BSE TSE Prion MAD COW TESTING IN THE USA COMPARED TO OTHER COUNTRIES?
1st a bit of history
SCIENCE NEWS JULY 13, 2004 / 5:02 PM
USDA advised against mad cow test in 2002
By STEVE MITCHELL, United Press International
"Why are we using Bio-Rad instead of Prionics if they are as bad as the (USDA) would have us believe with all these 'inconclusives?'" asked Terry Singletary, coordinator of CJD Watch, an advocacy group for patients and family members. His mother died of a rare form of CJD called Heidenhain Variant, which has not been linked with mad cow disease.
SCIENCE NEWS MAY 11, 2004 / 10:15 PM
USDA orders silence on mad cow in Texas
By STEVE MITCHELL, United Press International
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
Consumer Health
Inspector to file charges against USDA
By Steve Mitchell Sep 6, 2005, 22:46 GMT
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 ittested 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.
Archived url link;
A big shout out to https://web.archive.org/ Thank You!
"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.
snip...
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;
NOT to forget ;
It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing. This was done to ensure that samples inappropriate for the rapid screen test were still tested, and also to monitor and improve upon IHC testing protocols. Of those 9,200 routine tests, one test returned a non-definitive result on July 27, 2005. That sample underwent additional testing at NVSL, as well as at the Veterinary Laboratories Agency in Weybridge, England, and results were negative. ......
http://www.aphis.usda.gov/lpa/issues/bse_testing/test_results.html
r i g h t ............
By Steve Mitchell
United Press International
Published 2/9/2004 7:06 PM
WASHINGTON, Feb. 9 (UPI) -- The federal laboratory in Ames, Iowa, that conducts all of the nation's tests for mad cow disease has a history of producing ambiguous and conflicting results -- to the point where many federal meat inspectors have lost confidence in it, Department of Agriculture veterinarians and a deer rancher told United Press International.
The veterinarians also claim the facility -- part of the USDA and known as the National Veterinary Services Laboratories -- has refused to release testing results to them and has been so secretive some suspect it is covering up additional mad cow cases. ...
-------- 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 resignations are unexpected. just pondering...TSS
-------- Original Message --------
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
snip...see full transmission;
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
2
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
3
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
4
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.
5 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
6
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
7
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
8
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
see archived url;
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.
snip...
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.
snip...
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.
SNIP...
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
snip...
FULL TEXT 130 PAGES
NEW URL LINK;
Panel questions Homeland Security inspection of food By Jerry Hagstrom, CongressDailyPM
Agriculture Department Inspector General Phyllis Fong and several members of the House Agriculture Appropriations Subcommittee expressed concern Wednesday about whether the Homeland Security Department is properly inspecting food and other agricultural items when they arrive in the United States. Neither Fong nor the committee members provided any hard evidence of problems, but Fong said she and the Homeland Security Department's inspector general were conducting a joint review of inspection functions. Once the province of USDA's Animal and Plant Health Inspection Service, they were transferred to Homeland Security when that department was created.
"We are still very concerned about whether that broader inspection is being carried out," Fong said in testimony.
Fong said the joint inquiry was only in the stage of field investigation and had reached no conclusions.
Rep. Marcy Kaptur, D-Ohio, suggested the inspector general focus on the impact of the inspections on plants from other countries. House Agriculture Appropriations Subcommittee Chairman Henry Bonilla, R-Texas, said he had asked the Government Accountability Office to investigate the food inspection process. Rep. Tom Latham, R-Iowa, who noted he also sits on the House Homeland Security Appropriations Subcommittee, said, "Apparently there are still some unresolved issues about what the heck [the department] is doing."
Under questioning from Agriculture Appropriations ranking member Rosa DeLauro, D-Conn., Fong acknowledged it was APHIS Administrator Ron DeHaven who made the decision not to conduct further tests on a Texas cow whose initial test for bovine spongiform encephalopathy, or mad cow disease, was inconclusive. Further tests ordered by the inspector general several months later showed that the cow had the disease.
DeLauro noted that when Japan stopped importing U.S. beef in December, USDA moved faster to deal with that issue than it had when the Texas cow was tested, a sign, she said, that USDA was more concerned about trade than human health.
