Tuesday, October 29, 2013


VARIANT CJD PRESENTS DIFFERENTLY IN OLDER PATIENTS, and the infamous UKBSEnvCJD only theory, i.e. God save the industry at all cost $$$



 J Neurol Neurosurg Psychiatry 2013;84:e2 doi:10.1136/jnnp-2013-306573.17 Association of British Neurologists (ABN) joint meeting with the Royal College of Physicians (RCP), London, 23–24 October 2013 017






Graham Mackay⇓, Richard Knight, Robert Will + Author Affiliations


Southern General Hospital, Glasgow; National CJD research and surveillance unit, Edinburgh Abstract Introduction Variant Creutzfeldt–Jakob (vCJD) has an established clinical phenotype and diagnostic criteria. However, this phenotype has largely been described in a cohort of young vCJD cases, with a median age of onset of 27.


Methods Having reviewed the 176 definite and probable vCJD cases referred to UK CJD surveillance, six older cases, over 55 years were found. The clinical records of these cases were reviewed.


Results The six older vCJD cases were all male. Two had received blood from donors confirmed to have had vCJD. Only two of these cases met the diagnostic criteria for vCJD in life. Three cases had atypical clinical histories without either early psychiatric symptoms or involuntary movements. Only one of five patients had the typical pulvinar sign on their MRI scan.


Conclusion No cases of vCJD were diagnosed in the UK in 2012. However, clinicians should be aware of the occurrence of vCJD, with less typical phenotypes, in older patients. vCJD should be considered in older patients dying with dementia deteriorating in under three years, with ataxia and a rapid final deterioration. Post mortem should be considered in such cases, given the public health risks among a population more prone to undergoing medical procedures.






The age distribution has a political aspect. Scientists sought to sell BSE-based CJD to politicians on the basis of its novelty: early onset, florid plaques, strain type 4 and so on. Now that they have made the sale, and with the Inquiry Report as received wisdom (?!?), it becomes timely to reveal an older case and that they had blown off 5 years of elderly demented data (which has far higher frequency than young and demented so potentially holds more nvCHD cases).


If nvCJD had been presented primarily a disease of the elderly demented (scarcely a charismatic group, fundraisers use a poster-child), it would have been met with near-total indifference and business as usual. Elderly are written off as likely to die soon of one thing or another anyway, and daftness is perceived as normal. Why spend money on diagnosing them?





Subject: The 'Chosen Ones' (nvCJD) will fall, young and old... but sporadic, will stay just that, $$$$$ 'sporadic' $$$$$


Date: Fri, 27 Apr 2001 09:38:12 –0700


From: "Terry S. Singeltary Sr."


Reply-To: Bovine Spongiform Encephalopathy


To: BSE-L@uni-karlsruhe.de


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


Thursday April 26 8:26 PM ET


Human Mad Cow Disease Claims Oldest Victim


LONDON (Reuters) - More elderly people will fall victim to the human form of mad cow disease, medical experts said on Friday after a 74-year-old man became the oldest victim of the fatal brain affliction.


Variant Creutzfeldt-Jakob disease (news - web sites) (vCJD) was diagnosed after an autopsy was requested for the 74-year-old man on the basis that some of his symptoms were not associated with dementia and he died just seven months after they began.


Professor James Ironside of the CJD Surveillance Unit at Western General Hospital in Edinburgh said the death of the unidentified man is unlikely to be an isolated event, saying more cases of the disease could occur in people in their 50s, 60s and 70s.


Most of the 95 cases of the brain-wasting illness reported in Britain have been in people decades younger than the oldest victim.


``This case has important implications for the surveillance of vCJD, and raises the possibility that cases of vCJD in the elderly might be missed,'' they said in a letter to The Lancet medical journal.


Symptoms of the illness, which include loss of co-ordination, confusion and personality changes, can be mistaken for dementia in older people. Cases of vCJD are usually confirmed by an autopsy, which is not commonly performed on the elderly.


Doctors ``should be aware that vCJD can arise in elderly patients so that appropriate investigations are done,'' the experts added.


Doctors should request scans and autopsies in suspected cases of vCJD in the elderly.


The elderly man, a retired electrician, had no family history of brain disease and was healthy until he complained of pains in his hands and then became forgetful and started having hallucinations and paranoid delusions.


But the scientists said he ate meat pies and sausages at least once every week and pate every month. Researchers suspect humans get vCJD, which was first identified in 1996, by eating meat contaminated with mad cow disease or bovine spongiform encephalopathy (BSE (news - web sites)).


Last month an inquiry into a cluster of vCJD deaths in central England said local butchering practices were the most likely cause of the vCJD cases.


Because of its long incubation period, which can be up to 30 years, scientists say it is impossible to predict how many people will be struck down by the disease. Estimates range from thousands to tens of thousands over the coming years.




Thursday, 26 April, 2001, 12:48 GMT 13:48 UK


Third French CJD victim dies


The Eboli family is suing governments over the disease A 19-year-old man has become the third victim in France to die of the human form of mad cow disease.


Arnaud Eboli died on Wednesday from variant Creutzfeldt-Jakob disease (vCJD), the human type of BSE, his family have announced.


Last year, a lawyer acting for Mr Eboli and Laurence Duahamel - another victim of the disease - sued the French, British and EU authorities alleging they had failed to take all the necessary steps to contain the epidemic.


The law suits - filed in a Paris civil court - accuse Britain of knowingly exporting possibly contaminated material, and France and the European Commission of not taking the threat of disease seriously enough.


Britain, where the outbreak of BSE has been most severe, has so far confirmed 97 deaths from vCJD and the Republic of Ireland one.


Feed investigation


The news of Mr Eboli's death comes a day after French magistrates placed under official investigation a firm allegedly distributing contaminated feed.


Youssef Chataoui, head of the French company Euro Feed, is accused of illegal involvement in trafficking meat-based animal feed.


Feed products were allegedly brought from France, Ireland and the Netherlands to Belgium, where they were relabelled.


France banned bone meal from animal feed in 1990 and further tightened its controls in 1996.


"This discovery, if confirmed, could explain the scientific mystery of how certain cows born after the ban on animal derivatives in their feed could develop mad cow disease," the Le Parisien newspaper commented.




someone inside the Gov. told me this recently, one who knows;



Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at..........


USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........


if you want to move this thing along and shake the earth....


then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........


I am not kidding!!!!


so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........


forget any action........ it is ALL gonna be sporadic!!!


And, if there is a case....... there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever travelled to the


UK/europe, etc. etc. ....


It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....


and this may be their biggest downfall.






> Feed investigation


> The news of Mr Eboli's death comes a day > after French magistrates placed under > official investigation a firm allegedly > distributing contaminated feed.



this is exactly why 'sporadic' will stay 'sporadic' $$$$$


 disgusted again in Bacliff, Terry S. Singeltary Sr., Bacliff, Texas USA








Volume 357, Number 9265 28 April 2001


Research letters


Variant Creutzfeldt-Jakob disease in an elderly patient


J W Lorains, C Henry, D A Agbamu, M Rossi, M Bishop, R G Will, J W Ironside


We report a case of variant Creutzfeldt-Jakob disease (vCJD) in a 74-year old man in whom diagnosis was made at necropsy. The occurrence of vCJD in an individual in this age group is unlikely to be an isolated event. Doctors need


to be aware that vCJD can arise in elderly patients so that appropriate investigations (including magnetic resonance imaging) can be done, and permission for neuropathological necropsy requested, in suspected cases.


This case could also have important implications for public health policy decisions and surveillance programmes that target the younger age range of vCJD cases.


Wirral Hospital, Clatterbridge (J W Lorains FRCP); National CJD Surveillance Unit, University of Edinburgh, Western General Hospital, Edinburgh, EH4 2XU, UK (C Henry MRCPI, M Bishop BSC, R G Will FRCP, Prof J W Ironside FRCPath); Wirral Hospital, Arrowe Park (D A Agbamu MRCPath); and Walton Centre, Liverpool (M Rossi FRCPath)


Correspondence to: Prof J W Ironside (e-mail:j.w.ironside@ed.ac.uk)








From: TSS (216-119-138-130.ipset18.wt.net)


Subject: Death toll may rise to one a day from madcow disease


Date: October 28, 2000 at 7:39 pm PST


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


Greetings List Members,


it seems old Prof. Will at the CJD surveillance unit may have to think twice now about Mrs. Soukups from the U.S., and probably many more...


kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA


October 29 2000 BRITAIN


Death toll may rise to one a day


Youngest CJD victim dies at 14


Jonathon Carr-Brown


BRITAIN'S youngest victim of CJD, 14-year-old Zoe Jeffries, died yesterday as scientists began to increase estimates of the possible death toll from the illness.


