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From: TSS ()
Date: July 11, 2005 at 11:43 am PST

In Reply to: THE MANIPULATION OF BSE/TSE SCIENCE IN PEER REVIEW JOURNALS ? posted by TSS on July 11, 2005 at 11:23 am:

----- Original Message -----
From: "Terry S. Singeltary Sr."
To: "Bovine Spongiform Encephalopathy"
Sent: Monday, July 11, 2005 1:46 PM

The BSE Inquiry / Statement No 67
Dr Iain McGill (scheduled to give oral evidence 08 June 98)
Statement by I S McGill
Curriculum Vitae
1. A brief CV is enclosed with this statement as Annex 1.
Periods particularly concerned with TSEs are as follows:
Spring/Summer 1988 Final Year Elective Research project
The astrocytic reaction in BSE and its comparison
with natural scrapie of sheep.
Royal Veterinary College (RVC), London University.
Performed at Pathology Dept, MAFF, CVL, Weybridge
Jan 1990 - Jun 1991 Veterinary Research Officer
Central Veterinary Laboratory (CVL), Weybridge.
Employer: MAFF
Funding Body: MAFF
Aug 1991 - Dec 1992 Post Doctoral Research Worker
Institute of Psychiatry, London University.
Employer: Institute of Psychiatry
Funding Body: AFRC
1994 - 1998 Director, Prion Interest Group
Independent Research Organisation.
Privately financed.
Incorporated as scientific wing of
Shift Ltd in 1995 : Company reg no 291 6731
Statement of Interests
2. I have no links of any nature with the farming community (other than
those from my work
with farms as a vet student or as a qualified vet) nor with the feedstock,
pet food or
rendering industries.
Advice to Governmental Committees
3. I have had no involvement in UK Governmental committees.I did, however,
act as
rapporteur for a conference of international experts held in 1990 at the
CVL. This was
held under the auspices of the Gibbs Committee, organised by Dr CJ Gibbs of
the National
Institutes of Health, Bethesda, USA. My draft report from this conference
was passed on
to MAFF. (The final report is at YB90/3.12/1.1)
How I became involved in work on TSEs.
4. In 1987/88, my final year at the RVC, the work of Gerald Wells and his
colleagues at the
CVL on BSE was the subject of much discussion. I approached Richard Barlow
Professor of Pathology at RVC, who had decades of experience in scrapie
research, with a
view to carrying out my final year elective research project outside the
RVC, with the
team at the CVL. He agreed to co-supervise a project with Gerald Wells.
5. The report of this work is available and also held in RVC library. The
external examiner
for this research was Dr W B Martin, at that time sitting on the Southwood
This research achieved first place in the year in professional examinations
and contributed
to the award of the Cecil Aulden Second Prize (second place throughout
6. Once qualified, I worked for 18 months in practice, and then returned to
the Pathology
Department of the CVL in January 1990, to continue my work with Mr Wells.
Commissioning and Funding
Work at CVL, Weybridge, commissioned by MAFF
7. At CVL most of the projects I worked on were commissioned and directly
funded by
MAFF. All the research I pursued was as an employee of MAFF, excepting work
my final year at the RVC, when I was supported by a student grant.
8. I think it is worthwhile making a few salient points about my day to day
work for MAFF.
The facilities of the Pathology Department and the quality of technical and
support were in general excellent and the scientists I worked with were of a
high calibre. Once the decision to fund a project had been reached, there
were no
restraints on rapidly seeking tangible results.
9. Publications arising from such work include references 2, 5, 7, 8 & 10 in
the list of
publications to be found at the end of this statement.
Uncommissioned Work at CVL, Weybridge
10. As I was not always encouraged to pursue work I regarded as essential, I
also worked on
projects (either practical or theoretical) beyond the narrow confines of
specific MAFF
commission. Often this was possible within my daily routine, but I would
have to ‘clock off’ from my MAFF job and work in my own time rather than
leave the
matter untouched.
11. Publications arising from non-commissioned work started whilst I was
still an employee of
MAFF include :
(i) Wood LJN, McGill IS, Done SH and Bradley R (1997). Neuropathology of
scrapie: a study of the distribution patterns of brain lesions in 222 cases
of natural
scrapie in sheep, 1982-1991; ref 12.
The project as a whole was commissioned by MAFF, but my own involvement was
voluntary (see para. 31).
(ii) Heretical Model of Scrapie (1991) paper to the annual conference of the
Association of veterinary Teachers and Research Workers, Scarborough 1991,
referred to in the Veterinary Record, 128, pp368-369.
See paras 52 et seq for details of research proposed to MAFF at this time.
(iii) Stack MJ, Aldrich AM, Davis LA (1997). Comparison of detergent and
enzyme combinations for the detection of scrapie-associated fibrils from the
nervous system of sheep naturally affected with scrapie. Journal of
Pathology, 1997, 116, pp.181-189 (J/CP/116/181).
12. Although this is not acknowledged in the published article, I introduced
Mick Stack to the
use of Subtilisin Carlsberg enzyme for SAF extraction, initially from
tissue. Following a theoretical discussion with Dr (now Professor) Ian Shaw
in 1991 I had
pioneered such use of this enzyme. My conceptual role (not commissioned by
MAFF) in
this work illustrates the sometimes unexpected fruits of the free pursuit of
scientific (as
opposed to Government) ideas.
Work at the Institute of Psychiatry funded by an AFRC Grant
13. Publications arising from this work include references 3, 4, 6 & 9 in
the attached list of
14. Two publications submitted to the Veterinary Record during this period
went unpublished.
(See para 22).
Constraints on publication of results
" Internal approval"
15. Every paper generated within MAFF is sent for approval by superiors; the
more serious
the topic (for example if the disease is zoonotic or notifiable), the higher
it is sent before
approval is given or refused. I only outline the system in operation within
MAFF at that
time, and it is not my intention to criticise individuals who were
performing their ascribed
roles within the structure of MAFF.
16. I would like to illustrate the process of ‘approval’ with reference to
the identification of
FSE and subsequent publication of findings. The first case of FSE was
discovered at
Bristol University by Janet Wyatt (now Bradshaw) working with Dr Geoff
Pearson and
