Monday, August 1, 2016

USDA Announces Reopening of Brazilian Market to U.S. Beef Exports and the Potential for Transmissible Spongiform Encephalopathy TSE prion disease

Release No. 0175.16


Contact: Office of Communications (202) 720-4623


USDA Announces Reopening of Brazilian Market to U.S. Beef Exports


WASHINGTON, Aug. 1, 2016 – The U.S. Department of Agriculture (USDA) has reached agreement with Brazil's Ministry of Agriculture, Livestock and Food Supply to allow access for U.S. beef and beef products to the Brazilian market for the first time since 2003. Brazil's action reflects the United States' negligible risk classification for bovine spongiform encephalopathy (BSE) by the World Organization for Animal Health (OIE) and aligns Brazil's regulations to the OIE's scientific international animal health guidelines.


"After many years of diligently working to regain access to the Brazilian market, the United States welcomes the news that Brazil has removed all barriers to U.S. beef and beef product exports," said Agriculture Secretary Tom Vilsack. "We are pleased that Brazil, a major agricultural producing and trading country, has aligned with science-based international standards, and we encourage other nations to do the same. Since last year alone, USDA has eliminated BSE-related restrictions in 16 countries, regaining market access for U.S. beef and pumping hundreds-of-millions of dollars into the American economy.


"The Brazilian market offers excellent long-term potential for U.S. beef exporters. The United States looks forward to providing Brazil's 200-million-plus consumers, and growing middle class, with high-quality American beef and beef products," Vilsack said.


Both countries will immediately begin updating their administrative procedures in order to allow trade to resume. U.S. companies will need to complete Brazil's regular facilities registration process.


In a separate decision, USDA's Food Safety and Inspection Service (FSIS) also recently determined that Brazil's food safety system governing meat products remains equivalent to that of the United States and that fresh (chilled or frozen) beef can be safely imported from Brazil. Following a multi-year science based review consistent with U.S. food safety regulations for countries that export meat, poultry and egg products to the U.S., FSIS is amending the list of eligible countries and products authorized for export to the United States to allow fresh (chilled or frozen) beef from Brazil.


The Brazilian agreement is just the latest example of USDA's ongoing efforts to knock down barriers to U.S. exports. In 2016 alone, these efforts have led to the reopening of the Saudi Arabian and Peruvian markets for U.S. beef, the South Korean market for U.S. poultry, and the South African market for U.S. poultry, pork and beef. In 2015, U.S. beef exports reached $6.3 billion thanks to aggressive efforts by USDA to eliminate BSE-related restrictions in 16 countries since January 2015, gaining additional market access for U.S. beef in Colombia, Costa Rica, Egypt, Guatemala, Iraq, Lebanon, Macau, New Zealand, Peru, Philippines, Saint Lucia, Singapore, South Africa, Ukraine, Vietnam and, now, Brazil.


The past seven years have represented the strongest period in history for American agricultural exports, with international sales of U.S. farm and food products totaling $911.4 billion between fiscal years 2009 and 2015.


Since 2009, USDA has worked to strengthen and support American agriculture, an industry that supports one in 11 American jobs, provides American consumers with more than 80 percent of the food we consume, ensures that Americans spend less of their paychecks at the grocery store than most people in other countries, and supports markets for homegrown renewable energy and materials. USDA has also provided $5.6 billion in disaster relief to farmers and ranchers; expanded risk management tools with products like Whole Farm Revenue Protection; and helped farm businesses grow with $36 billion in farm credit. The Department has engaged its resources to support a strong next generation of farmers and ranchers by improving access to land and capital; building new markets and market opportunities; and extending new conservation opportunities. USDA has developed new markets for rural-made products, including more than 2,500 biobased products through USDA's BioPreferred program; and invested $64 billion in infrastructure and community facilities to help improve the quality of life in rural America. For more information, visit





 “This is absurd,” said Bullard adding, “Brazil produces far more beef than it can consume. This is why, with the world’s second largest cattle herd, which far and away dwarfs the size of the U.S. herd, Brazil is the world’s third largest beef exporter, behind only India and Australia. And like India and Australia, Brazil’s imports of U.S. beef for longer than a decade before it closed its borders to U.S. beef in 2003 were miniscule.


“To say that the Brazilian market affords U.S. cattle producers with economic opportunities would be laughable if not for the significant risk associated with Vilsack’s weakening of our longstanding import restrictions for countries like Brazil that continue to battle foot-and-mouth disease (FMD) and other dangerous livestock diseases.”


Bullard claims that one of the reasons it has taken so long for the USDA to approve raw beef imports from Brazil was because Brazilian cattle and their resulting beef continued to exceed tolerance levels for pesticides such as Ivermectin.


“Brazil lacks the resources and infrastructure to maintain health and safety standards that are at least equal to that of the United States,” said Bullard adding, “That is why the USDA lowered the U.S. standard to that of mere equivalency – which essentially means “close enough.”


“This reckless action by the Secretary, which helps multinational meatpackers leverage down U.S. cattle prices with increased imports that do not meet identical U.S. safety standards is yet another in a long line of failures by the USDA to do anything to strengthen the economic condition of the U.S. cattle industry.


“The Secretary capitulated on country-of-origin labeling (COOL) and continues to weaken U.S. import standards that protect our cattle herd and our customers from foreign diseases, including his most recent proposal to relax our import standards for raw beef from Namibia, Africa. He has refused to protect the competitiveness of the U.S. cattle market from antitrust and anticompetitive practices of the monopolistic meatpackers. He has refused to reform the beef checkoff program that funds a lobbying group that represents the economic interests of multinational meatpackers. And, under the Secretary’s watch, our industry continues to experience an alarming exodus of cattle farmers and ranchers, feedlot numbers have declined by the tens of thousands, domestic beef production has fallen to the lowest level since before NAFTA, and the U.S. cattle herd shrank to the lowest level in over 70 years.


“Even the Secretary’s depiction of exports over the past seven years as they relate to this particular announcement is deceitful at best. While the Secretary boasts that ‘the past seven years have represented the strongest period in history for American agricultural exports,’ this irresponsible statement purposely omits the fact that while the dollar value of beef and cattle exports did increase over the past seven years, they were decisively overwhelmed by record imports, which caused the trade deficit for our industry to grow from less than $1 billion in 2009 to more than $2.5 billion in 2015.


“We couldn’t be more disappointed in the Secretary’s actions, which clearly demonstrate that he is advocating the interests of multinational meatpackers at the expense of independent U.S. farmers and ranchers and consumers,” concluded Bullard.


# # #


R-CALF USA (Ranchers-Cattlemen Action Legal Fund, United Stockgrowers of America) is the largest producer-only cattle trade association in the United States. It is a national, nonprofit organization dedicated to ensuring the continued profitability and viability of the U.S. cattle industry. For more information, visit or, call 406-252-2516.


Posted by R-Calf USA on Monday, August 1st, 2016 @ 1:03PM Categories: Latest News, News Releases, Trade



r-calf deleted my posts, I had three. then r-calf put one of my post back up, the one that suited them the most. all r-calf wanted to hear about was Brazil, nothing about the USA. that’s too bad...tss


Terry Singeltary first up, see past history of mad cow political wrangling here;



Brazil: mad cow threat or trade war trashing? 05 Feb 01 By Phil Stewart Reuters


The timing alone is suspicious. Just one day after Canada failed to win a fresh World Trade Organization review of Brazil's aircraft subsidy program, it announced Friday that mad cow fears justify a temporary ban on Brazilian beef imports. The move was unprecedented. Brazil, home to the world's biggest cattle herd, has never had a case of mad cow disease. Yet it not only lost the Canadian market, but also the U.S. and Mexican markets since Canada's decision applied to the entire NAFTA trade bloc.


Now the big question on everybody's mind is whether Brazil is truly a threat to food safety -- as Canada contends -- or if this is merely the first shot in a trade war between the two countries.


"Canada is highly suspect. Had trade relations with Brazil been better, Canada would never have taken this line of action," said political analyst Andre Pereira Cesar.


Canada's official line is that Brazil was too slow in passing on information on the country's 160 million head of cattle. Canada, on behalf of NAFTA, asked for the documents in May 1998 -- and only received them after it informed Brazil of the ban last week. The lack of information, Canada argued, was enough of a health risk to merit a temporary ban.


