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Editorial
BSE: the further we go, the less we know
  1. Cristina Acín, BVet, PhD
  1. Animal Pathology, Universidad de Zaragoza, C/ Miguel Servet 177, Zaragoza, 50013, Spain
  1. e-mail: crisacin{at}unizar.es

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BOVINE spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE) that during the last three decades has overturned all the paradigms of surveillance, diagnosis, legislation and public concern. Several origins of the disease have been postulated, but epidemiological evidence has led to feeding of cattle with feedstuffs contaminated with prions (Wilesmith and others 1988) being the only credible hypothesis. Indeed, the total ban of meat and bone meal (MBM) in ruminant feedstuffs (regulation 999/2001) (European Commission [EC] 2001) was and is the only measure that has resulted in a spectacular decrease of the BSE epidemic (EC 2011). Nevertheless, the debate about the precise source of those prions has been kept alive over the years: were British classical scrapie strains able to endure chemical and physical treatments of MBM, or was a BSE strain already present in the bovine population and was it its recycling in MBM that triggered the appearance of the disease? Cattle BSE is transmissible by the oral route not only to cattle (Wells and others 1994), but also to sheep (Foster and others 1993), but what about transmissibility of scrapie to cattle by the oral route? It seems reasonable to think that, if sheep scrapie was the source of BSE, the experimental transmission of scrapie to cattle by …

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