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
excellentunfortunately, 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 infectionsI 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
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
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
humansrelative, 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 strainswe 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 1a
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 coercionthe 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