Volume 1: Findings and Conclusions
3. The early years, 1986-88
What was the cause of BSE?
The scrapie theory

182 The CVL had only one qualified epidemiologist in 1987, Mr John Wilesmith, who headed a small Epidemiology Department. He knew nothing of BSE until late in May, when he was asked by Dr Watson to investigate its epidemiology. There were then 6 confirmed cases on 4 farms, but as we have seen the numbers were about to escalate.

183 Mr Wilesmith prepared a questionnaire, rolled up his sleeves and set off in person to visit farms on which BSE suspects had been reported. Soon Mr M Cranwell had to be seconded from Starcross VIC in Exeter to assist him. By this time, unknown to Mr Wilesmith, thousands of cattle had been infected by recycling of earlier cases and were incubating the disease. Mr Wilesmith assumed, quite naturally, that each new case was an index case (that is, arising as a fresh incident) and that there was some common factor causing all of them. The search was on for that common factor. Vaccines, hormones and organophosphates were considered but ruled out: the disease had been found in cattle exposed to none of these.

184 From the outset feed was a runner. In August Mr Wilesmith noted that lamb MBM was used in commercial dairy rations, but added that it was not a recent introduction. This was a major conundrum. If feed was the cause, what novel ingredient or feature had suddenly started to make the feed infective?

185 Mr Wilesmith carried out calculations which indicated that the exposure of the cattle population to the BSE agent was likely to have begun in the winter of 1981-82. Had anything occurred at about this time to explain the disease?

186 Further investigations were put in hand to explore, with the help of the feed and rendering industries, why it might be that cattle feed had suddenly started infecting cattle. By the end of April 1988 Mr Wilesmith had reached no conclusion on this. He had, however, concluded that feed was the source of infection and that the source of infection in the feed was MBM made from sheep affected by scrapie. He set out these conclusions in a report, recommending a temporary ban on the inclusion of MBM in cattle and sheep feedstuffs, while further enquiries were made.

187 Mr Wilesmith and his colleagues are to be congratulated on the rapid identification of cattle feed as the cause of the cases of BSE that were being reported, and on the advice of a ban on feeding MBM to cattle and sheep. As we shall see, this advice was promptly implemented and cut off most of the source of infection, turning an escalating disease into one that would peak and decline.

188 Mr Wilesmith had, however, made some tentative conclusions which were to prove erroneous. He concluded that the cases being reported were all index cases. He concluded that the common source of infection was scrapie-infected feed which would result in the incidence of BSE rising sharply over a short period of time before maintaining a constant incidence. In a paper published at the end of 1988 he identified a number of factors which might explain why cattle feed had become infective around 1981-82. These included an increase in the amount of scrapie-infected sheep going for rendering and changes in the rendering process which had reduced the temperature applied. In the following year he refined these ideas and decided that particular significance attached to one specific change in the rendering process. The use of solvent to extract tallow had been widely abandoned at just about the right time to explain the outbreak of the disease. This process might well have played an essential role in inactivating the scrapie agent. When Mr Wilesmith learned of this change he commented that it was 'too good to be true'. In that, he was correct.

189 Mr Wilesmith's tentative conclusions were reasonable on the data available to him at the time, but they were wide of the mark, as he was in due course to acknowledge. The cause of infection of the cases being reported was not the scrapie agent in the feed, but the BSE agent itself. The cases were not first generation cases, but the consequence of recycling of BSE. Far from the incidence of BSE infection being likely to prove constant, it had been escalating year on year and was, in 1988, infecting cattle at a rate that probably exceeded 10,000 cases a month.

190 Changes in rendering processes may have had some effect on inactivation of the BSE agent, but they were not decisive or even significant.

191 Mr Wilesmith's tentative conclusions were widely accepted. They led to misconceptions, some of which have survived to the present day. We will deal with them shortly. They receive detailed consideration in Volumes 2 and 3.

The scrapie theory

192 The conclusion that BSE had been transmitted from scrapie-infected sheep was generally accepted. It was a reassuring conclusion. Sheep affected by scrapie had been eaten by humans for 200 years or more, without apparent ill effect. It was likely that scrapie in cattle would prove similarly innocuous. Although, as the years passed, evidence mounted that discredited the scrapie theory, this was never made clear to the public and most people are still under the impression that cattle caught BSE from scrapie-infected feed.

193 The conclusion that rendering changes had permitted the BSE agent to survive unscathed, whereas previously it had been inactivated, is also still widely accepted. There are two variations on this theme:

1. Some accuse the Government of having recklessly relaxed the Regulations governing rendering, or of having failed to impose a sufficiently rigorous regulatory regime.
2. Some accuse the rendering industry of having put the safety of their product at risk by cutting corners in order to cut costs.

194 Neither of these accusations is valid. There was no relaxation by the Government of rendering standards. Up to 1981 the rendering industry was largely unregulated. In 1981 Regulations were introduced that set minimum standards for the product of renderers, to be checked by regular sampling. The Regulations were strengthened in 1989. ¹ A more complex alternative involving the licensing of rendering plants was not pursued, but this would not have addressed the problem of BSE and the proposed criteria for the grant of licences would not have prevented it. That problem was not foreseen, nor was it reasonably foreseeable.

195 By the same token the changes made by the rendering industry to their processes did not, overall, make them more vulnerable to BSE. Neither the old nor the new processes would have inactivated the BSE agent. No rendering process has yet been devised which can guarantee to do so, though infectivity is reduced.

196 The theory that the rate of infection would have reached a plateau led to the conclusion in 1989 that the scale of the problem could be related to the rate at which cases were being reported. The Southwood Working Party on Bovine Spongiform Encephalopathy reported that year on the basis that the effect of recycling could be 'minimal and undetectable', in which case 350 to 400 cases a month could be expected. In early 1993 cases were being reported at a rate of around 1,000 a week. ²

197 These misconceptions involve no criticism of Mr Wilesmith. They demonstrate that in 1987 and 1988 lack of data made it impossible to appreciate the nature and extent of the disaster that had already occurred.