Avian Pathology.pptx

Course Title: Avian Pathology (Theory)

List of economically important diseases affecting poultry farms: Age wise
0-2 weeks
*Pullorum disease
*E. coli infection
Avian encephalomyelitis
*Aspergillosis
*Nutritional deficiencies
2-8 weeks
*E. coli infection
** Infectious Bursal Disease
**Marek’s disease
**New Castle Disease
*Fowl Pox
Infectious Bronchitis
Avian Influenza
***Chicken infectious anaemia
***Hydropericurdium -hepatitie
syndrome
*Aspergillosis
*Coccidiosis
*Nutritional encephalomalacia
*Known to occur in Bangladesh
**Re-emerged with enhanced virulence
*** Newly emerged diseases

8-20 weeks
*Fowl Cholera
*Fowl typhoid
Infectious coryza
*Marek’s disease
*New Castle Disease
Infectious laryngotracheitis
Avian Influenza
>20 weeks
*Fowl Cholera
*Pullorum disease
Infectious coryza
*New Castle Disease
Infectious laryngotracheitis
Avian Influenza
***Lymphoid leukosis/Avian leukosis/
Big liver and spleen disease
*Known to occur in Bangladesh
**Re-emerged with enhanced virulence
*** Newly emerged diseases
List of economically important diseases affecting poultry farms: Age wise

Vertically Transmitted Diseases of Poultry
•Pullorum disease
•Fowl typhoid
•Marek’s disease
•Lymphoid leukosis/Avian leukosis/ Big liver and spleen disease
•Avian Influenza
•Chicken infectious anaemia
•Hydropericurdium- hepatitis syndrome/ Lichi disease/ Angara disease
•Mycoplasmosis/ Chronic Respiratory Disease (CRD)
Subclinical diseases causing drop in egg production
•Egg drop syndrome 1976
•Infectious Bronchitis
•Avian encephalomyelitis
•New Castle Disease
•Avian Influenza
•Mycoplasmosis/ Chronic Respiratory Disease (CRD)
•Malnutrition
•Stress

Bacterial Diseases of Poultry
Salmonellosis
Pullorum disease
Fowl typhoid
Colibacillosis
Colisepticemia
Coligranuloma
Air saculitis
Omphalitis
Pasturellosis
Infectious coryza
Tuberculosis
Streptococcosis
staphylococcosis

Salmonellosis
• Is caused by Gram – ve bacteria Salmonella of Enterobacteriaceae family
• It consists of over 2400 serologically different variants (serotypes).
• Avian salmonellosis could be classified in two groups.
• The first one include infections called
• pullorum disease caused by S. pullorum and fowl typhoid caused by
S. gallinarum.
• The second group comprises infections caused by multiple motile
Salmonella serotypes most frequently S. Enteritidis and S. Typhimurium
isolates that are considered together as paratyphoid.

Salmonellosis (Pullorum disease)
•Pullorum disease is caused by S. pullorum (Gram negative, nonmotile,
Rod)
•Transmission:
•Infected egg (Vertical transmission)
•Ingestion (Horizontal transmission)
•Symptoms:
•Chicks huddling near the source of heat
•whitish diarrhoea
•Mortality 50-100% within 1st week of age (early chick mortality)

In young
• Septicemic course: no or few lesions
• Pasted white feces in the vent
• Gray nodules in lung, liver, gizard wall, heart, intestinal or cecal wall,
spleen, peritonium
• Swollen hock joints
• Plagues or cecal cheesy cores of debris in the lumen of intestine and
ceca
•Creamy or caseous yolk sac contents
Gross Lesions

In Adults
•Liver: Enlearged, congested and
presence of haemorrhagic streaks
•Heart: Necrotic foci or nodules in
cardiac muscles and pericarditis
•Yolk: Unabsorbed, yolk sac content may
be cheesy, yellow or dark red.
Gross Lesions

•Ovary: Heamorrhagic, misshapen, discolored
cystic ova, sometimes angular and attached
by stalk. Peritonitis may occur from detached
ova
•Lung and Gizzard: Necrotic foci or nodule.

