Wednesday, August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?

August 20, 2008

Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ?

MAD COW DISEASE, WHO STARTED IT, when and where did it start first ?

WAS/IS there a cover-up attempt ?

WILL the next administration here in the USA hold any sort of Congressional hearings or have a BSE Inquiry of sorts into the Bush Administrations handling of BSE in the USA (any and all strains of TSE) ?

OR, will it be the same old O.I.E. B.S.E. M.R.R. nonsense of 'don't look, don't find, mentality $$$


I am puzzled by several things. IF I remember correctly, the last two mad cows _documented_ in the U.S.A., this was before the surveillance and testing for BSE was shut down to almost nothing, for obvious reasons i.e. the findings back to back of the two atypical BSE cases, but I am puzzled by the fact that no detailed pathology of _both_ the Texas and the Alabama cow have been released, that I am aware of?

I am also puzzled by the fact that no more attention has been given to the fact of several statements and facts that in fact have come about, to simply go ignored? kind of reminded me of the infamous sporadic CJD in farmers and their wives with BSE herds.

But Confucius is confused again. my questions, who really started mad cow disease and or when and where did it really start? IT seems to me that this is not a questions that has been answered. ONE could look at the U.K. BSE epidemic as the point of origin, but if you go back, typical and atypical TSE in the bovine seems to have started way back. It could go all the way back to the U.S.

HAS the continuous rendering U.K. first theory (continuous rendering technology shipped to U.K. some 5 years and used there first before the U.S.A. started using) been proven, as the key to the start, or just an enhancement of sorts i.e. low temps, minus the oils, and was it true that the U.S. did NOT start using it before the U.K. ? and does it really matter ? could the TSE agent have survived and spread regardless ??? seems from the latest study on the TSE agent surviving the Biodiesel Production process, seems then it would not matter.

Friday, August 15, 2008 Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production

Looking further into this 'continuous rendering'. I first wrote about it here ;

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

2 January 2000


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;


NOW, to go back and read this document in full ;

Qualitative Analysis of BSE Risk Factors in the United States February 13, 2000 at 3:37 pm PST (BSE red book)

However, going back even further, it seems mad cow disease (a strain BEFORE the U.K. BSE first appeared) was in the U.S.A. spreading for a long time among mink, and after a careful review of the eating habits and diets, it turned out the mink were being fed >95%+ dead stock downer cow ration. the mink developed mad mink disease or what is now called Transmissible Mink Encephalopathy or TME, you can see this data here ;

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.

A Quantitative Assessment of the Possible Role of Nonambulatory Cattle in Transmissible Spongiform Encephalopathy in the United States March 6, 2000 at 1:05 pm PST

SO, we know some sort of TSE in fact was circulating among the USA cattle as far back as 1985. We can also tie feed of dead stock downer cows i.e. >95%+ dead stock downer cow rations. But these mink were proven to have had TME first in 1965, and shortly after that in 1971 it was proven that sheep scrapie would also transmit to mink. however, it was later found that the minks diet was NOT from sheep, after it was proven what the diet was i.e. dead stock downer cows.

Transmissible Mink Encephalopathy TME (MAD MINK DISEASE)

NOW, in 1979, it was proven that indeed U.S. scrapie strain that was transmitted to U.S. cattle, did NOT produce a Transmissible Spongiform Encephalopathy (TSE) like the U.K. B.S.E., but a TSE unlike the U.K. B.S.E. SO what does all this tell us? it tells me that there is a possibility that a strain of mad cow disease was circulating in the U.S.A. long, long, before originally thought, only left to be ignored, while incubating and spreading.

3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE.339 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture.340 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre.341 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle,

*** did not produce the same clinical signs of brain lesions characteristic of BSE. ***

3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988,342 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988–89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA.343 It was also felt that the results of such an experiment would be hard to interpret. While a negative result 337 Fraser, H., Bruce, M., Chree, A., McConnell, I. and Wells, G. (1992) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice, Journal of General Virology, 73, 1891–7; Bruce, M., Chree, A., McConnell, I., Foster, J., Pearson, G. and Fraser, H. (1994) Transmission of Bovine Spongiform Encephalopathy and Scrapie to Mice: Strain Variation and the Species Barrier, Philosophical Transactions of the Royal Society of London, Series B, Biological Sciences, 343, 405–11 338 Bruce, M., Will, R., Ironside, J., McConell, I., Drummond, D., Suttie, A., McCordie, L., Chree, A., Hope, J., Birkett, C., Cousens, S., Fraser, H. and Bostock, C. (1997) Transmissions to Mice Indicate that ‘New Variant’ CJD is Caused by the BSE Agent, Nature, 389, 498–501 339 Clark, W., Hourrigan, J. and Hadlow, W. (1995) Encephalopathy in Cattle Experimentally Infected with the Scrapie Agent, American Journal of Veterinary Research, 56, 606–12 340 YB88/10.00/1.1 341 Cutlip, R., Miller, J., Race, R., Jenny, A., Katz, J., Lehmkuhl, H., Debey, B. and Robinson, M. (1994) Intracerebral Transmission of Scrapie to Cattle, Journal of Infectious Diseases, 169, 814–20 342 YB88/6.21/1.2 343 YB88/11.17/2.4 SCIENCE 84 would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE.344 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest.345 3.59 Nevertheless, from the first demonstration of transmissibility of BSE in 1988, the possibility of differences in the transmission properties of BSE and scrapie was clear. Scrapie was transmissible to hamsters, but by 1988 attempts to transmit BSE to hamsters had failed. Subsequent findings increased that possibility.

doi:10.1016/S0021-9975(97)80022-9 Copyright © 1997 Published by Elsevier Ltd.

Second passage of a US scrapie agent in cattle

R.C. Cutlip, J.M. Miller and H.D. Lehmkuhl

United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Ames, Iowa, USA

Received 10 September 1996; accepted 31 July 1997. Available online 25 May 2006.


Scrapie and bovine spongiform encephalopathy are similar chronic neurodegenerative diseases of sheep and cattle. An earlier study showed that, on first passage in cattle, a US scrapie agent caused an encephalopathy that was distinct from bovine spongiform encephalopathy (BSE). The present report describes a second passage in cattle, carried out because diseases caused by the spongiform encephalopathy agents often change in character with additional passages in abnormal hosts. For this work, young calves were inoculated intracerebrally with a pooled suspension of brain from cattle that had died of encephalopathy after experimental inoculation with brain from scrapie-affected sheep. The second passage disease was essentially identical with the first passage disease, as judged by clinical signs, histopathological findings and distribution of "prion protein scrapie" (PrPsc). This represents additional evidence to suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.

IT seems that Cutlip, Miller, Lehmkuhl et al, it seems by this statement ;

'suggest that the US sheep scrapie agent tested is incapable of causing BSE in cattle.'

THAT the USA is home free from TSEs, however, how many scrapie strains are in the USA, including the atypical. we know atypical scrapie Nor-98 has been in the USA for a while, only detected recently. but did this study include all USA scrapie strains typical and atypical ??? I dont think so. also, this TSE strain that is produced by USA scrapie, could it be more virulent, and how many phenotypes are there ??? we know that the atypical BSE is more virulent, so I dont understand what seems to be 'jubilation' of the small study that shows that in fact the USA scrapie DOES produce a Transmissible Spongiform Encephalopathy TSE, it just happens to be unlike that of the UK BSE phenotype, and I would have expected nothing less, considering the many different strains. but I don't think these findings makes the USA mad cow free. IN fact, I find that by these findings, TSE in the USA bovine could have gone way back before the UK BSE epidemic, and I think it's just possible that the USA started this epidemic of TSEs.

let's look at the new atypical scrapie that has been in the U.S.A. i.e. the NOR-98-like;-) strain ;

PLEASE NOTE, (FIGURE 6), Scrapie Confirmed Cases in FY 2008 MAP, PA 3, 1**, Two cases-state of ID UNKNOWN, 1 case Nor98-like**

NOT to forget the 5 cases of the NOR-98 atypical scrapie documented in the USA in 2007, in five different states. WHICH pathologically looks like some sub-types of sporadic CJD, of which Stanely Prusiner warns of a public health risk ;

***The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.

Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.

Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005)


NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 007


Sunday, June 15, 2008

A descriptive study of the prevalence of atypical and classical scrapie in sheep in 20 European countries

Research article

another question, just how long have these atypical BSE TSEs been around in the bovine ???

let's look at another case of atypical BSE in Germany way back in 1992 ;

Subject: atypical BSE reported in 1992 and conviently slaughterd and incinerated and then swept under rug for about 12 years Date: April 26, 2007 at 1:08 pm PST 1992






2. The Collinge/Will dispute appears to rumble on. Dr. Collinge had told Dr. Tyrrell that Dr. Will's response to his criticism about sharing material had been ''quite unacceptable'' (in spite of it's apparently conciliatory tone). Apparently Professor Allen was now going to try and arrange a meeting to resolve the dispute. No action here for MAFF, although Mr. Murray may be interested.

3. Dr. Tyrrell regretted that the Committee had not seen the article on BBD. However he felt that for the time being NO specific action was called for. The most important need was to consider the possibility that the condition might be transmissible. As we have discussed, I suggested that we might circulate a paper to the members of the committee giving our appreciation of this condition (and perhaps of other non-BSE neurological conditions that had been identified in negative cases) and of any necessary follow up action. IF any Committee member felt strongly about this, or if the issue CAME TO A HEAD, we would call an interim meeting. He was happy with this approach. I would be grateful if Mr. Maslin could, in discussion with CVL and veterinary colleagues draft such a note, which will presumably very largely follow what Mr. Bradley's briefing paper has already said, taking account of DOH comments, We can then clear a final version with DOH before circulating it to Committee members.


This is a highly competitive field and it really will be a pity if we allow many of the key findings to be published by overseas groups while we are unable to pursue our research findings because of this disagreement, which I hope we can make every effort to solve.


2. The discovery might indicate the existence of a different strain of BSE from that present in the general epidemic or an unusual response by an individual host.

3. If further atypical lesion distribution cases are revealed in this herd then implications of misdiagnosis of 'negative' cases in other herds may not be insignificant.


This minute is re-issued with a wider distribution. The information contained herein should NOT be disseminated further except on the basis of ''NEED TO KNOW''.

R Bradley




Texas BSE Investigation Final Epidemiology Report August 2005

State-Federal Team Responds to Texas BSE Case

JUNE 30, 2005

(please note 7+ month delay in final confirmation so the BSE MRR policy could be set in stone first. $$$...tss)


The U.S. Department of Agriculture confirmed June 29 that genetic testing had verified bovine spongiform encephalopathy (mad cow disease) in a 12-year-old cow that was born and raised in a Texas beef cattle herd.

Subsequent epidemiological investigations resulted in the culling and testing of 67 adult animals from the index herd. Bio-Rad tests for BSE were conducted on all 67 animals by the National Veterinary Services Laboratory (NVSL) in Ames, Iowa. All tests were negative.

On July 12, Texas officials lifted the quarantine on the source herd. At press time, USDA's Animal and Plant Health Inspection Service was tracing animals of the same age that had left the ranch.


The BSE-positive animal was a Brahman-cross cow born and raised in a single Texas herd. The location of the ranch was not disclosed.

On Nov. 11, 2004, the 12-year-old cow was taken to a Texas auction market. Because of its condition, the cow was sent to Champion Pet Foods in Waco, Texas. The company produces several blends of dog food, primarily for the greyhound industry.

On Nov. 15, the animal arrived dead at Champion. Under procedures established by USDA's intensive surveillance program, a sample was sent to the USDA-approved Texas Veterinary Medical Diagnostic Testing Laboratory (TVMDL) at Texas A&M University.

Between June 1, 2004, and June 1, 2005, TVMDL tested nearly 34,000 samples from Texas, New Mexico, Arkansas and Louisiana. They tested the sample from Champion on Nov. 19 using a Bio-Rad ELISA rapid test for BSE. Initial results were inconclusive.

Because of the inconclusive results, a representative from USDA took the entire carcass to TVMDL where it was incinerated. USDA's Animal and Plant Health Inspection Service (APHIS) began tracing the animal and herd.

The sample was then sent to the National Veterinary Services Laboratory for further testing. Two Immunohistochemistry (IHC) tests were conducted and both were negative for BSE. At that point APHIS stopped their trace.

USDA scientists also ran an additional, experimental IHC "rapid" tissue fixation test for academic purposes. This test has not been approved internationally.

Some abnormalities were noted in the experimental test, but because the two approved tests came back negative, the results were not reported beyond the laboratory.

Monitoring by OIG

USDA's Office of Inspector General (OIG) has been monitoring implementation of the BSE expanded surveillance program and evaluating the following:

* Effectiveness of the surveillance program;

* Performance of BSE laboratories in complying with policies and procedures for conducting tests and reporting results;

* Enforcement of the ban on specified risk materials in meat products;

* Controls to prevent central nervous system tissue in advanced meat recovery products;

* Ante mortem condemnation procedures; and

* Procedures for obtaining brain tissue samples from condemned cattle.

While reviewing voluminous records, OIG auditors noticed conflicting test results on one sample-rapid inconclusive, IHC negative, experimental reactive.

Sample retested

At the recommendation of the Inspector General, the sample was retested during the week of June 5 with a second confirmatory test, the Western Blot. The results were reactive.

USDA scientists then conducted an additional IHC confirmatory test, using different antibodies from the November 2004 test. On Friday, June 10, Secretary of Agriculture Mike Johanns publicly announced the results as a "weak positive."

On June 16 an official with USDA's National Veterinary Services Laboratory hand-carried samples for further testing to the Veterinary Laboratory Agency (VLA) in Weybridge, England. Since 1991, the VLA has been a BSE reference laboratory for the World Organization for Animal Health (OIE).

Experts from the Weybridge lab confirmed the accuracy of the results of USDA's November confirmatory IHC test, concurring that the case could not have been confirmed on the basis of this sample. They also examined the November experimental IHC test and interpreted the results to be positive.

Weybridge also conducted additional tests, including IHC, OIE-prescribed Western Blot, NaTTA Western Blot and Prionics Western Blot tests.

To better understand the conflicting results, USDA also conducted Bio-Rad and IDEXX rapid screening tests, IHC and OIE-prescribed Western Blot. USDA also used DNA sequencing to determine the prion protein gene sequence of the animal.

Texas even had a 'secret' test that showed that mad cow positive; experimental IHC test results, because the test was not a validated procedure, and because the two approved IHC tests came back negative, the results were not considered to be of regulatory significance and therefore were not reported beyond the laboratory. . A Western blot test conducted the week of June 5, 2005, returned positive for BSE.

48 hr BSE confirmation turnaround took 7+ months to confirm this case, so the BSE MRR policy could be put into place. ...TSS

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

Subject: re-USDA's surveillance plan for BSE aka mad cow disease

Date: Mon, 02 May 2005 16:59:07 -0500

From: "Terry S. Singeltary Sr."

To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000505/!, mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000505/!,

Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............


There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...

Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 xxx xxx xxxx

Date: June 14, 2005 at 1:46 pm PST In Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:

Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS


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


Date: Mon, 22 Nov 2004 17:12:15 -0600

From: "Terry S. Singeltary Sr."

To: Carla EverettReferences: <[log in to unmask]><[log in to unmask] us>

Greetings Carla, still hear a rumor;

Texas single beef cow not born in Canada no beef entered the food chain?

and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update?


can you confirm??? terry


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

Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

Date: Fri, 19 Nov 2004 11:38:21 -0600

From: Carla Everett

To: "Terry S. Singeltary Sr."References: <[log in to unmask]>

The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas.


At 09:44 AM 11/19/2004, you wrote:

Greetings Carla,

i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from

TEXAS. can you comment on this either way please?

thank you,

Terry S. Singeltary Sr.>>


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

Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???

Date: Mon, 22 Nov 2004 18:33:20 -0600

From: Carla Everett

To: "Terry S. Singeltary Sr."References: <[log in to unmask]><[log in to unmask] us><[log in to unmask]> <[log in to unmask]us> <[log in to unmask]>

our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.

At 06:05 PM 11/22/2004,

you wrote:

why was the announcement on your TAHC site removed?

Bovine Spongiform Encephalopathy:

November 22: Press Release title here

star image More BSE information


Carla Everett wrote:

no confirmation on the U.S.'inconclusive test...

no confirmation on location of animal.>>>>>>


FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.

FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.

FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.

Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).

FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.

To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.

Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.

FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.


NO need to go any further there, the USA has proven the above statement was in fact their position i.e. THE TRIPLE SSS POLICY, SHOOT, SHOVE, AND SHUT THE HELL UP!

