Avian Encephalomyelitis

  • Uploaded by: Dr.Kedar Karki ,M.V.Sc.Preventive Vet.Medicine CLSU Philippines
  • 0
  • 0
  • May 2020
  • PDF

This document was uploaded by user and they confirmed that they have the permission to share it. If you are author or own the copyright of this book, please report to us by using this DMCA report form. Report DMCA


Overview

Download & View Avian Encephalomyelitis as PDF for free.

More details

  • Words: 474
  • Pages: 37
AVIAN ENCEPHALOMYELITIS Dr.Kedar Karki

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;

Clinical signs - 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

Risk of introduction •    AE could be introduced through the import of sub-clinically infected adult breeding stock, infected dayold chicks or hatching eggs.

Control / vaccines •  Immunization 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 immunization, but sometimes recurs after several years of freedom.

Related Documents

Avian
December 2019 17
Avian Flu
May 2020 14
Avian Influenza
May 2020 19
Avian Flu
May 2020 12

More Documents from ""