Thursday, April 19, 2012

Wendy Grant, who has died aged 89, was a neuropathologist who became one of the first scientists to warn the public that BSE, also known as Mad Cow Disease

Wendy Grant

Wendy Grant, who has died aged 89, was a neuropathologist who became one of the first scientists to warn the public that BSE, also known as Mad Cow Disease, could be incubating in the human population.

Wendy Grant
Image 1 of 2
May 1990: In one of the most celebrated images of the BSE crisis, Agriculture minister John Selwyn Gummer and his 4 year old daughter Cordelia tuck into beefburgers on a visit to the East Coast Boat Show. Photo: PA
Wendy Grant
2 OF 2 Wendy Grant
The disease was first identified in cows in 1985. Two years later government scientists suggested the most likely source was cattle feed made from the remains of dead sheep with scrapie, a similar brain disease. In 1988 John MacGregor, then agriculture minister, imposed a ban on cattle feed derived from dead animals.

A month before the ban came into force, however, a junior doctor, Tim Holt, became the first to suggest, in an article in the British Medical Journal, that BSE might pose a significant threat to human health, after he and a colleague discovered that some butchers were selling cow brains for human consumption. He suggested that the use of brains in British food should be banned.

Wendy Grant, a retired consultant neuropathologist and an expert in slow viruses (associated with diseases with long incubation periods of months to years) was alarmed by Holt’s piece, particularly when she discovered, through slaughterhouse workers, that cattle brains were being added to meat products such as pies, pâtés and stock cubes. As one of the few people to have read the literature on scrapie and the human equivalent, Creutzfeldt-Jakob disease (CJD), she realised that government assurances about BSE, “namely 'we have lived with scrapie for two and a half centuries and it has not done us any harm’,” were based on the false premise that cattle brains and sheep brains were dealt with in the same way at abattoirs, “which they obviously were not”. Humans, she argued, had not been seriously exposed over the centuries to the scrapie agent as sheep brains are seldom removed to be eaten. But when she wrote to the government pressing the need for an inquiry into the dangers of contamination, she was ignored.

In February 1989 a report by a committee chaired by Sir Richard Southwood highlighted “unnatural feeding practices” in modern intensive farming but concluded that it was “most unlikely” that BSE might be transmitted to humans, though the risk could not be entirely ruled out. The day the report was published Wendy Grant appeared on the BBC warning that infected tissues of cattle were still going into human food. The risks of humans contracting the disease were being underplayed, she maintained, pointing out that experimental work on scrapie-infected brains had revealed that it is very easy to infect almost any mammal, including apes, “and we are just another ape”. “Who knows?” she added, “some of us may be incubating it already.”

The government’s immediate response to growing public concern was to impose a ban on the use of offal in baby foods, but in an article Wendy Grant accused it of using baby foods “to divert the public from thinking about other foods and thus to imply they are safe, which they are not”. The official inquiry into the BSE scandal later identified her article as one of the influences that drove the government towards the decision in November 1989 to ban the use of cows’ brain and spinal cord for human consumption.

As ministers and the food industry battled to reassure consumers that British beef was “perfectly safe” and that eating it carried “no conceivable risk”, Wendy Grant, like other scientists involved, found herself the victim of a smear campaign, treated with hostility by Ministry of Agriculture officials and accused of being “out of date”.

But she refused to go away. When, in 1990, she discovered that, under pressure from the meat lobby, ministers had agreed that brains could be removed from cattle by splitting open the skulls, she pointed out that this frequently resulted in bits of brain being splattered on to meat destined for human consumption. Slaughtered cattle, she said, should be decapitated and the intact heads incinerated.
In 1994 she described it as “incomprehensible” that the brains of calves under six months old were still being allowed into the human food chain and called for an immediate ban: “We should not be eating the offal even from calves, because we do not yet know whether the disease is passed from mother to calf,” she said. Two years later government scientists confirmed that cows could indeed pass on BSE to their calves.

The turning point came after the first recorded death from what was later described as new variant Creutzfeldt-Jakob Disease (vCJD), on May 21 1995. Within a year 10 cases had been identified and on March 20 1996, the Health Secretary Stephen Dorrell made the announcement that these cases were most probably linked to the consumption of BSE-infected beef or beef products. In June, in the face of a worldwide ban on exports of British beef imposed by the EU, the government agreed to implement a more thoroughgoing slaughter programme and more effective removal of potentially infective materials from carcases.