others. Material was referred to Gerald Wells in April 1990 for his expert
opinion and he
passed histological sections to me for comment.
17. Over the next six months, the Bristol and Liverpool Veterinary Schools
(and possibly
others) and the CVL independently examined their archives of feline brains
to determine
whether this disease existed prior to the BSE epidemic, or whether it was a
new disease.
Neuropathological evidence suggested it was a new disease. This, along with
epidemiological and biochemical data, led Gerald Wells and myself to prepare
a paper for
an international TSE conference in Brussels including the indication that
there might be a
causal link between BSE and FSE. The abstract of this paper was faxed to
Brussels prior
to the conference for publication in a booklet for delegates. This abstract
(ref 5) includes
the suggestion of this link.
18. Following the conference, we prepared the full paper we had presented,
for publication in
a book of this European Commission-sponsored conference and sent it to our
for approval. (The correspondence which ensued in April and May 1991 is
found at
YB91/4.16/1.1;YB91/4.22/2.1;YB91/4.30/1.1;YB91/5.3/3.1). Specifically,
despite detailed
arguments supporting our statements, the following ultimatum was faxed to us
from the
then Assistant Chief Veterinary Officer, making it plain that he was taking
into account the
views of the then CVO:
“We are not willing for the paper to be published unless these references
removed. This may be unacceptable to the authors, in which case permission
publish is refused.”
19. Despite protestations that the body of the text would no longer agree
with the already
published abstract, and our detailed knowledge on the subject
notwithstanding, the edict
stood. We were left with little alternative but to amend the paper, which by
this time had
missed the original deadline for submission and was in danger of not being
published at all
(see correspondence above).
20. Subsequent to its publication in the conference book (ref 5), the paper
was also published
in a refereed journal (ref 7). The original abstract from ref 5 was then
also altered to agree
with the altered text. Specifically the words “with BSE” were removed from
the phrase
“epidemiological association with BSE”. I had left MAFF before this paper
was ever
21. This episode was described in Dispatches (Channel 4, 9pm Thursday 11th
1997), and on two separate occasions in. The Independent newspaper
and YB98/1.26/1.1).
Outright rejection of manuscripts submitted for publication, during
"Refereeing/Scrutineering" by Journals
22. The peer review system is in itself generally reasonable. However, an
issue of real concern
is that the Veterinary Record , the main channel of information for the
profession, failed to provide an open forum for discussion of the TSEs
throughout the
period of the terms of reference of the Inquiry.
23. The following is a chronology of papers submitted to the Veterinary
Record, but which
went unpublished:
1988: Letter entitled ‘Scrapie, Time to take HB Parry Seriously’
24. In this letter I stated that BSE had been officially confirmed as a TSE
(when much of the
veterinary profession still favoured a variety of alternate hypotheses). I
also suggested
that scrapie should be made a notifiable disease, and drew attention to the
work of HB
'James' Parry and the possibility that natural scrapie in sheep might be of
genetic origin.
25. I withdrew the letter following advice from Professor Barlow (who as far
as I can recall
had been contacted by MAFF and the Veterinary Record) that it might not be
in my
interests to pursue publication at that moment in time.
26. I received a letter from the then editor, Edward Boden, questioning my
permission to
release the information that BSE was indeed a proven TSE. I had no
permission, though
was unaware that any was needed, to inform my profession of this urgent and
1992: McGill and Wood
27. This paper summarises views as to why an open debate on TSEs and in
particular scrapie
were and remain essential. We drew attention to the work of Parry, Prusiner
and others,
and outlined novel explanations for recent research findings in light of
such work. We
suggested that not all the relevant questions were being asked in the
interpretation of data.
In particular, the possibility that the infectious agent was being generated
de novo from the
genome (the PrP gene) in certain families of sheep, was still not being
considered, despite
a body of scientific data going back over 30 years. It was to be a further 5
years before
publications from Government laboratories would start to cite Parry’s work
as a possibly
correct theory.
28. The refereeing process for this work was at the time not transparent,
and I have yet to be
informed as to why this remains unpublished.
29. 1992 Book review commissioned - on “Sub-Acute Spongiform
Encephalopathies” Eds.
Bradley, Savey & Marchant, Kluwer Academic Publishers, Dorchelt, for the
of the European Communities.
30. On 13th May 1992, I was commissioned by the Veterinary Record to review
this book
(YB92/5.13/1.1). After approximately 100 hours work for this review, an
decision was taken not to publish. Ironically, this book contained the very
paper by
Gerald Wells and myself over which "censorship" has been alleged.
Prolonged delay during "Refereeing/Scrutineering" of manuscripts submitted
1997 Wood McGill Done and Bradley (ref 12).
31. This work was started in 1990 to screen for putative BSE in sheep, by
James Wood, a
colleague in the Pathology Department at CVL, although it was not finally
published until
1997. James sought my assistance in light of my greater experience in TSE
pathology. I
worked many many months to get this paper into print (YB95/6.29/2.1;
refereeing process took two years, hardly an acceptable delay for crucial
work in this
field. The referees’ comments (YB95/6.29/2.2) themselves require scrutiny.
scrutineer seemed to referee the paper in a balanced way, whilst the other
seemed more
intent on pushing his/her own opinions onto the paper.
32. Publication was finally expedited in the summer of 1996, when the
politically sensitive
question of whether or not BSE had indeed gone into the sheep population
started to be
asked in the public domain. This paper finally appeared (with some important
and watering down) in 1997, seven years after it was started, and two years
after it was
submitted. It was jointly funded by MAFF and the Prion Interest Group.
33. Had my ongoing research into sheep scrapie been funded and/or the McGill
and Wood
