Manual on bovine spongiform encephalopathy
Bovine spongiform encephalopathy (BSE) was first recognized and defined as a pathological entity in the United Kingdom in November 1986 (Wells et al., 1996). Initial epidemiological investigations and examination of archived brains indicated that the first cases occurred around April 1985. Subsequently, the largest freeborn epidemic of a transmissible spongiform encephalopathy (TSE) occurred which has had severe economic effects and has caused concern for public health. The initial clinical signs of this fatal neurological disease are non-specific, typically involving behavioural changes. As the clinical phase progresses the disease is typified by alterations in mental state and of sensation and ataxia. The majority of affected animals reach the advanced stages within two to three months from the onset, when slaughter on welfare grounds becomes necessary (Wilesmith et al., 1988). The disease affects adult animals, with a peak age at onset of four to five years of age. Both se xes and all breeds are equally susceptible. BSE can only be confirmed post-mortem by pathological examination of brain tissue. Histological examination of the hind brain has been the primary method for the statutory diagnosis in the United Kingdom (Wells et al., 1989). The histological changes are typical of the TSEs. Microscopic lesions in the central nervous system consist of bilaterally symmetrical, non inflammatory vacuolation of neuronal perikarya and grey matter neuropil. BSE is transmissible by parenteral inoculation of inbred strains of mice (Fraser et al., 1988) and cattle (Dawson, Wells and Parker, 1990). In cattle the incubation period is approximately 18 months using brain homogenates from natural terminal cases.
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| Format: | Texto biblioteca |
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| Published: |
Rome (Italy) FAO
1998
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| Subjects: | bovine spongiform encephalopathy, spongiform encephalopathy, animal diseases, disease transmission, epidemiology, symptoms, disease surveillance, diagnosis, disease control, public health, |
| Online Access: | http://www.fao.org/3/w8656e/W8656E.HTM |
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| Summary: | Bovine spongiform encephalopathy (BSE) was first recognized and defined as a pathological entity in the United Kingdom in November 1986 (Wells et al., 1996). Initial epidemiological investigations and examination of archived brains indicated that the first cases occurred around April 1985. Subsequently, the largest freeborn epidemic of a transmissible spongiform encephalopathy (TSE) occurred which has had severe economic effects and has caused concern for public health. The initial clinical signs of this fatal neurological disease are non-specific, typically involving behavioural changes. As the clinical phase progresses the disease is typified by alterations in mental state and of sensation and ataxia. The majority of affected animals reach the advanced stages within two to three months from the onset, when slaughter on welfare grounds becomes necessary (Wilesmith et al., 1988). The disease affects adult animals, with a peak age at onset of four to five years of age. Both se xes and all breeds are equally susceptible. BSE can only be confirmed post-mortem by pathological examination of brain tissue. Histological examination of the hind brain has been the primary method for the statutory diagnosis in the United Kingdom (Wells et al., 1989). The histological changes are typical of the TSEs. Microscopic lesions in the central nervous system consist of bilaterally symmetrical, non inflammatory vacuolation of neuronal perikarya and grey matter neuropil. BSE is transmissible by parenteral inoculation of inbred strains of mice (Fraser et al., 1988) and cattle (Dawson, Wells and Parker, 1990). In cattle the incubation period is approximately 18 months using brain homogenates from natural terminal cases.
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