New Oxford Veterinarian Sentenced For Defrauding The U.S. Department Of Agriculture
PRESS RELEASE
New Oxford Veterinarian Sentenced For Defrauding The U.S. Department Of Agriculture
Tuesday, June 6, 2023
For Immediate Release U.S. Attorney's Office, Middle District of Pennsylvania HARRISBURG – The U.S. Attorney’s Office for the Middle District of Pennsylvania announced that Dr. Donald Yorlets, age 68, of New Oxford, Pennsylvania, was sentenced to 24 months of probation, including 12 months of home detention, and a $50,000 fine by U.S. District Court Judge Jennifer P. Wilson for defrauding the U.S. Department of Agriculture between 2016 and 2019 by submitting false blood samples for bovine disease testing and by issuing false Certificates of Veterinary Inspection for the animals.
According to U.S. Attorney Gerard M. Karam, federal law requires that each cow transported in interstate or international commerce be first tested for various bovine diseases, such as Bovine Tuberculosis, Brucellosis, Bovine Leucosis and Bovine Viral Diarrhea. Bovine Tuberculosis and Brucellosis are communicable diseases that can be transmitted to humans under certain circumstances. Bovine Tuberculosis is screened for by what is known as a Caudal Fold skin test. The test must be administered by a USDA accredited veterinarian and involves the injection of a tuberculin substance under the skin and checking it for a reaction 72 hours later. Testing for Brucellosis, Bovine Leucosis and Bovine Viral Diarrhea requires the drawing of blood and the submission of samples to an accredited laboratory for analysis.
Animals transported in international commerce can only be exported with an International Certificate of Veterinarian Inspection (ICVI). To lawfully issue an ICVI, a USDA accredited veterinarian must verify that each animal has been physically examined, tested for disease, vaccinated and medically treated as required by the USDA prior to shipment.
Yorlets conspired with Daniel and Benjamin Gutman, owners of a livestock exporting business known as Gutman Brothers Dairy Cattle, to avoid the disease testing requirements by falsely representing he tested every cow for Bovine Tuberculosis when, in fact, he did not. Yorlets also submitted hundreds of non-authentic, bovine blood samples to a PA Department of Agriculture testing laboratory in Harrisburg for testing and by issuing false Certificates of Veterinary Inspection for the untested animals. The false blood test results and Certificates enabled the sellers to quickly export hundreds of untested cows to Mexico, Canada, Qatar, and Puerto Rico.
The investigation began in 2017 when the Pennsylvania Veterinary Laboratory (PVL) in Harrisburg became suspicious that dozens of blood specimens submitted by Dr. Yorlets were not authentic. To confirm their suspicions the PVL sent 804 blood samples submitted by Dr. Yorlets to the USDA’s National Veterinary Services Laboratory (NVSL) in Iowa for Antibody Profile testing.
Each animal has a unique Antibody Profile in its blood. If all of the Yorlets’ blood specimens were genuine, Antibody Profile testing should have shown that all 804 blood samples had a unique Antibody Profile. However, the NVSL’s testing only found 70 unique Antibody Profiles in the 804 samples. The results confirmed that Dr. Yorlets’ repeatedly submitted the same blood samples for different animals and issued false Certificates of Veterinary Inspection for hundreds of cows that were never tested. This allowed the sellers to export the animals quickly and reduce expenses incurred in keeping the animals on domestic feeder lots.
Yorlets was a Pennsylvania licensed veterinarian since 1981. His veterinary license was suspended for six months following his guilty plea on August 31, 2020, and he was removed from the U.S. Department of Agriculture’s National Veterinary Accreditation Program.
Daniel Gutman and Benjamin Gutman, both residents of Maryland, were each sentenced to 30 months in prison for a conspiracy to defraud and commit offenses against the United States. Collectively, they were ordered to pay $1,938,646.42 in fines and forfeiture.
The case was investigated by the USDA’s Office of Inspector General and the Department of Homeland Security. Assistant United States Attorney Ravi Romel Sharma prosecuted the case.
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Updated June 6, 2023
THIS always fascinates me, when USDA officials et al, when a situation likes this arises, they can't even say the word, Bovine Spongiform Encephalopathy BSE Transmissible Spongiform Encephalopathy TSE Prion disease, aka mad cow disease, so i thought i might say it for them, and list my concerns of these same type breaches in safety protocol for the BSE TSE Prion.
It reminds me of the infamous Westland Meat Co. and Hallmark Meat Co., where downer cows, the most high risk cattle for mad cow disease BSE, were processed for THE NATIONAL SCHOOL LUNCH PROGRAM, and fed to our children all across the Nation, for over 4 years, and then tried to blame that recall on...wait for it...wait for it...ANIMAL ABUSE!
for THE NEXT 50 YEARS, Mothers and Fathers across the Nation will have to wonder if their children will come down with CJD TSE Prion. i don't make this stuff up folks, i will post that here now, then get on on the FAKE TESTING FOR CATTLE DISEASE IN THE USA.
LAST BUT NOT LEAST, THE MOST FRIGHTENING THING OF ALL, 50 YEARS PARENTS WILL HAVE TO WAIT TO SEE IF THEIR CHILDREN COME DOWN WITH CJD TSE PRION!
This is where STUPID meets the road imo, where you have politicians trying to take chocolate milk from THE SCHOOL LUNCH PROGRAM, claims it's bad for our baby's.
BUT IT'S PERFECTLY OK TO FEED OUR CHILDREN, FOR FOUR FUCKING YEARS, THE MOST HIGH RISK CATTLE FOR BSE MAD COW DISEASE, VIA THE SAME SCHOOL LUNCH PROGRAM...i don't make this stuff up people!
In the USA, USDA et al sometimes serves SRMs up as appetizers or horderves.
Thursday, November 28, 2013
Department of Justice Former Suppliers of Beef to National School Lunch Program Settle Allegations of Improper Practices and Mistreating Cows
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)
IF THIS LINK IS STILL DEAD, go to the archived one next...terry
what other tests has this Pennsylvania Veterinarian faked i.e. Scrapie, BSE, CWD, and is this the norm?
where have i heard this same song and dance before i.e. FAKE BSE TESTING? i have heard this before somewhere???
YES, I remember a few reports from the OIG, GAO, and fake BSE testing.
FDA Statement FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
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ooops!
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
see archived url link here;
"FDA will soon be improving the animal feed rule, to make this strong system even stronger."
LMAO!!! (see why down further...terry)
CATTLE ON FEED IN TEXAS
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
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Note: On Dec. 23, 2003, the U.S. Department of Agriculture reported that a cow in Washington state had tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease). As a result, information on this Web page stating that no BSE cases had been found in the United States is now incorrect. However, because other information on this page continues to have value, the page will remain available for viewing.
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.
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.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.
FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
see archived url link here;
PAST US MAD COW CASES AND TRACEABILITY PROBLEMS, WHAT'S IT GOING TO TAKE?
AUG. 11, 2017
***>Assuming no other factors influenced the levels of correct diagnosis and that the numbers estimated for 1997 to 1999 were a true representation of the potential under-diagnosis of the entire epidemic up until 1999, then the total number of missed cases positive for BSE could have been in the region of 5,500.
***>As a result, using more sensitive diagnostic assays, we were able to diagnose BSE positive cattle from the years 1997-1999 inclusive that were originally negative by vacuolation. From these data we have estimated that approximately 3% of the total suspect cases submitted up until the year 1999 were mis-diagnosed.
YOU know, Confucius is confused again LOL, i seem to have remembered something in line with this here in the USA...
USDA did not test possible mad cows
By Steve Mitchell
United Press International
Published 6/8/2004 9:30 PM
WASHINGTON, June 8 (UPI) -- The U.S. Department of Agriculture claims it tested 500 cows with signs of a brain disorder for mad cow disease last year, but agency documents obtained by United Press International show the agency tested only half that number.
"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."
THIS WAS DONE FOR A REASON!
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
TEXAS 2ND MAD COW THAT WAS COVERED UP, AFTER AN ACT OF CONGRESS, AND CALLS FROM TSE PRION SCIENTIST AROUND THE GLOBE, THIS 2ND MAD COW IN TEXAS WAS CONFIRMED
THE USDA MAD COW FOLLIES POSITIVE TEST COVER UP
JOHANNS SECRET POSTIVE MAD COW TEST THAT WERE IGNORED
OIG AND THE HONORABLE FONG CONFIRMS TEXAS MAD AFTER AN ACT OF CONGRESS 7 MONTHS LATER
TEXAS MAD COW
THEY DID FINALLY TEST AFTER SITTING 7+ MONTHS ON A SHELF WHILE GW BORE THE BSE MRR POLICY, i.e. legal trading of all strains of TSE. now understand, i confirmed this case 7 months earlier to the TAHC, and then, only after i contacted the Honorable Phyllis Fong and after an act of Congress, this animal was finally confirmed ;
During the course of the investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE. 200 adult animals of interest were determined to have left the index farm. Of these 200, APHIS officials determined that 143 had gone to slaughter, two were found alive (one was determined not to be of interest because of its age and the other tested negative), 34 are presumed dead, one is known dead and 20 have been classified as untraceable. In addition to the adult animals, APHIS was looking for two calves born to the index animal. Due to record keeping and identification issues, APHIS had to trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter channels, four are presumed to have entered feeding and slaughter channels and one calf was untraceable.
NEW URL LINK;
Executive Summary In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.
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Trace Herd 3 The owner of Trace Herd 3 was identified as possibly having received an animal of interest. The herd was placed under hold order on 7/27/05. The herd inventory was conducted on 7/28/05. The animal of interest was not present within the herd, and the hold order was released on 7/28/05. The person who thought he sold the animal to the owner of Trace Herd 3 had no records and could not remember who else he might have sold the cow to. Additionally, a search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. The animal of interest traced to this herd was classified as untraceable because all leads were exhausted.
Trace Herd 4 The owner of Trace Herd 4 was identified as having received one of the COI through an order buyer. Trace Herd 4 was placed under hold order on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05. There were 233 head of cattle that were examined individually by both State and Federal personnel for all man-made identification and brands. The animal of interest was not present within the herd. Several animals were reported to have died in the herd sometime after they arrived on the premises in April 2005. A final search of GDB records yielded no further results on the eartag of interest at either subsequent market sale or slaughter. With all leads having been exhausted, this animal of interest has been classified as untraceable. The hold order on Trace Herd 4 was released on 8/23/05.
Trace Herd 5 The owner of Trace Herd 5 was identified as having received two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67 head of cattle in multiple pastures. During the course of the herd inventory, the owner located records that indicated that one of the COI, a known birth cohort, had been sold to Trace Herd 8 where she was subsequently found alive. Upon completion of the herd inventory, the other animal of interest was not found within the herd. A GDB search of all recorded herd tests conducted on Trace Herd 5 and all market sales by the owner failed to locate the identification tag of the animal of interest and she was subsequently classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 5 was released on 8/8/05.
Trace Herd 6 The owner of Trace Herd 6 was identified as possibly having received an animal of interest and was placed under hold order on 8/1/05. This herd is made up of 58 head of cattle on two pastures. A herd inventory was conducted and the animal of interest was not present within the herd. The owner of Trace Herd 6 had very limited records and was unable to provide further information on where the cow might have gone after he purchased her from the livestock market. A search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. Additionally, many of the animals presented for sale by the owner of the herd had been re-tagged at the market effectually losing the traceability of the history of that animal prior to re-tagging. The animal of interest traced to this herd was classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 6 was released on 8/3/05.
Trace Herd 7 The owner of Trace Herd 7 was identified as having received an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7 contains 487 head of cattle on multiple pastures in multiple parts of the State, including a unit kept on an island. The island location is a particularly rough place to keep cattle and the owner claimed to have lost 22 head on the island in 2004 due to liver flukes. Upon completion of the herd inventory, the animal of interest was not found present within Trace Herd 7. A GDB search of all recorded herd tests conducted on Trace Herd 7 and all market sales by the owner failed to locate the identification tag of the animal of interest. The cow was subsequently classified as untraceable. It is quite possible though that she may have died within the herd, especially if she belonged to the island unit. The hold order on Trace Herd 7 was released on 8/8/05.
NEW URL LINK;
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.
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4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
NEW URL LINK;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II and Food Safety and Inspection Service Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
UNITED STATES DEPARTMENT OF AGRICULTURE OFFICE OF INSPECTOR GENERAL Washington, D.C. 20250 January 25, 2006 REPLY TO ATTN OF: 50601-10-KC
TO: W. Ron DeHaven Administrator Animal and Plant Health Inspection Service Barbara Masters Administrator Food Safety and Inspection Service ATTN: William J. Hudnall Deputy Administrator Marketing Regulatory Program Business Services William C. Smith Assistant Administrator Office of Program Evaluation, Enforcement, and Review FROM: Robert W. Young /s/ Assistant Inspector General for Audit
SUBJECT: Animal and Plant Health Inspection Service - Bovine Spongiform Encephalopathy (BSE) Surveillance Program - Phase II and Food Safety and Inspection Service - Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III This report presents the results of our audit of the enhanced BSE surveillance program and controls over specified risk materials and advanced meat recovery products. Your written response to the official draft report, dated January 20, 2006, is included as exhibit G with excerpts of the response and the Office of Inspector General’s (OIG) position incorporated into the Findings and Recommendations section of the report, where applicable. We accept the management decisions for all recommendations. Please follow your agency’s internal procedures in forwarding documentation for final action to the Office of the Chief Financial Officer (OCFO). We are providing a separate memorandum to the agencies and OCFO that provides specific information on the actions to be completed to achieve final action. We appreciate your timely response and the cooperation and assistance provided to our staff during the audit USDA/OIG-A/50601-10-KC/ Page i
Executive Summary
Animal and Plant Health Inspection Service - Bovine Spongiform Encephalopathy (BSE) Surveillance Program - Phase II and Food Safety and Inspection Service - Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Results in Brief This report evaluates elements of the interlocking safeguards in place to protect United States (U.S.) beef from Bovine Spongiform Encephalopathy, widely known as BSE or "mad cow disease." Since 1990, the U.S. Department of Agriculture (USDA), Animal and Plant Health Inspection Service (APHIS), has led a multi-agency effort to monitor and prevent BSE from entering the food supply. After discovering a BSE-positive cow in December 2003, APHIS expanded its BSE surveillance program. To further protect the food supply, USDA banned materials identified as being at risk of carrying BSE (specified risk materials (SRM)), such as central nervous system tissue. As part of this effort, USDA’s Food Safety and Inspection Service (FSIS) required beef slaughter and processing facilities to incorporate controls for handling such materials into their operational plans. Onsite FSIS inspectors also inspect cattle for clinical signs in order to prevent diseased animals from being slaughtered for human consumption. To evaluate the effectiveness of the safeguards, we assessed APHIS’ implementation of the expanded surveillance program, as well as FSIS’ controls to prevent banned SRMs from entering the food supply.
In June 2004, APHIS implemented its expanded surveillance program; participation by industry in this surveillance program is voluntary. As of May 2005, over 350,000 animals were sampled and tested for BSE. To date, two animals tested positive for BSE; one tested positive after implementation of the expanded surveillance program.
USDA made significant efforts to implement the expanded BSE surveillance program. Much needed to be done in a short period of time to establish the necessary processes, controls, infrastructure, and networks to assist in this effort. In addition, extensive outreach and coordination was undertaken with other Federal, State, and local entities, private industry, and laboratory and veterinary networks. This report provides an assessment as to the progress USDA made in expanding its surveillance effort and the effectiveness of its controls and processes. This report also discusses the limitations of its program and data in assessing the prevalence of BSE in the U.S. herd.
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40 ELISA test procedures require two additional (duplicate) tests if the initial test is reactive, before final interpretation. If either of the duplicate tests is reactive, the test is deemed inconclusive.
41 Protocol for BSE Contract Laboratories to Receive and Test Bovine Brain Samples and Report Results for BSE Surveillance Standard Operating Procedure (SOP), dated October 26, 2004.
42 The NVSL conducted an ELISA test on the original material tested at the contract laboratory and on two new cuts from the sample tissue.
43 A visual examination of brain tissue by a microscope.
44 A localized pathological change in a bodily organ or tissue.
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PLEASE SEE FLAMING EVIDENCE THAT THE USDA ET AL COVERED UP MAD COW DISEASE IN TEXAS ;
PAGE 43;
Section 2. Testing Protocols and Quality Assurance Controls
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FULL TEXT 130 PAGES
Audit Report
Animal and Plant Health Inspection Service
Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II
and
Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
Our prior report identified a number of inherent problems in identifying and testing high-risk cattle. We reported that the challenges in identifying the universe of high-risk cattle, as well as the need to design procedures to obtain an appropriate representation of samples, was critical to the success of the BSE surveillance program. The surveillance program was designed to target nonambulatory cattle, cattle showing signs of CNS disease (including cattle testing negative for rabies), cattle showing signs not inconsistent with BSE, and dead cattle. Although APHIS designed procedures to ensure FSIS condemned cattle were sampled and made a concerted effort for outreach to obtain targeted samples, industry practices not considered in the design of the surveillance program reduced assurance that targeted animals were tested for BSE.
In our prior report, we recommended that APHIS work with public health and State diagnostic laboratories to develop and test rabies-negative samples for BSE. This target group is important for determining the prevalence of BSE in the United States because rabies cases exhibit clinical signs not inconsistent with BSE; a negative rabies test means the cause of the clinical signs has not been diagnosed.
APHIS agreed with our recommendation and initiated an outreach program with the American Association of Veterinary Laboratory Diagnosticians, as well as State laboratories. APHIS also agreed to do ongoing monitoring to ensure samples were obtained from this target population.
Although APHIS increased the samples tested from this target group as compared to prior years, we found that conflicting APHIS instructions on the ages of cattle to test resulted in inconsistencies in what samples were submitted for BSE testing. Therefore, some laboratories did not refer their rabies negative samples to APHIS in order to maximize the number tested for this critical target population. In addition, APHIS did not monitor the number of submissions of rabies negative samples for BSE testing from specific laboratories.
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An NVSL official stated that APHIS is not concerned with rabies negatives samples from cattle less than 30 months of age. This position, however, is contrary to APHIS’ published target population.
Our prior audit recognized the significant challenge for APHIS to obtain samples from some high-risk populations because of the inherent problems with obtaining voluntary compliance and transporting the carcasses for testing. USDA issued rules to prohibit nonambulatory animals (downers) from entering the food supply at inspected slaughterhouses. OIG recommended, and the International Review Subcommittee33 emphasized, that USDA should take additional steps to assure that facilitated pathways exist for dead and nonambulatory cattle to allow for the collection of samples and proper disposal of carcasses. Between June 1, 2004, and May 31, 2005, the APHIS database documents 27,617 samples were collected showing a reason for submission of nonambulatory and 325,225 samples were collected with reason of submission showing "dead."
APHIS made extensive outreach efforts to notify producers and private veterinarians of the need to submit and have tested animals from these target groups. They also entered into financial arrangements with 123 renderers and other collection sites to reimburse them for costs associated with storing, transporting, and collecting samples. However, as shown in exhibit F, APHIS was not always successful in establishing agreements with non-slaughter collection sites in some States. APHIS stated that agreements do not necessarily reflect the entire universe of collection sites and that the presentation in exhibit F was incomplete because there were many collection sites without a payment involved or without a formal agreement. We note that over 90 percent of the samples collected were obtained from the 123 collection sites with agreements and; therefore, we believe agreements offer the best source to increase targeted samples in underrepresented areas.
We found that APHIS did not consider industry practices in the design of its surveillance effort to provide reasonable assurance that cattle exhibiting possible clinical signs consistent with BSE were tested. Slaughter facilities do not always accept all cattle arriving for slaughter because of their business requirements. We found that, in one State visited, slaughter facilities pre-screened and rejected cattle (sick/down/dead/others not meeting business
Downers and Cattle that Died on the Farm standards) before presentation for slaughter in areas immediately adjacent or contiguous to the official slaughter establishment. These animals were not inspected and/or observed by either FSIS or APHIS officials located at the slaughter facilities.
FSIS procedures state that they have no authority to inspect cattle not presented for slaughter. Further, APHIS officials stated they did not believe that they had the authority to go into these sorting and/or screening areas and require that the rejected animals be provided to APHIS for BSE sampling. Neither APHIS nor FSIS had any process to assure that animals left on transport vehicles and/or rejected for slaughter arrived at a collection site for BSE testing. FSIS allows slaughter facilities to designate the area of their establishment where federal inspection is performed; this is designated as the official slaughter establishment.34
We observed animals that were down or dead in pens outside the official premises that were to be picked up by renderers. Animals that were rejected by plant personnel were transported off the premises on the same vehicles that brought them to the plant.35
A policy statement36 regarding BSE sampling of condemned cattle at slaughter plants provided that effective June 1, 2004, FSIS would collect BSE samples for testing: 1) from all cattle regardless of age condemned by FSIS upon ante mortem inspection for CNS impairment, and 2) from all cattle, with the exception of veal calves, condemned by FSIS upon ante mortem inspection for any other reason.
FSIS Notice 28-04, dated May 20, 2004, informed FSIS personnel that, "FSIS will be collecting brain samples from cattle at federally-inspected establishments for the purpose of BSE testing." The notice further states that, "Cattle off-loaded from the transport vehicle onto the premises of the federally-inspected establishment (emphasis added), whether dead or alive, will be sampled by the FSIS Public Health Veterinarian (PHV) for BSE after the cattle have been condemned during ante mortem inspection. In addition, cattle passing ante mortem inspection but later found dead prior to slaughter will be condemned and be sampled by the FSIS PHV."
APHIS has the responsibility for sampling dead cattle off-loaded onto plant-owned property that is adjoining to, but not considered part of, the "official premises.37 FSIS procedures38 provide that "Dead cattle that are off-loaded to facilitate the off-loading of live animals, but that will be re-loaded onto the transport vehicle, are not subject to sampling by FSIS.
While performing our review in one State, we reviewed the circumstances at two slaughter facilities in the State that inspected and rejected unsuitable cattle before the animals entered the official receiving areas of the plants. This pre-screening activity was conducted in areas not designated by the facility as official premises of the establishment and not under the review or supervision of FSIS inspectors. The plant rejected all nonambulatory and dead/dying/sick animals delivered to the establishment. Plant personnel refused to offload any dead or downer animals to facilitate the offloading of ambulatory animals. Plant personnel said that the driver was responsible for ensuring nonambulatory animals were humanely euthanized and disposing of the carcasses of the dead animals. Plant personnel informed us that they did not want to jeopardize contracts with business partners by allowing unsuitable animals on their slaughter premises.
In the second case, one family member owned a slaughter facility while another operated a livestock sale barn adjacent to the slaughter facility. The slaughter facility was under FSIS’ supervision while the sale barn was not. Cattle sometimes arrived at the sale barn that were sick/down/dead or would die or go down while at the sale barn. According to personnel at the sale barn, these animals were left for the renderer to collect. The healthy ambulatory animals that remained were marketed to many buyers including the adjacent slaughter facility. When the slaughter facility was ready to accept the ambulatory animals for processing, the cattle would be moved from the sale barn to the slaughter facility where they were subject to FSIS’ inspection.
We requested the slaughter facilities to estimate the number of cattle rejected on a daily basis (there were no records to confirm the estimates). We visited a renderer in the area and found that the renderer had a contract with APHIS to collect samples for BSE testing. In this case, although we could not obtain assurance that all rejected cattle were sampled, the renderer processed a significant number of animals, as compared to the slaughter plants’ estimates of those rejected. Due to the close proximity (less than 5 miles) of the renderer to the slaughter facilities, and the premium it paid for dead cattle that were in good condition, there was a financial incentive for transport drivers to dispose of their dead animals at this renderer.
USDA/OIG-A/50601-10-KC Page 25
In our discussions with APHIS officials in Wisconsin and Iowa, they confirmed that there were plants in their States that also used pre-screening practices. On May 27, 2005, we requested APHIS and FSIS to provide a list of all slaughter facilities that pre-screened cattle for slaughter in locations away from the area designated as the official slaughter facility. Along with this request, we asked for information to demonstrate that either APHIS or FSIS confirmed there was a high likelihood that high-risk animals were sampled at other collection sites.
In response to our request, the APHIS BSE Program Manager stated that APHIS did not have information on slaughter plants that pre-screen or screen their animals for slaughter suitability off their official plant premises. To their knowledge, every company or producer that submits animals for slaughter pre-sorts or screens them for suitability at various locations away from the slaughter facility. For this reason, USDA focused its BSE sample collection efforts at other types of facilities such as renderers, pet food companies, landfills, and dead stock haulers. Further, in a letter to OIG on June 14, 2005, the administrators of APHIS and FSIS noted the following:
"…we believe that no specific actions are necessary or appropriate to obtain reasonable assurance that animals not presented for slaughter are being tested for BSE. There are several reasons for our position. First, we do not believe that the practice is in fact causing us to not test a significant enough number of animals in our enhanced surveillance program to invalidate the overall results. Second, OIG has concluded that because of the geographical proximity and business relationships of the various entities involved in the case investigated, there is reasonable assurance that a majority of the rejected cattle had been sampled. Third, it is also important to remember that the goal of the enhanced surveillance program is to test a sufficient number of animals to allow us to draw conclusions about the level of BSE (if any) in the American herd…We believe that the number we may be not testing because of the "pre-sorting" practice does not rise to a significant level. The number of animals tested to date has far exceeded expectations, so it is reasonable to infer that there are few of the animals in question, or that we are testing them at some other point in the process…APHIS estimated…there were approximately 446,000 high risk cattle…[and APHIS has]…tested over 375,000 animals in less than 1 year. This indicated that we are missing few animals in the high-risk population, including those that might be pre-sorted before entering a slaughter facility’s property."
snip...
APHIS notes that for the current surveillance program, it had established regional goals and APHIS was not trying to meet particular sampling levels in particular States. However, we believe that it would be advantageous for APHIS to monitor collection data and increase outreach when large geographical areas such as the above States do not provide samples in proportion to the numbers and types of cattle in the population.
We also disagree with APHIS/FSIS’ contention that because they have tested over 375,000 of their 446,000 estimate of high risk cattle, few in the high-risk population are being missed, including those that might be pre-screened before entering a slaughter facility’s property. In our prior audit, we reported that APHIS underestimated the high-risk population; we found that this estimate should have been closer to 1 million animals (see Finding 1). We recognize that BSE samples are provided on a voluntary basis; however, APHIS should consider industry practice in any further maintenance surveillance effort. Animals unsuitable for slaughter exhibiting symptoms not inconsistent with BSE should be sampled and their clinical signs recorded. However, this cited industry practice results in rejected animals not being made available to either APHIS or FSIS veterinarians for their observation and identification of clinical signs exhibited ante mortem. Although these animals may be sampled later at other collection sites, the animals are provided post mortem without information as to relevant clinical signs exhibited ante mortem. For these reasons, we believe APHIS needs to
USDA/OIG-A/50601-10-KC Page 27
observe these animals ante mortem when possible to assure the animals from the target population are ultimately sampled and the clinical signs evaluated.
snip...
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
see archived url link;
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE)
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 scheduledfor May 2007.
