Monday, November 30, 2009

Taiwan, USDA, and USA beef, what the consumer does not know, could kill them

The beef referendum is necessary

By Yu Ying-fu

Monday, Nov 30, 2009, Page 8 A referendum proposal on US beef launched by civic groups including the Consumers’ Foundation, the Homemakers’ Union and Foundation, the John Tung Foundation and the National Health Insurance Surveillance Alliance has passed the first application threshold and is proceeding to the second stage.

The proposed referendum suggests rejecting the Department of Health’s decision to allow imports of US bone-in beef, ground beef, bovine internal organs, spinal cord, etc, starting today. It further seeks to reopen negotiations with the US over beef imports.

For the referendum application to proceed, its proponents must collect the signatures of 5 percent of the total number of people who were eligible to vote in the most recent presidential election.

Gathering the signatures of hundreds of thousands of people across the country is no simple feat. As a lawyer, I have experience handling consumer complaints, for example against the Taipei City Government’s bus office and Eastern Multimedia Group.

I helped distribute official signature forms for the present proposal for a referendum on US beef. But based on my past experience, I am concerned that the signature drive will fail.

The proposed referendum says that the protocol on US beef imports signed by Taiwan and the US in Washington on Oct. 22 allows imports of bone-in beef, ground beef, processed beef products not contaminated with specific risk materials, central nervous system parts and meat scraps stripped by machine from cows less than 30 months old.

This deal sparked fear among consumers, while pan-blue and pan-green politicians have opposed the protocol, as have several county and city governments.

The government’s decision to relax restrictions on the import of bone-in beef, internal organs and other beef products from the US despite documented cases of bovine spongiform encephalopathy (BSE, also called mad cow disease) there — and political meddling by the government and the National Security Council in the decisions of experts at the health department are not appropriate in a democracy.

Taiwan’s Centers for Disease Control (CDC) say that treatment for variant Creutzfeldt-Jakob disease (vCJD), which is caused by abnormal prions from infected meat, cannot be cured. There is no treatment to slow or halt the course of the disease. Anyone infected with vCJD is on the road to inevitable death.

The only way to be sure of not getting the illness is to avoid eating beef products from BSE-affected countries.

To this day there have been no cases of the abnormal prion in Taiwan. Once in Taiwan, however, how would Taiwan get rid of it?

The government insists that US bone-in beef is safe, yet when the Ministry of Audit delivered a report on Oct. 27 to the legislature on the central government’s final account for last year, Auditor-General Lin Ching-long (???) said that, as of last year, the health department did not have enough personnel, funding or equipment to inspect and test US beef imports.

Furthermore, the prion can escape detection by specialized tests. This is because concentrations of the prion in certain body parts are so low that no technology exists that can guarantee that meat is free of it.

The prion’s presence can only be detected within six months of the onset of BSE. Cows less than 30 months old may be in the incubation stage of the illness, making the prion undetectable.

Health authorities have no way of guaranteeing that US beef is free of the disease, so assurances that consumers will be protected are nothing but empty talk.

Since the government is not capable of effectively testing imported beef, it should not have relaxed restrictions. Doing so puts consumers at risk.

This is a matter of consumer rights and a question of life or death for us and for future generations.

If not enough people sign the petition for this referendum proposal, Taiwan will be an object of disdain for the South Koreans. At least the South Koreans took to the streets in the hundreds of thousands to fight imports of US beef.

Yu Ying-fu is a lawyer.


Taiwan - Inquiry into US beef imports 30 Nov 2009

Premier Wu Den-yih (???) yesterday called for “mutual respect” between Taiwan and the US, as Taipei moved to adopt measures to block imports of US ground beef and bovine offal.

Wu dismissed remarks made by American Institute in Taiwan (AIT) Chairman Raymond Burghardt when he met with Legislative Speaker Wang Jyn-ping (???) on Monday that the controversy surrounding Taiwan’s relaxation of US beef imports was a “phony issue,” saying it was a “real issue of concern to the public.”

“We respect what [Burghardt] said, but we think and feel differently about this issue as he is an American and from a beef-­exporting country,” Wu told reporters at the Executive Yuan.

“When people still have doubts over the safety of US ground beef and bovine offal, of course the government has to prohibit imports of such products,” Wu said. “We respect [Burghardt’s] views, and we hope he can understand the public sentiment.”

Taiwan recently signed a protocol with the US to expand market access for US beef to include bone-in beef and other beef products that have not been contaminated with “specific risk materials.”


In response to a public outcry, the government promised to adopt administrative means to block ground beef and bovine offal, a move supported by the Chinese Nationalist Party (KMT) lawmakers, but a stance that has put them at odds with their Democratic Progressive Party (DPP) counterparts, who have proposed amending the Act Governing Food Sanitation (???????) to statutorily ban the imports.

Wu said the KMT’s version of the amendments — requiring all imports of ground beef and intestines be thawed for examination in a way that will effectively destroy the products — could create a win-win-win situation to safeguard public health, conform to the spirit of the WTO and respect the Taiwan-US protocol.

“I think there would be no reason for the US to oppose [administrative measures] targeting ground beef and bovine offal, which account for between 1 and 3 percent of its exports, nor would it let [the controversy] pose a negative influence on imports of its bone-in beef into Taiwan,” the premier said.


Meanwhile, Legislative Speaker Wang Jin-pyng (???) said yesterday it was unlikely the legislature would deal with a number of proposed amendments to the Act Governing Food Sanitation seeking to ban “risky” beef products from the US before the local elections next Saturday.

“We can sit down and discuss the proposals after the elections or the legislature will be paralyzed as a result,” Wang told reporters.

Wang made the remarks after the DPP once again occupied the speaker’s podium and threatened to boycott plenary sessions through next Saturday.


The DPP has paralyzed the plenary session since Nov. 3, making it impossible for any bills to clear the legislative floor over the past three weeks.

By law, the legislature should review and pass the central government’s fiscal budget request by the end of next month.

The deadlock continued because the DPP and the KMT still could not agree on the wording of the proposals.

The DPP would like to enshrine a ban on “risky” US beef products in the law, while the KMT wants to authorize the government to draw up measures to inspect bovine products from places where the risk of mad cow disease has been under control.

The KMT caucus condemned the DPP for paralyzing the plenary session again.

At a press conference, KMT caucus whip Lin Yi-shih (???) accused the DPP of refusing to negotiate relevant proposals even if the KMT had proposed a week ago to “ban the import of beef materials or products that are found risky or inedible.”

Showing reporters a number of snapshots of yesterday morning’s plenary session, KMT caucus secretary-general Lu Hsueh-chang (???) said only three DPP legislators — Chai Trong-rong (???), Yeh Yi-jin (???) and Kuo Wen-cheng (???) — participated in the boycott, while the remaining 25 DPP lawmakers were absent.

Lu accused the DPP of manipulating the controversy for political gain in the elections.

Meanwhile, KMT Legislator Kung Wen-chi (???) alleged that the DPP mobilized supporters to paralyze his phone lines in protest against his proposed amendment to the act.

Kung’s proposal sought to “draw up measures to inspect beef products from areas where the risk of mad cow disease has been under control.”

Kung said his cellphone and the phone at his office had been paralyzed by angry callers since an anonymous Netizen posted an article on Coolloud — a Web site for civic groups to publicize press releases and press conference notices — calling on the public to call the 22 KMT legislators endorsing Kung’s proposal.

Meanwhile, Taiwan Solidarity Union (TSU) Chairman Huang Kun-huei (???) said yesterday that Burghardt could not be more erroneous on the safety of US beef, demanding the US envoy recant his statement that US beef was safe for human consumption.

“It is possible that because Burghardt does not live on the continental US, he has lost touch with the current situation [of beef safety] and needs to be taught a lesson,” Huang said.

The TSU said the Consumer Union — a US-based consumer protection foundation — is engaged in a dispute with the US Food and Drug Administration (FDA), arguing that the US private meat plants should be allowed to conduct their own tests on cattle for bovine spongiform encephalopathy (BSE).

Huang said that the Consumer Union has long questioned the safety of US beef because of the prevalent practice of using chicken excrement as part of cow feed.

Such a practice has been blamed for being a source of BSE and other neurological diseases found in US cattle, Huang said.

Although the Consumer Union has formally asked the FDA to allow private meat establishments to conduct their own BSE tests, which the TSU said would only cost US$0.10 per test, the US government has flatly refused to do so, he said.

“Burghardt was obviously dead wrong when he said US beef is safe for human consumption and that no one in the US worries about its safety. He must recant his statement because, Mr Burghardt, you are wrong,” Huang said.

Source: taipeitimes

'Flash mob' US beef protest held outside Presidential Office

BLOGGERS WITH A BEEF: Protesters said it was the beginning of a campaign in which they hoped to stage a daily 'flash mob' protest at MRT stations By Ko Shu-ling STAFF REPORTER Monday, Nov 30, 2009, Page 3 A small group of bloggers and Internet users staged a “flash mob” protest in front of the Presidential Office yesterday afternoon to oppose the government’s decision to relax restrictions on US bone-in beef and beef products.

Chen Tai-yuan (???), who led the nine-strong protest, said yesterday was just the beginning of a long campaign and they hoped to stage at least one flash mob protest a day at mass rapid transit system (MRT) stations. Videos of the protests would be posted on YouTube, he said.

