For many people, the possibility that sheep are infected with BSE hardly bears contemplating. Yet contemplate we must, for if we do find that BSE is spreading insidiously in British sheep, the implications for human health are potentially enormous.
The problem lies with the existing measures designed to protect consumers of sheep products from exposure to an agent that we now know is infectious to humans and is invariably fatal. These measures are illogical, inconsistent and inadequate to deal with a threat that might be increasing because the eradication of BSE from sheep would be much harder than from cattle.
The Food Standards Agency (FSA) accepts that existing control measures would be inadequate if BSE were found in sheep but continues to describe the risk as theoretical and appears unwilling to tighten the controls until evidence is forthcoming that the risk is real. This "wait and see" approach seems to fly in the face of the "precautionary principle".
Because there is no simple test, it may be years before we know if BSE is spreading in sheep, and it could be difficult to prove that it is not. The longer we have to wait for positive evidence, the greater the number of consumers that could have been exposed without adequate protection. Allow me to explain.
BSE belongs to the group of brain diseases known as the transmissible spongiform encephalopathies (TSEs), of which scrapie in sheep is the prime example. My involvement with the TSEs goes back to 1962, initially as part of the one tiny group of scientists in the world studying scrapie and, since 1988, as a full-time consultant who was a founder member of the government's Spongiform Encephalopathy Advisory Committee (Seac) in 1990 and served it until 1998.
One of my first jobs, in 1988, was with a client in the pet-food industry, who wanted a simple way of minimising whatever risks there might be of infecting cats and dogs with BSE. At the same time, the government was considering the public-health implications of BSE, and my advice was sought in 1989.
We didn't have much to go on. It looked as if we might be in for a large BSE epidemic. Whatever its origin, studies of scrapie in rodents showed exactly why we had to assume that BSE in cattle might differ from sheep scrapie in being a risk to humans.
Crucially, we knew that the scrapie-like agents only multiply to high levels in a small number of tissues. Therefore the theoretical risks to humans and pets could be reduced greatly by excluding from the food chain just six tissues from all cattle that were over six months of age at the time of slaughter. These tissues (brain, spinal cord, spleen, thymus, tonsil and intestines) became known as the specified bovine offals (SBO), and they were banned from human food in the winter of 1989/90.
The SBO ban was introduced purely on the "precautionary principle" because of the grave danger that, if we ever did find evidence that BSE was a risk to man, it would come too late to do anything about it. Action was needed to minimise the risks without banning beef products outright.
I remember writing a defence of the SBO ban in an article for The Independent in March 1990, in which I explained the essential dilemma as follows: "On the one hand, it would be wrong to assume that there is no risk whatsoever. On the other, any preventative action has to be taken knowing that it may be quite unnecessary."
Without doubt, the SBO ban was the strongest measure we took to protect consumers from apparently healthy cattle that were incubating BSE. We did not know for sure that it was needed until 1996, when the link between BSE and vCJD was established.
Seac immediately turned its attention to the possibility that BSE had infected sheep. We already knew that sheep had been exposed to the same type of BSE-infected feeds as cattle but to a lesser extent. That exposure was greatly reduced after 1988 when the use of these feeds was banned from sheep as well as cattle. The feed ban was the primary measure to control BSE and, by 1996, the dramatic reduction in the BSE epidemic was obvious. So what was the problem? Even if a few sheep had been infected before the feed ban, most would have been slaughtered years ago.
Unfortunately it wasn't that simple. In 1996, we were aware of experiments showing that it was quite easy to transmit BSE into sheep experimentally by feeding them relatively small amounts of brain from BSE-infected cattle. This made it more likely that food-borne infection of sheep with BSE had occurred.
However the key question was: had a sufficient number of breeding sheep been infected to start a process of natural spread of BSE in the same way that scrapie spreads from sheep to sheep?
We knew that there was little natural spread of BSE from cattle to cattle (which is why the epidemic continues to decline), but now we had to assume just the opposite for BSE in sheep. We also knew that any spread of BSE in sheep would be "masked" by the thousands of cases of scrapie that occurred each year and that we could do nothing to stop that.
I remember a strong sense of déjà vu as we faced a dilemma precisely equivalent to that in 1989, except that the uncertainty was no longer the risk of BSE to humans, but the spread of BSE from sheep to sheep. And, quite apart from BSE, Seac was also concerned that a mutant strain of scrapie could arise at any time that would then be naturally selected in sheep and pose a risk to humans far greater than existing scrapie strains.
The ideal solution would be the total eradication of all TSE infectious agents from the national flock. This is the ultimate objective of the current national scrapie plan, but it could take 20 years or more to achieve.
Immediate action was needed to protect public health. Because the rate of spread of BSE from sheep to sheep was likely to be much slower than the rapid course of the BSE epidemic, Seac adopted an incremental approach starting with all sheep and goat heads (except the tongue). These were banned from human consumption in September 1996.
The next step was taken by the European Commission, because the problems of scrapie and BSE were not confined to the United Kingdom. Unfortunately, the proposals made by the commission in December 1996 were rejected, and it took years of argument to arrive at the current legislation on sheep offals, which became effective in January 2001.
The snag is that the current rules are illogical, inconsistent and fall far short of the original SBO ban. Since the SBO ban was based on our knowledge of scrapie in sheep, surely the ban on sheep tissues should at least be the same or equivalent? Why, for example, is spleen banned from sheep of all ages and tonsils from sheep only over 12 months of age, while other potentially risky tissues, such as intestines, are not banned at all?
And what should we do about the large lymph nodes? Lymph nodes were not included in the original SBO ban but, from January 1996, some of these had to be removed from exported British beef from cattle over 2.5 years of age. We now know that several tissues from BSE-infected sheep, including lymph nodes, pose a greater risk than the same tissues from infected cattle.
In a recent statement, the FSA acknowledged that the current controls would be inadequate if evidence was found that BSE was now present in the national sheep flock. The statement informed consumers of a study that may or may not show that some sheep were infected with BSE in the late 1980s or early 1990s. Because the study is ongoing and the results inconclusive, the FSA stated that "The risk of BSE in sheep therefore remains theoretical" and that "We are not advising consumers not to eat lamb". But things could change at any time.
Why play this waiting game? If the decision to improve the protection of consumers rests on knowing that there is a risk, it could be too late because it might be many years before the spread of BSE is detected in sheep. The technical difficulties are well described in a Seac sub-group report, Research and Surveillance for TSEs in Sheep, published in April 1999. Indeed, there are good scientific reasons why BSE might spread in sheep for many years without ever being recognised.
Would it not be wise to assume that BSE is present in sheep and to improve the control measures now? That would put us in a much better position if and when convincing evidence of a risk emerged.
Dr Richard H Kimberlin is a former director of the Neuropathogenesis Unit in EdinburghReuse content