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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),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
see archived url link;
Office of the United States Attorney District of Arizona
FOR IMMEDIATE RELEASE For Information Contact Public Affairs
February 16, 2007 WYN HORNBUCKLE Telephone: (602) 514-7625Cell: (602) 525-2681
CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD COW DISEASESURVEILLANCE PROGRAM
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Evidence uncovered during the government’s investigation established that Farm Fresh Meats and Farabee submitted samples from cattle outside the Targeted Cattle Population. Specifically, FarmFresh 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.
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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 ofAgriculture, Office of Inspector General. The prosecutionis being handled by Robert Long, Assistant U.S. Attorney, District ofArizona, Phoenix.CASE NUMBER: CR-07-00160-PHX-EHC RELEASE NUMBER: 2007-051(Farabee)# # #
http://www.usdoj.gov/usao/az/press_rele ... 51(Farabee).pdf
NEW URL LINK;
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
CORPORATION AND ITS PRESIDENT PLEAD GUILTY TO DEFRAUDING GOVERNMENT’S MAD COW DISEASE SURVEILLANCE PROGRAM
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
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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)
# # #
Subject: Re: BSE USA FONG OIG ON THE TEXAS MAD COW DeHaven tried to cover-up ''USDA was more concerned about trade than human health''
Date: March 1, 2006 at 2:55 pm PST
UNITED STATES DEPARTMENT OF AGRICULTURE OFFICE OF INSPECTOR GENERAL STATEMENT OF THE HONORABLE PHYLLIS K. FONG INSPECTOR GENERAL Before the HOUSE APPROPRIATIONS SUBCOMMITTEE ON AGRICULTURE, RURAL DEVELOPMENT, FOOD AND DRUG ADMINISTRATION, AND RELATED AGENCIES March 1, 2006
snip...
For release only by the House Committee on Appropriations Good morning, Mr. Chairman and Members of the Subcommittee. I thank you for inviting me to testify before you today to discuss the activities of the Office of Inspector General (OIG) and to provide information about our oversight of the Department of Agriculture’s (USDA) programs and operations. I would like to introduce the members of the OIG senior management team who are here with me today: Kathy Tighe, our new Deputy Inspector General; Robert Young, Assistant Inspector General for Audit; Mark Woods, Assistant Inspector General for Investigations; and Suzanne Murrin, Assistant Inspector General for Policy Development and Resources Management. I welcome this opportunity to provide the Subcommittee with an overview of the highlights of our audit and investigative activity over the past year. Fiscal Year 2005 presented many difficult challenges for the USDA and our country’s agricultural producers and consumers. In addition to administering programs relied upon by farmers and rural communities and managing the $128 billion in public resources entrusted to the Department, USDA assumed significant responsibilities responding to the hurricanes that ravaged the Gulf Coast in 2005 and addressing the threat of plant and animal disease. To best serve the Department, our Congressional oversight committees, and the general public, OIG has formally prioritized, organized, and planned our work according to three
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central objectives. I will present my testimony to the Subcommittee according to the framework of these three objectives: supporting Safety, Security, and Public Health in USDA programs and operations; protecting Program Integrity as USDA provides assistance to individuals and entities; and improving the Department’s Management of Public Resources. I. Safety, Security, and Public Health The BSE Surveillance Program and SRM Controls We recently issued our second report focusing on the Department’s efforts to establish and enforce effective, interlocking safeguards to protect producers and consumers from Bovine Spongiform Encephalopathy (BSE), commonly referred to as “mad cow disease.” Our February 2006 report reviewed the Animal and Plant Health Inspection Service’s (APHIS) implementation of its expanded BSE surveillance program and the Food Safety and Inspection Service’s (FSIS) controls to prevent banned specified risk materials (SRM) from entering our Nation’s food supply. We found that USDA made significant efforts to implement and improve the expanded surveillance program. The Department faced many challenges in a short period of time to establish the necessary processes, controls, and infrastructure needed for this massive effort. In our recent report, we discuss specific areas where we believe corrective actions were not fully effective in addressing our prior findings and recommendations on issues such as obtaining representative samples of the U.S. herd, identifying and obtaining samples from high-risk surveillance streams, and ensuring the completeness/accuracy of data. The Department
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has responded to our report with immediate actions. For example, at the Secretary’s direction, APHIS revised its testing protocols to provide for additional confirmatory procedures when inconclusive test results occur. Also, both APHIS and FSIS agreed with all OIG recommendations, and they have corrected, or have developed action plans to correct, the program weaknesses identified. APHIS’ Implementation of the Expanded Surveillance Plan APHIS obtained significantly more samples for testing than it originally anticipated would be needed to achieve its stated level of confidence in estimating the prevalence of BSE in the U.S. herd. The voluntary nature of the surveillance program, however, makes it difficult to determine how successful USDA was in obtaining a representative proportion of high-risk cattle for testing. OIG found that APHIS’ various statistical approaches to determining the prevalence of BSE mitigate some, but not all, of the limitations associated with its data and the agency’s underlying assumptions in the design and implementation of its surveillance program. The accuracy of the underlying data is critical to the development of a future maintenance surveillance program. We recommended that APHIS disclose the limitations in its surveillance program and underlying data when it makes its final assessment of the prevalence of BSE in the U.S. We also found that USDA needed to strengthen its processes to ensure the quality and capability of its BSE testing program, especially when inconclusive test results occur. We recommended that USDA re-evaluate and adjust its testing protocols based on its
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evaluation of emerging science and strengthen its proficiency testing and quality assurance reviews at participating laboratories. Evaluation of FSIS Processes Regarding SRMs To examine FSIS’ inspection procedures to enforce regulations to prevent risk materials in meat products, OIG reviewed the SRM plans of several meat processing facilities, observed FSIS inspections, and evaluated the effectiveness of controls during the slaughter process. FSIS technical experts assisted us in these reviews. We did not identify SRMs entering the food supply during our plant visits. However, we could not determine whether required SRM procedures were followed or were adequate due to the lack of specificity in the plans. We found that the plants lacked documentation of compliance with SRM control procedures and FSIS actions to validate such compliance. In addition to the control issues we identified regarding SRM procedures at slaughter and processing establishments, we found that FSIS’ information system could not readily provide FSIS with the data it needed to identify trends in SRM violations. The expanded stage of USDA’s BSE surveillance program is now nearing its end. Accordingly, it is important that the issues we have raised be considered as USDA completes its BSE surveillance program and reports on the prevalence of BSE in the U.S. herd. The Department has responded to our report with immediate action and agreed to address all of our findings and recommendations.
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Assessing USDA Controls for Beef Exported to Japan On January 20, 2006, Japanese officials announced that they had banned any further imports of beef products from the United States, based on the discovery that a U.S. plant had shipped a veal product containing vertebral column material that was prohibited by the terms of an agreement with Japan. On the same date, in response to Japan’s decision, the Secretary announced 12 actions USDA would undertake to facilitate resuming trade. These actions include delisting and investigating the plant that exported the ineligible product, requiring a second signature on export certificates, providing training to inspection personnel on export certification, and holding meetings with inspection officials and industry representatives to reaffirm program requirements. Shortly thereafter, the Secretary requested OIG to audit the adequacy of USDA’s coordination and control processes for the Beef Export Verification (BEV) program for Japan. OIG’s report, issued on February 16, 2006, concluded that the Agricultural Marketing Service (AMS) and FSIS could strengthen their controls over the BEV program by improving processes used to communicate BEV program requirements, clearly defining roles and responsibilities, and implementing additional oversight of FSIS inspection personnel. In response to our recommendations, the agencies agreed to an array of actions. AMS agreed to maintain a list of specific, export-eligible products for each facility with an approved BEV program; to systematically notify FSIS when any establishment is approved/delisted from a BEV program; and to review all establishments in the BEV program to ensure that they adhere to program requirements. FSIS agreed to
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clarify the roles and responsibilities of FSIS personnel involved at each stage of the export verification process; expedite the development of export certification training; and increase supervisory oversight of the export certification process. OIG believes that the full implementation of these measures will strengthen and improve the Department’s compliance with BEV program requirements. Assessment of the Equivalence of the Canadian Beef Inspection System Last year, my testimony discussed OIG’s findings from our audit of APHIS’ oversight of the importation of beef products from Canada. Our work on that audit led us to conduct an evaluation of FSIS’ assessment of the equivalence of the Canadian food safety inspection system, which we issued in December 2005. The then FSIS Administrator and the Under Secretary for Food Safety had identified concerns with the Canadian inspection system in late 2003. Our audit determined that FSIS did not fully address the issues raised by USDA officials in a timely manner. For example, in July 2003 FSIS found that Canadian inspection officials were not enforcing certain pathogen reduction and HACCP system regulations. These same types of concerns were identified again in June 2005. At the time of our audit, FSIS did not have protocols for evaluating deficiencies in a foreign country’s inspection system which could be used to question the system’s equivalence to U.S. standards. In addition, FSIS had not instituted compensating controls (such as increased port-of-entry testing) to strengthen public health protections while
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deficiencies were present. During the period of January 2003–May 2005, 4.4 billion pounds of Canadian processed product entered the U.S., even though FSIS officials questioned the equivalence of the Canadian inspection system. FSIS agreed with OIG’s five recommendations, which included implementing protocols to determine which deficiencies would lead FSIS to question whether a foreign country’s inspection system is equivalent to the U.S. system. In response to the report, FSIS committed to develop these protocols by March 2006 and to implement them immediately thereafter. Oversight of FSIS Recalls For the past several years we have testified about our continuing work regarding adulterated beef product recalls. In July 2004, a Pennsylvania firm initiated a recall of approximately 170,000 pounds of ground beef patties because of mislabeling. Approximately one-fourth of this product was made, in part, from beef trim from Canada which was not eligible for import to the U.S., following the detection of a Canadian cow with BSE. In May 2005, we reported on the adequacy of FSIS’ effectiveness checks and the agency’s oversight of the recall. Overall, we concluded that FSIS had strengthened its procedures regarding the agency’s oversight of recalls. However, we noted that FSIS personnel did not determine the amount of product purchased by firms on 26 of the 58 completed effectiveness checks. This resulted in reduced assurance that mislabeled product was completely retrieved from distribution. Agency officials concurred with the firms’ assertions that the product had been removed from the marketplace. In response to
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our recommendations, FSIS agreed to provide more specific direction to its personnel on identifying and evaluating the amount of product purchased. The Subcommittee has been interested in OIG’s investigation of a Pennsylvania company’s recall of meat products. This remains an ongoing civil fraud investigation and we will be pleased to provide information on its resolution to the Subcommittee upon its conclusion.
snip. ...9 of 34 pages. ...tss
http://appropriations.house.gov/_files/FongTestimony.pdf
see updated archived url link;
Comments on technical aspects of the risk assessment were then submitted to FSIS.
Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.
This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
NEW URL LINK;
Owens, Julie From: Terry S. Singeltary Sr. [flounder9@verizon.net]
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 8/3/2006
Greetings FSIS, I would kindly like to comment on the following ;
NEW URL LINK;
Suppressed peer review of Harvard study October 31, 2002.
October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024
NEW URL LINK;
Sunday, February 14, 2010
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
snip...SEE FULL TEXT;
BSE research project final report 2005 to 2008 SE1796 SID5
SUNDAY, MARCH 21, 2021
Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005 Singeltary's Regiew 2021
Subject: Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Tue, 30 Aug 2005 12:38:40 -0500 Content-Type: text/plain Parts/Attachments: text/plain (51 lines)
##################### Bovine Spongiform Encephalopathy #####################
From: TSS ()
Subject: Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005
Date: August 30, 2005 at 10:28 am PST
Release No. 0336.05 Contact: USDA Jim Rogers 202-690-4755 FDA Rae Jones 301-827- 6242
U.S. Department of Agriculture (USDA) Food and Drug Administration (FDA)
Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005
The U.S. Department of Agriculture's Animal and Plant Health Inspection Service (APHIS) and the U.S. Department of Health and Human Services' Food and Drug Administration (FDA) have completed their investigations regarding a cow that tested positive for bovine spongiform encephalopathy (BSE) in June 2005. The agencies conducted these investigations in collaboration with the Texas Animal Health Commission and the Texas Feed and Fertilizer Control Service.
Our results indicate that the positive animal, called the index animal, was born and raised on a ranch (termed the "index farm") in Texas. It was a cream colored Brahma cross approximately 12 years old at the time of its death. It was born prior to the implementation of the 1997 feed ban instituted by FDA to help minimize the risk that a cow might consume feed contaminated with the agent thought to cause BSE. The animal was sold through a livestock sale in November of 2004 and transported to a packing plant. The animal was dead upon arrival at the packing plant and was then shipped to a pet food plant where it was sampled for BSE. The plant did not use the animal in its product, and the carcass was destroyed in November 2004.
APHIS attempted to trace all adult animals that left the index farm after 1990, as well as all progeny born within 2 years of the index animal's death. Together, these animals are called animals of interest.
During the course of the investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE. 200 adult animals of interest were determined to have left the index farm. Of these 200, APHIS officials determined that 143 had gone to slaughter, two were found alive (one was determined not to be of interest because of its age and the other tested negative), 34 are presumed dead, one is known dead and 20 have been classified as untraceable. In addition to the adult animals, APHIS was looking for two calves born to the index animal. Due to record keeping and identification issues, APHIS had to trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter channels, four are presumed to have entered feeding and slaughter channels and one calf was untraceable.
To determine whether contaminated feed could have played a role in the index animal's infection, FDA and the Texas Feed and Fertilizer Control Service conducted a feed investigation with two main objectives: 1) to identify all protein sources in the animal=s feed history that could potentially have been the source of the BSE agent, and 2) to verify that cattle leaving the herd after 1997 were identified by USDA as animals of interest and were rendered in compliance with the 1997 BSE/ruminant feed rule.
The feed history investigation identified 21 feeds or feed supplements that were used on the farm since 1990. These feed ingredients were purchased from three retail feed stores and were manufactured at nine feed mills. This investigation found that no feed or feed supplements used on the farm since 1997 were formulated to contain prohibited mammalian protein. Due to this finding, FDA has concluded that the animal was most likely infected prior to the 1997 BSE/ruminant feed rule.
The investigation into the disposition of herd mates from this farm involved visits to nine slaughter plants and eight rendering plants. The investigation found that all of the rendering plants were operating in compliance with the BSE/ruminant feed rule. A review of the inspection history of each of these rendering firms found no violations of the FDA feed ban rule.
APHIS and FDA are very pleased with the results of their investigations, which show the animals of interest did not present a threat to livestock and that the ruminant feed rule is being followed. The U.S. maintains an interlocking system of safeguards designed to prevent BSE from entering the human and animal food chain. USDA also remains vigilant in its attempt to find BSE in the United States. To date, there have been more than 450,000 animals tested in the last 14 months and only two BSE positive animals found in this country.
For more information on USDA's epidemiological investigation and a copy of the report, please visit the APHIS website at http://www.aphis.usda.gov/lpa/issues/bse/bse.html
For more information on FDA's feed investigation, please visit the FDA's website at http://www.fda.gov/cvm/texasfeedrpt.htm
Last Modified: 08/30/2005
http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retrievecontent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/1/_th/J_2_9D/_s.7_0_A/7_0_1OB?PC_7_2_5JM_contentid=2005%2F08%2F0336.xml&PC_7_2_5JM_navtype=RT&PC_7_2_5JM_parentnav=LATEST_RELEASES&PC_7_2_5JM_navid=NEWS_RELEASE#7_2_5JM
see archived url link;
TSS
#################### https://lists.aegee.org/bse-l.html ####################
Subject: Report on Food & Drug Administration Dallas District Investigation of Bovine Spongiform Encephalopathy Event in Texas 2005
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Tue, 30 Aug 2005 16:26:26 -0500 Content-Type: text/plain Parts/Attachments: text/plain (535 lines)
##################### Bovine Spongiform Encephalopathy #####################
From: TSS ()
Subject: Report on Food & Drug Administration Dallas District Investigation of Bovine Spongiform Encephalopathy Event in Texas 2005
Date: August 30, 2005 at 2:15 pm PST
Report on Food & Drug Administration Dallas District Investigation of Bovine Spongiform Encephalopathy Event in Texas 2005
Executive Summary:
On June 24, 2005, USDA informed FDA that a cow in Texas tested positive for Bovine Spongiform Encephalopathy (BSE). Information provided by APHIS was that the BSE positive cow was born and raised in a herd in Texas and was approximately 12 years old. The animal was sampled for BSE at a pet food plant in Texas on November 15, 2004, as part of USDA’s enhanced surveillance program. The animal was disposed of by incineration and did not enter the human food or animal feed chains. Although the positive animal posed no risk to the animal feed supply, FDA, APHIS, the Texas Animal Health Commission (TAHC), and the Texas Feed and Fertilizer Control Service (TFFCS) conducted a feed investigation with two main objectives. The first objective was to identify all protein sources in the animal’s feed history that could potentially have been the source of the BSE agent. The second objective was to verify that cattle leaving the herd after 1997 that were identified by USDA/APHIS as animals of concern (e.g. progeny and feed cohorts), were rendered at facilities in compliance with the regulation (21 CFR 589.2000) that prohibits most mammalian protein in feed for ruminants that became effective August 4, 1997 (herein called BSE/Ruminant Feed rule).
The feed history investigation identified 21 feed products that had been used on the farm since 1990. These feed products were purchased from three retail feed stores and had been manufactured at nine different feed mills. The investigators visited these establishments to collect information on formulations, shipping invoices, and use of ruminant meat and bone meal (MBM) on the premises both pre-1997 feed ban and post-1997 feed ban. This investigation found no feed products used on the farm since 1997 that had been formulated to contain prohibited mammalian protein.
The investigation identified one feed which contained an animal protein source that could not be identified. The investigation also found one feed mill that supplied feed to the farm that had used ruminant MBM in feed formulations for non-ruminant species after the BSE/Ruminant Feed rule went into effect, which is permitted under the rule, and that several feed mills had used ruminant MBM in feeds prior to the feed ban. Although the investigation did not identify a specific feed source as the likely cause of this animal’s infection, it is probable that the most likely route of exposure for this animal was consumption of an animal feed containing mammalian protein prior to the implementation of the BSE/Ruminant Feed rule in 1997.
The investigation into the disposition of herd mates from this farm involved visits to nine slaughter plants and eight rendering plants. The investigation found that all rendering plants were operating in compliance with the BSE/ruminant feed ban regulation. A review of the inspection history of each of these rendering firms found no violations.
Background of Investigation:
When notified on June 24, 2005, FDA Headquarters and Dallas District management officials immediately began making contacts with their Federal, State and Local counterparts to plan for and initiate follow-up investigational activities to determine the feed history in this herd and to assure the safety of the animal feed supply by evaluating current and historic compliance with the BSE/ruminant feed ban rule.
APHIS established a joint Incident Command Post and FDA Dallas District staffed this post full time with a Supervisory Investigator charged with coordinating activities between FDA, APHIS, TAHC and TFFCS. Coordination conference calls were set up with all Federal and State agencies involved in the investigation to keep everyone apprised of investigational developments.
Animal Tracing Activities and Renderer Follow-up Inspections:
One of APHIS’ primary objectives was to identify and trace the animals of interest (animals of interest would include any animals which could have been potential birth cohorts or feed cohorts of the index animal, or potential offspring of the index animal within the two years prior to the positive diagnosis) from the index herd. This objective included the identification of points of sale and ultimately the actual slaughter facilities for animals of interest that left the farm. As the trace information was developed, APHIS shared this information with FDA. Further information on animal of interest identification and tracing can be found in the USDA Texas BSE Final Epidemiology report.
APHIS identified nine slaughter establishments receiving these animals of interest. Eight of the slaughter establishments were located in the State of Texas and one was located in the State of Georgia. Dallas District Investigators notified USDA/FSIS of our plans to visit each slaughter establishment to identify rendering facilities receiving materials from these slaughter establishments during the timeframe they received animals of interest. Dallas District also issued an assignment to Atlanta District to visit and inspect the one slaughter/renderer establishment located in the State of Georgia.
Eight renderers and one protein source broker were identified as receiving materials from these slaughter establishments. Each rendering facility identified was inspected for current compliance with the mammalian protein feed ban rule. Each firm’s operations during the period of time of receipt of these animals post 1997 were evaluated from a historical viewpoint and no evidence of noncompliance was detected.
In all, FDA visited nine slaughter facilities, eight rendering facilities and one broker of these materials. All facilities inspected were found to be in compliance with the BSE/ruminant feed ban rule
Following is a graphical representation of the animal product follow-up work performed.
Feed Investigation:
As information was learned about the index herd, FDA Investigators working with TAHC officials conducted multiple interviews with the producer of the animal regarding possible feeds, feed sources, animal husbandry practices, and other events which may have changed normal feeding practices over the course of the index animal’s life in the herd and any other information which may have been helpful in identifying the possible sources of feed for this animal and herd. FDA corroborated this information through interviews at the retail feed supply stores where the producer purchased feeds.
Follow-up at these retail feed supply stores identified 21 possible feed products the producer may have used during the history of the herd. Fifteen purchased feed products were identified, along with hay, native grass, rice straw, soybean meal, milk replacer/colostrum and bagged corn. These products were identified as originating from nine different manufacturers. Each of these manufacturers was inspected by FDA Dallas District and TFFCS Investigators.
Feed manufacturers were located throughout the State of Texas. An assignment was also issued to another FDA District to visit a Corporate Headquarters facility in an effort to review archived feed formulations and labels. During each of these inspections, the firm’s current compliance with the BSE/ruminant feed ban rule was evaluated and attempts were made to determine the protein sources used in feeds on the index farm. Many of the feeds investigated were manufactured and used prior to the implementation of the BSE/ruminant feed ban rule in 1997. Feed products of particular interest included any which may have contained a protein source and the primary focus was on identifying any possible mammalian protein source material in those feed products. We found that ruminant feeds that had contained mammalian meat and bone meal (MBM) prior to the BSE/ruminant feed ban rule had been discontinued or reformulated upon the implementation of these rules. There is no regulatory requirement for a feed mill to archive formulations for that length of time, so in those instances where an actual formulation could not be obtained, experienced employees of the firms were interviewed and their recollections recorded.
Of all the feeds in use by the producer since 1997, none were discovered to have contained prohibited material (mammalian protein). Since the age of the index animal was determined to be approximately 12 years, investigating and reconstructing a feed history over such a long period of time is challenging. This ranch is a beef cow-calf operation and minimal feed records were maintained. Due to the nature of this investigation, it is difficult to determine what feeds were in use at specific times and what the formulation of those feeds were at the time they were fed. A feed history was developed through interviews with the producer and other farm personnel since they did not maintain any feed history documentation. Interviews with personnel at retail establishments disclosed incomplete records and cash sales that did not always identify the purchaser. Dallas District investigated any and all feed ingredients that were identified as being fed or potentially fed over the course of the last 15 years of this herd’s operation. Feeds discovered during this investigation with potential mammalian protein sources are as below:
One feed, used prior to 1996, before the implementation of the feed ban, was suspected to contain mammalian meat and bone meal, but this could not be confirmed as no formulation records were available.
The producer recalled using a particular feed sporadically during the 1980’s and 1990’s, however, he could not remember the name or manufacturer of the feed and had no records identifying the product. It is not known whether this feed contained an animal protein source. Attempts to identify this feed through interviews with retail sources were unsuccessful.
The producer identified one feed product that has been used since the year 2000 which contains fish meal as a protein source. Further investigation revealed that this product had contained mammalian meat and bone meal prior to 1997, but that it had been reformulated at that time using fish meal to replace the MBM.
A tabular representation of the feed inspection follow-up activities is presented below:
Feed Dates of Use Protein Source Current BSE Inspection BSE Compliance History
Feed #1 - Range Meal 1980’s - 2000 Unknown - Unable to determine actual manufacturer, no records available from producer N/A N/A
Feed #2 - High Protein Starter Feed 2001 to present Feather meal BSE Compliant BSE Compliant
Feed #3 - High Protein Starter Feed ~1995 - 2001 Feather meal BSE Compliant BSE Compliant
Feed #4 - Cottonseed cake Prior to 1990 Cottonseed meal BSE Compliant BSE Compliant
Feed #5 - Cottonseed cake Early 1980’s - 1990’s Cottonseed meal BSE Compliant BSE Compliant
Feed #6 - Limiter 2001 to present Feather meal BSE Compliant BSE Compliant
Feed #7 - Creep pellets Prior to 1970 Likely feather meal - no formulation could be obtained N/A N/A
Feed #8 - Lick tub Since 2000 MBM prior to 1997 Fish Meal since 1997 BSE Compliant BSE Compliant
Feed #9 - Cottonseed meal Continuously Cottonseed meal BSE Compliant BSE Compliant
Feed #10 - Range Cubes Continuously since 1990 Feather meal BSE Compliant BSE Compliant[1]
Feed #11 - Sulfur Salt Block Continuously Minerals; calcium - all non-animal derived BSE Compliant BSE Compliant
Feed #12 - Lick tub Continuously since 1995 Feather meal BSE Compliant BSE Compliant
Feed #13 - Beef Supplement Prior to 1996 Prior to 1997, suspect MBM - Not able to confirm, no formulation available BSE Compliant Same manufacturer as Feed #10[1]
Feed #14 - Mineralized Salt Continuously since 1998 Minerals; calcium - all non-animal derived BSE Compliant BSE Compliant
Feed #15 - Soybean meal Since 2000, sparingly Soybean meal N/A N/A
Feed #16 - Corn Continuously Corn N/A N/A
Feed #17 - Rice straw 1996, during dry year Rice straw N/A N/A
Feed #18 - Hay Continuously Hay N/A N/A
Feed #19 - Milk Replacer Since 2000, Infrequent use Dehydrated colostrums, whey N/A N/A
Feed #20 - Grass Continuously Native grass N/A N/A
Feed #21 - Soybean meal Since 2000, sparingly Soybean meal N/A N/A
Dallas District previously documented one incident of the accidental addition of mammalian protein to a feed that was to be used for cattle at this facility. This incident was isolated to the manufacture of one lot of a custom cattle feed. A cross contamination error resulted in mammalian meat and bone meal being accidentally included in a feed. The error was detected soon after production. The firm acted swiftly in recalling the product and purchasing the animals that had consumed the feed. No products entered the human food or ruminant feed chain.
Dallas District Compliance History with BSE Feed Ban Rules:
Prior to 1997, feed manufacturers were not required to differentiate between protein sources used in ruminant and non-ruminant feeds. For a period of time following the implementation of the BSE/ruminant feed ban rule, some feed manufacturers continued to use both prohibited material and non-prohibited material within the same facility, employing separation and cleanout procedures to minimize cross-contamination. Although the regulations allow this practice, the potential for cross-contamination of ruminant feeds is greater. Most feed mills have found this practice to be difficult and have abandoned this practice.
Since the implementation of the BSE/ruminant feed ban rule in 1997, Dallas District and its State partners have inspected every known or registered feed manufacturer located in the states of Texas, Oklahoma and Arkansas. Further, every rendering operation and feed manufacturer actually processing with prohibited materials has been inspected annually. The compliance rate of the industry has been excellent.
