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AVIAN INFLUENZA

By:fouad almasri

Etiology
Classification: Family orthomyxoviridae Genous influenzavirusA

Morphology:

Spherical to pleomorphic (filamentous) Surface glycoprotein projections: 1) rod-shaped trimers of hemagglutinin 2)mushroom-shaped tetramers of neuraminidase (NA) Helical Nucleocapsid Eight segments, single stranded,negativesense RNA genome

Clinical signs:

AI virus pathotype: (MPAI or HPAI) Extremely variable clinical signs Depend on other factors including: host species age sex concurrent infections acquired immunity environmental factors

Respiratory tract infection Excessive lacrimation Coughing Sneezing WILD BIRD no clinical signs Rales DOMESTIC POULTRYclinical Rattles

MPAIV

Huddling signs Ruffled feathers Depression abnormalities in the Decreased activity In layers and breeders, hens: respiratory organ Decreased feed and Increased broodiness water consumption Decreased egg production digestive organ Occasionally diarrhea

urinary organ Reproductive organ exhibit generalized clinical signs

HPAIV
wild birds and domestic ducks: HPAI viruses

replicate poorly limited degree few clinical signs. chickens, turkeys, related galliformes: clinical signs reflect virus Replication damage to multiple visceral organs cardiovascular system nervous system

HPAIV(Cont.)
Clinical manifestations depending on: Extent of damage to specific organs and tissues less fulminating disease: birds survive for 37 days Nervous disorders: Tremors of head and neck Inability to stand Torticollis Opisthotonus Unusual positions of head and appendages Houses may be unusually quiet Reduction in normal vocalizations Depression is common as are significant declines in feed and water consumption. Drops in egg production

Gross pathology (MPAI)

In poultry Most frequent lesions Respiratory tract Especially sinuses congested and occasionally Tracheal mucosa hemorrhaged . Air sacculitis

are characterized as catarrhal, fibrinous, serofibrinous, mucopurulent, or fibrinopurulent inflammation The infraorbital sinuses may be swollen, and mucus to ucopurulent nasal discharge

Gross pathology (Cont.)


Enteritis ceca and/or intestine (turkeys) Inflammatory exudates (in the oviducts) Reductions in calcium deposition with in the eggshells Misshapen and fragile with loss of pigmentation Ovaries beginning with hemorrhage in the large follicles The oviduct may be edematous and contain catarrhal to fibrinous luminal exudates Swollen kidneys and visceral urate deposition

Gross pathology (HPAI)


(if death is per acute, no gross lesions may be observed)

Visceral organs and the skin: Edematous Hemorrhagic Necrotic lesions Swelling of the head, face, upper neck, and feet Subcutaneous edema Petechial to ecchymotic hemorrhages Hemorrhage, cyanosis non feathered skin (especially wattles and combs) Hemorrhages on serosal or mucosal surfaces especially prominent are hemorrhages on the epicardium, in pectoral muscles, and in mucosa of the proventriculus and ventriculus

Gross pathology (HPAI) (Cont.)


Necrotic foci are common in pancreas, spleen, and heart, and occasionally in liver and kidney The kidney lesions may be accompanied by urate deposits Lungs have focal ventral to diffuse interstitial pneumonia with edema. The lungs can be congested or hemorrhagic The cloacal bursa and thymus are usually atrophic.

Microscopic pathology (MPAI)

Ventromedial fibrinocellular to peribronchiolar lymphocytic pneumonia In severe cases The pneumonia may be diffuse with air capillary edema. Heterophilic to lymphocytic tracheitis and bronchitis Lymphocyte depletion Necrosis or apoptosis of lymphocytes in the cloacal bursa, thymus, spleen Viral antigen is rarely seen in lymphocytes in necrotic respiratory epithelium, renal tubule epithelium, and pancreatic acinar epithelium

Microscopic pathology (HPAI)

Affected tissues: brain, heart, lung, pancreas, and primary and secondary lymphoid organs Lymphocytic meningoencephalitis with focal gliosis Neuronal necrosis Neuronophagia are common Focal degeneration to multifocal-diffuse coagulative necrosis of cardiac myocytes has been reported, usually with accompanying lymphohistiocytic inflammation

Microscopic pathology (HPAI)

(Cont.)

Necrosis in: skeletal myofibers kidney tubules vascular endothelial cells corticotrophic cells of adrenal pancreatic acinar cells Lesions in respiratory tract: vary widely from minimal to severe. Nonfeathered skin: Numerous microthrombi within dermal and hypodermal capillaries and small blood vessels. Epidermis has various stages of vesicle formation progressing to full thickness necrosis.

DIAGNOSIS

A definitive diagnosis of avian influenza is established by: 1) direct detection of AI viral proteins or genes in specimens such as tissues, swabs, cell cultures, or embryonating eggs 2) isolation and identification of AI virus. A presumptive diagnosis can be made by etecting antibodies to AI virus.

Sample Selection and Storage

collect and store internal organs separately from the respiratory and intestinal tract tissues In the case of systemic infections produced by HP AI viruses, virtually every organ can yield virus because of the high levels of viremia or replication in parenchymal cells Samples detection within 48 hours after collection:, kept at 4C Samples must be held for additional time, storage at -70C Before testing for virus, tissues should be ground as a 5 10% suspension in the transport medium and clarified by low-speed centrifugation.

Direct Detection of AI Viral Proteins or Nucleic Acids

A human influenza test (Directigen, Becton-Dickinson) This antigen capture enzyme immunoassay was found to be specific and sensitive Monoclonal antibodies are useful for localizing viral antigen in tissues by immunoperoxidase staining Polymerase chain reaction methods have been described that are up to 100- fold more sensitive than virus isolation procedures

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