Chanting “Oppose toxic beef! Just say no! Relaunch negotiations,” participants in black lay on the ground for two minutes playing dead. They staged two protests, an hour apart.

Chen said they wore black to signify a funeral for President Ma Ying-jeou (???) and his administration, which he said had failed to protect the health of the public.

“Vegetarians can get mad cow disease,” he said. “There is a proven case in India.”

While the administration has reassured the public on the safety of US bone-in beef and beef products, Chen said he was not convinced.

“If it is safe, why did Taichung Mayor Jason Hu (???) say he would only eat US beef if President Ma eats it,” he said.

When asked whether he would eat US beef if Ma ate it in public to vouch for its safety, Chen said if Ma was willing to risk his own life that was his business.

Chen said he looked at the matter from two perspectives. One was whether US beef was safe and the other was how the administration had conducted its negotiations with Washington.

On the safety of US beef, Chen said Japan had sent food safety experts to the US to examine the slaughter of cattle younger than 20 months old and the expenses had been paid for by the US government. Taiwan, on the other hand, was conducting random checks at its own expense.

“Why? Are we second-class citizens or something?” he said. “Where is our dignity?”

Participants in yesterday’s protest said they supported the cause, but did not want their faces to be seen.

An 18-year-old who covered his face with a denim jacket said media exposure would not be good for his modeling career. Another participant wearing a surgical mask, black sunglasses and a baseball cap said he was not a supporter of the Democratic Progressive Party, but he believed in the ban on US bone-in beef. His position, however, ran counter to that of his company, a TV station.

Peng Lung-san (???), a motor scooter mechanic, lamented the fact that ordinary people were powerless, saying the government did whatever it wanted in its own interests.

Speaking from his own experience, Peng said the Taipei City Government had turned a deaf ear to his pleas not to demolish his apartment to make way for a new, bigger building complex. He said the city approved of such projects under the pretext of “urban planning.”


I would like comment on the facts about USA and BSE and CJD aka mad cow disease, and the rights of the Honorable People of Taiwan and all consumers. This same old song and dance has been played out time and time again, if it not be Taiwan, it was Korea, if not Korea, it was Japan, Canada, ... etc. etc.

It's all about only one thing, TRADE! Science has nothing to do with it. When the BSE GBR risk assessments and trade there from was abolished, when the OIE and the USDA made legal the trading of all strains of TSE globally, the consumer lost. AS with just what happened recently with the atypical Scrapie NOR-98, USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 FROM THE ANIMAL HEALTH CODE. IT can be traded freely now. AS with the atypical BSE cases in the USA, USDA et al have twisted this too into nothing more than an old cow prion disease, not to worry, with the cart before the horse again. When in fact atypical BSE seems to be more virulent than the typical BSE, with both the atypical l-BSE and h-BSE and the typical c-BSE, all documented in North America. The USA has systematically tried to cover up all cases of mad cow disease in the USA, but they failed to do it. A few were accidently reported, and then only with an act of Congress, were they confirmed. IF not for the OIG and the Honorable Phyllis Fong, that mad cow in Texas (the second one, the first stumbling and staggering mad cow in Texas in 2001 they refused to test at all, and sent it to be rendered), that 2nd Texas mad cow would have never been confirmed. The way it was, it took 7 months and literally an act of Congress to confirm it. Then the Alabama mad cow showed up. There is a long line of mad cow cover ups in the USA. They have been documented and ignored. The thing about Transmissible Spongiform Encephalopathy, it's the long, very long incubation period from time of exposure, to clinical symptoms, and then to death, for the ones that do become clinically affected, death is absolute, it is 100% fatal. But for some, they become exposed, and never go clinical. It is a false sense of security, that left unchecked, could come back to haunt the world. Most every scientist around the Globe knows full well that the USA Enhanced BSE surveillance program of 2004, and the Harvard BSE Risk Assessment of BSE in the USA, both were terribly flawed, and proven to be so. There is no doubt that the total of some 800,000+ BSE test were meaningless, due to these flaws, and proven to be so. The August 4, 1997 partial and voluntary mad cow feed ban in the USA was also terribly flawed, and proven to be so. For Pete's sake were are still feeding cows to cows in the USA in 2009. THE USDA et al let our children for 4 years feed on dead stock downer cows through the school lunch program, the most high risk cattle for mad cow disease. WHO will watch the children for the next 5+ decades for CJD. Sporadic CJD has been on the rise year and year in the USA, from 28 in 1996 and earlier to 205 cases in 2008, which includes 38 cases with type determination pending in which the diagnosis of vCJD has been excluded. nvCJD (which is vCJD now), is human BSE i.e. nvCJD from UK cattle. When UK sheep scrapie was transmitted to UK cattle, typical c-BSE was born, and nvCJD to humans there from. HOWEVER, when USA sheep scrapie was transmitted to USA cattle, your typical UK c-BSE was not the outcome, but something pathologically different. SO, Confucius ask, why then would USA human mad cow, look like UK nvCJD. It would NOT. There are many strains of scrapie, some 20+ different strains, with the atypical scrapie (NOR-98), and BSE in sheep. with the recent decisions of the OIE and the USDA et al on Nor-98, and deregulating that TSE, simply for trade, is like putting the horse before the cart, because they do not have the science to date to validate this human gamble. TYPICAL scrapie transmits to primate by their non-force oral consumption. TO my knowledge, to date, there have been no oral transmission studies done on atypical Scrapie NOR-98. WHAT about CWD? very little is known about CWD in the USA. now, there are two documented strains of CWD in cervids. CWD transmits to primates. WHAT about TME i.e. mad mink disease also in the USA? all these TSE have been rendered and fed to animals for human and animal consumption for over a decade. sporadic CJD rising in the USA of unknown route and sou ce. sporadic CJD in young and old people in the USA. I don't pretend to have all the answers, but I do know one thing, we have floundered way too long, and too export these TSE around the globe is just damn wrong in my opinion, and the consumers of these Countries receiving our highly potentially tainted products must have all the facts, not just part of them. WE must not allow the OIE and the USDA do what the U.K. did, that is export their tainted mad cow products around the Globe, except this time they just made it legal. There is much more to this nightmare than just the oral consumption, we must think 'friendly fire' there from. ...TSS

>>> In the papers, the government alleges the meatpacking plant slaughtered and processed downer cows for nearly four years — from January 2004 to September 2007 — at the average rate of one every six weeks...<<<

do you actually believe all these schools recalled this meat because of a few cattle being abused ?

see list ;

FNS All Regions Affected School Food Authorities By State United States Department of Agriculture Food and Nutrition Service National School Lunch Program March 24, 2008 School Food Authorities Affected by Hallmark/Westland Meat Packing Co. Beef Recall February 2006 - February 2008

Members of The HSUS are also concerned about the meat products provided to their children through the National School Lunch Program. More than 31 million school children receive lunches through the program each school day. To assist states in providing healthful, low-cost or free meals, USDA provides states with various commodities including ground beef. As evidenced by the HallmarkNVestland investigation and recall, the potential for downed animals to make their way into the National School Lunch Program is neither speculative nor hypothetical.


Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.


95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.


We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.




3.56 A further difference in the transmission properties of the two diseases was the pattern of disease caused in the brains of experimental animals. Mice inoculated with scrapie material from geographically and temporally distinct sources were found to have variable brain lesions, whereas mice inoculated with BSE material similarly derived from different sources all had very similar patterns of disease. 30 These results showed that, unlike scrapie, only one strain of BSE was present in the inocula derived from different sources. As the current hypothesis suggested that scrapie had transmitted to cattle at a number of geographically separate sites, it might have been expected that several strains of BSE would have been evident, given that over 20 strains of scrapie were known. Since 1996, strain-typing studies in mice have shown that the lesion profile produced by BSE is different to all known scrapie strains. 31

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. 32 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 The results were not published at this point, since the 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. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE.

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, 35 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. 36 It was also felt that the results of such an experiment would be hard to interpret. While a negative result 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. 37 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. 38 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.

Tuesday, November 17, 2009


Tuesday, November 17, 2009



Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 2009

Tuesday, November 10, 2009

Surveillance On the Bovine Spongiform Encephalopathy and rabies in Taiwan and USA

Monday, November 16, 2009

CANADA, USA, specified risk materials (SRMs), Environment, Fertilizer, AND Politics, just more BSe

Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009

Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009

----- Original Message ----- From: "Terry S. Singeltary Sr." To: Sent: Thursday, November 05, 2009 9:25 PM Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009



OIE Scrapie Chapter Revision • Current draft recognizes Nor98-like scrapie as a separate disease from classical scrapie • USDA provided comments on the draft to OIE,%20Thomas.pdf

Atypical scrapie/Nor 98 October 2009

Last year, after examining member country submissions and investigating rigorous scientific research, the World Organisation for Animal Health (OIE) decided that Nor 98 should not be listed in its Terrestrial Animal Health Code. The Code sets out trade recommendations or restrictions for listed diseases or conditions, and the OIE determined there was no need for such recommendations around Nor 98.