1992 paper been published, stimulating debate and further investigations,
this paper would
most certainly have appeared by 1995. Further work based on it could have
by 1997 whether or not, and if so to what extent, BSE had gone into sheep.
34. In addition, the work may by now have led to a rapid diagnostic test and
a great deal of
information on the actual (as opposed to the theoretical/experimental)
causes of sheep
scrapie and the fundamental biology of this entire group of diseases. Some
of the work
suggested in 1991 has still not been started.
Aspects of TSE work with which I was involved
Analysis of the astrocytic response in BSE and its comparison with natural
35. I worked as a neuropathologist with Gerald Wells to establish that
astrocytic reaction, one
of the fundamental triad of neuropathological changes occurring in TSEs, was
present in BSE. This work was accomplished using antibodies to GFAP (a
component characteristic of astrocytes) to quantify previously qualitative
that an astrocytic reaction was present. The astrocytic reaction in natural
sheep scrapie
was assessed in parallel.
Published: 1988 RVC library.
1991 (Wells, Wilesmith and McGill) - details of astrocytic response in BSE
1997 (Wood, McGill, Done and Bradley) - details of astrocytic response in
natural sheep
Surveillance for emerging scrapie-like diseases in animals in the UK
36. Working with Gerald Wells and other pathologists from the State
Veterinary Service, I
was involved with surveillance for neurological disease of animals in the
UK. This was
with particular reference to surveillance for, and subsequent confirmation
of TSEs.
During my time of employment, novel TSEs arose in domestic cats and in
exotic ungulates
in zoological collections. I also became involved in the investigation of a
putative TSE in
hound packs detected by Robert Higgins.
FSE, and BSE in exotic ungulates published in reviews:
1991 (Wells and McGill) ref 5
1992 (Wells and McGill) ref 7
FSE discussed in para 15.
37. Putative TSE in hounds - work started 1990 –(see para 41)
Robert Higgins, a Veterinary Investigation Officer at Thirsk, had been
working on a
hound survey in 1990. Gerald Wells and I myself received histological
sections from this
survey along with the accompanying letter (YB90/11.28/1.1) dated November
1990. This
letter details spongiform changes found in brains from hunt hounds failing
to keep up with
the rest of the pack, along with the results of SAF extractions from fresh
brain material
from these same animals. SAFs were not found in brains unless spongiform
changes were
also present. The spongiform changes were not pathognomonic (ie. conclusive
proof) for
prion disease, as they were atypical, being largely present in white matter
rather than grey
matter in the brain and spinal cord. However, Tony Scott, then head of
microscopy work on TSEs, had no doubt that these SAFs were genuine and that
hounds therefore must have had a scrapie-like disease. I reviewed all the
sections myself
(original notes appended) and although the pathology was not typical, I
could not exclude
the possibility that this was a scrapie-like disorder, as white matter
vacuolation is seen in
TSEs and Wallerian degeneration was also present in the white matter of the
another feature of scrapie.
38. I reviewed the literature on hound neuropathology, and discovered that
micrographs and
descriptive neuropathology from papers on ‘hound ataxia’ mirrored those in
material from
Robert Higgins’ hound survey. Dr Tony Palmer (Cambridge) had done much of
work, and I obtained original sections from hound ataxia cases from him.
This enabled me
provisionally to conclude that Robert Higgins had in all probability
detected hound ataxia,
but also that hound ataxia itself was possibly a TSE. Gerald Wells confirmed
in ‘blind’
examination of single restricted microscopic fields that there was no
distinction between
the white matter vacuolation present in BSE and scrapie cases, and that
occurring in
hound ataxia and the hound survey cases.
39. Hound ataxia had reportedly been occurring since the 1930’s, and a known
risk factor for
its development was the feeding to hounds of downer cows, and particularly
bovine offal.
Circumstantial evidence suggests that bovine offal may also be causal in
FSE, and TME in
mink. Despite the inconclusive nature of the neuropathology, it was clearly
evident that
this putative canine spongiform encephalopathy merited further
40. The inconclusive results in hounds were never confirmed, nor was the
link with hound
ataxia pursued. I telephoned Robert Higgins six years after he first sent
the slides to CVL.
I was informed that despite his submitting a yearly report to the CVO
including the
suggestion that the hound work be continued, no further work had been done
since 1991.
This was surprising, to say the very least.
41. The hound work could have provided valuable evidence that a scrapie-like
agent may have
been present in cattle offal long before the BSE epidemic was recognised.
hound survey remains unpublished.
Histopathological support to various other published MAFF experiments
42. These included neuropathological examination of material from
experiments studying the
attempted transmission of BSE to chickens and pigs (CVL 1991) and to mice
Neuropathological findings in cattle with clinically suspect but
histologically unconfirmed
bovine spongiform encephalopathy
43. This was my main project during my employment at MAFF.
44. At this time, approximately 10% of cattle suspected of having BSE were
not being
diagnosed as BSE-positive. The purpose of this work was to establish what
other diseases
were being clinically mistaken for BSE and causing these cattle to be taken
as suspects
under the BSE Order.
45. Upon closer examination, three of the 200 ‘BSE-negative’ brains proved
positive for
spongiform changes diagnostic of BSE (see YB87/12.14/1.2; YB87/12.15/2.1).
represents an overall diagnostic accuracy of 99.85%, exceeding the 99.6%
published for the same standard diagnostic technique. Despite this, at the
behest of MAFF
managers, the emphasis of the study and its provisional title had to be
changed, from
accurately representing the whole negative 10%, to a study examining this
10% minus any
mention whatsoever of BSE-affected cattle going undiagnosed. I therefore had
reluctantly locate and analyse three new BSE-negative suspect brains.
46. Discussion of this would according to MAFF officials have resulted in
‘lack of clarity’ and
opened up debate as to the accuracy of diagnosis.
