BSE origins remain obscure, but the epidemic is clearer

Perhaps the most telling aspect of Professor Gabriel Horn's July 2001, report investigating the origins and spread of BSE in the UK is what it revealed about how little is really known even now, while at the same time putting back into the public arena a number of ideas that scientists had previously hypothesized.Two conclusions stood out. First that an unmodified scrapie agent cannot be discounted as the origin of BSE, thus alerting policy makers to the fact that there could — possibly — be public health issues associated with sheep. This finding overturns a key conclusion from the Phillips' Inquiry into BSE, which said late last year that it was not plausible that an existing form of scrapie gave rise to BSE.Secondly, the report argued that cattle might have become infected early in life because meat and bone meal was included in feed for calves in their first few weeks of life in the UK, but seemingly – though this is not absolutely certain – not elsewhere in the world. The idea that cattle are more susceptible when young is, says Danny Matthews, head of molecular biology at the Veterinary Laboratories Agency (VLA), one that was first mooted in 1988/89. "My personal opinion is that the critical question is actually whether an unmodified scrapie agent caused BSE, and that is neither proven nor disproved. But it makes the difference as to whether we can continue to live with scrapie or we must try to eradicate it from sheep," says Mauritzio Pocchiari, head of the transmissible spongiform encephalopathies unit at the Italian National Health Institute in Rome and head of the country's CJD surveillance unit.Currently, the VLA is conducting an experiment on ten calves which had their brains injected with material from the brains of sheep that died from scrapie in the early 1970s. Two cattle have succumbed to a BSE-type disease, but the experiment still has a long time to run, says Matthews.Whilst the origins of BSE remain obscure, Horn's committee is clear that meat and bone meal (MBM) is the vector (each successive ban saw a decrease in new cases) and makes a strong case for BSE having arisen in the UK because of a combination of three reasons, seemingly unique to the country.First, the inclusion of meat and bone meal in the feed of young cattle. Secondly, a change in rendering practices that led to a 10-fold increase in the amount of infective agent that survived rendering and thus could have contributed to the spread of BSE (a finding that also overturns a conclusion of The Phillips Report). Thirdly, the sheep population is high in the UK, and, if the proportion of sheep carcasses in meat and bone meal is proportionately high, there would have been a high level of scrapie-infected material. The latter is a factor if scrapie, not a spontaneous mutation as suggested by the Phillips Inquiry, is the origin of BSE.Although the idea that cattle became infected very young was first put forward many years ago, the Philips inquiry into the BSE crisis missed the fact that feeding MBM to calves was largely restricted to Britain. As a result, the finding of the Horn Committee has surprised many senior figures in the research community. "It is new to me that it was a specific UK practice to feed MBM to young calves at that time," says Peter Smith, an epidemiologist at the London School of Hygiene and Tropical Medicine and acting chairman of the government's Spongiform Encephalopathy Advisory Committee (SEAC).Smith agrees that young calves could be more likely to catch BSE than older cows. "The modelling of the epidemic essentially suggests that," he says. "It is hard to explain the models unless you postulate that susceptibility is greatest in the early months of life."Definitively determining the origin of BSE after all this time may be difficult, says Matthews, who argues that computer models testing the theoretical predictions of each hypothesis — there are about 20 — against the actual behaviour of the epidemic are the more promising avenue toward understanding BSE.To complement computer studies, Smith says that the age-related susceptibility hypothesis should be tested with new pathogenesis studies in animals. "There is a shortage of experimental material on age susceptibility and it may be key to understanding the human epidemic." He says that researchers currently have "no idea" why variant Creutzfeldt-Jakob disease (vCJD), the human equivalent of BSE, seems to affect mainly young people.But others are not convinced by the new suggestion. "I don't think this can explain why BSE occurred in the UK and not elsewhere," says Malcolm Ferguson-Smith, a veterinary scientist at Cambridge University and co-author of the Phillips report. He points out that we can never be sure that many other countries in Europe did not feed MBM to calves in the 1970s. The animal feed industry rarely holds paperwork for more than a number of years, so there are no written records.To reach its conclusions, the Horn Committee interviewed senior nutritionists working in the livestock industry feed industry during the 1970s and onwards. But, "the committee has been unable to discover any written evidence bearing on this crucial information," the report admits.

BSE origins remain obscure, but the epidemic is clearer

The long awaited Horn report on the BSE epidemic throws up as many questions as it answers.

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