Results:
In total FDA, along with TFFCS, conducted 33 inspections, investigations and interviews of the producer, retail feed establishments, feed manufacturers, corporate headquarters, slaughter facilities, renderers and a protein source broker. The FDA Dallas District follow-up to this incident resulted in the coordination of efforts of multiple Federal and State agencies. This report is the physical output of many hours of research, planning and coordination. All of the inspections conducted confirmed the feed manufacturers and rendering operations to be in compliance with the current BSE/ruminant feed ban rule.
Dallas District conducts annual inspections of all feed mills and rendering facilities who handle, use or produce PM for feed use. Inspections performed since the initiation of the BSE/ruminant feed ban rules in 1997 have confirmed a high degree of industry wide compliance with these important safeguards. The district also routinely coordinates and shares information regarding feed inspections with the TFFCS who are also responsible for the evaluating feed ban compliance in the state of Texas.
Food and Drug Administration August 30, 2005
http://www.fda.gov/cvm/texasfeedrpt.htm
see archived url link here;
Subject: TRANSCRIPT OF JOHANNS ABOUT THE TEXAS MAD COW BSe Release No. 0339.05
August 30, 2005
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Tue, 30 Aug 2005 21:03:28 -0500 Content-Type: text/plain Parts/Attachments: text/plain (522 lines)
##################### Bovine Spongiform Encephalopathy #####################
From: TSS ()
Subject: TRANSCRIPT OF JOHANNS ABOUT THE TEXAS BSe Release No. 0339.05
Date: August 30, 2005 at 6:48 pm PST
Release No. 0339.05 Contact: USDA Press Office (202) 720-4623
TRANSCRIPT OF TECHNICAL BRIEFING WITH AGRICULTURE SECRETARY MIKE JOHANNS, USDA CHIEF VETERINARY OFFICER DR. JOHN CLIFFORD (ANIMAL AND PLANT HEALTH INSPECTION SERVICE), AND CENTER FOR VETERINARY MEDICINE DIRECTOR DR. STEVE SUNDLOF (FOOD AND DRUG ADMINISTRATION), UPDATE ON NATIONAL ANIMAL IDENTIFICATION SYSTEM AND BSE EPIDEMIOLOGY INVESTIGATION, WASHINGTON, DC -- AUGUST 30, 2005 SEC. MIKE JOHANNS: Thank you very much, and good afternoon everyone, and thank you for joining us. I will begin today with an announcement about the National Animal Identification System, and then what I'd like to do from there is ask Dr. John Clifford to report on the conclusion of the investigation related to the cow that tested positive for BSE in June of this year.
Many of you have heard me say before that I am deeply committed to the spirit of public service that involves listening, really listening, to the people whom we serve. We may not always agree with each other, but as public servants it is important that we listen. That's why I've been traveling around the country doing a Farm Bill listening tour to hear from the entire ag community about what's on their mind, what we're doing right, and what we might do better.
Well, today I'd like to tell you about some of the listening we've done on the National Animal Identification System. That's a good place for me to start. The system is one of the most important infrastructure initiatives in animal agriculture today. Our goal is to work hand-in-hand with producers and the states to enhance our collective ability to quickly identify animals that may be of concern in a disease outbreak.
When this system is fully implemented, we expect to be able to identify all potentially affected animals and premises within 48 hours of a disease detection.
You'd be hard-pressed to find anyone working in animal agriculture today who doesn't believe that's a worthy objective and an important investment for us to make. After all, the faster we identify affected animals and premises, the faster we are able to contain the disease.
But as with any major initiative touching so many segments of the industry, there are differing views on some pretty fundamental questions like whether data in the system should be publicly or privately held, how can we protect confidentiality of the data, and whether the data collection should be a voluntary system or a mandatory system.
Last year the USDA held a series of listening sessions around the country, some 16 in all as a matter of fact, to hear what folks around the country had to say. We also formed a special subcommittee under the Secretary's Advisory Committee on Foreign Animal and Poultry Diseases that has widespread producer representation.
And in May as you know we published a detailed thinking paper outlining our proposed strategy for getting a mandatory system in place and framing some additional questions for stakeholders to contemplate.
In their responses, producers expressed concern about confidentiality when it comes to animal movement information. Without question, the participation of producers is absolutely essential to the success of an animal identification system. That's why we paid attention when producers asked that animal movement data be privately held.
Based on the feedback, I'm putting forth guiding principles today that allow animal movement data to be maintained in a private system that can be readily accessed when necessary by state and federal animal health authorities. This allows the industry to continue developing databases that house animal movement information, and we envision those databases feeding a single, privately-held animal tracking repository that we can access.
This initiative, or innovative approach, addresses producers' concerns while at the same time enabling federal and state officials to access information that we may need for disease control purposes.
There are a number of concepts being discussed in the private sector about how this should work and how it should be funded. USDA is not favoring any one of them over the other. USDA will be scheduling a stakeholder meeting this fall to clarify expectations for the private tracking system and discuss user requirements in system specifications.
In the meantime, USDA will be finalizing and releasing the program standards that were presented in the thinking paper. Beyond that, we will be looking to industry to come together to drive this leg of the journey.
I believe strongly this is the right approach. This system has always been about government and private partnership. USDA has invested a great deal, nearly $19 million in 2004, to get the infrastructure started. Most of that went to cooperative agreements with states and with tribes. For Fiscal Year 2005, we've invested another $33 million with about half of that going to additional cooperative agreements. And there's another $33 million in the President's 2006 Budget for additional infrastructure building.
We are making great progress in the area of premise registration with 100,000 premises now registered and plans to begin later this year allocating blocks of animal identification numbers to tag manufacturers.
With today's announcement, we begin work on the next step in developing the animal identification system, tracking animal movements. The only way the system will work is if stakeholders have a role in designing it, if all are truly, fully invested. The piece of the system that is the most producer-dependent is this piece dealing with tracking animal movements, and so it simply makes good sense for producers to design and to maintain that piece of the system.
Ultimately we know we will end up with a system that embodies the best that the private system and government have to offer.
I would be happy to answer your questions about the National Animal Identification System in just a moment.
But just briefly while we're speaking of tracing animals, I did want to mention that we've completed our epidemiological investigation related to the BSE animal identified in June. This very thorough investigation has been a tremendous example of partnership at the federal, state, and, I might add, the industry level. And we appreciate that.
It's worth nothing that this investigation would have taken far less than two months if we had the National Animal Identification System in place. That delay is not significant in terms of human or animal health because BSE is not a contagious disease. But the time it has taken to identify, locate, and test animals of interest is significant to our efforts to reopen export markets, because a number of trading partners have been reluctant to make decisions until the investigation is complete.
I am pleased that we are now in a position to close the investigation, communicate this information to our trading partners, and then move forward. I have with me today Dr. John Clifford, our chief veterinarian, along with Dr. Steve Sundlof of the Food and Drug Administration, to provide you with information about their conclusions. So I'll now turn the microphone to Dr. Clifford.
DR. JOHN CLIFFORD: Thank you, Mr. Secretary. As you said, the announcement of the guiding principles for the future of a public/private partnership for animal ID is a giant step forward for a national animal identification system. Because it was developed through the integration of premises registration, animal registration, and animal tracking, the NAIS has always been viewed as a government/industry partnership. Today's announcement affirms our commitment and eagerness to work with the industry to achieve the goals of the NAIS.
Now I want to turn to the completion of the epidemiological investigation that was conducted following the BSE detection in Texas in June. Many people worked very hard on the investigation, and I'd like to thank the Veterinary Services employees involved, our colleagues from the Food and Drug Administration, the owners of the animals, along with the Texas Animal Health Commission and the Texas Feed and Fertilizer Control Service for their outstanding work.
This investigation is another great example of federal, state, and local partners cooperating to help protect livestock health in this country.
I'll now summarize our findings. Our results indicate that the positive animal, called the "index animal." was born and raised on a ranch, termed the "index farm," in Texas. It was a cream-colored Brahma cross, approximately 12 years of age at the time of its death. It was born prior to the implementation of FDA's mandatory ruminant-to-ruminant feed ban in the U.S., and that ban was implemented in August 1997.
The animal was sold through a livestock sale in November of 2004 and transported to a packing plant. The animal was dead upon arrival. The animal was therefore refused by the packing plant. This refusal was consistent with USDA's safeguards to protect the meat supply from BSE.
The animal was then shipped to a pet food plant where it was sampled for BSE. The plant did not use the animal in its product, and the carcass was destroyed.
APHIS's epidemiological investigation attempted to trace all adult animals that left the index farm after 1990. The investigation also attempted to trace all progeny born within two years of the index animal's death.
Together these animals are called "animals of interest." These steps are consistent with the guidance for epidemiological investigations and to detections of BSE issued by the International Animal Health governing body or the OIE.
During the course of this investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE.
A total of 200 additional adult animals of interest were determined to have left the index farm. Of these 200, APHIS determined that 143 animals were slaughtered, 2 animals were found alive but one was determined not to be of interest because of its age, and the other tested negative for BSE. 34 animals were presumed dead, 1 is known dead, and the remaining 20 are classified as "untraceable."
In addition to the adult animals, we also looked for two calves born to the index animal. Due to record-keeping and identification issues, we had to trace 213 calves. Of these 213, 208 entered feeding and slaughter channels, 4 are presumed to have entered feeding and slaughter channels, and 1 calf was untraceable.
As you know, BSE is not a contagious animal disease. This disease is spread through contaminated feed. To determine whether contaminated feed could have played a role in the index animal's infection, FDA and the Texas Feed and Fertilizer Control Service conducted a thorough feed investigation.
For a summary of the findings of the feed investigation, we have Dr. Steve Sundlof here from the FDA.
Before I turn things over, though, I will say that we are extremely pleased with the results of the epidemiological investigation. It shows there was no widespread problem associated with the index herd, and as you will hear more about in a moment, that the ruminant feed ban in the United States is solid. It also affirms that USDA's interlocking system of safeguards to prevent BSE from entering the food chain is working as it should.
We remain vigilant, as well, as in our efforts to determine the prevalence of BSE in the United States. To date there have been only 2 BSE-positive animals found in this country in more than 452,000 animals tested in the last 14 months.
All evidence is that the prevalence is extremely low and continues to decline given the length of time the ruminant feed ban has been in effect.
With that, I will turn things over to Dr. Steve Sundlof from the Food and Drug Administration.
DR. STEVE SUNDLOF: Thank you, Dr. Clifford. I will read an opening statement as well.
On June 24, 2005, the USDA informed the FDA that a cow in Texas tested positive for bovine spongiform encephalopathy. The animal was disposed of by incineration and did not enter the human food or animal feed chains. Although the animal posed no risk to the animal feed supply, FDA, along with USDA's Animal and Plant Health Inspection Service, the Texas Animal Health Commission, and the Texas Feed and Fertilizer Control Service conducted a feed investigation with two main objectives.
The first objective was to identify all protein sources in the animal's feed history that could potentially have been the source of the BSE agent.
The second objective was to verify that cattle of interest leaving the herd after 1997 were rendered at facilities that were in compliance with the 1997 regulation that prohibits most mammalian protein in the feed for ruminants, which hereafter we will call the BSE Ruminant Feed Rule.
The feed history investigation identified 21 products that had been used on the farm since 1990. These feed products were purchased from three retail feedstores and had been manufactured at nine different feed mills.
The investigators visited these establishments to collect information on formulation, shipping invoices, and the use of ruminant meat and bonemeal on the premises, both before the 1997 feed ban and after the 1997 feed ban.
This investigation found no feed products used on the farm since 1997 had been formulated to contain prohibited mammalian protein. The investigation identified one feed which contained an animal protein source that could not be identified and the investigation also found one feed mill that supplied feed to the farm and that used ruminant meat and bonemeal in feed formulations for nonruminant species after the BSE ruminant feed rule went into effect, and this was permitted under the rule.
And there were several feed mills that had used ruminant meat and bonemeal prior to the 1997 feed ban but had ceased to use that material after the 1997 feed ban.
The investigation into the disposition of herd-mates from this farm involved visits to nine slaughter plants and eight rendering plants. The investigation found that all rendering plants were operating in compliance with the BSE ruminant feed rule. A review of the inspection history of each of these rendering firms found no violation.
And those are my prepared comments.
SEC. JOHANNS: Very good. Thank you, both of you. And with that I think we're ready to open it up to some questions.
OPERATOR: Thank you. If you have a question you can do so by pressing *1 on your touchtone phone. Anytime you wish to cancel your question you can do so by pressing *2. Please be mindful to record your name as well as your affiliation when announced.
First question comes from Libby Quaid.
REPORTER: Hi. Thank you. A question for Dr. Sundlof with FDA. Your agency promised more than a year and a half ago to close loopholes in the feed ban. When will FDA act on that promise, and what will FDA do to close the loopholes?
DR. SUNDLOF: Thank you. Yes, we have been working on the proposed rule. We announced July 14 of 2004, in an advanced notice of proposed rulemaking, that we intended to move forward with a modification of the feed rule that would prohibit specified risk materials in all animal feeds. I can report that there's been quite a great deal of progress on that, and that we hope that a rule will be forthcoming within the next month or two.
REPORTER: Can you say what that rule will entail? Will it be different from what the ANPR was?
DR. SUNDLOF: It will -- well, the ANPR dealt with a whole lot of issues. And so I can't say it will be different, but I think you'll find it's consistent with what we announced in the ANPR.
MR. JIM ROGERS: Next question, please?
OPERATOR: Next question comes from Daniel Goldstein of Bloomberg News.
REPORTER: Yeah, hi. This question is for the Secretary. Last month or earlier this month the USDA released about 1,000 incidents where there was a case of meat plants not following the rules or violations for specified risk materials. And you spoke of some reluctance on the part of trading partners to reopen trade while there was a BSE investigation happening.
Has there been any reluctance on the part of these trading partners to reopen because of some of these violations?
SEC. JOHANNS: There hasn't been. They've asked for information. We supply that information, we answer whatever questions they have. There's an interest in it, I can say that, but I haven't had any trading partner say, 'We're not going to open the border,' or 'We're considering closing the border if they've opened it already.'
So at least at this stage it's been more of a situation where they were interested and we provided the information.
MR. ROGERS: Next question, please?
OPERATOR: Next question comes from Ron Hays of Clear Channel.
REPORTER: Yes. I guess my question is regards to some of the comments that have been made by the Japanese in recent days, Japanese Food Safety Commission. Seemingly some of their panel members questioning our feed ban and saying they're fearful that we might have as "bad of a situation as they had in Britain" is one quote we saw from the Japanese media. You know. Can anybody address-- what assurances can we make to them and to folks in this country that we are effective on our feed ban and right across the board?
SEC. JOHANNS: I'll ask Dr. Sundlof to address that in just a second, but I would just offer a thought.
That's just simply not the case. I mean, it just simply is not, not the case. We've worked very intensely, as you know, with the Japanese over many, many months now to deal with their questions and to address whatever concerns they raised. With the Japanese we've even gone beyond what international rules require. We agreed that we would start trading with animals at 20 months and under, and even the international standards don't require that.
In 452,000 animals tested in the last 14 months we've had two BSE-positive animals. So again, we'll respectfully address their question, but quite honestly I don't see any scientific basis for the issue they're raising.
Doctor, you can offer a thought if you would.
DR. SUNDLOF: Thank you, Mr. Secretary.
Well, let me just say that we've had a very effective feed ban in place since 1997. It's been over eight years now this month. And we have really focused our efforts on enforcing the ban and making sure that compliance with the feed ban was high.
And we reported on several occasions that compliance when we go out and investigate -- we did over 6,800 inspections in the last year and are projecting to do even more in the upcoming years -- that their physical inspections, where inspectors go out and do a physical examination of the feed plants or the renderers, in all cases we find the compliance by the industries affected is greater than 99 percent. So it's an extremely high compliance rate. It's hard to get any better than that.
The fact that both of these cattle that were BSE-positive in the United States were born at or before the feed ban and probably very likely consumed contaminated feed well before 1997-- there's just no indication the feed rule is not effective.
MR. ROGERS: Our next question, please?
OPERATOR: Next question comes from Steve Kay of Cattle Buyers Weekly.
REPORTER: Gentlemen, I want to go back to the proposed rule by AFDA because the question of Ron Hayes mentioned what members of Japan's Prion Subcommittee were referring to in part, and one of their concerns that we were still, we the U.S. are still allowing meat and bonemeal to be fed to nonruminants.
Now the advanced notice by FDA Dr. Sundlof suggests or proposes a ban on SRMs from all animal feed. Can you tell me, if you proceed with that, is that going to satisfy Japan, do you think? How is USDA going to convey to Japan that we might be moving in this way, because if this rule becomes a final rule but doesn't take effect for another year or more is Japan going to say, Well, we'll reopen our border in a year when this takes effect? I mean, how is all this going to play out?
SEC. JOHANNS: Well, I'll offer another thought and then Dr. Sundlof, I'd ask you to offer your thoughts.
Japan would not be justified under any science, any view of the world, to adopt that viewpoint. Again I point out with Japan we at the USDA, actually before I arrived, but made a decision to agree with Japan that we would start with the trade of animals 20 months and under.
In the history of the world we haven't found an animal that tested positive for BSE 20 months and under. They just simply have no risk here. So that approach would not be justified by international standards, it would not be justified by scientific standards. It really is time for Japan, in my opinion, to step up here and go through a science-based process and reopen the border, and hopefully we're nearing the end of that very kind of process.
Doctor, any thoughts?
DR. SUNDLOF: Thank you again, Mr. Secretary. I don't have the insight to know what the Japanese government is going to do, based on what the feed rule or the proposed feed rule will convey. But the rule is very much risk-based. It uses the Harvard Risk Assessment to actually quantitate the risk and the risk reduction of the proposed measures that we will be publishing soon. And so I would agree with the Secretary that on the basis of science, the science is clearly laid out in the proposed rule and under a risk assessment that has undergone significant peer review by the scientific community.
So I think if the decisions are going to be based in science then I think we will have a very defensible position.
MR. ROGERS: Next question, please.
OPERATOR: Next question comes come from Kerry Young of Bloomberg.
REPORTER: Hi. I just had a question on why it's taking so long to get the revised feed ban out there.
SEC. JOHANNS: Dr. Sundlof, if you could address that?
DR. SUNDLOF: Okay, thank you again. Well, one of the reasons was -- there's actually a number of reasons. Back in January 2004 when, within a month after the first case in the U.S. was reported, the Secretary of Health and Human Services at that point made a statement that the FDA would propose modifications to the feed rule that would eliminate plate waste, poultry litter, cattle blood and require that all facilities that manufacture with ruminant meat and bonemeal be dedicated to non-ruminants and not prepare any ruminant feed in those mills.
Within a week after the Secretary's announcement, the International Review Team that was advisory to the Secretary of Agriculture made recommendations that were very much different than that which the Secretary had announced the week prior. Based on that, we decided at that point to go through an advanced notice of proposed rulemaking to get all the information out, all the recommendations that the International Review Team has made, and discuss those from a risk basis.
And as a result of that, we are now into rulemaking.
One other thing that was a reason for the delay is that during this time USDA was in the middle of their intense surveillance activity to try and determine the prevalence of BSE in U.S. cattle. And that was done, the questions that were before us were--the International Review Team based their recommendations on assumptions that there was significant infectivity in the U.S. cattle herd. The results of the USDA surveillance tend to cast doubt on that assumption, and so it had a major effect on which was the correct regulation or what were the correct measures that would be commensurate with the real risk?
So those are some of the reasons it has been delayed. It's a complicated regulation. It involves a lot of material that will have to be disposed of in some environmentally friendly way, and so we have to be very thoughtful about how we propose a rule that has minimal environmental impacts but yet does the greatest amount to reduce the actual risk to BSE in cattle.
SEC. JOHANNS: If I could just add something that obviously is very, very relevant and very important. Again, that's to point out that in the last 14 months we've tested 452,000 high-risk animals. These are the animals, that present themselves for testing, that experience would show from other countries would have the highest chance of being a BSE situation. We've had two out of that identify as positive. And both of those animals were born before the feed ban.
So it's obviously the decision, some years ago now, to impose the first generation of feed ban was the right decision.
MR. ROGERS: Next question, please.
OPERATOR: Next question comes from Sally Schuff from Feedstuffs.
REPORTER: Yes. This is Sally Schuff at Feedstuffs. Thank you for taking the question.
The question is a two-part question for Dr. Clifford and Dr. Sundlof. Dr. Clifford, you said when the second case was announced the test results were more similar to the Western blot test, was more similar to results found in France than in the United Kingdom, leading to some question about what strain of BSE she might have. My question to you is, has that been resolved yet? Do you have any more positive identification on the strain?
My question for Dr. Sundlof is, have you identified the source of the meat and bonemeal that was fed prior to the feed ban? Was it domestic or imported?
DR. CLIFFORD: This is John Clifford. I'll answer the first part. From a regulatory standpoint, this is a case of BSE. Looking from a molecular standpoint, there's further work that's being done internationally on some of these cases. And--but from our standpoint, this is a case of traditional BSE that we would find. So that's the way we're approaching this.
OPERATOR: Next question comes from Karen Robinson of Dallas Morning News.
REPORTER: Hello, this is Karen Robinson Jacobs with the Dallas Morning News. I wanted to go back to the Texas cow, and if you could tell us maybe a little more slowly how much cattle or meat from this particular index ranch got into the human food chain, how much got into the pet food chain, and how concerned should consumers be that they may have eaten something already before the test even began?
DR. CLIFFORD: This is John Clifford. I'd begin by saying if you look at what we know internationally, it's not very common at all. In fact it's rare to have more than one single case of BSE found within a herd. So from that standpoint alone, the risk is extremely small. In addition you have other safeguards in place. We have had a feed ban in place since 1997. It's been in place for 8 years, and then there's other cross-cutting protections as well from the food safety side that Dr. Ken Peterson's on if he wants to address as well.
But as far as actual poundage, I don't think it's possible for us to give you that actual number. There was two calves of interest that we traced. Due to the lack of appropriate records at the time, we actually traced 213 calves. Of those, it's estimated that 212 of those animals went into the feeding and slaughter channels. Those animals would have been slaughtered likely prior to 30 months of age, which we know that it's extremely small risk of having BSE prior to 30 months of age.
And also internationally and in the research community, while it's never been proven that offspring can get this disease through maternal transmission -- it's never been proven or disproven actually -- but it's thought very much from the international experts and the research it is extremely rare if it does happen.
Both of these calves were born very well prior to this animal being slaughtered. This animal did not show any clinical signs typical of BSE -- sampled and destroyed. This animal did not show any clinical signs or evidence of BSE which would make it even more unlikely that these two offspring would have any risk of having BSE.
The other 200 head that were traced were retraced as a result also of a lack of records. We were looking at cattle of interest over a five-year period of time of which this animal was born. Her approximate age was 12. We expanded one year of that and made her 11 to 13, and then we'd go another year beyond that. So we looked at animals basically in the age range of 10 to 15 years of age to remove those from the herd. And we traced every adult animal that we could from 1990.
Many of those animals would not even be of concern because they would not have received any feed at the time that she was in the herd or would have not been a birth cohort and born at the same time that she was.
So of those, 143 were reported as slaughtered, and we confirmed that 131 were definitely slaughtered; 34 were presumed dead, and 20 of those were untraceable. So again, we feel that the risk is extremely small. We do not feel that the public or our pet food industry should have any concerns relative to this issue.
MR. ROGERS: Next question, please.
OPERATOR: Next question comes from Chuck Abbott of Reuters.
REPORTER: Good afternoon. I'm curious -- what, Mr. Secretary, what you're going to do about the downer ban which is still now a preliminary rather than a permanent rule. When will you decide on the downer ban? How sweeping will it be? And what's going to happen to the surveillance testing program? It has run some months beyond its originally envisioned lifetime. I'll stop there.
SEC. JOHANNS: The surveillance program, as you know, was really open-ended. So I might debate with you a little bit on your last thought there. But here's what I would say. I am not prepared to bring the surveillance program to a conclusion, have not made a final decision on the downer ban. As you know, we've started now with the testing of the 20,000 healthy animals. We hope to have that done in the next 60 days.
Dating from the time of my confirmation hearing really until now, my view was to get the surveillance program in the kind of shape that we wanted, make sure that we'd touched all the bases. And then, in addition to that, do the additional testing of the 20,000 healthy animals and then, once we have all the information together, make a decision on some of those pending issues.
So that's where it's at.
MR. ROGERS: All right. I'd like to thank everyone for calling today. If you have further questions for the U.S. Department of Agriculture, you can call me, Jim Rogers, at 202-690-4755. If you have questions for the Food and Drug Administration, please contact my counterpart Ray Jones at 301-827-6246. This concludes the call for today, and I thank you all for participating.
Last Modified: 08/30/2005
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see archived url link here;
https://animalhealthreportpriontse.blogspot.com/2021/03/investigation-results-of-texas-cow-that.html
Subject: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 1)
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Wed, 31 Aug 2005 13:19:28 -0500 Content-Type: text/plain Parts/Attachments: text/plain (878 lines)
##################### Bovine Spongiform Encephalopathy #####################
From: TSS ()
Subject: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 1)
Date: August 31, 2005 at 11:08 am PST
Texas BSE Investigation
Final Epidemiology Report
August 2005
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Table of Contents
Executive Summary............................................................................................................. 3
Background of the Investigation......................................................................................... 3
BSE Response Plan .............................................................................................................. 3
Definition of At-Risk Cattle.................................................................................................... 3
Definition of Cattle of Interest ............................................................................................... 4
Definition of Feed Cohort...................................................................................................... 4
Definition of Birth Cohort...................................................................................................... 4
Definition of At-Risk Progeny................................................................................................ 4
Epidemiology Investigation of Index Herd: Farm A....................................................... 5
Background........................................................................................................................... 5
Progeny................................................................................................................................. 6
Birth Cohort ........................................................................................................................... 6
Feed Cohort ........................................................................................................................... 6
Removal of Cattle from the Index Farm............................................................................ 7
Tracing of Progeny .............................................................................................................. 7
Tracing of Birth Cohorts..................................................................................................... 8
Tracing of Cattle of Interest................................................................................................ 9
Calculation of Minimum Estimated Ages .............................................................................. 9
Trace Herds ........................................................................................................................ 10
Trace Herd 1........................................................................................................................ 10
Trace Herd 2........................................................................................................................ 10
Trace Herd 4........................................................................................................................ 11
Trace Herd 5........................................................................................................................ 11
Trace Herd 6........................................................................................................................ 11
Trace Herd 7........................................................................................................................ 12
Trace Herd 8........................................................................................................................ 12
Analysis of Data on Presumed Dead and Untraceable Animals.................................... 12
Appendix 1 – Final Trace-Out Diagram.............................................................................. 13
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Executive Summary
In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from November 2004, that had originally been classified as negative on the immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot). The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation with the Texas Animal Health Commission (TAHC), established an incident command post (ICP) and began response activities according to USDA’s BSE Response Plan of September 2004. Response personnel removed at-risk cattle and cattle of interest (COI) from the index herd, euthanized them, and tested them for BSE; all were negative. USDA and the State extensively traced all at-risk cattle and COI that left the index herd. The majority of these animals entered rendering and/or slaughter channels well before the investigation began. USDA’s response to the Texas finding was thorough and effective.