Fowl typhoid
•Fowl typhoid is caused by S. gallinarum
(Gram negative, nonmotile, Rod)
•Transmission:
•Infected egg(Vertical transmission)
•Ingestion (Horizontal transmission)
•Age: Adult birds (3-6 months)
•Symptoms:
Dullness
 Loss of appetite
 Fever
Yellowish diarrhoea
Cyanosed comb and wattle
Mortality rate:n10-50%

Fowl typhoid (Gross Lesions)
Acute fowl typhoid:
•Enlarged and bronze greenish tint of
liver, sometime mottled with
multiple milliary necroses
•Splenomegaly (2-3 times bigger)
sometimes with grayish-whitish
nodules on the surface
•Enteritis in anterior part of small
intestine with ulcerations

Chronic fowl typhoid:
• Ova: Frequently affected follicles are
deformed and appear like thick,
discolored, pendulated masses
• Necrotic or Nodular lesions in heart,
pericardium
• Lung may show grayish areas of
consolidation
Fowl typhoid (Gross Lesions)

Pathogenesis of Salmonellosis
Horizontal transmission through oral route Vertical transmission through ovary
Enter into the intestine Enter into the ovum and infect them
Bacteria adhere with the intestinal
epithelial cells (fimbrae and mannos
resistant hemagglutinin)
Resulting diarrhoea and the virulence of
the organism depends on the initial
degree of mucosal invasiveness
Infected eggs serve as the source of
infection during the chick development
Resulting early chick mortality
Incubation period: 4-5 days

Colibacillosis
• Etiology: Escherichia coli (Gram negative, motile,
rod)
• Age: All (common in young growing birds)
• Transmission:
• Ingestion
• Inhalation
• Fecal contamination of egg
• Vertically transmitted by eggs
• Clinical Conditions:
 Airsaculitis
 Omphalitis (High early
mortality)
 Coliseptisemia
 Coligranuloma
Enteritis
Salphangitis
Synovitis and arthritis
Panophthalmitis
Pericarditis
Cellulitis

Colibacillosis (Gross lesions)
 Airsaculitis: (5-6 weeks of age)
• Thickened and caeseous exudates in
the air sac
• Adherence pericarditis
• Fibrinous perihepatitis
 Omphalitis (Yolk sac infection)/ Naval
infection: (early age)
•Reddish and oedematous tissue in the
umbilical region
•Abnormal and unabsorbed yolk sac
•Peritonitis
•Bloated and macerated abdominal
cavity

Colibacillosis (Gross lesions)
 Coliseptisemia: (Young to mature
birds)
• Green colored liver with small
necrotic foci
• Swollen parenchymatous organs
• Pericarditis
• Peritonitis
 Coligranuloma:
• Nodules occur along the
intestinal tract, mesentery, liver
• Resembles to TB

Pasturellosis/ Fowl cholera/ Avian cholera/Avian
hemorrhagic septicemia
• Etiology: Pasteurella multocida (Gram negative, non-motile, capsulated
and bipolar)
• Age: 8 weeks to adult
• Transmission:
• Horizontal transmission through ingestion and inhalation via nasal
exudate, faeces, contaminated soil and equipments.
• Morbidity and Mortality: may be upto 100%
• Infected birds will die after 6-12 hours of contact with bacteria

Symptoms:
Acute fowl cholera
•Death may be the first indication of disease
•Fever, anorexia, ruffled feathers
•Mucous discharge from the mouth and increased respiratory rate
•Whitish watery to greenish mucoid diarrhea
•Cyanosis in comb and wattles often occurs immediately prior to death

Chronic fowl cholera
•Wattle, sinuses, leg or wing joints, foot pads, and sternal bursae often become swollen
• Cheesy exudate accumulation in conjunctival sac and pharynx
•Tracheal rales and dyspnea

Fowl cholera (Gross Lesions)
Acute fowl cholera:
•Absent in very acute case
•Petechial haemorrhages in heart, anterior part of
the small intestine, the gizzard or the abdominal fat
•In liver multiple milliary or submilliary focal
coagulation necrosis
•Serofibrinous exudation with congestion in lung
•In layers (commercial or breeders), acute
oophorites with regressing follicles with peritonites

Chronic fowl cholera:
•Yellowish caseous exudate in Localized
infections such as hock joints, foot pads,
peritoneal cavity, oviduct,conjunctival sac,
middle ear and cranial bones

Acute fowl cholera:
•Absent in very acute case
•Petechial haemorrhages in heart, anterior part of
the small intestine, the gizzard or the abdominal fat
•In liver multiple milliary or submilliary focal
coagulation necrosis
•Serofibrinous exudation with congestion in lung
•In layers (commercial or breeders), acute
oophoritis with regressing follicles with peritonitis

Infectious coryza
•Etiology: Hemophillus paragallinarum
(Gram negative, bipolar, filamentous
coccoid) , aerobic
•Transmission: Horizontal transmission
•Direct contact (Air born transmission)
•Ingestion of contaminated water
•Age: Adult birds (8->20 weeks)
•High morbidity and lower mortality
•Symptoms:
Sneezing and dyspnoea with open
mouth breathing
Swollen face (Facial edema) and wattle
Nasal and lacrimal mucoid secretion.

