Select Committee on Agriculture Minutes of Evidence

Examination of witnesses (Questions 400-419)



  400. Is it still the view of your advisers that the original source of the outbreak was the case at Heddon-on-the-Wall, at the pig farm?
  (Professor King) Why do I not pass it to one of the experts: Alex?
  (Dr Donaldson) I have no information to the contrary. That premise had animals with lesions which were 12 days old, or thereabouts, and the virus isolated from there was the same as that isolated from the abattoir at Essex; we have characterised the particular viruses involved.

  401. You are aware of statements made by others that there appear to have been cases in sheep, including one case which was sheep sent for export, I think, which indicated an earlier provenance of the virus within the sheep flock?
  (Dr Donaldson) I am aware of information, through our World Reference Laboratory, that French scientists claim that they tested sheep originating in the United Kingdom and found that there were antibodies in them; antibodies would be formed as a consequence of infection. We have asked for those antisera to verify the test results; that is more than a month ago, and we have not received the antisera.

  402. So, when you said you had no evidence, you meant that perhaps you might be able to obtain evidence through that request but it has not yet arrived?
  (Dr Donaldson) That is correct.

  403. Assuming that the origin of the outbreak was at Heddon-on-the-Wall, can all of the outbreaks that have happened since be traced back, through some contact or other, to that source, or are there any mysteries that we have not been able to trace back?
  (Dr Ferguson) Certainly, for the early stage of the epidemic, MAFF did a very good job of doing exactly that sort of tracing, particularly through the livestock markets, Longtown, Welshpool and the other ones, which were so influential in causing the epidemic to spread. And just returning to the question of infected areas, I think one of the reasons the infected areas were made so wide early on was because it was known that the markets were playing such an important role and the infection was so disseminated, even if we had not seen it yet in areas. I think, more recently, there have been the occasional outbreaks geographically distant from existing ones, particularly around the Cumbria region but also elsewhere, going into the Forest of Dean and Gloucestershire, which have not had such a clearly identifiable source. But given that we know the virus can spread a considerable distance, whether wind-borne or whether on vehicles, or being transported by man, then that is not all that surprising.

  404. Have you been able to identify the most common sources of transit, transmission, from this; you have mentioned that there are a variety, and at various times statements have been made that wind-borne transmission has actually been surprisingly low, in incidence, in this particular outbreak, and that it appears likely that relatively close contact is the most common transmission route?
  (Dr Donaldson) I think this particular epidemic is no different from any other involving foot and mouth disease, in that the most common mechanism of spread is contact between infected and susceptible animals. In this particular epidemic, sheep, in particular, have played a major role in that, and, I think, if one is looking for a major factor in spread, it has been the involvement of sheep, in which the disease is often clinically very mild, or even inapparent. Enormous numbers of sheep moved in the early stages and, I think, contributed both to the scale of the epidemic and the speed of its spread.

  405. One might say that that might indicate the importance of tracking down this French data with some degree of urgency, because, as you have said, and certainly from my own experience, this disease is extremely difficult to spot in sheep, and I have had many cases drawn to my attention where the disease has been and gone without anyone noticing it, because it is so similar to other infections that a sheep can have. If we turn to the modelling exercise that was done on 23 March, I assume that the reason why it was done only some month and a bit after the first outbreak was the poverty of data that would have been available to produce any adequate models; is that right?
  (Dr Ferguson) In part. Personally, I had started developing, and I am sure the other groups were looking at the sorts of models which could be done, but in the initial meeting at the Food Standards Agency, which I think was 8 March, we did discuss the fact that more data would be required. And, in fact, by the time we actually started the analysis properly, about 14 March, or so, when we received the data, we did actually receive quite good quality data despite the fact case numbers were small, particularly the contact tracing data; that data took time to collect, and it was vital to the analyses, and I am sure Dr Woolhouse would agree with that. And so, yes, there is a limit to what could have been done earlier. Possibly, had we been involved very slightly earlier, we could have done something a week or so before, but certainly no more than that.