Sutton reported that USDA has urged the World Organization for Animal Health (OIE) to categorize Nor98-like scrapie as a separate disease from classical scrapie. Currently, the OIE has proposed a draft revision of their scrapie chapter that would exclude Nor98-like scrapie from the chapter. USDA will be submitting it's comments on this proposal soon.

see full text ;

Monday, November 30, 2009


Tuesday, August 04, 2009 Susceptibilities of Nonhuman Primates to Chronic Wasting Disease

Sunday, April 12, 2009

CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains

Wednesday, March 18, 2009

Detection of CWD Prions in Urine and Saliva of Deer by Transgenic Mouse Bioassay

Thursday, July 23, 2009

UW Hospital warning 53 patients about possible exposure to rare brain disease

10.3201/eid1505.081458 Suggested citation for this article: Angers RC, Seward TS, Napier D, Green M, Hoover E, Spraker T, et al. Chronic wasting disease prions in elk antler velvet. Emerg Infect Dis. 2009 May; [Epub ahead of print]

Chronic Wasting Disease Prions in Elk Antler Velvet

Wednesday, March 18, 2009

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

NOT only muscle, but now fat of CWD infected deer holds infectivity of the TSE (prion) agent. ...TSS

just follow the different topics and urls to the science and transmission studies. the transmission studies do not lie. only the politicians do. ...

and you don't even want to go to the mad cow issue and or the scrapie issue, and why should you $$$ your a sports writer, and this is much bigger than any of us will ever be, it was said long ago BSE would never be found in the USA. and due to the incubation period, it probably will not. but the BSE issue is just one phenotype. h and l and c BSE have all been found in North America.......... it's a damn political foot ball game, and we loose, and the animals loose $$$

Monday, July 13, 2009

Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease


Monday, July 06, 2009

Prion infectivity in fat of deer with Chronic Wasting Disease

Friday, February 20, 2009

Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease

Saturday, September 06, 2008

Chronic wasting disease in a Wisconsin white-tailed deer farm 79% INFECTION RATE

Contents: September 1 2008, Volume 20, Issue 5

snip...see full text ;

Tuesday, January 27, 2009

Chronic Wasting Disease found in a farmed elk from Olmsted County ST. PAUL, Minn. FOR IMMEDIATE RELEASE: Monday, January 26, 2009

Saturday, January 24, 2009

Research Project: Detection of TSE Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: 2008 Annual Report

2008 CWD Laboratory Testing for Wild White-tailed Deer,1607,7-186-25806-202922--,00.html

Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations

Thursday, December 25, 2008 Lions and Prions and Deer Demise

Monday, August 24, 2009

Third International CWD Symposium July 22-24, 2009 - Park City, Utah ABSTRACTS

Tuesday, July 21, 2009

Transmissible mink encephalopathy - review of the etiology

Saturday, December 01, 2007

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model


Thursday, October 15, 2009

Transmissibility studies of vacuolar changes in the rostral colliculus of pigs


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?

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009

August 10, 2009


I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. North America seems to have the most species with documented Transmissible Spongiform Encephalopathy's, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and source and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is no recourse, to date. But, while sub-clinical, how many can one exposed human infect? Can humans exposed to CWD and scrapie strains pass it forward as some form of sporadic CJD in the surgical and medical arenas? why must we wait decades and decades to prove this point, only to expose millions needlessly, only for the sake of the industries involved? would it not have been prudent from the beginning to just include all TSE's, and rule them out from there with transmission studies and change policies there from, as opposed to doing just the opposite? The science of TSE's have been nothing more than a political circus since the beginning, and for anyone to still believe in this one strain, one group of bovines, in one geographical location, with only one age group of human TSE i.e. nvCJD myth, for anyone to believe this today only enhances to spreading of these human and animal TSE's. This is exactly why we have been in this quagmire.

The ones that believe that there is a spontaneous CJD in 85%+ of all cases of human TSE, and the ones that do not believe that cattle can have this same phenomenon, are two of the same, the industry, and so goes the political science aspect of this tobacco and or asbestos scenario i.e. follow the money. I could go into all angles of this man made nightmare, the real facts and science, for instance, the continuing rendering technology and slow cooking with low temps that brewed this stew up, and the fact that THE USA HAD THIS TECHNOLOGY FIRST AND SHIPPED IT TO THE U.K. SOME 5 YEARS BEFORE THE U.S. STARTED USING THE SAME TECHNOLOGY, to save on fuel cost. This is what supposedly amplified the TSE agent via sheep scrapie, and spread via feed in the U.K. bovine, and other countries exporting the tainted product. BUT most everyone ignores this fact, and the fact that the U.S. has been recycling more TSE, from more species with TSEs, than any other country documented, but yet, it's all spontaneous, and the rise in sporadic CJD in the U.S. is a happenstance of bad luck ??? I respectfully disagree. To top that all off, the infamous BSE-FIREWALL that the USDA always brags about was nothing more than ink on paper, and I can prove this. YOU can ignore it, but this is FACT (see source, as late as 2007, in one recall alone, some 10,000,000 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE TO BE FED OUT, and most was never recovered. This was banned blood laced, meat and bone meal. 2006 was a banner year for banned mad cow protein going into commerce in the U.S. (see source of FDA feed ban warning letter below). I stress that the August 4, 1997 USA mad cow feed ban and this infamous BSE firewall, was nothing more than ink on paper, it was never enforceable.

I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub- clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE one strain TSE in cows, and the nv/v CJD one strain TSE humans, and the one geographical location source i.e. U.K., and that all the rest of human TSE are just one single strain i.e. sporadic CJD, a happenstance of bad luck that just happens due to a twisted protein that just twisted the wrong way, IN 85%+ OF ALL HUMAN TSEs, when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al, and that no other animal TSE transmits to humans ??? With all due respect to all Scientist that believe this, I beg to differ. To continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. 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? Tissue infectivity and strain typing of the many variants 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. ...

please see history, and the ever evolving TSE science to date ;

Saturday, June 13, 2009

Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009

Thursday, November 05, 2009

Incidence and spectrum of sporadic Creutzfeldt-Jakob disease variants with mixed phenotype and co-occurrence of PrPSc types: an updated classification

Tuesday, August 11, 2009

Characteristics of Established and Proposed Sporadic Creutzfeldt-Jakob Disease Variants

Brian S. Appleby, MD; Kristin K. Appleby, MD; Barbara J. Crain, MD, PhD; Chiadi U. Onyike, MD, MHS; Mitchell T. Wallin, MD, MPH; Peter V. Rabins, MD, MPH

Background: The classic Creutzfeldt-Jakob disease (CJD), Heidenhain, and Oppenheimer-Brownell variants are sporadic CJD (sCJD) phenotypes frequently described in the literature, but many cases present with neuropsychiatric symptoms, suggesting that there may be additional sCJD phenotypes.

Objective: To characterize clinical, diagnostic, and molecular features of 5 sCJD variants.

Design: Retrospective analysis.

Setting: The Johns Hopkins and Veterans Administration health care systems.

Participants: Eighty-eight patients with definite or probable sCJD.

Main Outcome Measures: Differences in age at onset, illness progression, diagnostic test results, and molecular subtype.

Results: The age at onset differed among sCJD variants (P=.03); the affective variant had the youngest mean age at onset (59.7 years). Survival time (P.001) and the time to clinical presentation (P=.003) differed among groups. Patients with the classic CJD phenotype had the shortest median survival time from symptom onset (66 days) and those who met criteria for the affective sCJD variant had the longest (421 days) and presented to clinicians significantly later (median time from onset to presentation, 92 days; P=.004). Cerebrospinal fluid analyses were positive for 14-3-3 protein in all of the affective variants, regardless of illness duration. Periodic sharp-wave complexes were not detected on any of the electroencephalography tracings in the Oppenheimer-Brownell group; basal ganglia hyperintensity was not detected on brain magnetic resonance imaging in this group either. All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.

Conclusions: The classic CJD phenotype and the Heidenhain, Oppenheimer-Brownell, cognitive, and affective sCJD variants differ by age at disease onset, survival time, and diagnostic test results. Characteristics of these 5 phenotypes are provided to facilitate further clinicopathologic investigation that may lead to more reliable and timely diagnoses of sCJD.

Arch Neurol. 2009;66(2):208-215



snip...see full text ;

Thursday, November 05, 2009

Incidence and spectrum of sporadic Creutzfeldt-Jakob disease variants with mixed phenotype and co-occurrence of PrPSc types: an updated classification

BSE (Mad Cow) Update: Do Reports of sCJD Clusters Matter?

snip... see full text ;

Friday, October 23, 2009

Creutzfeldt-Jakob Disease Surveillance Texas Data for Reporting Years 2000-2008

Sunday, August 10, 2008

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

Research Project: Detection of Transmissible Spongiform Encephalopathy Agents in Livestock, Wildlife, Agricultural Products, and the Environment Location: Foodborne Contaminants Research

Project Number: 5325-32000-008-00 Project Type: Appropriated

Start Date: Apr 07, 2008 End Date: Apr 30, 2012

Objective: We will develop highly sensitive diagnostic tests to detect transmissible spongiform encephalopathy (TSE) in livestock and wildlife animal species prior to the onset of clinical disease. We will also develop tests to confirm the presence or absence of TSE disease agents in ingredients of animal origin and decontaminated environments.

