Examination of Witnesses (Questions 40-59)|
WEDNESDAY 22 MAY 2002
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.
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.
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.
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
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.
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 calvescalves are weaned on to this artificial
powder which contains animal fatscontain a risk of exposure
there, whereas our experience is that that is not a significant
50. Everything else is common to feed or the
other issues that you mentioned earlier as possible sources of
(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.
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
(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
(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
58. Then you would see a period of further research,
and then you would stop your research because your tests are not
(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