But in the background is a seething feud between Brazil and Canada over aircraft subsidies. Canada has already won the right from the WTO to impose sanctions of $233.5 million a year on Brazil over its ProEx aircraft export subsidy program.


Canada alleges ProEx has unfairly helped Brazil's top civilian aircraft manufacturer, Embraer , and robbed sales from Canada's Bombardier Inc. Canada has repeatedly stressed that the ban on Brazilian beef has nothing to do with the subsidy dispute. But Brazilian officials see things very differently.


On Monday, Brazilian Foreign Minister Celso Lafer issued a statement threatening it would respond if Canada did not not reverse its decision. Brazil exports $5.5 million in processed beef to Canada annually, and some $82.5 million to the U.S.


"If Canada persists in acts that effectively damage Brazil's foreign trade, the Brazilian government reserves the right to take measures it judges convenient," Lafer said, without elaborating. Meanwhile, Agriculture Minister Marcus Vinicius Pratini de Moraes extended his stay in the United States to appeal to officials in Washington on Monday -- bypassing Canada entirely.


According to U.S. Department of Agriculture's representatives in Brazil, the South American country's cattle seem just fine. "We've done a preliminary review of the information and there doesn't appear to be any problem," said William Westman, chief Brazil counselor for the USDA's Foreign Agricultural Service (FAS) at the U.S. Embassy in Brasilia. "From what we've seen from the preliminary results, there's not an issue here."


Mad cow disease, or bovine spongiform encephalopathy (BSE), has led to more than 80 deaths in humans and many scientists believe that people who catch the illness do so because they ate BSE-infected beef. Mad cow has never been reported in the U.S. or in Brazil.


Diplomatic sources in Brasilia said they expect NAFTA nations to scrap the ban on Brazil within six to eight weeks -- the standard review period for phytosanitary reports. But no doubt, damage has already been done. Trade relations between the two countries have clearly worsened -- making a trade war that much more likely. In this environment, the chances of the Bush Administration laying the groundwork for a Free Trade Area of the Americas stretching from Alaska to Argentina are that much more bleak.


Brazil decries beef ban February 5, 2001 By ADALID CABRERA LEMUZ, Associated Press Brazil on Monday invited foreign experts to inspect its cattle herds for signs of mad cow disease and insisted there's no reason for a ban on Brazilian beef imports imposed by the United States and other countries. Brazilian cattle feed in pastures and not on ground cattle parts that have been blamed for spreading the disease in European countries, said Farm Defense Secretary Luiz Carlos de Oliveira. Brazil "is willing to open its borders to allow sanitary specialists to verify that there is not the slightest risk of contamination," he said.


Meanwhile, Agriculture Minister Marcus Vinicius Pratini de Moraes was in Washington to push for a suspension of the ban on imports of Brazilian beef products. He was to meet with U.S. Secretary of Agriculture Ann Veneman and offer data showing that Brazil is free of bovine spongiform encephalopathy, or mad cow disease...


"We're concerned about the domino effect that the U.S. ban could have on Brazilian beef imports in other markets," local news agency Agencia Estado quoted Pratini as saying.


On Friday, Canada suspended Brazilian beef imports until the risk of mad cow was fully assessed. The United States and Mexico quickly followed suit. The Canadian Food Inspection Agency said the ban was a precautionary step and there is no evidence mad cow disease has infected Brazilian cattle.


Still, the ban could hurt Brazil's exports just as the country is striving to improve its trade balance. The United States imported some $82 million in processed meat from Brazil last year and Canada purchased $5.5 million, the Agriculture Ministry said. Together, the two countries account for about 10 percent of Brazil's beef exports.


Opinion (webmaster): Canada's action, quickly followed by the US and Mexico, may have opened up a whole new era in BSE, whereby countries deliberately trash each other's cattle industry for unrelated tariff retaliation purposes.


TSEs are diseases believed by many scientists to occur roughly at a one in a million rate per year in all species of mammals due to de novo mutation. Short of knocking out the prion gene with genetic engineering, a background rate of one per million cows of BSE is unavoidable, just like background radioactivity from potassium-40 in rocks. This would be true even of a strictly grass and soy fed animal -- cow cannabalism is strictly an amplification mechansim, not an origination. The strains of BSE arising in this manner would not necessarily resemble British BSE in their properties. The risks to humans from these strains, if any, are unknown. However, health risks cannot be catastrophic because CJD remains a fairly rare disease, even allowing for under-reporting, and the fact that cattle were domesticated millenia ago.


Putting the shoe on the other foot, what if -- in a flurry of worldwide press releases -- Pitcairn Island, with Namibia and Tajikistan joining in, abruptly outlawed Canadian beef products because of alleged BSE risks. After all, unlike Brazil, Canada has reported a confirmed case of BSE (December 1993 cow in Alberta imported from UK in 1987), fails to use the Prionics gold standard surveillance test, and was a member of the Group of 70 countries on the receiving end of British meat and bone meal exports. (Canada imported 125 tons, the US 20 tons, Brazil zero, according to Her Majesty's Excise and Custom table published by the Sunday London Times on 5 Feb 01 -- see below.)


Canada would no doubt be mighty annoyed at Pitcairn Island.


Food fights are different than tariffs on airline parts: the aspersions cast linger on long after the event. Many people hear the initial story but not the followup clarification. Garbage can circulate for years on chat rooms. Canada could have substantive reasons for banning Brazilian beef that they have not yet disclosed: these need to be disclosed. Yes, Canada is following the precautionary form (extreme version): Brazil may indeed have non-zero risk -- but what country has been totally spared?


Now while most of the world frets over containment of the globalization of both BSE and its accompaning nvCJD, other elements have long seen a profiteering opportunity. For every country where domestic producers are hurt, there is another country that benefits. For example, USDA's Glickman was quick to publicly assure the British at the height of their troubles of the continuing availability of US beef.


However, innuendo, if that is all it is, of a developing country that just happens to have the world's largest beef herd that Mexico and the US endorsed this week is an unwelcome escalation that serves no one. Where is this going to end -- with the global consumer not trusting anyone's beef?



Brazil and the USA will be swapping BSE TSE Prions like two lovers swapping spit now...


Friday, October 30, 2015


Brazil Agriculture minister to visit Saudi Arabia over BSE mad cow trade



Life | Sat May 10, 2014 2:58pm EDT Related: Health, Brazil


Brazil confirms second case of atypical mad cow disease


 Brazil has confirmed a second case of atypical mad cow disease, a year after several countries banned Brazilian beef imports when a similar case of the disease was confirmed.


The agriculture ministry said late Friday that a lab in Weybridge, England approved by the World Animal Health Organization confirmed it was a spontaneous case of atypical bovine spongiform encephalopathy (BSE), or mad cow disease, with no link to contaminated feed.



LAUGH OUT LOUD LOL OR LAUGH MY ASS OFF LMAO !!! that last part is a total pipe dream, a myth...tss


now some facts about atypical BSE mad cow disease and feed. that spontaneous myth is just that, a myth, one that keeps faltering, see why ;



Monday, May 5, 2014


Brazil BSE Mad Cow disease confirmed OIE 02/05/2014



Thursday, September 26, 2013


Brazil evaluate the implementation of health rules on animal by-products and derived products SRM BST TSE PRION aka MAD COW DISEASE



Friday, December 07, 2012





Wednesday, December 19, 2012


Scientific Report of the European Food Safety Authority on the Assessment of the Geographical BSE Risk (GBR) of Brazil



Wednesday, January 29, 2014


Another Suspect case of Creutzfeldt-Jakob disease investigated in Brazil





 (Adopted by the International Committee of the OIE on 23 May 2006)


 11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,



 Wednesday, March 11, 2015


 OIE and Centers for Disease Control and Prevention Reinforce Collaboration



 Friday, April 4, 2014


 China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa and Saudi Arabia still retain BSE-related closures



 Thursday, May 30, 2013


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


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




 The OIE is nothing more than a trading brokerage for the Transmissible Spongiform Encephalopathy TSE prion disease aka mad cow type disease. Frances is still in the midst of a mad cow disease outbreak with atypical BSE cases still growing. mad cow disease is so bad in France, as with the USA, they stopped testing for mad cow disease (France altogether and the USA to figures so low, you would only detect a case of mad cow disease, only by chance).


 from the inside looking out ;


 Quote: Maybe familirise yourself with the OIE. The primary concern is animal health of the world they are the animal version of the WHO. It is a long way down from that ivory tower but here we go, until pressured by the USA representatives a country could not export animals for 6 years after finding a BSE/BASE positive animal so under the old rules the US would not be able to export anywhere in the world for another 4 1/2 years. Who got the risk levels system put in to allow some trade - your US representatives. You guys want to change rules - OK , but you do not get special rules that only apply to the US. As i have told you before Sand h I market all my own slaughter animals and you know that, so don't do the whole holier than thow act.


