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


Examination of Witnesses (Questions 40-59)

DR PETER NASH, MR PETER SOUL AND DR MANDY BAILEY

WEDNESDAY 22 MAY 2002

Diana Organ

  40. If you are fairly convinced that it is young calves that are susceptible to the disease, and you are fairly convinced that it has come from feed but you are not absolutely sure about that, and the animals exhibit the disease when they are older, how do we know that there are not vast numbers of cattle that go into the food chain that are incubating or developing this disease, and it does not show because those that go into the food chain are slaughtered before 30 months? You are telling us that we are pretty sure that CJD new variant does come from the consumption of beef, so how are we to know that we are safe eating beef? It may be that there are cattle that are developing this disease. We are showing 20 that have been born after August 1996 when they are five or six years old that showed it.
  (Mr Soul) It is quite clear that very large numbers of cattle that are incubating the disease have been going into the food chain.[1] That is why we have had the measures in place to protect public health, and those measures are, for example, the specified risk material controls. We wanted to be absolutely certain that any tissues that might have infectivity in them were removed from the food chain.

  41. So people that are now developing and exhibiting new variant CJD are recent cases, since the measures have been brought into place to protect the public.
  (Mr Soul) The assumption would be that they were exposed to infectivity before the public health protection measures came into place or before they were fully effective.

  42. That is an assumption; we do not know that, do we? It is not through eating meat that has been off the bone and that has been from a carcass that has been treated in the way that we now treat our carcasses.
  (Dr Bailey) I think there is some additional evidence. First of all, we do not know how long the incubation period is in people, although we do in cattle. I mentioned earlier that one of the pieces of experimental work that we have done is to look at how the disease develops in cattle and which tissues show signs of the abnormal prion protein, and which of these tissues are infective when they are injected into both mice and indeed calves, because we have done bio-assays with calves as well as with mice. When you look at the time course of the disease in the animal and when tissues become infective, and which tissues become infective, based on the evidence that is available, that is why we remove the specified risks material. We would not think that meat that is available for sale now contains infectivity. We have not found prions or infectivity in muscle tissue, and that has been repeated by other researchers, not just those funded by DEFRA. I think we do have a greater degree of evidence available than perhaps was indicated.

  43. You say that you do know about the length of time in cattle that the disease is in, but we know very little about the length in new variant CJD in humans. Do you not think we ought to be doing some research into how long it takes between being infected and displaying that disease?
  (Dr Bailey) I am not sure how we do it in humans.

  44. Can we not do it from the post mortem evidence we have from those that have actually had the disease?
  (Dr Bailey) But we do not know when they were infected. We do not know when the challenge was made.
  (Mr Soul) This is a Department of Health area, but they have carried out surveys, for example, of tonsils and appendices and so on to try and get some sort of indication of this where any information might be available. Can I just add one other point about the risk to humans? It appears that the infectivity does not develop in bovine until really quite late in the incubation stage, so although we have said that animals that were incubating the disease were going into the food chain, really and truly, the risk of them having any infectivity in them does not appear to occur until perhaps only two or three months before they develop clinical signs. This is why, not having animals under 30 months going into the food chain, there is an added protection over and above the SRM controls.

Chairman

  45. Let us just be clear about this, because this is a very emotional area. The notion that you might have a cow which was somehow harbouring infection in its meat which we might eat and then years later the disease might come out is simply not the case. Let us be clear about that. In so far as infectivity exists, it exists in certain tissues and those tissues are removed. Would you like to make that statement as categorically as you can.
  (Mr Soul) Yes. All the research that has been done indicates that that is the case.

David Taylor

  46. I was going to ask whether or not there had been pointers from the various clusters of new variant CJD, including five in my own county of Leicestershire and I think there was a cluster in south Yorkshire as well. Does not that not give some pointers to the period of incubation?
  (Dr Nash) Again, we are on DoH territory here, but there was a thorough study done of the Leicestershire cluster, as I understand it, and others may know better than I do, but I think that did point to likely infectivity during the 1980s, if I remember correctly, which would be before the BSE controls were introduced, and possibly even before we knew that we had BSE.

