened membrane over heart
(pericarditis); lesions of pneumonia may be
present
M.Arslan CS Page 84
14. Vaccination Schedule
Broiler
Age Vaccine Dose ml/bird Route
5-7 ND 0.025 E/D
8-12 IBD
16-17 HPS 0.5 I/M or S/C
20-22 ND Lasota D/W
28-30 IBD
LAYER
1 MD 0.3 S/C
5-7 ND+IB 0.025 E/D
8-12 IBD
18-20 IBD D/W
20-22 ND Lasota
32-34 IBD
38-40 ND Lasota
7th week Fowl Pox 1 dip of prong W/W
8 Coryza S/C , I/M
11 ND+IB 0.025 DW
14 Coryza S/C , I/M
16 ND+IB+EDS
After every 2 months ND Lasota 0.5 D/W
BREEDER
1 MD 0.3 S/C
2 ND+IB 0.025 E/D
10 ND Lasota
14 IBD
18 AI S/C , I/M
M.Arslan CS Page 85
22 ND Lasota 0.5 DW
24 HPS I/M
26 IB DW
38 AI S/C , I/M
40 IBD DW
6-8 wk MG S/C , I/M
7 ND Lasota DW
8 Fowl Pox 1 dip of prong W/W
9 IB 0.5 D/W
10 ILT 0.025 E/D
11 Coryza 0.5 S/C in neck
12 ND DW
13 AE
14 IB
15 MG .25 S/C , I/M
17 Coryza 0.5 S/C in neck
21 ND+IB+IBD+EDS 0.5 I/M in breast
15. ANTI-COAGGULANTS
EDTA 2mg/ml
Heparin
Sodium citrate 20mg/ml
Sodium oxalate
Potassium citrate
Potassium oxalate
16. Disinfectants
Class Members Conc. Residual Organic matter

activity
Hypochlorides 1;32, 1;40 Poor Poor
Idophores Pyodine, 2% Poor Poor

Povidon,Tinc.Iodine,
M.Arslan CS Page 86
Betadyne
Alcohals Ethyl alcohol 70-95% Low Low
QAC NH4 0.2-3% Yes No
Peroxides H2O2 No No
Aldehydes Form-,Glutar-,Estaldehyde 0.1-2% Yes Yes
Phenolics Excellent
Corrosive Irritant Toxic --cidal
Hypochlorides YES YES YES V. F. B
Idophores YES YES YES BVS
Alcohals NO NO NO G+ve,G-ve
QAC NO NO NO Enveloped Virus
Peroxides NO NO NO Anaerobic bacteria
Aldehydes YES YES YES
Phenolics V
17. Ethnovetrenary medicines of Poultry
Disease Plant product

ND Capsicum annum, Casia fistula, cassia sibernaria
Fowl Cholera Adansonia digitata
Fever Allium sativum
Coughung, Gasping, Ginger
Sneezing
Lameness Ginger (citta spp.)
Ulcerative Enteritis Glycerazia glabba, Alovera
Coccidiosis Amla, Lagnaria vulgaris
Diarrhea Sana atalica
Enteritis Alovera
Endoparasite Capsicum
Ectoparasite Derris aleptica
Ervous signs Zee maize
M.Arslan CS Page 87
Viral disease Aniseed
Anti-toxic Sylmarine(milk thistle plant)
Soothing effect Eucalyptus (product available “mercobeth”)
M.Arslan CS Page 88
POULTRY
SEROLOGY
M.Arslan CS Page 89
Blood Collection in Poultry
Objective
 Flock health monitoring
 To study cause of disease
 To check antibody titer
 To check chemical profile of bird
 To check seroprevelance of disease
Blood Collection Specifications

 Whole blood (cell study)
 Plasma (chemical study)
 Serum (Titer)
Minimum requirements for Blood Collection

 3 mL syringes
 Needles (the higher the gauge, the smaller the diameter of the needle). The 25 gauge
x 1 inch length is preferable for most birds.
 Blood collection vials
 Mini cooler (for transportation of blood samples to the laboratory)
How Much Blood Can One Collect

 1% of its body weight in grams
Blood Collection Sites in birds

i. Brachial vein(largest vein under wing)
ii. Jugular vein (the vein on the side of outstretched neck)
iii. Medial metatarsal vein (The vein on the inner leg, above the hock)
Measures after Blood Collection

 To obtain whole blood and plasma, gently mix the drawn blood by inverting the tube
a few times. This will ensure proper mixing of the anticoagulant with the whole
blood.
M.Arslan CS Page 90
 To obtain serum, place the blood vial on a slanted surface for 10 to 15 minutes to
allow for clotting
 The plasma and serum samples can be spun by centrifugation
ANTI-COAGGULANTS
EDTA 2mg/ml
Heparin
Sodium citrate
Sodium oxalate 20mg/ml
Potassium citrate
Potassium oxalate
Blood Collection from Chicken