"We are taking years to deal with public health," DeLauro said. "If APHIS is in charge of avian influenza and we have the kinds of problems existing here, it doesn't bode well for public safety."
http://www.govexec.com/dailyfed/0306/030106cdpm2.htm
see archived url;
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
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
Thursday, April 6, 2023
WOAH OIE CHAPTER 11.4 . BOVINE SPONGIFORM ENCEPHALOPATHY Article 11.4.1.
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
see my full submission;
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
Greetings again APHIS et al,
I would kindly like to again, post my concern or urgency, on why said information is so critical, and why the 3 year extension is so critical, especially today, with the recent mad cow cases in the UK, Switzerland, Brazil, Spain, and The Netherlands all atypical BSE cases, and the fact the OIE is so concerned with the recent science about atypical L-type BSE and atypical H-type BSE, both of which can transmit orally, (see OIE BSE atypical in my reference materials), new outbreak of a new Prion disease in a new livestock species, i.e. the camel. The fact Chronic Wasted Disease CWD TSE Prion of Cervid, is spreading across the USA, with no stopping it in the near future, now with 10 different strains, a spillover into cattle or sheep would be devastating, and the ramifications of human zoonosis there from, has great concern throughout the scientific community. The fact that the USA BSE feed ban was and is a joke today (see why, with the fact that CWD positive deer could enter the food/feed chain for other ruminants and what the DEFRA says), how the BSE surveillance and testing has failed us so terribly bad to date, by testing only 25k bovines a year for BSE, you will not find BSE until it's too late, again. THIS is all why INFORMATION COLLECTION is so vital for BSE and all human and animal Transmissible Spongiform Encephalopathy TSE Prion disease.
''The purpose of this notice is to solicit comments from the public (as well as affected agencies) concerning our information collection. These comments will help us:''
(1) Evaluate whether the collection of information is necessary for the proper performance of the functions of the Agency, including whether the information will have practical utility;
(2) Evaluate the accuracy of our estimate of the burden of the collection of information, including the validity of the methodology and assumptions used;
(3) Enhance the quality, utility, and clarity of the information to be collected; and
(4) Minimize the burden of the collection of information on those who are to respond, through use, as appropriate, of automated, electronic, mechanical, and other collection technologies; ...end
The question should be, what will the burden be, if WE DON'T COLLECT SAID INFORMATIONS ON BSE, and we find ourselves again facing a BSE epidemic?
I want to bring your attention too, and emphasize;
(3) Enhance the quality, utility, and clarity of the information to be collected; and...
I remember that infamous TEXAS MAD COW that instead of a 48 turnaround at Weybridge, said suspect positive, was declared NEGATIVE, until an Act of Congress and the Honorable Phyllis Fong overrode Texas negative test, sent that BSE sample to Weybridge, and 6 MONTHS LATER ON A 48 HOUR TURNAROUND (BSE REDBOOKS), that BSE sample was CONFIRMED POSITIVE (see history in my references).
Let's not kid ourselves, the BSE ENHANCED BSE SURVEILLANE efforts way back was a total failure, that's why it was shut down, too many atypical BSE cases were showing up.
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, 2023, down 4% from last year. The number of milk cows in the United States increased to 9.40 million. U.S. calf crop was estimated at 34.5 million head, down 2% from 2021. Jan 31, 2023.
ALL it would take is one BSE positive, yet alone a handful of BSE cases, this is why the Enhanced BSE was shut down, and the BSE testing shut down to 25k, and the BSE GBRs were replaced with BSE MRRs, after the 2003 Christmas Mad cow, the cow that stole Christmas, making it legal to trade BSE, imo.
THE world was set back to square one with the BSE Minimal Risk Regions, from the BSE GBRs.
WE must enhance our BSE Surveillance and BSE Testing, and the FDA PART 589 TSE PRION FEED BAN must be revised to include Cervid by-products and SRM, and it should be made MANDATORY, AND THIS SHOULD BE WELL DOCUMENTED with information collection.
said 'burden' cost, will be a heavy burden to bear, if we fail with Bovine Spongiform Encephalopathy BSE TSE Prion disease, that is why this information collection is so critical...
Singeltary References
see full submission of concerns;
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.
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.
#
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, 2023, down 4% from last year. The number of milk cows in the United States increased to 9.40 million. U.S. calf crop was estimated at 34.5 million head, down 2% from 2021. Jan 31, 2023.