The announcement of a public inquiry into the affair under the senior judge Lord Phillips in 1997 was welcomed by campaigners and when it was published in 2000, it vindicated Wendy Grant and other scientists who had persisted in voicing their concerns. The report concluded that the government had misled the public about the dangers of British beef and the chances of mad cow disease being spread to humans for years. It also said that bureaucratic delays had hampered the response to the crisis.
But Wendy Grant only felt able to give the report a qualified welcome: If action had been taken to ban cattle brains from the human food chain in 1989 when she had first warned of the possibility of transmission, there would have been fewer vCJD victims: “They should have listened to me,” she said. Since vCJD was first reported in 1996, a total of 217 patients from 11 countries have been identified. Altogether, since the disease became notifiable in 1996, 176 people in Britain have died from the disease, but uncertainties relating to the potential length of the incubation period complicate predictions of the future number of cases.

Helen Grant, always known as Wendy, was born in Ealing, west London on May 11 1922. Her parents were involved in relief work with refugees and her father had spent some time in prison in the First World War, as a conscientious objector.

Wendy was educated at schools in France, Austria, New Zealand and finally at Bedales, where she became head girl. After taking a degree in Medicine at Cambridge, she did her clinical training at University College London. She decided to specialise in neuropathology and in 1970 joined the Middlesex Hospital as a consultant. In 1985 she moved to Charing Cross Hospital as a senior lecturer and honorary consultant in neuropathology.

A life-long opponent of boxing, Wendy Grant was able to demonstrate that the part of the brain most affected by punching corresponds with the areas attacked by other neurological conditions such as Parkinsons. When Cassius Clay, alias Muhammad Ali, degenerated into an incoherent wreck within 10 years of retiring and the sport’s defenders claimed he was not punch drunk but was suffering from Parkinson’s, she observed that if he was indeed suffering from Parkinsons, it was a convenient coincidence. “Boxing is bad for the brain full stop,” she said.

Wendy Grant married, in 1945, Alick Elithorn, but the marriage was later dissolved. She is survived by a son. A daughter predeceased her.

Wendy Grant, born May 11 1922, died March 14 2012


The BSE Inquiry / Statement No 410

Dr Helen Grant

Issued 13/05/1999 (not scheduled to give oral evidence)



1. My credentials in the matters of BSE and CJD are:

a. 1970-1982 Consultant Neuropathologist at the Middlesex Hospital.

b. 1985-1989 Consultant Neuropathologist at the Charing Cross Hospital.

c. I have carried out six autopsies on CJD victims and reported on a similar number of cerebral biopsies from CJD patients.

1. Through my interest in slow viruses (particularly with reference to multiple sclerosis) I was one of only a few people to be aware of both Scrapie and CJD in 1988.

2. I have never had any formal links with the farming community, renderers, pet food manufacturers, etc. However, slaughterhouse workers began telephoning me as early as February 1989 after they learned through the media of my concern and knowledge about TSEs. Several of them rang me because they had had no instructions from the Health and Safety Executive about precautions to be taken to avoid infection from BSE carcases. (I have kept some of the correspondence with these workers together with my list of precautions to be taken in abattoirs).

3. I asked the slaughterhouses workers in detail to explain the routine slaughtering practices and was astonished to learn that sheep’s brains were generally left inside the skull whereas cattle brains were routinely removed to be added to our "meat products" – meat pies, pates, tinned items and stock cubes. I therefore feared that this almost indestructible infective agent was being swallowed by all beef eaters in the UK in large doses which would inevitably infect genetically susceptible people.

4. I was horrified because I suddenly realised why Government assurances about BSE – namely "we have lived with scrapie for two-and-a-half centuries and it has not done us any harm so we won’t have any trouble with BSE" – were based on a false premise which was that cattle brains and sheep’s brains were dealt with in the same way in the abattoirs which they obviously were not. Since sheep’s brains were seldom removed from the skulls (which is why cattle caught scrapie in the first place) we humans have never been seriously exposed over the centuries to the scrapie agent. Simple economics is the reason: sheep’s brains are too small to make the intricate process of their removal worthwhile.

5. I appeared on the BBC nine o’clock television news on February 27, 1989 (the day the Southwood Report was published) in my capacity as consultant neuropathologist at Charing Cross hospital. I was asked among other things to comment on the possible human hazard of BSE and I warned that I thought there was a risk because cattle brains were going into our food chain. I added: "Who knows? Some of us may be incubating it already." Some of us were.

