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

Examination of Witness (Questions 224 - 239)



  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.


  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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