 With all due respect, it is obvious that you know little about the OIE and how it actually works. Having been to their offices in Paris and talked personally with the Head of the Animal Test Section, you would choke if you knew how many lobby groups attend that office daily. There is a steady stream of paid lobby groups that have one goal in life and that is to sway the Section Heads of each department within the OIE to suit the needs of different jurisdictions around the world, which curiously enough, also includes the USA and Canada. Anyone can go there and chat with them - providing they can provide valid cause to be let in. To say that the only goal of the OIE is animal health is actually only part of their function. They are more than that and my discussions with Dr. Diaz there has showed me that. But to blindly make a statement regarding what they do when you have no idea what they actually do is like eating the skin of the orange and not knowing what is actually under.


 Interestingly you state that the US Government applied pressure (to the OIE) I assume and that is a great example of the lobby groups doing their job. So, at the end of the day, one can safely assume that it is the pressure applied by certain influential lobby groups that will determine a likely outcome to an apparent OIE directive. Man alive, isn't it great to live in a democracy wherein the people get to make the choices and not just some "other" interested party or group - say like........Cargill or Tyson for example?


 So, one last question, question?


 Who wags the tail of that dog?? And for what reason other than one that is purely associated with trade and international agreements and greed?


 And you think it is so simply explainable.




 Subject: UPDATED WHO Guidelines include tissues from Cervidae affected with Chronic Wasting Disease (CWD)


 snip...see full text ;


Sunday, October 18, 2015


*** World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research




Thursday, December 17, 2015


Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738 10 December 2015



Saturday, December 12, 2015





*** Transmissible Spongiform Encephalopathy TSE PRION UPDATE USA update 2016 ***


Saturday, July 23, 2016





Tuesday, July 26, 2016


*** Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016



Monday, June 20, 2016


*** Specified Risk Materials SRMs BSE TSE Prion Program



Saturday, July 16, 2016


*** Importation of Sheep, Goats, and Certain Other Ruminants [Docket No. APHIS-2009-0095]RIN 0579-AD10


*** WITH great disgust and concern, I report to you that the OIE, USDA, APHIS, are working to further legalize the trading of Transmissible Spongiform Encephalopathy TSE Pion disease around the globe.


THIS is absolutely insane. it’s USDA INC.



Wednesday, May 25, 2016


USDA APHIS National Scrapie TSE Prion Eradication Program April 2016 Monthly Report Prion 2016 Tokyo Update



*** Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.



Saturday, April 23, 2016


SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 TOKYO


Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X



Monday, May 02, 2016


*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***



Sunday, July 17, 2016





Saturday, May 28, 2016


*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***



*** NIH awards $11 million to UTHealth researchers to study deadly CWD prion diseases Claudio Soto, Ph.D. ***


Public Release: 29-Jun-2016



Tuesday, July 12, 2016


Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE, TSE, Prion Zoonosis Science History


see history of NIH may destroy human brain collection



Terry S. Singeltary Sr.

Wednesday, March 2, 2016

RANCHO He did not know that they were placing healthy cow heads next to suspect carcasses BSE TSE Prion

Subject: RANCHO “He did not know that they were placing healthy cow heads next to suspect carcasses,” Singleton’s defense team wrote.




Yardman only one not paid in Rancho diseased cow scheme


By Dan Flynn | March 1, 2016


Sentencing continues tomorrow in the criminal prosecution of the four men whose scheme to circumvent USDA inspection in 2013 caused diseased cattle to end up as human food.


The owner of Rancho Veal, Robert “Bob” Singleton, and Rancho Feeding Corp. yardman Eugene Corda will appear for sentencing on Wednesday in U.S. District Court for Northern California in San Francisco. Felix Sandoval Cabrera, foreman at the Petaluma, CA, slaughterhouse, will be the last to be sentenced on March 9.


Rancho owner Jesse “Babe” Amaral was the first to be sentenced. On Feb. 10 Amaral was sentenced to a year and day in federal prison to be followed by two years of supervised released including one year at a half-way house.


four men agreed to plead guilty to a single count of conspiracy to distribute adulterated, misbranded, and un-inspected meat. In exchange, the government agreed to drop multiple charges brought in an August 2014 indictment, including fraud and conspiracy.


Their scheme to process diseased cattle, mostly with eye cancers, caused a massive 8.7-million-pound meat recall in February 2014. The slaughterhouse was closed and eventually sold. Recall expenses and other damages cost Rancho’s business associates millions.


The need for a trial went away when the defendants all pleaded guilty. Sentencing documents, however, are beginning to fill in some of the details that would have come out at trial.


Singleton and Amaral met at cattle auctions in the early 1970s and decided to become business partners.


The real property of the Petaluma slaughterhouse was owned by Singleton Investments Inc., and was managed by both the Rancho Veal Corp., also owned by Singleton, and the Rancho Feeding Corp,, owned by Amaral.


Singleton was the cattle buyer at auctions, and also sold processed meat to vendors though his Rancho Veal Corp. Amara’s Rancho Feeding Corp. was the “USDA establishment,” permitted to slaughter and process cattle for human consumption.


Rancho Feeding had “custom slaughter agreements” with Rancho Veal, contracts where it agreed to manage the slaughterhouse and comply with all USDA regulations.


Cabrera, Rancho’s foreman who’d studied to be a USDA inspector, worked for Amaral for more than 30 years.


The 79-year old Singleton claims to have heard about the scheme from the 78-year old Amaral sometime in early 2013. Shortly thereafter, Singleton learned from Amaral that he’d directed Cabrera to bypass ante mortem (before death) inspection procedures if the foreman believed a cow was likely to be marked by an inspector as a “suspect” for condemnation.


Singleton claims not to have known that Amaral and Cabrera had employees carving the “USDA Condemned” stamps out of cattle that had been condemned. Nor did he know that, at Amaral’s direction, Corda was swapping un-inspected cattle showing symptoms of eye cancer for cattle that had already passed ante mortem inspection.


“He did not know that they were placing healthy cow heads next to suspect carcasses,” Singleton’s defense team wrote.


However, there was much Singleton did know.


He “knew Amaral, Cabrera, and Corda were somehow effectively circumventing inspection, and (Singleton) failed to ask questions or take responsibility for putting a stop to the unlawful scheme,” according to court documents. Amaral instructed Singleton to pay Cabrera $50 for every cow he “slipped” past USDA inspection.


“The evidence shows that Corda did not know his codefendants were also processing condemned cattle, or that Ranch’s owners were defrauding farmers in a separate scheme, and he was not charged with those counts in the indictment,” according to the sentencing memorandum filed by Assistant U.S. Attorney Hartley M.K. West.


“Corda also did not profit from his role beyond his regular paycheck, whereas Rancho’s owners and the kill floor foreman, Cabrera, did.”


West says Amaral and Singleton profited from the sale of the “eye cows” and condemned cattle and Amaral from a separate false invoicing scheme.


“Corda was not paid and did not seek compensation.” West wrote. “He was simply trying to keep his job by doing what Amaral told him.”


The government is recommending that the 65-year old Corda be sentenced to three years probation including six months of home confinement, which will apparently allow him to work and take his wife to chemotherapy for treatment of a re-occurrent breast cancer.


Corda worked for Amaral for 30 years, a man he described as “strong-minded” and “dominant and forceful.” Singleton became another of his boss’s in 1997, and like Amaral was known for his lifetime in the cattle business.


“At no time did I ever believe the two men would involve me in a scheme that would threaten the food supply,” Corda said in his pre-sentencing letter to the judge. He eventually realized Amaral and Cabrera had come up with a way to get cattle through without inspection.


Singleton admits he trusted Amaral and Cabrera. Amaral had run the kill floor of the small slaughterhouse for 45 years and Singleton believed his business partner could “distinguish between safe and unsafe conduct,”according to Singleton’s lawyers. They said Singleton especially trusted Cabrera’s expertise in meat inspection.