6. I was called to give evidence to the House of Commons Agriculture Select Committee on 13 June 1990 (IBD 1 Tab 7 p 42). On re-reading it, I see no reason to change anything in my evidence except the numbers of animals mentioned. The Government of the day was hardly disposed to ask my advice about BSE on a regular basis given my critical attitude since early 1989. But the then Labour Opposition, understandably anxious for information, turned to me frequently. Opposition Members included David Clark MP, Ron Davies MP and Ian McCartney MP. It was my technical information which helped Ron Davies MP to make his effective speech about BSE in the House of Commons on 17 May 1989 (M 7 Tab 7). Shortly afterwards, the Minister for Agriculture, John MacGregor, announced that legislation would be brought in to ban all cattle brains from human food (YB 89/6.13/5.1-5.2). The long summer recess delayed this legislation and the "specified offals" ban was finally enacted on 9 November 1989 (L2 Tab 4) (9 February 1990 in Scotland) (L10 Tab 9). Of course this was more than a year (15 months) after cattle had been protected in the same way.

7. Apart from my involvement with CJD I have of course been interested in that worldwide scourge, multiple sclerosis (MS). This led me to ponder the question of "slow virus infection – now labelled "prion infection" (an inaccurate title. In my opinion prion is a short title for an organism which causes Transmissible Spongiform Encephalopathy (TSE) such as scrapie, CJD, BSE, Kuru and others. Prion diseases has therefore become widely used instead of the cumbersome alternative (YB 94/4.25/10.1)) – which is one of the aetiological factors involved in MS. Scrapie, the ovine TSE, was then and still is by far the most extensively researched slow virus infection. I therefore read up all the papers on the subject as they appeared during the 1950s, ‘60s and ‘70s and was therefore immediately aware of the human hazard posed by the BSE catastrophe. Vets generally did not know about CJD (why should they?) and neuropathologists were mostly ignorant of scrapie. I happened to know about both in those early days due to my interest in "slow viruses".

8. I was in receipt of no extra funds beyond those provided by the NHS and the University of London to run my laboratories and pay my salary as a senior lecturer/honorary Consultant and I suffered no constraints over my publications, lectures to my students, or statements to the media. However, I became increasingly aware after 1988 that questioning official dogma about BSE brought difficulties to one’s career. I was myself about to retire from the Charing Cross Hospital, where I worked as a Consultant Neuropathologist, but I observed with horror that the good reputations of dissenting scientists in the field, not least Dr Stephen Dealler and especially Dr Harash Narang were systematically undermined.

9. My primary function has been to teach medical under-graduates and post-graduates about diseases of the brain and nervous system and, of course, to fulfil my clinical functions as a consultant neuropathologist at two London teaching hospitals. This, of course, meant that I conducted both biopsies and autopsies including those on patients with CJD: it was not primarily to publish scientific articles. My scientific publications include only one case which I think in retrospect may be CJD before that was known to be an infection with this agent. ("Post Traumatic Dementia": Helen C Grant, Behrman et al. Archiv für Psyciatre und Zeitschrift für die ges. Neurologie. 1965; 207: 128) More importantly I have carried out several biopsies and autopsies on CJD patients. My duties also included the initiation and supervision of research projects. When my trainees and PhD students published their resulting scientific papers I took the view that the work was theirs, they should get the credit (not I) and therefore I made it a matter of principle not to add my name as co-author.

10. I corresponded frequently from February 1989 onwards with Government ministers including John MacGregor, Donald Thomson, Gillian Shepherd and Angela Browning. But I received only short and reassuring replies containing what I believed to be inaccurate information. Because official bodies treated my early warnings with hostility, I soon learned that the only way to convey my concerns was to contribute relevant letters to the broadsheet newspapers and to speak to responsible members of the press, the broadcasting services and informed members of Opposition parties.

11. Since February 1989 I have answered innumerable letters from members of the public understandably anxious – if not panicky – about the effect on their diets of the outbreak. They came/come from a cross-section of the community: parents ("is the milk safe?"), restaurateurs, doctors, butchers, journalists, Education Committees. Since I retired finally in March 1989 I have had the time to answer them all eventually.

12. The BSE/CJD problem is quite incomprehensible without knowledge of the facts set out in Annex 1. The infective agent has unique and sinister properties.