  406. What other factors are put into the model? We have mentioned that there are a large number of variables affecting the way in which this disease is spread: weather conditions, the geography of the area, the precise breed of animal that is infective, and so on. What assumptions are placed in the various models? I recognise also there are at least three different models that are being used?
  (Professor King) I wonder if I could just stress that point, first of all. There are four teams of modellers involved and each of them is working quite independently, although there is a common source of information. John Wilesmith, at MAFF, has been the common source of information, and John himself is a modeller and so he has been doing modelling as well. But, in terms of the input, I am going to leave you to these two here.
  (Dr Ferguson) I would say I agree. It depends on exactly which model you are talking about, and you have trade-offs, basically, with modelling. You can build a very complex model which describes every little bit of detail; the problem is, there, you need very big computers to run it on, and quite often, with the level of detail you have to put into it, you do not have actually the precise quantitative parameter values to make that model worthwhile. So there is a trade-off in how much complexity you put in. In terms of the model I have been involved in developing, it is one of the simpler ones, it allows partially for the spatial spread, so it allows you to look at ring-culling, comparing policies; it does not go down to the details of looking at all differences between individual animal breeds or species, necessarily, but does account for some. You can then apply it though to look at, say, one of the key differences, which is regional heterogeneity, by applying it to the different regions. Other models—and Bryan Grenfell, from Cambridge, is not here today, so I will try to speak for him—have put more detail in, in terms of describing transmission between individual farms, as a kind of random process, allowing for more heterogeneity: differences between farms, in terms of numbers of animals, different species. That is a much more complex model; potentially it has more power, but it takes a lot more computer power to run it, and you can do many fewer things with this in a fixed amount of time. So there is a trade-off. One of the encouraging things though is, in terms of the broad conclusions of all the modelling efforts, and I will hand over to Mark, for the last two, to describe what he has been doing, they have been so broadly similar, in terms of their . . .

  407. I was going to say; from what you have said, in spite of the fact they are using different techniques—
  (Dr Ferguson) Yes; they have been broadly similar.

  408. From the graphs you produced, they produced roughly the same outcomes?
  (Dr Ferguson) Roughly the same results. It is, of course, easy, to some extent, and I understand this both from the lay person's point of view and from the experimentalist's point of view, to say: "Well, you haven't taken account of this key factor". And I think one of the long experiences of doing this sort of mathematical modelling for infectious diseases and other systems is you can get a surprisingly good insight into the behaviour of these diseases, actually leaving out a lot of the detail, and sometimes it is best to do that if you want a rapid answer. But I will let Mark Woolhouse also speak to the same issue.
  (Professor King) What I wanted to say is the following, that the group represented by the gentlemen on my left are the most fleet-footed of the modellers, and the reason is not only that they work right through the night but that their model is a relatively simple one, it is what we call a `mean-field' model, and the field there is not spaces on a farmland. On the other hand, what gave me confidence was the fact that the more detailed models, such as the Cambridge model and the Wilesmith model, were producing results which were broadly very compatible with the Imperial College model. This allowed me then to talk in great detail to the Imperial College modellers and say, "Would you please try a variation, for example, the 24-hour cull, what if we let it go up, what if we bring it down; equally, the 48-hour cull, what if we let that relax down to seven days, what effect does it have; what if we don't have a ring-cull and just a 24-hour cull?" So all of these results were available because of the fast capability of the Imperial College model. But the essential thing to me was that I was getting the same answers from the others, however slow. I do not know if Mark wants to add something.
  (Professor Woolhouse) I hope we are not one of the slower ones. I think the crucial thing about using mathematical models to advise policy-makers is that different models have different strengths in answering different questions. The question we were all asked, at the meeting on March 23, was a very simple question for an epidemiologist, "Is this epidemic out of control?" The answer was a unanimous "Yes," by our definition, which Professor King gave you earlier. The next question we were asked was, "Would a culling policy be appropriate for controlling this epidemic?", and the unanimous answer there was that a 24-hour culling policy was essential. And, in fact, going back to an earlier question of yours, that was actually known before any of the modellers got in, there was published literature to that effect. But "Was a 24-hour culling policy essential?", answer "Yes," unanimously; and "Would it be enough?", answer "No, not on current estimates." And that, of course, was the basis for introducing the contiguous cull.

  409. Without taking the slightly political tone of Owen, opposite, one of the factors in this, well, the key factor, is the data that you put into your model, and, clearly, there must be some influence, if you are tracking the number of outbreaks, which is what you are doing, if you classify outbreaks in slightly different ways. So, through the success of the policy that has been engaged in, which is to cull out neighbouring, contiguous farms, where the outbreak has not happened but would otherwise have done if those measures had not been taken, to some extent, you produce a self-fulfilling process, in which the number of outbreaks appears to go down because you are culling out the ones that would otherwise have been counted in that data. It might be useful for you to explain?
  (Professor Woolhouse) I can answer that specifically. What we have been able to do is to explore different interpretations of the data, to test the data for robustness regarding the models; we have done that extensively. Epidemiologists are very cynical, we do not always believe field data collected in a rush, we always test the data, we check for quality, we say, "Well, what if this wasn't true, would the scenario still hold?". And, again, after extensive simulations, we would argue, yes. One important thing about our results is that they are conservative, in the sense that we would not claim the epidemic was under control, for example, when it was not. We would not claim that a control policy would be more effective than it would be; we think this is very important for helping policy-makers. So all our estimates and projections are conservative, in those senses.

