Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005 Singeltary's Regiew 2021
Subject: Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Tue, 30 Aug 2005 12:38:40 -0500 Content-Type: text/plain Parts/Attachments: text/plain (51 lines)
##################### Bovine Spongiform Encephalopathy #####################
From: TSS () Subject: Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005 Date: August 30, 2005 at 10:28 am PST
Release No. 0336.05 Contact: USDA Jim Rogers 202-690-4755 FDA Rae Jones 301-827- 6242
U.S. Department of Agriculture (USDA) Food and Drug Administration (FDA)
Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005
The U.S. Department of Agriculture's Animal and Plant Health Inspection Service (APHIS) and the U.S. Department of Health and Human Services' Food and Drug Administration (FDA) have completed their investigations regarding a cow that tested positive for bovine spongiform encephalopathy (BSE) in June 2005. The agencies conducted these investigations in collaboration with the Texas Animal Health Commission and the Texas Feed and Fertilizer Control Service.
Our results indicate that the positive animal, called the index animal, was born and raised on a ranch (termed the "index farm") in Texas. It was a cream colored Brahma cross approximately 12 years old at the time of its death. It was born prior to the implementation of the 1997 feed ban instituted by FDA to help minimize the risk that a cow might consume feed contaminated with the agent thought to cause BSE. The animal was sold through a livestock sale in November of 2004 and transported to a packing plant. The animal was dead upon arrival at the packing plant and was then shipped to a pet food plant where it was sampled for BSE. The plant did not use the animal in its product, and the carcass was destroyed in November 2004.
APHIS attempted to trace all adult animals that left the index farm after 1990, as well as all progeny born within 2 years of the index animal's death. Together, these animals are called animals of interest.
During the course of the investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE. 200 adult animals of interest were determined to have left the index farm. Of these 200, APHIS officials determined that 143 had gone to slaughter, two were found alive (one was determined not to be of interest because of its age and the other tested negative), 34 are presumed dead, one is known dead and 20 have been classified as untraceable. In addition to the adult animals, APHIS was looking for two calves born to the index animal. Due to record keeping and identification issues, APHIS had to trace 213 calves. Of these 213 calves, 208 entered feeding and slaughter channels, four are presumed to have entered feeding and slaughter channels and one calf was untraceable.
To determine whether contaminated feed could have played a role in the index animal's infection, FDA and the Texas Feed and Fertilizer Control Service conducted a feed investigation with two main objectives: 1) to identify all protein sources in the animal=s feed history that could potentially have been the source of the BSE agent, and 2) to verify that cattle leaving the herd after 1997 were identified by USDA as animals of interest and were rendered in compliance with the 1997 BSE/ruminant feed rule.
The feed history investigation identified 21 feeds or feed supplements that were used on the farm since 1990. These feed ingredients were purchased from three retail feed stores and were manufactured at nine feed mills. This investigation found that no feed or feed supplements used on the farm since 1997 were formulated to contain prohibited mammalian protein. Due to this finding, FDA has concluded that the animal was most likely infected prior to the 1997 BSE/ruminant feed rule.
The investigation into the disposition of herd mates from this farm involved visits to nine slaughter plants and eight rendering plants. The investigation found that all of the rendering plants were operating in compliance with the BSE/ruminant feed rule. A review of the inspection history of each of these rendering firms found no violations of the FDA feed ban rule.
APHIS and FDA are very pleased with the results of their investigations, which show the animals of interest did not present a threat to livestock and that the ruminant feed rule is being followed. The U.S. maintains an interlocking system of safeguards designed to prevent BSE from entering the human and animal food chain. USDA also remains vigilant in its attempt to find BSE in the United States. To date, there have been more than 450,000 animals tested in the last 14 months and only two BSE positive animals found in this country.
