Select Committee on Agriculture Memoranda

Letter to the Committee Chairman from Dr A G Dickinson (R 11)

  I have not submitted any evidence to your Committee and this letter is intended to explain why. The enclosed copy of Hugh Pennington's Review of the Phillips Report [not printed] explains my involvement with TSE research, which has been longer than for anyone else world-wide.

  I was one of the half-dozen who put a great deal of effort into arguing for a BSE Inquiry to be set up, as I had been close to the subject over several decades. The Phillips Report has, with one major exception, been widely regarded as excellent—unfortunately, its science section is unsatisfactory in many respects. This is not surprising because this subject is at the frontier of knowledge and Lord Phillips deliberately excluded from his team anyone with direct involvement in TSE research (he rightly criticises various BSE committees for doing this).

  Some still disapprove of there having been a public inquiry, but they do not realise that the alternative was that we would now be half way through a High Court action lasting twice as long as Phillips took, with adversarial methods potentially doing untold co-lateral damage to both groups of victims (livestock farmers and vCJD families), but almost certainly failing to reveal the main aspects leading to the epidemic (I speak from the experience of having raised the warning, seven years in advance, that human growth hormone could be CJD-contaminated).

  From the wording of your Committee's invitation for the submission of written evidence, the Phillips Report is being assumed to be a sound basis from which to asses the "scale and focus of MAFF's research into TSEs". Because I am trying to be as constructive as possible, I hope that you will not be offended by commenting that it seems to me that the nearly impossible is being attempted. Unless the breadth of this subject is thoroughly understood by those concerned, along with all the technical limitations involved in interpreting the research, "scope and focus" cannot be judged. With the aim of being helpful, I will include a few examples of important unresolved issues which could provide a constructive basis for your inquiry.

  Since I started in this research in 1955, of the many committees intended to appraise or fund TSE work, there have been hardly any that have been of value. Many have had very wasteful or harmful consequences, because they comprised busy "experts" from other fields, who recommended the current scientific band-wagons (in 1955 for a scrapie vaccine or in 1988-89 ill-considered overemphasis on PrP) or the blatantly obvious (the need since 1960 for diagnostic tests). However, by making recommendations they succeeded in deflecting funds from other important aspects. During the BSE epidemic there has been extensive waste of the large, mainly MAFF-controlled, research funds. This is a view shared by many of those with proven TSE-research expertise, some of whom are still involved in the research and therefore too prudent or intimidated to publicise their opinions.

  There were two types of reason why BSE funding has been very wastefully focused. One, from the late 1980s, was the plethora of research committees controlling the policy and funds, hardly any of whose members were familiar with the subject, but who were mesmerised by the hype surrounding the protein, PrP. In 1971 I discovered the crucial role of this protein in the pathogenesis of the disease and published this along with a range of predictions, most of which have now been confirmed. You may be assuming that the molecular nature of TSE agents has been "proved" to be, simply, a modified form of this protein (a so-called "rogue protein"), but the number of those who doubt this is steadily growing, if only for the reason that this hypothesis has never been able to explain the facts, and such anomalies progressively increase in number. This short-sighted view of molecular aspects deflected funding away from several important areas. One vital aspect from which work was deflected for a decade after 1988 was the investigation of substances (polyanions) which have the prospect of providing therapies for TSE infections—I drew the Inquiry's attention to this lapse in my Statement.

  The second reason for considerable waste of funds was that staff at the Central Veterinary Lab, who were inexperienced with TSE research, controlled early decisions. An example of where this proved very costly was their misjudged decision to base routine BSE diagnosis on neuropathology, rather than on our quick, cheap 1986 biochemical assay, which would, importantly, also have been applicable to tissue from dead cattle that was unsuitable for neuropathology.

  The foregoing relates to the past but is symptomatic of the present. Three current examples are given below under separate headings. The first example still remains as the most important issue needing active debate and good experiments, because it may become necessary to undo public misconceptions about whether or not the BSE strain of agent per se is more dangerous to humans than other TSE strains. The impression created since 1996 by governments and the media has certainly been that it is a more dangerous strain, but where is the hard evidence?

 (1)   The unresolved question is whether the TSE strain that causes BSE and vCJD is intrinsically more easily transmitted to other species, including humans, than other TSE strains. [This issue was presented to the BSE Inquiry in paragraphs 4-9 of my Statement.]

  The misleading word that has been most popular with the media in recent years to describe BSE being transferred to another species is that it "jumped". I am certain that a more accurate term is that it was "pushed". In order to "push" one of these types of agents across to another species, the greater the amount of infective agent involved, the more likely it is to achieve infection of the other species. My assessment of the current situation with the transfer of BSE to humans, is that the whole picture could be explained solely in terms of the enormous scale of the BSE epidemic having massively exposed people to the otherwise very small risk of being infected.

  It is only because of the precautionary principle that the provisional assumption has to be made that the BSE strain is very much more liable to infect humans than strains that have been present in sheep for hundreds of years. For 15 years we have urgently needed to know the relative risk of the BSE strain to humans—relative, that is, compared with other strains of TSEs. I am not aware of any properly designed experiments with this objective: enquiries whether some are, at last, in progress have been unproductive.