IN Texas the Triple SSS policy is alive and well. most all downers and sick cattle that drop are burried right where they drop in Texas ;

"Anthrax is under-reported, because many ranchers in this area automatically dispose of carcasses and vaccinate livestock when they find dead animals that are bloated or bloody--common signs of the disease," said Dr. Fancher. "Anthrax is a reportable disease, however, and it's important to know when an outbreak occurs, so other ranchers can be notified to vaccinate.


Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

PLEASE SEE FULL TEXT ;Monday, June 16, 2008 Mad Cows and Computer Models: The U.S. Response to BSE

Docket APHIS-2006-0041 Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities Docket Type Rulemaking Document APHIS-2006-0041-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines Public Submission APHIS-2006-0041-0006 Public Submission Title Comment from Terry S Singletary Sr Views Add Comments How To Comment


MY personal belief, since you ask, is that not only the Canadian border, but the USA border, and the Mexican border should be sealed up tighter than a drum for exporting there TSE tainted products, until a validated, 100% sensitive test is available, and all animals for human and animal consumption are tested. all we are doing is the exact same thing the UK did with there mad cow poisoning when they exported it all over the globe, all the while knowing what they were doing. this BSE MRR policy is nothing more than a legal tool to do just exactly what the UK did, thanks to the OIE and GW, it's legal now. and they executed Saddam for poisoning ???

go figure....

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

OIE Recognition of the BSE Status of Members RESOLUTION No. XXI (Adopted by the International Committee of the OIE on 27 May 2008)

From: Terry S. Singeltary Sr.

To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000505/!x-usc:mailto:FREAS@CBER.FDA.GOV

Cc: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000505/! ; mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000505/!

Sent: Friday, December 01, 2006 2:59 PM

Subject: Re: TSE advisory committee for the meeting December 15, 2006 [TSS SUBMISSION


ONE FINAL COMMENT PLEASE, (i know this is long Dr. Freas but please bear with me)

THE USA is in a most unique situation, one of unknown circumstances with human and animal TSE. THE USA has the most documented TSE in different species to date, with substrains growing in those species (BSE/BASE in cattle and CWD in deer and elk, there is evidence here with different strains), and we know that sheep scrapie has over 20 strains of the typical scrapie with atypical scrapie documented and also BSE is very likely to have passed to sheep. all of which have been rendered and fed back to animals for human and animal consumption, a frightening scenario. WE do not know the outcome, and to play with human life around the globe with the very likely TSE tainted blood from the USA, in my opinion is like playing Russian roulette, of long duration, with potential long and enduring consequences, of which once done, cannot be undone.

These are the facts as i have come to know through daily and extensive research of TSE over 9 years, since 12/14/97. I do not pretend to have all the answers, but i do know to continue to believe in the ukbsenvcjd only theory of transmission to humans of only this one strain from only this one TSE from only this one part of the globe, will only lead to further failures, and needless exposure to humans from all strains of TSE, and possibly many more needless deaths from TSE via a multitude of proven routes and sources via many studies with primates and rodents and other species. ...

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

snip... 48 pages...

US atypical BSE - further details

As reported in the last BSE Report (Which? BSE May 2006) French research findings

concerning the two most recent cases of BSE in the USA suggest that these cases were

not typical of BSE in cattle and may reflect a sporadic form of the disease.

In the two US cases, discovered in herds in Texas and Alabama, threre was an absence

of telltale spongy lesions caused by prions. In addition, the prions in brain tissue

samples from these cows seemed to be distributed differently from the classic form.

Laboratory studies on mice in France showed that both the classic and atypical strains

could be spread from one animal to another, but the atypical strain might happen

spontaneously in cattle. The Texas and Alabama cows were older animals, as were

some of the other animals in Europe with seemingly atypical forms of BSE.31

Linda Detwiler, a former Agriculture Department veterinarian who consults for major

food companies, cautioned against making that assumption. "I think it's kind of early to

say that would be the case," Detwiler said. Other theories, she said, suggest the

atypical strain might come from a mutation of BSE or even from a related disease in


The US Agriculture Department has stated that whatever the cause there is no reason

to change federal testing or control measures. "It's most important right now, till the

science tells us otherwise, that we treat this as BSE regardless," the department's chief

veterinarian, John Clifford, said in an interview. ...

USDA officials have declined in the past to provide such details, but released information Friday [2 Jun 2006] after a French researcher revealed earlier this week that the cases in Texas last year 2005 and Alabama last spring 2006 were identical to "atypical" cases of BSE found in France.

Neurology 1999;52:1757 © 1999 American Academy of Neurology


Expedited Publication

A subtype of sporadic prion disease mimicking fatal familial insomnia P. Parchi, MD, S. Capellari, MD, S. Chin, MD, PhD, H. B. Schwarz, MD, N. P. Schecter, MD, J. D. Butts, MD, P. Hudkins, MD, D. K. Burns MD, J. M. Powers, MD and P. Gambetti, MD

Neurology, Vol. 70, Issue 11, 884-885, March 11, 2008 CLINICAL/SCIENTIFIC NOTES

SPORADIC FATAL INSOMNIA IN A FATAL FAMILIAL INSOMNIA PEDIGREE S. Capellari, P. Parchi, P. Cortelli, P. Avoni, G. P. Casadei, C. Bini, A. Baruzzi, E. Lugaresi, M. Pocchiari, P. Gambetti, and P. Montagna

Moreover, the mutation was also lacking in the proband father's DNA and the type of PrPSc (figure) in her brain was compatible with sporadic, not genetic FI ...



S. Capellari1a, P. Cortelli1, P. Avoni1, G.P. Casadei2, A. Baruzzi1, E. Lugaresi1, M. Pocchiari3, P. Gambetti4, P. Montagna1, P. Parchi1. 1Department of Neurological Sciences, University of Bologna, Bologna, Italy; 2Department of Cell Biology and Neurosciences, ISS, Roma, Italy; 3Servizio di Anatomia Patologica, Ospedale Maggiore, Bologna, Italy, 4Division of Neuropathology, CWRU, Cleveland, OH, USA. a mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000505/!

We describe a case of sporadic fatal insomnia (sFI) occurring in a family in which several members carried the D178N mutation in the PRNP gene and died of fatal familial insomnia (FFI). A 43-year-old woman presented with an 11-month history of diplopia, withdrawal, confusion, memory loss, unsteady gait and inability to sleep with episodes of agitation and dream enactment. After a progressive course characterized by cognitive impairment, marked gait ataxia, signs of autonomic hyperactivity, and myoclonus the patient died 24 months after the onset of symptoms. The patient did not have any personal contact with FFI affected relatives and her closest one was a paternal uncle, the son of her grand-grand mother. Analyses of DNA from various tissues of endo- ecto- and meso-dermal origin, including 5 different regions of the CNS revealed no pathogenic mutations and methionine homozygosity at codon 129 of PRNP. Brain histopathology and PrPSc typing showed typical features of FI such as thalamic and olivary atrophy, focal spongiform degeneration limited to the cerebral cortex, relative sparing of basal ganglia and cerebellum, and relatively low amount of PrPSc type 2A accumulation. sFI represents the rarest among the sporadic human TSE subtypes described to date with less than twenty cases described worldwide and only three cases diagnosed in Italy since the establishment of TSE surveillance. Similarly, only six unrelated FFI families have been observed in Italy to date, making the probability of a chance association between sFI and FFI in the same family extremely low. Thus, we believe that our observation emphasizes the importance of undiscovered factors modulating the susceptibility to human prion diseases. Supported by the EU Network of Excellence "NeuroPrion" (FOOD-CT-2004-506579).

Manuscript Draft Manuscript Number: Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Article Type: Personal View Corresponding Author: Mr. Terry S. Singeltary, Corresponding Author's Institution: na First Author: Terry S Singeltary, none Order of Authors: Terry S Singeltary, none; Terry S. Singeltary Abstract: TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. 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 2007.


WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE?


Volume 12, Number 12-December 2006

Perspective On the Question of Sporadic or Atypical Bovine Spongiform Encephalopathy and Creutzfeldt-Jakob Disease

Paul Brown,* Lisa M. McShane,? Gianluigi Zanusso,? and Linda Detwiler§ *Bethesda, Maryland, USA; ?National Institutes of Health, Bethesda, Maryland, USA; ?University of Verona, Verona, Italy; and §Virginia-Maryland Regional College of Veterinary Medicine, College Park, Maryland, USA


In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.