Background of the Investigation
On June 10, 2005, USDA announced that the November 2004 inconclusive BSE sample tested positive on SAF immunoblot. The SAF immunoblot was run at USDA’s National Animal Disease Center (NADC) upon the recommendation of USDA’s Office of the Inspector General. Samples were sent to a World Organization for Animal Health (OIE) reference laboratory for BSE in Weybridge, England, for confirmatory tests. Farm A, located in Texas, was the suspected farm of origin for the index cow and was placed under hold order on June 20, 2005 pending confirmation of the positive results and DNA analysis of the herd. Weybridge confirmed the BSE positive on June 24, 2005. The carcass of the index cow had been disposed of by incineration in November 2004. Cattle from several units on Farm A were bled for DNA testing (a unit is a part of the business entity of a farm. For example, a pasture on which a group resides may be a unit). Farm A was confirmed as the farm of origin for the index cow on June 29, 2005, and an ICP was established in Texas to coordinate the response. Removal of at-risk cattle from the index herd, and tracing of atrisk cattle and COI that had left the index herd, commenced immediately.
BSE Response Plan
The September 2004 BSE Response Plan outlines the necessary tracing and removal of atrisk cattle and, in some cases, COI, in response to the identification of a BSE-positive animal. Response personnel removed at-risk animals from the index farm and traced atrisk animals and COI in accordance with the response plan.
Definition of At-Risk Cattle
At-risk cattle were cattle that were confirmed to be: part of the birth cohort; part of the feed cohort; or progeny of the positive cow born within 2 years prior to the positive test. Response personnel removed at-risk cattle from the herd, euthanized them, and tested them for BSE; all were negative.
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Definition of Cattle of Interest
In many cases, at-risk cattle could not be definitively identified. Response personnel then analyzed herd inventories and herd records to identify a group of cattle that include all potential at-risk cattle and any other cattle that could not be distinguished from at-risk cattle. All of these cattle (at-risk cattle and any additional cattle as necessary) were defined as COI. COI that fell into the appropriate age range and could be part of the birth or feed cohort were removed from the herd, euthanized, and tested for BSE; all were negative.
Definition of Feed Cohort
The feed cohort consisted of all cattle which, during their first year of life, were reared with the positive animal during its first year of life and consumed the same feed during that period. In the index herd, this definition applied to cattle in any unit that were weaned and fed with calves from the other units for a short period of time and then later returned to their respective units of origin from 1991-1995 (the range of years that could have coincided with the first year of life of the index cow).
Definition of Birth Cohort
In most cases, it was impractical or impossible to definitively determine which cattle were exposed to a feed source. Accordingly, response personnel used a birth cohort to determine which cattle to consider at-risk. The birth cohort included all cattle born on the positive animal’s birth premises within 1 year before or after the BSE-positive animal’s date of birth.
Since the index cow was approximately 12 years of age, but an exact date of birth did not appear in the herd records, response personnel used a potential age range of 12 years with 1 year added to each end of that age (age 11 to 13) to sufficiently cover the most likely age range of the animal. In addition, if the positive animal moved from the birth premises to any other premises during its first year of life, all cattle of less than 1 year of age that were present on such additional premises were also considered to be at-risk. Using the age range of the index animal, all cattle born on the index premises from 1990-1995 were part of the birth cohort of the index animal.
Definition of At-Risk Progeny
Since the index cow was not confirmed to have been exhibiting clinical signs of BSE prior to her positive test results, the at-risk progeny as defined by the OIE were those offspring that were born within the 2 years prior to the positive test result. Those 2 years prior to the positive test result would have included her calves from 2002, 2003, and 2004. According to the owner, the index cow produced her last calf either in Fall 2003 or Spring 2004, and the calf prior to that was born either in Fall 2002 or Spring 2003. Tracing activities focused on these two calves as at-risk progeny.
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Epidemiology Investigation of Index Herd: Farm A
Background
The index cow was an approximately 12-year-old yellow or cream-colored Brahma cross that originated from Farm A located in Texas. The cow was sold through a livestock sale on 11/11/04, purchased by an order buyer, and was transported to a packing plant on Monday, 11/15/04. When the truck arrived at the packing plant during the late afternoon of 11/15/04, the index cow and one other were found dead on the truck and were transported to a pet food plant later that day where they were sampled for BSE testing as part of the enhanced BSE surveillance.
DNA analysis of blood samples taken from five of the six units of cattle that comprise Farm A yielded four animals from two different units that were genetically related to the index cow and confirmed Farm A as her herd of origin.
The herd on Farm A consisted of mixed breed beef cattle that are traditionally not used as seedstock replacement animals. Market records and preliminary tracing indicated that most animals that left the index herd either went to slaughter within a few days of sale or, in the case of younger animals, entered into known rendering and slaughter channels immediately following sale. There were only 11 cows identified during the investigation that were traced from Farm A into other herds where they had been used as replacement cows. The owner of Farm A raised this cow from birth and stated that the cow had never been off the premises prior to its sale. She was marketed because of poor body condition (the animal’s condition had not improved despite the early weaning of her 2003/2004 calf). The owner stated that the cow had always been excitable and had fallen while she was being loaded to go to the market, but that this was not unusual behavior for her in his opinion. In addition there was a report of this cow being down in the alley at the livestock market on 11/11/04, but she apparently got up again and was able to be loaded onto the truck to go to the packing plant. When questioned about any previous history of neurological signs in cattle on the farm, the owner reported that no cattle on the farm had ever shown any neurological signs, nor had there been any cases of rabies on the index farm.
Index Herd Census
Farm A consisted of 6 units (Units A through F) containing a total of about 217 adult cattle and approximately 100 to 120 calves. Early in the investigation, response personnel discovered that an additional unit belonging to the owner’s son and located adjacent to Unit F could also contain COI. This group, Unit G, contained 16 adult cattle and made a seventh unit that became included in the investigation.
On 6/22/05, the first three of the original six units were sampled for DNA testing to confirm the herd of origin of the index cow. Those first three units consisted of: Unit A contained 62 head with some older cattle (more likely than the other units to provide a DNA match); Unit B with 28 head (3-year-old unit); and Unit C with 25 head (2-year-old unit). Two additional units were sampled for DNA on 6/23/05; Unit D with 31 head and Unit E with 30 head, both of which contained older animals.
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The sixth unit, Unit F, containing 41 head, was purchased in 1993 from another source. Because it did not have animals that were genetically related to the other 5 units, this unit was not sampled for DNA testing. Unit F, and adjacent Unit G, contained COI because the weaned heifers from those units were commingled and fed with weaned heifers from the other units for a short period of time before they were returned to their respective units of origin. This practice of weaning and feeding together fit the definition of a feed cohort.
Progeny
The owner did keep some replacement heifers and, although he was relatively sure that he had not kept any offspring from the yellow cow because of her excitable demeanor, DNA analysis of the herd revealed several animals in the herd that may have been older offspring of the index cow. While the owner sold 12 calves at the sale with the index cow on 11/11/04, her last calf was not in that group. According to the owner, the index cow’s last calf was born either in Fall 2003 or Spring 2004, weaned early, and sold through the livestock market some time between February and October 2004. The calf prior to that would have been born either in Fall 2002 or Spring 2003 and was sold at the livestock market sometime between January and December 2003.
Birth Cohort
The owner of Farm A kept very few herd records; this made finding documentation on this cow’s birth cohort difficult. The birth cohort, by definition, included all cattle born on the positive animal’s birth premises within 1 year, before or after, the positive animal’s date of birth. The index cow was approximately 12 years of age in November 2004, but there was no exact birth date in the herd records. A potential age range of 11 to 13 years was used to sufficiently cover the animal’s most likely age. Using this range, all cattle born on the index premises between 1990 and 1995 were considered part of the birth cohort. In lieu of the owner’s records, herd records from Veterinary Services’ Generic Database (GDB) were used to compile a list of brucellosis calfhood vaccination (CV) tag numbers from the index herd that corresponded to animals to be included in the birth cohort. There were 121 animals identified through GDB as having been calfhood vaccinated on the index farm between 1991 and 1994. The owner of Farm A did not calfhood vaccinate after 1994. Moreover, calfhood vaccinates include only heifers. Therefore, the list of 121 animals was not a complete list of all birth cohorts. However the tracing that response personnel conducted on other COI was designed to account for the remainder of the birth cohorts.
Feed Cohort
Animals in Units A, D, and E, that were weaned and fed with the positive cow between 1991-1995, were already considered at-risk as part of the defined birth cohort. Animals in Units B and C were 3-year-olds and 2-year-olds, respectively, and were too young to be either birth or feed cohorts. Although Unit F was purchased separately and did not contain animals genetically related to the other units, calves from Unit F were weaned and fed for a short period of time with weaned calves from other units and all calves were later returned to their respective units of origin. Since Unit F was not purchased until 1993, the feed cohort consisted of those animals in Unit F that could have been weaned and fed with the index cow in 1993 or 1994. Additionally, Unit G contained possible feed cohorts that could have been weaned and fed with the index cow between the years of 1991 and 1995.
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Feed
The feeding regimen for the cattle in this herd consisted of natural pasture, hay, mineral supplement, syrup tubs occasionally, and a breeder’s supplement (predominantly a name brand manufactured breeder’s cube). The Food and Drug Administration (FDA) investigated all sources of feed and supplements used on Farm A. In-depth investigations and site visits were conducted by FDA involving retail feed stores, feed manufacturers, slaughter plants, renderers, and brokers. A more detailed account of the investigation is contained in FDA’s final report.
Removal of Cattle from the Index Farm
Any animal still present within the index herd that could have been a possible birth cohort or feed cohort of the index cow was targeted for removal as an at-risk animal. Units A, D, E, F, and G, all of which were known to contain older animals, were inventoried. Identification tags, tattoos, and brands were recorded, and all animals were aged based on their dentition and any man-made identification. Cattle whose estimated age indicated that they could have been part of the index cow’s birth or feed cohort were removed from the herd, euthanized, and tested for BSE; all were negative.
Units B and C were exempt from the cohort removal process because they contained only 3-year-old and 2-year-old animals respectively. Although the DNA analysis of animals in Units A through E determined that there were 2 animals present that could have been offspring of the index cow, their estimated age by dentition revealed that they were not of the appropriate age to be at-risk progeny. This verified the owner’s claim that he had sold the index cow’s last two calves at the livestock market and they were not currently present in the index herd.
After sorting by age, response personnel identified and removed the following numbers of cows from the herd on 7/6/05: Unit A, 11 cows; Unit D, 11 cows; Unit E, 7 cows. The same process was applied to Units F and G and the following numbers of cows were identified and removed from the herd on 7/7/05: Unit F, 28 cows; Unit G, 10 cows. Of the 67 animals removed from the herd as possible birth cohorts and/or feed cohorts of the index cow, 42 were definitively identified as belonging to the birth cohort due to the presence of a calfhood vaccination tag or tattoo that corresponded to the appropriate birth cohort years. All 67 animals were euthanized on 7/6/05 and 7/7/05 and samples were subsequently sent to USDA’s National Veterinary Services Laboratories (NVSL) for BSE testing. All samples were run on the ELISA test and confirmed negative on 7/8/05 and 7/9/05. Upon confirmation of negative results, disposal of carcasses was completed by burial in an approved landfill facility. The index farm was released from hold order on 7/11/05.
Tracing of Progeny
The 2003/2004 progeny of the index cow was known to have left the farm through a specific livestock market sometime between February and October 2004. The 2002/2003 progeny of the index cow left the farm through the same market sometime between January
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and December 2003. Response personnel learned early in the investigation that animals from the index farm were sold not only under the index farm owner’s name and that of his wife, but also by other members of the owner’s immediate family. Additionally, there were no herd records to indicate the gender of the two at-risk progeny. Therefore, market records for February through October 2004 and January through December 2003 were obtained for all calves sold both by Farm A’s owner and by members of his immediate family; response personnel traced all such calves to determine their disposition. With the index herd being composed of mixed breed beef cattle, the calves that left the farm were genetically unsuitable for use as replacement animals or for sale as breeding stock, a fact that was confirmed by the trace work and the documentation of the final disposition of the calves of interest.
Response personnel ultimately identified 213 calves of interest to be traced. Of these, 208 were confirmed to have entered known rendering/slaughter channels, 4 were presumed to have entered rendering/slaughter channels, and 1 was purchased in cash through a livestock market with no buyer name or contact information (this animal was classified as untraceable. See Appendix 1). A calf was categorized as presumed to have entered rendering/slaughter channels if it passed through at least one livestock market subsequent to its original sale and could not be individually traced due to unknown resale date and new backtag, but all calves resold matching that description during an appropriate date range were purchased by known rendering/slaughter order buyers.
It was not possible to DNA test the calves that entered known rendering and slaughter channels – most were of an age in which they were likely to have been slaughtered prior to the time of the investigation. There were no calves traced to farms outside of rendering and slaughter channels.
Tracing of Birth Cohorts
Since there were essentially no records maintained on the index farm, it was necessary to compile the list of known birth cohorts using brucellosis CV tag numbers for this herd from the period 1991 to 1994. The calves vaccinated during that time period were part of the index cow’s birth cohort and tracing activities centered on finding those animals. There were 121 animals whose CV tag number and/or tattoo included them as part of the birth cohort. Of those 121 animals, 67 animals were definitively accounted for (42 were found in the index herd, removed, and tested BSE negative; 25 were identified as having left Farm A through the market system and were traced, 11 of those were reported slaughtered, 13 were classified as presumed dead, and 1 was found alive, euthanized, and tested BSE negative). Of the remaining 54 animals from the birth cohort, there may have been several that died within the index herd, but the majority likely left the herd without identification and would have been either re-tagged at the livestock market or consigned directly to slaughter without identification. To account for these remaining birth cohorts, all adult cattle that left the index farm since 1990 were traced as COI.
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Tracing of Cattle of Interest
The investigation revealed that many animals left Farm A, arrived at markets without any identification tags, and were subsequently re-tagged at the market. Due to lack of farm records, it is unknown which of these re-tagged animals may have belonged to the birth cohort. As a result, all animals that may have left Farm A since 1990 were traced as COI. Additionally, animals from the index farm were sold not only under the index farm owner’s name and that of his wife, but also by other members of the owner’s immediate family; therefore, cattle sold from the index farm by all pertinent family members were traced. There were some older animals that left the index farm but were able to be excluded from further trace work because they were known not to have been part of the birth cohort or feed cohort of the index cow despite their being of the appropriate age. The index farm owner’s late father had maintained a herd of cattle separate from the index farm but which was added to the index farm in 1997. Complete herd test data and CV data from the GDB was obtained for the father’s herd and those animals were excluded from the tracing activities.
There were a total of 200 COI traced: 143 were reported to have been slaughtered (131 of those were confirmed as having been slaughtered), 1 is known to have died previously and was buried, 2 were found alive (1 was a known birth cohort that tested negative, 1 was determined not to be one of the cattle of interest due to her young age), 34 were classified as presumed dead, 20 were classified as untraceable. (See Appendix 1). Animals were confirmed at slaughter using GDB slaughter testing data or the hard copies of slaughter testing Form 4-54.
An animal was classified as presumed dead if records that could be used to advance the tracing of the animal were exhausted or did not exist, and the age of the animal at the time of the investigation was estimated to be at least 11 years old or older. Since the index herd was not a purebred or seedstock operation, and animals leaving the herd were unlikely to be purchased as replacement cattle, standard industry practices indicated that most adult animals that had left the herd would have been culled and slaughtered by the time they were in this age group. Additionally, this age cutoff was arrived at through review of market records and the specific years in which Farm A sold cattle through the market. An animal was classified as untraceable if all records to advance the tracing of the animal were exhausted or did not exist, and the age of the animal at the time of the investigation was estimated to be less than 11 years of age (the animal, therefore, could not be presumed dead).
Calculation of Minimum Estimated Ages
Throughout the tracing process, personnel used minimum estimated ages of the 200 COI to evaluate whether those individuals could be old enough to be part of the birth or feed cohort of the index cow. Since Farm A’s owner maintained no records on the ages of animals, GDB data assisted in assigning minimum estimated ages. Animals that were wearing brucellosis CV eartags could be aged quite accurately because the exact CV date was recorded in the GDB and those animals would have been vaccinated between 4 to 12 months of age. The GDB also contained lists of individual eartags for all animals on the
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index farm that were included in complete herd brucellosis testing in 1991, 1993, and 1994. Cattle included in those herd tests would have been at least 18 months of age at the time of the test and their minimum age today could be extrapolated from that data. Finally, the GDB also contained livestock market testing data that could also be used to assign a minimum age because the animal would have been at least 18 months of age on date the earliest brucellosis market test was conducted. The minimum ages calculated for the cattle of interest were used later in an analysis by USDA’s Centers for Epidemiology and Animal Health (CEAH) to determine the probable disposition of untraceable and presumed dead animals based on their age.
Trace Herds
Response personnel made every attempt to trace COI to their final dispositions (which, in most cases, was slaughter). If an animal was traced to a herd owner and the owner could not provide information that indicated that the animal of interest was not currently present within his/her herd, the owner’s herds were placed under hold order pending a herd inventory to determine whether or not the animal of interest had been retained. There were eight herds identified as the last traceable location of the animal of interest and were, therefore, subjected to herd inventories in an attempt to locate the animal.
When an animal of interest was located within a herd, the age of the animal was estimated using dentition and any man-made identification. If the animal fell into the appropriate age range to be a possible birth cohort or feed cohort of the index cow, the animal was removed from the herd and tested. If an animal of interest was located within the herd and fell into the appropriate age range to be a possible at-risk progeny of the index cow, the animal was sampled for DNA testing.
Trace Herd 1
The owner of Trace Herd 1 was identified as having received one of the adult COI from the index herd. Trace Herd 1 contained 909 head of cattle in multiple pastures and was placed under hold order on 7/21/05. Upon completion of herd inventory, the animal of interest was not found within the herd. A GDB search of all recorded herd tests conducted on Trace Herd 1 and all market sales by the owner failed to locate the identification tag of the animal of interest and she was subsequently classified as untraceable. The hold order on Trace Herd 1 was released on 8/8/05.
Trace Herd 2
Trace Herd 2 was identified as having received one of the adult COI from the index herd. Trace Herd 2 contained 19 head of cattle on one pasture and was placed under hold order on 7/25/05. The owner of Trace Herd 2 identified the animal of interest by her eartag while he was feeding his cattle out of a bucket and individually penned her for inspection by field personnel. While the cow was identified as one of the animals that had left the index farm, her age by dentition was estimated to be only 5 years old, which was too young to have placed her as part of the birth or feed cohort of the index animal. She was classified as found alive but determined not to be one of the COI; the hold order on Trace Herd 2 was released on 7/26/05.
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Trace Herd 3
The owner of Trace Herd 3 was identified as possibly having received an animal of interest. The herd was placed under hold order on 7/27/05. The herd inventory was conducted on 7/28/05. The animal of interest was not present within the herd, and the hold order was released on 7/28/05. The person who thought he sold the animal to the owner of Trace Herd 3 had no records and could not remember who else he might have sold the cow to. Additionally, a search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. The animal of interest traced to this herd was classified as untraceable because all leads were exhausted.
Trace Herd 4
The owner of Trace Herd 4 was identified as having received one of the COI through an order buyer. Trace Herd 4 was placed under hold order on 7/29/05. A complete herd inventory was conducted on 8/22/05 and 8/23/05. There were 233 head of cattle that were examined individually by both State and Federal personnel for all man-made identification and brands. The animal of interest was not present within the herd. Several animals were reported to have died in the herd sometime after they arrived on the premises in April 2005. A final search of GDB records yielded no further results on the eartag of interest at either subsequent market sale or slaughter. With all leads having been exhausted, this animal of interest has been classified as untraceable. The hold order on Trace Herd 4 was released on 8/23/05.
Trace Herd 5
The owner of Trace Herd 5 was identified as having received two COI and was placed under hold order on 8/1/05. Trace Herd 5 is made up of 67 head of cattle in multiple pastures. During the course of the herd inventory, the owner located records that indicated that one of the COI, a known birth cohort, had been sold to Trace Herd 8 where she was subsequently found alive. Upon completion of the herd inventory, the other animal of interest was not found within the herd. A GDB search of all recorded herd tests conducted on Trace Herd 5 and all market sales by the owner failed to locate the identification tag of the animal of interest and she was subsequently classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 5 was released on 8/8/05.
Trace Herd 6
The owner of Trace Herd 6 was identified as possibly having received an animal of interest and was placed under hold order on 8/1/05. This herd is made up of 58 head of cattle on two pastures. A herd inventory was conducted and the animal of interest was not present within the herd. The owner of Trace Herd 6 had very limited records and was unable to provide further information on where the cow might have gone after he purchased her from the livestock market. A search of GDB for all cattle sold through the markets by that individual did not result in a match to the animal of interest. Additionally, many of the animals presented for sale by the owner of the herd had been re-tagged at the market effectually losing the traceability of the history of that animal prior to re-tagging. The animal of interest traced to this herd was classified as untraceable due to all leads having been exhausted. The hold order on Trace Herd 6 was released on 8/3/05.
12
Trace Herd 7
The owner of Trace Herd 7 was identified as having received an animal of interest and was placed under hold order on 8/1/05. Trace Herd 7 contains 487 head of cattle on multiple pastures in multiple parts of the State, including a unit kept on an island. The island location is a particularly rough place to keep cattle and the owner claimed to have lost 22 head on the island in 2004 due to liver flukes. Upon completion of the herd inventory, the animal of interest was not found present within Trace Herd 7. A GDB search of all recorded herd tests conducted on Trace Herd 7 and all market sales by the owner failed to locate the identification tag of the animal of interest. The cow was subsequently classified as untraceable. It is quite possible though that she may have died within the herd, especially if she belonged to the island unit. The hold order on Trace Herd 7 was released on 8/8/05.
Trace Herd 8
Trace Herd 8 received an animal of interest, which happened to be a known birth cohort of the index cow, from Trace Herd 5. Trace Herd 8 consists of 146 head of cattle that were placed under hold order on 8/4/05. A herd inventory was conducted, the birth cohort was found alive in the herd, and she was purchased and euthanized. The hold order on Trace Herd 8 was released on 8/4/05. The cow was sampled on 8/5/05 and BSE tested by ELISA at NVSL. Results were negative (as reported on 8/6/05); carcass disposal was completed by alkaline digestion.
Analysis of Data on Presumed Dead and Untraceable Animals
CEAH performed an analysis of the minimum estimated ages of those COI that were classified as either presumed dead or untraceable to determine the likely disposition of those animals based on their ages. Moreover, CEAH performed an analysis of the likely disposition of the one calf that was classified as untraceable during the investigation.
13
Appendix 1 – Final Trace-Out Diagram
http://www.aphis.usda.gov/lpa/issues/bse/epi-updates/bse_final_epidemiology_report.pdf
see archived url link;
TSS
#################### https://lists.aegee.org/bse-l.html ####################
Subject: Re: Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Tue, 30 Aug 2005 13:34:30 -0500 Content-Type: text/plain Parts/Attachments: text/plain (735 lines)
##################### Bovine Spongiform Encephalopathy #####################
THE FONG EFFECT OR THE FONG SYNDROME
Friday, July 29, 2005
Ames lab to take over testing for mad cow disease Published: 07/29/2005 3:52 PM
By: Associated Press - Associated Press
AMES, IA - Scientists at the National Veterinary Services Laboratories here soon will begin conducting their own Western blot tests, eliminating the need to travel to Weybridge, England, when initial rapid testing detects mad cow disease.
"I think the change is good because we're more likely to know exactly what we're dealing with on each case," said Dr. Randall Levings, director of the labs.
The change is a response to an order from U.S. Agriculture Secretary Mike Johanns.
"We took those as our marching orders," Levings said.
Mad cow disease, formally known as bovine spongiform encephalopathy, or BSE, attacks a cow's nervous system. It is characterized by spongelike holes in the brain, the result of misshapen proteins called prions that kill brain cells.
The only way it is known to spread is by cattle eating infected brain and nerve tissue from other cows. That's why the government in 1997 banned the use of cattle feed that contains remnants of other cows. Of the three cases of mad cow confirmed in the United States, all three cows were born before the feed ban, Levings said.
Since January 2004, the government has tested more than 400,000 cows for the disease, using a rapid screening test and a test known immunohistochemistry, or IHC.
Rapid testing of a sample involves removing normal proteins and adding chemicals that bind to the abnormal proteins, making them visible. The IHC test involves staining paper-thin brain tissue samples to highlight the abnormal protein.
The Western blot test, conducted at Weybridge destroys normal proteins in the brain, leaving only the abnormal prions.
In June, the nation's Office of Inspector General ordered a review of the Ames lab's testing procedures after a sample last fall tested positive in England, but negative in Ames.
A rapid test on the sample in Ames detected the presence of BSE, but the following IHC test was negative. Ames workers also relayed the results of the test, but did not complete formal paperwork.
A version of mad cow disease, known as variant Creutzfeld-Jakob, has killed about 150 people worldwide, most of them in Britain, where there was an outbreak in the 1990s.
"We're taking all of the right steps," Levings said. "It would not be a risk to human or animal health in this country. It's not high. It's very, very low."
http://www.crgazette.com/2005/07/29/Home/News/madcowtesting.htm
SO, Johann's/GW et al have perfected the BSE/TSE testing protocols and they don't need anyone else to tell them what to do. this was proven with the TEXAS mad cow cases alone, r i g h t...... $$$ IF this is the case, why is Weybridge having to confirm our inconclusives ??? this is frightening.
IF not for the Honorable Phyllis Fong, that cow would have never been proven positive, well, documented anyway, it was proven positive time and time again...
The Fong Syndrome strikes again.
GW's BSE/TSE MRR policy a recipe for disaster.
USA in dire straights.
God help us... TSS
No Sacred Cows: Phyllis Fong Takes on the Beltway and Mad Cow Disease News Report, AsianWeek Staff Report, Asian Week, Jul 06, 2005
Newly appointed Agriculture Secretary Mike Johanns appears to be headed for a showdown with veteran Inspector General Phyllis K. Fong for ordering new tests for mad cow disease in the nation’s beef supply.
Since the tests Fong ordered have returned positive, several countries have once again stopped buying U.S. beef, provoking uproar in the cattle industry.
Reacting to industry pressure, Johanns now claims Fong requested the tests without his knowledge or approval and added: “It caught me by surprise, to be very honest with you. I believe the secretary should be involved in all decisions of this significance.”
Fong, the senior officer of the Inspector General’s office of the USDA was sworn in on December 2, 2002 after serving as Inspector General for the Small Business Administration. Like Johanns, she is appointed by the president and confirmed by the Senate. The Inspector General’s office is an independent arm of the department that performs audits and investigations.
When she ordered the re-testing of the latest case, she issued a statement saying she was also probing “the performance of [laboratories] in complying with procedures for conducting tests.” With the cow that was suspected of having the disease, she reported: “Auditors noted an unusual pattern of conflicting test results on one sample.”