Jeffries, from Wigan, Greater Manchester, contracted the disease two years ago. She became the country's 81st person confirmed to have died from CJD, the human equivalent of "mad cow" disease.


Her death coincided with a series of predictions and discoveries by government advisers and scientists. These include:


A death rate of one person a week by next September, rising to one a day by 2003.


A rise in the minimum number of deaths in Britain to 1,000, 10 times higher than previously forecast.


The emergence of two potential new clusters of the disease - in Glasgow, where so far five people have died from new variant CJD (nvCJD), and in Doncaster where there have been two CJD deaths. Regarded as statistically significant, these follow the discovery of a cluster in Queniborough, Leicestershire, where five have died.


The death of a 79-year-old American woman from CJD who spent part of the 1970s in the same area of Leicestershire, and the death of a 74-year-old from nvCJD.


Deaths among older people from nvCJD raise the possibility that the disease may have a longer incubation period than previously thought, which would indicate a higher death toll than previously forecast.


Scientists had believed that most people were infected in the late 1980s but there is now evidence from the Phillips inquiry into BSE, published last week, that the disease may have entered the food chain in the 1970s.


The latest developments have led Professor John Collinge, a member of the government's advisory body on BSE and CJD, to revise the minimum number of expected deaths from 100 - which will be reached early next year - to 1,000. "The longer the incubation period, the more potentially worrying it could be." said Collinge.


However, he emphasised that accurate predictions are impossible because of uncertainty over key causal factors including the dose of BSE-tainted meat that is needed to infect a victim, the route of exposure, the incubation period, genetic susceptibility and the extent of species barrier.


Research by Professor Roy Anderson, another advisory committee member, initially put the range of deaths between 100 and 136,000. In August he said the most likely number was about 6,000 and predicted that deaths of hundreds of thousands of people were unlikely.


These figures have, however, been criticised by scientists including Dr Stephen Deallar, a pathologist at Burnley hospital, Lancashire, who in the 1970s was one of the first to guess how BSE entered the food chain. "I think Collinge's revision is on the optimistic side," he said. "This is going to keep doubling for a number of years to come."


The death of the 74-year-old, believed to be from North Yorkshire, could have significant implications, he said. "If this man ate hamburgers in the 1970s and has been incubating it for 30 years, the doubling process is going to go on longer with a much bigger pool of people."


The death of Jeffries highlights the difficulties of diagnosing nvCJD four years after the government acknowledged both its existence and the poor standard of care that victims have received.


Her symptoms emerged in June 1998. Her mother, Helen Jeffries, said: "One morning Zoe got up and just didn't do anything. She just cried.


"It was as though she went to bed one person and got up a different one."


It was not until June 1999 that doctors from the CJD Surveillance Unit diagnosed her illness as nvCJD.


Although her mother said she was filled with remorse because she had fed her daughter cheap beef burgers, she criticised the lack of information and knowledge about BSE and CJD.


"It's just as if someone had stuck a knife into Zoe's body," she said. "I really do think she has been murdered."










Sunday, August 09, 2009


***CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009 ***





Wed, 29 Nov 2000 14:14:18 -0500


a private email from the late Dr. Gibbs, a true pioneer in the research of human/animal TSEs and one that never wavered on helping the families and victims of this horrible disease, and one that helped me many times in trying to seek out the truth;


Subject: Re: Hello Dr. Gibbs...........


Date: Wed, 29 Nov 2000 14:14:18 –0500


From: "Clarence J. Gibbs, Jr., Ph.D."


To: "Terry S. Singeltary Sr." References: 3a254430.9fb97284@wt.net


Hi Terry:


326 E Stret N.E., Washington, D. C. 20002.


Better shrimp and oysters than cards!!!!


Have a happy holiday and thanks for all the information you bring to the screen.


Joe Gibbs














Saturday, October 19, 2013


***A comparative study of modified confirmatory techniques and additional immuno-based methods for non-conclusive autolytic Bovine spongiform encephalopathy cases




Monday, September 02, 2013


Atypical BSE: role of the E211K prion polymorphism




Location: Virus and Prion Research Unit




Wednesday, September 25, 2013


Inspections, Compliance, Enforcement, and Criminal Investigations BSE TSE PRION 2013






















line to take, sporadic CJD


















ii. on page 2 the sentence ''He had drunk pooled milk from the herd which included that from the affected animal'' will mislead the uninformed. It needs to be made clear that milk from a cow which is suspected to be affected with BSE cannot be drunk or added to the bulk milk produced by the rest of the herd.


iii. in the final paragraph I suggest that the phrase ''and a causal link with BSE is at most conjectural'' BE DELETED: the first paragraph of the sentence would then stand as a clear statement that the CJD case was likely to have been a CHANCE PHENOMENON.






''DH is aware of a second case of CJD in a dairy farmer who has had BSE in his herd. We cannot comment on the details of the case, but we know of nothing to suggest this is anthing other than a sporadic case of CJD. .........











The numbers concerned are very small, and it is not possible to draw any conclusions from such small numbers. This issue is being considered by the Government's expert advisers....





THE FARMER IS THOUGHT TO HAVE HAD AT LEAST TWO CASES OF BSE IN HIS HERD, which were diagnosed in 1992. The farmer is reported to have asssisted in calving and to have drunk milk from his herd. This does not suggest that this is anything other than a sporadic case of CJD. ...












3. Neither Dr Will nor the CJD surveillance unit intend to disclose the existence of this case or make any comment at present unless it attracts media attention.










The second annual report on CJD surveillance in the UK, which is about to be published, gives occupational history details of 29 definite and probable CJD cases recorded in people who had a history of employment at any time in particular occupational groups of potential significance for the occurrence of the disease. The 29 cases were amongst 95 diagnosed over a 3 year period: the other 66 cases did not fall into such occupational groups.


These relevant details are:-
















snip... full text ;






Rocky Mountain oysters, mountain oysters, prairie oysters, Montana tendergroin or swinging sirloin






1. The article in the Daily Mail of 12 August again raises the question of a CAUSATIVE LINK BETWEEN BSE AND CJD. This follows the death of a second farmer from CJD...




I am, however, concerned about how DH and MAFF would respont to public concern generated if there are further CJD cases among farmers.




4. Unwelcome, though it maybe to the Tyrrell Committee, I think they must be asked at their next meeting to give further thought to what they might advise the Department and MAFF if ANOTHER FARMER (or TWO) DEVELOPS CJD. OR, if a butcher or abattoir worker develops the disease.


5. Although the Committee were given plenty of advance warning about the second farmer, they may NOT BE SO FORTUNATE NEXT TIME ROUND. Some Contingency planning on the Committee's response to a further case of CJD in a farmer seems essential. At the same time the Committee should consider if there is SPECIAL RISK TO FARMERS, FOR EXAMPLE THEIR HISTORICAL HABIT OF CHEWING CATTLE NUTS, that might be implicated. .....(oh my GOD...tss)






Ministers will note from this that experts are of the view, that there is unlikely to be a direct link between the cases of BSE, and the occurance of CJD in the farmer.


(NOTE CJD increasing over 3 years. ...TSS)






'AGE AT ONSET' is therefore likely to be a reflection of particulary aetiological factors, about which, for sporadic CJD at least, much is yet unknown. IT has therefore been suggested that examination of the f/d i/p of other groups with TSE's, and comparison with that of CJD subsets might help to elucidate aetiological mechanisms for sporadic CJD in particular; i.e. ALMOST A REVERSAL OF THE ORIGINAL UNDERTAKING.








2. The Tyrrell Committee met on 7 October and the significance of the two cases of CJD reported in dairy farmers who had BSE-affected animals on their farms was discussed at some length, AS WERE THE IMPLICATIONS OF A THIRD (OR FORTH) similar case.