Site Age Needle (mm)/gauge Volume that might
be taken
Heart Adult 17/22;50 At least 20 ml
Heart 3 weeks 22;19 5ml
Heart Day-old 22;19 0.5-1 ml
Wing Adult 21/20;37.5 At least 20 ml
Right Jugular vein 3 weeks 23;37.5 1-2 ml
M.Arslan CS Page 91
Serodiagnostic Tests
HA & HI TESTS
T o check antibody level in serum against agglutinating virus
Washing of RBC’s
 Take blood in Falcon tube and centrifuge at 700 rpm for 3 mins
 Remove supernatant along with buffy coat
 Add same amount of normal saline as supernatant is removed
 Dissolve button by gentle shaking
 Again centrifuge at 700 rpm for 3 mins
 Repeat this for 3 times
 Give 3 washes to RBC’s
 Take 1 ml washed RBC & add in graduated flask contain 99 ml normal saline to make
1% washed RBC
HA
Objective
 For quantification of antigen

 For quantification of cut-off point (threshold level) of antigen
 To dilute viruses
 Sub-sequent test is HA
Procedure
Take 50 ul N.saline in all wells of titration plate
Take 1.5-2 ml N.saline in vaccine vial to bring it in liquid form
Take 50 ul antigen in 1st well from stock solution and make 2-fold series dilution upto 11th well&
discard 50 ul from 11th well
Give incubation at 370C for 20-25 minutes

AGGLUTINATING BACTERIA
Results
Mycoplasma
th st
Button formation will start from 12 well to 1 well
Brucella
50% button formation is desired
M.Arslan CS Page 92
i.e 5th well is desired well
4HA=32
HA=8
This means that 1 ml from stock sol. And 7 ml from N.sallin
HI
OBJECTIVE
 TO KNOW IMMUNE STATUS OF FLOCK

 TO KNOW LEVEL OF ANTIBODIES THAT IS PROTECTIVE & GIVE MINIMUM
REACTION
Principle
Inhibit agglutination of RBC’s by making complexes of antigen & antibodies to threshold level,
where agglutination starts (Ag + RBC). These are protective levels.
Procedure
 Take 50 ul N.saline in all wells

 Take 50 ul serum in 1st well & make 2 fold series dilution upto 10th welland discard 5o ul
from 10th
 Add 50 ul antigen in 1-11 wells from working solution
 Incubate at 370C for 20 minutes
 Add 50 ul washed RBC’s to all wells
 Incubate for 5 mins at 370C
Results
 Button formation is from 1st to 12th

 I well before from 50% button formation is desired
M.Arslan CS Page 93
IHI/IHAI
This test is for non-haemagglutinating viruses & bacteria .
i.e
i. Birna virus (IBD)

ii. Herpes virus (ILT, MD)
iii. Rinder pest virus
Objective
To know immune status of flock against non-agglutinating virus or bacteria\
Principle
Artificial antigen/ epitope are produced which are responsible for immunity and pathogenecity.
Procedure
 Prepare washed RBC’s

 Make a coupling solution
Tanic acid (0.05 conc.) : Normal Saline
1 : 25000
 Take equal amount of RBC’s , Tanic acid & agent

(pathogen)
 Incubate it at 370C for at least 45 minutes Coupling Agent
 Take 50 µl Normal saline in 1-12 wells
Tannic acid
 Take 50 µl serum in 1st well & make 2 fold series
dilution upto 10th well Chromium chloride
 Add 50 µl antigen complex 1-11 well Glutraldehyde
 Incubate at 370C for 15 mins
 Give washing as given to RBC’s to remove non-used
RBC’s, antigen & tanic acid particles for clear results
Results
Results are like HA.
M.Arslan CS Page 94
Agar Gel Precipitation Test
Principle
Soluble antigen make precipitation in gel.
Apparatus
Serum, ag, agarose gel, glasswares
Gel concentration
For larger molecules, use diluted concentration of gel and use higher concentration for smaller
molecules.
Preparation of gel
 1 gram agrose + 100 ml Normal saline + boil for I minute + cool down
 When temperature is 400C , poured it into petri dish, there will be layer formation
 Make wells in semi solid gel
Procedure
 Take known serum in central well & samples in side wells or known antigen in central
well & serum samples in side wells
 Give incubation of 24 hours
Results
There will be precipitation line b/w central & positive well
How to develop known serum??
Inject killed vaccine in rabbit & give repeated exposure & then collect serum.
Difco
Agar gel in which molecules can run
Precipitation
Phenomenon in which Ag & Ab make white colored complex which can be seen by naked eye.
Complement Fixation Test
M.Arslan CS Page 95
This test is used to identify antigen or antibody except serum containing hemolytic agents
(babesia, anaplasma, streptococcus)
Complement Fixation Tes