The Veterinary Laboratories Agency in Weybridge, England, an outside testing agency, confirmed that a sample from an animal in November 2004 tested positive for bovine spongiform encephalopathy, or mad cow disease.
Yet Johanns, who took the reins of the Agriculture Department early this year in a Bush cabinet shake-up, insists that Fong has overstepped her bounds. “I was asked by the Senate and the president to operate the department,” Johanns said. “She could recommend; she could strongly urge. But then the question is whether it’s an operational decision.”
He reportedly learned of Fong’s order from his chief of staff after the new testing was already under way. He charges that it’s up for debate whether Fong had the authority to order the new tests, and asserts: “It’s my domain.”
This is not the first time Fong has found herself in the eye of the storm.
After allegations of misconduct arose in the handling of the first cow with mad cow disease, Fong launched a criminal investigation.
“Currently we are investigating allegations surrounding the actual state of the diseased cow before it went to slaughter,” Fong testified last year before the House subcommittee on agriculture appropriations. “So that’s a criminal investigation that’s open, ongoing, active and it’s focused on that issue.”
Fong’s investigation concluded that there was no criminal negligence, but in July she released an audit of the USDA’s testing program and concluded it had serious flaws that could undermine its credibility and lead to questionable estimates of how widespread the disease is in America.
Fong recently re-opened investigations started during the administration of Johanns’ predecessor, Ann Veneman. Veneman began a reform push on testing U.S. beef, but her efforts eventually ran aground amid battles between competing interests, including the beef industry, scientists and consumer activists.
The two behind-the-scenes audits follow complaints by several cow-state senators over policies and procedures in testing for mad cow disease.
Fong said in a statement that “our field work is ongoing” with results expected “late this summer.”
USDA’s Top Cop
As a young girl, Phyllis Fong had a hankering for the law. Those interests began in her childhood, kindled by her father.
“When I was growing up, I remember searching, as all kids do, for a career path that matched my talents,” she said in an article for the USDA. “And my father said to me, at one point in high school, that he really thought law school would be right for me, that I would be a tremendous lawyer. I had never thought about that as an option.”
Fong’s family had emigrated from Hawai‘i to China generations before, in the mid-1800s. Unlike a lot of APA families who insist that the children follow in the family business, Fong recalls, “He was a doctor and yet he did not suggest I go into medical school. I think he was tired of my arguing with him about everything!”
“I had a wonderful experience growing up. They call Hawai‘i a melting pot because of its multi-racial and multi-cultural society. I always felt that everyone there had the opportunity to become anything. It didn’t matter what color, what sex, what race, what ethnic heritage you were, if you were interested in something you could pursue it,” she said.
An unusual route led to her toward the senior job as USDA’s Inspector General. After studying Asian studies and finishing her law degree, she intended to become an international lawyer specializing in trade and immigration.
But when Fong arrived in Washington, D.C., she got a job with the U.S. Civil Rights Commission, which at the time was studying immigration policy. One thing led to another, and a colleague who was the Inspector General at the U.S. Small Business Administration asked her to become her special assistant
“I realized this was a good opportunity. Who can be against going after fraud and abuse? Who can be against economy and efficiency in government?” Fong has been in the field ever since, and oversees about 600 employees divided almost evenly between investigators and auditors.
Name: Phyllis K. Fong
Salary: $136,900
Position: Inspector General, USDA. She’s responsible for conducting and supervising audits and evaluations, as well as investigations and law enforcement efforts.
Birthplace: Philadelphia, Pennsylvania
Family: Married, two daughters, ages 4 and 7
Education: BA degree in Asian Studies, Pomona College; Juris Doctorate, Vanderbilt University School of Law
Past Experience: She was Inspector General of the U.S. Small Business Administration from 1999-2002 after holding several positions with the SBA, including Assistant Inspector General for Management and Legal Counsel and Assistant Inspector General for Management and Policy. In the early 1980s, she had served as assistant general counsel for the Legal Services Corporation and, before that, as an attorney with the U.S. Commission on Civil Rights.
Hobbies/Interests: Needlepoint
Priorities: “To instill the message within USDA that OIG’s mission is not just to audit and investigate. Our mission is to work in partnership with the Department to manage programs more effectively and deal with fraud and abuse.”
The Associated Press and USDA contributed to this report.
http://news.pacificnews.org/news/view_article.html?article_id=67ea9860e23ed4 d55409d8d845e3b40b
Subject: Re: USDA/APHIS JUNE 2004 'ENHANCED' BSE/TSE COVER UP UPDATE DECEMBER 19, 2004 USA
Date: Thu, 30 Dec 2004 12:27:06 -0600
From: "Terry S. Singeltary Sr.
BSE-L
snip...
OH, i did ask Bio-Rad about this with NO reply to date;
-------- Original Message --------
Subject: USA BIO-RADs INCONCLUSIVEs
Date: Fri, 17 Dec 2004 15:37:28 -0600
From: "Terry S. Singeltary Sr."
@bio-rad.com
Hello and Bio-Rad,
Happy Holidays!
I wish to ask a question about Bio-Rad and USDA BSE/TSE testing and there inconclusive. IS the Bio-Rad test for BSE/TSE that complicated, or is there most likely some human error we are seeing here?
HOW can Japan have 2 positive cows with No clinical signs WB+, IHC-, HP- , BUT in the USA, these cows are considered 'negative'?
IS there more politics working here than science in the USA?
What am I missing?
-------- Original Message --------
Subject: Re: USDA: More mad cow testing will demonstrate beef's safety
Date: Fri, 17 Dec 2004 09:26:19 -0600 From: "Terry S. Singeltary Sr."
snip...end
Experts doubt USDA's mad cow results
snip...END
WELL, someone did call me from Bio-Rad about this, however it was not , but i had to just about take a blood oath not to reveal there name. IN fact they did not want me to even mention this, but i feel it is much much to important. I have omitted any I.D. of this person, but thought I must document this ;
Bio-Rad, TSS phone conversation 12/28/04
Finally spoke with ;
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email: XXXXXXXXXXXXXXXXXX
at approx. 14:00 hours 12/28/04, I had a very pleasant phone conversation with XXXX XXXXX about the USDA and the inconclusive BSE testing problems they seem to keep having. X was very very cautious as to speak directly about USDA and it's policy of not using WB. X was very concerned as a Bio-Rad official of retaliation of some sort. X would only speak of what other countries do, and that i should take that as an answer. I told X I understood that it was a very loaded question and X agreed several times over and even said a political one.
my question;
Does Bio-Rad believe USDA's final determination of False positive, without WB, and considering the new atypical TSEs not showing positive with -IHC and -HP ???
ask if i was a reporter. i said no, i was with CJD Watch and that i had lost my mother to hvCJD. X did not want any of this recorded or repeated.
again, very nervous, will not answer directly about USDA for fear of retaliation, but again said X tell me what other countries are doing and finding, and that i should take it from there. "very difficult to answer"
"very political"
"very loaded question"
outside USA and Canada, they use many different confirmatory tech. in house WB, SAF, along with IHC, HP, several times etc. you should see at several talks meetings (TSE) of late Paris Dec 2, that IHC- DOES NOT MEAN IT IS NEGATIVE. again, look what the rest of the world is doing.
said something about Dr. Houston stating;
any screening assay, always a chance for human error. but with so many errors (i am assuming X meant inconclusive), why are there no investigations, just false positives?
said something about ''just look at the sheep that tested IHC- but were positive''. ...
TSS
-------- Original Message --------
Subject: Your questions
Date: Mon, 27 Dec 2004 15:58:11 -0800
From: To: flounder@wt.net
Hi Terry:
............................................snip
Let me know your phone number so I can talk to you about the Bio-Rad BSE test. Thank you
Regards
Bio-Rad Laboratories 2000 Alfred Nobel Drive Hercules, CA 94547 Ph: 510-741-6720 Fax: 510-741-5630 Email:
=================================
snip...end...TSS
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
To: paffairs@oig.hhs.gov, HHSTips@oig.hhs.gov, contactOIG@hhsc.state.tx.us
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box , Bacliff, Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to:
Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results
posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS
Date: June 14, 2005 at 1:46 pm PST In
Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced.
June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns.
Three days later same mad cow found in November turns out to be positive.
Both resignation are unexpected.
just pondering... TSS
MAD COW IN TEXAS NOVEMBER 2004. ...TSS
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update?
I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
terry
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 –0600
From: Carla Everett
To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas.
Carla At 09:44 AM 11/19/2004, you wrote:
>Greetings Carla,
>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from
>TEXAS. can you comment on this either way please?
>>thank you,
>Terry S. Singeltary Sr.
>>
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett
To: "Terry S. Singeltary Sr."
References: ...sniptss
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something. At 06:05 PM 11/22/2004,
you wrote:
>why was the announcement on your TAHC site removed?
>>Bovine Spongiform Encephalopathy:
>November 22: Press Release title here
>>star image More BSE information
>>>>terry
>>Carla Everett wrote:
>>>no confirmation on the U.S.' inconclusive test...
>>no confirmation on location of animal.>>>>>>
==========================
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update? I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
terry
==============================
Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 21:07:51 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett
References: <419E14E2.5040104@wt.net> <6.0.0.22.2.20041119113601.02682730@tahc.state.tx.us> <41A2724F.3000901@wt.net> <6.0.0.22.2.20041122174504.02796d38@tahc.state.tx.us> <41A27EBC.4050700@wt.net> <6.0.0.22.2.20041122183204.02801d88@tahc.state.tx.us>
ok, thank you Carla. i hate rumors and 'inconclusive' announcements. kind regards, terry Carla Everett wrote:
> our computer department was working on a place holder we could post
> USDA's announcement of any results. There are no results to be
> announced tonight
> by NVSL, so we are back in a waiting mode and will post the USDA
> announcement
> when we hear something.
> > > At 06:05 PM 11/22/2004, you wrote:
> >> why was the announcement on your TAHC site removed?
>> >> Bovine Spongiform Encephalopathy:
>> November 22: Press Release title here
>> >> star image More BSE information
>> >> >> >> terry
>> >> Carla Everett wrote: no confirmation on the U.S.' inconclusive test...
>>> no confirmation on location of animal.
I still want my Texas mad cows confirmed BY WB! TSS
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 21:07:51 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett
References: <419E14E2.5040104@wt.net> <6.0.0.22.2.20041119113601.02682730@tahc.state.tx.us> <41A2724F.3000901@wt.net> <6.0.0.22.2.20041122174504.02796d38@tahc.state.tx.us> <41A27EBC.4050700@wt.net> <6.0.0.22.2.20041122183204.02801d88@tahc.state.tx.us>
ok, thank you Carla. i hate rumors and 'inconclusive' announcements.
kind regards, terry
Carla Everett wrote:
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.
At 06:05 PM 11/22/2004, you wrote:
why was the announcement on your TAHC site removed?
Bovine Spongiform Encephalopathy: November 22: Press Release title here star image More BSE information
terry
Carla Everett wrote:
no confirmation on the U.S.' inconclusive test... no confirmation on location of animal.
I still want my Texas mad cows confirmed BY WB!
TSS
see archived url link
http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/08/0339.xml
see archived ulr link
http://www.usda.gov/documents/vs_bse_ihctestvar.pdf
archived url link
http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0217.xml
see archived BSe here;
USDA regulations, any cow that exhibits signs of central nervous system (CNS)
According to a 1997 Animal and Plant Health Inspection Service (NHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "it is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
May 13,2004
Page 2
snip...
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:
http://democrats.oversight.house.gov/images/stories/documents/20040607142914-86912.pdf
see archived url link;
48 HOUR BSE TEST TURN AROUND TURNS INTO ALMOST A YEAR, from Nov. 2004 when Texas TAHC first announced BSE postive, then took it back, and then almost one year later, Nov. 2005, a final BSE positive confirmation was announced, after only scientist around the globe, and literally an act of Congress took place by the Honorable Fong order the sample retested. ...Thank YOU!
http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0218.xml
archived BSe link
http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0206.xml
see archived link
see more BSe MRR policy wrangling...this whole time of this suspect BSE sample, imo, was to set in place the BSE MRR, from the BSE GBRs...imo...terry
ONE YEAR LATER, finally confirmed $$$
Release No. 0233.05 Contact: USDA Press Office (202) 720-4623
Printable version Email this page
TRANSCRIPT OF MEDIA CONFERENCE WITH REMARKS MADE BY AGRICULTURE SECRETARY MIKE JOHANNS, DR. JOHN CLIFFORD, CHIEF VETERINARY OFFICER, ANIMAL PLANT HEALTH INSPECTION SERVICE, AND DR. DANNY MATTHEWS, TSE PROGRAM MANAGER, VETERINARY LABORATORIES AGENCY, WEYBRIDGE, ENGLAND - WASHINGTON D.C. - JUNE 24, 2005
SNIP...
"So let me start first with the test results. As you are aware, last November we had an inconclusive report from a rapid screening test. USDA then conducted two IHC confirmatory tests, and both came out negative. A few weeks ago an additional confirmatory test was conducted, and that test is referred to as the Western blot test.
"On June 10 I learned that test was reactive and shared those results at that time.
"We now have the test results from the lab in Weybridge, England, as well as the results from additional testing in our own lab, and again I am here today to share those results with you.
"The results confirm the presence of BSE in this animal, an animal that was blocked from entering the food supply thanks to the firewalls that are in place. It is critically important to note that this animal was identified as a high risk animal. A sample was taken, and the carcass was incinerated.
http://www.usda.gov/wps/portal/usda/usdahome?contentidonly=true&contentid=2005/06/0233.xml
archived url link
-------- Original Message --------
Subject: RE: Greetings again Professor Aguzzi ... TSS
Date: Fri, 11 Mar 2005 09:19:49 +0100
From: "Adriano Aguzzi" T o: "'Terry S. Singeltary Sr.'"
Dear Mr. Singeltary
I sympathize with your wish to have the most sensitive assay implemented. However, the situation is not as simple as one might think. In the case of homogeneously distributed agent, biochemical detection of PrPSc is indeed likely to be more sensitive than immunohistochemistry. In the case of variegated, punctate distribution of the agent, morphological methods may indeed be an asset.
There are also issues of feasibility. In my laboratory, we routinely run phosphotungstic acid precipitation followed by Western blotting. However, this is an extraordinarily cumbersome procedure. The sensitivity is increased vastly, but the amount of work needed is also amazing. There is no way I could see our own procedure implemented for mass screening of millions of cows - unless one would draft a veritable army of laboratory technicians.
For all these reasons, while I see all your points, I feel unable to offer a strong public opinion in favor or against any specific methods. The final decision needs to take into account a variety of complex factors, and that is why I believe that it is best left to a panel of experts rather than to a public discussion.
Best regards Adriano Aguzzi
____________________________
Prof. Adriano Aguzzi (MD PhD hc FRCP FRCPath) Institute of Neuropathology, University Hospital of Zürich Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland Tel. ++41-1-255 2107 Tel. (direct line): 2869 Fax: ++41-1-255 4402, cellular: +41-79-320 1516 http://www.unizh.ch/pathol/neuropathologie/
-----Original Message-----
From: Terry S. Singeltary Sr. [mailto:flounder@wt.net] ;
Sent: Thursday, March 10, 2005 20:18
To: adriano@pathol.unizh.ch
Subject: Greetings again Professor Aguzzi ... TSS
Greetings again Professor Aguzzi,
A kind greetings from Texas. I hope you do not mind, but I must ask you several questions that will put you in the hot seat. Someone with credibility must come forward, such as yourself and speak out about the fact of the non scientific approach that USDA et al has take after the first diagnosis of BSE in the USA. This being, the refusal to use Western Blot on any suspicious or inconclusive BSE/TSE test. IHC is like a brain biopsy on trying to diagnose a CJD case. IF you take the sample from a part of the brain that is not that tainted, you will not get a reading. WB is much more sensitive, especially now with the Phospohtugstic acid precipitation step. IF Prusiners CDI was validated, who knows, that might even be more sensitive. Bottom line, we need you to come forward and state publicly ''the facts'' about USDA et al decision not to use WB on not only questionable samples, but on ALL samples. would you be willing to comment on this, to me or someone from the media (under the understanding it will be for the public)? I have several questions for you??? This is very very important in terms of human health (i.e. that nov. pos. pos. incl. neg cow).
P.S. there is one other top TSE scientist that has come forward and said what the USDA et al did with that cow was ''not logical''. (this will not be published for another 3 or 4 weeks). ONE other TOP TSE scientist saying the same thing would be much better for the public to hear and understand. anyway, does not hurt to ask, and i hope you come through here for us. I know this is a very loaded question, but times a wasting, and human health is at risk here...
thank you, with kindest regards,
I am sincerely,
Terry S. Singeltary Sr.
##################### Bovine Spongiform Encephalopathy #####################
I would like to add to the first paragraph of Adriano Aguzzis comments. We have seen cases in Europe, where a positive result obtained with our Western blot rapid test(Prionics-Check WESTERN)could not be confirmed with IHC, but with the OIE-Western blot procedure, and we have also seen cases where the result could be confirmed by IHC but not by OIE-Western blot. As Adrino Aguzzi pointed out both IHC and OIE-Western have their limitations, but when combined and when performed well they pick up BSE reliably. In case of doubt, i.e. if a rapid test comes out consistently positive but an initial attempt of confirmation with IHC (or OIE-Western) fails, we recommend to routinely do a second test with the respective alternative method. This is the procedure most national reference centers, which are responsible for final confirmation of BSE cases, are following. Regards Markus Moser Prionics
-------- Original Message --------
Subject: Q&A Dr. Jean-Philippe Deslys USDA REFUSAL TO USE WB ON TEXAS COW WITH BSE SYMPTOMS (FULL TEXT)
Date: Fri, 22 Apr 2005 11:53:47 -0500
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTS.UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy #####################
Q&A Dr. Jean-Philippe Deslys
1. What is the standard regime for testing of suspect animals in the EU?
The regime is an initial screening by a high-output test, the Bio-Rad test. If a result raises suspicion, a confirmatory test is conducted with the Western blot test.
2. How long has this been the case?
Its a fairly recent development. Only recently has the Western blot test become sensitive enough, with the addition of phospohtungstic acid precipitation step. The Bio-Rad test (which Deslys helped develop) is extremely sensitive, and the standard Western blot is extremely reliable with high-signal test results. However, it had to be made more sensitive for low-signal (samples with low density of malformed prions) samples. It has been made more sensitive.
Reproducibility is the problem with the IHC test. It is not standardized; depending on the lab and its protocols, or even on the technician involved in the test, one can get conflicting results.
3. Is there a way to measure the three tests in sensitivity, accuracy and objectivity?
Historically, yes. The IHC was the gold standard at one point, but we have shifted to the Western blot. It requires less work, it is more sensitive and its results are reproducible. IHC relies on localization. If you have a weak signal case, you may get lucky and test a spot with a high concentration of prions. But the opposite it true too; you can miss an infection by testing a sample with low concentrations. Western blot is much better for low signal situations.
4. The USDA in 2003 used the Western blot to confirm the BSE case in Washington state, and it sent samples to the U.K. for independent testing. In the case this November, which it announced was negative, it instead used the IHC test and did not send samples to the U.K. Is this good science?
Its not logical. If you have two consecutive questionable screenings, you do another test. I can only advise, its managements duty at USDA to make the decisions. But when you have a discrepancy between the rapid test and the IHC, it is only logical to confirm it with another test.
5. We are hearing now about a new strain of BSE, atypical BSE or aBSE. Or BaSE. We have heard that IHC, the so-called gold standard, cannot detect the variant. Is this true?
Yes. There have been a few cases, one in Italy, one in Belgium, one here in France. It seems to only affect very old animals. The distribution in the brain is very different than we see with BSE, it looks very different. The IHC test will come back negative.
This his a very recent phenomenon. I have no opinion on its virulence. We do not know where it comes from. It could be a version of sporadic infection. Western blot caught them, but we would not even know it existed if we werent running systematic testing in the EU.
BSE was around for a long time before we caught it and by then, it was everywhere. It had become highly infectious. It probably amplified due to low-temperature rendering. The disease was recycled through the food chain, and was given time to amplify. By the time it was identified, even good cooking couldnt eliminate it.
I cant stress enough that systematic testing is necessary. Withdrawing all positives from the food chain is the best way to break the cycle.
What can happen with testing of only cattle that are clearly at risk is that several can remain undetected. Canada has tested about 30,000 head of cattle and has three positives. That would indicate that there are probably undiscovered cases. And what happens then is that the disease is allowed to amplify. You have to maintain testing.
When people choose to protect their economic interests over public health, it can have a boomerang effect. It happened all through Europe. They always deny; its not OUR problem, it is our neighbors problem. And then a single case is discovered and the public reacts. The economic results are devastating. It would be better to just assume BSE is present and use systematic testing as protection. That way, the public is reassured that it is not entering the food supply.
By systematic testing, I mean doing as we do in the EU, which is to test every animal over 30 months of age when it is slaughtered. In Europe, three times as many cases of BSE have been caught by systematic testing as by clinical testing (of clearly sick animals). In 2004, eight clinical cases were discovered, 29 were discovered at rendering plants, and 17 at slaughter. We should be using these tests as a weapon to protect the public and to give them assurance that the food supply is being protected.
6. USDAs list of specified risk materials excludes some products, like blood and bone meal, that are banned in the EU and UK. Is our feed supply safe?
With SRMs, where do you stop? Tests have found prions in meat, nerves travel through meat, and so on. The main infectivity is in the brain and the spinal cord. A blood and bone meal ban in animal feed is not really necessary, because except in cases of highly infective animals, it is unlikely that they are dangerous in themselves. If you combine systematic testing and targeted SRM removal, the brain and the spinal column in cattle over 30 months, you can have a compromise that is both safer and less costly than expanded feed bans.
Certainly, you can stop the spread of BSE with a total ban on offal. But it has to be a total ban. It cant be given to sheep or swine or poultry. It would be very expensive and virtually impossible to accomplish. You can have farmers using the wrong feed or transportation errors.
Systematic testing makes far more sense. I think of it as a thermometer. It not only allows us to catch the disease, it also allows us to monitor its progress. We can watch the levels of infectivity and if they start going up instead of down, we can take measures.
To an extent, our environment is contaminated. About 10 percent of wild animals test positive for TSEs. If you recycle these agents, they can evolve and get more dangerous. This is probably what happened with BSE. It wasnt very dangerous until it evolved to the disease we know today.
People complain that testing is very expensive. It is much more expensive to kill and test whole herds.
7. In your opinion, is infected feed the sole method of transmission of BSE, apart from the very rare maternal transmission?
Feed is the main problem. However, we are seeing some other possibilities, including through fat and greases. Calves are fed milk extracts, with the cream removed. To make it nutritious, they are using fat and grease from cattle.
(FOLLOW QUESTION: Would that allow BSE to develop into an infective level in cattle younger than 30 months, assuming they might be getting infected at a younger age?)
8. You were involved in a study that tested two primates who were fed infected brain tissue. One eventually died of TSE; the other survived. The press reported that the main finding was that it would take something on the order of 1.5 kilograms of infected matter to create an infection, but that seems to be an oversimplification. Could you explain it further?
The findings suggest that as little as five grams is enough to infect. The 1.5 kilo figure is the amount of infected tissue that would have to be ingested from an animal that would be below the threshold of infection, and would test negative. In other words, even though a younger animal may be developing the disease, it would take a considerable amount of tissue to transmit the disease.
An animal could be just below the testing level, and not be particularly dangerous. But that is why you have to keep testing. Once it reaches the threshold, it can become highly infective.
9. BSE is a pretty horrifying disease, but overall, it has killed less than 200 humans, and only a handful in recent years. Listeria, by comparison, kills thousands every year. Overall, how do you rate the threat from BSE?
The overall risk is not particularly high. Over two million infected animals went into the food chain in Europe, 400,000 of them before the SRMs, the brains and spinal column, were removed from the carcass. Less than 200 died, and less than 4,000 are at risk of developing the disease. What we know now is that one particle is not going to kill you. There has to be condensation of the prions to be truly dangerous.
This is not a sterile world. But the danger is that now that the crisis appears to be over, attention will turn elsewhere and that will allow the disease to amplify again. Just as we stopped paying attention to AIDS when medication seemed to control it, then were surprised when a new and more infectious and aggressive strain appeared, we could be surprised by a more serious strain of BSE. That is why I support systematic testing for the long term. The object is to keep levels of BSE low, and to recognize the danger if it suddenly pops back up. ...END
TSS
######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
-------- Original Message --------
Subject: US CHOICE OF MAD COW TEST QUESTIONED
Date: Wed, 24 Mar 2004 16:12:06 -0600
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
US CHOICE OF MAD COW TEST QUESTIONED
The US plans to measure the incidence of mad cow disease in its cattle with a test that its own officials have said gives too many false positives. Some experts fear the choice reflects an official desire to downplay the impact of the first positive BSE tests that emerge, when they turn out not to be confirmed.
Last week the US Department of Agriculture (USDA) approved two tests, including one made by the Californian firm BioRad, for screening up to 300,000 cattle for BSE, starting in July. No more tests will be licensed for months. Announcing the testing plan, chief veterinary officer Ron DeHaven cautioned that "there will be positive results", many of them false.
BioRad's antibody-based test for the prion protein that causes BSE has given numerous false positives in Belgium and Germany. And in Japan only 8 of 113 cattle that repeatedly tested positive with BioRad were confirmed by slower tests that do not give false positives.
The USDA even wrote last May that "it is well known" that tests like BioRad's give false positives. It states that other kinds of quick tests are more suitable for testing for very low levels of BSE, which are expected in the US.
The second quick test approved by the USDA, made by Maine-based IDEXX, could also in theory give false positives. It remains unclear how reliable it is, because there has been little practical experience with the test so far. It is not yet approved for use in Europe, where the vast majority of BSE tests are done.
Debora MacKenzie, Brussels correspondent, New Scientist. tel +32-2-245-0412 fax +32-2-245-0552 mobile +32-49-754-0444
http://www.newscientist.com/ ;
=====================
Greetings,
odd that the USDA et al approves two US-OWNED tests that are _known_ to give false positives, when they know other rapid TSE test are much more reliable. IT's like they purposely do not want to find any TSE in the USA bovine, so they pick the worst test available. The USDA own experts think BioRad is not suitable for supposedly BSE/TSE free and low incidence areas, so why did they choose this test and or the IDEXX, which i dont think has even been submitted to the EU for evaluation and has no commercial experiance to my knowledge. You could almost get the feeling they are deliberately skipping over Prionics for the least supperior TSE rapid test. I believe the Canadians finally did choose prionics. maybe paul or marcus might comment? seems if North America is going to be a consolidated BEEF trading market amongst themselves and expect to export there tainted products everywhere, they could at least come up with the same TSE rapid Test. how can one use a less reliable test and the other use a more reliable test, and it all be the same? i know there is a word Dehaven used, but it slips my mind now, (consolidated markets) that's not it, but you get the just of my thoughts, i think;-)...TSS
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
-------- Original Message --------
Subject: Re: US CHOICE OF MAD COW TEST QUESTIONED
Date: Thu, 25 Mar 2004 00:53:39 +0100
From: Moser Markus Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
Regarding your question about Canada's BSE-test choice for their official BSE surveillance, I can confirm that they chose the Prionics-Check Western rapid test. Regards Markus
CONTINUED
-------- Original Message --------
Subject: Re: US CHOICE OF MAD COW TEST QUESTIONED
Date: Thu, 25 Mar 2004 01:11:04 +0100
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
Dear Terry,
odd that the USDA et al approves two US-OWNED tests that are _known_ to give false positives, when they know other rapid TSE test are much more reliable.
the BioRad-test seems to be the most sensitive rapid BSE test and it is clear that you "get" false positive results when you try to confirm its results with a less sensitive method like immune histochemistry. Poorly trained technicians of course may produce some false positives with the BioRad-test, but immune histochemistry produces many false negatives especially in the hands of not very experienced people. Generally the false negative and not the much fewer false positive results are the problem of all actually available BSE tests.