“Quite frankly, Bob did not trust the federal inspectors working at Rancho at the time, and believed that Cabrera had a better idea of what was a passable cow than those inspectors.” His attorneys said they offered that perspective “to illustrate the Bob at the time never believed that dangerous meat would ever be passed through to consumers.”


“Today Bob deeply regrets his conduct and the significant harm it caused,” wrote the attorneys from Orrick, Herrington & Sutcliffe LLP in San Francisco.


Due largely due to his being the first to fully cooperate in the investigation, the government is recommending Singleton be sentenced to three months in prison and three months of home detention followed by two years of supervised release with 50 hours of community service.


Singleton wants a “non-custodial sentence of probation.”


Whether he stays out of jail may depend upon whether the judge accepts Singleton’s view of the “loss calculation.” The recall of 8.7 million pounds of meat included the production of an estimated 15,600 head of cattle processed by Rancho over the course of a year.


That resulted in a loss of more than $2.5 million.


However, Singleton’s defense argues that the government’s investigation found 180 cows were affected by the criminal conduct and from that number, they could have “profited no more than $90,000.” There is a ten-fold increase in the impact on the sentencing calculation between the two numbers ($90,000 versus $2.5 million)


Singleton has also reached settlement agreements with all but one of companies that were financial harmed by Rancho’s scheme and resulting recall. The payments he has agreed to include: •RBR Meats/Riteway, $1.5 million; •BN Ranch, $450,000; •Tillamook Country Smoker, $7,720; and •Argus, $3,000.


Singleton’s attorneys have been unable to get a response from Advance Pierre Foods, the only remaining “victim entity.”


“Quite simply, Bob has no more money left, and no ability to pay a fine or further restitution,” his attorneys wrote. “After he pays agreed-to restitution and legal fees, Bob will be in debt.”


The government wants a separate restitution hearing scheduled after tomorrow if any unresolved issues remain after sentencing.


© Food Safety News



Three month sentence imposed on Rancho’s other owner


By Dan Flynn | March 3, 2016


Ranchocow_406x250U.S. District Court Judge Charles R. Breyer has sentenced 79-year old Robert W. Singleton to a “custodial term” of three months to be followed by one year of supervised probation for his role in a scheme to process cattle condemned by USDA, usually for cancerous eyes.


In a 15-minute sentencing hearing, Singleton was also ordered to pay a $100 court assessment. The judge did not impose any fine, and put restitution off to May 31.


Breyer ordered Singleton to self-surrender to the U.S. Marshals on or before May 31, but granted him permission to attend a family reunion in Reno, NV, before reporting. Singleton has been under instructions not to leave the jurisdiction of the U.S. District Court for Northern California.


Singleton was the first to cooperate with the government investigation of infractions at the Petaluma slaughterhouse. His business partner of more than 30 years, Jesse “Babe” Amaral operated the slaughterhouse as the Rancho Feeding Corp., while Singleton’s Rancho Veal Corp. purchased cattle at auctions and sale barns. Amaral came up with the idea of moving condemned animals past USDA inspectors and pocketing the money.


Breyer also sentenced a Rancho yardman, 65-year old Eugene D. Corda, to three months probation with a $100 assessment. Corda moved cattle into place as directed by a foreman, but eventually figured out what was going on. The judge granted Corda permission to continue feeding cattle for Amaral.


Amaral was sentenced last month to a year and day in federal prison. After that he will be on supervised probation for two years with the first year spent in a re-entry or half way house.


Only Rancho foreman Felix Cabrera remains to be sentenced. He will appear before Judge Breyer next week.


In lieu of a trial, all four defendants negotiated agreements with the government to plead guilty to distributing adulterated, misbranded, and un-inspected meat. All were also required to cooperate with investigators.


Rancho recalled 8.7 million pounds of meat in early February 2014, covering more than 13 months production back to Jan. 1, 2013.



>>> *** “He did not know that they were placing healthy cow heads next to suspect carcasses,” Singleton’s defense team wrote. ***<<<


where have I heard this before ???




Thursday, November 18, 2010




Galen Niehues, an inspector for the Nebraska Department of Agriculture, (NDA), was convicted of mail fraud for submitting falsified reports to his employer concerning inspections he was supposed to perform at Nebraska cattle operations. Niehues was tasked with performing inspections of Nebraska ranches, cattle and feed for the presence of neurological diseases in cattle including Bovine Spongiform Encephalopathy (BSE), also known as “Mad Cow Disease”. Niehues was to identify cattle producers, perform on-site inspections of the farm sites and cattle operations, ask producers specific questions about feed, and take samples of the feed. Niehues was to then submit feed samples for laboratory analysis, and complete reports of his inspections and submit them to the NDA and to the Federal Food and Drug Administration (FDA). An investigation by the FDA and NDA revealed Niehues had fabricated approximately 100 BSE inspections and inspection reports. When confronted, Niehues admitted his reports were fraudulent, and that had fabricated the reports and feed samples he submitted to the NDA. Niehues received a sentence of 5 years probation, a 3-year term of supervised release, and was required to pay $42,812.10 in restitution.








A 6 year old, home bred (HB), Friesian x Holstein cow in a dairy herd in Aberdeenshirer submitted as a suspect BSE case in the negative study (SE0203), has been diagnosed as BSE negative on standard, statutory (obex only), diagnostic criteria at CVL.


Further examination by Dr Jeffrey at Lasswade, as required by the project design, has revealed vacuolar change in the septal nucleus and putamen which co-localised with PrP immunoreactivity. No significant lesions were found in any other part of the brain, neither was PrP found in the medulla.


It is important to note that examination of four brain blocks used earlier in the epidemic would not have detected the lesion but a 16 block study (as used in the very days of BSE) would.




The herd of origin has had 15, HB, suspect cases of BSE since July 1989 and a further case is still alive.


2. Of the 15, eight have been confirmed by standard histopathology and seven diagnosed negative (including the above case).


3. Fixed brain tissue from the negative cases exists at Lasswade (because they always collect whole brain in Scotland) but has not so far been examined further. No frozen tissue was collected so neither SAF nor PrP detection (by immunoblotting) has been attempted.


4. Mr Wells agrees with Dr Jeffrey's and Dr Simmons' findings.




1. The brain tissue from the negative cases will be examined in detail by conventional histopathology and ICC.


2. Kevin Taylor and his veterinary colleagues have been alerted to the situation.




1. TRANSMISSION Attempt transmission from the 'case' to standard mice strains. (Note: In regard to strain typing, formalin may have modified strain phenotype - we need to discuss with NPU). Further transmission studies (eg in cattle) might be suggested if primary transmission in mice fails. These proposals have funding implications.


CODE 18-77




2. PrP GENOTYPING - Although only fixed brain tissue is available we are considering genotyping from parents/offspring/fixed brain. As a first step we are attempting to extract DNA from the fixed brain and to amplify the PrP gene by PCR.


3. John Wilesmith has interrogated the data base for the herd history. Other than the high proportion of negative cases nothing significant is apparent.


4. Familial relationships between suspect (including positive and negative) cases in this herd could be examined and tracings of breeding animals initiated.


5. Consideration might be given to collecting frozen spinal cord from new cases in this herd or in dispersals from it for (SAF/PrP examination).




1. At present it is unclear whether or not this is a singleton incident or whether the other negative cases in this herd show a similar lesion.


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


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


4. If this is a new strain all the implications need to be considered including whether or not to proceed with the further investigation of future cases negative for BSE on obex examination alone and from which whole brains are available (as in Scotland) or collected in the future. Also perhaps investigation of the tissue distribution of infectivity in these animals might be considered.


5. Animal and public health controls in place should be sufficient since all tissues (other than brain for diagnosis) are incinerated.


We observe that Dr Tyrrell would wish to be informed of this at an early opportunity and that the SEAC would wish to discuss it at their meeting in April.






17 February 1993


CVO - for information and comment on further action please


cc Mr K C Taylor


Dr B J Shreeve




This minute is re-issued with a wider distribution.


The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".


Mr Scudamore


Mr R C Lowson


Dr D Matthews


Mr I Robertson


Dr K MacOwan


Mr C Randall


Mr J W Wilesmith


Mr G A H Wells


Dr M Jeffrey


Dr M Simmons

























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




The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...





