Unfortunately, there are a few problems with the accepted wisdom concerning BSE:

• It is now known that none of the rendering processes used, before or after the 1980s, completely inactivates the infectivity of prions. Therefore cattle would have been exposed to scrapie prions in all countries worldwide where scrapie was present and MBM was used, not just in the UK in the 1980s. For example, the incidence of scrapie in the USA is hard to determine but in the 8 years after the level of compensation for slaughter of infected sheep was raised to $300 in 1977, the reported number of cases went up 10 fold to a peak of about 50 affected flocks a year.

BSE is not scrapie:

• The biological properties of the scrapie and BSE agents are distinct, e.g. transmissibility to different animal species and pattern of lesions produced in infected animals (Bruce ME. et al. Transmissions to mice indicate the 'new variant' CJD is caused by the BSE agent. Nature 389: 498-501, 1997). There is no evidence to support the assumption that BSE is scrapie in cows. The only feasible interpretation based on present knowledge is that BSE originated as an endogenous bovine (cow) prion which was amplified by the feeding of cattle-derived protein in MBM back to cows.

  Thus the emergence of BSE in the UK appears to have been due to 'bad luck' compounded by poor husbandry practices, i.e. use of MBM in ruminant feed.

© AJC 1997.