3. The Committee were unable to identify any possible risk factors over and above those that they had already considered, both in general and with particular of TASTING THE FEED does continue but there was no consensus about the value of advising farmers to discontinue this practice. Feed currently in use does not pose a risk because of the ruminant-ruminant feed ban.










In view of the CONCERN that exposue to BSE OR SCRAPIE MAY POSE A RISK TO HUMANS, it is proposed investigate the relationship between sporadic creutzfeldt-jakob disease.....








3. While Committee may have no leads to pursue on why farmers might be at increased risk, I hope they understand the urgency with which they will need to respond if or when a THIRD FARMER DEVELOPS CJD.


















Dr. Dealler





























I have informed Dr Tyrrell that we have now written to Dr Hueston to invite him to serve on the Committee and he was very pleased to hear this. He was also in favour of our idea of having a deputy Chairman who could take any emergency meetings eg IF THERE WERE TO BE ANOTHER CJD CASE IN AGRICULTURE. I suggested that either Dr. WIll or Dr Kimberlin were likely candidates and he thought that this was about right. He felt that on balance he would prefer Dr Will who he thought took a more cautious line and was LESS DOGMATIC. .....


















IP PS(L) wishes to probe this further we think it best to explain the matter VERBALLY. The problem is how to present the findings in this year's annual report in a way which avoids unnecessary public alarm and limits the scope for media scare stores. (or the facts...TSS)








''This year's findings show a number of associations but the strongest is for veal.''




''This is of considerable concern given recent developments. In particular, Ministers will be particularly concerned about the European dimension given the recent troubles with the Germans.''


YOU can see the beginning of the ukbsenvCJD only theory beginning to unfold now. full text of this ukbsenvcjd only conspiracy can be seen here. ...TSS












Dear Mr Elmhirst,




Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.


The Surveillance Unit is completely independent outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.




The statistical results regarding the consumption of venison was put into perspective in the body of the report and was NOT MENTIONED AT ALL IN THE PRESS RELEASE. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of VENISON was highlighted only by the media i.e. in the News at one television programme.


I believe that a further statement about the report, or indeed statistical links between CJD and consumption of Venison, would increase, and quite possibly GIVE DAMAGING CREDENCE, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.






see buttered and watered down report here that caters to industry instead of human safety...TSS








''This year's findings show a number of associations but the strongest is for veal.''




In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and increased risk of CJD. When some account was taken of possible confounding, the association between veal eating and risk of CJD emerged as the strongest of these associations statistically. These findings concerning dietary history are particulary difficult to interpret for two reasons.


1. .........BSeee...........TSS


2. .........BSeee...........TSS


(I.E. BSeee = bull sh!t encephalopathy or government cover-up i.e. God save the industry at all cost, including human health. ...TSS)


THUS, the reported veal eating habits of confirmed CJD cases appear virtually identical to suspect cases later judged not to have the disease. This provides good circumstantial evidence to support the hypothesis that the apparent association between veal consumption and CJD is due to recall bias. Analysis of other apparent dietary risk factors for CJD, including venison, has provided similar evidence of recall bias.




In summary, the analysis of the dietary case-control study demonstrates a strong association between a lifetime history of veal consumption and the risk of developing Creutzfeldt-Jakob disease. HOWEVER this result may well be due to recall bias and analysis of clinical and molecular bilogical features does not provide supportive evidence for the hypothesis that veal eating is a risk factor for CJD. ...












He says that when he worked at MAFF, ''the way it was structurally set up was not that science would drive the politics, but that the politics will drive the science. And that's wrong.''






11/3/96 DGRC alerts DTI Ministers and CSA to discovery of nvCJD on basis of letter from MRC Chief Executive dated 11/3/96



BIRTH OF THE UKBSEnvCJD ONLY THEORY, the birth of the 'BIG LIE' begins. ...tss









5. This case may raise fears of a link between BSE and CJD. Current advice is that there is no scientific evidence of a link between BSE in cattle and CJD in humans. Furthermore advice from the Spongiform Encephalopathy Advisory Committee is that they are satisified that all necessary safeguards are in place to minimise further spread of spongiform encephalopathies in animals and to prevent any risk of transmission to humans. ...






To ask the Secretary of State for Health, how many people under the age of 20 years in each of the last five years have suffered from Creutzfeldt-Jakob disease; and of these how many had not had any growth treatment previously.




We are not aware of any people under the age of 20 in the UK suffering from Creutzfeldt-Jakob Disease in the last five years.












As we discussed, a general line could be added, _if pressed_, to the line you have already received, as follows;


"We are confident that no-one from the CJD Surveillance Unit would discuss with any patient's relatives matters relating to BSE or to contact with the press"...(_and consider adding_..."in the way that has been reported."










4. In addition, Channel 4 is due to broadcast "Dispatches" (made by Fulcrum Productions) tomorrow evening, 26 January. The programme will cover the above issues. Paragraph 2 of a letter from Fulcrum (at D) includes transcript of an interview recorded for the programme with the teenage girl's relative. A copy of the reply from Dr Will, head of the CJD Surveillance Unit, to Fulcrum is also enclosed. The points Dr will makes are fully endorsed by the Department. It is worth noting that Dr Will had earlier spent a considerable amount of time briefing Fulcrum on the CJD Surveillance Unit's activities and on general CJD issues.


5. The implication of a cover-up with respect to the diagnosis in this case and possible links with BSE cannot be substantiated. ...














A TEENAGE GIRL may have caught the human form of MAD COW DISEASE by eating a contaminated burger it was claimed last night.


VICKY RIMMER, 16, has the killer Creutzfeldt-Jakob disease (CJD).
























I have interviewed Mrs Rimmer at my constituency surgery


IF there is nothing to hide, why is there so much SECRECY? WHY is the Government and other Bodies trying to stop any CHANCE OF PEOPLE CONNECTING THE TWO DISEASES. The B.S.E. problem is obvious, but if the correct measures are taken, surely the problem could be contained, however, as it stands the lack of investigation and interest of the possibility of B.S.E. and C.J.D. being linked is open for speculation and surely someone has to account for peoples lives! WHY is so much trouble being taken to convice people that B.S.E. and C.J.D. are not linked? Guilty Conscience perhaps ? - or cover up?






22 FEBRUARY 1994






Alleged Case of Creutzfeld Jakob Disease: Victoria Rimmer.


(now story changes that biopsy shows she does not have CJD...tss)






now story changes to ;




7. The Parliamentary Secretary is invited to note the recent statements made on __________ and the present position which remains that CJD cannot be confirmed, in this case at this stage.






3. The Medical Director at ___________________ Hospital advised the Department on 6 June that the results of ___________________ brain biopsy had been received and that it showed NO EVIDENCE OF CJD. ______________ Hospital subsequently issued a statement to the press to this effect and this was publicised widely in the press (doc 1). News coverage which followed suggested that the statement made by ________________ Hospital had been misleading (doc 2). Enquires have been made of the Medical Director at _______________ Hospital who has CONFIRMED THAT THE STATEMENT ISSUED BY THE HOSPITAL WAS ISSUED IN ERROR. The facts are that two pathology reports on the same piece of brain tissue were recieved. The first report indicated that CJD was unlikely, The second report indicated that CJD was possible, PERHAPS EVEN LIKELY, but that no definitive diagnosis could be made before a post mortem was undertaken.










IN light of Asante/Collinge et al findings that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;


 -------- Original Message --------


Subject: re-BSE prions propagate as


either variant CJD-like or sporadic CJD


Date: Thu, 28 Nov 2002 10:23:43


-0000 From: "Asante, Emmanuel A" To: "[log in to unmask]"


Dear Terry,


I have been asked by Professor Collinge to respond to your request. I am


a Senior Scientist in the MRC Prion Unit and the lead author on the


paper. I have attached a pdf copy of the paper for your attention. Thank


you for your interest in the paper.


In respect of your first question, the simple answer is, yes. As you


will find in the paper, we have managed to associate the alternate


phenotype to type 2 PrPSc, the commonest sporadic CJD.


It is too early to be able to claim any further sub-classification in


respect of Heidenhain variant CJD or Vicky Rimmer's version. It will


take further studies, which are on-going, to establish if there are


sub-types to our initial finding which we are now reporting. The main


point of the paper is that, as well as leading to the expected new


variant CJD phenotype, BSE transmission to the 129-methionine genotype


can lead to an alternate phenotype which is indistinguishable from type


2 PrPSc.


I hope reading the paper will enlighten you more on the subject. If I


can be of any further assistance please to not hesitate to ask. Best wishes.