Barring the discovery of a specific molecular signature (as in variant CJD), the most convincing clue to an association will come from the observation of trends over time of the incidence of typical and atypical BSE and of sporadic and variant CJD. With 4 diseases, each of which could have increasing, unchanging, or decreasing trends, there could be 81 (34) possible different combinations. However, it is highly likely that the trends for typical BSE and variant CJD will both decrease in parallel as feed bans continue to interrupt recycled contamination. The remaining combinations are thus reduced to 9 (32), and some of them could be highly informative.

For example, if the incidence of atypical BSE declines in parallel with that of typical BSE, its candidacy as a sporadic form of disease would be eliminated (because sporadic disease would not be influenced by current measures to prevent oral infection). If, on the other hand, atypical BSE continues to occur as typical BSE disappears, this would be a strong indication that it is indeed sporadic, and if in addition at least 1 form of what is presently considered as sporadic CJD (such as the type 2 M/V subtype shown to have a Western blot signature like BASE) were to increase, this would suggest (although not prove) a causal relationship (Figure 5).

Recognition of the different forms of BSE and CJD depends upon continuing systematic testing for both bovines and humans, but bovine testing will be vulnerable to heavy pressure from industry to dismantle the program as the commercial impact of declining BSE cases ceases to be an issue. Industry should be aware, however, of the implications of sporadic BSE. Its occurrence would necessitate the indefinite retention of all of the public health measures that exclude high-risk bovine tissues from the animal and human food chains, whereas its nonoccurrence would permit tissues that are now destroyed to be used as before, once orally acquired BSE has disappeared.

10 people killed by new CJD-like disease

Public release date: 9-Jul-2008 [ Print Article E-mail Article Close Window ]

Contact: Claire Bowles mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000505/! 44-207-611-1210 New Scientist

10 people killed by new CJD-like disease A NEW form of fatal dementia has been discovered in 16 Americans, 10 of whom have already died of the condition. It resembles Creutzfeldt-Jakob disease - with patients gradually losing their ability to think, speak and move - but has features that make it distinct from known forms of CJD.


Since Gambetti's team wrote a paper describing an initial 11 cases referred to his centre between 2002 and 2006 (Annals of Neurology, vol 63, p 697), another five have come to light. "So it is possible that it could be just the tip of the iceberg," Gambetti says.

Sunday, August 10, 2008

Thursday, July 10, 2008 A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008

Thursday, July 10, 2008 A New Prionopathy update July 10, 2008

A New Prionopathy OR more of the same old BSe and sporadic CJD

Communicated by: Terry S. Singeltary Sr.

[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents. Characterization of these agents should be given a high priority. - Mod.CP],F2400_P1001_PUB_MAIL_ID:1010,39963

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.


MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:


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?


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.

Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

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.

Terry S. Singeltary, Sr Bacliff, Tex

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

2 January 2000

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

15 November 1999

British Medical Journal vCJD in the USA * BSE in U.S.

Creutzfeldt Jakob Disease


Sunday, April 20, 2008

Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008

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

see full text ;

CJD TEXAS (cjd clusters)


The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

Research Project: STUDY OF ATYPICAL BSE Location: Virus and Prion Diseases of Livestock

Project Number: 3625-32000-086-05 Project Type: Specific C/A

Start Date: Sep 15, 2004 End Date: Sep 14, 2009


Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.

Sunday, March 16, 2008

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE

Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. Firm initiated recall is ongoing. REASON Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.



PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007 CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified. RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete. REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.



REASON Possible contamination of dairy feeds with ruminant derived meat and bone meal. VOLUME OF PRODUCT IN COMMERCE 1,484 tons DISTRIBUTION

TN and WV

FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA

Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.

FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.

FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.

Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.


Topics that will be covered in ongoing or planned reviews under Goal 1 include:

soundness of BSE maintenance sampling (APHIS),

implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),


The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.



HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008


Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...


Visit to USA ... info on BSE and Scrapie


AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.


2005 DEFRA Department for Environment, Food & Rural Affairs

Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail:


Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518

21 November 2001

Dear Mr Singeltary


Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.

As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.

Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.

Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less

critical. For more details see-

As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.

Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK

You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.

I hope this is helpful

Yours sincerely 4





b) Fibrillar material closely similar to SAF, found in BSE/Scrapie, was observed in 19 (4.3%) cases, all of which were hounds > 7 years of age. 14/19 of these suspected SAF results correlated with cases in the unresolveable histopathological category.


The following proposals address the hypothesis that the hound survey observations represent a PrP related or scrapie-like disease of dogs in which the pathological response, and possible the spread of infectivity, is neuroanatomically localized. By inference this could also mean that the disorder is clinically silent and non-progressive.

NOW, back to that mad mink disease i.e. TME outbreaks in the U.S.A., and the fact that 40% DIED OVER 8-10 WEEKS TIME !


Creutzfeldt-Jakob Disease (Variant) and Bovine Spongiform Encephalopathy (Prion Diseases) Description Since 1996, strong evidence has accumulated for a causal relationship between ongoing outbreaks, primarily in Europe, of a disease in cattle called bovine spongiform encephalopathy (BSE, or "mad cow disease") and a disease in humans called variant Creutzfeldt-Jakob disease (vCJD). Both disorders, which are caused by an unconventional transmissible agent, are invariably fatal brain diseases with incubation periods typically measured in years (1). Transmission of the BSE agent to humans, leading to vCJD, is believed to occur via ingestion of cattle products contaminated with the BSE agent; the specific foods associated with this transmission are unknown. However, a recently published case-control study involving 132 vCJD cases in the United Kingdom (UK) showed evidence of an increased risk for vCJD associated with the frequency of consuming beef products likely to contain mechanically recovered meat and head meat (such as burgers, meat pies, and sausages) (2). Bioassays and molecular tests have enabled identification of what World Health Organization consultants have classified as "high-infectivity" and "lower infectivity" tissues of cattle with BSE (3). The high-infectivity tissues include the brain, spinal cord, retina, optic nerve, and dorsal root and trigeminal ganglia, suggesting that these tissues can pose a relatively high risk of transmission. The lower infectivity tissues include peripheral nerves (e.g., sciatic and facial nerves), tonsils, nictitating membrane (third eye lid), distal ileum, bone marrow, and possibly thigh muscle. The latter tissue from one cow with BSE transmitted disease to highly BSE-sensitive transgenic mice at a rate indicative of trace levels of infectivity.

USDA CERTIFIED DEAD STOCK DOWNER COW SCHOOL LUNCH PROGRAM, the most HIGH RISK animal for BSE mad cow disease, and even more risky here in the USA, where the last two cases of mad cow disease was of the _atypical_ BSE, in Texas and Alabama. THE atypical BSE is more virulent to humans than the U.K. BSE strain. ...TSS

YOU really did not think that the Nations largest beef recall in history was because of a few abused cows did you ???

WHAT ABOUT THE children and CJD, from vaccines to baby food ;


Sunday, May 18, 2008


Sunday, May 18, 2008

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

Infectivity of bovine materials used in medicinal products and the importance of inoculation route

3.221 The risk from infectivity present in medicinal products was considered by the Southwood Working Party. They noted that ‘the greatest risk . . . would be from the parenteral injection of material derived from bovine brain or lymphoid tissue’.538 (As described previously, it was generally accepted that the oral route was considerably less efficient than the parenteral route.539)

3.222 In reality, different routes exist within the parenteral category – intracerebral, intraperitoneal, intramuscular, intravenous, intraspinal and subcutaneous. Experiments in 1978 looking at several of these routes found the efficiency between them to vary. Intracerebral and intraspinal were generally the most efficient, followed by intravenous, intraperitoneal and then subcutaneous.540 The fact that certain medicinal products could be injected directly into the body (most commonly intramuscularly) meant that in theory they would pose a greater risk than beef products in food.

3.223 Various cattle tissues were of relevance to medicinal products, including insulin, heparin, surgical catgut sutures and serum. The consideration given to these materials prior to March 1996 is addressed in vol. 7: Medicines and Cosmetics.