It is therefore not so easy to say, if the BioRad-test produced a false positive or if the confirming test produced a false negative result and which of them is more reliable. I for sure would not eat the meat of a cow which was seemingly false positive tested with the BioRad-test.
IT's like they purposely do not want to find any TSE in the USA bovine, so they pick the worst test available.
The BioRad-test is definitively not the worst test available (have a look on the EU results) and when a government does not want to get positive results, it uses immune histochemistry instead.
The USDA own experts think BioRad is not suitable for supposedly BSE/TSE free and low incidence areas, so why did they choose this test and or the IDEXX, which i dont think has even been submitted to the EU for evaluation and has no commercial experiance to my knowledge.
Are you sure that USDA has experts for BSE testing?
You could almost get the feeling they are deliberately skipping over Prionics for the least supperior TSE rapid test. I believe the Canadians finally did choose prionics. maybe paul or marcus might comment?
The Prionics western blot test is also a good rapid test which of course does not produce false positive results. In addition this test allows to see new variants of BSE, which would not be seen with the BioRad. But at least in Europe its positive results become confirmed by the OIE Western blot exactly as the BioRad results. Because of this control step the BioRad test cannot produce significantly more problems.
seems if North America is going to be a consolidated BEEF trading market amongst themselves and expect to export there tainted products everywhere, they could at least come up with the same TSE rapid Test. how can one use a less reliable test and the other use a more reliable test, and it all be the same? i know there is a word Dehaven used, but it slips my mind now, (consolidated markets) that's not it, but you get the just of my thoughts, i think;-)...TSS
Not the minor differences between the rapid tests are the problem, but the much to low testing numbers and the prefered IHC-testing in the USA. In Germany we test every month as many as the USA is going to test per year (mostly with BioRad) - and we have only 13 million cattle.
kind regards
Roland
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
-------- Original Message --------
Subject: Re: US CHOICE OF MAD COW TEST QUESTIONED
Date: Thu, 25 Mar 2004 02:51:09 +0100
From: Moser Markus Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######## Bovine Spongiform Encephalopathy #########
Dear Roland
Immunohistochemistry, correctly executed, is the gold standard, together with the OIE Western blotting method. It allows detection of infection even in cases where prion aggregates can only be detected in few individual cells. It is certainly not less sensitive than either Bio-Rad or Prionics. In fact, the abundant data on all three methods indicate equal diagnostic sensitivity (if sampling is done appropriate: note that immunohistochemistry has to be conducted on different tissue samples, since the tissue has to be formalin fixed). In case a BSE case obtained with a rapid test cannot be confirmed in a first approach with one of the gold standard methods, the second method will be used. I agree, that the sensitivity of immunohistochemistry can be negatively influenced e.g. by only looking at a limited number of slides or by not carefully examining the slides for prion aggregates. However, if a rapid test is not confirmed by immunohistochemistry due to a sloppy analysis, it will still show up in the OIE Western blot. Nevertheless, it is of course possible, that a true positive result cannot be confirmed e.g. if only the tissue sample used for the initial testing contained prion aggregates, which is theoretically possible, since the aggregates are not evenly distributed in the tissue. This is why it is not formally possible to disproof with 100% certainty an initial positive diagnosis (and you are right: it's certainly wise to rather not eat any suspicious animals). Nevertheless, false positives cannot in general be attributed to faulty confirmatory tests, but to the fact that the ELISA method simply produces a certain rate of false positives, which is why we offer rapid BSE tests on both platforms, the ELISA and the Western technology. And we make it clear to our customers, that when choosing the Prionics-Check LIA (the ELISA based test) coping with occasional false positive results will be inevitable. The LIA is therefore mostly used in European countries, with well established levels of BSE, while the Prionics-Check Western is also used in BSE-free countries (where a maximum positive predictive value is important to support the conclusion of low frequency or absence of BSE, which would otherwise be difficult for the reason you indicated and I mentioned above, i.e. due to the reason that it is hard to formally disprove an initial diagnosis with absolute certainty). Regards, Markus
-------- Original Message --------
Subject: Re: ''INCONCLUSIVE'' IS NEGATIVE or so they claim...OFFICIAL REPORT
Date: Tue, 1 Feb 2005 16:59:27 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@LISTSERV.KALIV.UNI-KARLSRUHE.DE
References: <41A3B789.6080907@wt.net> <41A4ED7C.4090501@wt.net>
##################### Bovine Spongiform Encephalopathy #####################
*** 2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006 ***
THURSDAY, FEBRUARY 23, 2012
EIGHT FORMER SECRETARIES OF AGRICULTURE SPEAKING AT USDA'S 2012 AGRICULTURE OUTLOOK FORUM INDUCTED INTO USA MAD COW HALL OF SHAME
THURSDAY, OCTOBER 22, 2015
Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened
2020 DECEMBER
WEDNESDAY, DECEMBER 9, 2020
Biden's pick Tom Vilsack Failed Terribly on Mad Cow BSE TSE Prion, why put him back as top Agriculture pick?
THURSDAY, DECEMBER 17, 2020
THE MAD COW BSE TSE PRION THAT STOLE CHRISTMAS DECEMBER 2003, WHAT REALLY HAPPENED, A REVIEW 2020
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
https://animalhealthreportpriontse.blogspot.com/2021/03/investigation-results-of-texas-cow-that.html
FSIS NOTICE 54-05 8/29/05
POLICY ON USE OF RESULTS FROM THIRD PARTY LABORATORIES
NOTE: This notice reissues the contents of FSIS Notice 52-03 in its entirety.
PURPOSE FSIS is periodically presented with positive results from a laboratory analysis conducted by a third party laboratory that indicate an adulterant is present in FSIS inspected and passed product. A third party laboratory is one not owned by, nor under contract with, the establishment providing the sample. Under very limited circumstances, FSIS may rely on a third party laboratory's positive result to take action on the product (e.g., request a recall or take regulatory action). This notice describes the circumstances in which FSIS considers it appropriate to rely on results from a third party laboratory.
POLICY ON THIRD PARTY LABORATORY RESULTS
In deciding whether to rely on third party laboratory results, FSIS will consider the following questions (also see attached flowchart (PDF only)):
Were the procedures used to collect, handle, and transport the sample equivalent to FSIS procedures? FSIS will request documentation of the procedures used and will assess whether the integrity of the sample or specimen could have been compromised during collection or transportation. Was the sample or specimen handled using a documented chain of custody establishing that the integrity of the sample or specimen was not compromised during transport from the point of collection to the laboratory or within the laboratory? FSIS will assess the documentation of the chain of custody to determine whether the people who handled the sample kept it intact and properly maintained throughout the process. Was there assurance that the results obtained by the third party laboratory are reliable and accurate for the analysis in question? FSIS will assess the available information about the laboratory (e.g., whether the laboratory is accredited under the International Organization for Standardization Standard 17025 (ISO 17025) and whether the analysis was performed in accordance with that accreditation) to determine whether the Agency can confidently rely on the laboratory's results. Was the sample or specimen analyzed in accordance with documented analytical methodology that has a sensitivity and specificity that are determined by FSIS to be equivalent to the FSIS laboratory methodology in question?
If the Agency finds that the answers to the four questions listed are "yes", FSIS would consider that there is an appropriate basis to rely on the results of the analysis by the third party laboratory. Thus, FSIS would be prepared to take action (e.g., request a recall or institute a regulatory action) on the basis of the results obtained by the third party laboratory.
If the Agency finds that the answer to number 1 or number 2 is "no" or "inconclusive", then the sample result is disregarded. If the answer to number 1 and number 2 is "yes", then FSIS considers the laboratory's results in the following manner:
If the answer to number 3 is "yes" and the answer to number 4 is "no", then FSIS will take a verification sample; If the answer to number 3 is "no" and the answer to number 4 is "no" then FSIS will disregard the sample results; and, If the answer to number 3 is "no" and the answer to number 4 is "yes" then FSIS will take a verification sample.
When taking verification samples, FSIS will make an effort, whenever possible, to collect an intact sample of the same exact product and lot code(s) from the same location at which the third party sample was collected.
NOTE: Even without reliable laboratory results, FSIS may decide on the basis of the available epidemiological and other evidence that there is reason to find that product is adulterated and, thus, to act against that product.
Philip S. Derfler /s/
http://www.fsis.usda.gov/regulations_&_policies/Notice_54-05/index.asp
see new archived url link here;
FSIS NOTICE 54-05
Decision Tree on Third Party Laboratory
Results FSIS receives lab result and
contacts the laboratory for the
following information
Is sample collection procedure documented,
followed and equivalent to FSIS?
Yes No
Is sample chain of custody OK? Disregard Results No
Yes
party laboratory are reliable and accurate for the analysis
in question?
Yes No
Are the sample analysis
procedures and performance
characteristics documented and
equivalent to FSIS?
Are the sample analysis
procedures and performance
characteristics documented and
equivalent to FSIS?
Yes No Yes No
Treat the sample result
as if it were an FSIS
laboratory sample result
Disregard Results
Collect a verification
sample for the FSIS
laboratory
Was there assurance that the results obtained by the third
http://www.fsis.usda.gov/oppde/rdad/fsisnotices/54-05_flowchart.pdf
see archived url link here;
BSE REDBOOK
Preliminary Notification
The director of NVSL is responsible for immediately notifying the APHIS, Veterinary Services (VS) deputy administrator when tests suggest a presumptive diagnosis of BSE. Once NVSL has made a presumptive diagnosis of BSE, APHIS and FSIS field activities will also be initiated. APHIS will receive notification (either confirming or not confirming NVSL's diagnosis) from the United Kingdom anywhere between 24 and 96 hours. (The international animal health community has recognized the United Kingdom's Central Veterinary Laboratory {CVL} as the world's reference laboratory for diagnosing BSE. Other countries, including Belgium, France, Ireland, Luxembourg, the Netherlands, Portugal, and Switzerland, have all sent samples to this lab to confirm their first case of BSE).
snip...
BSE Response Team
The BSE Response Team will complete the informational memorandum for the Secretary. The Team will prepare the letter to the Office of International Epizootics (OIE), the international animal health organization, for signature by the APHIS, VS Deputy Administrator. OIE requires that all countries submit official notification within 24 hours of confirming a diagnosis of BSE. The BSE Response Team and the office of the APHIS, VS Deputy Administrator would coordinate a teleconference to inform all APHIS regional directors and AVIC'S. The BSE Response Team and the office of the FSIS, OPHS Deputy Administrator would coordinate a teleconference to inform all regional and field FSIS offices. The BSE Response Team would coordinate a teleconference to notify other Federal agencies. The BSE Response Team would coordinate a teleconference to notify key industry/consumer representatives. The BSE Response Team and APHIS International Services would notify foreign embassies. The BSE Response Team would establish a toll-free 800 telephone line for industry representatives, reporters, and the public. The BSE Response Team would coordinate with APHIS Legislative and Public Affairs and USDA office of Communications to issue a press release the day the diagnosis is confirmed. The press release would announce a press conference to be held the morning after the diagnosis is confirmed......
THE END
From: Terry S. Singeltary Sr. (216-119-138-126.ipset18.wt.net)
Subject: Hunkering down in the APHIS BSE Situation Room...
Date: February 14, 2000 at 9:04 am PST
Subject: hunkering down in the APHIS BSE Situation Room
Date: Wed, 12 May 1999 01:55:54 -0800
From: tom Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
i am looking now a bizarre Oct 98 internal USDA publication describing a james bond-type US effort to control media should the long-anticipated first case of BSE in the US be admitted.
'Players' on the 27 member BSE Response Team are to be flown in from all over the country to a BSE Headquarters 'situation room' apparently an underground bunker in Riverdale, Maryland under the command of the Assistant Secretary of Marketing.
Authentic press releases are already prepared and ready to go out after a few specifics have been filled in. They are spelled out in a separate document, the BSE Red Book, aka BSE Emergency Disease Guidelines.
Aphis' National Veterinary Services Laboratories (NVSL) activates team assembly. From the time a bovine brain sample is submitted, it takes 14-18 days to confirm a diagnosis of BSE. In the first 10-13 days, NVSL have enough information to determine the need for additional tests. If a provisional BSE diagnosis is made, the sample is 'hand-carried' (are they going to tell the airline and customs?) to the Central Veterinary Laboratory in England for confirmation, where they are expecting a 24 to 96 hour turn-around.
I guess that means we can get the white tiger brain analyzed by Friday despite the 22 year delay to date. Maybe we could throw in a few cougar brains from NE Colorado too.
A Team Member is designated to silently monitor this listserve and www.mad-cow.org (among others) -- for what, it doesn't say. The Freedom of Information Act request from the East Coast consumer group turned up numerous top-secret USDA downloads from that site and Dealler's.
After 24 hours of secret briefings for 'select industry and trading partners' (to allow them to take positions on the commodities markets opposite the 'non-select' industry and trading partners?), a press conference will be held the next day.
There are plans to trace the cow, its lineage, its herdmates, the renderer, traceout of product, buyout of herd, farm of origin, to get the state involved to quarantine the herd (pre-arranged for all 50 states), expectations for trade bans, notification of OIE within 24 hours, media 800 numbers, spokespersons and backups, notify CDC, FDA, NIH, and many other commendable activities. The Flow Chart is a sight to behold, I will try to scan it in tomorrow.
In short, that cow is going to be toast by the time the public first hears about it.
The Plan does not speak to the scenario in which the CVL says, yes, this is bovine spongiform encephalopathy all right but it is one of your strains, not ours. Invoking their Absence of Evidence is Evidence of Absence principle, there may be no perceived need for public disclosure in this case.
USDA is caught completely unprepared if BSE first turns up in a US zoo animal. These animals could easily be diagnosed outside the "system" and be the subject of a publicity-seeking lab press release. I think this is a more likely scenario because the US has likely imported many thousands of zoo animals with advanced infections from Britain and France and there has been zero monitoring. Unlike with downer cows, anyone with the right colleagues can get ahold of a fallen zoo animal. Zoo animals enter the food chain in some cases after being rendered.
Another scenario would be some stock market speculator obtaining the Red Book and issuing a flurry of bogus but authentic-looking press releases that included bogus 800 and hacked USDA web links. The press here is so lazy and so accustomed to putting out public relation handouts as news that the objectives would be accomplished for a few hour (or days, depending on the Response Team's paralysis vis-a-vis off-flow chart events). Some people think a practise run for this happened in the Indiana case a year or two back.
The first case of nvCJD in an American will also be a public relations fiasco. In the dim bulb of the public mind, any American with mad cow disease would have gotten it from eating meat here. USDA has no way to prove that the victim acquired it on a three week trip to England in 1987. This will sound lame even to the press. All CJD is synonymous with mad cow disease in the public perception; the more often the different kinds are explained, the more their suspicions are aroused. The first case of nvCJD in an American will simply validate what they already know and just be viewed as an overdue admission from the government.
tom
___________________________________________________________
From: Terry S. Singeltary Sr. (216-119-130-102.ipset10.wt.net)
Subject: When a case of B.S.E. is found in the U.S/Response to Disease outbreak...'redbook'
Date: March 13, 2000 at 10:13 am PST
BSE Red Book 2.1-26
5.0 Response to Disease Outbreak
snip...see full report of From: Terry S. Singeltary Sr. (216-119-130-102.ipset10.wt.net)
Subject: When a case of B.S.E. is found in the U.S/Response to Disease outbreak...'redbook'
Date: March 13, 2000 at 10:13 am PST
"FDA will soon be improving the animal feed rule, to make this strong system even stronger."
LMAO!!! (see why down further...terry)
Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
LINE TO TAKE
3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:-
"There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.
DO Hagger RM 1533 MT Ext 3201
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
SO, what about that mad cow feed ban in the USA since 1997???
here's a few, i stopped tracking them after all the FOIA got just too burdensome...see;
scroll to bottom and see USA repeating our same failures, over and over again...8. 21 CFR Part 589.2000
8. 21 CFR Part 589.2000 Failed Mad Cow Feed Ban in USA (these are just a few examples of 100s i have filed...terry)
BANNED MAD COW FEED IN COMMERCE IN ALABAMA
Date: September 6, 2006 at 7:58 am PST PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
b) Performance Chick Starter, Recall # V-131-6;
c) Performance Quail Grower, Recall # V-132-6;
d) Performance Pheasant Finisher, Recall # V-133-6.
CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006. Firm initiated recall is complete.
REASON
Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html
PRODUCT Bulk custom dairy pre-mixes,
Recall # V-120-6 CODE None RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete. REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 350 tons
DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006 RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6 CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons
DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6 CODE
a) Bulk
b) None
c) Bulk
d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006. Firm initiated recall is ongoing.
REASON
Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
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.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
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.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
WEDNESDAY, MARCH 29, 2023
The use of animal by-products in a circular bioeconomy: Time for a TSE road map 3?
BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
Thursday, April 6, 2023
WOAH OIE CHAPTER 11.4 . BOVINE SPONGIFORM ENCEPHALOPATHY Article 11.4.1.
Wednesday, May 24, 2023
WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification
Monday, May 22, 2023
BSE TSE Prion MAD COW TESTING IN THE USA COMPARED TO OTHER COUNTRIES?
SATURDAY, JUNE 03, 2023
Pennsylvania CWD Since July 1, 2022, 400+ Wild Deer Test Positive, Captive Deer Total CWD?
RECENT CASES OF MAD COW DISEASE IN 2023;
WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification
United States of America - Bovine spongiform encephalopathy - Immediate notification
GENERAL INFORMATION
COUNTRY/TERRITORY OR ZONE
COUNTRY/TERRITORY
ANIMAL TYPE
TERRESTRIAL
DISEASE CATEGORY
Listed disease
EVENT ID 5067
DISEASE Bovine spongiform encephalopathy
CAUSAL AGENT Bovine spongiform encephalopathy prion, atypical strain, L-type
GENOTYPE / SEROTYPE / SUBTYPE
USDA Announce A Case Of Mad Cow Disease BSE
May 2, 2023
Docket No. APHIS–2023–0027 Notice of Request for Revision to and Extension of Approval of an Information Collection; National Veterinary Services Laboratories; Bovine Spongiform Encephalopathy Surveillance Program Singeltary Submission
ONLY by the Grace of God, have we not had a documented BSE outbreak, that and the fact the USDA et al are only testing 25K cattle for BSE, a number too low to find mad cow disease from some 28.9 million beef cows in the United States as of Jan. 1,
see full history of mad cow disease in the USA;
BSE TESTING ONLY 25K ANNUALLY WILL NOT FIND BSE CIRCULATING IN THE USA CATTLE HERDS, UNLESS IT'S REAL BAD...THAT'S WHEN YOU HAVE PROBLEMS, AND YOUR JUST TRYING TO HOLD THE NUMBERS DOWN...IMO...terry
Sample Size Estimate for BSE Ongoing Surveillance
July 20, 2006
snip...
In addition, we aim to meet the objective of conducting ongoing surveillance at a level that meets or exceeds OIE surveillance recommendations. We believe this objective is reached by the following sampling strategy, which is sufficient to detect BSE at 1 infected animal per 1,000,000 adult cattle in the population with a high degree of confidence.
Sample Size to Meet OIE Surveillance Recommendations
APHIS is committed to maintaining BSE surveillance that at least meets OIE guidelines. The OIE surveillance guidelines for BSE recommend a target number of surveillance points for Type A surveillance based on the size of a country’s cattle population. These points are accrued over 7 consecutive years, and are weighted according to the surveillance stream and age of the animal sampled. For a large cattle population, using the design prevalence of 1 case per 100,000 adult cattle and 95 percent confidence, 300,000 total points over 7 years, or 42,857 points per year, are required for Type A surveillance (OIE 2005).
KEY POINTS In addition to a stringent feed ban imposed by the Food and Drug Administration in 1997 as well as the removal of all specified risk material which could harbor BSE, USDA has a strong surveillance program in place to detect signs of BSE in cattle in the United States. In fact, we test for BSE at levels greater than World Animal Health Organization standards. The program samples approximately 25,000 animals each year and targets cattle populations where the disease is most likely to be found. The targeted population for ongoing surveillance focuses on cattle exhibiting signs of central nervous disorders or any other signs that may be associated with BSE, including emaciation or injury, and dead cattle, as well as non-ambulatory animals. Samples from the targeted population are taken at farms, veterinary diagnostic laboratories, public health laboratories, slaughter facilities, veterinary clinics, and livestock markets.
***> OIG case # NY-3399-56 REDACTED, VT
***> ''Enclosed is OIG's notification that they have scheduled an investigation of the following individual. REDACTED is alleged to have provided possibly inaccurate test results involving diseased sheep. However, because the results were determined to be inconclusive, no actual violation was actually committed.''
FRIDAY, FEBRUARY 20, 2015
APHIS Freedom of Information Act (FOIA) Appeal Mouse Bio-Assays 2007-00030-A Sheep Imported From Belgium and the Presence of TSE Prion Disease Kevin Shea to Singeltary 2015
Comment #6: WHAT happened to the test results and MOUSE BIO-ASSAYS of those imported sheep from Belgium that were confiscated and slaughtered from the Faillace's, what sort of TSE did these animals have?
Response: It is not clear how the test results referred to in this comment are relevant to the Harvard BSE Risk Assessment Update. Sheep were not considered in the risk assessment.
Comment #7: WHY is it that the Farm of the Mad Sheep of Mad River Valley were quarantined for 5 years, but none of these farms from Texas and Alabama with Atypical TSE in the Bovine, they have not been quarantined for 5 years, why not, with the real risk of BSE to sheep, whom is to say this was not BSE ?
Response: This comment pertains to policy. As such, it is not addressed here.
[PDF]Owens, Julie Page 1 of 98 8/3/2006 - USDA Food Safety ...
www.fsis.usda.gov/.../2006-0011-1.p... Cached
Food Safety and Inspection Service Loading... by F Greetings - 2006 - Related articles Aug 3, 2006 -
Subject: [Docket No. FSIS-2006-0011] ... [Federal Register: July 12, 2006 (Volume 71, Number 133)]. [Notices] ..... group as compared to prior years, we found that conflicting APHIS instructions .....
WHY is it that the Farm of the Mad Sheep of Mad River Valley were quarantined for 5 years, but none of these.
http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf
https://www.fsis.usda.gov/shared/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf
THURSDAY, AUGUST 20, 2020
Why is USDA "only" BSE TSE Prion testing 25,000 samples a year?
USDA Announces Atypical L-Type Bovine Spongiform Encephalopathy BSE Detection
The U.S. Department of Agriculture (USDA) is announcing an atypical case of Bovine Spongiform Encephalopathy (BSE), a neurologic disease of cattle, in an approximately five-year-old or older beef cow at a slaughter plant in South Carolina. This animal never entered slaughter channels and at no time presented a risk to the food supply or to human health in the United States. Given the United States’ negligible risk status for BSE, we do not expect any trade impacts as a result of this finding.
USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Laboratories (NVSL) confirmed that this cow was positive for atypical L-type BSE. The animal was tested as part of APHIS’s routine surveillance of cattle that are deemed unsuitable for slaughter. The radio frequency identification tag present on the animal is associated with a herd in Tennessee. APHIS and veterinary officials in South Carolina and Tennessee are gathering more information during this ongoing investigation.
Atypical BSE generally occurs in older cattle and seems to arise rarely and spontaneously in all cattle populations.
This is the nation’s 7th detection of BSE. Of the six previous U.S. cases, the first, in 2003, was a case of classical BSE in a cow imported from Canada; the rest have been atypical (H- or L-type) BSE.
The World Organization for Animal Health (WOAH) recognizes the United States as negligible risk for BSE. As noted in the WOAH guidelines for determining this status, atypical BSE cases do not impact official BSE risk status recognition as this form of the disease is believed to occur spontaneously in all cattle populations at a very low rate. Therefore, this finding of an atypical case will not change the negligible risk status of the United States, and should not lead to any trade issues.
The United States has a longstanding system of interlocking safeguards against BSE that protects public and animal health in the United States, the most important of which is the removal of specified risk materials - or the parts of an animal that would contain BSE should an animal have the disease - from all animals presented for slaughter. The second safeguard is a strong feed ban that protects cattle from the disease. Another important component of our system - which led to this detection - is our ongoing BSE surveillance program that allows USDA to detect the disease if it exists at very low levels in the U.S. cattle population.
More information about this disease is available in the BSE factsheet.
#
FRIDAY, MAY 19, 2023
USDA Announces Atypical L-Type Bovine Spongiform Encephalopathy BSE Detection
SATURDAY, MAY 20, 2023
Tennessee State Veterinarian Alerts Cattle Owners to Disease Detection Mad Cow atypical L-Type BSE
Wednesday, May 24, 2023
WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification
Monday, March 20, 2023
WAHIS, WOAH, OIE, REPORT United Kingdom Bovine Spongiform Encephalopathy Atypical H-Type
WAHIS, WOAH, OIE, REPORT Switzerland Bovine Spongiform Encephalopathy Atypical L-Type
Switzerland Bovine Spongiform Encephalopathy Atypical L-Type
Switzerland - Bovine spongiform encephalopathy - Immediate notification
BRAZIL BSE START DATE 2023/01/18
BRAZIL BSE CONFIRMATION DATE 2023/02/22
BRAZIL BSE END DATE 2023/03/03
SPAIN BSE START DATE 2023/01/21
SPAIN BSE CONFIRMATION DATE 2023/02/03
SPAIN BSE END DATE 2023/02/06
NETHERLANDS BSE START DATE 2023/02/01
NETHERLANDS BSE CONFIRMATION DATE 2023/02/01
NETHERLANDS BSE END DATE 2023/03/13
Tuesday, May 30, 2023
World Organisation for Animal Health 90th General Session of the World Assembly of Delegates BSE TSE Prion 2023
WEDNESDAY, JUNE 7, 2023
Adams County veterinarian gets probation, house arrest, fine for submitting false bovine blood samples to PA Dept. of Agriculture
Donald Yorlets admitted to conspiring to falsify testing designed to prevent transmission of communicable diseases to cows that were being shipped internationally.
''FDA will soon be improving the animal feed rule, to make this strong system even stronger.''
DEFRA
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip.....
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip.....
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip.....
