Avian Influenza

In chickens and turkeys the incubation period is hours to a few days, and some birds die suddenly with no warning. Others show marked depression, loss of appetite, a sharp fall or stop in egg laying with soft-shelled or misshapen eggs, coughing, sneezing, blood-tinged discharge from the nose and mouth, greenish diarrhoea and nervous signs. The comb, wattles and head become swollen and bluish, and the shanks and feet show bruise-like haemorrhages. Domestic ducks and geese are often infected with few signs. At necropsy there is oedema and cyanosis of the head, subcutaneous haemorrhage on the legs, and pinpoint haemorrhages on internal organs; peracute deaths may show no lesions.

High pathogenicity avian influenza (HPAI) is caused by influenza A viruses (genus Alphainfluenzavirus, family Orthomyxoviridae) that carry the H5 or H7 haemagglutinin. They arise when H5 or H7 low pathogenicity strains, which usually circulate in wild waterfowl and cause mild or silent infection, mutate after reaching poultry. The defining genetic change sits at the cleavage site of the haemagglutinin protein, a sequence that governs how widely the virus is distributed in the body. The result in chickens and turkeys is a systemic illness with oedema, cyanosis and haemorrhage in the skin and internal organs, killing most birds within days. The viruses keep changing by point mutation (antigenic drift) and by reshuffling of their eight gene segments (antigenic shift).

Most or all bird species can be infected. Wild aquatic birds are the natural reservoir of low pathogenicity strains, while the Asian lineage H5 (goose/Guangdong) viruses now circulate in wild birds and have been carried by migration across Eurasia, Africa, the Americas and Antarctica. Asian lineage H5N1 remains endemic in poultry in certain countries in Asia and the Middle East. Virus is shed in faeces and respiratory secretions and spreads by direct contact, contaminated feed, water and equipment, and movement of infected poultry. Outbreaks in endemic regions tend to recur in colder months. Mammals including cats, dairy cattle and marine mammals are infected sporadically. Human infection is rare and linked to close contact with infected birds. HPAI in birds of any subtype must be reported to WOAH.

Infectious bronchitis, Newcastle disease, mycoplasmosis, fowl cholera and aspergillosis all need to be ruled out. HPAI lesions are variable and resemble those of other systemic avian diseases, so no clinical or necropsy feature is decisive. Separation rests on the laboratory: RT-PCR or antigen tests on oropharyngeal, tracheal or cloacal swabs or tissues, then subtyping and sequencing of the haemagglutinin cleavage site or virulence testing in young chickens to tell HPAI from low pathogenicity strains.

Respiratory tract, digestive tract, skin of head, comb, wattles, shanks and feet, reproductive tract (egg production), central nervous system, lungs, spleen, kidney, liver, heart, mammary gland (cattle)

Strict biosecurity: keep poultry away from wild birds, contaminated water and fomites; all-in/all-out management; quarantine new birds. Vaccination is used in some countries under official control with surveillance. Cull, clean and disinfect on outbreak.

Mortality in chickens and turkeys may approach 90-100% (MSD, CFSPH), whereas WOAH describes flock mortality as often around 50%. No treatment is used; affected poultry flocks are culled. Survivors are usually in poor condition.