For more information on USDA's epidemiological investigation and a copy of the report, please visit the APHIS website at http://www.aphis.usda.gov/lpa/issues/bse/bse.html
For more information on FDA's feed investigation, please visit the FDA's website at http://www.fda.gov/cvm/texasfeedrpt.htm
Last Modified: 08/30/2005
http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB/.cmd/ad/.ar/sa.retrievecontent/.c/6_2_1UH/.ce/7_2_5JM/.p/5_2_4TQ/.d/1/_th/J_2_9D/_s.7_0_A/7_0_1OB?PC_7_2_5JM_contentid=2005%2F08%2F0336.xml&PC_7_2_5JM_navtype=RT&PC_7_2_5JM_parentnav=LATEST_RELEASES&PC_7_2_5JM_navid=NEWS_RELEASE#7_2_5JM
TSS
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Subject: Re: Investigation Results of Texas Cow That Tested Positive for Bovine Spongiform Encephalopathy (BSE) Aug. 30, 2005
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Tue, 30 Aug 2005 13:34:30 -0500 Content-Type: text/plain Parts/Attachments: text/plain (735 lines)
##################### Bovine Spongiform Encephalopathy #####################
THE FONG EFFECT OR THE FONG SYNDROME
Friday, July 29, 2005
Ames lab to take over testing for mad cow disease Published: 07/29/2005 3:52 PM
By: Associated Press - Associated Press
AMES, IA - Scientists at the National Veterinary Services Laboratories here soon will begin conducting their own Western blot tests, eliminating the need to travel to Weybridge, England, when initial rapid testing detects mad cow disease.
"I think the change is good because we're more likely to know exactly what we're dealing with on each case," said Dr. Randall Levings, director of the labs.
The change is a response to an order from U.S. Agriculture Secretary Mike Johanns.
"We took those as our marching orders," Levings said.
Mad cow disease, formally known as bovine spongiform encephalopathy, or BSE, attacks a cow's nervous system. It is characterized by spongelike holes in the brain, the result of misshapen proteins called prions that kill brain cells.
The only way it is known to spread is by cattle eating infected brain and nerve tissue from other cows. That's why the government in 1997 banned the use of cattle feed that contains remnants of other cows. Of the three cases of mad cow confirmed in the United States, all three cows were born before the feed ban, Levings said.
Since January 2004, the government has tested more than 400,000 cows for the disease, using a rapid screening test and a test known immunohistochemistry, or IHC.
Rapid testing of a sample involves removing normal proteins and adding chemicals that bind to the abnormal proteins, making them visible. The IHC test involves staining paper-thin brain tissue samples to highlight the abnormal protein.
The Western blot test, conducted at Weybridge destroys normal proteins in the brain, leaving only the abnormal prions.
In June, the nation's Office of Inspector General ordered a review of the Ames lab's testing procedures after a sample last fall tested positive in England, but negative in Ames.
A rapid test on the sample in Ames detected the presence of BSE, but the following IHC test was negative. Ames workers also relayed the results of the test, but did not complete formal paperwork.
A version of mad cow disease, known as variant Creutzfeld-Jakob, has killed about 150 people worldwide, most of them in Britain, where there was an outbreak in the 1990s.
"We're taking all of the right steps," Levings said. "It would not be a risk to human or animal health in this country. It's not high. It's very, very low."
http://www.crgazette.com/2005/07/29/Home/News/madcowtesting.htm
SO, Johann's/GW et al have perfected the BSE/TSE testing protocols and they don't need anyone else to tell them what to do. this was proven with the TEXAS mad cow cases alone, r i g h t...... $$$ IF this is the case, why is Weybridge having to confirm our inconclusives ??? this is frightening.
IF not for the Honorable Phyllis Fong, that cow would have never been proven positive, well, documented anyway, it was proven positive time and time again...
The Fong Syndrome strikes again.
GW's BSE/TSE MRR policy a recipe for disaster.
USA in dire straights.