Emmanuel Asante


<> ____________________________________


Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial


College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG


Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:


[log in to unmask] (until 9/12/02)


New e-mail: [log in to unmask] (active from now)






full text ;








in the USA, a 16 year old in 1978;




(20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. see second url below)


in France, a 19 year old in 1982;


in Canada, a 14 year old of UK origin in 1988;


in Poland, cases in people aged 19, 23, and 27 were identified in a retrospective study (published 1991), having been originally misdiagnosed with a viral encephalitis;


Creutzfeldt's first patient in 1923 was aged 23.






20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A 19 year old died from sCJD in France in 1985. There is no evidence of an iatrogenic cause for those cases....












Dear Bob,


An otherwise enjoyable dinner last night as guest of the Association of Clinical Pathology was marred by a conversation with a neuropathologist who was just about to write CMO with details of a case of CJD he had just seen. When first mentioning the case, he claimed she was only 36, but after a few more glasses of wine he became less certain of that and thought she could have been older. Locally, they made quite an assoctiation with BSE, since she ws a farmers wife on that farm that, atypically for that area of S Yorkshire, had several BSE cases. I was told the clinical and pahtological pictures were typical of CJD. ...




cover-up of 4th farm worker ???















now story changes from;


SEAC concluded that, if the fourth case were confirmed, it would be worrying, especially as all four farmers with CJD would have had BSE cases on their farms.




This is not unexpected...


was another farmer expected?





4th farmer, and 1st teenager









Over a 5 year period, which is the time period on which the advice from Professor Smith and Dr. Gore was based, and assuming a population of 120,000 dairy farm workers, and an annual incidence of 1 per million cases of CJD in the general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an individual in the general population to develop CJD. Using the actual current annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5 TIMES.


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 farm 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 sub-population is 10 TIMES, and taking an annual incidence of 0.7 per million, IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than that in the general population...








Vickey Rimmer, 16, DID NOT DIE FROM nvCJD, she died from a form of sporadic CJD, whatever the hell that is. and there have been 16 year old die from sporadic CJD in the USA as well.


SIMPLY PUT, the ukbsenvcjd only theory was wrong from day one. the elderly are expendable, pets and kids are not.


Science was dictated by 'big buisness' after the Vickey Rimmer case with the ukbsenvcjd only myth.




18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 7 December 2006 are now available.




64. A member noted that at the recent Neuroprion meeting, a study was presented showing that in transgenic mice BSE passaged in sheep may be more virulent and infectious to a wider range of species than bovine derived BSE.


Other work presented suggested that BSE and bovine amyloidotic spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS SIMILAR IN NATURE TO A MUTATION FOUND IN CASES OF SPORADIC CJD.







3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse


Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University


Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years.


***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans.***


6:30 Close of Day One








There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.


He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.





MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE (the last two cases of mad cow disease in the USA were in Alabama, and Texas, both of which were atypical BSE).




Please remember, the last two mad cows documented in the USA i.e. Alabama and Texas, both were of the 'atypical' BSE strain, and immediately after that, the USDA shut down the testing from 470,000 to 40,000 in the U.S. in 2007 out of about 35 million cattle slaughtered. also, science is showing that some of these atypical cases are more virulent to humans than the typical UK BSE strain ;



***Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.***


Progress Report from the National Prion Disease Pathology Surveillance Center


An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD


April 3, 2008





 According to Professor James Ironside of the National CJD Surveillance Unit, Miss Rimmer's case was "unique" and tests showed signs of both vCJD and new variant CJD.


"Our understanding of the case is not complete. It is one of the most unusual and difficult cases I have ever come across," he explained.


"The characteristics of the disease suffered by Miss Rimmer do not fall neatly into any category.


"The investigations that we have performed so far would indicate that this case, unique as it is, has more similarities to sporadic CJD than to new variant."




Mr Hughes returned a verdict of death by natural causes and concluded that Miss Rimmer died of bronchial pneumonia caused by CJD. ...













Wednesday, October 09, 2013






Thursday, October 10, 2013


*** CJD REPORT 1994 increased risk for consumption of veal and venison and lamb ***





***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.






***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.






Sunday, August 25, 2013


***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission




Sunday, July 21, 2013


*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?




NOW, let’s take a look at what the science is saying on the risk factors of human TSE prion disease from CWD prion disease of cervids.


first, from the cdc/nih et al prion gods, and what they said on human cwd potential, and what that might look like ;


now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????


“Our conclusion stating that we found no strong evidence of CWD transmission to humans”



From: TSS (216-119-163-189.ipset45.wt.net)




Date: September 30, 2002 at 7:06 am PST


From: "Belay, Ermias"




Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"


Sent: Monday, September 30, 2002 9:22 AM




Dear Sir/Madam,


In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.


That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.


Ermias Belay, M.D. Centers for Disease Control and Prevention



-----Original Message-----




Sent: Sunday, September 29, 2002 10:15 AM


To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV




Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS


Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41


A prion disease of cervids: Chronic wasting disease


Sigurdson CJ.




*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,




full text ;





Monday, February 09, 2009


Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD





Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain


Date: August 25, 2007 at 12:42 pm PST


our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.




Wednesday, March 18, 2009


Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II







Saturday, October 19, 2013


ACA Council Meets to Endorse Several Proposed USAHA Resolutions (CWD TSE PRION DISEASE)




Monday, October 14, 2013


Researchers estimate one in 2,000 people in the UK carry variant CJD proteins




WHAT about the sporadic CJD TSE proteins ?



WE now know that some cases of sporadic CJD are linked to atypical BSE and atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all it’s sub-types $$$



Sunday, August 11, 2013


Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013


*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010




Sunday, October 13, 2013


CJD TSE Prion Disease Cases in Texas by Year, 2003-2012




Tuesday, September 24, 2013


NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)


*** Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15 ***




Saturday, July 6, 2013


*** Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy


Research Article




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 • www.cdc.gov/eid • Vol. 17, No. 5, May 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.








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




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)




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).





Suspect symptoms


What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?


28 Mar 01


Like lambs to the slaughter 31 March 2001 by Debora MacKenzie Magazine issue 2284. Subscribe and get 4 free issues. FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.


Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.


Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.


"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.


Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.


Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.


As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.


"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.


But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.


People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.


But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."


There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.


Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.




Wednesday, February 16, 2011










Sunday, December 12, 2010


EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010







AS of June 30, 2011,








see updated APHIS scrapie report ;




Tuesday, February 01, 2011


Sparse PrP-Sc accumulation in the placentas of goats with naturally acquired scrapie


Research article




Date: Tuesday, February 01, 2011 5:03 PM


To: Mr Terry Singeltary


Subject: Your comment on BMC Veterinary Research 2011, 7:7


Dear Mr Singeltary


Thank you for contributing to the discussion of BMC Veterinary Research 2011, 7:7 .


Your comment will be posted within 2 working days, as long as it contributes to the topic under discussion and does not breach patients' confidentiality or libel anyone. You will receive a further notification by email when the posting appears on the site or if it is rejected by the moderator.


Your posting will read:


Mr Terry Singeltary,




Scrapie cases Goats from same herd USA Michigan


Comment: " In spite of the poorly defined effects of PRNP genetics, scrapie strain, dose, route and source of infection, the caprine placenta may represent a source of infection to progeny and herd mates as well as a source of persistent environmental contamination. "


Could this route of infection be the cause of the many cases of Goat scrapie from the same herd in Michigan USA ?


Has this been investigated ?


(Figure 6) including five goat cases in FY 2008 that originated from the same herd in Michigan. This is highly unusual for goats, and I strenuously urge that there should be an independent investigation into finding the common denominator for these 5 goats in the same herd in Michigan with Scrapie. ...


Kind Regards, Terry



Thursday, January 07, 2010


Scrapie and Nor-98 Scrapie November 2009 Monthly Report Fiscal Year 2010 and FISCAL YEAR 2008




In FY 2010, 72 cases of classical Scrapie and 5 cases of Nor-98 like Scrapie were confirmed...