47. Although this may seem a minor consideration, it illustrates the
kneejerk and perhaps
unnecessary culture of secrecy operating within MAFF at that time.
48. As it was also a theoretical possibility that cases of BSE might exist
without the
characteristic spongiform changes, a further purpose of this work was to
examine selected
cases using immunocytochemistry for PrP to determine if any had BSE but
lacked the
characteristic pathology. Although the sensitivity of the technique used has
dramatically since then, none were found at this time, and this was one of
the important
findings of the paper which was published.
49. In a number of informal conversations at that time, managers within MAFF
let me know
that the upper echelons of MAFF “had had it up to here with you scientists
finding out
about new diseases”. As a Veterinary Research Officer employed in disease
surveillance, I
had considered that to be my job.
Published 1993 (McGill and Wells) ref 10
Theoretical models of TSE diseases
50. Published in the Veterinary Record 1991 (J/VR/128/368) as editorial of
conference. In 1991 Martin Alder, new editor of the. Veterinary Record ,
published a very
favourable account of my theoretical paper presented at AVTRW 1991 in
under the heading “Heretical Model of Scrapie”. The Chairman of this session
was Bill
Blakemore, Cambridge Vet School. It was printed (after consultation with me)
in an
editorial article “Fruits of Research On Show in Scarborough”. He devoted
more column inches to work by myself and Kenton Morgan than to work reported
NPU, although they had presented far more papers. It was to be the last time
my name
would appear in the Veterinary Record until 1997.
Unpublished 1988, 1992
Establishing that human prion disease can exist without characteristic
51. This was the first conclusive proof that prion diseases can indeed exist
without any of the
characteristic pathology, extending the phenotypic diversity of prion
Published 1992 (Lantos, McGill et al) ref. 6
Setting up in vitro models of human prion diseases (GSS, familial CJD) in
cells in culture
(Resigned half way through project)
Neuropathology of natural sheep scrapie.
Started 1990, submitted 1995, published 1997 (Wood, McGill et al) ref 12
See para 11 for details of this work.
Contact with / Advice to Government
Contact with CVL / MAFF
52. I maintained regular contact with scientists at the CVL until 1997.
53. I cannot catalogue all the information, advice or recommendations I
offered to MAFF or
CVL between 1988 and 1997, as there is too much to include. However, I could
with the following summary of two substantive suggestions for research.
Research on the biochemical/physical nature of “strains”
54. Prior to their publication as an editorial in the Veterinary Record, a
summary of these
ideas was presented to the CVL management for funding as a ‘blue sky’ PhD
project in
Spring 1991. The proposal was not taken up. This was the first occasion on
which I
proposed research to the Government in writing.
An abattoir survey for incidence of BSE
55. I suggested in 1990 that to improve the provision of control material I
should collect 20
cattle heads from a local abattoir.The purpose of this was to provide
material to act as controls for our (CVL’s) BSE work. However,
examination of these brains might also have given an indication of the
number of cattle
incubating BSE which were entering the human food chain. This research had
been recommended in the Interim Report of the Tyrrell Committee, June 89.
56. I was instructed a few days after suggesting this to my head of
department that I was not
the first person to have thought of that, and that a decision had been taken
not to do that
research. I was also instructed, for some reason, not to put it in writing.
57. Budgets could hardly have been an issue contributing to the rejection of
this proposal, as
tongueless cattle heads were free, being banned from human consumption.
Contact with AFRC
58. I had contact with the AFRC in several capacities:
My work at the Institute of Psychiatry was funded by an AFRC grant.
Attending BSE Programme conferences in 1992 and 1994.
Submitted a further grant application to the AFRC in 1991.
59. This proposal was to continue research on natural scrapie, with which I
had been involved
at CVL (eventually published 1997; ref 12). I was to collaborate with John
(molecular neurobiologist) and David Male (co-author of the standard
Immunology text
worldwide: Roitt, Brostoff and Male). All five referees gave positive
statements about the
proposal, which was alpha-rated (see YB92/12.10/1.1 and YB92/12.17/1.1).
60. This was the second time that I suggested substantial investigations on
the TSEs to the
government in writing. Once more the proposal was not taken up.
61. In view of the continuing uncertainties as to the degree to which BSE
has affected the
sheep population, it would perhaps have been wise to fund this application
at that time.
62. Some of this work has still not been initiated, although the paper
(Wood, McGill et al
1997), after a two year delay from submission to publication, and the
original 1992 AFRC
grant submission, both described a unique series of characterised sheep
brains affected
with naturally occuring TSEs. The majority of them are natural scrapie
although further
work on this series of brains would give an indication of whether BSE was
also occurring
in sheep in the 1980s and early 1990s. Events have moved forward since this
application was submitted, both in the nvCJD and scrapie fields, but this
still represents a
crucial question in the epidemiology of both scrapie and BSE which remains
This work should, in my opinion, be initiated forthwith, and further work
based on these
results pursued vigorously as results are obtained.Refer to discussion also
at para 31.
Additional Comments
63. I could perhaps sum up MAFF’s approach to BSE with an observation which
is by no
means original:
“Absence of evidence” is not the same as “evidence of absence”
1. McGill IS (1986) The Shortcut to Elitism. The Guardian, December 1st,
2. Wells GAH, Wilesmith, JW & McGill IS (1991) Bovine spongiform
encephalopathy - a neuropathological perspective. Brain Pathology, 1, 69-78
3. McGill IS (1991) Bovine Spongiform Encephalopathy. In: Practical Food
Ed. Dickens T, Croner Publications Ltd, Kingston, UK, pp. 435-436
4. McGill IS & Whatley SA (1991) Understanding the causes of brain disease.
Independent, August 16th, p. 20
5. Wells GAH & McGill IS (1991) Recently described scrapie-like
encephalopathies of