These are sero proteins which are fixed by Ag & Ab complex. These proteins are mainly
responsible for inflammatory reaction & cause lyses of RBCs.
Principle
Ag & Ab complex will activate the complement system.
Amboceptors
These are ant-species antibodies (Antibodies are produced against cells of another species)
Development of Amboceptors
 Prepare Hyper immune serum
Day Dose of RBC (ml) Route Conc. Of RBCs

1 0.2
3 0.4
5 0.6 I/V 0.5-1 %
7 0.8
9 1
 Isolation of Serum
i. After 9 days of injection wait for 2-3 weeks, after it collect serum from that
animal (rabbit). This serum will contain amboceptors
ii. Destroy complement by heating it at 560C for 15 mins maximum(& minimum 3
mins)
Quantification of amboceptors
 Add 50ul normal saline in 1 -12 wells

 Add 50ul hyper immune serum in 1st well and make 2 fold series dilution up to 11th well
M.Arslan CS Page 96
 Add 50ul sheep RBC in 1 -12 wels
 Incubation
Result
The 1 well next of 50% agglutination is desired
i.e
50% agglutination is 5th well the 6th is desired well
6th=64 (5 ml RBC+1 ml serum)
Sensitized RBCThe 1 well next of 50% agglutination is desired
i.e
50% agglutination is 5th well the 6th is desired well
6th=64 (5 ml RBC+1 ml serum)
Sensitized RBC
 RBC coated with amboceptors this is indication system

 Complement of rabbits serum is inactivated because it will cause lysis of sensitized
RBCS if not activated
Opsonization
Adherence of Ag+ Ab
Quantification of complement protein
 Take complement through guinea pig serum

 Take normal saline from 1- 12th well
 Add 50ul guinea pig in 1st well and make 2 fold series dilution up to 11th well
 Add sensitized RBCS in 1-12th wells
 Incubation at 37oC for 20 mint
M.Arslan CS Page 97
Results
Hemolysis will start from 1st well and then decrease gradually. The well having button
formation is desired i.e
6th=64
4 HA
4 hemolytic units=64
1 ________________ =64/4=16
16 (1ml serum + 15ml normal saline) → working solution
Reagents for test review
1. Development of amboceptors
2. Quantification of amboceptors
3. Sensitized RBCS
4. Quantification of complement
5. Ab (serum)
6. Live vaccine (antigen)
Procedure
 take normal saline in 1 -12th well

 Take 50ul target serum in 1st well and make 2 fold serial dilution up to 9th well
 Add antigen in 1-10th well
 Add complement in 1-11 well
 Give incubation at 37o C for 20 mints
 Add 50ul sensitized RBCS in 1 -12 wells
Results
If AB are specific to AG then there is no lysis of EBCS
M.Arslan CS Page 98
Review of CFT
Quantification of amboceptors
 Add normal saline from 1-12th well

 Add serum from 1 to 11th wells
 Add sheep RBCS from 1 to 12th well
 Incubate
Quantification of complement
 Add normal saline from 1 to 12th wells

 Add guinea pigs RBCS in 1 to 11th wells
 Add sensitized RBCS from 1 to 12th wells
 Incubate
Test
 Add normal saline from 1 to 12th wells

 Add target serum from 1 to 9th well
 Add antigen from 1 to 10th well
 Add complement from 1 to 11th well
 Incubation
 Add sensitized RBCS from 1 to 12th well
Bacterial neutralization test

Principle
 Specific AB binds specific Ag
Objectives
 To identify the strain of Ag

 To infer bacterial disease challenges
M.Arslan CS Page 99
The mononuclear antibodies taken from SPF and use in this test
Requirements
 Animals  Incubation
 AG  Trypton water
 Inactivated serum  Sterile test tube
Procedure
 Add 0.25 ml normal saline in 1 to 12th wells

 Add inactivated serum in 1st well and make 2 fold serial dilution up to 11th wells
 Add 0.5 ml bacteria of 1.5 ratio diluted
 Incubation
 Inject these into animals through inter venues rout at 0.1 ml dose rate
Results
If AB neutralized Ag then no deformities in animals
 E .coli = pink colonies

