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Avian Influenza A respiratory infection of chickens and turkeys that is characterized by upper respiratory involvement, mortality and decreased egg production.

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Presentation on theme: "Avian Influenza A respiratory infection of chickens and turkeys that is characterized by upper respiratory involvement, mortality and decreased egg production."— Presentation transcript:

1 Avian Influenza A respiratory infection of chickens and turkeys that is characterized by upper respiratory involvement, mortality and decreased egg production in adults. Infects most species of birds (also other species). 1983 outbreak of virulent AI (Fowl Plague) in chickens in Pennsylvania and surrounding states resulted in $60 million eradication program. Several more recent breaks, including Mexico and Hong Kong. On January 22, 2012, China reported its second human death due to bird flu. Pandemic flu viruses have some avian flu virus genes and usually some human flu virus genes. Both H2N2 and H3N2 are pandemic strains.

2 Influenza Viruses Etiology VIRAL - Orthomyxovirus type A They are enveloped, negative stranded RNA viruses All subtypes (but not all strains of all subtypes) of influenza A virus are adapted to birds. Influenza A viruses can be divided into 15 Haemagglutinin (H) antigens. 9 Neuraminidase (N) antigens. Extremely variable in virulence Extreme antigenic variability brought about by genetic reassortment in host cells. 2 Pathotypes: HPAI, LPAI

3 Etiology – H5 and H7 are the most dangerous – Amino acid sequence at H cleavage site is important Highly virulent AI viruses cause the disease fowl plague – H5N2 - Pennsylvania "break". – H5N1 - Hong Kong outbreak – 1997-98 These viruses are extremely virulent. Hens may be found dead on the nest.

4 Ecology of Avian Influenza Viruses The greatest variety of AI viruses has been isolated from wild birds, particularly from waterfowls. Serve as reservoirs and gene pools These birds perpetuate only viruses of low pathogenecity Natural host of AI viruses to which the viruses are well adapted. Waterfowls are resistant to the disease induced by HPAI viruses.

5 Ecology of Avian Influenza Viruses Domestic Poultry does not appear to be the natural host of these viruses, therefore the degree of adaptation to the host is low and this could possibly explain why documented virus mutation has virtually always occurred in domestic poultry

6 Incubation Period Variable - few hours to days Depends on virulence of the virus and the route of exposure

7 What is the difference between HPAI, LPAI and H5N1? All HPAI viruses examined to date have had a motif with multiple basic amino acids (arginine and lysine) at the HA0 cleavage site. In contrast, the cleavage motifs of LPAI viruses typically have only two basic amino acids, at positions – 1 and –4 from the cleavage site.

8 H5N1 is the technical term for a particularly lethal sub- type of avian influenza, Unlike seasonal influenza, in which infection usually causes only mild respiratory symptoms in most people, H5N1 infection may follow an unusually aggressive clinical course, with rapid deterioration and high fatality. Primary viral pneumonia and multi-organ failure have been common among people who have become ill with H5N1 influenza. Of the few avian influenza viruses that have crossed the species barrier to infect humans, H5N1 virus has caused the largest number of reported cases of severe disease and death in humans.

9 Course of Disease 1-2 weeks - depends on strain of virus.

10 Method of Spread Contact with infected birds Waterfowl are the original reservoir Ethnic slaughter house and distribution also very important – Live bird markets are a problem

11 Morbidity Variable

12 Mortality Usually doesn't exceed 10% unless fowl plague (high path) virus. Then can reach 80-100% mortality.

13 Clinical Signs Non-Specific: Decreased feed consumption Decreased egg production Mild to severe rales Sinusitis Edema of head and wattles Diarrhea Whitens the shell of broiler breeder eggs.

14 Postmortem Lesions Fairly non-specific: Variable depending on strain of virus. Sinusitis with mucopurulent to caseous exudate. Fibrinopurulent pericarditis. Congestive, hemorrhagic and necrotic changes on the skin and the intestinal tract. Hemorrhages in trachea, lungs, proventriculus, gizzard, viscera and heart.

15 Differential Diagnosis Mycoplasma Newcastle Infectious Bronchitis Ornithosis (Chlamydia psittaci ) Turkey rhinotracheitis (TRT)/ Avian pneumovirus (APV) Determination of the H and N type and virulence are essential for control programs

16 Diagnosis Serology – Agar gel precipitation (AGP) and ELISA Detects all types – Hemagglutination-inhibition (HI) Detects only homologous hemagglutinin type Virus isolation – hemagglutinating virus PCR Immunochemistry Histopathology - non-specific, Clinical Signs

17 Treatment None

18 Prevention Biosecurity – Isolation rearing. – Depopulate infected flocks. – All strains are reportable. – Bury the birds. Vaccination Killed vaccines are available for certain approved areas. – Protect only against homologous H type

19 Control Biosecurity – Quarantine – Intensify disinfecting measures Monitoring/Surveillance Stamping Out / Depopulation Vaccination - only for LPAI and not for HPAI because it might prolong the shedding of the virus Proper Disposal


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