Scrapie Nor-98 like case in California FY 2011 AS of December 31, 2010.


Scrapie cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat cases = 21 Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS cases)


Last herd with infected goats disignated in FY 2008 Michigan 8 cases




Tuesday, February 01, 2011


Sparse PrP-Sc accumulation in the placentas of goats with naturally acquired scrapie


Research article





"In spite of the poorly defined effects of PRNP genetics, scrapie strain, dose, route and source of infection, the caprine placenta may represent a source of infection to progeny and herd mates as well as a source of persistent environmental contamination."


Could this route of infection be the cause of the many cases of Goat scrapie from the same herd in Michigan USA ?


Has this been investigated ?


(Figure 6) including five goat cases in FY 2008 that originated from the same herd in Michigan. This is highly unusual for goats, and I strenuously urge that there should be an independent investigation into finding the common denominator for these 5 goats in the same herd in Michigan with Scrapie. ...


Kind Regards, Terry





Scrapie Nor-98 like case in California FY 2011 AS of December 31, 2010.


Scrapie cases in goats FY 2002 - 2011 AS of December 31, 2010 Total goat cases = 21 Scrapie cases, 0 Nor-98 like Scrapie cases (21 field cases, 0 RSSS cases)


Last herd with infected goats disignated in FY 2008 Michigan 8 cases







----- Original Message -----


From: "BioMed Central Comments"




Sent: Wednesday, February 16, 2011 4:13 AM


Subject: Your comment on BMC Veterinary Research 2011, 7:7


Your discussion posting "Scrapie cases Goats from same herd USA Michigan" has been rejected by the moderator as not being appropriate for inclusion on the site.


Dear Mr Singeltary,


Thank you for submitting your comment on BMC Veterinary Research article (2011, 7:7). We have read your comment with interest but we feel that only the authors of the article can answer your question about further investigation of the route of infection of the five goats in Michigan. We advise that you contact the authors directly rather than post a comment on the article.


With best wishes,




Maria Kowalczuk, PhD Deputy Biology Editor BMC-series Journals


BioMed Central 236 Gray's Inn Road London, WC1X 8HB


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BMC Veterinary Research






Tuesday, February 01, 2011


Sparse PrP-Sc accumulation in the placentas of goats with naturally acquired scrapie


Research article




Tuesday, April 30, 2013


Transmission of classical scrapie via goat milk


Veterinary Record2013;172:455 doi:10.1136/vr.f2613




Friday, May 10, 2013


Evidence of effective scrapie transmission via colostrum and milk in sheep




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, November 30, 2009






Thursday, December 20, 2012






*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.



Thursday, May 30, 2013


World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease


U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease






I ask Professor Kong ; Thursday, December 04, 2008 3:37 PM


Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment ''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....'' Professor Kong reply ;




''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''



Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA END...TSS



Thursday, December 04, 2008 2:37 PM



"we have found that H-BSE can infect humans."


personal communication with Professor Kong. ...TSS



BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.



Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.







please see below from PRION2013 ;



*** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.


AD.56: The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice



Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki Okada, Shirou Mohri and Takashi Yokoyama National Institute of Animal Health; Tsukuba, Japan


H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE, and has been detected in several European countries, and North America. Transmission studies of H-type BSE led to the emergence of the classical BSE (C-BSE) phenotypes during passages in inbred wild type and bovinized PrP-overexpressing transgenic mice. In this study, we conducted serial passages of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice (TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage were constant (~= 220 d), no clear differences were observed in their biological and biochemical properties. However, at the forth passage, 2 different BSE phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the other is longer survival times. TgBoPrP mice with longer incubation period showed the H-type phenotype of PrPsc profile and pathology. However, those of shorter incubation period were different phenotypes from previously existed BSE prions (C-BSE, L-type BSE, and H-type BSE).


*** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.





please see ;



Thursday, August 15, 2013


The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice




Sunday, September 1, 2013


*** Evaluation of the Zoonotic Potential of Transmissible Mink Encephalopathy


We previously described the biochemical similarities between PrPres derived from L-BSE infected macaque and cortical MM2 sporadic CJD: those observations suggest a link between these two uncommon prion phenotypes in a primate model (it is to note that such a link has not been observed in other models less relevant from the human situation as hamsters or transgenic mice overexpressing ovine PrP [28]). We speculate that a group of related animal prion strains (L-BSE, c-BSE and TME) would have a zoonotic potential and lead to prion diseases in humans with a type 2 PrPres molecular signature (and more specifically type 2B for vCJD)




Together with previous experiments performed in ovinized and bovinized transgenic mice and hamsters [8,9] indicating similarities between TME and L-BSE, the data support the hypothesis that L-BSE could be the origin of the TME outbreaks in North America and Europe during the mid-1900s.





Monday, October 10, 2011


EFSA Journal 2011 The European Response to BSE: A Success Story




EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.







see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;




Thursday, August 12, 2010


Seven main threats for the future linked to prions


First threat


The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.


***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.


Second threat














Tuesday, July 2, 2013


APHIS USDA Administrator Message to Stakeholders: Agency Vision and Goals Eliminating ALL remaining BSE barriers to export market




Sunday, August 21, 2011


The British disease, or a disease gone global, The TSE Prion Disease


(see video here)






(see video at bottom)




Sunday, September 6, 2009








Creutzfeldt-Jakob Disease Public Health Crisis









JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733


Diagnosis and Reporting of Creutzfeldt-Jakob Disease


Terry S. Singeltary, Sr Bacliff, Tex


Since this article does not have an abstract, we have provided the first 150 words of the full text.


KEYWORDS: creutzfeldt-jakob disease, diagnosis. To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.


References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.




Published March 26, 2003


RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States


Terry S. Singeltary, retired (medically)


I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?


Published March 26, 2003






BY Philip Yam


Yam Philip Yam News Editor Scientific American www.sciam.com


Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.




Laying Odds


Are prion diseases more prevalent than we thought?


Researchers and government officials badly underestimated the threat that mad cow disease posed when it first appeared in Britain. They didn't think bovine spongiform encephalopathy was a zoonosis-an animal disease that can sicken people. The 1996 news that BSE could infect humans with a new form of Creutzfeldt-Jakob disease stunned the world. It also got some biomedical researchers wondering whether sporadic CJD may really be a manifestation of a zoonotic sickness. Might it be caused by the ingestion of prions, as variant CJD is?


Revisiting Sporadic CJD


It's not hard to get Terry Singeltary going. "I have my conspiracy theories," admitted the 49-year-old Texan.1 Singeltary is probably the nation's most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union's Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.madcow. org Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people's health.


Singeltary has similar inclinations. ...






Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9


June 2003


BY Philip Yam




Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.








14th ICID International Scientific Exchange Brochure -


Final Abstract Number: ISE.114


Session: International Scientific Exchange


Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009


T. Singeltary


Bacliff, TX, USA




An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.




12 years independent research of available data




I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.




I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.




CJD Singeltary submission to PLOS ;


No competing interests declared.


see full text ;






The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003 doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI


Tracking spongiform encephalopathies in North America




Xavier Bosch


“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt—Jakob ...







 -------- Original Message --------


Subject: Tracking spongiform encephalopathies in North America LANCET INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003


Date: Tue, 29 Jul 2003 17:35:30 –0500


From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy


To: BSE-L@uni-karlsruhe.de


Volume 3, Number 8 01 August 2003




Tracking spongiform encephalopathies in North America


Xavier Bosch


My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.


49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD)the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.


Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.


Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.


To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.


Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.


Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.


Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.


Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.


Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.


CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.






> > > he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source. < < <


actually, that quote was from a more recent article in the Journal of Neurology (see below), not the JAMA article.



Full Text


Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734.





Re: vCJD in the USA * BSE in U.S.


15 November 1999 Terry S Singeltary, NA


In reading the recent article in the BMJ about the potential BSE tests being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize me, that the U.S. has been concealing vCJD. There have been people dying from CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for some time. It just seems that when there is one found, they seem to change the clarical classification of the disease, to fit their agenda. I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt Jakob disease.


Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so bad at times, it would take 3 of us to hold her down, while she screamed "God, what's wrong with me, why can't I stop this." 1st of symptoms to death, 10 weeks, she went blind in the first few weeks. But, then they told me that this was just another strain of sporadic CJD. They can call it what ever they want, but I know what I saw, and what she went through. Sporadic, simply means, they do not know.


