C853 - AVIAN ENCEPHALOMYELITIS

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C853 - AVIAN ENCEPHALOMYELITIS

Nature of the disease
Avian encephalomyelitis (AE) is a viral disease of young chickens caused by a virus from the Hepatovirus family and characterised by central nervous system signs (Epidemic Tremors). It can be the cause of significant economic loss.
Classification
FAO List C disease
Susceptible species
AE occurs naturally in chickens, turkeys, pheasants and Japanese quail.
Distribution
AE has been reported from virtually all developed countries, including New Zealand, Australia, USA and New Caledonia.
Clinical signs 
Chickens of all ages are susceptible, but clinical signs of encephalitis only develop in those younger than four weeks. The disease is similar in turkeys and chickens. Under field conditions disease is most common in the 1–2 week age group. Following initial dull expression of the eyes, the following signs are seen:

- progressive ataxia with the chick losing control of legs, sitting on its haunches and falling onto its side;

- tremor of the head and neck.

Ataxia progresses to paralysis and death results from inability to feed or drink, or through being trampled.

Some birds recover, and others may survive with persistent clinical signs.

In susceptible adult birds, infection is usually sub-clinical, although there may be a transient drop in egg production.

Post-mortem findings 

In chicks dying of AE there are no characteristic gross lesions. Histological examination of brain and spinal cord reveals characteristic encephalomyelitis with neuronal degeneration, perivascular cuffing and gliosis.

Differential diagnosis 
  • Newcastle disease
  • St Louis encephalitis
  • ricketsiosis
  • vitamin E deficiency
  • vitamin A deficiency
  • riboflavin deficiency
  • perosis
Specimens required for diagnosis 
Samples of brain tissue should be collected for histopathology, fluorescent antibody testing and/or virus isolation.

Serum sample from young chicks should be collected for ELISA test.

Transmission   
AE virus is transmitted both vertically and horizontally i.e. through the egg and by contact. Eggs laid by hens with sub-clinical infection will carry the virus. While hatchability drops, eggs will hatch and chicks will develop clinical disease soon after. Affected chicks shed virus in faeces and will infect susceptible in-contact chicks. 

To date wild birds have not been incriminated as reservoirs.

Risk of introduction   
AE could be introduced through the import of sub-clinically infected adult breeding stock, infected day-old chicks or hatching eggs.
Control / vaccines  
Immunisation with unattenuated live virus or with inactivated vaccine has been successfully used to control AE in both chickens and turkeys. If live king water. Breeder chickens are vaccinated at 10-16 weeks of age. Pheasants are vaccinated at 5-10 weeks of age and bobwhite quail at 6-10 weeks of age virus is administered to breeding pullets before they come into lay, their progeny will be protected by maternal antibody. 

The disease can be eliminated from flocks by immunisation, but sometimes recurs after several years of freedom.

References
  • Epidemic Tremor, In Merck Veterinary Manual, National Publishing Inc. Eight ed, 1998, Philadelphia, p 1971
  • Office International des Epizooties, 2002