Examination of Witness (Questions 224
- 239)
WEDNESDAY 7 NOVEMBER 2001
PROFESSOR ROY
ANDERSON
Chairman: Professor Anderson, we are sorry that
you have had such a long wait to come before us, but we have been
very eager to discuss matters with you. I am not going to do a
long introduction, I think we are going to carry on where we have
just left off, which is, as you will know, obviously, the key
issue here, with Diana.
Diana Organ
224. Good afternoon, Professor Anderson. Professor
Anderson, what experience do you have in the sort of course of
animal diseases?
(Professor Anderson) The group at Imperial College
deals with the epidemiology and control of infectious diseases
very broadly. My own first involvement was something like 20 years
ago, when I was asked by then MAFF to look at bovine TB and to
recommend some control options for that disease and, in particular,
some research. Subsequent to that, the group in 1996 was asked
by Government to become involved in the analysis of the BSE epidemic,
which gave us (a) a great deal of experience of interacting with
MAFF, and (b) quite a lot of experience to do with livestock databases.
The fundamental principles underpinning the spread of human infectious
diseases are very, very similar to those in the veterinary field;
so the science is indeed very, very similar.
225. And on the basis of your expertise in that
field, you actually drew up a model of the expected path of this
disease, and as a result of that came to the conclusion, am I
right, that the only way to flatten the curve and the disease
was to have a contiguous cull?
(Professor Anderson) No, that is not strictly true.
The precise course of events, post the announcement on 20 February,
a number of staff in the research group were quite interested
in trying to look at the course of the foot and mouth epidemic,
two in particular, and I encouraged them to do so. One of those
individuals, Dr Christl Donnelly, had published a very important
paper the previous year on foot and mouth, a retrospective analysis
of the Taiwan and the 1967 epidemic in Great Britain, and that
pointed to one very, very simple fact, which was speed was of
the essence. So our first focus was on what is the vital importance
of removing the index premise and what timescale should it be
removed within, and that is the problem we started with. And then,
subsequent to that, we discovered, very early on, that with the
character of the current epidemic, if that was the only control
policy, it was unlikely to constrain the epidemic from spreading
very, very extensively throughout the UK.
226. But we have heard that different foot and
mouth outbreaks are different, the virus is different, the strain
is different, so to take what had happened with the Taiwan outbreak
does not necessarily apply for what is going to happen, with what
happened in the UK in the spring and summer of 2001. And we have
heard, as Professor King said, that it was not so airborne. And
we cannot necessarily take what happened in a previous example,
with a different strain, and say one policy fits all?
(Professor Anderson) I totally agree; you are absolutely
correct. And one of the interesting bits of Dr Donnelly's paper
was a comparative analysis of Taiwan with the 1967 epidemic in
Great Britain, and the conclusion of that paper was different
in some respects but the one thing that was very, very important
was the message, time is of the essence with a fast-spreading
virus. And so our initial focus was on that problem, and indeed
we asked for data on the time taken for identification, or report
of the case, to laboratory confirmation and then to subsequent
slaughter of the index premise; and when that information came
back it indicated there were some quite serious problems.
227. Have we not got another problem, that because
in our rush to carry out the contiguous cull we actually destroyed
the evidence, because we slaughtered everything, so we did not
test everything, so we do not know whether the animals that were
disposed of had no virus or had old virus or had new virus, so
how can we actually take the evidence to support what we might
do in the future if we actually destroyed the very evidence we
needed to know for further scientific work on it?
(Professor Anderson) That is a very good question,
actually, and one of the suggestions of my own research group
to do with bovine TB control was that a set of experiments were
done with different control measures in different parts of the
country. Unfortunately, bovine TB is a very different kettle of
fish, it spreads very, very slowly, and you do have the option
of doing experiments, trying out different methods. My own personal
view is, if any hesitation had taken place in the early part of
March to mid March about what a possible course of action would
have been, the vast majority of the dense premises with livestock
in the UK would have been affected by foot and mouth; so you have
not got the luxury, unfortunately, in this particular case, of
doing experiments—trying different methods in different
regions. There are two other points related to this, from the
previous discussion, which I wanted to bring up in relation to
the questions, because I think they are important. First of all,
everybody is using the word `modelling'. It is important to make
the point that, for example, my own department is a very interdisciplinary
department, it ranges from molecular biologists through to field
veterinary scientists, through the clinical/medical epidemiological
area. Modelling was a tool in a set of interdisciplinary skills
that were applied to this problem, they included the establishment
for DEFRA of a robust and carefully checked database on cattle
and livestock, they included the statistical estimation of parameters
about the performance of control policies at a particular point
in time, and they included also doing a series of scientific reviews
for the Office of Science and Technology on rather important issues,
such as how good are the vaccines, how long does the virus live
outside the host, and etc. So it is important to register that
this was not just modelling, this was a very interdisciplinary
approach. Now the second point, Mr Chairman, if I could just add
this one, testing is vital. From the medical area, I know very,
very well that an accurate and precise diagnostic test early on
in an epidemic's development is key to successful control. You
have heard quite a bit of discussion of Professor Brown's method,
and I sat through the talk about the validation of it recently,
and it performed extremely poorly. The story is much more complicated
than that; it is not just how it performs on a clinical case,
it is how it performs day one, day two, day three, after that
animal has acquired the virus. Because the titre is extremely
low, the density of the virus is very low early on. And at the
moment we are still in the dark about the performance of these
tests; and my own guess is that, with current technology in this
area, we are never going to be able to pick up very, very early
infections, except with a bit of luck. And I would like to come
back, Chairman, if I could, to the BSE sheep-testing story, because
there are some important additional scientific problems there
too. Sorry, that is a lengthy response.
