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Control measures for BSE have been effective in significantly reducing the number of cases since the disease was recognised 25 years ago. In a workshop at this year's AHVLA conference, held in Surrey from September 13 to 15, speakers considered the advances and knowledge gaps in the understanding of the disease and ways in which policies across Europe could be adapted to reflect changing circumstances. Arianwen Morris reports
BOVINE spongiform encephalopathy (BSE), a progressive degenerative neurological disease of cattle, was first detected in the UK in 1986 as a result of passive surveillance of farm animal diseases by the Veterinary Investigation Service of the Ministry of Agriculture, Fisheries and Food (MAFF) and submission of material to veterinary pathologists at the Central Veterinary Laboratory in Weybridge.
Discussing the history of the disease, Gerald Wells, the retired head of neuropathology at the Animal Health and Veterinary Laboratories Agency (AHVLA), noted that, in 1987, a paper had been published in Veterinary Record drawing attention to strong resemblances between BSE and the encephalopathies recorded in several other species, such as scrapie in sheep.
Early epidemiological investigations produced evidence that the BSE epidemic had resulted from the use of infectious meat and bone meal in cattle feed and a feed ban was introduced in the UK in 1988 preventing the inclusion of ruminant proteins in ruminant rations. Initially, the hypothesis that BSE was caused by prions had not been widely accepted.
In 1996, a novel form of the human TSE Creutzfeldt–Jakob disease (CJD), termed variant CJD (vCJD), was identified in human beings, giving rise to concerns that BSE had zoonotic potential. Control measures for BSE were tightened as a result and, later the same year, a total ban on feeding any mammalian proteins to farmed animals was enforced.
‘The UK epidemic peaked in 1991 to …
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