  47. Following on my colleague's question, because the period of incubation is uncertain, we cannot be at all confident at this point about the scale of new cases in terms of new variant CJD, can we, and whether or not those numbers are in fact in decline?
  (Dr Bailey) No, that is correct. There have been various predictions. Again, this is a Department of Health area rather than ours. Various published papers give different predictions. All of the cases that have been found so far have had a particular genetic make-up, and it is possible, as is the case with kuru, that you get two peaks, because you get cases of this genetic make-up now, and then you get another peak of cases with a different genetic make-up at a later time point where the incubation point is longer. So it is very difficult to make any firm predictions.

Mr Jack

  48. Will we ever get to zero cases of BSE?
  (Dr Nash) That would certainly be our hope.
  (Mr Soul) It depends, does it not, on whether sporadic disease occurs? As we said earlier, one of the theories for the origin of the disease is that you get sporadic cases in cattle, and if that is the case, there could always be a case occurring in the future.

  49. What are you doing to be in touch with your counterpart scientists in other Europe Union countries which have not had the numerical outbreak that we have had but where clearly the disease is spreading? Are the factors which you have identified as being associated with the spread of the disease parallelled by, for example, the French experience, or is there anything different in other European countries that ought to give us cause for concern?
  (Mr Soul) The first point to make is that our central veterinary laboratory here is the Community reference laboratory for BSE, so that is a very good way of linking in with what is going on in the science in other countries, and there are very good liaison arrangements, not only with Europe but with other interested countries throughout the world. As to the differences, the only thing that strikes me immediately is that certainly the Danes and the Germans have a theory that animal fats in milk replacer powder fed to calves—calves are weaned on to this artificial powder which contains animal fats—contain a risk of exposure there, whereas our experience is that that is not a significant factor.

  50. Everything else is common to feed or the other issues that you mentioned earlier as possible sources of infectivity?
  (Mr Soul) That is right, yes. Again, they had confidence in, for example, the processing standard that they applied to their meat and bonemeal. They thought that that was sufficient to eliminate infectivity, but I think now they understand that it is not 100 per cent, and they understand as well that cross-contamination is a significant factor, whereas previously they had tended to rule it out. So yes, their experience is mirroring ours.

Mr Simpson

  51. I wonder if you could help the Committee with a bit of boring detail. Dr Bailey, you are Head of the BSE Division of DEFRA and you, Dr Nash, are a Director of the TSE directorate. Does that mean, in terms of the DEFRA wiring diagram, that you are co-equal, or is one of you senior to the other?
  (Dr Nash) I am Acting Director, and that has under it two divisions. There is Mandy's division, which is the BSE Division, which deals with cattle and general matters, and there is a sheep TSE Division, which is the other main division, which is responsible for the National Scrapie Plan, for example.

  52. How many people directly come under you in terms of what I would call, in old-fashioned terms, straight civil servants and for that matter those whom I would regard as vets and scientists?
  (Dr Nash) Coming under me, which is the policy TSE directorate, there are approximately 80 people altogether. We work very closely with Peter Soul, whose division is not part of my policy directorate, but we work very closely with the veterinary side.
  (Mr Soul) I have a deputy and four veterinary advisers working for me. I have one vacancy.

  53. You are head of the veterinary TSE team, so there are other vets within DEFRA?
  (Mr Soul) Yes, working to the Chief Veterinary Officer. There are a number of different veterinary teams in varying divisions covering different areas like tuberculosis, brucellosis, epizootic diseases and so on.