ALL it would take is one BSE positive, yet alone a handful of BSE cases, this is why the Enhanced BSE was shut down, and the BSE testing shut down to 25k, and the BSE GBRs were replaced with BSE MRRs, after the 2003 Christmas Mad cow, the cow that stole Christmas, making it legal to trade BSE, imo.
Document APHIS-2023-0027-0001 BSE Singeltary Comment Submission
see full submission;
NOW before you go off and start repeating BSE TSE Prion science that is almost 50 years old, let's be perfectly clear what science is saying today, and especially what the WAHIS/WOAH/OIE et al are saying about the atypical BSE strains... OIE Conclusions on transmissibility of atypical BSE among cattle
Given that cattle have been successfully infected by the oral route, at least for L-BSE, it is reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle are exposed to contaminated feed. In addition, based on reports of atypical BSE from several countries that have not had C-BSE, it appears likely that atypical BSE would arise as a spontaneous disease in any country, albeit at a very low incidence in old cattle. In the presence of livestock industry practices that would allow it to be recycled in the cattle feed chain, it is likely that some level of exposure and transmission may occur. As a result, since atypical BSE can be reasonably considered to pose a potential background level of risk for any country with cattle, the recycling of both classical and atypical strains in the cattle and broader ruminant populations should be avoided.
Annex 7 (contd) AHG on BSE risk assessment and surveillance/March 2019
34 Scientific Commission/September 2019
3. Atypical BSE
The Group discussed and endorsed with minor revisions an overview of relevant literature on the risk of atypical BSE being recycled in a cattle population and its zoonotic potential that had been prepared ahead of the meeting by one expert from the Group. This overview is provided as Appendix IV and its main conclusions are outlined below. With regard to the risk of recycling of atypical BSE, recently published research confirmed that the L-type BSE prion (a type of atypical BSE prion) may be orally transmitted to calves1 . In light of this evidence, and the likelihood that atypical BSE could arise as a spontaneous disease in any country, albeit at a very low incidence, the Group was of the opinion that it would be reasonable to conclude that atypical BSE is potentially capable of being recycled in a cattle population if cattle were to be exposed to contaminated feed. Therefore, the recycling of atypical strains in cattle and broader ruminant populations should be avoided.
4. Definitions of meat-and-bone meal (MBM) and greaves
Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.
''H-TYPE BSE AGENT IS TRANSMISSIBLE BY THE ORONASAL ROUTE''
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA?, what if?
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Sheep are susceptible to the agent of TME by intracranial inoculation and have evidence of infectivity in lymphoid tissues
Author item CASSMANN, ERIC - Oak Ridge Institute For Science And Education (ORISE) item MOORE, SARA - Oak Ridge Institute For Science And Education (ORISE) item SMITH, JODI - Iowa State University item Greenlee, Justin
Submitted to: Frontiers in Veterinary Science Publication Type: Peer Reviewed Journal Publication Acceptance Date: 11/14/2019 Publication Date: 11/29/2019 Citation: Cassmann, E.D., Moore, S.J., Smith, J.D., Greenlee, J.J. 2019.
Sheep are susceptible to the agent of TME by intracranial inoculation and have evidence of infectivity in lymphoid tissues.
Frontiers in Veterinary Science. 6:430. https://doi.org/10.3389/fvets.2019.00430. DOI: https://doi.org/10.3389/fvets.2019.00430
Interpretive Summary: Prion diseases are protein misfolding diseases that are transmissible between animals. The outcome of prion infection is irreversible brain damage and death. Transmission can occur between animals of the same or different species, however, transmission between different species is usually less efficient due to the species barrier, which results from differences in the amino acid sequence of the prion protein between the donor and recipient species. The present work evaluated whether transmissible mink encephalopathy (TME) can infect sheep. Our results demonstrate that sheep are susceptible to the TME agent and that the TME agent has similar properties to the agent of L-type atypical bovine spongiform encephalopathy (L-BSE). This work supports the ideas that L-BSE is a possible source for TME in mink and that the practice of feeding cattle with neurologic disease to mink should be avoided. This information is important to farmers who raise cattle, sheep, or mink.