Approach: The threat of BSE continues to affect export economics for US meat. Meanwhile scrapie continues to influence sheep profits and herd biosecurity, and CWD is spreading throughout North America. Thus U.S. animal industry stakeholders have identified detection of the TSE infectious agent (prions) as a priority biosecurity research issue essential for prevention of TSE diseases. We will build on our previous successes using mass spectrometry (MS) for high-sensitivity and specificity in detection of PrPsc as a marker for TSE infectivity in blood using a hamster scrapie model. We will also develop a novel PrP-null mouse strain and related myeloma cell culture system for production of monoclonal antibodies (MAb), which may be specific for PrPsc. We will then choose MS or MAb and validate our novel diagnostic for preclinical diagnosis of scrapie in sheep blood. Whereas MS and MAb methods rely on dissolved samples, contamination of agricultural products and environmental surfaces is associated with solid samples. So we will produce a cell culture based assay for TSE infectivity that is surface-adsorbed. After using the relatively convenient hamster model for early development, we will validate this technology for detection of scrapie in sheep brain on meat-and-bone meal and stainless steel. All work with infectious material will take place within our APHIS-approved BL2 biocontainment facilities labs at the Western Regional Research Center (WRRC), while mass spectrometry will be performed on non-infectious material under BL1 containment. Replacing 5325-32000-007-00D (3/19/2008).

2008 Annual Report



and foremost, we must do these things properly. ...

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

Tuesday, November 10, 2009

Surveillance On the Bovine Spongiform Encephalopathy and rabies in Taiwan

AHRI.,No.40 : 51-63 (2004)

Surveillance of Transmissible Spongiform Encephalopathy and Rabies in 2004

Shu-Hwae LEE, Kwok-Rong TSAI, Kuo-Hui CHANG, Jen-Chieh CHANG, Che-tun HUNG, Lu-Jen TING , Wastson H. T. SUNG

Animal Health Research Institute, Council of Agriculture, Executive Yuan

We have applied histopathology, immunohistochemistry, Western immunoblot assay, and enzyme-linked immunosorbent assay techniques in the continuous surveillance program of bovine spongiform encephalopathy (BSE). Among the 859 cattle brains, 826 brains were collected randomly from the abattoirs, 3 from the M. tuberculosis-contaminated farms, 6 from the sick cows imported from Canada, 1 from the bovine ephemeral fever virus infected cattle and 23 from the culling old cattle in Taiwan in 2004. Cattle developed central nervous signs or showed other symptoms were also included. All of the brains were negative. Additionally, histopathological observation and direct immunofluorescent antibody were also applied to examine 1 rabies-suspected case with nervous symptom and 79 brain tissues of stray dogs in 2004. Rabies viral antigens and typical lesion were not detected in all tissues indicating free status of rabies in Taiwan. On the other hand, 3,204 sera samples including 1,380 samples from domestic dogs and 1,821 samples from stray dogs were examined by the enzyme-linked immunosorbent assay. Results showed that the sera-positive rate of domestic and stray dogs were 58.6% (809/1,380) and 35.9% (654/1,821), respectively.

Key words: TSE, rabies, surveillance

REPORT NO. AHRI report No38

Topic Surveillance On the Bovine Spongiform Encephalopathy and rabies in Taiwan in 2002

Department Animal Health Research Institute, Council of Agriculture, Executive Yuan

Author LEE Shu-Hwae, Kou-Hei CHANG, Kwok-Rong TSAI, Lu-Jen TING, Jong-Rong SHIAU, Shih-Yuh LIN

We have established a fast and accurate screening technique based On immunopathology to detect bovine spongiform encephalopathy (BSE) from bovine and ovine brain tissues standard operation procedures for the screening of BSE and rabies were established too. By following these procedures, the risk of BSE from imported food and the spread and damage of BSE and rabies would be greatly reduced. A total of 647 cattle brains aged older than 30 months (4.2-year-old in average) were screened in 2002. Totally, 1,385 brain sections colleced from the abanoirs and M. tuberculosis contaminated farms scattered through 11 counties, including Taoyang, Taichung, Chunghwa, Yunling, Nantao, Tainan, Pingtung, Ilan, Taitung, Panfu, and Kingmen, were examined. None of those samples showed spongiform change in pathology. Besides, enzyme-linked immunosorbent assay and Westem immunoblot assay were used to examine 647 cattle brains and 90 cattle brains collected since 1999 to 2002, also showing negative results in prion protein. These results would be submitted to the World Organisation for Animal Health to claim that Taiwan is a BSE free area. Fifty-Six canaine brains were also examined in histopathological sections and stained with direct immunofluorescent antibodies, showing negative results. An enzyme-linked immunosorbent assay was applied to detect the specific antibodies to rabies in 4,317 dog serum. samples. Among those serum samples, 1,946 samples were from domestic dogs and 2,371 were from stray dogs. Result revealed that 41.0% of domestic dogs and 21.4 % of stray dogs were positive in ELISA.

Keyword bovine spongiform encephalopathy; rabies; Surveillance; Taiwan

REPORT NO. AHRI report No36

TOPIC Surveillance on Bovine Spongiform Encephalopathy in Taiwan in 1998-2000

Department Animal Health Research Institute, Council of Agriculture, Executive Yuan

Author Lee, Shu-Hwae , Kou-Hei Chang, Min-Chao Weng, Jei-Fu Su and Shih-Yuh Lin

In order to fulfill the Office International des Epizooties (OIE) requirements for the statement of free area of bovine spongiforrn encephalopathy (BSE), 85 cattle brains were collected from the abattoirs, rendering plants and the cattle herds infected by M. tuberculosis located in 8 prefectures of Taiwan. Cattle developed CNS signs or showed other symptoms were also included. A total of 850 brain histologic tissue sections (10 sections/brain) were examined. None of the 850 brain tissue sections showed evidence related to spongiform change. Then, thirty out of the 85 brain tissue sections were examined further by the Western blot diagnostic kit. No evidence of prion was found. These results could therefore provide for OIE to recognize Taiwan as a free Country of BSE.

Keyword Bovine spongiform encephalopathy, M. tuberculosis, brain tissue sections

AHRI report No.37

Topic Establishment of the Laboratory Diagnostic Techniques and Monitormg of Bovine Spongiform Encephalopathy in Taiwan

Department Animal Health Research lnstitute, Council of Agriculture

Authur Kuo-Hui Chang*, Shu-Hwae Lee, Min-Chao Weng, Jei-Fu Su, Shih- Yuh, Lin

Summary To prevent bovine spongiform encephalopathy (BSE) from entering our country, we have established the BSE laboratory diagnostic techniques, including the laboratory biosafety, histopathology, immunohistochemistry, Western immunoblot assay, and enzyme-linked immunosorbent assay. We have also applied those techniques to the continuous surveillance program of BSE. A total of 127 cattle brains were collected from the abattoirs, rendering plants, and M. tuberculosis-conaminated farms located in 10 counties of Taiwan during 1998 to 2001. Cattle developed central nerous signs or showed other symptoms were also included. All the brains were examined and present negative results.

Keywords bovine spongiform encephalopathy, mad cow disease, prion, laboratory diagnostic techniques

Pathological Diangosis and Services for Animal Diseases in Taiwan in 2002

Republic of Korea Livestock and Products Sem-Annual 2008 This article provides the cattle industry data from the USDA FAS Livestock and Products Semi-Annual 2008 report for the Republic of Korea. A link to the full report is also provided. The full report includes all the tabular data, which we have omitted from this article.


Annual and Semi







Report Highlights: Imports of beef are projected to remain stable in 2008 at 310,000 metric tons. Increases in domestic inventory will alleviate some of the unmet demand for animal protein. Lower international pork prices in the United States and increasinly lower tariffs for Chilean pork will make imported pork and pork products more price competitive this year. Total imports of pork are forecast at 452,000 tons, an increase of 2.5 percent from 2007. The domestic livestock industry is facing higher feed prices this year and will likely increase slaughter rates from those initially forecasted.

Situation and Outlook The political landscape in Korea is changing. On February 25, a new conservative president, Lee Myung-bak, was sworn into office after 10 years of liberal rule. During his campaign the new president made a “747” jumbo election pledge to revive Korea's economy by achieving seven percent annual growth, per-capita national income of $40,000 and making Korea the world’s seventh largest economy in 10 years. Currently, exports are still strong, but the world economy is slowing and Korea may begin to feel the effects in the second half of this year. Imports are forecast to rise considerably this year due to high oil, grain and raw material prices. As a result, the economic forecast for 2008 is expected to be just under five percent.

With a new president, comes a new government. The new Minister for Food, Agriculture, Forestry & Fisheries (MIFAFF),, Jung Un-chun (also spelled Chung Woon-chun) has stated that “the country’s agriculture policy should no longer be passive and protective, but instead should be proactive and aggressive.” As a result, Jung’s nomination drew mixed reviews from rank-and-file farmers. The new Minister is likely to deal with the beef issue, while at the same time explore ways to provide additional debt relief to farmers in order to gain their support for the Korea-U.S. free trade agreement.

