Science: A killer in sheep's clothing
Is the Government pulling the wool over our eyes? Experts are now facing one of their biggest fears: that BSE has been passed from cattle to sheep.
Steve Connor is the Science Editor of The Independent and i. He has won many awards for his journalism, including five-times winner of the prestigious British science writers’ award; the David Perlman Award of the American Geophysical Union; four times highly commended as specialist journalist of the year in the UK Press Awards; UK health journalist of the year and a special merit award of the European School of Oncology for his investigations into the tobacco industry. He has a degree in zoology from the University of Oxford and has a special interest in genetics and medical science, human evolution and origins, climate change and the environment.
Friday 20 November 1998
Next week, the Spongiform Encephalopathy Advisory Committee (Seac), which is charged with that task, is expected to publish its latest advice on one of the most difficult questions it has had to consider: has BSE infected sheep? It is expected that the committee will recommend further research to investigate whether the cattle disease has affected another link of the human food chain, but the advice will probably fall short of recommending additional measures designed to limit the consumption of sheep offal.
Professor Almond, the head of Seac's subcommittee on BSE in sheep, was blamed for generating a scare that does not exist. But to a great extent, the furore that erupted over his comments in a BBC radio interview can be traced back to the many statements the previous government issued over BSE in cattle. Time and again we were told that BSE was almost certainly caused by scrapie - an endemic brain disorder of sheep - crossing into cattle that had eaten infected feed made with sheep-derived meat and bone meal.
This scenario also offered the government some comfort. They argued that sheep scrapie has been known about in Britain for at least 200 years and had never in that time been linked with any human diseases. The government argued that "scrapie in cattle", as BSE was sometimes called, was just like scrapie in sheep, and so posed no conceivable risk to human health.
Statements from the Ministry of Agriculture, Fisheries and Food (Maff), the government department most keen to play down the fears over BSE, never missed an opportunity to equate BSE with scrapie. One statement issued in February 1990, to announce research showing that BSE can be transmitted to mice, said: "Similar results were obtained some years ago in relation to experimental transmission studies of sheep scrapie to sheep and to mice. The BSE results therefore provide further evidence that BSE behaves like scrapie, a disease which has been in the sheep population for over two centuries without any evidence whatsoever of being a risk to human health."
The complacency of this approach, however, was shattered in March 1996 when the government, under the advice of Seac, had to concede that BSE was the most likely cause of an unusual form of Creutzfeldt-Jakob disease (CJD), a fatal brain disorder in humans. Subsequent research in laboratory mice confirmed this. To date, nearly 30 young people have died of new variant CJD.
Almost as soon as the announcement was made, people began to wonder again about the government's scrapie-to-BSE logic. If scrapie was supposed to have started BSE, then surely BSE could have got back into sheep because they, too, were fed the same infected meat and bone meal that amplified the disease in cattle. And if BSE in cattle could cause human disease, then surely there must be a risk from BSE in sheep?
Members of Seac met in July 1996 to hammer out their first public response to a worrying new dimension to the BSE crisis. At this meeting the experts considered details of experiments showing that it was possible for sheep to be artificially infected with BSE by eating less than a gram of infected bovine brain. What was more, the symptoms of BSE in sheep looked identical to scrapie yet its molecular biology was similar to BSE in cattle. This meant that sheep that look as if they have scrapie - which is harmless to humans - may actually have BSE, which is potentially lethal.
The only way to distinguish BSE from scrapie is by a complex, and expensive, set of experiments in mice that can take years to complete. In the absence of any simple test, Seac was left with the unenviable task of recommending a course of action based on absolutely no knowledge about the scale of the problem. Its first step was to ban parts of the sheep thought to be most infective - the brain, spinal cord and spleen.
Farmers and meat traders greeted the decision with derision. What was the point of taking measures which would scare the public for a highly theoretical risk that may not even exist? In fact Seac could have gone further. The specified bovine-offal ban includes a far wider range of prohibited cattle tissues. Scientists who work on scrapie know that the infection can be detected in sheep's intestines, thymus, tonsils and, most importantly, lymph glands which are scattered throughout the body. If Seac really wanted to minimise the risk, it could have extended the sheep-offal ban to include some or all of these tissues.
"It's a question of balance," says Professor Almond. "The balance the committee took in 1996 in relation to this conjectural possibility that there may be BSE in sheep was to go for a risk-reduction strategy, not a risk-minimisation strategy."
Some experts, however, view the current status quo as illogical. If there is a risk of BSE in sheep, why not introduce the same health measures designed to protect the public against the cattle epidemic? "If you were suggesting that we must extend the offal ban on sheep to the level comparable to that in cows, we would argue that we can't do that without severe disruption to the industry and causing alarm in the eyes of the public," Professor Almond says. "And you'd be doing that in the full knowledge that you hadn't got a single scrap of evidence that there was BSE in sheep."
The problem for the sheep farmers, however, is that Seac has already caused alarm in the eyes of the public by raising the issue of BSE in sheep in the first place. But, as Professor Almond admits, not having looked for BSE in sheep does not mean it is not there. The real problem is that if BSE is now present in sheep, it is almost certainly becoming an endemic disease, being transmitted like scrapie from one animal to another, rather than the result of a one-off infection from contaminated feed.
Professor Almond's subcommittee is seeking ways of actively searching for BSE in the nation's sheep using new and as yet highly experimental tests that might be able to distinguish it from scrapie. The problem is trying to interpret a negative result. Unless every animal is tested, not finding BSE in a sample population does not necessarily mean it does not exist.
The British breeding flock is more than 20 million animals, and many thousands would have to be sampled at random to get a reasonably accurate idea of whether BSE is a significant problem. If BSE affects only a few per cent of the flock, even sampling several thousand animals could just miss them entirely.
Concern over BSE becoming, like scrapie, endemic to British sheep is the nightmare scenario Seac members are forced to contemplate. As Professor John Collinge, a Seac member and inventor of a prototype BSE/scrapie test currently undergoing field trials, says: "For these reasons, and because sheep offal has not been subjected, to date, to the same comprehensive restriction from the human diet as specified bovine offal, we consider a search for the BSE strain in current cases of field scrapie in the UK to be essential."
The sentiments are echoed by Sir John Pattison, the chairman of Seac: "I think we gain nothing by sitting down and thinking through the issues theoretically. We've done that. We now have to gather more data and see where that takes us." The issue of BSE in sheep is not, unfortunately, going to go away just yet.
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