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

8. 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

9. Morbidity
Variable

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

11. 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.

12. 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.

13. 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

14. 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

15. Treatment
None

16. 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

17. 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