God help us... TSS
No Sacred Cows: Phyllis Fong Takes on the Beltway and Mad Cow Disease News Report, AsianWeek Staff Report, Asian Week, Jul 06, 2005
Newly appointed Agriculture Secretary Mike Johanns appears to be headed for a showdown with veteran Inspector General Phyllis K. Fong for ordering new tests for mad cow disease in the nation’s beef supply.
Since the tests Fong ordered have returned positive, several countries have once again stopped buying U.S. beef, provoking uproar in the cattle industry.
Reacting to industry pressure, Johanns now claims Fong requested the tests without his knowledge or approval and added: “It caught me by surprise, to be very honest with you. I believe the secretary should be involved in all decisions of this significance.”
Fong, the senior officer of the Inspector General’s office of the USDA was sworn in on December 2, 2002 after serving as Inspector General for the Small Business Administration. Like Johanns, she is appointed by the president and confirmed by the Senate. The Inspector General’s office is an independent arm of the department that performs audits and investigations.
When she ordered the re-testing of the latest case, she issued a statement saying she was also probing “the performance of [laboratories] in complying with procedures for conducting tests.” With the cow that was suspected of having the disease, she reported: “Auditors noted an unusual pattern of conflicting test results on one sample.”
The Veterinary Laboratories Agency in Weybridge, England, an outside testing agency, confirmed that a sample from an animal in November 2004 tested positive for bovine spongiform encephalopathy, or mad cow disease.
Yet Johanns, who took the reins of the Agriculture Department early this year in a Bush cabinet shake-up, insists that Fong has overstepped her bounds. “I was asked by the Senate and the president to operate the department,” Johanns said. “She could recommend; she could strongly urge. But then the question is whether it’s an operational decision.”
He reportedly learned of Fong’s order from his chief of staff after the new testing was already under way. He charges that it’s up for debate whether Fong had the authority to order the new tests, and asserts: “It’s my domain.”
This is not the first time Fong has found herself in the eye of the storm.
After allegations of misconduct arose in the handling of the first cow with mad cow disease, Fong launched a criminal investigation.
“Currently we are investigating allegations surrounding the actual state of the diseased cow before it went to slaughter,” Fong testified last year before the House subcommittee on agriculture appropriations. “So that’s a criminal investigation that’s open, ongoing, active and it’s focused on that issue.”
Fong’s investigation concluded that there was no criminal negligence, but in July she released an audit of the USDA’s testing program and concluded it had serious flaws that could undermine its credibility and lead to questionable estimates of how widespread the disease is in America.
Fong recently re-opened investigations started during the administration of Johanns’ predecessor, Ann Veneman. Veneman began a reform push on testing U.S. beef, but her efforts eventually ran aground amid battles between competing interests, including the beef industry, scientists and consumer activists.
The two behind-the-scenes audits follow complaints by several cow-state senators over policies and procedures in testing for mad cow disease.
Fong said in a statement that “our field work is ongoing” with results expected “late this summer.”
USDA’s Top Cop
As a young girl, Phyllis Fong had a hankering for the law. Those interests began in her childhood, kindled by her father.
“When I was growing up, I remember searching, as all kids do, for a career path that matched my talents,” she said in an article for the USDA. “And my father said to me, at one point in high school, that he really thought law school would be right for me, that I would be a tremendous lawyer. I had never thought about that as an option.”
Fong’s family had emigrated from Hawai‘i to China generations before, in the mid-1800s. Unlike a lot of APA families who insist that the children follow in the family business, Fong recalls, “He was a doctor and yet he did not suggest I go into medical school. I think he was tired of my arguing with him about everything!”
“I had a wonderful experience growing up. They call Hawai‘i a melting pot because of its multi-racial and multi-cultural society. I always felt that everyone there had the opportunity to become anything. It didn’t matter what color, what sex, what race, what ethnic heritage you were, if you were interested in something you could pursue it,” she said.
An unusual route led to her toward the senior job as USDA’s Inspector General. After studying Asian studies and finishing her law degree, she intended to become an international lawyer specializing in trade and immigration.
