Avian Encephalomyelitis
Also known as: AE— Epidemic tremor in chickens—Avian encephalomyelitis virus (AEV)
| Scientific Classification | |
|---|---|
| Kingdom | Virus |
| Family | Picornaviridae |
| Genus | Hepatovirus |
| Species | Avian encephalomyelitis-like virus 1 |
Introduction
Avian Encephalomyelitis (AE) is commonly known as epidemic tremor in chickens. It is caused by Avian encephalomyelitis-like virus 1 (AEV), which is a single-stranded RNA (ssRNA) virus belonging to the Picornaviridae family. It was formerly classified as an enterovirus but is now considered a Hepatovirus as its genome ecodes for a single polyprotein (2134 amino acids), which shares greater resemblance to that of the hepatitis A viruses than the other picornavirus genera. The virus has a non-enveloped capsid with icosahedral symmetry and is approximately 26 nm in diameter and has buoyant density of 1.31 g/ml in caesium chloride [1]. There is only one serotype of AEV, which is not related antigenically to other avian picoronaviruses, which is why it has been referred to in the past as an enteroviruses or enterovirus-like viruses.
Avian Encephalomyelitis (AE)is of economic concern to breeders and layers as it causes a decrease in egg production in laying hens, a decrease in egg hatchability, neurological diseases in chicks under three weeks of age and affected chicks that that survive are considered unlikely to be profitable.
Signalment
The domestic host for AEV is the chicken but it can also infect species of partridge, turkey, quail, guineafowl and pheasants. The infection causes the most serious disease in chicks under 3 weeks of age and older chicks show fewer clinical signs. Laying hens show a temporary reduction in their productivity . The incubation period varies from 5 to 14 days depending on the route of infection.
Clinical Signs
The disease causes a range of neurological signs in chicks under 3 weeks, ranging from ataxia, rapid tremor of the head and neck, drooping of the wings, weakness, paralysis, exercise intolerance to blindness and changes in vocalisation. It also causes weight loss, lameness, and unthriftiness. Affected chicks sit on their hocks, and cannot move well and many fall over onto their sides. Mortality can be as high as 25% with higher morbity rates of up to 60%. Older chicks show fewer neurological signs and in laying hens the disease causes a temporary reduction (2 weeks) in egg production and a decrease in droppings.
Epidemiology
The virus replicates in the epithial cells of the alimentary tract and is circulated in the bloodstream to other organs and the central nervous system (CNS). The virus is shed within 3 days of oral ingestion and in young chicks can continue to be shed for over two weeks. Shedding ceases once specific antibody's are produced. The disease is spread horizontally, via the faecal-oral route and chicks from non-immune layers under the age of three weeks are neurologically affected. Vertical transmission can also occur from infected layers to their chicks. The virus may be shed for several weeks. Once a bird becomes infected with the disease or is vaccinated it is immune to AE for life, some birds are left blind. AE is not considered a zoonosis.
Diagnosis
The following methods have been used to help diagnose Avian Encephalomyelitis; Virus Neutralization test, Agar Gel test, Embryo Susceptibility test and more recently an Elisa test. All of the tests show the presence of antibodies and indicate exposure to the disease and not necessarily a current infection. Diagnosis can be confirmed by either histopathology or by virus isolation. Classic diagnosis is typically made by the presence of brain lesions shown histologically.
Grossly, lymphocytic infiltration of the muscular region of the ventriculus has also been noted as well as perivascular infiltration within the brain and chord, with the exception of the cerebellum, where lesions can be found only in the nucleus cerebellaris. Pathognomonic lesions can be found within the midbrain and rotundua and ovidalis nucleus (microglisosis) and proventriculus (dense nodules within the muscular wall). Lesions can also be present in the pancreas.
Differential diagnosis: include Newcastle disease (ND), Equine encephalomyelitis infection, nutritional disturbances ( rickets, encephalomalacia, riboflavin deficiency), and Marek’s disease [2]
Distribution
Worldwide, the disease has been documented in Africa, Asia, Australia, Europe, and North and South America.
Treatment
There is no treatment for chicks infected with avian encephalomyelitis (AE). [2]. Surviving chicks will be immune to AE for life.
Control
In regions where AE is prevalent an effective way of preventing AE is to vaccinate pullets several weeks before they come into lay. Vaccination protects the flock from a reduction in egg production and prevents vertical transmission of the virus to chicks by providing the chicks with a sufficient level of maternal derived antibodiesas because there is only one serotype for the AEV. There are live and attenuated vaccinations available which can be administered in drinking water or as an eye drop, the latter being more effective. vaccination by eye-drop of only 10% of a flock gave the same results as drinking water application [3]
References
- ↑ Tannock, G.A., Shafren, D.R., (1994) Avian encephalomyelitis: a review. Avian Pathology, 23(4):603-620; 85 ref.
- ↑ 2.0 2.1 Calnek, B.W.(2003). Avian Encephalomyelitis. In: Saif, Y.M., Barnes, H.J., Glisson, J.R., Fadly, A.M., McDougald, L.R., Swayne, D.E., eds. Diseases of Poultry. Ames, Iowa, USA: Iowa State Press, 271-282.
- ↑ Shafren, D.R., Tannock, G.A., Groves, P.J. (1992) Antibody responses to avian encephalomyelitis virus vaccines when administered by different routes. Australian Veterinary Journal, 69(11):272-275; 10 ref.
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