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 . 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.

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

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.

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.

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

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

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

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

Morbidity Variable

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

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. Shell color isn't being laid down in the oviduct. Destroy infected eggs.

Postmortem Lesions 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 proventriculus and heart.

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

Diagnosis Serology Virus isolation – hemagglutinating virus PCR 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

Treatment None

Prevention and Control 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

Control Biosecurity Monitoring/Surveillance 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