Difference between revisions of "Avian Encephalomyelitis"
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| − | + | Also known as: '''''AE'''''— '''''Epidemic tremor in chickens''''' | |
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| − | Also known as: '''''AE''''' — '''''Epidemic | ||
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==Introduction== | ==Introduction== | ||
| − | Avian Encephalomyelitis (AE) is commonly known as epidemic tremor in chickens | + | Avian Encephalomyelitis (AE) is commonly known as epidemic tremor in chickens and is caused by a hepatovirus [[avian encephalomyelitis-like virus 1| '''''avian encephalomyelitis-like virus 1''''']] (AEV). The disease is of economic concern to breeders and layers as it causes a decrease in egg production in laying hens and causes neurological diseases in chicks under three weeks of age. |
| − | + | The disease is spread commonly via the '''horizontal''', 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 layer to their chicks. The virus may be shed for several weeks and cause a decrease in egg hatchability. Once a bird becomes infected with the disease or is vaccinated it is immune to AE for life as there is only one serotype for the AEV. Some birds however can become blind. AE is not considered a zoonosis. | |
==Signalment== | ==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. | + | 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== | ==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 | + | 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'''. |
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==Diagnosis== | ==Diagnosis== | ||
| − | The following methods have been used to help diagnose Avian Encephalomyelitis | + | 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 indicate the presense of antibodies but not necessarily the presence of the disease. Diagnosis can be confirmed by either histopathology or by virus isolation. Classic diagnosis is typically made by the presence of brain lesions shown histologically. |
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| − | All of the tests | ||
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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. | 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 | + | '''Differential diagnosis''': include [[Newcastle Disease Virus| Newcastle disease (ND)]], [[Equine Viral Encephalitis| Equine encephalomyelitis infection]], nutritional disturbances ([[Rickets| rickets]], encephalomalacia, riboflavin deficiency), and [[Mareks Disease| Marek’s disease]] <ref name="Calnek, 2003">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.</ref> |
==Distribution== | ==Distribution== | ||
'''Worldwide''', the disease has been documented in Africa, Asia, Australia, Europe, and North and South America. | '''Worldwide''', the disease has been documented in Africa, Asia, Australia, Europe, and North and South America. | ||
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==Treatment== | ==Treatment== | ||
| − | There is '''no treatment''' for chicks infected with avian encephalomyelitis. Surviving chicks will be '''immune to AE for life'''. | + | There is '''no treatment''' for chicks infected with avian encephalomyelitis (AE). Affected chicks that that survive are considered unlikely to be profitable <ref name="Calnek, 2003" />. Surviving chicks will be '''immune to AE for life'''. |
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==Control== | ==Control== | ||
| − | In regions where AE is prevalent | + | 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 antibodies. 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 <ref name="Shafren, 1992">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.</ref> |
| − | + | ==References== | |
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| − | {{ | + | {{Learning |
| − | | | + | |flashcards = [[Avian Encephalomyelitis Flashcard]] |
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}} | }} | ||
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| − | + | [[Category:Avian Encephalomyelitis]] | |
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| − | [[Category: | + | [[Category:To Do - CABI review]] |
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Revision as of 20:45, 22 June 2011
Also known as: AE— Epidemic tremor in chickens
Introduction
Avian Encephalomyelitis (AE) is commonly known as epidemic tremor in chickens and is caused by a hepatovirus avian encephalomyelitis-like virus 1 (AEV). The disease is of economic concern to breeders and layers as it causes a decrease in egg production in laying hens and causes neurological diseases in chicks under three weeks of age.
The disease is spread commonly via the horizontal, 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 layer to their chicks. The virus may be shed for several weeks and cause a decrease in egg hatchability. Once a bird becomes infected with the disease or is vaccinated it is immune to AE for life as there is only one serotype for the AEV. Some birds however can become blind. AE is not considered a zoonosis.
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.
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 indicate the presense of antibodies but not necessarily the presence of the disease. 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 [1]
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). Affected chicks that that survive are considered unlikely to be profitable [1]. 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 antibodies. 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 [2]
References
- ↑ 1.0 1.1 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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