Imports of beef are projected to rema in stable in 2008; although the forecast was dropped slightly on account of higher slaughter rates. This increase in domestic production will result in a 5 percent increase in consumption compared to last year. The unmet demand for beef in Korea is quite high given that per capita consumption in 2007 (7.5 kg) is still below the 2003 level (8.1 kg) and well below the level in the United States (about 30.5 kg).

Increased swine slaughter in 2008 resulting in higher expected domestic production is the main reason that the forecast for pork imports was lowered. Imports of pork will increase year on year due to lower international prices. Increased U.S. swine production and the steady decline in tariff rates for Chilean pork will make imported pork more price competitive this year. The demand for pork, even though it is at record levels (19.7 kg), probably still has room for growth.

Domestic prices for live cattle and swine depend on slaughter rates. Higher prices for imported corn and soybeans, ingredients used locally in compound livestock feeds, will increase costs for the farmer. Judging by past history, farmers are likely to sell off their cattle at higher rates if their costs increase. Higher slaughter rates will result in lower live animal prices and lower wholesale prices for beef and pork; however, this does not necessarily translate into lower retail prices for the consumer. Retail prices tend to remain stable, changing only when external pressures force retailers to lower their prices. Absent U.S beef, the price of imported beef will increase as the higher costs of production in exporting countries are passed on to buyers.

Beef and Beef Products Production Inventory levels are expected to remain high regardless of whether or not U.S. beef returns to the market in 2008. Korea's total cow beginning stock levels in 2008 are five percent higher than those compared to this same time last year. High cow numbers will permit farmers to increase their herd sizes in 2008. In addition, 595,000 head of Hanwoo were artificially inseminated in the second half of 2007, an increase of 19.7 percent from the same period in 2006. With such high insemination rates and beginning stock levels, the total inventory is not expected to come down until at least 2009.

The conclusion of the KORUS FTA negotiations in early April 2007 and the brief resumption of U.S. beef imports that began in April 2007 after the bone chip issue was partially resolved had a huge impact on domestic beef prices. Live cow prices dropped over four percent from an average of 4,960,000 won (about $5,221, at an exchange rate of US$1=950 won) per head in April 2007 to 4,786,000 won (about $5,038) in May 2007, after the arrival of the first beef shipment on April 23, 2007. This decline continued until U.S. beef was shut off again on October 5, 2007. Since then, however, prices have begun to move upward again.

The price drop provoked farmers to sell off their stock and send cattle to slaughter. During the four month period (May-August) after U.S. beef imports resumed and prior to the Korean Thanksgiving Holidays (October), beef cattle slaughter jumped 6.7 percent in 2007 compared to the same period in 2006. The cow-steer slaughter ratio jumped to 45.9:54.1 during this four-month period, compared to 44.7:55.3 during the same period in 2006 and the 2006 annual average ratio of 43.3:56.7. Despite the short-term panic, Korea still maintains a very high level of Hanwoo inventory; however increased feed grain prices will have a direct effect on production costs and in the long run will cause less competitive farmers to stop producing cattle.

Korea was recognized by the World Organization for Animal Health (OIE) as being free from Foot & Mouth Disease (FMD) in 2002. Korea has requested that other countries, including the United States recognize its OIE status.

Korea’s beef self-sufficiency ratio has increased from 36.1 percent in 2003 to 46.9 percent in 2007; however, this is not because of an increase in production but rather a drop in consumption. The high price of beef in Korea has resulted in decreased demand for all beef, domestic and imported. When U.S. beef enters the market, as seen in 2007, the effect is more competition, more choice and lower prices for consumers resulting in increased demand that may actually be beneficial to the domestic industry. Increased availability of beef does not replace current suppliers, it expands the whole market. There is a market for Hanwoo beef that will remain even if U.S. beef is present; but not all consumers can eat Hanwoo beef given the cost. After the market was liberalized in 2000, Hanwoo production did not go away and even in 2007, with some U.S. beef available, Hanwoo sales actually increased and production grew.

Source: U.S. Meat Export Federation/Korea and the National Agric ultural Cooperative Federation Consumption Beef consumption is projected to continue to increase in 2008 as it did in 2007 due to higher domestic production. Prices dropped slightly in 2007 due to the availability of U.S. beef from May to October and this contributed to an increase in consumption of beef from all origins.

Korean consumers are still concerned about the safety of U.S. beef. The chart of U.S. beef retail sales shows that with each finding of backbone, sales dropped. According to a recent survey, 85.5 percent of consumers stated that they worry about the safety of U.S. beef.

According to the Ministry of Agriculture and Forestry (MAF), Korean consumers purchased beef 1.59 times per month in 2007 (up from 1.53 times per month in 2006) and spent an average of 36,100 Korean won per purchase (up from 27,980 Korean won in 2006). Consumers seem to be willing to spend more to purchase beef than they are to purchase pork or poultry. In addition, MAF is providing support to livestock producers to develop brands that provide consumers with more information about the meat they are buying. The awareness of brands is growing. In 2007, 34.5 percent of consumers said they were aware of beef brands, a marginal increase from 34.4 percent in 2006. In a recent survey, over half stated that they were willing to pay an additional 5-10 percent more for a branded meat product.

Source: U.S. Meat Export Federation/Korea Very little beef is consumed in the form of processed meat in Korea and virtually all beef is purchased for direct cooking, either in the form of Korean barbeque, soup, and other Korean dishes. Only 600 tons of imported beef rounds from Australian and New Zealand are processed into beef jerky by a domestic company.

The most popular cuts of beef are bone-in short ribs, loins and chuck rolls. Short ribs are consumed mainly for Korean barbeque or kalbi. Loins are also used for Korean barbeque while chuck roll is used for making bulgoki, shaboo shaboo and steak. As Koreans like to barbeque their beef, well marbled beef receives higher prices over lean meat. Also, as consumers are accustomed to grainfed beef, they prefer such beef over grass-fed. Thus, Australia which used to supply grass-fed beef is now switching to grain-fed beef. Grass-fed beef is often marinated in order to cover the grass flavor that Koreans do not like. There is also a preference for fresh chilled beef rather than frozen beef. During the period when U.S. beef was banned, not only did the total amount of short rib imports drop, but Australian clod replaced chuck rolls for bulgoki.

Source: U.S. Meat Export Federation/Korea Trade Total imports of beef and beef products in 2008 are forecast at 310,000 metric tons (carcass weight equivalent). Since a commercially viable protocol for U.S. beef currently does not exist, this report makes no projection regarding imports of U.S. beef. Therefore, imports of beef from current sources are projected to remain stable from last year. The current 2008 forecast is down from the previous 2008 forecast when it was expected that a small amount of U.S. boneless beef would be imported.

The total beef import market has never really returned to the level prior to the ban on U.S. beef at the end of December 2003. Despite aggressive marketing of grain fed beef by Australia, total beef imports are still far below the 2003 level.

U.S. Beef Imports Before the BSE ban was imposed at the end of 2003, beef was the top U.S. agricultural export to Korea and Korea was the third largest beef market for the United States. A beef protocol for deboned skeletal muscle meat was established in January 2006 and after an audit of all 36 plants eligible to export by the Korean quarantine authorities, the market was theoretically opened in September 2006. After three successive shipments, each one rejected due to bone fragment findings; Korea published slightly less onerous inspection procedures in March 2007. The new procedures indicated that all shipments would be subject to 100% inspections with x-ray machines, but that the rejections will only be limited to the box and not the entire shipment. These new inspection procedures enticed U.S. exporters to begin shipping boneless U.S. beef. On August 1, a vertebral column finding, a bone that Korea considered specified risk material (SRM) resulted in a quarantine inspection suspension for one month. This suspension was lifted on August 24; however, it was reinstated on October 5 when another vertebral column was found. This latest suspension is anticipated to remain until a bone-in protocol is negotiated. There is about 5,000 tons of beef that is in the bonded area; this beef has arrived, but has not been inspected.

Beef Tariffs and the Korea-U.S. Free Trade Agreement The Korea-U.S. free trade agreement was concluded on April 1, 2007; however, neither the Korean National Assembly nor the U.S. Congress has ratified the agreement. Although the continued quarantine inspection suspension limits the ability of the United States to ratify this agreement, it does have some significant benefits for U.S. red meat exporters.

Korean tariffs on imports of beef muscle meats will decline to zero from the current 40 percent tariff in 15 equal annual reductions. A trade level similar to Korea's average imports from 2001 to 2003 of 182,800 metric tons of U.S. muscle meats valued at $569 million; implementation of the Korea-U.S. free trade agreement translates into a tariff savings of $15 million in year one of the agreement. Once tariffs are completely phased out, the annual tariff savings will be an estimated $1,300 per ton.

The agreement does includes a quantity safeguard of 270,000 tons for beef muscle meats, growing at a compound 2-percent annual rate to a final safeguard level of 354,000 tons in 15 years. In year 16 and beyond, safeguards will no longer apply. In 2003, the United States exported a record 224,000 metric tons of beef to Korea. This amount is still far below the trigger level in year one.

Korean tariffs on beef offal also decline in 15 equal annual reductions from their current 18- or 17-percent levels.

