A letter to the now defunct Select
Committee on Agriculture, which was not meant to be published, but was by mistake!

(Many thanks to Alan Beat's Smallholders' Newsletter for this important letter See www.smallholders.org )

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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