533 SEAC 22/5 534 Wells, G. (1998) Preliminary Observations on the Pathogenesis of Experimental Bovine Spongiform Encephalopathy (BSE): An Update, Veterinary Record, 142, 103 535 Wells, G., Hawkins, S., Green, P., Spencer, Y., Dexter, I. and Dawson, D. (1999) Limited Detection of Sternal Bone Marrow Infectivity in the Clinical Phase of Experimental Bovine Spongiform Encephalopathy (BSE), Veterinary Record, 144, 292–4 536 Scott, M.R., Will, R., Ironside, J., Nguyen, H.-O., Tremblay, P., DeArmond, S.J. and Prusiner, S.B. (1999) Compelling Transgenetic Evidence for Transmission of Bovine Spongiform Encephalopathy Prions to Humans, Proceedings of the National Academy of Sciences of the USA, 96, 15137–42 537 Scott, M.R., Safar, J., Telling, G., Nguyen, H.-O., Groth, D., Torchia, M., Kochler, R., Tremblay, P., Walther, D., Cohen, F., DeArmond, S. and Prusiner, S. (1997) Identification of a Prion Protein Epitope Modulating Transmission of Bovine Spongiform Encephalopathy Prions to Transgenic Mice, Proceedings of the National Academy of Sciences of the United States of America, 94, 14279–84 538 IBD1 tab 2 para. 5.3.3 539 Kimberlin, R. and Walker, C. (1989) Pathogenesis of Scrapie in Mice after Intragastric Infection, Virus Research, 12, 213–20; Diringer, H., Beekes, M. and Oberdieck, U. (1994) The Nature of the Scrapie Agent: The Virus Theory, Annals of The New York Academy of Science, 724, 246–58; Prusiner, S., Cochran, S. and Alpers, S. (1985) Transmission of Scrapie in Hamsters, Journal of Infectious Diseases, 152, 971–8 540 Kimberlin, R.H. and Walker, C.A. (1978) Pathogenesis of Mouse Scrapie: Effect of Route of Inoculation on Infectivity Titres and Dose-Response Curves, Journal of Comparative Pathology, 88, 39–47

Sunday, May 18, 2008


***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

Thursday, June 05, 2008

Review on the epidemiology and dynamics of BSE epidemics

Vet. Res. (2008) 39:15 DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article


And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.


Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) [23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland [56]. It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

full text 18 pages ;

please see full text ;

EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA)

Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.

The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90's when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.

snip...see full text ;

June 12, 2008


FDA Has Provided Few Details on the Resources and Strategies Needed to Implement its Food Protection Plan

What GAO Found

NOW, I suppose my final question, or maybe it is not a question, just a quarter for my thoughts. Confucius thought of the day is this, how in the hell can Canada continue to document mad cow disease, and after all of the above, by some God Giving miracle, the U.S.A. just cannot for the life of all of us, find a single case of mad cow disease, since the only two home grown atypical BSE cases in Texas and Alabama $$$ With the amount of trading back and forth for the past decades between Canada and the U.S.A. of live cattle, and feed, it would almost be mathematically impossible for the U.S.A. not to have documented more mad cows than they have done so to date. ITs a phenomenon unlike know other I have witnessed. it is a miracle.

now, my final comment is not a comment at all, just what a high ranking official inside the USDA told me 8 years ago, and still holds true today $

2000 - 2001

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 agressively 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 theUS! As for the BSE conference call... I think you did agreat 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.) ... END

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in the USA.

and they meant it. ...

Pathologist: Carol Richardson

DIAGNOSIS: 1. Moderat spongiform encephalopathy- acute.
2. Mild renal nephrosis - peracute

REMARKS: These acute changes suggest a toxicity of some description. The non-suppurative reactions are far more chronic, mild and non-specific.

Owner of animal, Mr. Stent



Attempts at virus isolation have proved negative.

Cases reviewed and discussed, ...No conclusion drawn....

GAH Wells

Subject: Carol Richardson $ BSE
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
Date: Wed, 1 Nov 2000 09:51:39 -0800
Content-Type: text/plain Parts/Attachments: text/plain (345 lines)

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

Greetings List,

dont know if this will help calm nerves a bit, but you might find what you want here, in one of those reference YB numbers. her hand-written notes on the case would be; YB85/9.10/3.1-3.2

It was not, therefore, immediately apparent from the post-mortem histopathological examination of the brain of one animal in this herd that it was the first and unprecedented case of a new disease. Even though it can now be seen, with hindsight, that such was the case.

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


The Stent farm cases

12. On 10th September, 1985 specimens (brain, kidney and spinal cord) from a cow owned by a Mr Stent of Pitsham Farm was referred to the CVL by the Winchester VI Centre (Mr J. Watkin-Jones, Veterinary Officer (VO)) for histopathological examination. Referrals from the VI Centres were dealt with on a rota system by the Consultative Pathology Unit (see paragraph 9 above). The veterinary pathologist on duty when the case came in to the Pathology Department was Ms Carol Richardson. At the time both Carol Richardson and I held the position of Senior Research Officer Grade II (SROII), both of us reporting directly to Ray Bradley. Carol Richardson worked in a section of the Department called Ruminant Reproductive Pathology and I believe that she had been working mainly on reproductive disorders in cattle and sheep, with a particular interest in research into infections producing foetal damage. She would, however, have dealt with scrapie cases through some of her previous work with Dr Stanley Terlecki, a former pathologist in the Department.

13. When such diagnostic cases came into CVL from a VI Centre the technician on duty at the time completed a VL99 card summarising the clinical history of the cow and the herd it originated from (based on information provided in the referral letter from the relevant VI Centre). The duty veterinary pathologist prepared the necessary pathological material for histological processing. Sections were then produced from the animal tissues for subsequent examination. The VL99 card for this particular case from Mr Stent's farm is found at YB85/9.10/3.1-3.2. This card and the prepared sections would then have been passed back to the duty veterinary pathologist for examination, which in this instance was Carol Richardson.

14. Carol Richardson conducted the histopathological examination and reported her findings on 19th September, 1985 (YB85/9.10/3.1-3.2). Her hand-written notes on the examination are on the VL99 card (see YB85/9.10/3.1-3.2). The final pathology report prepared by Carol Richardson, which was sent to Mr Watkin-Jones at Winchester VI Centre, is found at YB85/9.19/3.2. It should be noted that the purpose of the pathology reports prepared by the veterinary pathologists for such referrals from VI Centres is to make morphological diagnoses based on an examination of specimens provided. As far as is possible the pathologist then tries to place the diagnosis in the context of the clinical history of the particular animal and its herd or flock to reach conclusions or speculations on an aetiological diagnosis (the cause of the observed changes). This is the purpose of the "Remarks" section of the pathology report. Carol Richardson's examination reported "moderate spongiform encephalopathy" and "mild renal nephrosis" (the morphological diagnoses) and she attributed these observed changes to "a toxicity of some description" (the possible aetiological diagnosis). This was what was reported to the VI Centre. It is notable that nowhere in her report does she mention scrapie or indicate that her observations lead her to suspect any "scrapie-like" disease. The fact that the report mentions "moderate spongiform encephalopathy" is not conclusive in that respect. As highlighted by my short paper on vacuolation previously referred to in paragraph 8, spongiform conditions of the brain can arise from several different causes, including as a reaction to the ingestion of toxic substances, so this observation was consistent with her suggested aetiological diagnosis.

15. At the time this case came in from Mr Stent's farm, I was attending a meeting of the Charles Davis DVM Foundation for Veterinary Pathology in Cheshire. As is often the practice between pathologists in the event of encountering unusual or unexplained findings, Carol Richardson left the specimens and her pathology report for me to examine immediately on my return. A copy of Carol Richardson's report of 19th September, 1985 as annotated in manuscript by myself, is found at YB85/9.19/3.1. When sections are left for colleagues to examine it is not expected that any particular action would be taken by the colleague on his or her own initiative in respect of those sections. The purpose would be simply to offer a view on the material and then return the sections and report to the original examining pathologist, as was the case in this instance. Carol Richardson was absent from the Department on sick leave from 29th December, 1986, and this subsequently became maternity leave on 31st May, 1987. She returned to the Department on 29th December, 1987. Had Carol Richardson felt strongly thatabout the observations she had originally made were those of scrapie in cattle, and my subsequent opinion on her report, I would have expected that she would have come back to me to discuss the matter subsequently or take the matter further herself. in the period between seeing my annotations on her original report on the Stent case in September 1985 and her absence at the end of December 1985.

16. My re-examination of the sections "reinforcedwas consistent with" her original diagnosis in so far as I agreed with her overall observations and that such observations were not artefactual i.e. caused as a result of post-mortem changes or in the preparation of sections. My conclusion was that the brain lesions observed in this case could not in my experience be attributed to a specific disease, but a speculative comment was made that they could possibly be the result of chronic bacteraemia or an endotoxaemia (the production of poisons in the blood due to infection). Whilst the clinical history as described by the referring VI Centre (see YB85/9.10/3.1) describes that seven out of 130 cows were "nervous", this does not equate necessarily to the occurrence of a specific neurological disorder. The history indicated the occurrence of complex metabolic problems within the Stent herd (see paragraph 17 below).