 Salmonella = white
 Mycoplasma = fry egg like colonies
o Death before 60 hrs is considered as acute death
o Symptoms will be observed after 24 hours
SPA
 Take serum on slide  Add colored antigen
 Incubate at room temperature
Results
Agglutination occurs in +ve samples
M.Arslan CS Page 100

Egg Inoculation Techniques
 Detect the virus
 Culture the virus
 Demonstrate the egg/embryo
 Check effect on embryo & growth
 9-12 days old embryos have a high amount of fluid of 20-24 ml
 9-10 days old embryo are required for this technique
Route of injecting Virus
 Chorioallontoic sac
 Yolk sac
 Amniotic sac
 Chorio allantoic membrane
CAM Route transmittable viruses
o NDV
o AIV
 Fluid to be injected 0.5 cc
 Needle 17 gauge
 Seal the pore with sterile wax & candle can be used for this purpose.
 Sterilize the area of 1 meter within performing area with ethanol
 Egg shell must be cleaned with pyodine
 Mark the egg with help of candler & inject from opposite side of mark with the help of insulin
syringe
 Take field virus to perform this inoculation by isolation the virus
 Incubate for 60-70 hours at 370 C , then candle the egg after every 24 hours
Culture of Virus
Virus is intracellular organism, so require special conditions to grow. So, it requires special conditions to
grow. Different viruses grow in different cavities of egg.
 Before inoculation one must know the pre-dilaction site

 Isolation of virus is done from field conditions, Then
i. Preservation
ii. Inoculation
iii. Incubation (at 370C for 72 hours)
iv. Harvesting

 Candle the eggs after every 24 hours and check results
Death time Reason
Before 24 hours - Non-specific

- May be due to mechanical injury
24-48 hors Virus is very virulent
48-72 hours Virus is less virulent
No death Virus is absent or Avirulent
 By candling, check that the embryo is feasible for collection or not.

 Death may be due to
i. Virus
ii. Bacteria
iii. Mechanical injury
Purification shows the cause of death of embryo. Needle cause injury to embryo which cause secondary
bacterial infection. This secondary bacterial infection leads to pus formation and ultimately purification
is there.
In bacterial death the embryo is putrefied while not in viral death
Bacterial growth may cause autolysis of embryo. In autolysis there are loose body organs, pus, smell(H 2S
gas),low fluid & bleeding.
Harvesting of Virus
Eggs select for harvesting,
i. Should not be putrefied

ii. Must have clear fluid
iii. Maximum fluid
iv. No blood mixing
v. Having high titer of virus
How the Titer is checked
Check the agglutination under microscope. Take a drop (50 µl) of virus & one drop of 3% washed RBCs
on slide & check under microscope.

Disadvantage of collecting low titer fluid
It will tend to lesser the titer of collected fluid. All fluid is collected in one bottle. So, when a low titer
fluid is added in bottle, it will cause some dilution of concentrated collected fluid.
Optimum Titer for Collection
1024 (10th well)
Harvesting protocol
 Keep the broader end upward b/c

i. Collection of fluid will be easy
ii. Embryos come down ward & fluid come upward
 Keep eggs in freezer for 2-3 hours
a. Before candling (keep a;; eggs in freezer)
Or
b. After candling (keep dead embryo containing eggs in
freezer)
B/C to clot the blood & for easy collection of fluid.
 Decaping of egg. Remove air cell membranes. Clear fluid must be visible, otherwise discard the
egg.
 Press embryo with small spoon to bring the fluid upward. Without pressing, there is 5-7 ml fluid
& by pressing the fluid will be 13 ml.
Harvesting from eggs containing blood
Take the fluid and centrifuge it. Then remove fluid to collect the virus.
Harvesting from embryo
Triturate the embryo & then centrifuge it. Collect the fluid. But to obtain virus from embryo, eggs should
be SPF.
Preservation
 Preserve at minus temperature (-200C)

 Make aliquots to preserve the fluid
 Make bundles of aliquots and preserve at -200C