Technical Abstract: Transmissible mink encephalopathy (TME) is a food borne prion disease. Epidemiological and experimental evidence suggests similarities between the agent of TME and L-BSE. This experiment demonstrates the susceptibility of four different genotypes of sheep to the agent of TME by intracranial inoculation. The four genotypes of sheep used in this experiment had polymorphisms corresponding to codons 136 and 171 of the prion gene: VV136QQ171, AV136QQ171, AA136QQ171, and AA136QR171. All intracranially inoculated sheep without comorbidities (15/15) developed clinical scrapie and had detectable PrPSc by immunohistochemistry, western blot, and enzyme immunoassay (EIA). The mean incubation periods in TME infected sheep correlated with their relative genotypic susceptibility. There was peripheral distribution of PrPSc in the trigeminal ganglion and neuromuscular spindles; however, unlike classical scrapie and C-BSE in sheep, ovine TME did not accumulate in the lymphoid tissue. To rule out the presence of infectious, but proteinase K susceptible PrPSc, the lymph nodes of two sheep genotypes, VV136QQ171 and AA136QQ171, were bioassayed in transgenic ovinized mice. None of the mice (0/32) inoculated by the intraperitoneal route had detectable PrPSc by EIA. Interestingly, mice intracranially inoculated with RPLN tissue from a VV136QQ171 sheep were EIA positive (3/17) indicating that sheep inoculated with TME harbor infectivity in their lymph nodes. Western blot analysis demonstrated similarities in the migration patterns between ovine TME and the bovine TME inoculum. Overall, these results demonstrate that sheep are susceptible to the agent of TME, and that the tissue distribution of PrPSc in TME infected sheep is distinct from classical scrapie.
Previous work has shown that the Stetsonville, WI outbreak of TME could have been precipitated by feeding mink a downer cow with atypical BSE; therefore, it very well may have originated from a cow with L-BSE. The agent of TME appears to remain stable, and it has a high transmission efficiency after a sequence of interspecies transmission events. Although C-BSE is the archetypal foodborne TSE, our findings indicate that L-BSE and bTME have greater transmission efficiencies in bovinized mice. Previous work has demonstrated that L-BSE also is more virulent than C-BSE in mice expressing the human prion protein [46, 55]. Although the documented incidence of L-BSE is low, the propensity of L-BSE and the TME agent to cross species barriers support the continued monitoring for atypical BSE.
***>This work supports the ideas that L-BSE is a possible source for TME in mink and that the practice of feeding cattle with neurologic disease to mink should be avoided. This information is important to farmers who raise cattle, sheep, or mink.<***
1985
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...
Specified Risk Materials DOCKET NUMBER Docket No. FSIS-2022-0027 Singeltary Submission Attachment
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
RECENT MAD COW CASES
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
The European Union summary report on surveillance for the presence of transmissible spongiform encephalopathies (TSE) in 2021
Published:
30 November 2022
Approved: 3 November 2022
Metadata
EFSA Journal 2022;20(11):7655
Keywords: TSE, BSE, CWD, scrapie, classical, atypical, surveillance
On request from: European Commission Question Number: EFSA‐Q‐2021‐00765
Contact: zoonoses@efsa.europa.eu
Abstract
This report presents the results of surveillance on transmissible spongiform encephalopathies (TSE) in cattle, sheep, goats, cervids and other species, and genotyping in sheep and goats, carried out in 2021 by 27 Member States (MS, EU27), the United Kingdom (in respect of Northern Ireland) (XI), and eight other non‐EU reporting countries: Bosnia and Herzegovina, Iceland, Montenegro, North Macedonia, Norway, Serbia, Switzerland and Turkey.
In total, 1,021,252 cattle were tested by EU27 and XI (−9%, compared with 2020 when data from the United Kingdom were not restricted to Northern Ireland), and 66,121 cattle by eight non‐EU reporting countries,
with two cases of H‐BSE in France and Spain, and four L‐BSE in France (2), Germany and Spain.
In total, 311,174 sheep and 118,457 goats were tested in the EU27 and XI (−6.4% and −1.8%, respectively, compared to 2020 when data from the whole United Kingdom were considered).
In sheep, 551 cases of scrapie were reported by 17 MS and XI: 448 classical scrapie (CS) by six MS [80 index cases (IC) with genotypes of susceptible groups in 97% of the cases], 103 atypical scrapie (AS) (96 IC) by 13 MS and XI.
In the other non‐EU reporting countries, 27,594 sheep were tested with 55 CS and 1 AS in Iceland and 8 AS in Norway.