"These 9,200 cases were different because brain tissue samples were preserved with formalin, which makes them suitable for only one type of test--immunohistochemistry, or IHC."




THE IHC test has been proven to be the LEAST LIKELY to detect BSE/TSE in the bovine, and these were probably from the most high risk cattle pool, the ones the USDA et al, SHOULD have been testing. ...TSS


USDA 2003


We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back. Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS.


Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.




Dr. Detwiler: It seems a good idea, but I'm not aware of it. Another important thing to get across to the public is that the negatives do not guarantee absence of infectivity. The animal could be early in the disease and the incubation period. Even sample collection is so important. If you're not collecting the right area of the brain in sheep, or if collecting lymphoreticular tissue, and you don't get a good biopsy, you could miss the area with the PRP in it and come up with a negative test. There's a new, unusual form of Scrapie that's been detected in Norway. We have to be careful that we don't get so set in the way we do things that we forget to look for different emerging variations of disease. We've gotten away from collecting the whole brain in our systems. We're using the brain stem and we're looking in only one area. In Norway, they were doing a project and looking at cases of Scrapie, and they found this where they did not find lesions or PRP in the area of the obex. They found it in the cerebellum and the cerebrum. It's a good lesson for us. Ames had to go back and change the procedure for looking at Scrapie samples. In the USDA, we had routinely looked at all the sections of the brain, and then we got away from it. They've recently gone back.


Dr. Keller: Tissues are routinely tested, based on which tissue provides an 'official' test result as recognized by APHIS .


Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't they still asking for the brain? But even on the slaughter, they're looking only at the brainstem. We may be missing certain things if we confine ourselves to one area.






Completely Edited Version PRION ROUNDTABLE


Accomplished this day, Wednesday, December 11, 2003, Denver, Colorado








Date: June 21, 2007 at 2:49 pm PST


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


An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services.


In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE),


*** the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle.


As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.




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


soundness of BSE maintenance sampling (APHIS),


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




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





Wednesday, July 15, 2015


Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?



***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.


***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.


IBNC Tauopathy or TSE Prion disease, it appears, no one is sure


Posted by flounder on 03 Jul 2015 at 16:53 GMT



*** Needless conflict ***


Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b


Published online 16 May 2012


Terry S. Singeltary Sr. said:


I kindly wish to submit the following please ;






see more on Rancho history here;


Friday, March 21, 2014


Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014 ?


“As of March 20, 2014, FSIS has completed all checks (effectiveness checks and disposition verification checks) for recalls 002-2014 and 013-2014 regarding Rancho Feeding Corporation. FSIS has determined that based on the number of successful checks (see Directive 8080.1, Attachment 1, Table 3) where businesses were notified of the recall and removed affected products from commerce that the recall activities were effective.”



Thursday, March 20, 2014





Thursday, March 6, 2014


TEXAS RECALL LIST MASSIVE FROM DEAD STOCK DOWNER CANCER COWS OFFAL from Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8, 2014 shipped to Texas, Florida, and Illinois UPDATE FEBRUARY 14, 2014



Thursday, February 27, 2014





Tuesday, February 11, 2014


California Firm Recalls Various Meat Products Produced Without the Benefit of Full Inspection Class I Recall 002-2014 and 013-2014 Health Risk: High Jan 13, 2014 and Feb 8, 2014



Saturday, September 21, 2013


Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT



>>>“Cabrera knocked the cancer eye cows, and he or another kill floor employee at his instruction slaughtered them and deposited their heads in the gut bin,” the indictment states. “Cabrera, or another kill floor employee at his instruction, placed heads from apparently healthy cows, which had been previously reserved, next to the cancer eye cow carcasses. <<<


where have I heard something similar before ?


Date: June 21, 2007 at 2:49 pm PST


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


An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE),


***the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle.


As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.




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


soundness of BSE maintenance sampling (APHIS),


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




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





-MORE Office of the United States Attorney District of Arizona


FOR IMMEDIATE RELEASE For Information Contact Public Affairs


February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625 Cell: (602) 525-2681




PHOENIX -- Farm Fresh Meats, Inc. and Roland Emerson Farabee, 55, of Maricopa, Arizona, pleaded guilty to stealing $390,000 in government funds, mail fraud and wire fraud, in federal district court in Phoenix. U.S. Attorney Daniel Knauss stated, “The integrity of the system that tests for mad cow disease relies upon the honest cooperation of enterprises like Farm Fresh Meats. Without that honest cooperation, consumers both in the U.S. and internationally are at risk. We want to thank the USDA’s Office of Inspector General for their continuing efforts to safeguard the public health and enforce the law.” Farm Fresh Meats and Farabee were charged by Information with theft of government funds, mail fraud and wire fraud. According to the Information, on June 7, 2004, Farabee, on behalf of Farm Fresh Meats, signed a contract with the U.S. Department of Agriculture (the “USDA Agreement”) to collect obex samples from cattle at high risk of mad cow disease (the “Targeted Cattle Population”). The Targeted Cattle Population consisted of the following cattle: cattle over thirty months of age; nonambulatory cattle; cattle exhibiting signs of central nervous system disorders; cattle exhibiting signs of mad cow disease; and dead cattle. Pursuant to the USDA Agreement, the USDA agreed to pay Farm Fresh Meats $150 per obex sample for collecting obex samples from cattle within the Targeted Cattle Population, and submitting the obex samples to a USDA laboratory for mad cow disease testing. Farm Fresh Meats further agreed to maintain in cold storage the sampled cattle carcasses and heads until the test results were received by Farm Fresh Meats.


Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, Farm Fresh Meats and Farabee submitted, or caused to be submitted, obex samples from healthy, USDA inspected cattle, in order to steal government moneys.


Evidence collected also demonstrated that Farm Fresh Meats and Farabee failed to maintain cattle carcasses and heads pending test results and falsified corporate books and records to conceal their malfeasance. Such actions, to the extent an obex sample tested positive (fortunately, none did), could have jeopardized the USDA’s ability to identify the diseased animal and pinpoint its place of origin. On Wednesday, February 14, 2007, Farm Fresh Meats and Farabee pleaded guilty to stealing government funds and using the mails and wires to effect the scheme. According to their guilty pleas:


(a) Farm Fresh Meats collected, and Farabee directed others to collect, obex samples from cattle outside the Targeted Cattle Population, which were not subject to payment by the USDA;


(b) Farm Fresh Meats 2 and Farabee caused to be submitted payment requests to the USDA knowing that the requests were based on obex samples that were not subject to payment under the USDA Agreement;


(c) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Data Collection Forms to the USDA’s testing laboratory that were false and misleading;


(d) Farm Fresh Meats completed and submitted, and Farabee directed others to complete and submit, BSE Surveillance Submission Forms filed with the USDA that were false and misleading;


(e) Farm Fresh Meats falsified, and Farabee directed others to falsify, internal Farm Fresh Meats documents to conceal the fact that Farm Fresh Meats was seeking and obtaining payment from the USDA for obex samples obtained from cattle outside the Targeted Cattle Population; and


(f) Farm Fresh Meats failed to comply with, and Farabee directed others to fail to comply with, the USDA Agreement by discarding cattle carcasses and heads prior to receiving BSE test results. A conviction for theft of government funds carries a maximum penalty of 10 years imprisonment. Mail fraud and wire fraud convictions carry a maximum penalty of 20 years imprisonment. Convictions for the above referenced violations also carry a maximum fine of $250,000 for individuals and $500,000 for organizations. In determining an actual sentence, Judge Earl H. Carroll will consult the U.S. Sentencing Guidelines, which provide appropriate sentencing ranges. The judge, however, is not bound by those guidelines in determining a sentence.


Sentencing is set before Judge Earl H. Carroll on May 14, 2007. The investigation in this case was conducted by Assistant Special Agent in Charge Alejandro Quintero, United States Department of Agriculture, Office of Inspector General. The prosecution is being handled by Robert Long, Assistant U.S. Attorney, District of Arizona, Phoenix. CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee) # # #



WE can only hope that this is a single incident. BUT i have my doubts. I remember when the infamous TOKEN Purina Feed Mill in Texas was feeding up to 5.5 grams of potentially and probably tainted BANNED RUMINANT feed to cattle, and the FDA was bragging at the time that the amount of potentially BANNED product was so little and the cattle were so big ;


"It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated."



On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed. ... FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.