animals - case definitions. In: Sub-acute Spongiform Encephalopathies, Eds.
R, Savey M & Marchant B, Kluwer Academic Publishers, Dorchelt, pp. 11-24.
6. Lantos P, McGill IS, Janota I, Doey J, Collinge J, Bruce M, Whatley SA,
Anderton BH, Clinton J, Roberts GW & Rosser N (1992) Prion protein
immunocytochemistry helps to establish the true incidence of prion disease.
Neuroscience Letters, 147, 67-71
7. Wells GAH & McGill IS (1992) Recently described scrapie-like
encephalopathies of
animals - case definitions. Research in Veterinary Science, 53, 1-10
8. Pollin MM, McGill IS & Wells GAH (1992) The differential
diagnoses of clinically suspect but unconfirmed BSE. Neuropathology and
Neurobiology, 18, 633 (abstract)
9. Guha M & McGill IS (1992) Book review of Black's Veterinary Dictionary
Edition), Ed, West GP, A & C Black, London. Reference Reviews, 6, 26
10. McGill IS & Wells GAH (1993). Neuropathological findings in cattle with
suspect but histologically unconfirmed bovine spongiform encephalopathy
Journal of Comparative Pathology, 108, 241-260
11. McGill IS (1995) Ayurvedic Medicine - The Documentary. Natural Medicine
News, Spring 1995
12. Wood LJN, McGill IS, Done SH and Bradley R (1997) Neuropathology of
a study of the distribution patterns of brain lesions in 222 cases of
natural scrapie in
sheep, 1982-1991. Veterinary Record 140, 167-174
13. McGill IS, Hobson J (1998) Multi-centre evaluation of a herbal skin gel
for veterinary
practice - a questionnaire survey. Veterinary Times, 28, 1, 20-21
14. McGill IS (1998) BSE and Censorship. The Independent January 26th 1998,
Education & Qualifications
1975 - 1982 Southend High School for Boys
GCE O-Levels (1980): 9 (6 A, 3 B)
GCE A-Levels (1982): Biology (A), Physics (A), Chemistry (A)
GCE S-Level (1982): Biology (2)
1982 - 1984 Royal Veterinary College, University of London
1984 - 1985 Kings College, University of London
B.Sc(Hons), II(i) Neuroscience and Immunology
1985 - 1988 Royal Veterinary College, University of London
B.Vet.Med., MRCVS.
Distinctions : Medicine , Clinical Pathology (Elective Subject)
First place for research project
Cecil Aulden Second Prize
Professional Experience
1988 - 1989 Veterinary Surgeon -- Blue Cross Animal Hospital, Victoria,
In addition to clinical duties, I upgraded clinical pathology services
within the hospital and established an interpretive service for laboratory
data for other clinicians.
1990 - 1991 Veterinary Research Officer -- MAFF Central Veterinary
Weybridge, Surrey.
In this post I worked as a neuropathologist with Gerald Wells and William
Hadlow, in a large
interdisciplinary team researching the prion diseases of animals.
My work concentrated on the neuropathological characterisation of Bovine
Encephalopathy (BSE), the prion diseases of other animals and their
differential diagnosis.
This gave me good general experience of neurological disease, its diagnosis
and pathological
characteristics in a wide range of animals and an introduction to many
fields of neuroscience
research. Although broad-based, my research in these varying disciplines was
centred on the
Prion protein and its gene, and associated molecular pathology in the prion
I described, amongst other things, the first cases in the UK of a chlamydial
disease of cattle
putatively equivalent to Sporadic Bovine Encephalomyelitis (see McGill and
Wells, 1993).
Additional responsibilities included:
Liaison with the Consultant Pathology Unit for neuropathological
surveillance, including
rabies diagnosis for the British Isles and characterisation of novel
diseases such as blue eared
pig disease.
Conducting occasional seminars introducing scrapie and BSE diagnosis for
visiting scientists
from abroad.
Rapporteur for The Gibbs Committee on Subacute Spongiform Encephalopathies
(held at
CVL in summer 1990).
Papers presented at AVTRW conferences at Scarborough (1990 & 1991), at
Community Seminar on Spongiform Encephalopathies, Brussels, (1991) and
International Pig
Veterinary Society, Holland, (1991).
Aug 91 - Dec 92 Research Worker (post-doctoral level)
Department of Neuroscience, Institute of Psychiatry, London
In this post I continued to follow my interest in the prion diseases, and
gained a good
grounding in both theoretical and practical molecular biology. I cloned PrP
genes from blood
samples taken from individuals with PrP mutations causal of familial CJD or
GSS and
transfected them into neuroblastoma cells in culture to investigate the
disease process in vitro.
I continued to work with colleagues from other disciplines, particularly
Neurology and
Neuropathology, and with Professor Peter Lantos and others established for
the first time that
prion disease can exist without its characteristic pathology (Lantos, McGill
et al, 1992).
Positions of responsibility included:
Lecturing on a course entitled "Molecular Mechanisms of Neurodegeneration",
to both
internal and external scientists, and as part of the London University M.Sc.
Lecturing on scrapie-like diseases as part of the London University M.Sc. in
Animal Health at
the RVC.
Liaison and research collaboration between the IOP and my previous employers
at CVL,
Sole responsibility for the organisation and funding of the 1992/1993
seminar series for the
Department of Neuroscience, in which leading researchers from around the UK
were invited
to give seminars.
Paper presented at AFRC BSEP meeting, Reading, April 1992.
1994 - Present Scientific and Veterinary Consultant
(Spring 94) Acted as neuropathological consultant for research on the
transmissibility of BSE in collaboration with Dr David White and
Professor Neil Eddington at the Royal Veterinary College, University
of London.
(Summer 94) Veterinary Surgeon, Blue Cross Animal Hospital (Victoria,
(Oct 94 - Dec 94) Lecturer in anatomy and histology, Optics Department, City
Islington College (London).
(1995) Re-established the Prion Interest Group (originally founded at the
Institute of Psychiatry in 1991) as a private organisation, continuing
research on prions.
Filmed and directed a documentary in India/Europe about Ayurvedic
Acted as a locum veterinarian for the PDSA and the Veterinary Centre
(Jan 96 - Present) Veterinary Consultant to Ayuvet (UK) Ltd., co-ordinating
clinical and
laboratory research into the Ayurvedic system of medicine and its
application in European veterinary medicine. Continued co-ordination
of the Prion Interest Group.
Issued on behalf of the witness by:
The BSE Inquiry Press Office
6th Floor Hercules House
Hercules Road
London SE1 7DU
Tel: 0171 261 8377 / 8383
Fax: 0171 803 0893