  It is often claimed that no scrapie strain has infected humans, but this is an unjustified extrapolation. What has been well established is that if any scrapie strain has passed from sheep to humans, this must be such a rare event that it has not been detected as a component of the 1:50,000 rate of incidence of CJD in humans. It seems reasonable to conclude that the scale of exposure of humans to scrapie strains during the 20th century will have been vastly less than that to the BSE strain during the epidemic. The simple observation that humans and several other species have become infected with BSE proves nothing about whether it transmits more easily to other species when the same doses of different strains of infective agent are compared. The cases seen in other species can be explained either by the massive scale of exposure to BSE agent afforded by the epidemic, or by the BSE strain having "higher infectiousness" for other species, or both. Its known greater thermal stability than other strains may well be an important aspect of this. The Phillips Report, unfortunately, jumps to a premature conclusion on this whole question, but that is not their only lapse.

  I am certainly not arguing that the BSE strain will prove to be no more dangerous to other species than most TSE strains—we must have hard facts. An extensive range of experiments is urgently needed, comparing the relative transmissibilities of various TSE strains with the BSE strain: these must cover a full range of doses of agent and species sources, and must examine several routes of potential infection. The work will need to be done in several species.

 (2)   The search for the BSE strain in the sheep population

  Whether or not it should be a very high priority to search for the BSE strain in British sheep (or even world-wide) depends on the outcome of work under the previous heading. There have been hints of MAFF contingency plans to deal with British flocks on a draconian scale should the BSE strain be found, which heightens the urgency of answering the underlying question. But, at least, the Phillips Report kills off over a decade of MAFF propagation of the unsupported claim that the BSE strain originated on many occasions from scrapie strains being transferred to cattle in Meat and Bone Meal. (Unfortunately, the Report backs an origin for BSE that is implausible in the extreme.)

  I was responsible for devising the type of strain-typing test needed for identifying different TSE strains and, with former colleagues at the Neuropathogenesis Unit (NPU), devised various means of separating component strains from mixtures. Nowhere else is there any such experience. It was a cause for amazement, therefore, when I heard that MAFF was funding attempts to search for particular strains in the UK sheep population by pooling the brains of sheep in batches, to economise this search. They will need considerable good luck with any such approach. I hope that they have run pilot trials with deliberate mixtures of a dozen known strains, along with the BSE strain, to test the proposition. At least, the NPU have declined to adopt any such method.

  This brain-pool approach sounds like another MAFF-associated emulation of the botched CVL design for cattle "maternal transmission" experiments, which largely wasted several million pounds and many years. Is it fair comment to recall that in 1986-87, as director of the NPU, I only had £75,000 for all our TSE research experiments, after paying salaries and overheads for nearly 40 staff?

 (3)   The National Scrapie Eradication Plan for GB

  The National Sheep Association know of my long-standing concern about the often unfounded speculations that have been damaging to their industry during the last decade.

  Late last year, I was shown a copy of the glossy MAFF booklet dealing with the scheme aimed to eradicate scrapie from British sheep by breeding from rams carrying a particular version of the gene which codes for the PrP protein. As I had done the pre-molecular groundwork for this, by 20 years of selecting sheep genetically for some variants of this gene, I am in a position to understand the potential complications. Indeed, it was long realised that the notion of a version of the gene that would "resist" all known (and future) strains of TSEs, may not be realistic. This was underlined by the fact that in 10 years of searching for a strain of scrapie agent that could break such a barrier, I had been lucky enough to find one, with approximately this property. Furthermore, this finding was not a surprise because the work with scrapie in mice had taught me to avoid the notion of genetic "resistance" to TSEs: this complication is fundamental to understanding of the whole subject and is widely unrecognised, for example on occasion by leading members of SEAC. The nagging possibility of "carrier-infections" with TSE agents is one aspect of this complication.

  Where the balance of judgement lies in the present context is dealt with in the response to the MAFF document appended to this letter, which is signed by four senior animal-disease scientists [not printed]. It came as a surprise that the booklet was issued as a "Consultation on proposals for Phase 1—a Ram Genotyping Scheme" when there appeared to have been several years of active support by MAFF for implementing this scheme. It seems to have the de facto status of an ongoing programme.

  In closing, I must query the implication underlying the stated objective of your Committee. A subject like BSE is far bigger than any single department should attempt to handle. A very significant error was that MAFF was intent on keeping exclusive control, for example, by their early determination to exclude the Government Chief Scientist.

  I consider it entirely inappropriate that any government department or group of departments (or their agencies) should control research on basic scientific issues, especially areas so near the frontier of knowledge. Such direct control should only involve practical and applied topics in well known areas. The research role of departments should focus almost entirely on having first-hand, comprehensive information about "who and where" there is success, but this must be staffed on criteria very different from present ones. Whitehall norms will need to be changed radically, where science is involved.

  The basic research should be funded so as to ensure its objectivity and freedom from coercion—the Research Councils, as originally created, were well conceived to achieve this. Radical changes are needed to avoid the administrative traps into which MAFF fell headlong, when it allowed a disease outbreak to turn into a huge epidemic.

25 January 2001

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