Infectious coryza (Gross Lesions)
•Acute catarrhal inflammation of mucous
membranes of nasal passages and sinuses
•Catarrhal conjunctivitis
•Airsacculitis
•Pericarditis
•Perihepatitis
•Sinusitis
•Valvular endocarditis
•Catarrhal exudates in trachea

Infectious coryza (Pathogenesis)
Infection through the ingestion or direct contact
The organism adhere with the cilliated mucosa of
upper respiratory tract
Colonization occur with the help of the capsule and
haemagglutination antigen
Proliferation and toxin release
Development of lesions

Clostridial infection (Necrotic enteritis)
•Etiology: Alpha toxins of Clostridium perfringens type A,C,E and F (anaerobic)
•Transmission: Horizontal
•Direct contact with contaminated litter
•Ingestion of contaminated feed and water
•Age: Adult birds (8->20 weeks), mortality upto 50%
•Symptoms:
•In peracute cases, death in 1–2hours
•Diarrheic and inappetant, anorexic and dehydrated
•Depression
•Reluctant to move
•Ruffled feathers

Necrotic enteritis (Gross Lesions)
•Small intestine is distended and friable
•Yellowish brown necrotic areas involving the whole intestine
•Intestinal mucosa has a focal-to-confluent pseudomembrane (“Turkish towel”
appearance)
•Petechial hemorrhage throughout the mucosa
•Pale necrotic foci in liver
•Distended gall bladder with inspissated material

Necrotic enteritis(Pathogenesis)
Infection throguh the cotaminated feed or litter material
The coccidial infection causes damage to the intestinal mucosa and produce an
anaerobic condition for Clostridium sp.
After entering throug the damaged intestine, the oganisms proliferate
and liberate toxins
Toxemia and development of lesions

Viral Diseases of Poultry
Newcastle Disease
Marek’s Disease
Avian Influenza
Infectious Bursal Disease
Infectious Bronchitis
Avian Pox
Avian Leucosis
Egg Drop Syndrome

Newcastle Disease
•Synonyms: Ranikhet Disease
•Etiology: Family Paramyxoviridae
• Species: Paramyxovirus
•This RNA virus, three types:
I. Lentogenic - mild virulent
II. Mesogenic- moderate virulant
III. Velogenic- highly virulent
•Transmission:
•Direct contact (Air born transmission)
•Inhalation
•Ingestion of contaminated food and water
•Age: Adult birds (8->20 weeks)
•Heavy Mortality (100%) with early chick
mortality
•Symptoms:
Yellow/greenish diarrhoea
Twitching of neck, Tremor
Paralysis
Respiratory distress with nasal discharge
 Birds appear depressed and lethargic with
ruffled feathers

Newcastle Disease(Pathogenesis)
Infection through the ingestion or direct contact
After entering into the body, the viruses reaches in the intestine and replication occur
Attachment of the viruses occur with the receptors present in intestinal wall mediated by
haemagglutinin glycoprotein
Then the virus membrane fuses with cell membrane with fusion glycoprotein
Thus neucleocapsid complex enters in the cells
During replication glycoprotein is cleaved for the progeny virus particles to be infective
The virulent viruses invade and replicate in many tissues and organs resulting the
production of infective viruses throughout the body and cause development of lesions

Newcastle Disease(Gross Lesions)
A. Velogenic Form:
•Petechial hemorrhage on the tip of
the proventicus papillae
•Haemorrhagic ulcers in the intestine
particularly at the ileocaecal junction
(caecal tonsils)
•Petechial haemorrhage on the serosal
surface of visceral organs.
B. Mesogenic Form:
•Congestion of the lungs and brain
•Pneumoencephalitis
•Mottling of spleen
C. Lentogenic From:
•Haemorrhagic lesions are few and
absent and low mortality
•Drop of egg production with
congestion of ovaries