But when Fong arrived in Washington, D.C., she got a job with the U.S. Civil Rights Commission, which at the time was studying immigration policy. One thing led to another, and a colleague who was the Inspector General at the U.S. Small Business Administration asked her to become her special assistant
“I realized this was a good opportunity. Who can be against going after fraud and abuse? Who can be against economy and efficiency in government?” Fong has been in the field ever since, and oversees about 600 employees divided almost evenly between investigators and auditors.
Name: Phyllis K. Fong
Salary: $136,900
Position: Inspector General, USDA. She’s responsible for conducting and supervising audits and evaluations, as well as investigations and law enforcement efforts.
Birthplace: Philadelphia, Pennsylvania
Family: Married, two daughters, ages 4 and 7
Education: BA degree in Asian Studies, Pomona College; Juris Doctorate, Vanderbilt University School of Law
Past Experience: She was Inspector General of the U.S. Small Business Administration from 1999-2002 after holding several positions with the SBA, including Assistant Inspector General for Management and Legal Counsel and Assistant Inspector General for Management and Policy. In the early 1980s, she had served as assistant general counsel for the Legal Services Corporation and, before that, as an attorney with the U.S. Commission on Civil Rights.
Hobbies/Interests: Needlepoint
Priorities: “To instill the message within USDA that OIG’s mission is not just to audit and investigate. Our mission is to work in partnership with the Department to manage programs more effectively and deal with fraud and abuse.”
The Associated Press and USDA contributed to this report.
http://news.pacificnews.org/news/view_article.html?article_id=67ea9860e23ed4 d55409d8d845e3b40b
FSIS NOTICE 54-05 8/29/05
POLICY ON USE OF RESULTS FROM THIRD PARTY LABORATORIES
NOTE: This notice reissues the contents of FSIS Notice 52-03 in its entirety.
PURPOSE FSIS is periodically presented with positive results from a laboratory analysis conducted by a third party laboratory that indicate an adulterant is present in FSIS inspected and passed product. A third party laboratory is one not owned by, nor under contract with, the establishment providing the sample. Under very limited circumstances, FSIS may rely on a third party laboratory's positive result to take action on the product (e.g., request a recall or take regulatory action). This notice describes the circumstances in which FSIS considers it appropriate to rely on results from a third party laboratory.
POLICY ON THIRD PARTY LABORATORY RESULTS
In deciding whether to rely on third party laboratory results, FSIS will consider the following questions (also see attached flowchart (PDF only)):
Were the procedures used to collect, handle, and transport the sample equivalent to FSIS procedures? FSIS will request documentation of the procedures used and will assess whether the integrity of the sample or specimen could have been compromised during collection or transportation. Was the sample or specimen handled using a documented chain of custody establishing that the integrity of the sample or specimen was not compromised during transport from the point of collection to the laboratory or within the laboratory? FSIS will assess the documentation of the chain of custody to determine whether the people who handled the sample kept it intact and properly maintained throughout the process. Was there assurance that the results obtained by the third party laboratory are reliable and accurate for the analysis in question? FSIS will assess the available information about the laboratory (e.g., whether the laboratory is accredited under the International Organization for Standardization Standard 17025 (ISO 17025) and whether the analysis was performed in accordance with that accreditation) to determine whether the Agency can confidently rely on the laboratory's results. Was the sample or specimen analyzed in accordance with documented analytical methodology that has a sensitivity and specificity that are determined by FSIS to be equivalent to the FSIS laboratory methodology in question?
If the Agency finds that the answers to the four questions listed are "yes", FSIS would consider that there is an appropriate basis to rely on the results of the analysis by the third party laboratory. Thus, FSIS would be prepared to take action (e.g., request a recall or institute a regulatory action) on the basis of the results obtained by the third party laboratory.