Autogenous vaccine
Objective
To control te disease by that virus which cause the disease
Diseases
i. HPS ii. IBH
Requirement Specification
 Liver (from infected flock)  Liver 50g/1000 doses
 Normal saline (37% or 40%)  Formalin 6 ml /1000 ml
 Formalin Antibiotic &  Gentamycin 1-3ml/1000 ml
 Antifungal agent
Dosage
 0.25-0.3 ml/bird
Procedure
o Take half amount of Normal Saline
& half amount of Liver
o Triturate in homogenizer for 15 mins
o Add required amount of formalin in
homogenate
o Add required amount of antibiotics
& antifungal agents
o Repeat the same procedure for
remaining liver & other materials
o Sieving with masculine cloth
o Add normal saline to fulfill the
volume

o Give a period of 16 hours to prepared vaccine (8 hours at 40C & 8 hours at room
temperature)
o Then inject to infected flock
Results
o Results will appears after 6 hours

o There are 50 % chances of recovery of flock. It depends upon the quality of formalin
used & other conditions which are used to make vaccine.
Adeno Virus
This virus is particularly intranucleaur & forms the intranucleaur inclusion

bodies

Terms Related to Poultry Pathology
Adjuvant
Material added to an antigen to increase its immunogenicity.
Agonist
Substance which changes the properties of cells via receptors at the cell membranes.
Amino acids
The "building blocks" from which protein are constructed.
Antibody
Proteins produced by an organism's immune system to recognize foreign substances.
Antigen
Any substance that stimulates an immune response by the body. The immune system recognizes such substances as
being foreign, and produces cellular antibodies to fight them. Antigen/antibody response is an important part of a
person's immunity to disease.
Adenocarcinoma
A cancer that develops from the glandular tissue of the body.
Assay
A quantitative or qualitative evaluation, or test, of a substance. Frequently used to describe
tests of the presence or concentration of infectious agents, antibodies, etc.
Attenuated
An attenuated vaccine is one that has been weakened by chemicals, or other processes (passages) so that it will produce
an adequate immune response without causing the serious effects of an infection.
AUC
The area under the concentration-time curve at steady-state over 24 h unless otherwise stated. It is equivalent to a single
dose AUC 0-∞
Bacteria
Tiny microorganisms that reproduce by cell division and usually have a cell wall. Bacteria can be shaped like a sphere,
rod, or spiral and can be found in virtually any environment.
Bioavailability (F)
The fraction of administered drug that reaches the systemic circulation.
Biodegradation
Decomposition or breakdown of a substance through the action of microorganisms (such as bacteria or fungi) or other
natural physical processes (such as sunlight).
Biopharmaceutics
The study of the factors influencing the bioavailability of a drug in man and animals and the use of this information to
optimize pharmacological and therapeutic activity of drug products.
Booster
Administration of an additional vaccination to help increase or speed the immune response to a previous vaccination.
Breeding flock
A flock that is composed of stock that has been developed for commercial egg or meat production and is maintained for
the principal purpose of producing chicks for the ultimate production of eggs or meat for human consumption.
Capsid proteins

Proteins that make up the shell of a virus particle that contains the genetic material.
Carcinogen
A substance that causes cancer.
Carrier
A person or animal that harbors a specific infectious agent without visible symptoms of the disease. A carrier acts as a
potential source of infection.
CAS Number
A CAS (Chemical Abstracts Service) Registry Number is a unique identifier of a chemical.
Each CAS Registry Number, is a unique numeric identifier, designates only one substance, has no chemical
significance and is a link to a wealth of information about a specific chemical substance.
CAS Registry
The largest and most current database of chemical substance information in the world containing more than 32 million
organic and inorganic substances and 59 million sequences.
CFU
Colony Forming Units. A measure of viable microbial populations
Challenge
The process of infecting an animal with a disease agent to test for protective immunity.
Cmax (level, concentration)
The highest concentration reached or estimated in the compartment of reference.
Consumption
Total domestic consumption in a given time period, includes domestic production, imports of chicken products and any
chicken products that are moved into the market from frozen stocks and excludes any exports and
Contaminant
A substance that is either present in an environment where it does not belong or is present at levels that might cause
harmful (adverse) health effects.
Cytokine
Proteins manufactured by cells of various lineages that, when secreted, drive specific responses (e.g., proliferation,
growth, or maturation) in other susceptible cells.
Decontamination
A general term for the destruction or removal of microbial contamination to render an item safe.
Deoxyribonucleic acid (DNA)
The chemical inside the nucleus of a cell that carries the genetic instructions for making living organisms.
Disinfection
A process used to reduce the number of micro-organisms.
Dose
The amount of a substance to which a person/animal is exposed over some time period. Dose is a measurement of
exposure. Dose is often expressed as milligram (amount) per kilogram (a measure of body weight) per day (a measure
of time).
Dose-response relationship
The relationship between the amount of exposure (dose) to a substance and the resulting changes in body function or
health (response).
EFSA
The European Food Safety Authority (EFSA), an agency of the European Union. Its permanent home is in Parma, Italy.
Its primary responsibility is to provide independent scientific advice on all matters concerning Food Safety.
Electrolytes

