An Assignment on Special Pathology

Submitted to:
Dr. D. k. Singh
Department of Pathology
IAAS, Rampur
Submitted by:
Mr. Suraj Subedi
B. V. Sc. & A. H. 5th Sem.
Roll No. 29
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Aflatoxicosis

It is pathogenic condition due to ingestion of food with aflatoxin which is highly toxic
and carcinogenic metabolite produced by fungi Aspergillus flavus and A. parasiticus.
Aflatoxicosis is acute and chronic type; acute due to ingestion of large quantity of aflatoxins
while chronic due to exposure of lower dose over a period of time. Aflatoxin binds to nucleic
acid and disrupts polyribosome and interfere nucleic acid and protein synthesis. It also causes
mutation in proto-oncogenic ot tumour suppressor genes esp. in hepato-cellular carcinoma. It
donot cause death directly although high levels nay be lethal like in case of acute cases.
There is decreased growth, poor feed conversion, and marked decrease in resistance to
infection. Chicken shows decreased egg production, reduced egg hatchability, and reduced
testicular wt. in breeder male with less sperm production.

Lesions
Acute: Severe hepatic necrosis, Edema and hemorrhage in gall bladder wall may be seen
Periportal necrosis: Chicken, ducklings, cats etc.
Midzonal necrosis: Rabbits
Centrilobular necrosis: Pigs, Cattle
Chronic: Marked proliferation of small bile ductules at periphery of hepatic lobule leading
to periportal fibrosis or cirrhosis; Nodular regeneration of hepatocytes and megalocytic
hepatocytes
Hepatic cell carcinoma in pigs

Diagnosis
• Aflatoxin detection in feed and blood serum. Aflatoxin detection by
a) Biological testing: bile duct hyperplasia
b) Chemical testing: total toxin estimation by flurotoxinometer
• Characteristic gross and histo-pathological finding
Aspergillosis

Aspergillosis is a systemic or deep mycoses caused by Aspergillus sps. These are

opportunistic pathogenic fungi and infection by spore inhalation, hematogenous spread is also
common. Aspergillus causes brooder pneumonia in fowl. It cause mastitis, placentitis &
abortion, rumenitis and gastritis in cattle. It also infects guttural pouches of horses and results
symptoms like recurrent epistaxis and visceral & locomotor disturbances. Granuloma may
spread to the cerebellum.

Lesions
• Active or invasive Aspergillosis cause necrosis and hemorrhage with purulent and
mononuclear inflammatory response.
• Invasion into wall of arteries leads to thrombosis and infarction.
• Tissue staining shows organism as large colonies of radiating hyphae or small colonies
of irregularly scattered hyphae and usually basophilic.
• Granulomas with central core of caseating necrosis and foreign body type giant cell.

Diagnosis
• Demonstration of fungi and slender branching septate hyphae in tissue section
• Recovering fungus from culture

Candidiasis

This is a pathogenic condition caused by spores of fungus Candida albicans. It is mainly

superficial mycoses of mucous membrane affecting mouth, esophagus, crop and
proventriculus in avian species. Less systemic infection but may affect GIT, lungs, liver,
kidneys or brain. It may also cause mastitis and abortion. It is more common in young
animals, debilitated patients and also as a complication of antibiotic therapy.

Lesions
• Grossly white pseudo membrane lying over the skin or mucous membrane
• Microscopically:

 Membrane composed of masses of entangled pseudohyphae (chains of yeast like

cell called blastoconidia or blastospores), septate hyphae and budding yeast like
organism.
 Leukocytic infiltration mainly neutrophil and lymphocytes beneath epidermis.
 Systemic candidiasis cause necrosis and suppuration rarely granulomatous

Diagnosis
Fungi demonstration: presence of blastoconidia and entangled pseudohyphae

Coccidiosis
 It is a disease caused by protozoa of genera Eimeria and Isospora. These are obligate
intracellular parasites common in cattle, sheep and poultry. The animal become infected by
ingestion of oocyst or sporulated oocyst which in S.I hatch to tiny sporozoytes and directly
invade the intestinal epithelium. They pass all their stages of life cycle in alimentary canal.
Coccidiosis in cattle is immunosuppressive which increases their susceptibility to other
common infections. The animal shows sign of sudden onset of bloody diarrhea with fever
followed by dehydration, emaciation and sometime death.

