Disease Information (11) (Provided by Prion Molecular Biology Lab, Foreign Animal Diseases Division) ( 07/05/11 ) | |||||
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Part | Charger | leeyh | date | 07/05/11 | |
Bovine spongiform encephalopathy
1. Definition / Geographical distribution
Bovine spongiform encephalopathy(BSE) is a progressive neurodegenerative disease of adult cattle. The disease is one of the transmissible spongiform encephalopathies (TSEs) or 'prion' disease. These diseases are characterized by long incubation periods, the accumulation in the central nervous system(CNS) of an abnormal isoform of a host-encoded prion protein (PrP). The source of the BSE epidemic is probably food supplements that were prepared with bone meal from dead sheep.
BSE was first diagnosed in England in 1986, and its annual case incidence in the UK peaked in 1992. Although the great majority of cases have occurred in cattle in the UK, smaller-scale epidemics, linked to the export of live cattle and MBM(meat and bone meal) from that country and subsequently from other BSE-infected countries, have occurred elsewhere in Europe. Increasing numbers of cases have been detected in other countries of Europe since 1999, when more sensitive surveillance programs were introduced. In 2001, the first cases in cattle born outside Europe were confirmed in Japan. In 2003, Canada reported its first indigenous case of BSE.
2. Clinical signs/Incubation period
The initial signs of BSE are non specific and largely behavioral. Consequently, the early clinical diagnosis is only possible after repeated observation and knowledge of normal behaviour.
Due to the long incubation period, signs usually appear when animals are between 2 and 7 years of age. BSE usually has an insidious onset and a slowly progressive clinical course extending over weeks to months. Apprehension, hyperaesthesia and ataxia are the main signs, and at least one of these signs is present in most BSE cases; they represent the most frequent changes in mental status, sensation, and posture and movement, respectively. Changes in mental status affect behaviour and temperament; the first sign of BSE may be when a normally placid animal becomes aggressive and kicks in the milking shed. Hypersensitivity can be to touch, sound and light. Ataxia affects mainly hind limbs. Other abnormalities of posture and movement include falling, tremor and abnormal head carriage. In advanced cases, generalized weakness and loss of condition can cause recumbency and signs of altered mental status and hyperaesthesia may no longer be obvious. The clinical history of any recumbent of chronically wasted animal should be sought, especially in an abattoir situation. There is often loss of body weight, condition and reduced milk production, despite continued appetite. The duration of the clinical disease can range from less that two weeks to as long as one year. The majority of cases will require euthanasia within two months of onset. The disease is invariably fatal. There is no treatment, or vaccine available.
3. Gross lesions / Diagnosis
There are no characteristic gross pathological changes associated with BSE. Histopathology reveals bilaterally symmetrical spongiform degeneration affecting the nerve cells of the brain stem nuclei. The degree of spongiform degeneration is variable, whereas the extent of reactive gliosis correlates with the degree of neuronal loss.
BSE is diagnosed through the detection of the abnormal prion protein in brain. The brainstem including the obex is required for testing. Tissues are to be submitted fresh. There are a number of tests available to establish a preliminary diagnosis of BSE : Western blot, ELISA, immunohistochemistry to detect the presence of abnormal prion protein.
There is no validated diagnostic test currently available for the BSE agent in live animals. Laboratory tests on tissue obtained at postmortem examination are therefore required for confirmation of this disease. Laboratory examination of brain and spinal cord samples collected at postmortem examination is essential to confirm a suspected case of BSE.
A complete diagnosis of the TSE as BSE of the type observed in the UK and continental Europe would result from a mouse bioassay demonstration infectivity associated with an incubation period and lesion profile consistent with the BSE agent.
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