Release No. 0545.09 Contact: Carol Guthrie (USTR) 202-395-3230 Chris Mather (USDA) 202-720-4631

Joint Statement from USTR and USDA Spokeswomen Regarding Expanded Market Access for U.S. beef in Taiwan

Washington, Nov. 2, 2009 - The Office of the United States Trade Representative and the U.S. Department of Agriculture today released a brief statement regarding Taiwan's announcement on the import of American beef. The following statement is from Carol Guthrie, Assistant United States Trade Representative for Public Affairs, and Chris Mather, USDA Director of Communications:

"After over two years of extensive negotiations and scientific and technical exchanges, the United States has been looking forward to an announcement from Taiwan authorities that Taiwan would fully open its market to American beef and beef products on the basis of the bilateral protocol we have negotiated. The Protocol that Taiwan promulgated today is science-based and follows the guidelines of World Organization of Animal Health (OIE) as well as the findings of Taiwan's own risk assessment on the safety of U.S. beef. We understand today that Taiwan also announced a number of other additional domestic measures regarding beef and beef products. We are currently reviewing these measures to ensure they allow Taiwan consumers the opportunity to enjoy the same safe American beef and beef products that American families eat. We look forward to working with our partners in Taiwan to ensure that Taiwan's domestic requirements are consistent with the Protocol, the science, the OIE guidelines, and Taiwan's international obligations."


USDA is an equal opportunity provider, employer and lender. To file a complaint of discrimination, write: USDA, Director, Office of Civil Rights, 1400 Independence Avenue, SW, Washington, DC 20250-9410 or call (800) 795-3272(voice), or (202) 720-6382 (TDD).

# USDA News 202 720-4623



NOW, let's look at some _facts_. they seem to get over looked some times, and from time to time, we should look at _all_ the facts. ...TSS

I. EXECUTIVE SUMMARY On December 12, 2005, after nearly two years of banning the export of beef from the United States, Japan resumed beef trade with the United States. On January 20, 2006, Japan government officials discovered 3 boxes of veal with vertebral column shipped from the United States. Vertebral column is not allowed under the specific trade agreement with Japan. The United States acknowledges this was unacceptable because it did not meet the terms of our agreement with Japan, but emphasized that the product did not present a health risk to the public.

Box 3.1 Key events in recent U.S.-Korea Beef Trade • Prior to Korea's ban on imports of U.S. beef following the discovery BSE in a Canadian-born cow in the state of Washington in late 2003, Korea imported an average of 5,670 tons of U.S. beef—primarily “short ribs”— per month. Product primarily consisted of “short ribs.” • In September 2006, Korea allowed U.S. shipments of boneless beef to resume, albeit with a “zero” tolerance policy for bone chips or other material considered “at risk.” In addition, Korea will not accept beef from animals over 30 months of age, which is a more stringent approach than international standards of the World Organization for Animal Health (also known as the OIE). • In late May 2007, OIE classified the United States as a “Controlled Risk” region for BSE. Controlled Risk is the second highest safety rating. • Korea rejected the first three shipments of U.S. beef after reopening its market in September 2006 upon finding bone fragments in several boxes. Typically beef is shipped in prepackaged boxes. U.S. beef is mechanically deboned, which invariably results in small bone fragments, although this is considered commercially acceptable in the industry. The entire shipment, instead of the individual boxes, was rejected. • In June 2007, several boxes of ribs were found in a shipment to Korea resulting in a “stoppage” of U.S. shipments. After a USDA investigation it was determined that the shipment was safe and was meant for U.S. domestic sale and mistakenly sent to Korea. Korea is presently accepting U.S. boneless beef and has indicated that it will only return individual boxes instead of entire shipments. • Negotiations are currently ongoing. Sources: World Organization for Animal Health (OIE). Official Animal Health Status, “Bovine Spongiform Encephalopathy”; Industry officials, e-mail and telephone correspondence with Commission staff, Washington, DC, June 2007; Johnston, Tom. “South Korea Reopens to U.S. Beef Imports,” June 8, 2007; and USDA, FAS, “Korea Lifts Suspension of Six U.S. Meat Plants,” June 25, 2007.

2006/12/01 11:45 KST

Seoul again rejects U.S. beef on bone chip discovery

SEOUL, Dec. 1 (Yonhap) -- South Korea said Friday it has rejected a shipment of three tons of U.S. beef because bone chips were found in the meat, the second case in just three weeks.

On Nov. 24, South Korea, the third-largest buyer of U.S. beef in 2003, rejected the first shipment of the meat to arrive here since lifting a three-year ban imposed out of fear of mad cow disease in September this year, saying it found bone fragments, which violated an agreement.

"The bones do not seem to be specified risk material, but it violates the agreement with the United States to ship only boneless beef," the National Veterinary Research & Quarantine Service said in a statement.

Under the agreement, U.S. beef suppliers to South Korea are required to ensure that bones, spinal cord and brains are removed from the meat. Also, the beef must come from cattle no older than 30 months.

Seoul imposed bans on U.S. beef after an animal with mad cow disease was found in the state of Washington in December 2003.

South Korea had been under pressure from the U.S. to resume beef imports amid negotiations for a free trade agreement with the U.S.

The two countries are aiming to conclude the talks by the first quarter of next year so President George W. Bush can approve it before his trade authority expires in July 2007.

A beef trade dispute may be one of the major hurdles in the upcoming talks to be held in Montana next week, watchers said.

Mad cow disease is a brain-wasting livestock illness. Hunans eating contaminated meat from infected animals can contract a fatal form of the disease.


specified risk material (SRM), would carry infectivity. For bovine animals the SRM are the skull including the brain, eyes, trigeminal ganglia, tonsils, thymus, spleen, and the spinal cord of animals over 12 months of age; the vertebral column (including dorsal root ganglia) of animals over 12 months of age, and the intestines (from duodenum to rectum) of animals of any age. The absence of an age limit for intestines resulted from experimental data demonstrating BSE infectivity in the distal ileum of animals very early after challenge with the BSE agent. The current list of SRM for the European Union is detailed in Appendix 3.

Another Bone Fragments Found in US Beef

By Kim Yon-se Staff Reporter The government said it found seven bone fragments in the third batch of beef shipment from the United States.

It is the third time that South Korea has found bone pieces since September when it decided to resume the import of American beef.

``The meat is from cattle slaughtered in Nebraska and processed in Iowa,¡¯¡¯ said Kang Mun-il, director general of the National Veterinary Research & Quarantine Service (NVRQS).

The quarantine service said that the fragments were found in the 10.2 tons of chuck short ribs from U.S. cattle. The NVRQS inspected only 5 percent, or 10 of the 651 boxes that arrived in Korea on Dec. 1.

Bone inclusion in shipments is a violation of import conditions between the two countries. The beef will be sent back to the U.S. or destroyed, the quarantine service said.

South Korea had refused U.S. beef due to its concern over a case of mad cow disease reported in the U.S. in 2003.

The government had said it would return or destroy the two previous shipments on Nov. 24. and Dec. 1 as a bone fragment and three fragments were found in the beef from Kansas and Nebraska, respectively.

``I heard that the U.S. also conducted an X-ray test _ on the third batch _ before shipment,¡¯¡¯ Kang said. ``The possibility that the U.S. failed to detect the bone fragments is high because they were so thin.¡¯¡¯

He rejected some reports that U.S. beef with bone fragments have already been consumed by some U.S. soldiers here and Koreans. He said, ``I think the reports are groundless as the beef should be destroyed or sent back.¡¯¡¯


12-06-2006 21:20

Note: Values may not sum to totals shown because of rounding. Includes HS 2304. The value of U.S. exports of animal feed preparations46 (mixed feeds) to Korea has increased 51 percent over the 2002 to 2006 period.47 The United States has been a leading supplier to Korea from 2002 to 2006 (table 3.5), and the immediate removal of Korean tariffs (4.2 or 5 percent) as a result of implementation of the FTA would likely improve the U.S. competitiveness against China and other leading exporters. The United States is the leading supplier of pet food48 exports to Korea, with a market share of more than 50 percent (table 3.6); Korea is the eighth-largest U.S. export market for pet foods.49 Korea’s pet food consumption is expected to increase over the next several years as the trend toward pet ownership becomes increasingly popular as disposable incomes continue to rise and multiple pet households become more common.50 The immediate removal of the 5 percent tariff on pet food under the FTA would likely allow the United States to increase its already dominant market share against leading competitors.