Lesion
• Grossly, intensely congested, eroded and bleeding area on certain portion of S.I. and
sometimes alternate with thickened mucosa.
• Depends upon initial infecting dose of oocyst and spread of infection during
schizogamy.
• Intense inflammation of lamina propria and sometimes sub mucosa and hemorrhage in
intestinal tract.
• Hyperplasia of intestinal epithelium which is cast into long papillary fold

• Adenomotous hyperplasia in rabbits, dog, sometimes in cat and dog

Diagnosis
• Presence of oocyst in fecal samples associated with sudden onset of bloody diarrhea

• Gross and microscopic lesions, organism demonstration in tissue section

Degnala

Degnala is a chronic gangrenous syndrome of buffaloes and cattle (morbidity and

mortality higher in buffalo), clinically similar to chronic ergotism and mainly caused by
Mycotoxicosis of Fusarium sps and other fungi like Trichothecium, Rhizopus, Aspergillus,
Penicillium etc. It appears only in winter season and in animals fed Fusarium contaminated
rice or wheat straw.

Symptoms
It is characterized by anorexia, lameness, reluctance to walk, edema, gangrenous
ulceration around the corona of hoof or tail, falling of the hoof, eruption or cracking of skin,
emaciation, recumbency and death. Hair loss from switch of tail, drop in milk production,
ascending drying of tail, sloughing of tissue of the tail end , drying curling sloughing of ear tip,
loss of hair, swelling reddening of coronet, grounding, frying and sloughing of skin of muzzle.

Lesions
• Grossly, edema and gangrenous manifestation of the extremities like ear lobes, tail,
tongue tip etc.
• Blood vessels are hard and thickened.

• The subcutaneous tissue contains excess straw colored fluid and there may be hydro
pericardium.
• Pm findings: edema and gangrenous manifestations of the extremities, ear lobes, tail
and tip of the tongue.
 • Microscopically
 vasculoocclusive and non-inflammatory blood vessels

 Dark blue tiny particles were seen on red blood cell (RBC) after Giemsa staining.
 Hematologically, increase of band neutrophil, giant platelet, hypoalbuminemia
and hyperglobulinemia were characteristics.

Diagnosis
• Clinical signs
• Gross and microscopic findings

• Hematology shows increase of band neutrophil, giant platelet, hypoalbuminemia and

hyperglobulinemia.
• isolation of fungus from infected feeds and straw

Rabies

Rabies is an acute viral encephalomyelitis, highly fatal with mortality close to 100%. Ity
is caused by Lyssa Virus and relatively fragile & susceptible to most disinfectant. This virus
spread by contamination of wound by fresh saliva, rare transmission by aerosol route.
Pathogenesis:
Variable incubation period, generally 1-2 months. Virus replicates in myocytes and shed
into extra- cellular spaces. Virus enters the nervous system at motor end plate and spread in
the axons of nerve cells to the ventral horn of spinal cord, replicates and spread to the brain
to disseminate the whole CNS. Brain stem, hippocampus, and cerebral cortex are
susceptible and neuronal destruction in these regions gives the disease symptoms.
Centrifugal viral spread in many tissues like salivary gland. Destruction of spinal neurons
results in paralysis and paralytic form. Viral invade in brain cause irritation to higher center
and cause manias, excitement, convulsion. Finally death results from respiratory paralysis.
Signs:
Typical sign of CNS disturbance. Signs are usually in 2 forms. In dumb or paralytic
form, animal falls into a stupor and has peculiar starring expression. Early paralysis of throat
muscles and mastication muscles usually with profuse salivation and inability to swallow.
Paralysis progresses to coma and death. In Furious form, typical mad-dog syndrome;
excessive salivation and saliva may be churned into foam. Death will be within 10 days after
appearance of the first symptoms.
Cattle, same general pattern with abrupt lactation stopping and characteristic
bellowing i.e. deep loud cry
Lesions:
• Limited to CNS. Main lesion site is brain stem, hippocampus & gasserian ganglion.
• Diffuse encephalitis with perivascular cuffing, neuronophagic nodules and other
changes.
• Gasserian ganglia have proliferating glial cells called "Babes nodules".
 • Spherical cytoplasmic inclusion bodies called "Negri bodies" seen in Hippocampus of
dogs and Cerebellum Purkinje cells of cattle.
• Degenerative changes in salivary gland leading to necrosis.
Zoonotic Implications:
Transmitted to humans, veterinarians being at specific risk so a major occupational
hazard for veterinarians who receive pro-exposure prophylaxis.
Diagnosis:
• Based on symptoms and lesions
• Isolation of symptomatic suspected dog and it die within 10 days, rabies suspected
• Lab diagnosis
 FAT: smears from hippocampus or cerebellum or gasserian ganglion
 Histological search for negri bodies
 Animal inoculation e.g. in mice intra cerebrally
 Peroxidase - Antiperoxidase staining techniques
Differential diagnosis: Canine Distemper, Canine Hepatitis, Toxoplasmosis