Substances that dissociate in water to form a cation (positively charged ion) and and anion (negatively charged ion).
ELISA (enzyme-linked-immunosorbent serologic assay)
A technique that relies on an enzymatic conversion reaction. It is used to detect the presence of specific substances,
such as enzymes, viruses, antibodies or bacteria.
Endemic
Disease that is widespread in a given population.
Enzootic
A disease which is constantly present in the animal community, but only occurs in a small number of cases.
Enzyme
Specialized proteins that act as catalysts for virtually all necessary chemical reactions that take place within the body.
Like all catalysts, enzymes unchanged by the reactions they promote, and will initiate many reactions until they are
degraded (usually by another enzyme).
Epidemic
The occurrence of cases of an illness in a community or region which is in excess of the number of cases normally
expected for that disease in that area at that time.
Epidemiology
The branch of medical science that deals with the incidence, distribution, and control of disease in a population.
Epitope
A molecular region on the surface of an antigen capable of eliciting an immune response and of combining with the
specific antibody produced by such a response.
Epizootic
An outbreak or epidemic of disease in animal populations.
Etiology
Causal association of a disease with an agent. The study of the cause of diseases.
FAO
The Food and Agriculture Organization of the United Nations (FAO) is a specialized agency of the United Nations that
leads international efforts to defeat hunger. Serving both developed and developing countries, FAO acts as a neutral
forum where all nations meet as equals to negotiate agreements and debate policy. FAO was founded on 16 October
1945 in Canada. The headquarters
FDA
Food and Drug Administration. The American drug regulatory authority.
Fibroblast
A cell derived from connective tissue.
Fomite
An object that is not harmful in itself but which can harbor pathogenic organisms and thus may be involved in
transmission of an infection.
Functio laesa
Loss of function; one of the cardinal signs of inflammation.
Gene
The functional and physical unit of heredity passed from parent to offspring. Genes are pieces of DNA, and most genes
contain the information for making a specific protein.
Gene-deleted
An organism with one or more genes removed from the genome to render it nonpathogenic so it can be used as a
vaccine.
Genotoxin

A substance that damages DNA. A genotoxin can cause mutations in DNA - mutagen, it can trigger cancer -
carcinogen, or it can cause a birth defect - teratogen.
Geographic information system (GIS)
mapping system that uses computers to collect, store, manipulate, analyze, and display data.
Glycoprotein
A biomolecule composed of a protein and a carbohydrate.
GMP
Good Manufacturing Practices: The part of quality assurance which ensures that products are consistently produced and
controlled to the quality standards appropriate to their intended use and as required by the marketing authorization.
Half Life
The period of time required for the concentration or amount of drug in the body to be reduced to exactly one-half of a
given concentration or amount.
Iatrogenic
Related to an abnormal state or condition produced in a patient through inadvertant or erroneous treatment.
Idiopathic
Denoting a disease of unknown cause.
IgA
IgA antibodies are found in areas of the body such the nose, breathing passages, digestive tract, ears, and eyes. IgA
antibodies protect body surfaces that are exposed to outside foreign substances. This type of antibody is also found in
saliva and tears. IgA activity is essentially related to the mucosa immunity.
IgG
One of many antibodies present in blood serum which is usually indicative of a recent or remote infection. IgG is most
prevalent about 3 weeks after an infection begins. It is the most important antibody in the secondary response.
IgM
One of many antibodies present in blood serum which is usually indicative of an acute infection. It is the first
immunoglobulin to be produced after the immune response takes place. IgM is the predominant isotype in the primary
response.
Immune system
All the organs, cells, biological substances and cell functions which, together, are responsible for defending the body
from extraneous elements.
In vitro
In an artificial environment outside a living organism or body.
In vivo
Within a living organism or body.
Incidence
The number of new cases of disease in a defined population over a specific time period.
Incidence
The number of new cases in a population during a specified time period.
Infection
The entry and development of an infectious agent in the body of a person or animal.
Kilobase (kb)
A measure of the size of a nucleic acid molecule. One kilobase = 1000 nucleotides. Animal virus DNAs range in size
from less than 2 kilobases (Circoviruses) up to several hundred (Poxviruses).
Live vaccine

