Select Committee on Environment, Food and Rural Affairs Minutes of Evidence

Examination of Witnesses (Questions 1-19)




  1. You will no doubt recall, as we all do vividly, that day however many years ago it was when the Secretary of State for Health stood up in the House of Commons and said that, in looking for the cause of the new variant CJD, one could not rule out that it had been transmitted by the consumption of meat from animals which had been infected with BSE. In everything we have learned since then, has that statement been reinforced, diluted, or has it remained the same? What is now the perception, given that many of the expectations for the spread of CJD appear not to have been fulfilled? If you were giving advice to a minister who had to make that statement now, what would the advice be?

  (Dr Nash) I think there are two aspects to that question. One is the link between BSE in cattle and CJD in humans, and the second aspect of the question is the consumption of beef as opposed to other modes of transmission. On the first of those questions, I would say that, if anything, the evidence is stronger now than it was then for a link between BSE in cattle and vCJD in humans. It is true that the evidence is circumstantial, but it is very strong, and it comes from three sources: first of all, the different types of infective tissue from BSE and from vCJD, when strain-typed in mice, give the same signature. Similarly, when western-blotting or phenotyping of those tissues occurs, again, the signature is the same. I think what is also interesting is that when these methods are applied to other forms of CJD, to sporadic CJD for example, in humans, or indeed when the methods are applied to scrapie in sheep, they do not give this signature. So this is quite powerful, albeit circumstantial evidence. Secondly, experiments have been carried out mainly in other countries on inoculating three types of monkeys with the material from BSE in cattle, and they have gone down with TSEs. In the one species where the brain was examined, it was reported to be extremely similar to the brain pattern of vCJD. The third type of evidence is the epidemiological evidence, that the countries which have had vCJD cases, primarily the UK, Ireland and France, coincide with the countries where BSE was recognised at an early stage, or in the case of France as well, of course, where there were imports of beef from the UK. The evidence is circumstantial, as I said, but it is very strong. On the second aspect, of whether, if there is a link, it is caused by the consumption of beef, we are not necessarily the best Department to ask that question, I have to say. I think there would be greater expertise and responsibility within the Department of Health. All I would say is that it is a plausible explanation that it is the consumption of beef, although there may be other routes of transmission—medical routes, for example—which, as I said, others would be expert in.

  2. Let us come to BSE. I have been looking back over the history, and I hope this summary is accurate. The Phillips Inquiry concluded that BSE probably started spontaneously in a cow and was spread by rendering. The alternative theory was that BSE was in sheep but was masked by scrapie, and that a small percentage of the prions in sheep are in fact BSE prions, and the scrapie prions are killed by heat and the BSE prions are not. Then there is a theory that the origin is in other animals, because things like big cats can develop spongiform encephalopathies spontaneously. Professor Ebringer argues forcibly that BSE is in fact caused by auto-immune response to the common organism Acinetobacter and is not transmissible to humans; that in fact, it resembles multiple sclerosis in its characteristics. The latest research appears to tell us that the maternal transmission we all thought we discovered did not take place at all. One asks oneself why there are so few cases of new variant CJD—perhaps the oral route is fairly inefficient as opposed to inoculation to the brain—and with the species barrier the doses are small. Have we the faintest idea about the origin of BSE?
  (Dr Bailey) Since the Phillips Inquiry, two independent groups of scientists have looked at this. There has been the Horn Report, which was published, which has considered the origin, and then the EU Scientific Steering Committee has also looked at the scientific evidence relating to the origin. I think the bottom line is that we really do not absolutely certainly know the cause, and there are several plausible hypotheses, some of which, Chairman, you have mentioned yourself. There are some that are less viable; for example, you mentioned the Ebringer one. But I think a common agreement is the prion theory. Prions are associated with the disease, and that is essential in the scientific opinion, that prions are a part of the thing. One has to differentiate between the spread of the disease, where again there is very good agreement that meat and bonemeal was the vector for the disease, and the origin itself, the first case. There is not absolute agreement on that.