Ovine random genotyping was reported by nine MS and genotypes of susceptible groups accounted for 7.9%.
In goats, 224 cases of scrapie were reported by six EU MS: 219 CS (30 IC) by six MS, and five AS (5 IC) by three MS.
In total, 5,854 cervids were tested for chronic wasting disease by eight MS; all resulted negative. Norway tested 21,670 cervids with two moose and one red deer positive. In total, 149 animals from four other species tested negative in Finland and Turkey.
© European Food Safety Authority
see full text;
SECOND, let's review the USDA/APHIS et al BSE, Scrapie, and CWD testing, past and present...
WEDNESDAY, NOVEMBER 30, 2022
USDA Bovine Spongiform Encephalopathy BSE, Scrapie, CWD, Testing and Surveillance 2022 A Review of History
TUESDAY, SEPTEMBER 07, 2021
Atypical Bovine Spongiform Encephalopathy BSE OIE, FDA 589.2001 FEED REGULATIONS, and Ingestion Therefrom
TUESDAY, SEPTEMBER 13, 2022
BSE pathogenesis in the ileal Peyer’s patches and the central and peripheral nervous system of young cattle 8 months post oral BSE challenge
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA
WEDNESDAY, JANUARY 12, 2022
Bovine Spongiform Encephalopathy BSE TSE Prion Origin USA, what if?
TUESDAY, MAY 31, 2022
USA Bovine Spongiform Encephalopathy BSE: description of typical and atypical cases
PLOS ONE Journal
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
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
SATURDAY, SEPTEMBER 24, 2022
Transmission of CH1641 in cattle
MONDAY, SEPTEMBER 19, 2022
589.2001 BSE TSE regulations which prohibits the use of high-risk cattle material in feed for all animal species 2022
FRIDAY, APRIL 1, 2022
USDA TAKES THE C OUT OF COOL, what's up with that?
MONDAY, JUNE 6, 2022
APHIS USDA History Highlight: APHIS Combats Bovine Spongiform Encephalopathy Published Jun 1, 2022
WEDNESDAY, DECEMBER 8, 2021
Importation of Sheep, Goats, and Certain Other Ruminants AGENCY: Animal APHIA, USDA, FINAL RULE [Docket No. APHIS–2009–0095] RIN 0579–AD10
WEDNESDAY, MARCH 24, 2021
USDA Animal and Plant Health Inspection Service 2020 IMPACT REPORT BSE TSE Prion Testing and Surveillance MIA
https://animalhealthreportpriontse.blogspot.com/2021/03/usda-animal-and-plant-health-inspection.html
SUNDAY, MARCH 21, 2021
Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005 Singeltary's Regiew 2021
https://animalhealthreportpriontse.blogspot.com/2021/03/investigation-results-of-texas-cow-that.html
THURSDAY, JANUARY 23, 2020
USDA Consolidates Regulations for NAHLN Laboratory Testing USDA Animal and Plant Health Inspection Service
sent this bulletin at 01/23/2020 02:15 PM EST
WEDNESDAY, APRIL 24, 2019
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019
Saturday, July 23, 2016
BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016
Tuesday, July 26, 2016
Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016
Monday, June 20, 2016
Specified Risk Materials SRMs BSE TSE Prion Program
*** 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
SEE MAD COW FEED VIOLATIONS AFER MAD COW FEED VIOLATIONS ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
WEDNESDAY, APRIL 24, 2019
***> USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019
SATURDAY, JUNE 1, 2019
Traceability of animal protein byproducts in ruminants by multivariate analysis of isotope ratio mass spectrometry to prevent transmission of prion diseases
CONTINUED IN FILE ATTACHMENT, about 27 pages...terry
SEE FULL SUBMISSION IN ATTACHMENT;
SRM Federal Docket Singeltary Submission 2019
downloads.regulations.gov/FSIS-2019-0021-0002/attachment_1.pdf
Tuesday, September 10, 2019
FSIS [Docket No. FSIS–2019–0021] Notice of Request To Renew an Approved Information Collection: Specified Risk Materials Singeltary Submission
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)
U.S., suppliers settle over school lunch beef linked to recall
By Reuter news service
Published: November 27, 2013
Livestock, Markets, News
Nov 27 (Reuters) – Several California companies and individuals tied to the largest beef recall in U.S. history agreed to settle charges of animal cruelty and the slaughtering of sick cattle for food, including beef supplied to the National School Lunch Program, the Justice Department said on Wednesday.