Marek’s Disease
Synonyms: Visceral leukosis/ Acute leukosis
Etiology:
Species: Alphaherpes virus
This is a DNA virus
Cell Associated virus, produce a tumor specific antigen in the
cell surface (MATSA, Marek’s Associated Tumor Specific
Antigen)
Source of infection: concentrated in the feather follicles and
shed in the dander (sloughed skin and feather cells).
Transmission:
Direct contact (Air born transmission)
Age:
Acute case: Broiler- 7 weeks and layer- in between 7 to 16 weeks
(Morbidity 90% and Mortality 100%)
Clinical case: 20-30 weeks (Morbidity3% and Mortality 3-10%)

Marek’s Disease
• Symptoms:
• Lameness, paralysis (both
unilateral and bilateral) and
hanging wings
• Torticollis (Twitching of the
neck due to paralysis of neck
muscles)
• Head turn upside down
• Tumor on skin

Marek’s Disease (Pathogenesis)
The virus enter into the susceptible host through respiratory tract and it is
picked by the phagocytic cells that leades to 4 phages of infection:
1. Early productive infection causes mainly degenerative changes i.e.
cytolytic changes.
2. Second phage of cytolytic productive restrictive infection coinciding
with permanent immunosuppression
3. Laten infection which coincides with the development of immune
responses. Mainly T-cells are infected in the latency although B-cells
may also involved
4. Proliferative phage involving the nonproductively infected lymphoid
cells which may progress to lymphoma formation. The
lymphoproliferative changes constitute the final responses and may
progress to tumor formation

Marek’s Disease (Gross Lesions)
•Thickening of nerves (Sciatic,
Brachial, Vagus ) with loss of cross
straitions
•Tumor of malignant lymphoma in
ovary/testes, liver, lungs, spleen,
muscles, heart, kidney, proventiculus
and intestine
•Tumor on skin (Distnict whitish
nodules, scab like, brownish crust
formation)

Avian Influenza
Synonyms: Avian flu / Bird flu / fowl plague
Etiology:
Species: Orthomyxo virus
This is a RNA virus
There is several subtypes based on Haemagglutinin(H) and
Neuraminidase (N) antigens
Source of infection: infected birds
Transmission:
Direct contact of infected birds which excretes viruses from RT,
conjunctiva and feces
Through ingestion of contaminated food and water
Age: Any
Low Pathogenicity Avian Influenza Viruses: The morbidity and mortality
is usually low
High Pathogenicity Avian Influenza Viruses: mortality can be as high as
100% in a few days

Avian Influenza
Symptoms:
• High Pathogenicity Avian Influenza Viruses:
• In peracute cases, clinical signs or gross lesions
may be lacking before death
• In acute cases, there is cyanosis and swelling of
head, comb and wattle
• red discoloration of the shanks and feet
• blood-tinged oral and nasal discharges
• Low Pathogenicity Avian Influenza Viruses:
• respiratory signs such as sneezing, coughing,
ocular and nasal discharge
• swollen infraorbital sinuses
• Rapid decreased in egg production or infertility,
ova rupture

Avian Influenza (Pathogenesis)
After entry in to the hosts, the viruses adsorb to the glycoprotein receptor
on the cell surface and enter into the cells by receptor mediated endocytosis
The tissue trophism of the viruses is involved in the pathogenesis which is
receptor specific
Pathogenesity of the viruses is due to haemagglutinin molecules which is
cleaved by proteases and the cleaved haemagglutinin is the deciding factor
for viral replication and for the production of pathogenic infective virion
particles
Due to presence of proteases, the viruses invade and replicate in tissues and
organs resulting in generalized disease and death

Avian Influenza (Gross Lesions)
Cyanosis and edema of the head, comb
and wattle
Subcutaneous ecchymotic hemorrhages
in feet and petechial hemorrhages on
visceral organs ( epicardium, sternal
surface)and in muscles (breast muscle)
Necrotic foci in liver, pancreas, spleen,
kidneys and intestine
Visceral gout
Nephrosis with swollen kidney
Sinusitis with caseous or mucopurulent
exudates
Caseous exudates in air sac

Infectious Bursal Disease
Synonyms: Gumboro disease
Etiology:
Species: Avibirna virus
This is a Double stranded RNA virus having two segments.
5 serotypes available
Source of infection: Contaminated feed and water and droppings of
infected birds
Route of Transmission:
Oral route mainly, but also the conjunctival and respiratory route
also important
Age:
Clinical case: 3 and 6 weeks of age (Morbidity 100% and
Mortality 80%)

Infectious Bursal Disease
Symptoms: Symptoms are varied due to
immunosuppression:
• Ruffeled feather with go off feed and
water
• Watery whitish diarrhoea with sticky vent
• Picking of vent
• On progress, there is severe depression,
trembling, incordination and ultimately
death