If the Agency finds that the answer to number 1 or number 2 is "no" or "inconclusive", then the sample result is disregarded. If the answer to number 1 and number 2 is "yes", then FSIS considers the laboratory's results in the following manner:
If the answer to number 3 is "yes" and the answer to number 4 is "no", then FSIS will take a verification sample; If the answer to number 3 is "no" and the answer to number 4 is "no" then FSIS will disregard the sample results; and, If the answer to number 3 is "no" and the answer to number 4 is "yes" then FSIS will take a verification sample.
When taking verification samples, FSIS will make an effort, whenever possible, to collect an intact sample of the same exact product and lot code(s) from the same location at which the third party sample was collected.
NOTE: Even without reliable laboratory results, FSIS may decide on the basis of the available epidemiological and other evidence that there is reason to find that product is adulterated and, thus, to act against that product.
Philip S. Derfler /s/
http://www.fsis.usda.gov/regulations_&_policies/Notice_54-05/index.asp
FSIS NOTICE 54-05
Decision Tree on Third Party Laboratory
Results FSIS receives lab result and
contacts the laboratory for the
following information
Is sample collection procedure documented,
followed and equivalent to FSIS?
Yes No
Is sample chain of custody OK? Disregard Results No
Yes
party laboratory are reliable and accurate for the analysis
in question?
Yes No
Are the sample analysis
procedures and performance
characteristics documented and
equivalent to FSIS?
Are the sample analysis
procedures and performance
characteristics documented and
equivalent to FSIS?
Yes No Yes No
Treat the sample result
as if it were an FSIS
laboratory sample result
Disregard Results
Collect a verification
sample for the FSIS
laboratory
Was there assurance that the results obtained by the third
http://www.fsis.usda.gov/oppde/rdad/fsisnotices/54-05_flowchart.pdf
FDA Statement FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
####
ooops!
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
CATTLE ON FEED IN TEXAS
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
---------------------------------------------------------------------------- ----
Note: On Dec. 23, 2003, the U.S. Department of Agriculture reported that a cow in Washington state had tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease). As a result, information on this Web page stating that no BSE cases had been found in the United States is now incorrect. However, because other information on this page continues to have value, the page will remain available for viewing.
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.
FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary
The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
It is clear that the designing scientists must
also have shared Mr Bradley's surprise at the results because all the dose
levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s145d.pdf
2
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100
grams) was probably given with the benefit of hindsight; particularly if one
considers that later in the same answer Mr Bradley expresses his surprise that it
could take as little of 1 gram of brain to cause BSE by the oral route within the
same species. This information did not become available until the "attack rate"
experiment had been completed in 1995/96. This was a titration experiment
designed to ascertain the infective dose. A range of dosages was used to ensure
that the actual result was within both a lower and an upper limit within the study
and the designing scientists would not have expected all the dose levels to trigger
infection. The dose ranges chosen by the most informed scientists at that time
ranged from 1 gram to three times one hundred grams. It is clear that the designing
scientists must have also shared Mr Bradley's surprise at the results because all the
dose levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts
[BBC radio 4 FARM news]
http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm
2) Infectious dose:
To cattle: 1 gram of infected brain material (by oral ingestion)
http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml
TSS
Subject: Report on Food & Drug Administration Dallas District Investigation of Bovine Spongiform Encephalopathy Event in Texas 2005
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Tue, 30 Aug 2005 16:26:26 -0500 Content-Type: text/plain Parts/Attachments: text/plain (535 lines)
##################### Bovine Spongiform Encephalopathy #####################
From: TSS ()
Subject: Report on Food & Drug Administration Dallas District Investigation of Bovine Spongiform Encephalopathy Event in Texas 2005
Date: August 30, 2005 at 2:15 pm PST
Report on Food & Drug Administration Dallas District Investigation of Bovine Spongiform Encephalopathy Event in Texas 2005
Executive Summary:
On June 24, 2005, USDA informed FDA that a cow in Texas tested positive for Bovine Spongiform Encephalopathy (BSE). Information provided by APHIS was that the BSE positive cow was born and raised in a herd in Texas and was approximately 12 years old. The animal was sampled for BSE at a pet food plant in Texas on November 15, 2004, as part of USDA’s enhanced surveillance program. The animal was disposed of by incineration and did not enter the human food or animal feed chains. Although the positive animal posed no risk to the animal feed supply, FDA, APHIS, the Texas Animal Health Commission (TAHC), and the Texas Feed and Fertilizer Control Service (TFFCS) conducted a feed investigation with two main objectives. The first objective was to identify all protein sources in the animal’s feed history that could potentially have been the source of the BSE agent. The second objective was to verify that cattle leaving the herd after 1997 that were identified by USDA/APHIS as animals of concern (e.g. progeny and feed cohorts), were rendered at facilities in compliance with the regulation (21 CFR 589.2000) that prohibits most mammalian protein in feed for ruminants that became effective August 4, 1997 (herein called BSE/Ruminant Feed rule).