17. Samples from three other cows in the Stent herd which had died or were killed on the farm had been referred to CVL for examination earlier in March, April and May of 1985 (CVL references VLO11453/85/0286, VLO11453/85/0640 and VLO12473/85/0831 respectively). Following, as far as I can recall, a telephone call from Mr J. Watkin-Jones, on 26th September, 1985 I reviewed the history of the submissions from the Stent herd and discussed them with him. This again, was standard practice where the VIS were investigating a persistent herd problem. A copy of my note of this event, together with the VI Centre referral letters and pathology reports for each case from the Stent farm (with manuscript comments made by myself at the time of this review) are found at YB85/9.26/1.1; YB85/9.10/3.1; YB85/9.19/3.1; YB85/4.31/1.1; YB85/5.9/1.1; YB85/4.6/1.1; YB85/4.16/1.1; YB85/2.13/1.1 and YB85/3.1/1.1 respectively. None of the samples for the three earlier cases included brain tissue and the main post-mortem finding in these cases was internal bleeding. Taken in isolation and in the light of these factors, the case in September 1985 did not at that time suggest that a new disease had been identified. Vacuolar changes in the brain of that particular animal were not severe and there was previous, and current, evidence of other disease problems. The herd from which these animals came had clearly experienced a lot of other health problems including haemorrhagic disorder (internal bleeding), hypocalcaemia (lack of calcium), septic arthritis (pus in joints), renal damage, bovine viral diarrhoea and peritonitis (inflammation of the abdominal cavity) associated with foetal death. This was a complex pattern in a dairy herd indicating that a variety of different diseases might be occurring. It was not, therefore, immediately apparent from the post-mortem histopathological examination of the brain of one animal in this herd that it was the first and unprecedented case of a new disease. Even though it can now be seen, with hindsight, that such was the case.

18. Further samples of nervous system tissues and other organs were received at CVL from a cow in the Stent herd on 10th September, 1986 (YB86/9.22/1.1-1.2). These were examined by Dr S. Done, a veterinary pathologist who joined the Pathology Department in 1983. A copy of the VL99 card for this case is found at YB86/9.22/1.1-1.2. Histopathogical examination of the central nervous system (CNS) tissues submitted from this case showed mild spongiform change in the medulla (hind brain). Other brain regions are described as having either no visible lesions or mild focal haemorrhage. See paragraph 31 for further discussion of this case.

4.The single case of BSE that I examined in September 1985 was the one and only case that I have seen.

5.The first officially reported case of BSE

Memory recalls a sequence of events the importance of which can only be made by informed judgement. The following account of an interesting and exciting event is taken largely from my memory. I have used copies of the original letter,case card, diagnostic report, accession books and my 1985 organiser diary to make this account as accurate as possible.

6.I had returned from annual leave and was on rota as duty pathologist. The senior technician of the diagnostic unit asked me to examine an adult bovine brain; the vet wanted a diagnosis a.s.a.p.

7.The history was of 7/130 cows showing nervous symptoms over the previous 5 months; most had gone for casualty slaughter and no gross abnormality had been seen in the viscera. (YB85/9.10/1.1).The Pathology Department had examined pieces of liver, kidney, heart and lung from three previous cases from this farm (YB85/2.15/1.1; YB85/4.9/1.1; YB85/5.3/1.1) (2 adults and 1 calf)and had found chronic mild hepatitis(1),acute hepatic necrosis (1) moderate pulmonary oedema (1) and chronic mild interstitial nephritis (2).

8.The history of these earlier cases was one of internal haemorrhage and samples had been sent for organic mercurial poisoning assay. There had been metabolic problems in this herd and active BVD infection in the calves. The case card numbers of these three cases can be seen in the cross-reference column on the case card of the September specimen- MS1509/85 (YB85/9.10/2.1). In addition to the nervous signs seen in this cow, abscessation of the stifle was also present. On gross examination, the brain was well fixed and relatively undamaged; pieces of spinal cord and a piece of kidney were included and were grossly unremarkable. The meninges appeared thickened but this was probably normal for an adult cow.

9.In the absence of gross abnormality, I made multiple incisions and took standard blocks (13) for histological processing and the production of H&E (see procedures) sections. Blocks of spinal cord and kidney were also sent for processing (11/9/85).

10.I have a set sequence for examining brain sections; when these sections were returned to me (13/9/85) I examined the frontal cerebrum first and progressed caudally scanning each section from dorsal to ventral surface. In this case there seemed to be a mild vacuolation of the cerebral neuropil. At this time Gerald Wells had been investigating the possibility that prolonged exposure of nervous tissue to 70% alcohol could produce neuropil vacuolation. Such prolonged exposure would occur over the week-end but I checked with the technician to ensure that such exposure had not occurred in this case before resuming my examination. I noted finding a mild multifocal non-suppurative peri-vascular infiltration with some eosinophils and in the caudal cerebrum mild focal gliosis. No abnormality was found in the thalamus (cranial midbrain) but mild neuropil vacuolation of the reticular formation in the colliculi. The medulla (a pathogonomic site for Scrapie in sheep) showed moderate neuronal and neuropil vacuolation. I found no abnormality in the cerebellum but the section of lumbar spinal cord showed mild neuropil vacuolation of the dorsal horns. There were two types of lesion in the section of kidney;a chronic mild /moderate non-suppurative interstitial reaction with tubular regeneration and fibrosis; a peracute reaction of a mild multifocal tubular necrosis with hydropic change (protein reabsorption).

11.These sections were reviewed by Gerald Wells in 1987 with essentially similar findings but more refined. (See case card at YB85/9.10/2.1).

12.Although I had never seen this type of lesion before in a cow I had frequently seen the combination of neuronal and neuropil vacuolation with this distribution in Scrapie. To me,this was Scrapie in a cow.

13.Before writing the report I sought a second opinion; I needed the opinion of a ruminant neuropathologist and therefore placed the sections, my findings and a request for re-examination on Martin Jeffrey’s bench. I was eager to hear his opinion and immediately after lunch went to collect the slides. Martin had left a note on which was written "Bovine scrapie". As I left his room I met him in the doorway. Apparently this was the first case he had seen but he informed me that Gerald had examined two cases and was expecting another two cases.

14.Interestingly, we apparently had more than one case here from different farms but obviously Gerald was dealing with it. In all my experience, there has not been a case of a novel disease in cattle affecting more than one farm initially: this should have caused alarm bells to ring. If there are several cases at different farms, it is important to cross-reference for the purposes of disease surveillance. A site visit to the Pitsham farm would have resulted in further well-preserved specimens, and more background information.

15.On the 17th-18th Sept. I drafted a batch of diagnostic reports including my report to Winchester VIC (YB85/9.19/1.1).

16.The report is a reiteration of my findings except that the histo-anatomical term `reticular formation’ should have been typed in the sentence above and not under the findings in the medulla. When it came to stating a diagnosis I decided that since the pathological term used for the clinical disease Scrapie of sheep is ovine spongiform encephalopathy then this "new" entity must also be classified as a "spongiform encephalopathy". I called it mild because again projecting onto the sheep situation with only a few sites affected the inclusion of mild as a descriptive term seemed correct. Although there was a chronic interstitial nephritis , I decided to highlight the peracute nephrosis which was probably related to a bacterial toxaemia associated with the stifle abcess.

17.From the history of the case on the Stent farm, it seemed as if the clinical course of the disease was fairly rapid in that metabolic disorders of short duration and heavy metal toxicities were being considered on the farm. Therefore, it seemed likely that the cause(s) of the spongiform changes were a result of an acute clinical disease (rather than a chronic illness) and in the absence of a more likely aetiology, toxicity seemed to be the most appropriate catagory that fitted both symptoms and findings.

18.I dismissed the possibility that a bacterial toxaemia had caused the spongiform change; in my limited experience of ruminant neuropathology, toxaemia was likely to produce frank neuronal necrosis rather than degenerative vacuolation (cf. Clostridial toxaemia).

19.The report was sent for typing; returned and despatched on the 19th September. The second copy and the original letter was filed on VlO 12467, the diagnostic file for cattle diseases. I asked the technician, Dorothy Wells (no relation to Gerald) to cross-reference with similar cases. I always asked the technician to do this, to enter the case numbers of similar cases on the pathology card. In this case I asked Dorothy to cross-reference for the two cases that Gerald had appaerntly already seen.