Issued on behalf of the witness by:

The BSE Inquiry Press Office 6th Floor Hercules House Hercules Road London SE1 7DU Fax: 0171 803 0893 Website: Email:

annex 1 (wiped clean from internet)

 however, my files have this ;

 ANNEX 1 to witness statement 410 of Dr. Helen Grant

Annex 1

Unique Properties of the scrapie/BSE/CJD Agent, the so-called "prion"
A. The transmissible organism which causes all the transmissible spongiform encephalopathies (TSEs) -- scrapie, BSE, CJD and Kuru -- is almost indestructible, unlike any other virus, bacterium, protozoon, fungus or parasite. For example, it still transmits scrapie after being 'fixed' in formaldehyde for ten years. Heating it to a very high temperature, exposing it to enormous doses of ultraviolet light, or to ionising radiation, do not affect it. Incineration is the only way of destroying it and even then the temperature must be very high indeed.

B. It proliferates only in the brain, eyes, spinal cord, pituitary and, in some mammals, the placenta. The transmission of these diseases is dose-related and although the virus usually enters the bloodstream from the stomach, and then visits all tissues for a few hours, it lingers and proliferates only in the brain etc. The red meat (muscle) of BSE-infected cattle has never transmitted the disease in the laboratory and we have not had any trouble from eating scrapie-infected muscle over the centuries.

C. It lurks for years in an outwardly completely healthy individual.

D. During this long 'incubation period' the brain etc. is infective which is why it was necessary to ban the brains etc. of all cattle from human foods.

E. It raises no antibodies -- which might then be tested for -- in the infected host.

F. There is officially no live test to reveal infected individuals. "Officially" because a live (urine) test has recently been devised and has been used successfully in 15 out of 15 humans who were subsequently shown to have suffered CJD. MAFF's vets refuse to make use of this live test and denigrate it whenever they are asked about it. It could also be used to screen blood donors.

G. Individuals' susceptibility to this organism is genetically determined. Not all types of sheep develop scrapie; not all types of cattle develop BSE and only some humans -- those of an unusual genotype -- will, if infected, develop CJD.

H. Scrapie, the orginal disease in sheep, has been easily transmitted by mouth to many experimental mammals including primates.

Humans are primates.

Items b (placenta), c, d and f establish that the Government's present 'culling' policy, which is not based on science, cannot possibly eradicate BSE.


Subject: ANNEX 1 to Witness statement 410 of Dr. Helen Grant

Date: Wed, 19 Jan 2000 15:58:39 -0600

From: "Terry S. Singeltary Sr." <>

Reply-To: Bovine Spongiform Encephalopathy <>


######### Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########

Greetings List Members,

I have often wondered about scrapie and it's possible relationship to sporadic CJD. A few things I thought interesting in this statement from Dr. Helen Grant, I would like to share with you.....snip...end...tss

556 In the first place there was the public reaction to the Report. This started with a broadcast on the day the Report was published from Dr Helen Grant, a consultant neuropathologist at Charing Cross Hospital in London, who commented on the risk posed by cattle brains that were going into the human food chain. In an article in The Guardian on 2 March 1989, she suggested that the Government was concentrating on baby food ‘to divert the public from thinking about other foods and thus to imply that they are safe, which they are not’.

 The press contrasted MAFF’s statement with views expressed by Dr Helen Grant, Consultant Neuropathologist:

My gut feeling is that some genetically susceptible people may have become infected with material by eating meat products.

Sunday, May 18, 2008



Sunday, May 18, 2008

BSE, CJD, and Baby foods (the great debate 1999 to 2005)

Sunday, May 18, 2008


R.I.P. DR. GRANT !!!

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.


The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

PMID: 6997404





A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates.

One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias" Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.



Nature. 1972 Mar 10;236(5341):73-4.

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

C. J. GIBBS jun. & D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

Nature. 1972 Mar 10;236(5341):73-4.

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

Gibbs CJ Jr, Gajdusek DC. Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

C. J. GIBBS jun. & D. C. GAJDUSEK National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

Wednesday, February 16, 2011




why do we not want to do TSE transmission studies on chimpanzees $


5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.




If the scrapie agent is generated from ovine DNA and thence causes disease in other species, then perhaps, bearing in mind the possible role of scrapie in CJD of humans (Davinpour et al, 1985), scrapie and not BSE should be the notifiable disease. ...

Thursday, November 18, 2010

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

Wednesday, January 19, 2011

EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011

Monday, June 27, 2011

Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease


Emerging Infectious Diseases • • Vol. 17, No. 5, May 2011

Experimental Oral Transmission of Atypical Scrapie to Sheep

Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos

To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals’ peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specifi c prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These fi ndings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.


Although we do not have epidemiologic evidence that supports the effi cient spread of disease in the fi eld, these data imply that disease is potentially transmissible under fi eld situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing fi nding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.

How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantifi ed, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confi rmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected.