228. Thank you. You made the point that speed
is of the essence if we were going to get ahead of this disease,
and obviously there were certain groups of people and individuals
that had, for them, very good reasons why they should hold out
against MAFF coming onto their premises and looking at what they
believed were their healthy animals and possibly involving them
in a contiguous cull. And, obviously, we are having next week
the Second Reading of the Animal Health Bill, which seeks to have
powers that would override that problem. Should we have had that
power, that Bill, before this outbreak of foot and mouth, and
would it have had a considerable impact on shortening the outbreak
and the severity of it?
(Professor Anderson) I think it would have had an
impact, and a series of the different groups who are involved
in the analysis are going to try to assess, given data on the
fraction of contested cases over time, what impact it would have
had. I think the general point, given the current agricultural
situation in Europe, not just Britain, where one has dense holdings
of animals, sometimes mixed holdings, one has considerable movement
of animals between countries, when you have a fast-spreading,
very dangerous infectious disease, I think all Governments require
the power to act very, very quickly for that. And also this problem
goes beyond just the issue of culling, it goes to a question that
came up earlier, which you raised, about BSE testing, and indeed
scrapie testing. I would like to see legislation which enabled
DEFRA to do a random sample, to go into farms and say, "I
would like to randomly sample your animals to test for BSE,"
or indeed scrapie. And that legislation is not available at the
moment.
229. And to do with the belief that you had
that the contiguous cull was the only way forward, what do you
say to those people that were from Devon and from, say, the Forest
of Dean, that actually held out in resistance against the contiguous
cull, and subsequently, when their animals were tested, were blood
tested, and they were cleared and there was no evidence of the
virus in their area, what do you say to them; are they just statistical
anomalies, or is it that actually if we tested all of these people
we would have found vast numbers of them did not need to have
their animals slaughtered?
(Professor Anderson) It is an important question,
but I think an equally important question is what do you say to
the third generation cases, the farmers who own the premises surrounding
the contiguous area; if you had not had the contiguous cull in
place, my scientific view is that foot and mouth would be endemic
by this stage in Great Britain. What do you say to all those other
farmers whose animals contracted the disease.
Chairman
230. You said, Professor Anderson, just a few
moments ago, that you wished to make some comments on the BSE
in sheep issue. I think it might be an appropriate time to do
that now?
(Professor Anderson) I thought Professor King dealt
with this very precisely and very accurately. There is, just one
supplementary, issue, which, from membership of SEAC for a number
of years, has been a cause for concern, and that is that these
tests are state of the art science, particularly this western
blot one which, looks at the relative weight of the rogue protein.
What is lost in all of this is that the current testing programmes
for BSE in Europe, using a test which is not validated with respect
to how sensitive it is in terms of the incubation period of the
disease. We know that it picks up late-stage cattle, when they
are beginning to show clinical signs of BSE, and therefore the
prevalence data that is on the European Union BSE website says,
Germany tested 900,000 cattle, X per cent were positive. Now that
is likely to be an underestimate, in my view, potentially large
underestimate, of what is present, because it is quite possible
that this test only detects late-stage disease. And what I would
like to see is that DEFRA is encouraged to validate these tests,
and that includes the western block one, in animals that are experimentally
infected, and you can test to see its sensitivity year one, year
two, year three, year four. Now, with BSE, material stored down
from animals who were exposed in such experiments is present in
Weybridge, and it would be very nice to see a little gentle encouragement
to do the validation of the testing by the stage of the incubation
period of the animal; because I have a horrible feeling that there
is a little bit of an underestimation in the European figures
that are currently published.
231. The Secretary of State will be where you
are this time next week, so it may well be that we have an opportunity
to put that point to her.
(Professor Anderson) It is a point that has been made
in SEAC, it is minuted in SEAC minutes, but I am not aware of
any action as yet.