  54. What I am getting at in a crablike way is that one of the things that emerged from the debate that we had on bovine TB yesterday was, of course, that the problem is that the Department is frequently fire-fighting in terms of having to take vets and others off, for example, dealing with testing for bovine TB to dealing with Foot and Mouth. First of all, has this been a problem, as has been claimed, and secondly, in terms of your TSE programme, have you sufficient resources or have you identified areas in which you need additional resources?
  (Dr Nash) First of all, on the effect of FMD, that certainly did make it difficult last year and delayed things. We had two major programmes to get off the ground. There was the EU BSE testing programme and there was the National Scrapie Plan. For example, in relation to the TSE testing programme, we did have to delay things, partly because of resources but partly also because of what was happening in the country. However, now we have actually overcome those problems and are complying with the EU requirements on testing and, as I said earlier, we have tested in the UK over 200,000 bovines. But I would not deny that that was a problem. As for the position now, it would always be nice to have more staff, but I think that the numbers we have, all things considered, are reasonable.
  (Mr Soul) I said I am carrying one vacancy at the moment, and in a small team like mine that is actually quite significant. We do have genuine difficulties in recruiting vets to come and work in central London. That is a fact. It is a problem for us. We would like more, so if you know of any way of encouraging them to come and work for me . . ..

  55. Many of us are attending a reception this evening with the British Veterinary Association. We will pass on your request. You are obviously shifting your research to concentrating on TSEs in sheep. Were you horrified by the kind of media coverage several months ago in which there was a suggestion that sheep was the next disaster area and that we were looking to see the destruction of a very large percentage of British sheep?
  (Dr Nash) Obviously, one is always concerned to see articles in the press if they exaggerate the position. However, I would say that the Food Standards Agency has had a deliberate policy of openness on the subject of BSE in sheep and has been very quick to put information into the public domain. We very much support that, and I think it has actually helped to have ongoing information going into the public domain and people know that nothing is being kept from them. I think actually a lot of the press articles have been helpful in informing the general public on this theoretical risk.

  56. You would regard it still as a theoretical risk.
  (Dr Nash) Yes.

  57. That is based upon current research?
  (Dr Bailey) Yes, it is. BSE has not been identified as naturally occurring in sheep. Clearly, experimentally you can inject it into sheep and get them to develop a BSE-like signature in the brain, but it has not been shown to occur naturally so far.

  58. Then you would see a period of further research, and then you would stop your research because your tests are not showing anything?
  (Dr Bailey) I think there are two elements to this question. There is the research programme itself, and one of the key factors in the research programme is to actually develop a test that can clearly and rapidly differentiate between BSE and scrapie. The method that is used to distinguish between the two at the moment is very largely based on bio-assay in mice, which takes a great deal of time; it takes two years to finish the study. Obviously, one of the key features is to develop a test which will enable us very quickly to distinguish between the two. There are some in development and there are some that are giving very promising indications that they are going to be able to do this by molecular means. That is the first thing. The second thing is that, as part of the EU surveillance requirements, we are now required to test a lot more sheep for TSEs, and where any of the animals prove positive, where of course it could be scrapie or BSE, it will have to be followed up with additional tests, and those are being developed, as I explained, to see whether they look more like BSE than scrapie. Also, all of the cases which are notified as scrapie cases, clinical cases out in the field, we are also examining very carefully with a whole range of different tests to reassure ourselves that they do not look like BSE as opposed to scrapie. So there are various elements to this occurring, and the more information we get on the incidence of scrapie in sheep, it will give us a better ability to predict, if it occurred, the likely prevalence of BSE in that group of animals.

  59. Rather like other colleagues, you are dealing with people who are having to do this in a fairly simple way. What you are saying to the Committee is that at present, from the research that you have carried out, there is no evidence of TSE in sheep, so that is a good sigh of relief for the farming community and for consumers, but you are saying also that, nevertheless, you are continuing research because there is always a possibility that it could get into sheep. Is that right?
  (Dr Bailey) Yes. I think the reason that we believe that it is possible that sheep could have got BSE is because we know that they can get it, because we have experimentally shown that, and they were exposed to meat and bonemeal in just the same way that cattle were, because obviously meat and bonemeal was incorporated into some of the feed that some sheep might have received. We also know from research work that in sheep scrapie can be maintained, and it is an endemic disease. Therefore, the way in which scrapie is maintained, it could mean that BSE too could be maintained in that way, by being passed on from sheep to sheep in some way. Because of this, we have to assume theoretically that it is a possibility, which is why we are continuing to do further research in this area, because it is a theoretical possibility.


1   Note by witness: This was the case in the past. However, it is estimated that less than one animal within 12 months of developing clinical disease may have entered the food chain per year since 2000. Back


 
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