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Volume 2: Science
3.
The nature and cause of BSE
Summary
3.244 In this chapter we have described the scientific investigation of the BSE epidemic and the conclusions drawn from those investigations. With the benefit of hindsight gained from recent research, we have been able to evaluate the conclusions reached at the time and have come to the following views:
- The infection responsible for the epidemic was spread in MBM.
- Its apparent presentation as an extended common source was due to the cattle-to-cattle recycling of the BSE agent over a number of years before the recognition of the disease.
- The BSE agent is not an unmodified form of scrapie. Rather, it seems to be a novel TSE agent that arose from a prion mutation in cattle, sheep or another species in the 1970s or earlier. Its origin might have been from a single point source in South West England.
- Changes in rendering were not responsible for a failure to inactivate the infective agent and were not responsible for the emergence of BSE in cattle.
- The infective agent is post-translationally modified prion protein, a self-replicating protein. Other as yet unknown factors may contribute to the development of BSE in infected animals.
- The minimum infective oral dose of the BSE agent has not been determined. It can be contained in less than 1 gram of brain from an affected animal.
- The BSE epidemic has been prolonged since the introduction of the ruminant feed ban in 1988 by a combination of factors of which contamination of cattle feed with MBM in feed designed for pigs and poultry seems to be the most important. The part played by maternal and lateral transmission remains uncertain.
- BSE differs from scrapie in that the lymphoreticular system appears to contain less infectivity as measured by bioassay. However, mouse bioassay is 1,000 times less sensitive than assay in cattle, by which the full range of tissue infectivity in cattle has yet to be determined.
- It is not known whether or not BSE has been transferred to the national sheep flock.
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