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Avian Influenza-Highly Pathogenic (HPAI), Fowl Plague

Extracted From:
A Pocket Guide to
Poultry Health
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By Paul McMullin
© 2004

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One of only two 'Class A' diseases of poultry targeted for emergency disease control measures by OIE, the equivalent of the World Health Organisation for animal diseases. This viral disease can cause exceptionally high mortality, especially in turkeys. In addition official control measures disrupt trade in poultry products from affected areas. The cause is a virus, Orthomyxovirus type A, its pathogenicity is variable, and isolates are designated sero-type/ species/location/reference number/year/subtype designation(H/N). Highly pathogenic forms are usually of the H groups 5 and 7 and may now be identified (if H5 or H7) by the presence of a sequence at the haemagglutinin cleavage site that codes for multiple basic amino acids.

The definitive classification of high pathogenicity is an intravenous pathogenicity test (IVPI) in 6-week-old chickens result of greater than 1.2 . This is a test in which the virus is inoculated into susceptible chickens that are then kept under observation. The higher the proportion of the chickens dying or showing signs the higher the IVPI. The virus infects chickens, turkeys, ducks, partridges, pheasants, quail, pigeons, and ostriches. Effectively all birds are considered to be at risk of infection. Apathogenic and mildly pathogenic influenza A viruses occur worldwide.

Highly pathogenic avian influenza A (HPAI) viruses of the H5 and H7 HA subtypes have been isolated occasionally from free-living birds. Outbreaks due to HPAI were recorded in the Pennsylvania area, USA, in the years 1983-84. More recently outbreaks have occurred in Australia, Pakistan, Mexico and, from December 1999, in northern Italy. A serious outbreak occurred in The Netherlands in 2003 with a few linked cases in Belgium and one in Germany. H5 viruses of low pathogenicity may become highly pathogenic usually after circulating in poultry flocks for a time (Pennsylvania, Italy). Because of this, and the high mortality that 'low-path' AI can cause in turkeys, OIE and other bodies are currently examining ways to improve control of LPAI. See current OIE records for up to date information on distribution of HPAI. Morbidity is high but mortality usually relatively low, 5-50%.

The route of infection is probably oral initially, but possibly by the conjunctival or respiratory route and the incubation period is 3-5 days. Transmission is by direct contact with secretions from infected birds, especially faeces, waterfowl, equipment, clothing, drinking water. The virus replicates mainly in respiratory tissues of chickens and turkeys but in the intestinal tract of clinically normal waterfowl. Avirulent in one species may be virulent in others. Broken contaminated eggs may infect chicks in the incubator simulating vertical transmission. The virus is moderately resistant, can survive 4 days in water at 22°C, over 30 days at 0°C. It is inactivated by a temperature of 56°C in 3 hours and 60°Cin 30 min, by acid pH, by oxidising agent and by formalin and iodine compounds. It can remain viable for long periods in tissues. Infections with other pathogens (e.g. Pasteurella) may increase mortality, even with 'low pathogenicity' strains.

Avian Influenza is a potential zoonosis. It can result in inapparent infection, conjunctivitis or severe pneumonia. The small number of human deaths associated with HPAI appear to have resulted from direct exposure to infected birds on farm or in markets.


  • Sudden death.
  • Marked loss of appetite, reduced feed consumption.
  • Cessation of normal flock vocalisation.
  • Drops in egg production.
  • Depression.
  • Coughing.
  • Nasal and ocular discharge.
  • Swollen face.
  • Cyanosis of comb/wattles.
  • Diarrhoea (often green).
  • Nervous signs such as paralysis.

Post-mortem lesions

  • Inflammation of sinuses, trachea, air sacs and conjunctiva.
  • Ovarian regression or haemorrhage.
  • Necrosis of skin of comb and wattles.
  • Subcutaneous oedema of head and neck.
  • Dehydration.
  • Muscles congested.
  • Haemorrhage in proventricular and gizzard mucosae and lymphoid tissue of intestinal tract.
  • Turkey lesions tend to be less marked than those of chickens, while ducks may be symptomless, lesionless carriers of highly pathogenic virus.


A presumptive diagnosis may be made on history and post­mortem lesions. Confirmation is by viral isolation in chick embryo, HA+, NDV-, DID+. Commercial Elisa test kits are now available. However, as with many such tests occasional false positive reactions can occur. The agar gel precipitation test is non-group-specific and is used to confirm any positives. Differentiate from Newcastle disease, fowl cholera, infectious laryngotracheitis, other respiratory infections, bacterial sinusitis in ducks.


None, but good husbandry, nutrition and antibiotics may reduce losses. Eradication by slaughter is usual in chickens and turkeys.


Hygiene, quarantine, all-in/all-out production, etc. Minimise contact with wild birds, controlled marketing of recovered birds. Vaccination is not normally recommended because, although it may reduce losses initially, vaccinated birds may remain carriers if exposed to the infection. Vaccines have been used in recent outbreaks in Mexico and Pakistan. To be effective inactivated vaccines must be the right subtype for the particular situation (H5 will not protect against H7 and vice versa). In outbreaks a regime of slaughter, correct disposal of carcases, cleaning, disinfection, isolation, 21-day interval to re-stocking should be followed. Survivors can be expected to have a high degree of immunity but may harbour virulent virus.

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