The settlements end a federal fraud lawsuit begun in February 2008 by the Humane Society of the United States, which had obtained a video that appeared to show inhumane cattle treatment and improper inspections of sick cattle at a Chino, California, plant run by Westland Meat Co. and Hallmark Meat Co.
Under the settlements, Westland agreed to enter a $155.68 million consent judgment, which its lawyer said is unlikely to be collected because the company is defunct, while its owner, Steve Mendell, agreed to pay $240,000.
The government also said M&M Management LLC, Cattleman’s Choice Inc., the estate of Cattleman’s late owner, Aaron “Arnie” Magidow, and Magidow’s widow JoAnn will pay $2.45 million. JoAnn Magidow was not accused of wrongdoing.
Two other defendants, Donald Hallmark Sr and Donald Hallmark Jr, settled in October 2012 for $304,130, the government said. The government joined the case in May 2009.
According to the lawsuit, Westland/Hallmark treated cattle inhumanely and falsely represented that it processed meat only from ambulatory cattle, when it also used “downer” cattle that can walk only with help. Such cattle are considered a greater risk to spread illness.
The case was tied to contracts from August 2003 to January 2008 under which the U.S. Department of Agriculture bought fresh and frozen beef from Westland/Hallmark for school lunches. The USDA now bans non-ambulatory cattle from entering the human food chain.
“Children across the country depend on the National School Lunch Program to provide them with a healthy meal each day,” Stuart Delery, assistant attorney general for the Justice Department’s civil division, said in a statement. “We all depend on companies providing food to the program to follow the rules designed to ensure those meals are safe to eat.”
Mark Troy, a partner at the law firm Crowell & Moring representing Westland, Mendell and M&M, said federal meat inspectors “had been on site 100 percent of the time and inspected every single cow,” but the government blamed Westland because workers had been caught on the video mistreating cows.
He said the Westland judgment is not expected to be paid because the company is out of business.
An uncollectible $497 million judgment was previously entered against Hallmark Meat, the Humane Society has said.
Edward Woods, a partner at Akin Gump Strauss Hauer & Feld representing Cattleman’s Choice, Arnie Magidow’s estate and JoAnn Magidow, in a statement said his clients “were able to reach a settlement with the U.S. for the costs of suit, a mere fraction of what the U.S. had been seeking.”
Both lawyers noted that a federal judge had earlier this year dismissed parts of the government’s case.
A February 2008 recall of Westland/Hallmark beef covered 143 million pounds (64.9 million kg) of meat over two years, of which 37 million pounds (16.8 million kg) had been bought for school lunches and other federal programs.
USDA officials at the time said much of the recalled beef had probably been consumed, but that there had been only a minor risk of illness from eating it.
Westland and M&M were based in Corona Del Mar, California, and Cattleman’s Choice in Commerce, California, the Justice Department said.
The case is U.S. ex rel. Humane Society of the United States v. Westland/Hallmark Meat Co et al, U.S. District Court, Central District of California, No. 08-00221.
ARS USDA Generation of human chronic wasting disease in transgenic mice
Publication Date: 9/26/2021
“We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.”
SUNDAY, APRIL 9, 2023
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
SEE A FEW HIGHLIGHTS;
''Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model.''
''Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission.'' ''These findings have strong implications for public health and CWD management.''
''We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions.''
''Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage.''
Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for ''infection. ''
''Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.''
''Indeed, such heterogeneity and distinct seeding activities and infectivity of abnormal PrP fragments was observed in VPSPr cases [20, 43].''
''This implies a high risk of exposure to this strain, e.g., through consumption or handling of infected carcasses, in contrast to rarer CWD strains, and therefore, an actual risk for human health.''
''Fecal shedding of infectious prions, if it occurs in humans, is particularly concerning because of potential human-to-human transmission and adaptation of hCWD.''
Overall, our findings suggest that CWD surveillance in humans should encompass a wider spectrum of tissues/organs tested and include new criteria in the diagnosis of potential patients.
***> PLEASE NOTE;
''Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defned by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profle and the N-terminal cleavage site.''
snip...
''CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable. Here, humanized mice inoculated with CWD deer isolates had an atypical onset of the disease with myoclonus (93.75%), before presenting typical clinical signs, generating prions that presented with either atypical biochemical signature (#321 and #3063), shed in feces (#327), or were undetectable by the classical detection methods. The fact that we could not establish a strong correlation between disease manifestation in tg650 mice inoculated with Wisc-1- or 116AG-CWD and the presence of abnormal PrP (Western blot, IHC or RTQuIC) might be explained by the presence of heterogeneous prions in the brains of infected mice with diferent seeding properties in vitro. Indeed, such heterogeneity and distinct seeding activities and infectivity of abnormal PrP fragments was observed in VPSPr cases [20, 43].''
VPSPr, GSS, and CWD zoonosis, concerns there from, where did i hear this concern before?
1. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
FRIDAY, APRIL 07, 2023
***> Case report: Two clusters of Creutzfeldt-Jakob disease cases within 1 year in West Michigan <***
TUESDAY, APRIL 11, 2023
Texas TAHC Chronic Wasting Disease Discovered in Deer Breeding Facilities in Frio and Hamilton Counties
TUESDAY, MARCH 21, 2023
Texas CWD seven new cases three separate deer-breeding facilities in Zavala, Washington and Gonzales counties 471 confirmed to date
THURSDAY, APRIL 27, 2023
TEXAS REPUBLICAN SB 1372 TAXPAYERS TO PAY FOR GAME FARMS CWD DEPOPULATION
MONDAY, MAY 15, 2023
TAHC Chapter 40, Chronic Wasting Disease and Scrapie Chapter 60, Singeltary Comment Submission
TEXAS CWD TSE PRION DETECTED IN 488 CASES TO DATE;
SCIENCE NEWS DEC. 30, 2003 / 3:31 PM
Mad Cow: Linked to thousands of CJD cases?
By STEVE MITCHELL, United Press International
https://www.upi.com/Science_News/2003/12/30/Mad-Cow-Linked-to-thousands-of-CJD-cases/47861072816318/
SCIENCE NEWS APRIL 1, 2005 / 4:48 PM
Groups seek to save NIH brain collection
By STEVE MITCHELL, Medical Correspondent
https://www.upi.com/Science_News/2005/04/01/Groups-seek-to-save-NIH-brain-collection/72961112392131/
SCIENCE NEWS APRIL 7, 2005 / 3:30 PM
NIH sends mixed signals on CJD brains
By STEVE MITCHELL, Medical Correspondent
SCIENCE NEWS MAY 31, 2005 / 5:26 PM
NIH says it will preserve CJD brains
By STEVE MITCHELL
2023
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.
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.
224 CHAPTER 14
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.''
NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER SURVEILLANCE TABLES OF CASES EXAMINED January 11th, 2023
Tables of Cases Examined National Prion Disease Pathology Surveillance Center Cases Examined¹
Updated quarterly.
Last updated on: January 11th, 2023
Year Total Neuropath Referrals² Prion Disease Sporadic Genetic Iatrogenic vCJD
1999 & earlier 383 232 202 27 3 0
2000 145 102 90 12 0 0
2001 209 118 110 8 0 0
2002 241 144 124 18 2 0
2003 259 160 137 21 2 0
2004 315 180 163 16 0 1³
2005 330 179 157 21 1 0
2006 365 179 159 17 1 2⁴
2007 374 210 191 19 0 0
2008 384 221 205 16 0 0
2009 397 231 210 20 1 0
2010 402 246 218 28 0 0
2011 392 238 214 24 0 0
2012 413 244 221 23 0 0
2013 416 258 223 34 1 0
2014 355 208 185 21 1 1⁵
2015 401 263 243 20 0 0
2016 395 277 248 29 0 0
2017 375 266 247 19 0 0
2018 308 221 202 18 1 0
2019 433 280 259 21 0 0
2020 366 252 227 24 1 0
2021 343 248 223 22 0 0
2022 307 199 165 13 0 0
TOTAL 83086 51567 46238 4919 14 4
Year CSF Only and RT-QuIC Positive10
2015 241
2016 360
2017 406
2018 431
2019 538
2020 494
2021 516
2022 492
TOTAL 3478
1Listed based on the year of death or, if not available, on the year of referral;
2Cases with suspected prion disease for which brain tissue was submitted;
3Disease acquired in the United Kingdom;
4Disease acquired in the United Kingdom in one case and in Saudi Arabia in the other;
5Disease possibly acquired in a Middle Eastern or Eastern European country;
6Includes 25 cases in which the diagnosis is pending (1 from 2020, 2 from 2021 and 21 from 2022), and 20 inconclusive cases;
7Includes 24 (3 from 2021 and 21 from 2022) cases with type determination pending in which the diagnosis of vCJD has been excluded.