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
PLoS One. 2020; 15(8): e0237410. Published online 2020 Aug 20. doi: 10.1371/journal.pone.0237410 PMCID: PMC7446902 PMID: 32817706
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
Nathaniel D. Denkers, Conceptualization, Data curation, Formal analysis, Investigation, Methodology, Validation, Visualization, Writing – review & editing,#1 Clare E. Hoover, Conceptualization, Data curation, Investigation, Writing – original draft, Writing – review & editing,#2 Kristen A. Davenport, Conceptualization, Data curation, Investigation, Writing – review & editing,3 Davin M. Henderson, Conceptualization, Data curation, Investigation, Methodology,1 Erin E. McNulty, Data curation, Investigation, Methodology, Writing – review & editing,1 Amy V. Nalls, Conceptualization, Investigation, Methodology, Writing – review & editing,1 Candace K. Mathiason, Conceptualization, Funding acquisition, Investigation, Supervision, Writing – review & editing,1 and Edward A. Hoover, Conceptualization, Data curation, Funding acquisition, Supervision, Writing – review & editing1,* Byron Caughey, Editor Author information Article notes Copyright and License information Disclaimer This article has been corrected.
See PLoS One. 2021 June 10; 16(6): e0253356. Associated Data Data Availability Statement
Abstract
The minimum infectious dose required to induce CWD infection in cervids remains unknown, as does whether peripherally shed prions and/or multiple low dose exposures are important factors in CWD transmission. With the goal of better understand CWD infection in nature, we studied oral exposures of deer to very low doses of CWD prions and also examined whether the frequency of exposure or prion source may influence infection and pathogenesis. We orally inoculated white-tailed deer with either single or multiple divided doses of prions of brain or saliva origin and monitored infection by serial longitudinal tissue biopsies spanning over two years. We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.
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In conclusion, we have attempted to model and better understand CWD infection relative to natural exposure. The results demonstrate: (a) that the minimum CWD oral infectious dose is vastly lower than historical studies used to establish infection; (b) that a direct relationship exists between dose and incubation time to first prion replication detection in tonsils, irrespective of genotype; (c) that a difference was not discernible between brain vs. saliva source prions in ability to establish infection or in resultant disease course; and (d) that the CWD infection process appears to conform more to a threshold dose than an accumulative dose dynamic.
Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle
G. A. H. Wells,1 T. Konold,1 M. E. Arnold,1 A. R. Austin,1 3 S. A. C. Hawkins,1 M. Stack,1 M. M. Simmons,1 Y. H. Lee,2 D. Gavier-Wide´n,3 M. Dawson1 4 and J. W. Wilesmith1 1 Correspondence G. A. H. Wells
g.a.h.wells@vla.defra.gsi.gov.uk
1 Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK
2 National Veterinary Research and Quarantine Service, Anyang, Republic of Korea
3 National Veterinary Institute (SVA), SE-75189 Uppsala, Sweden
Received 27 July 2006
Accepted 18 November 2006
The dose–response of cattle exposed to the bovine spongiform encephalopathy (BSE) agent is an important component of modelling exposure risks for animals and humans and thereby, the modulation of surveillance and control strategies for BSE. In two experiments calves were dosed orally with a range of amounts of a pool of brainstems from BSE-affected cattle. Infectivity in the pool was determined by end-point titration in mice. Recipient cattle were monitored for clinical disease and, from the incidence of pathologically confirmed cases and their incubation periods (IPs), the attack rate and IP distribution according to dose were estimated. The dose at which 50 % of cattle would be clinically affected was estimated at 0.20 g brain material used in the experiment, with 95 % confidence intervals of 0.04–1.00 g. The IP was highly variable across all dose groups and followed a log-normal distribution, with decreasing mean as dose increased. There was no evidence of a threshold dose at which the probability of infection became vanishingly small, with 1/15 (7 %) of animals affected at the lowest dose (1 mg).
snip...
DISCUSSION
The study has demonstrated that disease in cattle can be produced by oral exposure to as little as 1 mg brain homogenate (¡100.4 RIII mouse i.c./i.p. ID50 units) from clinically affected field cases of BSE and that the limiting dose for infection of calves is lower than this exposure...
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P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmzas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Lwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat Energie Atomique, France; 3Instituto Superiore di Sanit, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study 'BSE in primates' supported by the EU (QLK1-2002-01096).
1.3. Determination of the Minimal Infectious BSE Dose in Non-human Primates
In a concerted European effort involving 5 laboratories including ours, the BSE-macaque model was then used to evaluate the minimal amount of BSE-infected material necessary to induce vCJD in primates. Results so far show that 5g of infectious BSE cattle brain is sufficient to induce the disease in all recipient animals by the oral route, with 500 mg yielding an incomplete attack rate10,11). The ID50 of BSE cattle brain is 200 mg for cattle12). These results suggest a low species barrier between cattle and non-human primates.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmzas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frdric Auvr, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Sals, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
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BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 01 mg 001 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was
inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of
bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and int****ritoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
It is clear that the designing scientists must
also have shared Mr Bradley's surprise at the results because all the dose
levels right down to 1 gram triggered infection.
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100 grams) was probably given with the benefit of hindsight; particularly if one considers that later in the same answer Mr Bradley expresses his surprise that it could take as little of 1 gram of brain to cause BSE by the oral route within the same species. This information did not become available until the "attack rate" experiment had been completed in 1995/96. This was a titration experiment designed to ascertain the infective dose. A range of dosages was used to ensure that the actual result was within both a lower and an upper limit within the study and the designing scientists would not have expected all the dose levels to trigger infection.
The dose ranges chosen by the most informed scientists at that time ranged from 1 gram to three times one hundred grams.
It is clear that the designing scientists must have also shared Mr Bradley's surprise at the results because all the dose levels right down to 1 gram triggered infection.
Notice of Request To Renew an Approved Information Collection: Specified Risk Materials DOCKET NUMBER Docket No. FSIS-2022-0027 Singeltary Submission
Greetings FSIS, USDA, et al,
Thank you kindly for allowing the public to comment on ;
(a) whether the proposed collection of information is necessary for the proper performance of FSIS’ functions, including whether the information will have practical utility;
(b) the accuracy of FSIS’ estimate of the burden of the proposed collection of information, including the validity of the method and assumptions used;
(c) ways to enhance the quality, utility, and clarity of the information to be collected; and
(d) ways to minimize the burden of the collection of information, including through the use of appropriate automated, electronic, mechanical, or other technological collection techniques, or other forms of information technology.
I will be commenting mostly on a, b, and c, because d, is wanting to minimize the burden of collection, and i do not think that is possible if ''These statutes mandate that FSIS protect the public by verifying that meat, poultry, and egg products are safe, wholesome, and properly labeled and packaged.'', is truly the intent of these statutes, and i would kindly like to explain why, and why it is so critical that these Specified Risk Materials SRM TSE Prion Statues are so important for public health, and WHY there is an urgent need to enhance them, considering the risk factors of Chronic Wasting Disease CWD TSE Prion in Cervid.
THIS collection of SRM materials information should be done all the time, year after year, and ending it EVER would be foolish, imo, not scientific, and will lead to future risk to public health, if you consider just how bad USDA/FSIS/APHIS/FDA failed so badly with the FDA PART 589 TSE PRION FEED BAN, the SRM REMOVAL, THE BSE SURVEILLANCE AND TESTING PROGRAMS, THEY FAILED ALL OF THEM TERRIBLY IMO, AND BY CONTINUING TO INSIST ON TESTING 25K CATTLE FOR BSE IS A DISASTER WATING TO HAPPEND IMO!
SPECIFIED RISK MATERS
Specified Risk Materials SRMs, are the most high risk infectious materials, organs, of a cow that is infected with Bovine Spongiform Encephalopathy, Transmissible Spongiform Encephalopathy, BSE TSE Prion. the atypical BSE strains are, like atypical L-type BSE are more infectious that the typical C-type BSE. Also, Science of the BSE TSE has evolved to show that there are more infectious tissues and organs than previously thought. I wish to kindly post all this evidence, as to show you why this information collection of SRMs are so vital to public safety, and why they should be enhanced for cattle, cervid, sheep, and goats, oh, and not to forget the new livestock prion disease in camel, the Camel Prion Disease CPD.
ONE other thing, you must remember, SCIENCE AND TRANSMISSION STUDIES have now shown that CWD and Scrapie can transmit to PIGS by Oral route. This should be included in any enhancement of the SRM or FDA PART 589 TSE PRION FEED ban.
NOT to forget Zoonosis of all of the above, i will post the latest science to date at the bottom of the attached files.
Thank You, terry
Singeltary further comments in attachment;
Specified Risk Materials DOCKET NUMBER Docket No. FSIS-2022-0027 Singeltary Submission Attachment https://downloads.regulations.gov/FSIS-2022-0027-0002/attachment_1.pdf Monday, December 5, 2022 Notice of Request To Renew an Approved Information Collection: Specified Risk Materials DOCKET NUMBER Docket No. FSIS-2022-0027 Singeltary Submission
SEE MAD COW FEED VIOLATIONS AFER MAD COW FEED VIOLATIONS ;
PUBLIC SUBMISSION
Use of Electronic Identification Eartags as Official Identification in Cattle and Bison APHIS-2021-0020-0001 Singeltary Submission
Comment from Singeltary Sr., Terry
Posted by the Animal and Plant Health Inspection Service on Mar 21, 2023
SEE ADDITIONAL COMMENTS IN ATTACHMENT;
Sunday, January 10, 2021
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission June 17, 2019
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al,
I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.
THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.
Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.
The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with 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. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.
WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.
WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.
AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...
APHIS Indemnity Regulations [Docket No. APHIS-2021-0010] RIN 0579-AE65 Singeltary Comment Submission
Comment from Singeltary Sr., Terry
Posted by the Animal and Plant Health Inspection Service on Sep 8, 2022
PDF]Freas, William TSS SUBMISSION File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [flounder@wt.net] Monday, January 08,200l 3:03 PM freas ...
2. WE have a new Prion disease outbreak, in a new Livestock species, in Africa, and apparently, it's fairly large.
Monday, November 14, 2022
Prion Diseases in Dromedary Camels (CPD) 2022 Review
3. PIGS
Title: Prion infectivity detected in swine challenged with chronic wasting disease via the intracerebral or oral route
Author item MOORE, S - Orise Fellow item Kunkle, Robert item SMITH, JODI - Iowa State University item WEST-GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 4/4/2016 Publication Date: N/A Citation: N/A
Interpretive Summary:
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of North American cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. In the US, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine, mink, and poultry still occurs. In addition, scavenging of CWD-affected cervid carcasses by feral pigs presents a potential risk for CWD exposure. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following oral or intracranial experimental challenge. At 8 weeks of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). At death a complete necropsy examination was performed, including testing of tissues for misfolded prion protein (PrPcwd) by western blotting (WB), enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry (IHC). None of the pigs developed clinical signs consistent with prion disease. Four >6 month intracranially challenged pigs (survival times 45-73 mpc) were positive by ELISA, two were also positive by WB, and one was positive by IHC. One >6 month orally challenged pig (64 mpc) was positive by ELISA. To further investigate the potential for infectivity, brain tissue from selected pigs was bioassayed in mice expressing porcine PRNP. Tissue from the two WB-positive >6 month intracranially challenged pigs produced positive bioassay results, albeit with low attack rates and variable incubation periods. Interestingly, bioassay of material from the longest surviving >6 month orally challenged pig (72 mpc), which was negative for PrPcwd by all other tests, produced a positive bioassay result. Bioassay of material from additional animals is currently underway. This study demonstrates that pigs can serve as potential hosts for CWD, although with low attack rates and scant PrPcwd accumulation.
Detection of infectivity in orally challenged pigs using mouse bioassay raises the possibility that naturally exposed pigs act as a reservoir of CWD infectivity, even though affected pigs do not develop overt clinical signs or readily detectable PrPcwd.
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP
Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.
Interpretive Summary:
The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.
''These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.''
ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
see full report;
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
2017 Annual Report
Objectives
Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.
Approach
The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.
Progress Report
All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.
Accomplishments
1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.
Review Publications
snip...
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation
Author item MOORE, SARAH - Orise Fellow item WEST GREENLEE, M - Iowa State University item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item Smith, Jodi item Kunkle, Robert item KANTHASAMY, ANUMANTHA - Iowa State University item Greenlee, Justin
Submitted to: Journal of Virology Publication Type: Peer Reviewed Journal Publication Acceptance Date: 7/6/2017 Publication Date: 9/12/2017 Citation: Moore, S.J., West Greenlee, M.H., Kondru, N., Manne, S., Smith, J.D., Kunkle, R.A., Kanthasamy, A., Greenlee, J.J. 2017. Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation. Journal of Virology. 91(19):e00926-17. https://doi.org/10.1128/JVI.00926-17. Interpretive Summary: Chronic wasting disease (CWD) is a fatal disease of wild and captive deer and elk that causes damaging changes in the brain. The infectious agent is an abnormal protein called a prion that has misfolded from its normal state. Whether CWD can transmit to swine is unknown. This study evaluated the potential of pigs to develop CWD after either intracranial or oral inoculation. Our data indicates that swine do accumulate the abnormal prion protein associated with CWD after intracranial or oral inoculation. Further, there was evidence of abnormal prion protein accumulation in lymph nodes. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. This information is useful to wildlife managers and individuals in the swine and captive cervid industries. These findings could impact future regulations for the disposal of offal from deer and elk slaughtered in commercial operations. U.S. regulators should carefully consider the new information from this study before relaxing feed ban standards designed to control potentially feed borne prion diseases.
Technical Abstract: Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following oral or intracranial experimental inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from pigs in all inoculated groups. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can serve as hosts for CWD, though with scant PrPSc accumulation requiring sensitive detection methods. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. https://www.ars.usda.gov/research/publications/publication/?seqNo115=339093
“Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk.”
“In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations.”
“These findings could impact future regulations for the disposal of offal from deer and elk slaughtered in commercial operations.”
“U.S. regulators should carefully consider the new information from this study before relaxing feed ban standards designed to control potentially feed borne prion diseases.”
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
LINE TO TAKE
3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:-
"There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.
DO Hagger RM 1533 MT Ext 3201
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
MONDAY, OCTOBER 10, 2022
Docket No: 2002N-0273 (formerly Docket No. 02N-0273) Substances Prohibited From Use in Animal Food and Feed Scientists Comments December 20, 2005
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
June 17, 2019
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al,
I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.
THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.
Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.
The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with 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. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.
WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.
WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.
AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...
Comment from Terry Singeltary Posted by the Animal and Plant Health Inspection Service on Jun 19, 2019
WEDNESDAY, JANUARY 1, 2020
USDA OIE BSE TSE PRION FDA PART 589 BSE TSE PRION aka MAD COW FEED BAN Failure 2020 UPDATE
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
THURSDAY, DECEMBER 17, 2020
THE MAD COW BSE TSE PRION THAT STOLE CHRISTMAS DECEMBER 2003, WHAT REALLY HAPPENED, A REVIEW 2020
MONDAY, NOVEMBER 30, 2020
***> REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRION
see updated concerns with atypical BSE from feed and zoonosis...terry
WEDNESDAY, DECEMBER 23, 2020
BSE research project final report 2005 to 2008 SE1796 SID5
Tuesday, May 30, 2023
World Organisation for Animal Health 90th General Session of the World Assembly of Delegates BSE TSE Prion 2023
PLEASE NOTE, THIS BLOG HAS BEEN PUT UNDER A WARNING, you can see why...
Docket No. APHIS–2023–0027 Notice of Request for Revision to and Extension of Approval of an Information Collection; National Veterinary Services Laboratories; Bovine Spongiform Encephalopathy Surveillance Program Singeltary Submission Document APHIS-2023-0027-0001 BSE Singeltary Comment Submission
see full submission;
Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
APHIS Indemnity Regulations [Docket No. APHIS-2021-0010] RIN 0579-AE65 Singeltary Comment Submission Singeltary Sr., Terry
Sep 8, 2022
FRIDAY, APRIL 07, 2023
Case report: Two clusters of Creutzfeldt-Jakob disease cases within 1 year in West Michigan
SEAC SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007 Singeltary Submission
sporadic CJD and BSE ?
December 2002
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante Jacqueline M. Linehan Melanie Desbruslais Susan Joiner Ian Gowland Andrew L. Wood Julie Welch Andrew F. Hill Sarah E. Lloyd Jonathan D.F. Wadsworth John Collinge
The EMBO Journal (2002)21:6358-6366 https://doi.org/10.1093/emboj/cdf653
Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.
Snip…
These studies further strengthen the evidence that vCJD is caused by a BSE-like prion strain. Also, remarkably, the key neuropathological hallmark of vCJD, the presence of abundant florid PrP plaques, can be recapitulated on BSE or vCJD transmission to these mice. However, the most surprising aspect of the studies was the finding that an alternate pattern of disease can be induced in 129MM Tg35 mice from primary transmission of BSE, with a molecular phenotype indistinguishable from that of a sub-type of sporadic CJD. This finding has important potential implications as it raises the possibility that some humans infected with BSE prions may develop a clinical disease indistinguishable from classical CJD associated with type 2 PrPSc. This is, in our experience, the commonest molecular sub-type of sporadic CJD. In this regard, it is of interest that the reported incidence of sporadic CJD has risen in the UK since the 1970s (Cousens et al., 1997). This has been attributed to improved case ascertainment, particularly as much of the rise is reported from elderly patients and similar rises in incidence were noted in other European countries without reported BSE (Will et al., 1998). However, it is now clear that BSE is present in many European countries, albeit at a much lower incidence than was seen in the UK. While improved ascertainment is likely to be a major factor in this rise, that some of these additional cases may be related to BSE exposure cannot be ruled out. It is of interest in this regard that a 2-fold increase in the reported incidence of sporadic CJD in 2001 has recently been reported for Switzerland, a country that had the highest incidence of cattle BSE in continental Europe between 1990 and 2002 (Glatzel et al., 2002). No epidemiological case–control studies with stratification of CJD cases by molecular sub-type have yet been reported. It will be important to review the incidence of sporadic CJD associated with PrPSc type 2 and other molecular sub-types in both BSE-affected and unaffected countries in the light of these findings. If human BSE prion infection can result in propagation of type 2 PrPSc, it would be expected that such cases would be indistinguishable on clinical, pathological and molecular criteria from classical CJD. It may also be expected that such prions would behave biologically like those isolated from humans with sporadic CJD with type 2 PrPSc. The transmission properties of prions associated with type 2 PrPSc from BSE-inoculated 129MM Tg35 mice are being investigated by serial passage.
Snip…
We consider these data inconsistent with contamination of some of the 129MM Tg35 mice with sporadic CJD prions. These transmission studies were performed according to rigorous biosafety protocols for preparation of inocula and both the inoculation and care of mice, which are all uniquely identified by sub-cutaneous transponders. However, crucially, the same BSE inocula have been used on 129VV Tg152 and 129MM Tg45 mice, which are highly sensitive to sporadic CJD but in which such transmissions producing type 2 PrPSc were not observed. Furthermore, in an independent experiment, separate inbred lines of wild-type mice, which are highly resistant to sporadic CJD prions, also propagated two distinctive PrPSc types on challenge with either BSE or vCJD. No evidence of spontaneous prion disease or PrPSc has been seen in groups of uninoculated or mock-inoculated aged 129MM Tg35 mice.
While distinctive prion isolates have been derived from BSE passage in mice previously (designated 301C and 301V), these, in contrast to the data presented here, are propagated in mice expressing different prion proteins (Bruce et al., 1994). It is unclear whether our findings indicate the existence of more than one prion strain in individual cattle with BSE, with selection and preferential replication of distinct strains by different hosts, or that ‘mutation’ of a unitary BSE strain occurs in some types of host. Western blot analysis of single BSE isolates has not shown evidence of the presence of a proportion of monoglycosylated dominant PrPSc type in addition to the diglycosylated dominant pattern (data not shown). Extensive strain typing of large numbers of individual BSE-infected cattle either by biological or molecular methods has not been reported.
Snip…see;
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" e.asante@ic.ac.uk
To: "'flounder@wt.net'" flounder@wt.net
Dear Terry,
I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, ***yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.
Emmanuel Asante
<<Asante et al 2002.pdf>>
____________________________________
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now)
____________________________________end
Deaths from sporadic CJD reported in Britain in the 1990s peaked at around 89 a year in 1998 and the number has stayed around the 80 mark ever since - far more than the 28 variant CJD cases in 2000, the worst year so far for variant CJD.
The number of people in the North-East officially confirmed to have died of vCJD is 13.
The number thought to have died of classical CJD is believed to number at least 200.
A spokesman for the Department of Health said: "These are interesting and potentially important findings, which we will need to consider in detail."
The £55m in compensation given by the Department of Health is not available for sporadic CJD victims or relatives, and there is no way yet scientists can distinguish between cases that arose from spontaneous changing in the form of the prion protein linked to both diseases, and those that might be diet-related.
Newcastle scientist Dr Harash Narang, who has spent many years researching CJD, said: "What Professor Collinge's research shows is that many of those who have been classified as dying from sporadic CJD in the past may in fact have died from BSE."
Page 2: Differences between classical CJD and vCJD....
BSE is 'linked' to CJD deaths
Differences between classical CJD and vCJD
Age when obvious symptoms occur after many years of incubation:
Identified in 1920s. Disease mainly of middle-aged and elderly. Incidence roughly one in a million, but steadily rising from 33 to 89 a year.
Identified in 1996. Average age late 20s. Found mainly in Britain: 130 cases with 122 deaths so far. Six in France, one each in Italy, Ireland, Canada, and United States.
Until now assumed a normal prion protein in the brain spontaneously changed into abnormal dangerous form. Recently suggested some cases possibly caused by surgical contamination during operations. BSE or similar diseases could now be factor.
Largely blamed on consumption of cheap cattle meat and offals during 1980s. Tough food controls meant to have significantly reduced risk. Concern remains over whether sheep might also have become infected with BSE and entered food chain.
Page 3: Duration of illness and symptoms...
BSE is 'linked' to CJD deaths
Duration of illness and symptoms
Time between obvious symptoms and death typically a few months. Loss of balance, sense of direction, and control over limbs and bodily functions. Fear, anxiety.
First symptoms often indicate psychological problems. Duration often well over a year. Several physical symptoms similar to sporadic CJD.
More questions, more victims
This weekend marked the seventh anniversary of the death of Peter Hall, of Chester-le-Street, from vCJD.
He was 20 years old and one of the first in the UK to be diagnosed with the new disease.
His parents, Frances and Derek, have been campaigning ever since and 18 months ago won a victory when the Government agreed to compensate the families of victims of vCJD.
Last night Frances, who is now secretary of the Human BSE Foundation, said: "When Peter died in 1996 I never thought that seven years later we still would not understand the disease that killed him.
"And yet here we are with yet more questions and more victims.
"This new study could have major implications for those who have died of CJD since BSE - particularly the young ones who until now were diagnosed with sporadic CJD.
"But it will take time and I suspect it will be years rather than months before we understand what is happening."
Page 4: Hospital report due out soon...
BSE is 'linked' to CJD deaths
Hospital report due out soon
An investigation into how North-East patients were potentially exposed to the deadly brain disease CJD is due to be published soon, health officials have confirmed.
A draft report into the incident at Middlesbrough General Hospital last year has been completed by Dr Bill Kirkup, regional director of public health in the North-East.
Dr Kirkup was asked by Chief Medical Officer Sir Liam Donaldson to investigate the incident, where 24 people were operated on with instruments used on someone who was later found to have CJD.
The hospital denies any procedural lapse as there was nothing to suggest the original patient had the disease prior to surgery. But the Department of Health said the instruments should have been quarantined to avoid contamination.
A DoH spokesman said: "There's a draft report that has been completed and we're hoping to be able to publish the findings shortly."
BMJ. 2002 Nov 9; 325(7372): 1055. doi: 10.1136/bmj.325.7372.1055/a PMCID: PMC1124571PMID: 12424157
Inquiry into handling of CJD alert welcomed Mark Hunter
Author information Copyright and License information Disclaimer
The chief executive of Middlesbrough General Hospital welcomed the launch of an independent inquiry into the hospital's handling of an alert involving Creutzfeldt-Jakob disease (CJD).
The alert arose when staff realised that instruments used on a patient who was later found to have the disease had been reused on 24 other patients.
Chief medical officer Liam Donaldson announced the inquiry last week as the Department of Health began frantically backtracking on its initial criticism of the hospital.
Having originally described the possible exposure of 24 patients to a risk of CJD infection as “an appalling incident” that reinforced the need to adhere to its “crystal clear guidance” on decontamination, the department later adopted a more conciliatory tone.
“This is a difficult and distressing situation for all the patients and families concerned, as well as for the dedicated staff at Middlesbrough General Hospital,” said Professor Donaldson. “I have asked the regional director of public health, Dr Bill Kirkup, to fully assess the facts and report to me shortly. His report will ensure that any measures necessary to improve local procedures or strengthen national policy are taken.”
Meanwhile, the medical director for South Tees Hospitals NHS Trust, Dr Paul Lawler, had made it clear to the press that the hospital had followed the Department of Health's guidance to the letter throughout the incident.
He said that the potential for contamination stemmed from a brain biopsy undertaken in July on an elderly woman who was later found to have the sporadic form of CJD.
“CJD was not suspected in this patient at the time of the operation,” stressed Dr Lawler. It was only when a “diligent” pathologist sent a sample of tissue to the CJD surveillance unit “to rule CJD out rather than confirm it” that the diagnosis was made.
In the intervening three weeks the instruments from the original biopsy were used on a further 24 patients.
“Once sporadic CJD was diagnosed we followed the procedure set down by the CJD incidents panel,” said Dr Lawler. This meant the immediate withdrawal of £90000 ($140000; €141000) worth of drills, craniotomy sets, and surgical instruments.
However, the 24 patients were not told that they were at potential risk of contamination until the story broke in the media last week, 12 weeks after the instruments were withdrawn.
The hospital's managers say that this was because they were waiting for a decision from the government's CJD panel on when and how to contact the patients.
The hospital has now contacted all the patients and will be allocating them “a named person at the trust who will fully support them for as long as they feel they need it.”
The trust's chief executive, Bill Murray, said: “We are deeply sorry for any distress caused to the patients and their families and will do everything we possibly can to help them through this difficult time.
“We welcome this independent inquiry.”
Sporadic CJD in Farmers, Farmers Wife, with BSE herd…
NEW URL LINK 2022
This was not simply another farmer but the third farmer......
NEW URL LINK 2022
http://web.archive.org/web/20090505233408/http://www.bseinquiry.gov.uk/files/yb/1995/06/21002001.pdf
suspect case of CJD in a farmer who has had a case of BSE in his beef suckler herd.
http://web.archive.org/web/20030331213802/http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf
NEW URL LINK 2022
http://web.archive.org/web/20090506063655/http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf
cover-up of 4th farm worker ???
http://web.archive.org/web/20030516083454/http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf
NEW URL LINK 2022
http://web.archive.org/web/20090506063655/http://www.bseinquiry.gov.uk/files/yb/1995/10/23006001.pdf
MONDAY, MAY 19, 2008
SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS
The risk of CJD increases with age; the 2016–2020 average annual rate in the United States was about 5 cases per million in persons 55 years of age or older.