Infectious Bursal Disease (Pathogenesis)
After infection, virus first reaches to liver and the enter into the blood
stream resulting viremia
Within hours, virus is found in macrophages and lymphoid cells in caeca,
Jejunum, duodenum and kupffer cells of liver and distributed to different
tissues including bursa
The virus causes destruction of affected lymphoid cells (mainly B cells and
their precursors) in the bursa of Fabricious, spleen and caecal tonsils
Bursal depletion at early age may results in impaired immune response
Causing immunosuppression leading to lowered resistance to diseases

Infectious Bursal Disease (Gross Lesions)
Petechial and echymotic haemorrhage
on the pectoral, thigh and leg muscles
Edematous and haemorrhagic bursae of
fabricius giving it blackish coloration
Gelatinous exudate around bursa
Haemorrhagic caecal tonsils
Mottled liver with severe congestion
Enlarged spleen and atrophied later on
Enlarged and haemorrhagic kidneys

Infectious Bursal Disease (IBD)
Symptoms: Symptoms are varied due to
immunosuppression:
• Ruffeled feather with go off feed and
water
• Watery whitish diarrhoea with sticky vent
• Picking of vent
• On progress, there is severe depression,
trembling, incordination and ultimately
death

Infectious Bronchitis (IB)
Etiology:
Species: Avian gammacoronavirus
Source of infection: respiratory discharges and feces
Aerosol, ingestion of contaminated feed and water, and
contact with contaminated equipment and clothing
Age:
Clinical case: All age (Morbidity typically 100% and mortality is
approximately 5%, although mortality rates can be as high as
60% when disease is complicated by concurrent bacterial
infection)

Infectious Bronchitis(IB) Clinical signs
 coughing, sneezing and having tracheal
rales and dyspnoea
 Nasal and ocular discharge (Chicks)
 Depressed and huddle under heat lamps
(Chicks)
 Drop in egg production
 Thin shelled egg
 Thin and watery yolk
 Feed consumption and weight gain are
reduced

Infectious Bronchitis (Pathogenesis)
After infection, virus first reaches to respiratory tract, replication
occur in trachea and lungs resulting viremia
Through blood stream it reaches to various organs like kidney,
oviducts etc.
Where it causes damage of kidney tubules leading to reduced
absorption of water, glucose and electrolytes causing dehydration
and acidosis. In reproductive tract causes damage resulting
production performance and reduced egg production

Infectious Bronchitis (Gross Lesions)
Serous, catarrhal or caseous exudates in respiratory tract
Caseous plague in bronchi
Air sacs contain foamy exudate initially, progressing to cloudy thickening
Cystic oviducts in young hen
In laying hen, oviduct of reduced weight and length and regression of the
ovaries
Swollen, pale kidneys, with the tubules and ureters distended with urates
and uroliths

Avian Pox
Synonyms: Fowl pox
Etiology:
Species: avian poxvirus
This is a Double stranded RNA virus having two segments.
5 serotypes available
Source of infection: Contaminated feed and water and droppings of
infected birds
Oral route mainly, but also the conjunctival and respiratory route
also important
Age:
Clinical case: 3 and 6 weeks of age (Morbidity 100% and
Mortality 80%)

Avian Pox (Clinical Signs)
• Nodules in featherless parts of
body (Comb, wattle and face)
• Yellowish cheese like materials in
the buccal cavity
• Swelling of eyelids leading to
blindness

Avian Pox (Pathogenesis)
After infection, virus first reaches to epithelial cells of upper respiratory
tract and mouth, which are highly susceptible for viruses
After entering in epithelial cell, it spreads from cell to cell which is helped by
the production of epidermal growth factor causing the proliferation of cells
producing pock lesion
Some viruses enters in blood circulation and cause viremia resulting reachin
to certain organ like liver and spleen

• Cutaneous pox (dry form):
• Dry pox starts as small whitish foci that
develop into wart-like nodules.
• The nodules eventually are sloughed and
scab formation precedes final healing
• Lesions are most commonly seen on the
featherless parts of the body (comb,
wattles, ear lobes, eyes, and sometimes the
feet)
• Diphtheritic pox (wet form):
• Wet pox is associated with the oral cavity
and the upper respiratory tract, particularly
the larynx and trachea.
• The lesions are diphtheritic in character
and involve the mucous membranes to
such a degree that when removed, an
ulcerated or eroded area is left.
Avian Pox(Gross Lesions)

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