20.I heard nothing further about my 1985 case.

21.I left the CVL at Christmas 1986, on maternity leave.

############ ############

see full discussion here ;


I am truly confused here.

a BSE consultant in 1983 ??? Confucius is confused yet again.

how can you be a consultant of something that has not happened yet ???

is this a typo, or what ??? what is R Bradley speaking of in 1983 ??? what is this BSE CONSULTANT in 1983???

i am confused, i thought the first mad cow documented was in 1985, first discovered in 1984, but misdiagnosed, then later discovered to be BSE, a new strain of TSE in the bovine, but the following document has thrown me ?



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


R Bradly Pathology 12 October 1983

also, see ;

1981 nervous disease in a Hereford calf (calves aged 7-14 days shoring progressive nervous signs of the hind limb weakness progressing to paraplegia. ...

From: TSS
Date: July 11, 2005 at 11:23 am PST - 10 - 19.

On 18th February, 1987 (YB87/2.18/1.1) I reported to Dr Watson and Dr Shreeve on a further case which we had received from Truro VIC. The brain had shown neuronal vacuolation and in brain extracts there were fibrils that were similar in size and appearance to SAFs from sheep with scrapie. The Virology Department was studying the brain further and considering a transmission study. A few weeks before this, I had discussed the possibility of a transmission study with Michael Dawson, a research officer in the Virology Department and an expert in viral diseases in sheep, and we were considering carefully the safety aspects. In my note I raised the question of whether we should disclose the information we had more widely to the VIS because this may assist in getting any other cases referred to CVL but there was the difficulty that we knew very little about the disorder and would be unable to deal with queries that might be raised.

20. On 23rd February, 1987 (YB87/2.23/1.1) I sent Mr Wells a note asking him to prepare a statement for publication in Vision, the in-house newsheet prepared by the VIS for the SVS, setting out details of what we had discovered. On 24th February, 1987 (YB87/2.25/2.1) Gerald Wells indicated in a note to me that he had discussed the proposed article with Mr Dawson and they both believed that it could be damaging to publish anything at that stage. They believed cases would be referred to CVL in any event because they were unusual and they did not feel "Vision" was an appropriate publication because its confidentiality was questionable and might lead to referrals to veterinary schools rather than CVL. Gerald Wells was also concerned about the resources available in his section to deal with referred cases. I replied (YB87/2.25/2.1) indicating a draft statement was needed by the Director before a decision on publication could be made. Gerald Wells prepared a draft statement (YB87/3.2/2.1) and sent it to me on 2nd March, 1987. In his cover note (YB87/3.2/1.1) he commented that he believed the distribution of any statement about the new disease outside of CVL to be premature because there was so little information available about the new disease. I passed on a copy of Gerald Wells' note to Dr Watson (YB87/3.2/3.1). I discussed the matter of publication with Dr Watson. No decision had been taken to publish any material at that stage and I sent a note to Gerald Wells letting him know the position and confirming that his views and those of Michael Dawson would be taken into account when a decision was taken.

- 11 -

21. In March, 1987 serious consideration was given to possible transmission (e.g. to hamsters) and other experiments (other than the collection of epidemiological data by the VIS and clinicopathology which had been in progress since the first cases were recognised in November, 1986).

22. On 23rd April, 1987 I sent a report (YB87/4.23/1.1) to Dr Watson and Dr Shreeve informing them that nine control brains were being examined for SAFs and a cow which appeared to be affected with BSE had been purchased for observation. The cow had come from the farm where the original cases had developed and had arrived at CVL on 22nd April, 1987.

23. On 15th May, 1987 Dr Watson informed me that the proposed "Vision" draft would be circulated to VICs in England and Wales if it was approved by management. On 22nd May, 1987 I was copied in on a note (YB87/5.22/2.1) from B.M Williams, (who I believe was Head of the VIS at this time but retired shortly after this), to Dr Watson. This confirmed that the draft prepared for publication in Vision was approved but that the final paragraph should be amended to make it clear that knowledge of the new disease should not be communicated to other research institutes or university departments. At a meeting with Dr Watson on 2nd June, 1987 he informed me that no communication should be made with NPU until after the meeting with the CVO on 5th June, 1987 (see my note of 3rd June, 1987 – YB87/6.3/1.1). We needed much more data and information to answer inevitable queries. ...

The Cultural Politics of Science and Decision-Making An Anglo-German Comparison of Risk Political Cultures

 The BSE Case

Kerstin Dressel
sine-Institute Munich, Germany

The following report include excerpts of a thesis submitted in fulfilment of the requirements for the degree of
Doctor rerum politicarum (Dr. rer. pol.)
at the Ludwig-Maximilians-University of Munich
supervisor: Prof Dr Ulrich Beck
Institute for Sociology, Munich, Germany
The British case study was prepared at the Centre for the Study of Environmental Change at Lancaster University, UK,
Supervisor: Prof Dr Brian Wynne
kindly supported by a grant of the Economic and Social Research Council, UK
Munich, 2nd October 2000
© Kerstin Dressel, 2000  all rights reserved.

suppressed peer review of Harvard study October 31, 2002


5.289 We have concluded, for the reasons given above, that Dr Narang's work received fair consideration by MAFF scientists. While we would pay tribute to Dr Narang's dedication to research into TSEs, we feel that he had a fair opportunity to demonstrate the validity of his work but did not succeed in doing so.

No way to treat a pioneer
Apr 20 2003
By Phil Doherty

A leading charity has called for a public inquiry into the way a top mad cow disease expert has been treated by the establishment.

Harash Narang was the first scientist to make the link between the illness and its human equivalent- variant Creutzfeldt-Jakob disease - in 1990.

Dr Narang says he was made redundant from his job at Newcastle's Public Health Laboratory Services after making his findings known.

He claims that he lost his post after the then Health Minister Stephen Dorrell ordered all the lab's work on the killer disease to cease.

Since he became a whistle-blower, he says, he has not been able to get lab time in the UK to continue his work.

Dr Narang has since moved to the United States.

He is now working at the CJD surveillance unit based at Case Western Reserve University in Cleveland, Ohio.

CJD Foundation head Noel Baldwin, who lost his son Patrick to the killer disease, said: "There is more and more information coming out that proves Dr Narang was right all along.


"He said years ago that CJD could be found in blood and passed on by transfusions and medical instruments. This has now been accepted.

"He argued that BSE could cause both sporadic as well as vCJD, and recent research has shown this to be correct. He also invented a urine test which shows if someone is harbouring the disease."

Mr Baldwin also rued the Government's decision to pull Medical Research Council funding from Dr Narang.

He said: "Now it looks as if the US will benefit financially from this ground-breaking research.
"The UK establishment has ignored him for more than 10 years. We believe those responsible should be made accountable for this because if they had listened to Dr Narang maybe some of those poor people wouldn't have died from this terrible disease.


"This is a national scandal that needs to be fully addressed by a public inquiry.
"We are planning to launch this campaign in the next few months and will be involving sympathetic MPs to get this issue aired in the House of Commons."


CJD doc jets off

Mar 9 2003

By Phil Doherty, Sunday Sun

The North scientist who first established a link between mad cow disease and its human form is quitting Britain.

Harash Narang has been head-hunted by a top US university to continue his research into variant Creutzfeldt-Jakob disease.

He was working for the Government's Public Health Laboratory Service in Newcastle when he revealed the link and later lost his job.

Dr Narang claimed he was made redundant because he went public with his findings, an allegation which has always been denied. He said: "I now have a job at the United States CJD Surveillance Centre based in Case Western Reserve University, Cleveland, Ohio.

"I'm very excited because it has excellent facilities and is one of the best CJD surveillance centres in the world.

The university is examining a urine test pioneered by Dr Narang which can show whether someone has CJD.

Currently only a post-mortem diagnosis can be made.

Dr Narang said: "Early indications show that my test has performed even better than anticipated. It is expected to be validated very shortly."

And he revealed: "I do not regret telling the truth all those years ago. If I had to do it again then I would."

Ken Bell, a financial backer of Dr Narang's work, claimed he had been forced to go abroad because he cannot get laboratory time in the UK.

He said: "Harash has been blackballed in the UK because he told the public the truth.
"The establishment will try anything to stop him working here. It's a disgrace."

Noel Baldwin, of the CJD Foundation charity, said: "He has been proved right about so many things . . . that CJD can be transmitted through blood, that BSE can cause both variant and sporadic CJD and that you can test for the disease through urine samples."

