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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 replied

(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 premature

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, 1987.

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 officials...TSS

----- 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


La Vonne Gallo
HighWire Press
1454 Page Mill Road
Palo Alto, CA 94304
fax: 650.725.9335


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