----- Original Message -----
From: "Terry S. Singeltary Sr."
Sent: Monday, July 11, 2005 1:31 PM

##################### Bovine Spongiform Encephalopathy

From: TSS ()
Date: July 11, 2005 at 11:23 am PST




All material for publication including written works to be published in
scientific journals, books, proceedings of scientific meetings, abstracts of
verbally delivered papers and the like should be scrutinized for risk to the
Ministry before dispatch to the publishers.............

full text;

- 10 -

19. On 18th February, 1987 (YB87/2.18/1.1) I reported to Dr Watson and Dr
Shreeve on a further

case which we had received from Truro VIC. The brain had shown neuronal
vacuolation and

in brain extracts there were fibrils that were similar in size and
appearance to SAFs from sheep

with scrapie. The Virology Department was studying the brain further and
considering a

transmission study. A few weeks before this, I had discussed the possibility
of a transmission

study with Michael Dawson, a research officer in the Virology Department and
an expert in

viral diseases in sheep, and we were considering carefully the safety
aspects. In my note I

raised the question of whether we should disclose the information we had
more widely to the

VIS because this may assist in getting any other cases referred to CVL but
there was the

difficulty that we knew very little about the disorder and would be unable
to deal with queries

that might be raised.

20. On 23rd February, 1987 (YB87/2.23/1.1) I sent Mr Wells a note asking him
to prepare a

statement for publication in Vision, the in-house newsheet prepared by the
VIS for the SVS,

setting out details of what we had discovered. On 24th February, 1987
(YB87/2.25/2.1) Gerald

Wells indicated in a note to me that he had discussed the proposed article
with Mr Dawson and

they both believed that it could be damaging to publish anything at that
stage. They believed

cases would be referred to CVL in any event because they were unusual and
they did not feel

"Vision" was an appropriate publication because its confidentiality was
questionable and might

lead to referrals to veterinary schools rather than CVL. Gerald Wells was
also concerned

about the resources available in his section to deal with referred cases. I

(YB87/2.25/2.1) indicating a draft statement was needed by the Director
before a decision on

publication could be made. Gerald Wells prepared a draft statement
(YB87/3.2/2.1) and sent it

to me on 2nd March, 1987. In his cover note (YB87/3.2/1.1) he commented that
he believed

the distribution of any statement about the new disease outside of CVL to be

because there was so little information available about the new disease. I
passed on a copy of

Gerald Wells' note to Dr Watson (YB87/3.2/3.1). I discussed the matter of
publication with Dr

Watson. No decision had been taken to publish any material at that stage and
I sent a note to

Gerald Wells letting him know the position and confirming that his views and
those of Michael

Dawson would be taken into account when a decision was taken.

- 11 -

21. In March, 1987 serious consideration was given to possible transmission
(e.g. to hamsters) and

other experiments (other than the collection of epidemiological data by the
VIS and

clinicopathology which had been in progress since the first cases were
recognised in November,


22. On 23rd April, 1987 I sent a report (YB87/4.23/1.1) to Dr Watson and Dr
Shreeve informing

them that nine control brains were being examined for SAFs and a cow which
appeared to be

affected with BSE had been purchased for observation. The cow had come from
the farm

where the original cases had developed and had arrived at CVL on 22nd April,

23. On 15th May, 1987 Dr Watson informed me that the proposed "Vision" draft
would be

circulated to VICs in England and Wales if it was approved by management. On
22nd May,

1987 I was copied in on a note (YB87/5.22/2.1) from B.M Williams, (who I
believe was Head

of the VIS at this time but retired shortly after this), to Dr Watson. This
confirmed that the

draft prepared for publication in Vision was approved but that the final
paragraph should be

amended to make it clear that knowledge of the new disease should not be
communicated to

other research institutes or university departments. At a meeting with Dr
Watson on 2nd June,

1987 he informed me that no communication should be made with NPU until
after the meeting

with the CVO on 5th June, 1987 (see my note of 3rd June, 1987 –
YB87/6.3/1.1). We needed

much more data and information to answer inevitable queries. ...