Mr Öpik

  410. I want to talk about control policies. One of your colleagues, Dr Paul Kitching, said, on Saturday evening on the Channel Four News, that there were big differences between this and the '67 outbreak. He said production of aerosol viruses from this particular virus is considerably reduced, work carried out at your institution had already shown that aerosol production of the strain was much less from pigs than from previous strains. And yet it does seem that the '67 outbreak has been the main driver of policy on this occasion, even though it does seem that there could be a case to argue that the virus had been on farms for a long time, in sheep. So the two questions I have got really are, to what extent is it appropriate for us to base our treatment of this outbreak on the '67 experience, and, secondly, if sheep may have had it for much longer than just a few days, why the urgency on the 24-hour cull?
  (Professor King) Can I stress, first of all, that it would be incorrect to say that our policy was based on the '67/'68 outbreak. We came in—and, I have to say, Chairman, I had the benefit of the most remarkable scientific help in this process; some of those people are represented here. I do not know that there was anything like that understanding of the outbreak in '67/'68. And we have been able to advise the policy-makers on how to proceed. So I do not think it would be right to say that. It has been based on the modelling. Now, before I pass you over to the others, what I have also reproduced for you are some of these graphs that I presented to the media during the outbreak, and the first, which is labelled `Two' in the top right-hand corner, each of these are the output of the nimble-footed group, the Imperial College group, and you will see that this was the stage of the outbreak when we were getting involved and saying it was out of control. Curve A represents the `out of control' epidemic, in which the turnaround is related to the fact that you are losing all the animals, you are not getting it under control. Curve B corresponds to the 24-hour cull being introduced; and Curve C is the output of the model with this 24- plus 48-hour. Now at the point when we first showed this data we had no clear indication as to which way this epidemic would proceed; but if you turn the page you will see where we are at the present day, so that the black points represent how the epidemic has proceeded. And I think you would have to agree that the modellers have done remarkably well, that since the policy was introduced we have followed Curve C rather more closely than we have followed Curve B, or A. The criticism, Chairman, of the scientists would be that the epidemic is going below Curve C, they did not get it quite right, the epidemic is decaying faster than they predicted.


  411. The Bank of England is in difficulty because inflation is lower than predicted, but I do not think you will be in too much difficulty if the epidemic is lower than predicted, somehow.
  (Professor King) I am not avoiding your question but I am trying to answer it in a slightly different way. What we have is theory, predicting an output, and then the measurements coming in; and, as an experimental and theoretical scientist, that is often how I proceed. What I would say here is, "Well, that model wasn't bad; now what was the input to the model?" and the input to the model was the best input that was available at the time, as has already been described to you, based on the tracing, the detailed tracing, that MAFF had been doing in the early stages. Now Dr Donaldson's team, at Pirbright, together with Paul Kitching, who is a member of my committee, have discovered more about the disease; and the net result is that, surprise, surprise, the epidemiologists, particularly the group on my left, are getting a better description of the way the disease is spreading. So if you turn to not Curve 4 but Curve 5 you will see the red curve is their latest prediction about how the epidemic proceeds, based on all of the most recent inputs, so they have now tweaked the model to include the most recent input from the animal biologists. Now, at this point,—

  412. It seems to be a very fortuitous arrival at June 7, if I may say so.
  (Dr Ferguson) This was not enforced on the model!