WE now know all that was a lie. WE know that literally Thousands of TONS of BANNED and most likely tainted product is still going out to commerce. WE know now and we knew then that .005 to a gram was lethal. WE know that CWD infected deer and elk, scrapie infected sheep, BSE and BASE infected cattle have all been rendered and fed back to livestock (including cattle) for human and animal consumption.


Paul Brown, known and respected TSE scientist, former TSE expert for the CDC said he had ''absolutely no confidence in USDA tests before one year ago'', and this was on March 15, 2006 ;


"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."


Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.


USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.


"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end



CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...





Tuesday, September 12, 2006 11:10 AM


"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."


OR, what the Honorable Phyllis Fong of the OIG found ;


Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain



Table 1. Animal feed ingredients that are legally used in U.S. animal feeds




Rendered animal protein from Meat meal, meat meal tankage, meat and bone meal, poultry meal, animal the slaughter of food by-product meal, dried animal blood, blood meal, feather meal, egg-shell production animals and other meal, hydrolyzed whole poultry, hydrolyzed hair, bone marrow, and animal animals digest from dead, dying, diseased, or disabled animals including deer and elk Animal waste Dried ruminant waste, dried swine waste, dried poultry litter, and undried processed animal waste products






Food-animal production in the United States has changed markedly in the past century, and these changes have paralleled major changes in animal feed formulations. While this industrialized system of food-animal production may result in increased production efficiencies, some of the changes in animal feeding practices may result in unintended adverse health consequences for consumers of animal-based food products. Currently, the use of animal feed ingredients, including rendered animal products, animal waste, antibiotics, metals, and fats, could result in higher levels of bacteria, antibioticresistant bacteria, prions, arsenic, and dioxinlike compounds in animals and resulting animal-based food products intended for human consumption. Subsequent human health effects among consumers could include increases in bacterial infections (antibioticresistant and nonresistant) and increases in the risk of developing chronic (often fatal) diseases such as vCJD. Nevertheless, in spite of the wide range of potential human health impacts that could result from animal feeding practices, there are little data collected at the federal or state level concerning the amounts of specific ingredients that are intentionally included in U.S. animal feed. In addition, almost no biological or chemical testing is conducted on complete U.S. animal feeds; insufficient testing is performed on retail meat products; and human health effects data are not appropriately linked to this information. These surveillance inadequacies make it difficult to conduct rigorous epidemiologic studies and risk assessments that could identify the extent to which specific human health risks are ultimately associated with animal feeding practices. For example, as noted above, there are insufficient data to determine whether other human foodborne bacterial illnesses besides those caused by S. enterica serotype Agona are associated with animal feeding practices. Likewise, there are insufficient data to determine the percentage of antibiotic-resistant human bacterial infections that are attributed to the nontherapeutic use of antibiotics in animal feed. Moreover, little research has been conducted to determine whether the use of organoarsenicals in animal feed, which can lead to elevated levels of arsenic in meat products (Lasky et al. 2004), contributes to increases in cancer risk. In order to address these research gaps, the following principal actions are necessary within the United States: a) implementation of a nationwide reporting system of the specific amounts and types of feed ingredients of concern to public health that are incorporated into animal feed, including antibiotics, arsenicals, rendered animal products, fats, and animal waste; b) funding and development of robust surveillance systems that monitor biological, chemical, and other etiologic agents throughout the animal-based food-production chain “from farm to fork” to human health outcomes; and c) increased communication and collaboration among feed professionals, food-animal producers, and veterinary and public health officials.




Sapkota et al. 668 VOLUME 115 | NUMBER 5 | May 2007 • Environmental Health Perspectives



NOW, what about the product that is not reported ?


HOW many more Farm Fresh Meats, Inc. and Roland Emerson Farabee's are out there that submitted bogus samples for the infamous June 2004 ENHANCED BSE MAD COW COVER-UP, but did not get caught ?


IT was not bad enough to have the USDA et al bungle there own BSE Testing Protocols up so bad, it took Weybridge and a year of hounding by s o m e, and finally an act of Congress to finally get that cow confirmed, but once caught there, i guess the next best thing would be to have bogus BSE testing samples submitted for testing from healthy USDA cattle, what next ? not to forget about the other stumbling and staggering Tejas mad cow they rendered without any test at all, and the other Tejas mad cow that took 7+ months and an act of Congress to finally get confirmed from Weybridge. my God, even the three stooges, laural and hardy put all together could have thought up all this. $$$


The beef import forecast for the second quarter was unchanged from last month’s, despite pressure from higher-than-expected domestic cow slaughter that has remained high through most of this period. Beef imports into the United States from Australia, New Zealand, and Uruguay provide additional processing beef that, along with domestic cow and bull beef, is mixed with 50-percent trim from fed cattle to make ground beef. Forecast beef exports were raised slightly, mainly on continued (though gradual) improvements in sales to major Asian markets. In late May the World Animal Health Organization – known by its French acronym, OIE – designated the United States as having “controlled risk status” for bovine spongiform encephalopathy, or BSE. This designation reflects the OIE’s view that beef produced in the United States is safe for export, since BSE control measures such as feed bans and removal of specified risk materials result in negligible risk to consumers. However, the OIE standards are only guidelines. Individual countries may adopt differing standards, and those countries that do accept OIE standards must still undertake the bureaucratic processes to revise their rules and procedures.



(Adopted by the International Committee of the OIE on 23 May 2006)


11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to then Central Bureau............



P.S. Thank You Honorable Phyllis Fong for trying to keep them straight anyway. ...TSS


Thursday, July 24, 2014


Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA



Saturday, June 12, 2010


PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse



infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et al TRIPLE MAD COW FIREWALL, 10 YEARS AFTER ;




Date: March 21, 2007 at 2:27 pm PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.


Firm initiated recall is ongoing. REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.






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


Firm initiated recall is complete. REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.







*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;



infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et al TRIPLE MAD COW FIREWALL, 16 YEARS AFTER ;


Sunday, December 15, 2013





Wednesday, September 25, 2013


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





Summary Report BSE 2012


Executive Summary



Saturday, August 4, 2012


Final Feed Investigation Summary - California atypical L-type BSE Case - July 2012



Saturday, August 4, 2012


Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation



LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow. This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$ ALABAMA MAD COW g-h-BSEalabama In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.




Saturday, August 14, 2010


BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)



her healthy calf also carried the mutation


(J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008).


This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks.


Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009



Owens, Julie


From: Terry S. Singeltary Sr. []


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


To: FSIS RegulationsComments


Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98






Thursday, November 28, 2013


Department of Justice Former Suppliers of Beef to National School Lunch Program Settle Allegations of Improper Practices and Mistreating Cows



seems USDA NSLP et al thought that it would be alright, to feed our children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high risk cattle for mad cow type disease, and other dangerous pathogens, and they did this for 4 years, that was documented, then hid what they did by having a recall, one of the largest recalls ever, and they made this recall and masked the reason for the recall due to animal abuse (I do not condone animal abuse), not for the reason of the potential for these animals to have mad cow BSE type disease (or other dangerous and deadly pathogens). these TSE prion disease can lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5 DECADES FOR CJD ???


Saturday, September 21, 2013


Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT



DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ??? this recall was not for the welfare of the animals. ...tss you can check and see here ; (link now dead, does not work...tss)



try this link ;



Sunday, November 13, 2011


*** California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock



Thursday, February 13, 2014


HSUS VS USDA ET AL BAN DOWNER CALVES FOR HUMAN CONSUMPTION (*veal) and potential BSE risk factor there from



Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014


Transmissible Spongiform Encephalopathy TSE Prion Disease have now been discovered in a wide verity of species across North America. typical C-BSE, atypical L-type BASE BSE, atypical H-type BSE, atypical H-G BSE, of the bovine, typical and atypical Scrapie strains, in sheep and goats, with atypical Nor-98 Scrapie spreading coast to coast in about 5 years. Chronic Wasting Disease CWD in cervid is slowly spreading without any stopping it in Canada and the USA and now has mutated into many different strains. Transmissible Mink Encephalopathy TME outbreaks. These Transmissible Spongiform Encephalopathy TSE Prion Disease have been silently mutating and spreading in different species in North America for decades.