Emerging Infectious Diseases • • Vol. 17, No. 5, May 2011

Thursday, March 29, 2012

atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

Monday, April 16, 2012

Continuing Enhanced National Surveillance for Prion Diseases in the United States

Subject: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68

Comment from Terry Singeltary

Document ID: APHIS-2008-0010-0008 Document Type: Public Submission

This is comment on Proposed Rule: Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products

Docket ID: APHIS-2008-0010 RIN:0579-AC68

Topics: No Topics associated with this document

View Document:


Document Subtype: Public Comment

Status: Posted

Received Date: March 22 2012, at 12:00 AM Eastern Daylight Time

Date Posted: March 22 2012, at 12:00 AM Eastern Daylight Time

Comment Start Date: March 16 2012, at 12:00 AM Eastern Daylight Time

Comment Due Date: May 15 2012, at 11:59 PM Eastern Daylight Time

Tracking Number: 80fdd617

First Name: Terry

Middle Name: S.

Last Name: Singeltary

City: Bacliff

Country: United States

State or Province: TX

Organization Name: CJD TSE PRION

Submitter's Representative: CONSUMERS


comment submission Document ID APHIS-2008-0010-0001 Greetings USDA, OIE et al, what a difference it makes with science, from one day to the next. i.e. that mad cow gold card the USA once held. up until that fateful day in December of 2003, the science of BSE was NO IMPORTS TO USA FROM BSE COUNTRY. what a difference a day makes$ now that the shoe is on the other foot, the USDA via the OIE, wants to change science again, just for trade $ I implore the OIE decision and policy makers, for the sake of the world, to refuse any status quo of the USA BSE risk assessment. if at al, the USA BSE GBR should be raise to BSE GBR IV, for the following reasons. North America is awash with many different TSE Prion strains, in many different species, and they are mutating and spreading. IF the OIE, and whatever policy makers, do anything but raise the risk factor for BSE in North America, they I would regard that to be highly suspicious. IN fact, it would be criminal in my opinion, because the OIE knows this, and to knowingly expose the rest of the world to this dangerous pathogen, would be ‘knowingly’ and ‘willfully’, just for the almighty dollar, once again. I warned the OIE about all this, including the risk factors for CWD, and the fact that the zoonosis potential was great, way back in 2002. THE OIE in collaboration with the USDA, made the legal trading of the atypical Nor-98 Scrapie a legal global commodity. yes, thanks to the OIE and the USDA et al, it’s now legal to trade the atypical Nor-98 Scrapie strain all around the globe. IF you let them, they will do the same thing with atypical BSE and CWD (both strains to date). This with science showing that indeed these TSE prion strains are transmissible. I strenuously urge the OIE et al to refuse any weakening to the USA trade protocols for the BSE TSE prion disease (all strains), and urge them to reclassify the USA with BSE GBR IV risk factor. SEE REFERENCE SOURCES IN ATTACHMENTS

SEE Terry S. Singeltary Sr. Attachment WORD FILE ;

Sunday, March 11, 2012

APHIS Proposes New Bovine Spongiform Encephalopathy Import Regulations in Line with International Animal Health Standards Proposal Aims to Ensure Health of the U.S. Beef Herd, Assist in Negotiations

Wednesday, April 4, 2012

Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine Products APHIS-2008-0010-0008 RIN:0579-AC68

pink slime and a ship of fools, with Governor Rick Perry at the helm.

john gummer of England, force fed his daughter mad cow beef. a few years later, a young friend of theirs (23) died from mad cow disease. NOW, Governor Rick Perry, shows he is as big a fool as John Gummer.

see more on this sad sad saga here ;

Wednesday, March 14, 2012


Sunday, August 28, 2011

Rick Perry, Texas, BSE aka mad cow disease, CJD, and 12 years of lies there from

BY the way, ammonia treated beef DOES NOT KILL MAD COW DISEASE !!!

> > > Ackerman says downed cattle are 50 times more likely to have mad cow disease (also known as Bovine Spongiform Encephalopathy, or BSE) than ambulatory cattle that are suspected of having BSE. Of the 20 confirmed cases of mad cow disease in North America since 1993, at least 16 have involved downer cattle, he said. < < <

don’t forget the children...

PLEASE be aware, for 4 years, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens.

who will watch our children for CJD for the next 5+ decades ???

WAS your child exposed to mad cow disease via the NSLP ???



you can check and see here ;

Saturday, March 5, 2011


Sunday, February 12, 2012

National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas

Monday, April 16, 2012

Continuing Enhanced National Surveillance for Prion Diseases in the United States