  3. I think it is commonly agreed that meat and bonemeal was the guilty party, but when you say there is not absolute agreement on the origin of BSE, you are being more assertive than perhaps the evidence permits. There just is no agreement. The simple matter is we do not know.
  (Dr Bailey) There is not agreement.

  4. So we are in a situation where we are looking at balance of probabilities in terms of the origin of the disease in cattle itself, and we are looking at balance of probabilities in terms of its transmission to humans as well. So we have two uncertainties, each of which rests upon actuarially the most likely probability. Is that an accurate assessment?
  (Dr Bailey) I think so, yes.

Mr Jack

  5. Just to follow up on that, when BSE first came about and there was a relationship established with CJD—if I might call it "old" CJD as opposed to the new variant—we did not seem to be too worried, but then we did become worried when the new variant arrived and there was the link we have just discussed with human beings. Have you any idea what caused the change to come about that we had a new variant of CJD, and given that CJD seems to be able to change its nature, should we be worried about that for the future?
  (Dr Nash) I think the old, sporadic type of CJD occurs all over the world, and occurs in older people and, as the name says, seems to be sporadic; there is no known cause and it seems to be an inevitable thing. When the new variant CJD came along, in a sense, there was much greater concern about this because of the fact that it seems to be linked, as I was saying earlier, to BSE in cattle, and affects younger people.

  6. What caused the old to become the new? Was there something which changed old CJD into new? I was interested to know whether that gave us any clue about the whole question of these transmissible spongiform encephalopathies.
  (Mr Soul) I just wanted to pick up on your point saying that we were not very worried. We were worried, and that is illustrated by the fact that major surveillance programmes were set up in a number of different countries to look hard at CJD, and of course, we found that a new variety of CJD had appeared, and in investigating that it was quite clear that that was different from the old type of CJD; it was genuinely a new phenomenon. That is where the link was then made that the most likely cause of that was in fact a connection with BSE in cattle. The old type did not change into the new type; the new type was a genuinely new phenomenon.

Mr Lepper

  7. From all that you have said so far, I imagine that you feel that SEAC was right when it recorded in its minutes of its meeting of 6 February this year the views of Dr Venters, published in the British Medical Journal in October last year, that the causal link between the BSE prion and new variant CJD is open to question. I assume that you feel that SEAC was right to be somewhat sceptical of Dr Venters' views.
  (Dr Bailey) I think that SEAC were correct in being somewhat sceptical. This item is really a matter for the Department of Health though. This was a topic that SEAC considered in providing advice for the Department of Health.

  8. Is there any part of the Government's research programme that is actually devoted to looking at other possibilities than the link between the BSE prion and new variant CJD? Has research got into a kind of rut, or are views such as Dr Venters'—and there may be others who are questioning—receiving funding to research?
  (Dr Bailey) Yes, the Government has provided funding in the past for alternative theories. For example, DEFRA, then MAFF, did provide funding for Professor Ebringer for the auto-immune theory. The Department has a policy of maintaining an open mind and funding work in support of alternative theories and hypotheses, provided that that work is scientifically sound and that it can demonstrate by the scientific principles used the questions it is seeking to address. It would be sent for external peer review to validate those points, but nonetheless, the Department has a policy of maintaining an open mind in these areas.

  9. So we are not in danger of there being a kind of established orthodoxy which we might come to regret at a later date because we have overlooked other things?
  (Dr Bailey) No, I do not think that is the case.


  10. You mentioned peer review. This is a new disease, as you have said. The number of scientists who are experts in it is presumably limited. One sometimes has the impression that all the scientists who are working on it are grouped together under the umbrella of something like SEAC, and it is really quite difficult to find people who are both expert and independent, able to bring that sort of peer review to bear. Can you reassure us that SEAC has not become a closed shop, sharing a particular view which is difficult to penetrate with alternative concepts?
  (Dr Bailey) Again, following up on some of the comments that were made in the Phillips Inquiry about consulting extensively the scientific community and not just focusing on one or two individuals, I think the Department has done this in recent years. If I may turn again to the comment about the Horn review of the origin of BSE, the members of that group were certainly not all people who were TSE scientists. They did have people who had expertise in other fields—geneticists at Cambridge and people who had experience in other kinds of neurological disease. That is one example. Certainly in terms of peer review of project proposals, our policy again is to consult those individuals who have expertise that is relevant, and this may not always be TSE expertise. For example, it may be in the diagnostics area, people who have expertise in different methodologies, scientific approaches to detecting things, or people who have experience, for example, in the environmental area or soil science. We are not just consulting people who have TSE expertise.