Korea, however, has SPS and technical barriers to trade (TBT) measures that have constrained U.S. pet food exports. Interpretation and implementation of the FTA’s TBT chapter and the actions of the standing committee established by the FTA’s SPS chapter would likely be important to fully realize these gains in market access.51 As a result of the U.S. outbreak of bovine spongiform encephalopathy (BSE) in 2003, Korea has banned U.S. exports of pet foods containing beef or other ruminant products. Additionally, Korea requires that U.S. exports of pet food containing animal proteins, including fish meal, need to be certified that they are entirely of U.S. origin. Consequently, animal proteins from other countries, which could be lower-cost, are prohibited in pet foods. In addition, pet food importers are required to provide a full ingredient list with percentages of each ingredient by weight for registration at provincial government offices. The absence of Korean safeguards to prevent disclosure of this proprietary information has disrupted U.S. exports of pet food to Korea.52 U.S. exports of distiller’s dried grains with solubles (DDGS) to Korea were negligible until 2004, but have risen sharply since then (table 3.7). A large proportion of DDGS are 53 Shurson, “Benefits and Limitations of Using DDGS in Swine Diets,” January 25, 2007. 54 ATAC for Grains, Feed, and Oilseeds, Advisory Committee Report, April 25, 2007, 6. 55 Ibid. 56 American Soybean Assoc., “American Soybean Association Applauds Korean Trade Agreement (April 3, 2007).” 57 National Oilseed Processors Assoc., “NOPA Strongly Supports Korea Free Trade Agreement (April 4, 2007).” 3-12 consumed domestically by the U.S. livestock industry, but its domestic use is presently constrained in animal rations because of nutritional limitations such as digestibility, protein quality, and energy values.53 As a result, the exportable surplus of DDGS has increased with the expansion of the U.S. ethanol industry, and the United States is now the leading exporter of DDGS to Korea with a market share of over 60 percent in 2006. The immediate removal of the 5 percent tariff on DDGS as a result of implementation of the FTA would further increase the competitiveness of the United States against China, the other primary supplier. This improved access would be expected to result in DDGS having a greater inclusion in feed rations in future years as Korea’s feed manufactures seek to diversify sources.54

----- Original Message -----
From: "Terry S. Singeltary Sr."
Sent: Wednesday, November 04, 2009 2:32 PM

[BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009

Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009

Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009



I wish to send you the following data on USA mad cow disease and cjd.

I am not anti-meat. I am anti-stupid, and stupid is as stupid does.

WHO WILL WATCH THE CHILDREN for CJD over the next 5 decades ?

FOR 4 years, the USDA fed dead stock downer cows, the most high risk cattle for mad cow disease and other dangerous pathogens to children all across the USA via the USDA certified dead stock downer cow school lunch program...


BOVINE SPONGIFORM ENCEPHALOPATHY (typical and atypical strains)

Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009

Sunday, September 6, 2009




CVM Annual Report Fiscal Year 2008: October 1, 2007-September 30, 2008


BSE Feed Rule Enforcement: A Decade of Success OFF TO A FAST START


Sent: Tuesday, November 03, 2009 5:14 PM


Date: March 21, 2007 at 2:27 pm PST




Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007


Cattle feed delivered between 01/12/2007 and 01/26/2007


Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

Firm initiated recall is ongoing.


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.


42,090 lbs.







The firm does not utilize a code - only shipping documentation with commodity and weights identified.


Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.


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.


9,997,976 lbs.


ID and NV



Thursday, March 19, 2009


Sunday, October 18, 2009

Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009

Thursday, October 15, 2009

Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009

Tuesday, July 14, 2009

U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST

WHERE did we go wrong $$$

Sunday, December 28, 2008

MAD COW DISEASE USA DECEMBER 28, 2008 an 8 year review of a failed and flawed policy

Monday, May 11, 2009

Rare BSE mutation raises concerns over risks to public health

SCRAPIE (typical and atypical strains)

Tuesday, November 10, 2009

A retrospective immunohistochemical study reveals atypical scrapie has existed in the United Kingdom since at least 1987

Brief Research Reports

NOR-98 ATYPICAL SCRAPIE 5 cases documented in USA in 5 different states USA 2007


Monday, September 1, 2008


CHRONIC WASTING DISEASE CWD (typical and atypical strains)

DOI: 10.3201/eid1509.090253 Suggested citation for this article: Race B, Meade-White KD, Miller MW, Barbian KD, Rubenstein R, LaFauci G, et al.

Susceptibilities of nonhuman primates to chronic wasting disease.

Emerg Infect Dis. 2009 Sep; [Epub ahead of print] Susceptibilities of Nonhuman Primates to Chronic Wasting Disease Brent Race,1 Kimberly D. Meade-White,1 Michael W. Miller, Kent D. Barbian, Richard Rubenstein, Giuseppe LaFauci, Larisa Cervenakova, Cynthia Favara, Donald Gardner, Dan Long, Michael Parnell, James Striebel, Suzette A. Priola, Anne Ward, Elizabeth S. Williams,2 Richard Race,3 and Bruce Chesebro3 Author affiliations: Rocky Mountain Laboratories, Hamilton, Montana, USA (B. Race, K.D. Meade-White, K.D. Barbian, C. Favara, D. Gardner, D. Long, M. Parnell, J. Striebel, S.A. Priola, A. Ward, R. Race, B. Chesebro); Colorado Division of Wildlife, Fort Collins, Colorado, USA (M.W. Miller); State University of New York Downstate Medical Center, Brooklyn, New York, USA (R. Rubenstein); New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA (G. LaFauci); American Red Cross, Rockville, Maryland, USA (L. Cervenakova); and University of Wyoming, Laramie, Wyoming, USA (E.S. Williams) 1These authors contributed equally to this article. 2Deceased. 3Co-senior authors.

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy, or prion disease, that affects deer, elk, and moose. Human susceptibility to CWD remains unproven despite likely exposure to CWD-infected cervids. We used 2 nonhuman primate species, cynomolgus macaques and squirrel monkeys, as human models for CWD susceptibility. CWD was inoculated into these 2 species by intracerebral and oral routes. After intracerebral inoculation of squirrel monkeys, 7 of 8 CWD isolates induced a clinical wasting syndrome within 33–53 months. The monkeys’ brains showed spongiform encephalopathy and protease-resistant prion protein (PrPres) diagnostic of prion disease. After oral exposure, 2 squirrel monkeys had PrPres in brain, spleen, and lymph nodes at 69 months postinfection. In contrast, cynomolgus macaques have not shown evidence of clinical disease as of 70 months postinfection. Thus, these 2 species differed in susceptibility to CWD. Because humans are evolutionarily closer to macaques than to squirrel monkeys, they may also be resistant to CWD.

Page 1 of 21


Oral Infection of Squirrel Monkeys

To test a more natural route of infection, we exposed squirrel monkeys orally to CWD. Of the 15 exposed squirrel monkeys, 1 (no. 345) was found dead in its cage at 69 mpi; it had shown no neurologic signs or weakness. Western blot results indicated PrPres in brain, spleen, and lymph nodes (Figure 2, panel D). The level of PrPres in the brain of monkey 345 was comparable with that in end-stage intracerebrally inoculated monkeys; body weight at necropsy indicated a 33% decrease over the final 10 months. The high levels of PrPres and the severe wasting indicate that CWD infection could have been the cause of death. A second monkey, 303, was euthanized at 69 mpi because of suspicion of TSE after 2 weeks of progressive weakness, wasting, and eventual anorexia. PrPres analysis confirmed PrPres in brain (Figure 2, panel D), spleen, and lymph nodes. For monkeys 303 and 345, levels of PrPres in the lymph nodes and spleens were 10–100-fold lower than those in brain.

Two other orally infected monkeys were euthanized during the first 69 mpi (Table 2). Monkey 301 was euthanized at 39 mpi, after rapid onset of lethargy and anorexia that led to severe dehydration. Results of Western blot analysis for PrPres were negative in brain (Figure 1, panel B), spleen, lymph nodes, heart, skeletal muscle, duodenum, jejunum, ileum, colon, salivary gland, kidney, lung, and tonsil. However, immunohistochemical analysis detected PrPres in the

Page 7 of 21

spleen and 1 mesenteric lymph node from this monkey, indicating a low level of infection (Figure 3, panels J,K). Monkey 614 was euthanized at 44 mpi because it did not recover from anesthesia related to routine tuberculosis screening. Neither Western blot nor immunohistochemical analysis detected PrPres in brain, spleen, or lymph nodes of this monkey.

Infection of Cynomolgus Macaques

We inoculated cynomolgus macaques both orally and intracerebrally with 3 CWD inocula representing elk, mule deer, and white-tailed deer (Table 3). Of the cynomolgus macaques, 1 (no. 609) was euthanized at 48 mpi after it became aggressive. Brain (Figure 2, panel B), spinal cord, spleen, and lymph nodes were negative for PrPres by Western blot and immunohistochemical analysis. All remaining CWD-inoculated cynomolgus monkeys are currently (at 70 mpi) neurologically asymptomatic and have stable or increased body weights.


Amino acid substitutions in PrP can alter susceptibility to TSE agents, including CWD (18,29,30). To determine whether the lack of susceptibility in several intracerebrally inoculated squirrel monkeys (Table 1) was caused by PrP gene polymorphisms, we sequenced the PrP genes from 23 squirrel monkeys. When compared with published squirrel monkey sequences (28,31), variation was seen at residue 164, in the number of octapeptide repeats, and at residue 19 of the signal peptide (Table 4). However, these genetic differences in PrP did not appear to account for the lack of susceptibility of monkey 310, which was infected with CWD genotype A, because this genotype was also found in 5 of the CWD-positive monkeys. Because we were not able to sequence PrP of monkey 628, we could not assess the role of PrP variation in the lack of disease.