The USDA, FDA, et al have assured us of a robust Triple BSE TSE prion Firewall, of which we now know without a doubt, that it was nothing but ink on paper. Since the 1997 mad cow feed ban in the USA, literally tons and tons of banned mad cow feed has been put out into commerce, never to return, as late as December of 2013, serious, serious breaches in the FDA mad cow feed ban have been documented. The 2004 enhanced BSE surveillance program was so flawed, that one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.


see ;



The BSE surveillance and testing have also been proven to be flawed, and the GAO and OIG have both raised serious question as to just how flawed it has been (see GAO and OIG reports). North America has more documented TSE prion disease, in different documented species (excluding the Zoo BSE animals in the EU), then any other place on the Globe. This does not include the very likelihood that TSE prion disease in the domestic feline and canine have been exposed to high doses of the TSE prion disease vid pet food. To date, it’s still legal to include deer from cwd zone into pet food or deer food. Specified Risk Material i.e. SRM bans still being breach, as recently as just last month.


nvCJD or what they now call vCJD, another case documented in Texas last month, with very little information being released to the public on about this case? with still the same line of thought from federal officials, ‘it can’t happen here’, so another vCJD blamed on travel of a foreign animal disease from another country, while ignoring all the BSE TSE Prion risk factors we have here in the USA and Canada, and the time that this victim and others, do spend in the USA, and exposed to these risk factors, apparently do not count in any way with regard to risk factor. a flawed process of risk assessment.


sporadic CJD, along with new TSE prion disease in humans, of which the young are dying, of which long duration of illness from onset of symptoms to death have been documented, only to have a new name added to the pot of prion disease i.e. sporadic GSS, sporadic FFI, and or VPSPR. I only ponder how a familial type disease could be sporadic with no genetic link to any family member? when the USA is the only documented Country in the world to have documented two different cases of atypical H-type BSE, with one case being called atypical H-G BSE with the G meaning Genetic, with new science now showing that indeed atypical H-type BSE is very possible transmitted to cattle via oral transmission (Prion2014). sporadic CJD and VPSPR have been rising in Canada, USA, and the UK, with the same old excuse, better surveillance. You can only use that excuse for so many years, for so many decades, until one must conclude that CJD TSE prion cases are rising. a 48% incease in CJD in Canada is not just a blip or a reason of better surveillance, it is a mathematical rise in numbers. More and more we are seeing more humans exposed in various circumstance in the Hospital, Medical, Surgical arenas to the TSE Prion disease, and at the same time in North America, more and more humans are becoming exposed to the TSE prion disease via consumption of the TSE prion via deer and elk, cattle, sheep and goats, and for those that are exposed via or consumption, go on to further expose many others via the iatrogenic modes of transmission of the TSE prion disease i.e. friendly fire. I pondered this mode of transmission via the victims of sporadic FFI, sporadic GSS, could this be a iatrogenic event from someone sub-clinical with sFFI or sGSS ? what if?


Two decades have passed since Dr. Ironside first confirmed his first ten nvCJD victims in 1995. Ten years later, 2005, we had Dr. Gambetti and his first ten i.e. VPSPR in younger victims. now we know that indeed VPSPR is transmissible. yet all these TSE prion disease and victims in the USA and Canada are being pawned off as a spontaneous event, yet science has shown, the spontaneous theory has never been proven in any natural case of TSE prion disease, and scientist have warned, that they have now linked some sporadic CJD cases to atypical BSE, to atypical Scrapie, and to CWD, yet we don’t here about this in the public domain. We must make all human and animal TSE prion disease reportable in every age group, in ever state and internationally, we must have a serious re-evaluation and testing of the USA cattle herds, and we must ban interstate movement of all cervids. Any voluntary effort to do any of this will fail. Folks, we have let the industry run science far too long with regards to the TSE prion disease. While the industry and their lobbyist continues to funnel junk science to our decision policy makers, Rome burns. ...end




Sunday, June 29, 2014


Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014



Saturday, June 14, 2014


Rep. Rosa DeLauro (D-CT) Calls for Briefing on Beef Recalled for Mad Cow Potential Rep. Rosa DeLauro (D-CT)



Thursday, June 12, 2014


Missouri Firm Recalls Ribeye and Carcass Products That May Contain Specified Risk Materials 4,012 pounds of fresh beef products because the dorsal root ganglia may not have been completely removed



Monday, July 28, 2014


Mitigating the Risk of Transmission and Environmental Contamination of Transmissible Spongiform Encephalopathies 2013 Annual Report



Tuesday, August 12, 2014





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




Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)


These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...


Table 9 presents the results of an analysis of these data.


There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).


Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.


There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).


The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).


There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).


The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).




It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).




In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...




In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)


snip...see full report ;



Thursday, October 10, 2013


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



PEO752/2 0097








25 MAR 1996




The Prime Minister held a meeting on Tuesday 19 March to discuss the latest scientific information on Bovine Spongiform Encephalopathy (BSE) and Creutzfeldt Jacob Disease (CJD), The Deputy Prime Minister, the Lord President, Chief Secretary, Lord Privy Seal, the Secretary of State for Health, the Secretary of State for Scotland, the Minister for Agriculture. the Financial Secretary, the Attorney General, the Minister for Food, the Chief Whip, Sir Robin Butler, Keith Meldrum (Chief Veterinary Officer), Professor Pattison (Chairman of SEAC), Dr Eileen Rubery (Department of Health), Richard Packer (MAFF), Lord McColl, John Ward, Howell James, Alex Allan, Jonathan Haslam, Robert Culpin (HM Treasury), Kenneth Mackenzie (Cabinet Office), Tim Sutton (HM Treasury) were also present.


The Deputy Prime Minister, the Chief Secretary to the Treasury and the Lord Privy Seal all announced that they had relevant interests in the form of cattle herds.


The Prime Minister began the meeting by commenting that some very difficult decisions needed to be taken to ensure that the correct balance was struck between treating this matter seriously and over-reacting. Colleagues needed to recall that there were many issues which remained unknown.


Professor Pattison said that his committee had considered the new information which had become available very carefully and had examined in detail all the possible options. ***The situation was that there were now nine cases of CJD which appeared to be different from classical CJD. There were, in addition, three other possibJe cases. The cases tended to be among the young but varied from those aged 18 to age 41. The new variant CJD showed. an atypical clinical picture with an unknown pathology. This had persuaded SEAC that the variant was distinct. No cases in the UK or abroad had been seen before which matched to this pattern. The Committee had considered the new methods of monitoring the occurrence of the disease and were aware lab techniques had improved, but they bad drawn the conclusion that they could not persuade themselves that it was more careful observation alone which had brought these cases to light.


This implied that there might be a new risk factor and in the view of the Committee the most likely explanation was that BSE was that risk factor. To date however the evidence was not available which proved that BSE could be linked to these cases. It appeared to the Committee to be the most likely explanation but they might be wrong. It might, for example, be that the new form had always been present in a low incidence but had remained unreported or there-might be an entirely separate new environmental factor. However, the committee was of the view that the most likely cause was something new in the cattle population in the mid-1980s which was causing something new in the human population in the mid-1990s. This was in their view likely to be exposure to BSE before the introduction of the SBO controls.


Professor Pattison noted that it was impossible to predict how many more cases there might be and it might well be eighteen months before the full extent of the problem could be ascertained. A dozen or so might be the limit or it might remain at a relatively low level as in cats and unlike in the cattle population it had not escalated. The cattle epidemic with escalating numbers was probably due to feeding cattle remains back to cattle. This had not happened with cats nor of course with humans.


The committee believed it was increasingly impossible to keep this information confidential. Members of the Committee had already had to attend two expert meetings where they had not been able to provide colleagues with the full story. Given the increasingly high risk of a leak it was the Committee's view that a controlled statement by the Government would be more appropriate. The Committee had considered whether extra restrictions on human consumption of beef or beef products would be necessary. They had not concluded that immediate measures were necessary other than to stress the importance of implementing existing controls as nearly perfectly as possible. The Committee would consider again at the weekend what more might be done. ranging from a do nothing option to the slaughter of the national herd.


Personally. Professor Pattison did not think that extreme measures would be necessary. In his view the committee was more likely to focus on controls concerning older cattle, together with further controls on mechanically recovered meat. ...snip...end...tss











Since there were indications that the news was about to break, there was no reason to prevent all members of the Committee joining the meeting in London...



Sunday, July 06, 2014


Dietary Risk Factors for Sporadic Creutzfeldt-Jakob Disease: A Confirmatory Case-Control Study


Conclusions—The a priori hypotheses were supported.


