Bovine Spongiform Encephalopathy

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BSE was first brought to the attention of Mr John Wilesmith, Head of the Epidemiology Unit at the CVL, in late May 1987, when Dr William Watson, Director of the CVL, asked him to investigate the epidemiology of the new disease. Data on the disease collected by Veterinary Investigation Centres were passed to Mr Wilesmith in early June. At this time, six cases on four farms had been confirmed by neuropathological examination.
Possible sources of infection from sheep and other species, especially animal protein in cattle feed, were considered, as well as genetic factors and semen used for artificial insemination. The prospect of scrapie having infected feed via MBM was specifically mentioned. This had previously been considered by Dr Alan Dickinson in relation to scrapie infection in sheep, but had not been investigated experimentally.
Mr Wilesmith was requested to take charge of the epidemiological investigation. He designed a questionnaire to assist in the systematic collection of data on factors which might be involved in the origin and spread of BSE. As the numbers of reported cases increased through voluntary notification, Mr Wilesmith visited farms with affected or suspected animals. By December 1987 he had compiled information on approximately 200 confirmed cases of BSE. 12 The first paper produced as a result of the analysis of this data was published in December 1988.

Results of the initial epidemiological investigations were published in the Veterinary Record in December 1988. In the paper, Mr Wilesmith concluded that, on the basis of current evidence, it appeared that MBM was the vehicle of infection. Although he had discounted autosomal dominant inheritance of the disorder, Mr Wilesmith was unable to comment on the occurrence and incidence of maternal transmission of the disease. Given the ages of the BSE cases at the time, and therefore the number of their offspring which would survive the minimum incubation period, he did not expect maternal transmission to have an effect on the annual incidence until at least 1990.
Analysis of the 1987 BSE data also revealed the spatial pattern of the emerging disease and provided clues as to where the infectivity might have originated. Mr Wilesmith noted that there was no evidence of an association between the occurrence of BSE and any single compounder of proprietary feedstuffs. A number of compounders were involved and they, in turn, received MBM from many different renderers. As cases of BSE occurred simultaneously in geographically separate regions supplied by different compounders, Mr Wilesmith suggested that each case was an index case, ie, the first case in a defined population. He also concluded that there was no evidence of cattle-to-cattle transmission, and that the distribution of cases seemed characteristic of an extended common source epidemic. Although this assessment was widely accepted at the time, and indeed still is by some, more recent analysis has suggested a different pattern for the BSE epidemic, and has raised questions over certain assumptions made at the time regarding the origin of the disease.

The analysis also looked at when the first cases of BSE might have arisen. All cases occurred in adult animals with an age range of 2 years 9 months to 11 years of age, with the highest incidence in 4-year-olds. As the first cases in the study were identified in 1985, this suggested that it was most likely that most of the cattle were first exposed to infection in 1981-82. Mr Wilesmith suggested a number of factors that might have combined to initiate the epidemic. These included:

  1. a dramatic increase in the sheep population in Great Britain;
  2. a probable (but unproven) increase in the prevalence of scrapie-infected flocks;
  3. a greater inclusion of sheep heads in material for rendering;
  4. a greater inclusion of casualty and condemned sheep in material for rendering;
  5. the introduction of continuous rendering processes during the 1970s and 1980s; and
  6. the decline in the practice of using solvent extraction of tallow in rendering since the mid-1970s.
Mr Wilesmith regarded the most important factor in the exposure of cattle to the scrapie agent as being the introduction of continuous rendering processes that might have resulted in the rendering of animal material at lower temperatures and/or for shorter periods, and therefore in the possible failure to inactivate the scrapie agent. From late 1987 onwards, Mr Wilesmith thought it most likely that BSE was originally derived from existing strains of scrapie. The alternative explanation that the emergence of BSE might have been due to a new mutant strain of scrapie, transmissible to cattle, was also considered by Mr Wilesmith, but discounted. He suggested that 'the form of the epidemic and the geographically widespread occurrence of BSE would require the simultaneous emergence of this mutant scrapie strain in a large number of flocks (or cattle herds) throughout the country', and that this theory was inconsistent with the data. Nonetheless, he observed some geographical variation in incidence at the start of the epidemic with a 'greater incidence in Southern England . . . especially in Kent'. He suggested that this might be due to variation among compounders in the use and inclusion rate of MBM in cattle feedstuffs.
The ruminant feed ban, which banned the use of ruminant-derived protein in ruminant feed in Great Britain, came into force on 18 July 1988. Following the introduction of the ban, Mr Wilesmith produced estimates on the likely course and extent of the epidemic. His predictions depended on a number of assumptions, which he recognised might not necessarily be correct. He first assumed that maternal transmission did not occur and then that the effect of the inclusion of infected cattle in the cattle food chain, ie, recycling of infection, was minimal. Given these assumptions, he concluded that the annual incidence would continue at a constant rate of the order of 2 cases per 10,000 adult cows per year until 1992, when the ruminant feed ban would result in a steady decline in the epidemic. It was these assumptions that Mr Wilesmith relayed to the Southwood Working Party.
The ruminant feed ban did result in a dramatic reduction after 1992 in the number of cases of BSE, indicating that Mr Wilesmith's conclusion that feed was the vector for the spread of the disease was correct. This was a major breakthrough in the understanding of BSE, and one that was instrumental in controlling it.



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