The Cultural Politics of Science and Decision-Making

An Anglo-German Comparison of Risk Political Cultures

 The BSE Case


Kerstin Dressel

sine-Institute Munich, Germany

The following report include excerpts of a thesis submitted in fulfilment of
the requirements for the degree of

Doctor rerum politicarum (Dr. rer. pol.)

at the Ludwig-Maximilians-University of Munich

supervisor: Prof Dr Ulrich Beck

Institute for Sociology, Munich, Germany

The British case study was prepared at the Centre for the Study of
Environmental Change at Lancaster University, UK,

Supervisor: Prof Dr Brian Wynne

kindly supported by a grant of the Economic and Social Research Council, UK

Munich, 2nd October 2000

© Kerstin Dressel, 2000  all rights reserved.

suppressed peer review of Harvard study October 31, 2002

SEEMS some might have been gearing up for the future BSE/TSE cover-up, well
before it was ever first documented. this is where i think the BSE/nvCJD
only theory was first born, in some back room with government and industry

----- Original Message -----
From: "Galyean, Michael"
Sent: Saturday, May 28, 2005 3:34 PM
Subject: FW: Prion biology relevant to bovine spongiform encephalopathy
(ANIMALSCI Feedback Form)

Dr. Novakofski:

I recevied the following message and comments regarding your recent paper on
prion biology published in the Journal of Animal Science. I hope you will
take the time to look over the comments and respond to Mr. Singeltary.


Michael Galyean
Journal of Animal Science


From: Terry S. Singeltary Sr. []
Sent: Thu 5/26/2005 9:20 AM
To: Amanda Kolling
Cc: Galyean, Michael
Subject: Re: Prion biology relevant to bovine spongiform encephalopathy
(ANIMALSCI Feedback Form)

I have forwarded this to Dr. Michael Gaylean as suggested.
thank you........

please note new email address

any questions or follow ups, please do not hesitate to write...

thank you,

kindest regards,
Terry S. Singeltary Sr.

----- Original Message -----
From: Amanda Kolling
To: Terry S. Singeltary Sr.
Sent: Thursday, May 26, 2005 8:11 AM
Subject: RE: Prion biology relevant to bovine spongiform encephalopathy
(ANIMALSCI Feedback Form)

Dear Mr. Singeltary,

Thank you for your comments. Contrary to a previous e-mail sent to you by an
employee of HighWire, the Journal of Animal Science does accept Letters to
the Editor. If you are interested in submitting this as a letter to the
editor, I urge you to contact our editor-in-chief, Dr. Michael Gaylean at

