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Following the detection of bovine spongiform encephalopathy (BSE) in the UK, epidemiological studies identified a foodborne source with meat and bone meal (MBM) as the likely vehicle of infection (Wilesmith and others 1988). Subsequent studies demonstrated that the infectious agent is a transmissible spongiform encephalopathy (TSE) strain with uniform neuropathological, molecular and biological properties (Simmons and others 1996, Bruce 2003, Vidal and others 2005, Green and others 2005a, Stack and others 2011a). Furthermore, transmission studies implicated the BSE agent as the cause of variant Creutzfeldt-Jakob disease in human beings (Bruce and others 1997). However, the origin of the agent remains unknown. One hypothesis suggests that it was a strain of sheep scrapie in the UK (Wilesmith and others 1988). Recycling of this agent in MBM, and inclusion of MBM in ruminant feed prior to control measures, would inevitably have resulted in exposure of sheep, raising concerns that the BSE agent may have been established in the sheep population, possibly manifesting in disease indistinguishable from scrapie (Schreuder and Somerville 2003). The present study was initiated in 1997 to determine the susceptibility of cattle to the oral exposure of scrapie-affected brain by using pools of brains from scrapie-affected British sheep sourced during the BSE epidemic.
All procedures were carried out in accordance with the Animal (Scientific Procedures) Act 1986, under licence from the UK Government Home Office.
Inocula comprised two pools of brains from sheep of various breeds (including Cambridge, Finn Dorset, Mule, Suffolk, Swaledale, Texel and Welsh Mountain) diagnosed with scrapie in the period 1996–2000. Some affected sheep may have consumed contaminated feed before the enhanced feed controls of 1996, banning the incorporation of mammalian MBM in farmed animal feed. Pools were segregated by PRNP alleles, principally at codon 136, into Valine (300 sheep, pool V) and …