Mr Mitchell

  11. You are going to have to help us with the science. Is it correct that there is a growing belief that there is a period of susceptibility among young calves, and that BSE is more likely to be acquired by young calves than by older cows?
  (Dr Bailey) The epidemiological evidence, when we have studied the incidence of individual cases in herds and the numbers of cases in herds, is that younger animals are more susceptible. The experimental work to directly test that has not been done, but DEFRA is currently funding work on age susceptibility and dose response in sheep, using both BSE and scrapie to challenge the sheep. So we are actually testing the age susceptibility in sheep.

  12. So we cannot say yet conclusively that there is a link between the age of a cow and susceptibility?
  (Dr Bailey) It has not been shown directly experimentally. As I said, the epidemiological evidence points in that direction.

  13. What impact would it have on the methods used to deal with the disease if such a link were proved?
  (Dr Bailey) I am not sure that it would have any major effect, given first of all that the disease itself takes a long time to develop within the animal, and given that the controls that we have in place provide consumer safety: the feed controls, which should mean that they can no longer be recycled; the food controls on meat and bonemeal; the over 30 months scheme—very few animals throughout the course of the entire epidemic developed the disease before 30 months—and the removal of specified risk material. I am not sure that the controls themselves would necessarily change in any way as a consequence of that.
  (Mr Soul) Even if we were absolutely confident that only calves below six months were susceptible, we could not then afford to change the control programme because we know that the risk of cross-contamination in the livestock feed industry is so huge. If there was any infectivity present in feed for adult animals, there is a very good chance that calves are going to get access to that at some stage on some farms.

  14. Research is now concentrating on this question of whether there is a period of susceptibility. What research has been done?
  (Dr Bailey) As I indicated, the research is being done with sheep actually, looking at different ages of challenge and also looking at the dose with respect to the different ages. The reason that we are doing the work primarily with sheep is because in sheep we believe that, in terms of maintaining scrapie within the flocks, sheep are exposed by vertical or lateral transmission, and therefore it is quite important to define this in the case of sheep.

  15. We gather that DEFRA has no plans to undertake new work on adult cattle. Why is that?
  (Dr Bailey) In terms of the age susceptibility question which you have just mentioned, we are doing work in sheep, and I know that does not give you a direct answer in cattle, but it will be very important to establish the principle. The second reason is that to undertake such an experiment in cattle would be very expensive and very time-consuming, because clearly you would have to maintain the cattle for a large number of years, five to seven years, and we would have to have large numbers of cattle involved in the experiment in order to do it. Obviously, resources are not unlimited and we have to consider relative priorities, and our view is, because we are addressing the issue and doing work with sheep, which is also answering other questions relevant to our sheep programme, it is not the highest of our priorities to do it in cattle.

  16. So if you prove the susceptibility period on sheep, it could also apply to cattle.
  (Dr Bailey) It would give an indication. We cannot make that absolute assumption, but it would give an indication.

  17. Does that mean that it is not now possible to exclude an unmodified scrapie agent as the agent responsible for BSE?
  (Dr Bailey) That was the conclusion of the Horn Committee, which looked at the origin.

Paddy Tipping

  18. You have been telling us helpfully about age susceptibility and that there is evidence for this, but no definitive proof. Could you extend the argument and say if there is evidence on this, when we look at vCJD, is there any evidence to suggest that that might be a factor there?
  (Dr Bailey) Obviously, it is quite possible that it also applies to new variant CJD, and the evidence is merely looking at the age profiles of the cases which develop new variant CJD. In the main, although there has been one case in an elderly man, they have been young people.

  19. So this is again survey work.
  (Dr Bailey) Yes.

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