My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following;


vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD.


The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?


CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997.


So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie. Cats becoming infected with a TSE. Have you ever read the ingredients on the labels of cat and dog food? But, they do not put these tissues from these animals in pharmaceuticals, cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and the many more products that come from bovine, ovine, or porcine tissues and organs. So, as I said, this CWD would be a small piece of a very big puzzle. But, it is here, and it most likely has killed. You see, greed is what caused this catastrophe, rendering and feeding practices. But, once Pandora's box was opened, the potential routes of infection became endless.


No BSE in the U.S.A.? I would not be so sure of that considering that since 1990;


Since 1990 the U.S. has raised 1,250,880,700 cattle;


Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of Oct. 4, 1999;


There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until Aug. 4, 1997 went to the renders for feed;


Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of Aug. 1999;


Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.


I believe all these TSE's are going to be related, and originally caused by the same greedy Industries, and they will be many. Not just the Renders, but you now see, that they are re-using medical devices that were meant for disposal. Some medical institutions do not follow proper auto- claving procedures (even Olympus has put out a medical warning on their endescopes about CJD, and the fact you cannot properly clean these instruments from TSE's), and this is just one product. Another route of infection.


Regardless what the Federal Government in the U.S. says. It's here, I have seen it, and the longer they keep sweeping it under the rug and denying the fact that we have a serious problem, one that could surpass aids (not now, but in the years to come, due to the incubation period), they will be responsible for the continued spreading of this deadly disease.


It's their move, it's CHECK, but once CHECKMATE has been called, how many thousands or millions, will be at risk or infected or even dead. You can't play around with these TSE's. I cannot stress that enough. They are only looking at body bags, and the fact the count is so low. But, then you have to look at the fact it is not a reportable disease in most states, mis-diagnosis, no autopsies performed. The fact that their one-in-a- million theory is a crude survey done about 5 years ago, that's a joke, under the above circumstances. A bad joke indeed........


The truth will come, but how many more have to die such a hideous death. It's the Government's call, and they need to make a serious move, soon. This problem, potential epidemic, is not going away, by itself.


Terry S. Singeltary Sr.


P.O. Box 42, Bacliff, Texas 77518 USA




Competing interests:None declared




U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...


2 January 2000


Terry S Singeltary


In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.


The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;


"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."


Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.


Something else I find odd, page 16;


"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."


A few more factors to consider, page 15;


"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."


"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."


"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."


Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow.


Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.


To be continued...


Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA


Competing interests:None declared




DER SPIEGEL (9/2001) - 24.02.2001 (9397 Zeichen) USA: Loch in der Mauer Die BSE-Angst erreicht Amerika: Trotz strikter Auflagen gelangte in Texas verbotenes Tiermehl ins Rinderfutter - die Kontrollen der Aufsichtsbehördensind lax.Link auf diesen Artikel im Archiv:




 "Löcher wie in einem Schweizer Käse" hat auch Terry Singeltary im Regelwerk der FDA ausgemacht. Der Texaner kam auf einem tragischen Umweg zu dem Thema: Nachdem seine Mutter 1997 binnen weniger Wochen an der Creutzfeldt-Jakob-Krankheit gestorben war, versuchte er, die Ursachen der Infektion aufzuspüren. Er klagte auf die Herausgabe von Regierungsdokumenten und arbeitete sich durch Fachliteratur; heute ist er überzeugt, dass seine Mutter durch die stetige Einnahme von angeblich kräftigenden Mitteln erkrankte, in denen - völlig legal - Anteile aus Rinderprodukten enthalten sind.


Von der Fachwelt wurde Singeltary lange als versponnener Außenseiter belächelt. Doch mittlerweile sorgen sich auch Experten, dass ausgerechnet diese verschreibungsfreien Wundercocktails zur Stärkung von Intelligenz, Immunsystem oder Libido von den Importbeschränkungen ausgenommen sind. Dabei enthalten die Pillen und Ampullen, die in Supermärkten verkauft werden, exotische Mixturen aus Rinderaugen; dazu Extrakte von Hypophyse oder Kälberföten, Prostata, Lymphknoten und gefriergetrocknetem Schweinemagen. In die USA hereingelassen werden auch Blut, Fett, Gelatine und Samen. Diese Stoffe tauchen noch immer in US-Produkten auf, inklusive Medizin und Kosmetika. Selbst in Impfstoffen waren möglicherweise gefährliche Rinderprodukte enthalten. Zwar fordert die FDA schon seit acht Jahren die US-Pharmaindustrie auf, keine Stoffe aus Ländern zu benutzen, in denen die Gefahr einer BSE-Infizierung besteht. Aber erst kürzlich verpflichteten sich fünf Unternehmen, darunter Branchenführer wie GlaxoSmithKline, Aventis und American Home Products, ihre Seren nur noch aus unverdächtigem Material herzustellen.


"Its as full of holes as Swiss Cheese" says Terry Singeltary of the FDA regulations. ...










Thursday, June 6, 2013






since our fine federal friends have decided not to give out any more reports on the USA breaches of the feed ban and surveillance etc. for the BSE TSE prion mad cow type disease in the USDA livestock, I thought I might attempt it. I swear, I just don’t understand the logic of the SSS policy, and that includes all of it. I assure you, it would be much easier, and probably better for the FDA and the USDA INC., if they would simply put some kind of report out for Pete’s sake, instead of me doing it after I get mad, because I am going to put it all out there. the truth.


PLEASE BE ADVISED, any breach of any of the above classifications OAI, VAI, RTS, CAN lead to breaches into the feed BSE TSE prion protocols, and CAN lead to the eventual suspect tainted feed reaching livestock. please, if any USDA official out there disputes this, please explain then how they could not. paperwork errors can eventually lead to breaches of the BSE TSE prion mad cow feed ban reaching livestock, or contamination and exposure there from, as well.


I would sure like to see the full reports of just these ;


4018 CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y


9367 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N


9446 DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N


9447 DEN-DO 3002857110 Weld County Bi-Products dba Fort Morgan Pet Foods 13553 County Road 19 Fort Morgan CO 80701-7506 OPR RE HP 12/7/2011 OAI N


see full list of the fda mad cow bse feed follies, toward the bottom, after a short brief update on the mad cow bse follies, and our good friend Lester Crawford that was at the FDA.


ALSO, I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$










Inspections conducted by State and FDA investigators are classified to reflect the compliance status at the time of the inspection, based upon whether objectionable conditions were documented. Based on the conditions found, inspection results are recorded in one of three classifications:


OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.


VAI (Voluntary Action Indicated) when inspectors find objectionable conditions or practices that do not meet the threshold of regulatory significance, but warrant an advisory to inform the establishment that inspectors found conditions or practices that should be voluntarily corrected. VAI violations are typically technical violations of the 1997 BSE Feed Rule. These violations include minor recordkeeping lapses or conditions involving non-ruminant feeds.


NAI (No Action Indicated) when inspectors find no objectionable conditions or practices or, if they find objectionable conditions, those conditions are of a minor nature and do not justify further actions.



 when sound science was bought off by junk science, in regards to the BSE TSE prion mad cow type disease, by the USDA, CFIA, WHO, OIE, et al. $$$


when the infamous, and fraudulently USDA, FSIS, APHIS, FDA, gold card was taken away that infamous day in December of 2003, all cards were off the table, it was time to change the science, and change they did. ...tss


snip. ...please see full text ;


 Thursday, June 6, 2013










January 28, 2007


Greetings APHIS,


I would kindly like to submit the following to ;




 January 28, 2007 - Regulations.gov






Owens, Julie


From: Terry S. Singeltary Sr. [flounder9@verizon.net]


Sent: Monday, July 24, 2006 1:09 PM


To: FSIS Regulations Comments


Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)


Page 1 of 98 8/3/2006


Greetings FSIS, I would kindly like to comment on the following ;





Response to Public Comments on the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005


INTRODUCTION The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp).


Comments on technical aspects of the risk assessment were then submitted to FSIS. Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary. This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment.