Dr Narang starts work at Case University later this month. Shu Chen, one of his future colleagues, said: "He will be a great asset to our CJD research."

Edmonton company boasts cheap BSE test Duncan Thorne , CanWest News Service; Edmonton Journal Published: Friday, July 21, 2006 EDMONTON -- An Edmonton company is confident it has a cheap, ground-breaking test for mad cow disease, but the test's British inventor who claims to have first made the link between BSE and the disease's human form insists he still holds the rights.

Despite their differences, inventor Harash Narang and BSE Prion Solutions Inc. agree the test holds amazing potential to quickly and inexpensively test live cattle for bovine spongiform encephalopathy better known as mad-cow disease. The only approved tests so far for mad cow and its human equivalent depend on removing brain samples after death. A test on live animals would open the way to guaranteeing disease-free herds.

"We have a test that not only works, but works each and every time," said Ron Arnold of BSE Prion Solutions Inc., adding formal validation may take up to two years and regulatory approval.
Narang, a former British government scientist who went public about human risks from BSE in 1990, started developing tests for detecting the disease in the late 1980s while at a public health laboratory. He had been studying cases of a fatal but rare human brain illness, Creutzfeldt-Jakob disease (CJD), when he started noticing some cases were different. He has said he was well on the way to establishing a link between BSE and the unusual CJD cases when he was ordered to stop his research. He has also claimed officials rejected his calls for increased testing for BSE and the new form of CJD, now known as variant CJD.

Narang developed three diagnostic tests, including an early version of the urine test that BSE Prion intends to bring to market.

A wide-ranging 1998 inquiry into Britain's response to the mad cow crisis found problems with Narang's claims. It cited evidence that fellow scientists could not get his test to work.
Even so, Narang continued development of the urine test. A British company, Biotec Global, sponsored much of his work. He is no longer part of the research, but work on it continues at the United States National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland. Narang and Case Western researchers reported in 2005 that the urine test could reliably detect a harmless form of the prion protein that is blamed for BSE and variant CJD. It could also detect the bad form if the prion was first added directly to the urine.

They said their findings "may lay the foundation for a future technique," if in fact the bad prion can turn up naturally in urine.

"It needs a lot of work still," Ayuna Dagdanova, one of the test's researchers at the U.S. prion surveillance centre, said from Cleveland.

Without solid data it's not possible to say if they are close to detecting BSE in urine, she said. "No one actually knows, but preliminary experiments show the possibility."

Arnold, a partner in Biotec, said Narang gave Biotec the patent rights in 2003 and it in turn gave BSE Prion the licence for the Americas and Europe.

"We've talked with patent attorneys in London and also in Newcastle. Everyone agrees that the documents and the transfer of ownership of the patents was done judiciously and was extremely well put together by the solicitors," said Arnold.

Edmonton company boasts cheap BSE test Duncan Thorne , CanWest News Service; Edmonton Journal Published: Friday, July 21, 2006 Narang, speaking from Newcastle, acknowledged signing papers, but said it was not clear what he was signing. He said he continues to pay the patent renewal fees.

Biotec has sunk more than $2 million into the research, but BSE Prion has not had to pay a licence fee, Arnold said. That's because the project is humanitarian, with plans to hand over any earnings for research purposes, in the form of grants and scholarships.

Narang, who holds shares in Biotec despite the ownership dispute, also said he also wants any profits to go into further research. Meanwhile, he said he's owed back pay and expenses for work he did over the past five years a claim Arnold rejects.

Edmonton Journal
© CanWest News Service 2006

Experimental Biology and Medicine 230:343-349 (2005) © 2005 Society for Experimental Biology and Medicine



Sensitive Detection of Prion Protein in Human Urine

Harash K. Narang*,2, Ayuna Dagdanova, Zhiliang Xie, Qiwei Yang and Shu G. Chen,1 * BioTech Global, 22-40 Brentwood Avenue, Newcastle Upon Tyne, NE2 3DH, UK; and Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, Ohio 44106
1To whom requests for reprints should be addressed at Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44106. E-mail:


Transmissible spongiform encephalopathies are a group of infectious diseases typically associated with the accumulation of a protease-resistant and ß-sheet-rich prion protein, PrPSc, in affected brains. PrPSc is an altered isoform derived from the host-encoded glycoprotein, PrPC. The expression of PrPC is the highest in brain tissue, but it can also be detected at low levels in peripheral tissue. However, it is unclear whether a significant amount of PrPC is released into body fluid and excreted into urine. We have developed a simple, rapid method for the reliable detection of PrPC in urine from normal subjects by Western blotting. Our method can easily and reliably detect PrPC in apparently healthy individuals using less than 1 ml of urine in which the amount of urinary PrPC is estimated to be in the range of low micrograms/liter.

SIMPLE FACT, if you don't test, you don't find.

WHERE might we have been if Narang's research (and others that were not 'in the round'), would have been supported from the start ???

WHY were there just these 'chosen few' that recieved funding and got into the 'peer review round' ???

(please note, i have heard through the grapevine that Narang has recently past away, i have not confirmed this, (came from a good source though), and i never saw this in the news, but i hope that i am wrong. if true, this would be a great loss to the TSE science). ...TSS

August 20, 2008

Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate

Emmanuel E. Comoy1*, Cristina Casalone2, Nathalie Lescoutra-Etchegaray1, Gianluigi Zanusso3, Sophie Freire1, Dominique Marcé1, Frédéric Auvré1, Marie-Magdeleine Ruchoux1, Sergio Ferrari3, Salvatore Monaco3, Nicole Salès4, Maria Caramelli2, Philippe Leboulch1,5, Paul Brown1, Corinne I. Lasmézas4, Jean-Philippe Deslys1

1 Institute of Emerging Diseases and Innovative Therapies, CEA, Fontenay-aux-Roses, France, 2 Istituto Zooprofilattico Sperimentale del Piemonte, Turin, Italy, 3 Policlinico G.B. Rossi, Verona, Italy, 4 Scripps Florida, Jupiter, Florida, United States of America, 5 Genetics Division, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America


Background Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne transmission of prions from slaughtered cattle with classical Bovine Spongiform Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic in aging cattle, were recently identified at slaughterhouses throughout Europe and North America, raising a question about human susceptibility to these new prion strains.

Methodology/Principal Findings Brain homogenates from cattle with classical BSE and atypical (BASE) infections were inoculated intracerebrally into cynomolgus monkeys (Macacca fascicularis), a non-human primate model previously demonstrated to be susceptible to the original strain of cBSE. The resulting diseases were compared in terms of clinical signs, histology and biochemistry of the abnormal prion protein (PrPres). The single monkey infected with BASE had a shorter survival, and a different clinical evolution, histopathology, and prion protein (PrPres) pattern than was observed for either classical BSE or vCJD-inoculated animals. Also, the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine.

Conclusion/Significance Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.

Citation: Comoy EE, Casalone C, Lescoutra-Etchegaray N, Zanusso G, Freire S, et al. (2008) Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate. PLoS ONE 3(8): e3017. doi:10.1371/journal.pone.0003017
Editor: Neil Mabbott, University of Edinburgh, United Kingdom
Received: April 24, 2008; Accepted: August 1, 2008; Published: August 20, 2008
Copyright: © 2008 Comoy et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

snip... FULL TEXT ;

>>>"the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine." <<<

DOI: 10.1051/vetres:2007053 c INRA, EDP Sciences, 2008 Review article


And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.


Cases of atypical BSE have only been found in countries having implemented large active surveillance programs. As of 1st September 2007, 36 cases (16 H, 20 L) have been described all over the world in cattle: Belgium (1 L) [23], Canada (1 H)15, Denmark (1 L)16, France (8 H, 6 L)17, Germany (1 H, 1 L) [13], Italy (3 L)18, Japan (1 L) [71], Netherlands (1 H, 2 L)19, Poland (1 H, 6 L)20, Sweden (1 H)21, United Kingdom (1 H)22, and USA (2 H)23. Another H-type case has been found in a 19 year old miniature zebu in a zoological park in Switzerland [56]. It is noteworthy that atypical cases have been found in countries that did not experience classical BSE so far, like Sweden, or in which only few cases of classical BSE have been found, like Canada or the USA.

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

full text 18 pages ;

please see full text ;

***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

Sunday, March 16, 2008

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE

HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory JUNE 2008


Tissue infectivity and strain typing of the many variants Manuscript of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...


Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate

to be continued. ...TSS

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

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