Infectivity of CWD-infected Squirrel Monkey Tissues in PrP Transgenic Mice

To determine whether passage of CWD in squirrel monkeys altered the tropism of the infectious agent, we inoculated tgDeerPrP mice and tg mice expressing human PrP (lines 66 and RM) intracerebrally with tissue homogenates from 3 CWD-positive squirrel monkeys (nos. 322, 308, and 301) with PrPres and from an intracerebrally inoculated cynomolgus macaque (no. 609). Clinical disease did not develop in any tgDeerPrP mice during 600–700 days (Table 5). The lack of transmission to tgDeerPrP mice from the 3 squirrel monkeys with detectable CWD PrPres indicated that either the infectivity levels were low in these squirrel monkeys or that the original cervid species tropism was altered by the passage in squirrel monkeys. Similarly, the

Page 8 of 21

lack of transmission to tg mice expressing human PrP implied that passage through squirrel monkeys did not facilitate adaptation to an agent with increased tropism for humans.


As new CWD foci continue to emerge among cervid populations, the risk for CWD transmission to humans needs to be assessed. We used 2 monkey species and 2 routes of inoculation to test the susceptibility of primates to 8 different pools of CWD. To date, we have verified CWD in 11 of 13 intracerebrally inoculated squirrel monkeys; average incubation period was 41 months (range 33–53 months). Using a single CWD pool, Marsh et al. noted infection in 2 of 2 squirrel monkeys 31–34 months after intracerebral inoculation (13). Intracerebral inoculation of squirrel monkeys with other TSE agents, including kuru, variant CJD, sporadic CJD, and sheep scrapie, had incubation periods of ˜24 months and attack rates of ˜100% (14,15,32). The extended incubation periods and lower attack rates for our squirrel monkeys may result from a partial species barrier to CWD.

The signs of wasting syndrome in CWD-infected monkeys were similar to those of CWD infection in cervids, in which loss of body condition is nearly always a major component of infection and neurologic deficits vary (2). The correlation of clinical signs between CWD in cervids and squirrel monkeys suggests that CWD might affect a common brain region in each species. We observed PrPres deposition in squirrel monkeys primarily in the frontal lobe of the cerebral cortex, claustrum, putamen, and thalamus. Cervids typically have the most abundant and predictable PrPres in the dorsal motor vagus nucleus (obex), olfactory cortex, and diencephalon (including thalamus, hypothalamus, metathalamus, and epithalamus) (2,33). A plausible hypothesis could be that disruption of regions within the hypothalamus and thalamus leads to a metabolic imbalance, resulting in a severe wasting syndrome. We did not observe a strong correlation between infectivity titer inoculated and attack incidence or incubation period (Table 1). One potential explanation is that the variation in speed of disease progression might not be relevant given the low number of animals in each group. A second possibility is that our squirrel monkeys varied at PrP alleles that may affect CWD susceptibility. However, analysis of 23 squirrel monkeys showed no PrP sequence differences

Page 9 of 21

correlating with susceptibility to CWD (Tables 1, 2, 4). A third possibility is that genes other than the gene for PrP might influence CWD susceptibility.

For humans, eating infected or contaminated tissue is a likely route of CWD exposure. In other animal models, oral transmission of TSE is generally 1,000-fold less effective than direct intracerebral challenge and results in longer incubation periods and lower efficiency of disease transmission. In our oral transmission experiments, we found evidence of CWD infection in 3 monkeys at >52 mpi; 2 at 69 mpi had abundant PrPres in brain and lower levels in spleen and lymph nodes, and 1 euthanized at 39 mpi had PrPres in lymphatic tissues only. Thus, transmission seems to be slower by the oral route than by the intracerebral route, and other orally infected monkeys may be affected in the future.

Cynomolgus macaques are evolutionarily closer to humans than are squirrel monkeys (17). At nearly 6 years postinoculation, no macaques have shown clinical signs of CWD. Intracerebral inoculation of cynomolgus macaques with BSE causes disease in 3 years; human variant CJD requires 2–3 years, and human sporadic CJD requires 5 years (16,34). However, oral inoculation of cynomolgus macaques with BSE agent required a minimum of 5 years before clinical disease was observed (35). Therefore, we cannot rule out CWD transmission to cynomolgus macaques.

The PrP gene sequence can influence cross-species transmission of prion disease. Therefore, we compared squirrel monkey and cynomolgus macaque PrP gene sequences to look for differences that might account for different susceptibilities of these monkeys to CWD. In the PrP gene excluding the signal peptide, deer differed from squirrel monkeys at 17 residues and from cynomolgus macaques at 16 residues, but 14 of these differing residues were identical in squirrel monkeys and macaques (Figure 4). Therefore, there are only 2 residues in cynomolgus macaques (100 and 108) and 3 residues in squirrel monkeys (56, 159 and 182) at which these monkeys differ from deer and also from each other. These residues might play a role in susceptibility differences seen in our study. Human exposure to CWD-infected cervids in past decades is likely. The highest levels of prion infectivity are present in the central nervous system and lymphatic tissues of CWD-infected cervids; contamination of knives, saws, and muscles with these tissues can easy occur when processing game. Despite the likelihood of exposures, epidemiologic studies of humans

Page 10 of 21

living in CWD-endemic areas of Colorado and Wyoming during 1979–2001 have not shown any increases in human TSE cases (36,37). Ongoing studies by the Colorado Department of Public Health and Environmental Human Prion Disease Surveillance Program, in conjunction with the University of Colorado School of Medicine, have also concluded that no convincing cases of CWD transmission to humans have been detected in Colorado (38). However, if CWD in humans appears like a wasting syndrome similar to that observed in the squirrel monkeys in our study, affected persons might receive a diagnosis of a metabolic disorder and never be tested for TSE. Fortunately, additional laboratory data are consistent with the epidemiologic data, and these results support the conclusion that a species barrier protects humans from CWD infection (11–13,20,36,37).

Thursday, September 10, 2009

Experimental oral transmission of CWD to red deer (Cervus elaphus elaphus): early detection and late stage distribution of protease-resistant protein

Thursday, September 24, 2009

Validation of Use of Rectoanal Mucosa-Associated Lymphoid Tissue for Immunohistochemical Diagnosis of Chronic Wasting Disease in White-Tailed Deer

Saturday, May 16, 2009

Chronic Wasting Disease Herd Certification Program Document ID APHIS-2006-0118-0096 APHIS-2006-0118-0096

Sunday, April 12, 2009

CWD UPDATE Infection Studies in Two Species of Non-Human Primates and one Environmental reservoir infectivity study and evidence of two strains



TO ASSUME that CWD transmission to humans will only look like nvCJD, and not sporadic CJD or any of it's sub-types, is incorrect, not scientific. ...TSS

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


full text ;

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

From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM

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

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

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

-----Original Message----- From: Sent: Sunday, September 29, 2002 10:15 AM To: [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask]; [log in to unmask]">[log in to unmask] Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

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

snip...see full text ;


Saturday, December 01, 2007

Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model

Volume 13, Number 12–December 2007 Research



(please note, the only reason FSE is not detected in the USA, is the lack of surveillance i.e. don't look, don't find. ...TSS)


(please note again, the only reason a TSE has not been _confirmed_ in a dog, i.e. don't look, don't find)


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.


worse still, there is serious risk the media could get to hear of such a meeting…


Crushed heads (which inevitably involve brain and spinal cord material) are used to a limited extent but will also form one of the constituent raw materials of meat and bone meal, which is used extensively in pet food manufacturer…



Thursday, October 15, 2009

Transmissibility studies of vacuolar changes in the rostral colliculus of pigs


Thursday, November 05, 2009

Incidence and spectrum of sporadic Creutzfeldt-Jakob disease variants with mixed phenotype and co-occurrence of PrPSc types: an updated classification

Friday, October 23, 2009

Creutzfeldt-Jakob Disease Surveillance Texas Data for Reporting Years 2000-2008

BSE (Mad Cow) Update: Do Reports of sCJD Clusters Matter?

snip... see full text ;


MARCH 26, 2003

Send Post-Publication Peer Review to journal:

Re: 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?


Volume 3, Number 8 01 August 2003


Tracking spongiform encephalopathies in North America

Xavier Bosch

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

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

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

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

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

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

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

UK and Europe regarding BSE.

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

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunterstwo of whom were friendswho died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison. CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans & the data seeking evidence of CWD transmission to humans have been very limited.

he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). 

I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.<<< href="">

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.


BY Philip Yam

Yam Philip Yam News Editor Scientific American


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

Sunday, August 10, 2008

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


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.

Friday, November 30, 2007


IT ALL STARTED, LEGALLY, RIGHT HERE, the legal trading of ALL TSE's, globally $$$

Docket APHIS-2006-0026 Docket Title Bovine Spongiform Encephalopathy; Animal Identification and Importation of Commodities Docket Type Rulemaking Document APHIS-2006-0026-0001 Document Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions, Identification of Ruminants and Processing and Importation of Commodities Public Submission APHIS-2006-0026-0012 Public Submission Title Comment from Terry S Singletary

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-2006-0041-0028 Public Submission Title Comment from Terry S Singletary


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 products 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.

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. ...

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-2006-0041-0028.1 Public Submission Title Attachment to Singletary comment

January 28, 2007

Greetings APHIS,

I would kindly like to submit the following to ;


Monday, October 26, 2009



NOW, consider all these animal TSEs, consider all these animals used in food for human and animals, consider all the exposed, then consider the 'pass if forward' modes of transmission, and an incubation period for up to 5 decades.

Thank You,

with kindest regards,

I am sincerely,

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