Best regards,

Amanda Kolling
Technical Editor,
Journal of Animal Science

At 09:11 AM 5/17/2005 -0700, Terry S. Singeltary Sr. wrote:
>Comments sent via JAS Feedback Page
> NAME: Terry S. Singeltary Sr.
> BROWSER: Mozilla/5.0 (Windows; U; Win98; en-US; rv:1.0.2)
> Gecko/20030208 Netscape/7.02
>J. Anim. Sci. 2005. 83:1455-1476
>© 2005 American Society of Animal Science
>Prion biology relevant to bovine spongiform encephalopathy1
>J. Novakofski*,2, M. S. Brewer{dagger}, N.
>Mateus-Pinilla{ddagger}, J. Killefer* and R. H. McCusker*
>* Departments of Animal Sciences and {dagger} Food
>Science and Human Nutrition, University of Illinois at
>Urbana­Champaign 61801-4737; and {ddagger} Illinois
>Natural History Survey, Center for Wildlife and Plant
>Ecology, Champaign, IL 61820
>2 Correspondence: 1503 South Maryland Dr. (phone:
>217-333-6181; e-mail:
>Bovine spongiform encephalopathy (BSE) and chronic
>wasting disease (CWD) of deer and elk are a threat to
>agriculture and natural resources, as well as a human
>health concern. Both diseases are transmissible
>spongiform encephalopathies (TSE), or prion diseases,
>caused by autocatalytic conversion of endogenously
>encoded prion protein (PrP) to an abnormal, neurotoxic
>conformation designated PrPsc. Most mammalian species
>are susceptible to TSE, which, despite a range of
>species-linked names, is caused by a single highly
>conserved protein, with no apparent normal function. In
>the simplest sense, TSE transmission can occur because
>PrPsc is resistant to both endogenous and environmental
>proteinases, although many details remain unclear.
>Questions about the transmission of TSE are central to
>practical issues such as livestock testing, access to
>international livestock markets, and wildlife
>management strategies, as well as intangible issues
>such as consumer confidence in the safety of the meat
>supply. The majority of BSE cases seem to have been
>transmitted by feed containing meat and bone meal from
>infected animals. In the United Kingdom, there was a
>dramatic decrease in BSE cases after neural tissue and,
>later, all ruminant tissues were banned from ruminant
>feed. However, probably because of heightened awareness
>and widespread testing, there is growing evidence that
>new variants of BSE are arising "spontaneously,"
>suggesting ongoing surveillance will continue to find
>infected animals. Interspecies transmission is
>inefficient and depends on exposure, sequence homology,
>TSE donor strain, genetic polymorphism of the host, and
>architecture of the visceral nerves if exposure is by
>an oral route. Considering the low probability of
>interspecies transmission, the low efficiency of oral
>transmission, and the low prion levels in nonnervous
>tissues, consumption of conventional animal products
>represents minimal risk. However, detection of rare
>events is challenging, and TSE literature is
>characterized by subsequently unsupported claims of
>species barriers or absolute tissue safety. This review
>presents an overview of TSE and summarizes recent
>research on pathogenesis and transmission.
>Key Words: Bovine Spongiform Encephalopathy . Chronic
>Wasting Disease . Prion
> >there is growing evidence that new variants of BSE are
>arising "spontaneously,"
>THERE is NO evidence of a 'spontaneous' TSE anywhere that
>is infectious and shows the pathology of any natural TSE.
>if i have missed something, could someone please site this
>science to me please.
> >Considering the low probability of interspecies
>transmission, the low efficiency of oral transmission,
>and the low prion levels in nonnervous tissues,
>consumption of conventional animal products represents
>minimal risk.
>I DISAGREE with all of the above. all one has to do is
>read transmission
>studies. scrapie infected sheep and goats, CWD infected
>deer and
>elk (who knows how many strains) and undocumented TSEs
>in the
>USA bovine have been rendered and fed to animals for
>consumption for decades. it's only a pipe dream that
>none of this
>was infectious. to think of a 'spontaneous' TSE as just
>up from nowhere, is like believing in Santa Claus. remember
>the USA scrapie research in Mission, Texas. IT did NOT look
>like BSE...
>1: J Infect Dis 1980 Aug;142(2):205-8
> Oral transmission of kuru, Creutzfeldt-Jakob
>disease, and scrapie to nonhuman primates.
> Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL,
>Gajdusek DC.
> Kuru and Creutzfeldt-Jakob disease of humans and
>scrapie disease of sheep and goats were transmitted to
>squirrel monkeys (Saimiri sciureus) that were exposed
>to the infectious agents only by their nonforced
>consumption of known infectious tissues. The
>asymptomatic incubation period in the one monkey
>exposed to the virus of kuru was 36 months; that in the
>two monkeys exposed to the virus of Creutzfeldt-Jakob
>disease was 23 and 27 months, respectively; and that in
>the two monkeys exposed to the virus of scrapie was 25
>and 32 months, respectively. Careful physical
>examination of the buccal cavities of all of the
>monkeys failed to reveal signs or oral lesions. One
>additional monkey similarly exposed to kuru has
>remained asymptomatic during the 39 months that it has
>been under observation.
>PMID: 6997404
>3. You will recall that the advice provided by
>Professor Smith in
>1993 and by Dr. Gore this month used the sub-population
>of dairy
>farm workers who had had a case of BSE on their farms -
>63,000, which is approximately half the number of dairy
>workers - as a denominator. If the above sums are
>repeated using
>this denominator population, taking an annual incidence
>in the general
>population of 1 per million the observed rate in this
>is 10 TIMES, and taking an annual incidence of 0.7 per
>that in the general population...
>It was, however, performed in the USA in 1979, when it
>was shown that
>cattle inoculated with the scrapie agent endemic in the
>flock of Suffolk
>sheep at the United States Department of Agriculture in
>Mission, Texas,
>developed a TSE quite unlike BSE. 32 <
>The findings of the initial transmission, though not of
>the clinical or
>neurohistological examination, were communicated in
>October 1988 to Dr
>Watson, Director of the CVL, following a visit by Dr
>Wrathall, one of
>the project leaders in the Pathology Department of the
>CVL, to the
>United States Department of Agriculture. 33
>The results were not published at this point, since the
>transmission to mice from the experimental cow brain
>had been
>inconclusive. The results of the clinical and
>histological differences
>between scrapie-affected sheep and cattle were
>published in 1995.
>Similar studies in which cattle were inoculated
>intracerebrally with
>scrapie inocula derived from a number of
>scrapie-affected sheep of
>different breeds and from different States, were
>carried out at the US
>National Animal Disease Centre. 34
>The results, published in 1994, showed that this source
>of scrapie
>agent, though pathogenic for cattle, did not produce
>the same clinical
>signs of brain lesions characteristic of BSE.
>Visit to USA ... info on BSE and Scrapie
>AS implied in the Inset 25 we must not _ASSUME_ that
>transmission of BSE to other species will invariably
>present pathology typical of a scrapie-like disease.
>In Confidence - Perceptions of unconventional slow
>virus diseases
>of animals in the USA - APRIL-MAY 1989 - G A H Wells
>WHY is USA insisting _now_ not to use WB, when on the
>1st _confirmed_
>case Dec. 23, 2003
>USA mad cow, WB was used ???
>maybe this is the reason ;
>JAPAN BSE # 8 & 9 cow
>8. 6/10/2003 Holstein Steer 13/10/2001 23 mths
>No clinical signs WB+, IHC-, HP-
>9. 4/11/2003 Holstein Steer 13/1/2002
>21 mths No clinical signs WB+, IHC-, HP-
>More information on the first 11 Japanese BSE-cases can
>be found on the

>website of the Japanese Embassy in the US:
>IN fact, the new strain of TSE in cattle BaSE, does not
>look like nvCJD in humans, but very similar
>to the sporadic CJD;
>BASE in cattle in Italy of Identification of a second
>bovine amyloidotic spongiform encephalopathy: Molecular
>similarities with sporadic Creutzfeldt-Jakob disease
>Adaptation of the bovine spongiform encephalopathy
>agent to primates and comparison with Creutzfeldt-
>Jakob disease: Implications for human health THE
>findings from Corinne Ida Lasmézas*, [dagger] ,
>Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*,
>Domíníque Marcé*, François Lamoury*, Nicolas Kopp
>[Dagger ] , Jean-Jacques Hauw§, James Ironside¶, Moira
>Bruce [||] , Dominique Dormont*, and Jean-Philippe
>Deslys* et al, that The agent responsible for French
>iatrogenic growth hormone-linked CJD taken as a control
>is very different from vCJD but is similar to that
>found in one case of sporadic CJD and one sheep scrapie
>Characterization of two distinct prion strains derived
>from bovine spongiform encephalopathy transmissions to
>inbred mice
>Terry S. Singeltary SR.
>P.O. Box 42
>Bacliff, Texas USA 77518


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Palo Alto, CA 94304
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