Occurrence: Worldwide. Species affected: All. Age affected: All.

Causes: Type A Orthomyxoviruses.

 

Effects: Reportable disease. Respiratory distress, coughing, sneezing, rales, depression, sinusitis, emaciation, feed refusal, nervous signs and diarrhoea. In layers, there is a drop in egg production and shell quality. Mortality is rapid with virulent strains.

 

Detailed causes:

All birds of all ages are susceptible to avian influenza.

 

The causative agent, orthomyxovirus, is a single-stranded RNA virus containing 8 segments, and 35 serotypes. Type A viruses are divided into subtypes according to the antigenic nature of haemagglutinin (HA) and neuraminidase (N). The HA is a viral protein which can attacht to the cell surface and the N an enzyme which can brake the virus-cell attachment. Viruses are identified by HA, N, species of animal and year isolated. Antigenic change is common by antigenic shift (reassortment of segments).

 

Mode of transmission

It is spread by aerosol via the respiratory tract and breathing contaminated faeces. It can also be spread by wild water fowl and contaminated fomites.

 

Special note

It is a notifiable disease, highly contagious, and spread by waterfowl. The virus is highly unstable and can alter pathotypes quickly by passage in various animal species. Migratory birds spread and transmit human and swine influenza viruses across continents. Ratites (ostriches, emus and rheas) are sometimes infected.

 

Clinical signs:

The incubation period is hours to days, depending on age, sex, species affected, concurrent infections and pathogenicity of virus.

 

Respiratory distress, coughing, sneezing, rales, depression, sinusitis, emaciation, off feed, nervous disorder and virulent stains (fowl plague). Multiple pathotypes can occur. A drop in egg production and shell quality, watery eyes, excessive lacrimation, oedema of head and face, and cyanosis may be observed.

 

Postmortem lesions

Lesions include mucous in trachea, air sacculities, swollen head or wattles, egg peritonitis, sinusitis, watery lungs, and fibrinous enteritis.

 

Pericarditis, necrosis of skin and GI tract; haemorrhages on wattles, combs and legs’necrotic foci on liver, spleen, kidney and lungs, and haemorrhages at junction of proventriculus and gizzard can be seen with fowl plaque.

 

Diagnosis:

The AGP and ELISA tests can be used for determining the presence of antibody in the sera.

 

Isolation and identification of virus from trachea or vent in embryonating eggs or tissue culture is needed. Test haemagglutinating ability of the virus mixed with chicken sera containing antibodies against influenza. The virus can be sub-typed using specific sera against all known HA and N.

 

It simulates mycoplasmosis, turkey coryza, VVND, ILT, ornithosis, and fowl chlorea.

 

Treatment and control:

 

Prevention

• Killed vaccine is available in limited areas.
• Quarantine, depopulation and eradication of virulent form is mandated under law in the US.
• Strict biosecurity is needed.
• Control of live birds market in large North Eastern US cities is important to prevent the spread of the virus.
• Recombinant AI vaccine available in Mexico contains H gene cloned into fowl pox vector.

 

Treatment

Broad-spectrum antibiotics are helpful to control secondary bacteria.

 

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