*Consumption of various meat products may be one method of transmission of the infectious agent for sCJD.



Seven main threats for the future linked to prions


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


Second threat





Monday, October 10, 2011


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




*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.






***In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.



***Infectivity in skeletal muscle of BASE-infected cattle



Friday, December 19, 2014


Rancho Alleged Cancerous Eyeball Case Going To Trial





***********OCTOBER 2015*************




THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.


O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations


Emmanuel Comoy, Jacqueline Mikol, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France


Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. ***We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. ***Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.




***thus questioning the origin of human sporadic cases...





***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***


***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***


P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification


Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan


To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).


Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.


Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.








***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.






Title: Transmission of scrapie prions to primate after an extended silent incubation period




item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -


Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573.


Interpretive Summary:


The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.


Technical Abstract:


Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health. In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.


***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.



***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.


***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.









Zoonotic Potential of CWD Prions


Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA


*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.




***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***




P.105: RT-QuIC models trans-species prion transmission


Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA


Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.


***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.




***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***







Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014


*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.


*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.




*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***



*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.



*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***


Monday, November 16, 2015


*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***




98 | Veterinary Record | January 24, 2015




Scrapie: a particularly persistent pathogen


Cristina Acín


Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’


From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).


Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.


Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.


The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).


In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.


Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).


In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.


The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).


Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).


So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?


What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.






98 | Veterinary Record | January 24, 2015



*** These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils.


*** These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.


New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication


The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.



Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production


Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.



Detection of protease-resistant cervid prion protein in water from a CWD-endemic area


The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.



A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing


Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE


In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.



*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***


Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3





Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.


Claudio Soto


Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.


Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.




***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.




Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.



Wednesday, December 16, 2015


Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission


Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission


Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1


1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK


Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.






Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).


Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.


This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.


PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.


In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.


Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification



Wednesday, December 16, 2015


*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission



Monday, January 4, 2016


Long live the OIE, or time to close the doors on a failed entity?



Monday, October 26, 2015





Thursday, October 22, 2015


Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened



Sunday, October 18, 2015


World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research



Terry S. Singeltary Sr. said:


re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy


2015-12-07 02:27 AM


Terry S. Singeltary Sr. said: re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy


Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)


I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.


First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.


Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.


where have we all heard this before? it’s been well documented via the BSE Inquiry. have they not learned a lesson from the last time?


we have seen this time and time again in England (and other Country’s) with the BSE mad cow TSE Prion debacle.


That ‘anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.


The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients who got pooled extracts injected from thousands of cadavers were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.


That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find ‘alarming’ is pathetic.


Sounds like the journalists had it right in the first place: ‘Alzheimer’s may be a transmissible infection’ in The Independent to ’You can catch Alzheimer’s’ in The Daily Mirror or ‘Alzheimer’s bombshell" in The Daily Express.


if not for the journalist, the layperson would not know about these important findings.


where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?


when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.


to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer’s, the price of poker goes up drastically.


so, who makes that final decision, and how many more decades do we have to wait?


the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?


Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.


FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.


in my opinion, it’s one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.


greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it’s bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.


my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer’s of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.


I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...


[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]




snip...see full Singeltary Nature comment here;



see Singeltary comments to Plos ;




BSE101/1 0136






From: . Dr J S Metiers DCMO


4 November 1992




1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.


2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible.


what are the implications for public health?


3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.






BSE101/1 0137


4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.


J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2



>>> The only tenable public line will be that "more research is required’’ <<<


>>> possibility on a transmissible prion remains open<<<


O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?


Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease


*** Singeltary comment PLoS ***


Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?


Posted by flounder on 05 Nov 2014 at 21:27 GMT



Sunday, November 22, 2015


*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis Abstract


Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.


Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00




*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery ***


Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.


Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.



Wednesday, February 10, 2016


*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***



Tuesday, February 23, 2016


Parks and Wildlife begins reducing deer population at Texas Mountain Ranch Chronic Wasting Disease CWD TSE Prion Update



*** I kindly would like to comment on a few statements from the TPWD et al ;



Terry S. Singeltary Sr. Bacliff, Texas USA 77518


Tuesday, February 23, 2016


ARKANSAS Detects First Chronic Wasting Disease CWD in a wild elk



Friday, February 05, 2016


*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION Detections in Farmed Cervids and Wild ***



Saturday, February 6, 2016


*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No. APHIS-2016-0007] Singeltary Submission ***



 USDA JUSTIFIES SCIENTIFIC SUPPRESSION AS ITS POLICY Confidential Agency Panel Approves Censorship and Media Gag Orders Posted on Feb 29, 2016 | Tags: Scientific Integrity, USDA




Washington, DC — Under its policy purporting to protect scientific integrity, the U.S. Department of Agriculture is entitled to do just the opposite, according to confidential findings by an internal agency panel released today by Public Employees for Environmental Responsibility (PEER). The panel rejected a complaint by one of its top entomologists that USDA purged controversial findings, blocked publication of research papers with policy implications, and forbade scientists from being interviewed by reporters. These conclusions come from a report by a five-member “Scientific Integrity Review Panel” convened to review the dismissal of a complaint filed by Dr. Jonathan Lundgren, a Senior Research Entomologist and Lab Supervisor for the USDA Agriculture Research Service based in South Dakota who has published research about adverse effects on monarch butterflies from widely-used neonicotinoid insecticides (or “neonics”). The panel agreed that Dr. Lundgren’s complaint should not be pursued because – The panel was told that charges of “reprisal” and retaliatory investigations were outside the scope of its review;


The panel found that USDA is entitled to prohibit scientists from speaking with reporters or even answering questions at conferences about the significance or ramifications of published studies; and


USDA’s Scientific Integrity Policy explicitly authorizes it to block publication of research containing “statements that could be construed as being judgments of or recommendations on USDA or any other federal government policy.” “This review confirms that what occurs inside USDA does not resemble what anyone else would consider ‘scientific integrity,’” stated Jeff Ruch, Executive Director of PEER which is suing USDA for its refusal to even consider a rulemaking petition seeking to strengthen the agency’s Scientific Integrity Policy. “Inside USDA, politics determines what scientific work will see the light of day.”


On February 12th, USDA Inspector General Phyllis Fong announced that her office had opened an investigation into a “significant volume” of complaints by agency scientists about censorship and interference with research on subjects that USDA upper management deemed sensitive.


The review panel report on the Lundgren complaint arises out of the first appeal of any USDA scientific integrity complaint. Dr. Lundgren filed his formal scientific integrity complaint in September of 2014. One month later, it was rejected as not even meriting an investigation. Dr. Lundgren immediately appealed but since USDA had never received an appeal on a scientific integrity complaint decision, the agency took an entire year to determine how to handle it. Yet under the guidelines finally developed – The panel does not investigate the complaint but instead simply reviews materials provided by agency management. In this case, no panel member even attempted to speak with Dr. Lundgren or any of the witnesses he identified;


There is no process for remedying any alleged scientific misconduct if it is ever confirmed; and


The panel findings are confidential and USDA will not release them under the Freedom of Information Act by maintaining that even final reports are “deliberative.”


“How will public confidence in the integrity of USDA science be enhanced when all of the reviews are kept secret?” asked Ruch, noting that a stated objective of the policy is to “ensure public confidence.” “Given how this complaint was handled, no wonder scientific integrity lapses inside USDA are never resolved and simply fester. Something now unmistakably clear is that no scientist in their right mind should report political manipulation of science inside USDA.”




Read the Scientific Integrity Review Panel report and approvals


See ruling that reprisal is outside the scope of USDA Scientific Integrity Policy


Examine USDA scientific integrity appeal guidelines


View transmittal letter to Dr. Lundgren asking him to keep it confidential


Look at Dr. Lundgren’s scientific integrity and whistleblower complaints


Revisit USDA refusal to consider strengthening its scientific integrity policy


Jonathan Latham, PhD


Executive Director The Bioscience Resource Project Ithaca, NY 14850 USA




Skype: jonathanlatham2 Tel: 1-607-319-0279


“The conscious and intelligent manipulation of the organized habits and opinions of the masses is an important element in democratic society. Those who manipulate this unseen mechanism of society constitute an invisible government which is the true ruling power of our country.”—Edward Bernays, Propaganda


-- end///


Terry S. Singeltary Sr. Bacliff, Texas USA 77518