Please bear the following points in mind:





-----Original Message-----


From: Terry S. Singeltary Sr. [mailto:flounder@wt.net]


Sent: Tuesday, February 18, 2003 12:45 PM


To: Freas, William


Cc: Langford, Sheila


Subject: Re: re-vCJD/blood and meeting of Feb. 20, 2003


Greetings FDA,


Variant Creutzfeldt-Jakob Disease Guidance Topic of Feb. 20 TSE Cmte.


[Committee Meeting on February 20, 2003]


FDA’s Transmissible Spongiform Encephalopathies Advisory Committee will meet Feb. 20 to hear updates on the implementation of the agency’s variant Creutzfeldt-Jakob Disease guidance and its effect on blood supply. FULL STORY>>


my name is Terry S. Singeltary Sr., and i lost my mother to hvCJD, one of six known phenotypes of sporadic CJD. i would like to observe this meeting or participate, but have no financial means to do so with. i am disabled from neck injury. anyway, i am not sure if a waiver of fees is possible? i belong to several groups trying to track the true extent of CJDs and trying to find the truth. with CJDs not being reportable but only in a handful of states, and the fact there is no CJD Questionnaire being issued to victims and their families that asks any questions pertaining to route and source, i think to track tainted blood will be futile. i had a major neck surgery in 2001 (3rd), and not _one_ question pertaining to CJD/TSE on any paperwork (and damn near died from MRSA after refusing blood and cadaver bone for fear of risk of CJD/TSEs, go figure, 7 weeks vancomycin via PIC long-line straight to heart). luckily i had informed my neurosurgeon and he did use some disposable instruments and a bone grinder that would not be used again. i would like to submit my concerns on the vCJD _only_ theory as being a total mistake, and that no one knows just how many strains are actually linked to tainted meat and the oral route (one of many potential routes). Asante/Collinge et al have major findings on sporadic CJD, why in the hell is this not making big news in the USA? ($$$) the fact that with the new findings from Collinge et al, that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc, the commonest sporadic CJD, i only ponder how many of the sporadic CJDs in the USA are tied to this alternate phenotype? these new findings are very serious, and should have a major impact on the way sporadic CJDs are now treated as opposed to the vCJD that was thought to be the only TSE tied to ingesting beef, in the medical/surgical arena. these new findings should have a major impact on the way sporadic CJD is ignored, and should now be moved to the forefront of research as with vCJD/nvCJD. the USA has many TSEs, the USA lacks sufficient testing for TSEs in cattle, and the USA still refuses to rapid TSE test USA cattle in sufficient numbers to find, when the late Dr. Richard Marsh had proven that mink had gone down with a TSE (TME), from being fed on 95%+ downer cattle. the GAO has also warned the industry and the FDA that the ruminant-to-ruminant feed ban has to significantly improved if they expect to keep BSE/TSEs out of USA cattle. Scrapie has increased significantly, and CWD is spreading. with the titre of infectivity for lethal dose getting smaller (.1 gram lethal), seems the risk of transmission through various potential routes and sources are rising. all this should warrant CJD/TSEs in humans in the USA to be made reportable on a National bases immediately, and a CJD questionnaire to all CJD/TSE victims and their families. to flounder on these two very important issues, will only allow the agent to spread further...




-------- Original Message --------


Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD


Date: Thu, 28 Nov 2002 10:23:43 -0000


From: "Asante, Emmanuel A" e.asante@ic.ac.uk


To: "'flounder@wt.net'" flounder@wt.net


Dear Terry,


I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.


Thank you for your interest in the paper.


In respect of your first question, the simple answer is, yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.


I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.


Emmanuel Asante






Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)








Freas, William


From: Terry S. Singeltary Sr. [flounder@wt.net]


Sent: Monday, January 08,2001 3:03 PM


To: freas@CBS5055530.CBER.FDA.GOV


Subject: CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)


Greetings again Dr. Freas and Committee Members,


I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version).


I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below).


So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here:


remember AIDS/HIV, 'no problem to heterosexuals in the U.S.?


no need to go into that, you know of this blunder:


DO NOT make these same stupid mistakes again with human/animal TSE's aka MADCOW DISEASE. I lost my Mom to hvCJD, and my neighbor lost his Mother to sCJD as well (both cases confirmed). I have seen many deaths, from many diseases. I have never seen anything as CJD, I still see my Mom laying helpless, jerking tremendously, and screaming "God, what's wrong with me, why can't I stop this". I still see this, and will never forget. Approximately 10 weeks from 1st of symptoms to death. This is what drives me. I have learned more in 3 years about not only human/animal TSE's but the cattle/rendering/feeding industry/government than i ever wished to.


I think you are all aware of CJD vs vCJD, but i don't think you all know the facts of human/animal TSE's as a whole, they are all very very similar, and are all tied to the same thing, GREED and MAN.


I am beginning to think that the endless attempt to track down and ban, potential victims from known BSE Countries from giving blood will be futile. You would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT SWIFTLY to find blood test for TSE's, whether it be blood test, urine test, eyelid test, anything at whatever cost, we need a test FAST.


DO NOT let the incubation time period of these TSEs fool you.


To think of Scrapie as the prime agent to compare CJD, but yet overlook the Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by scrapie from a vaccine made of scrapie infected sheep brains, would be foolish. I acquired this full text version of the event which was recorded in the Annual Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. from the BVA and the URL is posted in my (long version).


U.S.A. should make all human/animal TSE's notifiable at all ages, with requirements for a thorough surveillance and post-mortem examinations free of charge, if you are serious about eradicating this horrible disease in man and animal.


There is histopathology reports describing “_florid_ plaques" in CJD victims in the USA and some of these victims are getting younger. I have copies of such autopsies, there has to be more. PLUS, sub-clinical human TSE's will most definitely be a problem.


THEN think of vaccineCJD in children and the bovine tissues used in the manufacturing process, think of the FACT that this agent surviving 6OO*C. PNAS -- Brown et al. 97 (7): 3418 scrapie agent live at 600*C


Then think of the CONFIDENTIAL documents of what was known of human/animal TSE and vaccines in the mid to late 80s, it was all about depletion of stock, to hell with the kids, BUT yet they knew. To think of the recall and worry of TSE's from the polio vaccine, (one taken orally i think?), but yet neglect to act on the other potential TSE vaccines (inoculations, the most effective mode to transmit TSEs) of which thousands of doses were kept and used, to deplete stockpile, again would be foolish.


--Oral polio; up to 1988, foetal calf serum was used from UK and New Zealand (pooled); since 1988 foetal calf serum only from New Zealand. Large stocks are held.


--Rubella; bulk was made before 1979 from foetal calf serum from UK and New Zealand. None has been made as there are some 15 years stock.


--Diphtheria; UK bovine beef muscle and ox heart is used but since the end of 1988 this has been sourced from Eire. There are 1,250 litres of stock.


--Tetanus; this involves bovine material from the UK mainly Scottish. There are 21,000 litres of stock.


--Pertussis; uses bovine material from the UK. There are 63,000 litres of stock.


--They consider that to switch to a non-UK source will take a minimum of 6-18 months and to switch to a non-bovine source will take a minimum of five years.


3. XXXXXXXXXXX have measles, mumps, MMR, rubella vaccines. These are sourced from the USA and the company believes that US material only is used.






BSE3/1 0251


4. XXXXXXXXXXX have a measles vaccine using bovine serum from the UK. there are 440,000 units of stock. They have also got MMR using bovine serum from the UK.


5. XXXXXXXXXXX have influenza, rubella, measles, MMR vaccines likely to be used in children. Of those they think that only MMR contains bovine material which is probably a French origin.


6. XXXXXXXXXXX have diphtheria/tetanus and potasses on clinical trial. These use veal material, some of which has come from the UK and has been made by XXXXXXXXXXX (see above).


I have documents of imports from known BSE Countries, of ferments, whole blood, antiallergenic preparations,




human blood plasma, normal human blood sera, human immune blood sera, fetal bovine serum, and other blood fractions not elsewhere specified or included, imported glands, catgut, vaccines for both human/animal, as late as 1998. Let us not forget about PITUITARY EXTRACT. This was used to help COWS super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease.






How much of this was used in the U.S.?


Please do not keep making the same mistakes;


'Absence of evidence is not evidence of absence'. What are the U.S. rules for importing and manufacturing vaccines, medicines and medical devices?


Does the U.S.A. allow sourcing of raw material of ruminants from the U.S.A.?


U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds.?