A vaccine that contains a living, yet weakened organism or virus.
Marker vaccine
A recombinant organism containing a foreign gene in which, when used as a vaccine, the foreign gene or antibodies to
the expressed protein from the foreign gene can be detected. Marker vaccines or animals receiving marker vaccines can
be detected with specific diagnostic tests.
Metabolism
The conversion or breakdown of a substance from one form to another by a living organism.
MHC (Major Histocompatability Complex)
MHC is the name given to a cluster of genes on chromosome 16 that influenza immune response.
MIC
The minimum inhibitory concentration (MIC) of an antibacterial is defined as the maximum dilution of the product that
will still inhibit the growth of a test microorganism.
MLC
The minimum lethal concentration (MLC) of an antibacterial is defined as the maximum dilution of the product that
will kill a test organism.
MRL
The maximum residue limit (MRL) is defined as the maximum concentration of a residue that is legally permitted or
acceptable in or on a food.
Mutagen
A substance that causes mutations (genetic damage).
Mutation
A change (damage) to the DNA, genes, or chromosomes of living organisms.
Nosocomial infection
An infection occurring in a patient which is acquired at a hospital or other healthcare facility. Commonly called a cross
infection.
Oligonucleotides
A linear nucleic acid fragment consisting of 2-10 nucleotides joined by phosphodiester bonds.
Oocyst
Egg stage of the coccidian parasite.
Outbreak
A sudden appearance of a disease in a specific geographic area.
Pandemic
An outbreak of disease that spreads throughout the world.
Pathogen organisms
Organism that cause disease
Pathogenicity
The ability to cause disease.
Pathognomonic
Characteristic or indicative of a disease, denoting especially one or more typical symptoms, pathological lesions.
Pharmacokinetics
The study of absorption, distribution, metabolism and excretion (ADME) of drugs and their corresponding
pharmacologic, therapeutic, or toxic responses in man and animals.
PK/PD

The quantitative relationship between a pharmacokinetic parameter (such as AUC, peak level) and a microbiological
parameter (such as MIC) is labelled as a PK/PD index (PDI).
Plaque Forming Unit (=PFU)
A measure of infectious virus particles. One plaque forming unit is equivalent to one infectious virus particle.
Plasma
The fluid portion of the blood, rich in soluble proteins with a wide range of functions.
Positive predective value
The number of truly positive cases in a population adjusted positive by a specific test procedure.
Prebiotics
Non-digestible food ingredients that benefically affect the host by selectively stimulating the growth and/or activity of
one or a limited number of bacteria in the colon, and thus improve host health.
Prevalence
The number of cases at a given time in a population at risk of exposure.
Primer
A short oligonucleotide sequence used in a polymerase chain reaction.
Probiotics
A probiotic is a culture of one or more micro-organisms, which benefit the host by stimulating the positive properties of
its natural occuring microflora in the gut. A probiotic is manufactured by fermentation technology.
Quarantine
Isolation or restriction of free movement imposed to prevent the spread of contagious disease.
Recombination
The creation by a process of intramolecular exchange, of chromosomes combining genetic information from different
sources, typically two genomes of a given species.
Reservoir
Any person, animal, arthropod, plant, soil or substance in which an infective agent normally lives and multiplies. The
infectious agent primarily depends on the reservoir for its survival.
RT-PCR
(reverse transcriptase polymerase chain reaction) Powerful technique for producing millions of copies of specific parts
of the genetic code of an organism so that it may be readily analyzed. More specifically, RT-PCR produces copies of a
specific region of complementary DNA that has been converted from RNA. The technique is often used to help in the
identificat
Sarcoma
A cancer developing from fibriblast.
Sensitivity
The ability of a test to detect a disease or pathogen. High sensitive tests may generate false positive results.
Specificity
The ability of a test to differentiate between the disease or pathogen of significance and other agents. High specific tests
may generate false positive results.
Standard operating procedures
The detailed written instructions that specify how a test or administrative procedure is to be performed, or how a piece
of equipment is operated, maintained and calibrated.
Sterilisation
A process used to render an object free from all living organisms.
Superantigens

Proteins produced by pathogens, including bacteria, mycoplasma and viruses that are capable of simulating large
numbers of T cells.
Synergistic effect
The combined effect of the substances acting together is greater than the sum of the effects of the substances acting by
themselves.
Table-egg layer
A domesticated chicken grown for the primary purpose of producing eggs for human consumption.
Teratogen
A substance that causes defects in development between conception and birth. A teratogen is a substance that causes a
structural or functional birth defect.
Titer
The concentration of a substance in a solution, or the strength of such a substance detected by titration. The term is
most likely to refer to antibody titer, which is a measure of the concentration of specific antibodies to selected microbes
that are circulating in an individual's bloodstream.
Toxicity
The capacity of a substance to confer morbidity or mortality.
Validation
Validation is defined as the establishing of documented evidence which provides a high degree of assurance that a
planned process will consistently perform according to the intended specified outcomes.
Vector
A carrier which transmits infective agent from one host to another. In recombinant DNA technology, it can be (1) a
self-replicating molecule of DNA that serves to transfer a gene of forgeign DNA fragment from one organism to
another (usually bacteria) or (2) a virus or bacteria containing a foreign gene thet is used to vaccinate an animal.
Virus
A virus is a minuscule cell parasite. Incapable of living independently, a virus penetrates a cell and takes control of the
cell’s machinery to reproduce itself, and, later, contaminate other cells.
Vitamins
Organic substances, which are necessary for the proper operation of vital functions in humans and animals. Vitamins
must be provided in the diet, since the anima l body is generally incapable of synthesising its own vitamins in sufficient
quantities.
WHO
World Health Organization. Agency of the United Nations, the aim of which is to promote health. Founded in 1947 and
based in Geneva.
Withdrawal period
The period necessary between the last administration of the veterinary medicinal product to animals, under normal
conditions of use, and the production of foodstuffs from such animals, in order to protect public health by ensuring that
such foodstuffs do not contain residues in quantities in excess of the maximum residue limits for active substance.
Xenogeneic
Derived or obtained from an organism of a different species.
Zoonotic
Relating to a disease that is communicable from animals to humans under natural conditions.