8The sporadic cases include 4504 cases of sporadic Creutzfeldt-Jakob disease (sCJD), 82 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 37 cases of sporadic Fatal Insomnia (sFI).
9Total does not include 301 Familial cases diagnosed by blood test only.
10Lists number of patients (deceased and alive) who have had a positive RT-QuIC and no neuropath examination.
For a downloadable PDF version of our quarterly table, please click the link below:
NPDPSC Table of Cases Examined
© 2023 Case Western Reserve University 10900 Euclid Ave. Cleveland, Ohio 44106 216.368.2000 Legal Notice | Privacy Policy PATHOLOGY Campus Location: Wolstein Research Building 5129 2103 Cornell Road Cleveland, OH 44106
Mailing Address: 10900 Euclid Ave. Cleveland, OH 44106-7288
Phone: 216.368.3611
Email: pathology@case.edu
Tables of Cases Examined | Pathology | School of Medicine | Case Western Reserve University case.edu
National Prion Disease Pathology Surveillance Center Cases Examined1 (September 20, 2022) Year Total Neuropath Referrals2 Prion Disease Sporadic Familial iCJD vCJD
1999 & earlier 383 232 202 27 3 0
2000 145 102 90 12 0 0
2001 209 118 110 8 0 0
2002 241 144 124 18 2 0
2003 259 160 137 21 2 0
2004 315 180 163 16 0 13
2005 328 179 157 21 1 0
2006 365 179 159 17 1 24
2007 374 210 191 19 0 0
2008 384 221 205 16 0 0
2009 397 231 210 20 1 0
2010 401 246 218 28 0 0
2011 392 238 214 24 0 0
2012 413 244 221 23 0 0
2013 416 258 223 34 1 0
2014 355 208 185 21 1 15
2015 401 263 243 20 0 0
2016 395 277 248 29 0 0
2017 375 266 247 19 0 0
2018 308 221 202 18 1 0
2019 434 281 259 22 0 0
2020 365 252 227 24 1 0
2021 343 248 223 22 0 0
2022 213 124 98 9 0 0
TOTAL 82116 50827 45568 4889 14 4
Year CSF Only & RT-QuIC Positive10
2015 140
2016 183
2017 227
2018 266
2019 311
2020 310
2021 341
2022 262
TOTAL 2040
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease acquired in the United Kingdom in one case and in Saudi Arabia in the other;
5 Disease possibly acquired in a Middle Eastern or Eastern European country;
6 Includes 28 cases in which the diagnosis is pending (1 from 2020, 3 from 2021 and 24 from 2022), and 20 inconclusive cases;
7 Includes 20 (3 from 2021 and 17 from 2022) cases with type determination pending in which the diagnosis of vCJD has been excluded.
8 The sporadic cases include 4437 cases of sporadic Creutzfeldt-Jakob disease (sCJD), 82 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 37 cases of sporadic Fatal Insomnia (sFI).
9 Total does not include 300 Familial cases diagnosed by blood only. 10 Lists number of patients (deceased and alive) who have had a positive RT-QuIC and no neuropath examination.
WEDNESDAY, JANUARY 25, 2023
Canada Creutzfeldt-Jakob disease surveillance system (CJDSS) report steady rise in cases as of January 2023 and STILL NO CASES REPORTED OF VPSPr CJD
NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER SURVEILLANCE TABLES OF CASES EXAMINED January 11th, 2023
Tuesday APRIL 05, 2022
Incidence of Creutzfeldt-Jakob Disease in the United States 1993-2014
Title: HUMAN and ANIMAL TSE Classifications i.e. mad cow
disease and the UKBSEnvCJD only theory
Article Type: Personal View
Corresponding Author: Mr. Terry S. Singeltary
Terry S. Singeltary Sr., Bacliff, Texas, 77518 flounder9@verizon.net Galveston Bay!