The U.S. rendering system would easily amplify T.S.E.'s: Have we increased the stability of the system (improved heat treatments) since the EU SSC report on the U.S.A. was published in july 2000?


What is done to avoid cross-contaminations in the U.S.A.?


How can the U.S. control absence of cross-contaminations of animal TSE's when pig and horse MBM and even deer and elk are allowed in ruminant feed, as well as bovine blood?


I sadly think of the rendering and feeding policy before the Aug. 4, 1997 'partial' feed ban, where anything went, from the city police horse, to the circus elephant, i will not mention all the scrapie infected sheep. I am surprised that we have not included man 'aka soyent green'. It is a disgusting industry and nothing more than greed fuels it.


When will the U.S.. start real surveillance of the U.S. bovine population (not passive, this will not work)?


When will U.S. start removing SRMs?


Have they stopped the use of pneumatic stunners in the U.S.?


If so, will we stop it in all U.S. abattoirs or only in those abattoirs exporting to Europe?


If not, WHY NOT?


same questions for removal of SRM in the U.S.A., or just for export?


If not, WHY NOT?


How do we now sterilize surgical/dental instruments in the U.S.A.?


Where have we been sourcing surgical catgut?


(i have copies of imports to U.S., and it would floor you) hen will re-usable surgical instruments be banned?


Unregulated "foods" such as 'nutritional supplements' containing various extracts from ruminants, whether imported or derived from




US cattle/sheep/cervids ("antler velvet" extracts!) should be forbidden or at least very seriously regulated. (neighbors Mom, whom also died from CJD, had been taking bovine based supplement, which contained brain, eye, and many other bovine/ovine tissues for years, 'IPLEX').


What is the use of banning blood or tissue donors from Germany, France, etc... when the U.S.A. continues exposing cattle, sheep and people to SRM, refuses to have a serious feed ban, refuses to do systematic BSE-surveillance?


The FDA should feel responsible for the safety of what people eat, prohibit the most dangerous foods, not only prohibit a few more donors - the FDA should be responsible for the safe sourcing of medical devices, not only rely on banning donors "from Europe" The 'real' risks are here in the U.S. as well, and nave been for some time.


We must not forget the studies that have proven infectivity in blood from TSE's.


The Lancet, November 9, 1985


Sir, --Professor Manuelidis and his colleagues (Oct 19, p896) report " transmission to animals of Creutzfeldt-Jakob disease (CJD) from the buffy coat from two patients. We also transmitted the disease from whole blood samples of a patient (and of mice) infected with CJD.1 Brain, Cornea, and urine from this patient were also infectious, and the clinicopathological findings2 are summarised as follows.




Samples,were taken aseptically at necropsy. 10% crude homogenates of brain and cornea in saline, whole blood (after crushing a clot), and untreated CSF and urine were innoculated intracerebrally into CF1 strain mice (20 ul per animal). Some mice showed emaciation, bradykinesia, rigidity of the body and tail, and sometimes tremor after long incubation periods. Tissues obtained after the animal died (or was killed) were studied histologically (table). Animals infected by various inocula showed common pathological changes, consisting of severe spongiform changes, glial proliferation, and a moderate loss of nerve cells. A few mice inoculated with brain tissue or urine had the same amyloid plaque found in patients and animals with CJD.3




Department of Neuropathology, Neurological Institute, Faculty of Medicine, Kyushu University, Fukuoka812, Japan


JUN TATEISHI (full text-long version)




CWD and transmission to man will be no different than other TSE's.


"Clearly, it is premature to draw firm conclusions about CWD assing naturally into humans, cattle and sheep, but the present esults suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has




caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs,"


G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O'Rourke3, L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M. Smits2 and B. Caughey1,7


or more recently transmission of BSE to sheep via whole blood Research letters Volume 356, Number 9234 16 September 2000


Transmission of BSE by blood transfusion in sheep Lancet 2000; 356: 999 – 1000


F Houston, J D Foster, Angela Chong, N Hunter, C J Bostock


See Commentary


"We have shown that it is possible to transmit bovine spongiform encephalopathy (BSE) to a sheep by transfusion with whole blood taken from another sheep during the symptom-free phase of an experimental BSE infection. BSE and variant Creutzfeldt-Jakob disease (vCJD) in human beings are caused by the same infectious agent, and the sheep-BSE experimental model has a similar pathogenesis to that of human vCJD. Although UK blood transfusions are leucodepleted--a possible protective measure against any risk from blood transmission-- this report suggests that blood donated by symptom-free vCJD-infected human beings may represent a risk of spread of vCJD infection among the human population of the UK."


"The demonstration that the new variant of Creutzfeldt-Jakob disease (vCJD) is caused by the same agent that causes bovine spongiform encephalopathy (BSE) in cattle1 has raised concerns that blood from human beings in the symptom-free stages of vCJD could transmit infection to recipients of blood transfusions (full text long version)" and...


"The large number of cases (1040), temporal clustering of the outbreaks (15 in the first 6 months of 1997), the high in-flock incidence, and the exceptional involvement of goats (390 cases), suggested an accidental infection. The source of the epidemic might have been TSE-contaminated meat and bonemeal, but eight flocks had never been fed any commercial feedstuff. Infection might have risen from the use of a formol-inactivated vaccine against contagious agalactia prepared by a single laboratory with brain and mammary gland homogenates of sheep infected with Mycoplasma agalactiae. Although clinical signs of TSE in the donor sheep have not been found, it is possible that one or more of them were harbouring the infectious agent. Between 1995 and 1996, this vaccine was given subcutaneously to 15 of the affected flocks (to one flock in 1994) ; in these animals the disease appeared between 23 and 35 months after vaccination. No information is available for herd 13 because it was made up of stolen animals. Sheep from the remaining three flocks (1-3, figure) did not receive the vaccine, thus suggesting a naturally occurring disease.” (again, full text long version).


IN SHORT, please do under estimate this data and or human/animal TSE's including CWD in the U.S.A.


A few last words, please.


The cattle industry would love to have us turn our focus to CWD and forget about our own home grown TSE in Bovines. This would be easy to do. Marsh's work was from downer cattle feed, NOT downer deer/elk feed. This has been proven.




There should be NO LESS THAN 1,000,000 tests for BSE/TSE in 2001 for U.S.A. French are testing 20,000 a week. The tests are available. Why wait until we stumble across a case from passive surveillance, by then it is to late. IF we want the truth, this is a must???


United States Total ,Bovine Brain Submissions by State,


May 10, 1990 thru October 31, 2000


Total 11,700


FROM 1.5 BILLION HEAD OF CATTLE since 1990 ???


with same feeding and rendering practices as that of U.K. for years and years, same scrapie infected sheep used in feed, for years and years, 950 scrapie infect FLOCKS in the U.S. and over 20 different strains of scrapie known to date. (hmmm, i am thinking why there is not a variant scrapid, that is totally different than all the rest)? just being sarcastic.


with only PARTIAL FEED BAN implemented on Aug. 4, 1997??? (you really need to reconsider that blood meal etc. 'TOTAL BAN')




AND PLEASE FOR GODS SAKE, STOP saying vCJD victims are the only ones tied to this environmental death sentence. "PROVE IT". It's just not true. The 'CHOSEN ONES' are not the only ones dying because of this man-made death sentence. When making regulations for human health from human/animal TSEs, you had better include ALL human TSE's, not just vCJD. Do NOT underestimate sporadic CJD with the 'prehistoric' testing available to date. This could be a deadly mistake. Remember, sCJD kills much faster from 1st onset of symptoms to death, and hvCJD is the fastest. Could it just be a higher titre of infectivity, or route or source, or all three?



Last, but not least. The illegal/legal harvesting of body parts and tissues will come back to haunt you. Maybe not morally, but due to NO background checks and human TSEs, again it i will continue to spread.



Stupidity, Ignorance and Greed is what fuels this disease. You must stop all of this, and ACT AT ONCE...








"different strains (of same disease), different routes of infection (of same disease), different infectivity levels (dose rate) of the (same disease) = different symptoms, different lengths of illness from 1st onset of illness to death, (of the same disease) + different cultures = different geographical locations = different strains (of same disease)...TSS"




DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)


The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why???? than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!!


Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....


Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!


And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...


Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and aggressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"


again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.


You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)


















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