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor:
In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally..
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
WEDNESDAY, FEBRUARY 8, 2023
NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER SURVEILLANCE TABLES OF CASES EXAMINED January 11th, 2023
MONDAY, APRIL 24, 2023 2023
CDC REPORTS CJD TSE Prion 5 cases per million in persons 55 years of age or older
Singeltary 1999
US scientists develop a possible test for BSE
BMJ 1999; 319 doi: https://doi.org/10.1136/bmj.319.7220.1312b (Published 13 November 1999)
Cite this as: BMJ 1999;319:1312
15 November 1999
Terry S Singeltary
NA
medically retired
Rapid Response:
Re: vCJD in the USA * BSE in U.S.
In reading the recent article in the BMJ about the potential BSE tests being developed in the U.S. and Bart Van Everbroeck reply. It does not surprize me, that the U.S. has been concealing vCJD. There have been people dying from CJD, with all the symptoms and pathological findings that resemble U.K. vCJD for some time. It just seems that when there is one found, they seem to change the clarical classification of the disease, to fit their agenda. I have several autopsies, stating kuru type amyloid plaques, one of the victims was 41 years of age. Also, my Mom died a most hideous death, Heidenhain Variant Creutzfeldt Jakob disease.
Her symptoms resemble that of all the U.K. vCJD victims. She would jerk so bad at times, it would take 3 of us to hold her down, while she screamed "God, what's wrong with me, why can't I stop this." 1st of symptoms to death, 10 weeks, she went blind in the first few weeks. But, then they told me that this was just another strain of sporadic CJD. They can call it what ever they want, but I know what I saw, and what she went through. Sporadic, simply means, they do not know.
My neighbors Mom also died from CJD. She had been taking a nutritional supplement which contained the following;
vacuum dried bovine BRAIN, bone meal, bovine EYE, veal bone, bovine liver powder, bovine adrenal, vacuum dried bovine kidney, and vacuum dried porcine stomach. As I said, this woman taking these nutritional supplements, died from CJD.
The particular batch of pills that was located, in which she was taking, was tested. From what I have heard, they came up negative, for the prion protein. But, in the same breath, they said their testing, may not have been strong enough to pick up the infectivity. Plus, she had been taking these type pills for years, so, could it have come from another batch?
CWD is just a small piece of a very big puzzle. I have seen while deer hunting, deer, squirrels and birds, eating from cattle feed troughs where they feed cattle, the high protein cattle by products, at least up until Aug. 4, 1997.
So why would it be so hard to believe that this is how they might become infected with a TSE. Or, even by potentially infected land. It's been well documented that it could be possible, from scrapie. Cats becoming infected with a TSE. Have you ever read the ingredients on the labels of cat and dog food? But, they do not put these tissues from these animals in pharmaceuticals, cosmetics, nutritional supplements, hGH, hPG, blood products, heart valves, and the many more products that come from bovine, ovine, or porcine tissues and organs. So, as I said, this CWD would be a small piece of a very big puzzle. But, it is here, and it most likely has killed. You see, greed is what caused this catastrophe, rendering and feeding practices. But, once Pandora's box was opened, the potential routes of infection became endless.
No BSE in the U.S.A.? I would not be so sure of that considering that since 1990;
Since 1990 the U.S. has raised 1,250,880,700 cattle;
Since 1990 the U.S. has ONLY checked 8,881 cattle brains for BSE, as of Oct. 4, 1999;
There are apprx. 100,000 DOWNER cattle annually in the U.S., that up until Aug. 4, 1997 went to the renders for feed;
Scrapie running rampant for years in the U.S., 950 infected FLOCKS, as of Aug. 1999;
Our feeding and rendering practices have mirrored that of the U.K. for years, some say it was worse. Everything from the downer cattle, to those scrapie infected sheep, to any roadkill, including the city police horse and the circus elephant went to the renders for feed and other products for consumption. Then they only implemented a partial feed ban on Aug. 4, 1997, but pigs, chickens, dogs, and cats, and humans were exempt from that ban. So they can still feed pigs and chickens those potentially TSE tainted by-products, and then they can still feed those by-products back to the cows. I believe it was Dr. Joe Gibbs, that said, the prion protein, can survive the digestinal track. So you have stopped nothing. It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent neurologically ill cattle, some with encephalopathy stamped on the dead slips, were picked up and sent to the renders, along with sheep carcasses. Speaking of autopsies, I have a stack of them, from CJD victims. You would be surprised of the number of them, who ate cow brains, elk brains, deer brains, or hog brains.
I believe all these TSE's are going to be related, and originally caused by the same greedy Industries, and they will be many. Not just the Renders, but you now see, that they are re-using medical devices that were meant for disposal. Some medical institutions do not follow proper auto- claving procedures (even Olympus has put out a medical warning on their endescopes about CJD, and the fact you cannot properly clean these instruments from TSE's), and this is just one product. Another route of infection.
Regardless what the Federal Government in the U.S. says. It's here, I have seen it, and the longer they keep sweeping it under the rug and denying the fact that we have a serious problem, one that could surpass aids (not now, but in the years to come, due to the incubation period), they will be responsible for the continued spreading of this deadly disease.
It's their move, it's CHECK, but once CHECKMATE has been called, how many thousands or millions, will be at risk or infected or even dead. You can't play around with these TSE's. I cannot stress that enough. They are only looking at body bags, and the fact the count is so low. But, then you have to look at the fact it is not a reportable disease in most states, mis-diagnosis, no autopsies performed. The fact that their one-in-a- million theory is a crude survey done about 5 years ago, that's a joke, under the above circumstances. A bad joke indeed........
The truth will come, but how many more have to die such a hideous death. It's the Government's call, and they need to make a serious move, soon. This problem, potential epidemic, is not going away, by itself.
Terry S. Singeltary Sr.
Bacliff, Texas 77518 USA
flounder@wt.net
Competing interests: No competing interests
Singeltary 2000
BMJ 2000; 320 doi: https://doi.org/10.1136/bmj.320.7226.8/b (Published 01 January 2000) Cite this as: BMJ 2000;320:8
02 January 2000 Terry S Singeltary retired
Rapid Response:
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well...
In reading your short article about 'Scientist warn of CJD epidemic' news in brief Jan. 1, 2000. I find the findings in the PNAS old news, made famous again. Why is the U.S. still sitting on their butts, ignoring the facts? We have the beginning of a CJD epidemic in the U.S., and the U.S. Gov. is doing everything in it's power to conceal it.
The exact same recipe for B.S.E. existed in the U.S. for years and years. In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25 page report by the USDA:APHIS:VS. It could have been done in one page. The first page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering technology and the lack of usage of solvents, however, large differences still remain with other risk factors which greatly reduce the potential risk at the national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the U.S., with nothing more than the cattle to sheep ratio count, and the geographical locations of herds and flocks. That's all the evidence they can come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous rendering technology which uses lower temperatures and accounts for 25 percent of total output. This technology was _originally_ designed and imported from the United States. However, the specific application in the production process is _believed_ to be different in the two countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two countries. The calculations are based on slaughter numbers, fallen stock estimates, and product yield coefficients. This approach is used due to variation of up to 80 percent from different reported sources. At 3.6 million tons, the United States produces 8 times more animal rendered product than the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and bone meal is more acute in both relative and absolute terms in the United Kingdom (Figures 27 and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61 thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in the United States. For sheep greater than 1 year, this is less than one-tenth of one percent of the United States supply."
"The potential risk of amplification of the BSE agent through cattle meat and bone meal is much greater in the United States where it accounts for 59 percent of total product or almost 5 times more than the total amount of rendered product in the United Kingdom."
Considering, it would only take _one_ scrapie infected sheep to contaminate the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug. 1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful of scrapie infected material is lethal to a cow.
Considering all this, the sheep to cow ration is meaningless. As I said, it's 24 pages of B.S.e.
To be continued...
Terry S. Singeltary Sr. Bacliff, Texas USA
Competing interests: No competing interests
Singeltary 2001
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor:
In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally..
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
Singeltary 2003
doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
Available online 29 July 2003.
Volume 3, Issue 8, August 2003, Page 463
Volume 3, Number 8 01 August 2003
Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.
49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.
To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.
Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.
Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.
Getting data on TSEs in the USA from the government is like pulling teeth, Singeltary argues. You get it when they want you to have it, and only what they want you to have.
Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings; adding that, the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure. The USA should develop a system modelled on that established in the UK, he points out.
Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters two of whom were friends who died from pathologically confirmed CJD, says that at present there are insufficient data to claim transmission of CWD into humans; adding that [only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further. Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.
CDC spokesman Ermias Belay says that the CDC will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat. He notes that although the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited.
Singeltary 2003
January 28, 2003; 60 (2) VIEWS & REVIEWS
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Terry S. Singeltary, retired (medically)
Published March 26, 2003
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
Singeltary 2007
The Pathological Protein: Mad Cow, Chronic Wasting, and Other Deadly Prion Diseases
by Philip Yam
''Answering critics like Terry Singeltary, who feels that the US undercounts CJD, Schonberger _conceded_ that the current surveillance system has errors but stated that most of the errors will be confined to the older population''...
Revisiting Sporadic CJD
It’s not hard to get Terry Singeltary going. “I have my conspiracy theories,” admitted the 49-year-old Texan.1 Singeltary is probably the nation’s most relentless consumer advocate when it comes to issues in prion diseases. He has helped families learn about the sickness and coordinated efforts with support groups such as CJD Voice and the CJD Foundation. He has also connected with others who are critical of the American way of handling the threat of prion diseases. Such critics include Consumers Union’s Michael Hansen, journalist John Stauber, and Thomas Pringle, who used to run the voluminous www.madcow.org Web site. These three lend their expertise to newspaper and magazine stories about prion diseases, and they usually argue that
223
prions represent more of a threat than people realize, and that the government has responded poorly to the dangers because it is more concerned about protecting the beef industry than people’s health.
Singeltary has similar inclinations, but unlike these men, he doesn’t have the professional credentials behind him. He is an 11th-grade dropout, a machinist who retired because of a neck injury sustained at work. But you might not know that from the vast stores of information in his mind and on his hard drive. Over the years, he has provided unacknowledged help to reporters around the globe, passing on files to such big-time players as The New York Times, Newsweek, and USA Today. His networking with journalists, activists, and concerned citizens has helped medical authorities make contact with suspected CJD victims. He has kept scientists informed with his almost daily posting of news items and research abstracts on electronic newsgroups, including the bulletin board on www.vegsource.com and the BSE-listserv run out of the University of Karlsruhe, Germany. His combative, blunt, opinionated style sometimes borders on obsessive ranting that earns praise from some officials and researchers but infuriates others—especially when he repeats his conviction that “the government has lied to us, the feed industry has lied to us—all over a buck.” As evidence, Singeltary cites the USDA’s testing approach, which targets downer cows and examined 19,900 of them in 2002. To him, the USDA should test 1 million cattle, because the incidence of BSE may be as low as one in a million, as it was in some European countries. That the U.S. does not, he thinks, is a sign that the government is really not interested in finding mad cows because of fears of an economic disaster.
Singeltary got into the field of transmissible spongiform encephalopathy in 1997, just after his mother died of sporadic CJD. She had an especially aggressive version—the Heidenhain variant—that first causes the patient to go blind and then to deteriorate rapidly. She died just ten weeks after her symptoms began. Singeltary, who said he had watched his grandparents die of cancer, considered her death by CJD to be much, much worse: “It’s something you never forget.” Her uncontrollable muscle twitching became so bad “that it took three of us to hold her one time,” Singeltary recalled. “She did everything but levitate in bed and spin her head.” Doctors originally diagnosed Alzheimer’s disease, but a postmortem neuropathological exam demanded by Singeltary revealed the true nature of her death.
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Classifying a disease as “sporadic” is another way for doctors to say they don’t know the cause. Normal prion proteins just turn rogue in the brain for no apparent reason. The term “sporadic” is often particularly hard for the victims’ families to accept, especially when the patient was previously in robust health. Maybe it was something in the water, they wonder, or in the air, or something they ate—the same questions CJD researchers tried to answer decades ago. The names “sporadic CJD” and “variant CJD” also confuse the public and raise suspicions that U.S. authorities are hiding something when they say there have been no native variant CJD cases in the country.
Singeltary suspected an environmental cause in his mother’s demise—a feeling reinforced a year later when a neighbor died of sporadic CJD. For years, the neighbor had been taking nutritional supplements that contained cow brain extracts. Researchers from the National Institutes of Health collected samples of the supplement, Singeltary recounted, and inoculated suspensions into mice. The mice remained healthy—which only means that those supplement samples tested were prion-free.
Scientists have made several attempts during the past few decades to find a connection between sporadic CJD and the environment. Often, these studies take the form of asking family members about CJD victims—their diet, occupation, medical history, hobbies, pets, and so forth—and comparing them with non-CJD subjects. Such case-control CJD studies have produced some intriguing—and sometimes contradictory—results. In 1985, Carleton Gajdusek and his NIH colleagues reported a correlation between CJD and eating a lot of roast pork, ham, hot dogs, and lamb, as well as rare meats and raw oysters.2 Yet they also recognized that the findings were preliminary and that more studies were needed.
Following up, Robert Will of the U.K. National CJD Surveillance Unit and others pooled this data with those from two other case-control studies on CJD (one from Japan and one from the U.K.). In particular, they figured the so-called odds ratio—calculated by dividing the frequency of a possible factor in the patient group by the frequency of the factor in the control group. An odds ratio greater than 1 means that the factor may be significant. In their study, Will and his collaborators found an increase of CJD in people who have worked as health professionals (odds ratio of 1.5) and people who have had contact with cows
Laying Odds 225
(1.7) and sheep (1.6). Unfortunately, those connections were not statistically significant: The numbers of pooled patients (117) and control subjects (333) were so small that the researchers felt the odds ratios needed to reach 2.5 to 8 (depending on the assumptions) before they could be deemed statistically significant. The only statistically significant correlations they found were between CJD and a family history of either CJD (19.1) or other psychotic disease (9.9), although the latter might simply be correlated because psychotic disease may be an early symptom of undiagnosed CJD.3 In contrast with earlier findings, the team concluded that there was no association between sporadic CJD and the consumption of organ meats, including brains (0.6).
Although these case-control studies shed a certain amount of light on potential risk factors for CJD, it’s impossible to draw firm conclusions. Obtaining data that produces statistically meaningful results can be difficult because of the rarity of CJD and hence the shortage of subjects. Human memory is quite fragile, too, so patients’ families may not accurately recall the lifestyle and dietary habits of their loved ones over the course of a decade or more. Consequently, researchers must cope with data that probably contain significant biases. In a review paper on CJD, Joe Gibbs of the NIH and Richard T. Johnson of Johns Hopkins University concluded that “the absence of geographic differences in incidence is more convincing evidence against major dietary factors, since large populations eschew pork and some consume no meat or meat products.” A CJD study of lifelong vegetarians, they proposed, could produce some interesting data.4
The inconclusive results of case-control studies do not completely rule out the environment as a possible cause of CJD. “Dr. Prusiner’s theory does fit much of the data of spontaneous generation of [malformed] PrP somewhere in the brain,” Will remarked—that is, the idea that sporadic CJD just happens by itself falls within the realm of the prion theory. Still, “it’s very odd, if you look at all the forms of human prion diseases there are, all of them are transmissible in the laboratory and could be due to some sort of infectious agent.”5 One of the great difficulties, he explained, is that “given that this is a disease of an extraordinarily long incubation period, are we really confident that we can exclude childhood exposure that is transmitted from person to person, as people move around? It’s difficult to be sure about that.” There might a “carrier state” that leaves people healthy yet still able to
226 CHAPTER 14
infect others. If so, “you would never be able to identify what’s causing the spread of the disease,” concluded Will, who hasn’t stopped looking for a possible environmental link. He has some preliminary data based on studies that trace CJD victims’ lives well before the time symptoms began—up to 70 years; they suggest some degree of geographic clustering, but no obvious candidates for a source of infection.
A Case for Undercounting
The difficulty in establishing causal links in sporadic prion diseases—if there are any in the first place—underlines the importance of thorough surveillance. The U.K. has an active program, and when a victim of CJD is reported, one of Robert Will’s colleagues visits and questions the victim’s family. “No one has looked for CJD systematically in the U.S.,” the NIH’s Paul Brown noted. “Ever.”6 The U.S., through the Centers for Disease Control and Prevention, has generally maintained a more passive system, collecting information from death certificates from the National Center for Health Statistics. Because CJD is invariably fatal, mortality data is considered to be an effective means of tabulating cases. The CDC assessed the accuracy of such data by comparing the numbers with figures garnered through an active search in 1996: Teams covering five regions of the U.S. contacted the specialists involved and reviewed medical records for CJD cases between 1991 and 1995. Comparing the actively garnered data with the death certificate information showed that “we miss about 14 percent,” said CDC epidemiologist Lawrence Schonberger. “That’s improving. Doctors are becoming more knowledgeable,” thanks to increased scientific and media attention given to prion diseases.7
The active surveillance study of 1996, however, only looked at cases in which physicians attributed the deaths to CJD. Misdiagnosed patients or patients who never saw a neurologist were not tabulated— thus CJD may be grossly underreported. Many neurological ailments share symptoms, especially early on. According to various studies, autopsies have found that CJD is misdiagnosed as other ills, such as dementia or Alzheimer’s disease, 5 to 13 percent of the time. The CDC finds that around 50,000Americans die from Alzheimer’s each year
Laying Odds 227
(about 4 million have the disease, according to the Alzheimer’s Association). Therefore, one could argue that thousands of CJD cases are being missed. (On the flip side, CJD could be mistakenly diagnosed as Alzheimer’s disease or dementia, but the number of CJD patients is so small that they wouldn’t dramatically skew the statistics for other neurological ills.)
In part to address the issue of misdiagnosis, CJD families have asked the CDC to place the disease on the national list of officially notifiable illnesses, which tends to include more contagious conditions such as AIDS, tuberculosis, hepatitis, and viral forms of encephalitis. Currently, only some states impose this requirement. CDC officials have discounted the utility of such an approach, arguing that it would duplicate the mortality data, which is more accurate than early diagnoses of CJD, anyway. Moreover, mandatory reporting of CJD cases does not necessarily guarantee the end to missed cases.8
One clue suggests that the passive system is undercounting CJD in the U.S.: racial difference. The number of black CJD victims is about 38 percent that of white victims. Rather than sporadic CJD being a onein-a-million lottery, it’s more like one-in-2.5-million for AfricanAmericans. Access to medical care might be one reason. Schonberger recounted that the CDC had asked other countries with substantial black populations to submit CJD figures for comparison but found that the surveillance in those countries was inadequate. “We haven’t been able to find any comparable literature on this issue, so it’s still up in the air,” Schonberger said. On the other hand, Alzheimer’s disease is more common among black people than whites, with an estimated higher prevalence ranging from 14 percent to almost 100 percent, according to a February 2002 report by the Alzheimer’s Association. Are some black CJD cases being misdiagnosed as Alzheimer’s?
Answering critics like Terry Singeltary, who feels that the U.S. undercounts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population. As Schonberger pointed out, no doctor would misdiagnose a 30-year-old CJD patient as having Alzheimer’s. The average age of the first 100 variant CJD victims was 29; should the epidemiology of vCJD change—if older people start coming down with it—then there would be problems. “The adequacy of our overall CJD surveillance would be greatly reduced should the proportion of older individuals affected by variant CJD substantially increase,” Schonberger explained.9
SNIP...SEE FULL TEXT;
''The average age of the first 100 variant CJD victims was 29; should the epidemiology of vCJD change—if older people start coming down with it—then there would be problems. “The adequacy of our overall CJD surveillance would be greatly reduced should the proportion of older individuals affected by variant CJD substantially increase,” Schonberger explained.9''
THE PATHOLOGICAL PROTEIN by Philip Yam
Singeltary Submission SEAC 2007
SEAC SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007 Singeltary Submission
This was 22 years to the day Mom died from the Heidenhain Variant of Creutzfeldt Jakob Disease i.e. hvCJD, when i made this submission to SEAC and this was their reply to my questions of concern about cjd in the USA, my how things have changed...terry
SEAC SPONGIFORM ENCEPHALOPATHY ADVISORY COMMITTEE Minutes of the 99th meeting held on 14th December 2007
ITEM 8 – PUBLIC QUESTION AND ANSWER SESSION 40. The Chair explained that the purpose of the question and answer session was to give members of the public an opportunity to ask questions related to the work of SEAC. Mr Terry Singeltary (Texas, USA) had submitted a question prior to the meeting, asking: “With the Nor-98 now documented in five different states so far in the USA in 2007, and with the two atypical BSE H-base cases in Texas and Alabama, with both scrapie and chronic wasting disease (CWD) running rampant in the USA, is there any concern from SEAC with the rise of sporadic CJD in the USA from ''unknown phenotype'', and what concerns if any, in relations to blood donations, surgery, optical, and dental treatment, do you have with these unknown atypical phenotypes in both humans and animals in the USA? Does it concern SEAC, or is it of no concern to SEAC? Should it concern USA animal and human health officials?”
41. A member considered that this question appeared to be primarily related to possible links between animal and human TSEs in the USA. There is no evidence that sCJD is increasing in the USA and no evidence of any direct link between TSEs and CJD in the USA. Current evidence does not suggest that CWD is a significant risk to human health. There are unpublished data from a case of human TSE in the USA that are suggestive of an apparently novel form of prion disease with distinct molecular characteristics. However, it is unclear whether the case had been further characterised, if it could be linked to animal TSEs or if other similar cases had been found in the USA or elsewhere. In relation to the possible public health implications of atypical scrapie, H-type BSE and CWD, research was being conducted to investigate possible links and surveillance was in place to detect any changes in human TSEs. Although possible links between these diseases and human TSEs are of concern and require research, there is no evidence to suggest immediate public health action is warranted. The possible human health risks from classical scrapie had been discussed earlier in the meeting. Members noted that there are effective channels of discussion and collaboration on research between USA and European groups. Members agreed it is important to keep a watching brief on new developments on TSEs.
Singeltary 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
August 10, 2009
Greetings,
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. North America seems to have the most species with documented Transmissible Spongiform Encephalopathy's, most all of which have been rendered and fed back to food producing animals and to humans for years. If you look at the statistics, sporadic CJD seems to be rising in the USA, and has been, with atypical cases of the sCJD. I find deeply disturbing in the year of 2009, that Human Transmissible Spongiform Encephalopathy of any strain and or phenotype, of all age groups, and I stress all age groups, because human TSE's do not know age, and they do not know borders. someone 56 years old, that has a human TSE, that has surgery, can pass this TSE agent on i.e. friendly fire, and or passing it forward, and there have been documented nvCJD in a 74 year old. Remembering also that only sporadic CJD has been documented to transmit via iatrogenic routes, until recently with the 4 cases of blood related transmission, of which the origin is thought to be nvCJD donors. However most Iatrogenic CJD cases are nothing more than sporadic CJD, until the source is proven, then it becomes Iatrogenic. An oxymoron of sorts, because all sporadic CJD is, are multiple forms, or strains, or phenotypes of Creutzfeldt Jakob Disease, that the route and source and species have not been confirmed and or documented. When will the myth of the UKBSEnvCJD only theory be put to bed for good. This theory in my opinion, and the following there from, as the GOLD STANDARD, has done nothing more than help spread this agent around the globe. Politics and money have caused the terrible consequences to date, and the fact that TSEs are a slow incubating death, but a death that is 100% certain for those that are exposed and live long enough to go clinical. once clinical, there is no recourse, to date. But, while sub-clinical, how many can one exposed human infect? Can humans exposed to CWD and scrapie strains pass it forward as some form of sporadic CJD in the surgical and medical arenas? why must we wait decades and decades to prove this point, only to expose millions needlessly, only for the sake of the industries involved? would it not have been prudent from the beginning to just include all TSE's, and rule them out from there with transmission studies and change policies there from, as opposed to doing just the opposite? The science of TSE's have been nothing more than a political circus since the beginning, and for anyone to still believe in this one strain, one group of bovines, in one geographical location, with only one age group of human TSE i.e. nvCJD myth, for anyone to believe this today only enhances to spreading of these human and animal TSE's. This is exactly why we have been in this quagmire.
The ones that believe that there is a spontaneous CJD in 85%+ of all cases of human TSE, and the ones that do not believe that cattle can have this same phenomenon, are two of the same, the industry, and so goes the political science aspect of this tobacco and or asbestos scenario i.e. follow the money. I could go into all angles of this man made nightmare, the real facts and science, for instance, the continuing rendering technology and slow cooking with low temps that brewed this stew up, and the fact that THE USA HAD THIS TECHNOLOGY FIRST AND SHIPPED IT TO THE U.K. SOME 5 YEARS BEFORE THE U.S. STARTED USING THE SAME TECHNOLOGY, to save on fuel cost. This is what supposedly amplified the TSE agent via sheep scrapie, and spread via feed in the U.K. bovine, and other countries exporting the tainted product. BUT most everyone ignores this fact, and the fact that the U.S. has been recycling more TSE, from more species with TSEs, than any other country documented, but yet, it's all spontaneous, and the rise in sporadic CJD in the U.S. is a happenstance of bad luck ??? I respectfully disagree. To top that all off, the infamous BSE-FIREWALL that the USDA always brags about was nothing more than ink on paper, and I can prove this. YOU can ignore it, but this is FACT (see source, as late as 2007, in one recall alone, some 10,000,000 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE TO BE FED OUT, and most was never recovered. This was banned blood laced, meat and bone meal. 2006 was a banner year for banned mad cow protein going into commerce in the U.S. (see source of FDA feed ban warning letter below). I stress that the August 4, 1997 USA mad cow feed ban and this infamous BSE firewall, was nothing more than ink on paper, it was never enforceable.
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route. This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub- clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE one strain TSE in cows, and the nv/v CJD one strain TSE humans, and the one geographical location source i.e. U.K., and that all the rest of human TSE are just one single strain i.e. sporadic CJD, a happenstance of bad luck that just happens due to a twisted protein that just twisted the wrong way, IN 85%+ OF ALL HUMAN TSEs, when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al, and that no other animal TSE transmits to humans ??? With all due respect to all Scientist that believe this, I beg to differ. To continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human. WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...
please see history, and the ever evolving TSE science to date ;
Saturday, June 13, 2009
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States 2003 revisited 2009
Singeltary 2010
Human Prion Diseases in the United States
Robert C. Holman ,Ermias D. Belay,Krista Y. Christensen,Ryan A. Maddox,Arialdi M. Minino,Arianne M. Folkema,Dana L. Haberling,Teresa A. Hammett,Kenneth D. Kochanek,James J. Sejvar,Lawrence B. Schonberger
Published: January 1, 2010
https://doi.org/10.1371/journal.pone.0008521
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
I kindly disagree with your synopsis for the following reasons ;
Singeltary 2014
Alzheimer's disease, iatrogenic transmission, what if?
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
*** 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
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
MONDAY, APRIL 24, 2023
Prion Disease on the Rise in the U.S., Now the question is, why?
''5 cases per million in persons 55 years of age or older.''