OMPHALITIS
Localized Form of Colibacilosis
Major Reasons of diseases

 Chicks from flock having Salpingitis or Oophritis
 Fecal contaminated eggs shells in incubator
 Unhealed Navel
 Improper incubator or brooding facility
Disease of young chicks

 Mortality is at peak for 1-6 days and then declines
 May cause 10-15% mortality
Clinical Signs
 Depressed birds
 Vent pasting
 Distended Abdomen
 Emaciation
 Dehydrated bird
 Increased navel with abnormal color, consistency and smell
PM Lesions
 Inflamed yolk sac
 Blood vessels of yolk sac are Prominent
 Swollen & dark Liver & kidney

 Congested lungs

 Hemorrhages in serosal surface of intestine
Possible Trasmission
 Bacteria transport from oviduct to egg in birds suffer with Salpingitis or Oophritis
 Feacal contamination of shell
 Unhealed navels
 From infected birds
Treatment
 Amoxicilin
M.Arslan CS

Poultry Pathology Salman Lateef

Uploaded by

Copyright:

Available Formats

Poultry Pathology Salman Lateef

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Poultry Pathology Salman Lateef

Uploaded by

Copyright:

Available Formats

POULTRY PATHOLOGY

UAF sub campus T T Singh

Course NO: patho-505

Course Title: Poultry Pathology

DELIEVERED BY: DR. SALMAN LATIF BUTT

Prepared by: M.Arslan CS (2009-ag-2062)

1. Diseases of poultry by Y.M. Saif

Sr. No Disease Page#

14. Bacterial Diseases 34

15. Protozoal Diseases 57

17. Nutritional Deficiencies 61

20. Poultry Serology 89

21. Terms 105

There are 5 sections of poultry diseases

Viral diseases are more important. Viruses are of 2 types

 Gram positive or Gram negative

 Causative agent is Paramyxovirus type 1

 Neurotropic (develop at latter stage of disease)

Strain Virulence Examples

Transmission True vertical= pathogen is

Clinical signs depend upon system which is affected by death of embryo

 Villi will be absent at Ulcer

The Lesions of ND may be comparable with

 Hit all system of body

 Mucoid hemorrhages (paint brush) in Trachea

Microscopic lesions Pychnotic Nuclei= condensed nuclei

 Extension of collecting ducts Karyolysis= absence of nucleus

 Glomerulonephritis Karyo hexis= division of nucleus

ILT (AVIAN DIPHTHERIA)

APV (TRT, SHS, PNEUMONITIS)

 Bloody discharge from nares

 Rhinitis (Inflammation of nasal mucosa)

 Paint brush hemorrhages in all intestine

 Pale yellow kidney

IBD (Avian Nephrosis, Gumboro)

CIA (Cytolytic Disease)

 Recovery of disease is after 28 days

HOW INCUBATION PERIOD IS MEASURED??

The virus is injected in peritoneum and observed its shedding in

Types of bone marrow

HPS (Angara Disease)

Mortality & Morbidity

Clinical signs The dead birds with

Gross lesions Anoxia

Differential diagnosis Toxin Binder

IBH (Inclusion Body Hepatitis)

Mycotoxin + HPS= Liver like IBH

Techniques for Toxin identification

Viral slowly spreading disease characterized by proliferative nodules lesions on unfeathered

1. Cutaneous form (dry form)

Mortality & Morbidity

 Swollen feather follicles

Treatment & Control

i. Rispon strain of HV-B

Neoplastic Diseases of Chicken

 MD could not come before 4-5

 No lameness of schaitic nerve

A.E (Avian Encephalomyelitis )