Mr Öpik

  413. Karl Popper would be proud of this, by the way.
  (Professor King) I think it would be fair to ask Dr Donaldson to respond to your questions.
  (Dr Donaldson) Going back to the comparison between the '67/'68 epidemic and the current one, a feature of what happened in '67/'68 was that there was an explosive start to the epidemic, I am sure you are aware of that; that was attributed subsequently to the fact that pigs were infected initially, and probably released very potent, or highly concentrated, plumes of airborne virus, which spread across the Cheshire Plain, from near Oswestry, which was the source, over an area of high cattle density. We know now that, when we are looking at airborne spread of foot and mouth disease, which is a feature of the disease, and a very important feature of the disease, the pattern of airborne spread is most commonly from pigs, at source, they are the powerful emitters, to cattle downwind, who are the most sensitive species to infection. Those features were also part of the current epidemic at the early stages, from the abattoir at Essex and also from the farm at Heddon-on-the-Wall, leading to the infection of sheep, from Heddon-on-the-Wall, and then the distribution through the rest of the country, particularly to Cumbria and then to Devon, and other parts. You referred to Paul Kitching's statement, that this current strain is excreted by pigs to a lesser amount than we have found with previous strains, that is correct; however, although it is excreted to a lesser extent, it is still excreted at a very significant level. My view about the modelling, and I have said this within the group, and my colleague Paul Kitching has also said it, is that we feel that the modelling does not take sufficient account of the very great differences there are between different species in the doses required to infect them and the amounts they subsequently excrete. It is not a surprise that the modelling has close agreement for different groups because they are modelling what I would call an hypothetical species, and I think that needs to be borne in mind. Since they are not taking great account of species, I would suggest that there is an inherent inaccuracy in the forecasts. Going back to the question, earlier, from Mr Mark Todd, about the input data, my colleague Paul Kitching and I have reservations about the quality of the input data, and we have expressed that within the science group also, and it relates primarily to the role of sheep; we have spoken about sheep earlier and the fact that identification of infected sheep is difficult, therefore, it is very hard, we would say, or almost impossible in certain instances, to know what the lead-in time has been on certain infected premises. There has been a trend of sheep to be infected, to spread the infection silently and then to infect cattle, and cattle are the indicator species. But putting a time-frame to the period from the recognition of disease in cattle back to the introduction of infection of the sheep is, I would suggest, very difficult and could have a wide amount of variation; and I think those factors need to be considered, in looking at the modelling.

  Mr Öpik: That is a very useful clarification, and if I may follow up with a few short questions relating to some of the tactics around the issue. First of all, really for the record, what would happen if we took no action at all, in the United Kingdom, would the disease eventually become endemic, die out, would there be an immunity in the stock; leaving aside any questions about export, I am simply asking from a technical standpoint?


  414. Just a dose of flu; that syndrome?
  (Professor King) If we took no action at all, in particular, not even vaccinating cattle, then I believe the answer is that we would move into an endemic situation.

Mr Öpik

  415. What would be the long-term—once again, leaving aside any export question?
  (Professor King) Long term, you would have the disease popping up continuously; that is what we would mean by endemic.

  416. And how bad would that be for the animal population, in terms of health?
  (Dr Donaldson) I think someone has used the term `common cold'. The only common feature between common cold in man and foot and mouth disease in animals is that the mechanism of spread from infected to susceptible in contact animals is that the spread is very like common cold, it is spread in droplets and droplet nuclei, and, in susceptible animals, in most cases but not all, most commonly they become infected by inhalation and infection starts in the respiratory tract and then goes elsewhere, eventually producing vesicles. If we were to relax the control measures, I think, almost inevitably, as Professor King has indicated, the virus would become endemic in the United Kingdom; then you would get into a situation of a pattern of spread of the virus through the population, the establishment of a natural immunity, the waning of that immunity over time, as animals are replaced, and then another wave of infection. In countries, in Africa and South America, where they have not had the resource to control the disease, it tends to cycle at periods of every three to five years, and that reflects a susceptible population coming through. Might I add one comment, going right back to the very first questions? "Why have the slaughter out policy?" The justification for the slaughter out policy, horrible as it may be, is that it is a well-proven method of eliminating the possibility of convalescent carrier animals, and I mean by that animals that could be persistently infected. Total stamping out of infected herds is the only way of guaranteeing that that will not happen. If it is not done, if there is partial slaughter, and by that I mean if only the diseased animals are killed, then there is a high probability that the incubating animals, and perhaps some recovered animals, will continue to harbour the virus, and so you are tipping the balance very much towards an endemic situation.

  417. I have got two other short ones, but just to conclude on this particular heretical thought; should we be considering, as one possible option, the acceptance of this disease as an endemic disease in the United Kingdom, and perhaps across Europe, in your judgement?
  (Dr Donaldson) Absolutely not. The traditional methods of controlling foot and mouth disease are well proven, and if properly applied should eliminate the virus.

  418. Thank you for that. Just one, very short, other question. We were informed, on Monday, in our Select Committee, that the laboratory tests were not necessarily very reliable; how reliable are the laboratory tests that you are using currently to determine whether the infection, in fact, was present in a sample?
  (Professor King) These are serology tests that you are now asking about, as distinct from the PCR tests?

  419. Correct; yes.
  (Professor King) PCR tests for the virus, the serology tests for the antibody, and the serology tests are performed at the Pirbright Laboratory, so it is back to Alex.
  (Dr Donaldson) There is no doubt in my mind that we are using the most appropriate, sophisticated, sensitive and specific tests which are available. We have something like 70 years' experience of developing and improving on tests for foot and mouth disease. I am not sure what the basis of your question is.

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