Mr Mitchell
232. Can I just ask, arising from the point
Diana made, we had this correspondence cited earlier, about evidence
from Alayne Addy, of 200 cases where they resisted contiguous
cull, and in none of those was any sign of foot and mouth infection
found. Now, on the basis of what Professor King told us, that
is to say, you are sacrificing 83 per cent, because you find evidence
of it in 17 per cent, you would have expected 34 cases of foot
and mouth in those 200 cases?
(Professor Anderson) But, as I said before, in the
paper published in Science by the Imperial group in April, and
also the paper published in Nature in October, it investigates,
if you did not do the contiguous cull, what would have been the
number of farms infected; and it is poorly understood that the
contiguous cull saved animal lives, so, of course, there was the
sacrifice of some uninfected animals, and I thought Professor
King and Dr Grenfell and Professor Woolhouse explained the science
behind that very, very clearly. But the point that is not generally
reported in the press is, the contiguous cull, in the view of
the scientists who were involved in this analysis and DEFRA scientists,
saved animal lives.
233. Who first asked you, and when, to construct
this model of the outbreak?
(Professor Anderson) I have to refer to some notes
about the time, because the facts are so important. The first
case was confirmed on February 20; on the 24th we had an informal
discussion in the department at Imperial, decided to encourage
some work to look at what the potential course of this epidemic
would be. In the last week of February, I had a `phone call from
Sir John Krebs at the Food Standards Agency, who said, "Are
you looking at this privately?" and I said, yes, we had;
he said, "Would it be helpful to organise a meeting to ensure
that you had prompt access to the data?" and we discussed
membership of that committee, who were the best people, not only
in Britain but more broadly, in Europe and the United States.
That committee was organised by Sir John Krebs. Subsequent to
that, we did some more work, very quickly, because it was quite
clear the epidemic was not under control, and at a subsequent
meeting of the Food Standards Agency, which John Krebs organised,
he invited David King. At that meeting, David King formally took
a detailed interest in the problem and constituted the Science
Group, and then for the following month we were asked questions
almost daily, particularly at one stage, about, if you did this
what impact would it have. And two young people, Christl Donnelly
and Neil Ferguson, worked seven days a week, very, very long hours,
to try to refine this model, estimate the parameters, put together
the database, to be able to respond to these more policy-orientated
questions. It was done on a faster timescale than I have ever
been involved in an infectious disease problem, and, as you can
understand, there was extreme nervousness in the research group
about making predictions of an epidemic's course on the initial
exponential rise, and all of us felt very, very uncertain about
what the future was, but we believed that the scientific methods
being used were the best available at that time.
234. I remember you coming before, in the previous
Select Committee, because it was at that place I first began to
realise the election was going to be in June, when I saw your
charts. But it is interesting. This model, it seems to me, led
directly to, and led you to advocate, the contiguous cull. It
is important, therefore, to know when this bump here emerged,
because suddenly the predictions start going down, based on the
assumption of `slaughter on infected and neighbouring farms within
48 hours'; so at what stage was that line, C, inserted?
(Professor Anderson) The results were given virtually
instantaneously to the Office of Science and Technology, so anything
they released that has a date on it, that probably is literally
about one day before the results were produced. So they transmitted
electronically as soon as the results were finished.
235. But that line was developed before the
contiguous cull was introduced?
(Professor Anderson) Yes.
236. A lot of the analysis depends on the information
you are feeding in, and you cannot have known at this early stage
how widespread the infection was beforehand, you cannot have known
whether it came from Heddon-on-the-Wall, or whether it was in
sheep in various areas, as has also been suggested; a lot of the
information you were feeding in to develop that prediction must
have been faulty?
(Professor Anderson) A lot of the information was
incomplete, it always is in epidemic processes. DEFRA very kindly
shared, via John Wilesmith at Weybridge, the information on the
contact tracing from the original market movements, and that gave
us a hint on, what is rather important, a spatial kernel of transmission.
It is the probability that the disease had transmitted a certain
distance. And what one could see from the very early stages of
the epidemic was there were many long-distance transmission events,
and, in my own experience of dealing with epidemic outbreaks,
that was very good information at that point in time; it was subsequently
revised, as more data came in, but, in terms of contact tracing
data, that was as good as you can get, and I was impressed that
DEFRA had actually got that so quickly.
237. There were other models as well, were there
not?
(Professor Anderson) Yes.
238. Did they point in the same way?
(Professor Anderson) My experience of scientific committees,
they often form a circle and shoot inwards, as it were, and this
was an unusual illustration, in my view, of totally different
scientific groups, using different methods, coming up with a broad
consensus in not only qualitative detail but quantitative detail,
and I had never seen that before.
239. And all pointing to contiguous kill?
(Professor Anderson) Yes.
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