The feed history investigation identified 21 feed products that had been used on the farm since 1990. These feed products were purchased from three retail feed stores and had been manufactured at nine different feed mills. The investigators visited these establishments to collect information on formulations, shipping invoices, and use of ruminant meat and bone meal (MBM) on the premises both pre-1997 feed ban and post-1997 feed ban. This investigation found no feed products used on the farm since 1997 that had been formulated to contain prohibited mammalian protein.
The investigation identified one feed which contained an animal protein source that could not be identified. The investigation also found one feed mill that supplied feed to the farm that had used ruminant MBM in feed formulations for non-ruminant species after the BSE/Ruminant Feed rule went into effect, which is permitted under the rule, and that several feed mills had used ruminant MBM in feeds prior to the feed ban. Although the investigation did not identify a specific feed source as the likely cause of this animal’s infection, it is probable that the most likely route of exposure for this animal was consumption of an animal feed containing mammalian protein prior to the implementation of the BSE/Ruminant Feed rule in 1997.
The investigation into the disposition of herd mates from this farm involved visits to nine slaughter plants and eight rendering plants. The investigation found that all rendering plants were operating in compliance with the BSE/ruminant feed ban regulation. A review of the inspection history of each of these rendering firms found no violations.
Background of Investigation:
When notified on June 24, 2005, FDA Headquarters and Dallas District management officials immediately began making contacts with their Federal, State and Local counterparts to plan for and initiate follow-up investigational activities to determine the feed history in this herd and to assure the safety of the animal feed supply by evaluating current and historic compliance with the BSE/ruminant feed ban rule.
APHIS established a joint Incident Command Post and FDA Dallas District staffed this post full time with a Supervisory Investigator charged with coordinating activities between FDA, APHIS, TAHC and TFFCS. Coordination conference calls were set up with all Federal and State agencies involved in the investigation to keep everyone apprised of investigational developments.
Animal Tracing Activities and Renderer Follow-up Inspections:
One of APHIS’ primary objectives was to identify and trace the animals of interest (animals of interest would include any animals which could have been potential birth cohorts or feed cohorts of the index animal, or potential offspring of the index animal within the two years prior to the positive diagnosis) from the index herd. This objective included the identification of points of sale and ultimately the actual slaughter facilities for animals of interest that left the farm. As the trace information was developed, APHIS shared this information with FDA. Further information on animal of interest identification and tracing can be found in the USDA Texas BSE Final Epidemiology report.
APHIS identified nine slaughter establishments receiving these animals of interest. Eight of the slaughter establishments were located in the State of Texas and one was located in the State of Georgia. Dallas District Investigators notified USDA/FSIS of our plans to visit each slaughter establishment to identify rendering facilities receiving materials from these slaughter establishments during the timeframe they received animals of interest. Dallas District also issued an assignment to Atlanta District to visit and inspect the one slaughter/renderer establishment located in the State of Georgia.
Eight renderers and one protein source broker were identified as receiving materials from these slaughter establishments. Each rendering facility identified was inspected for current compliance with the mammalian protein feed ban rule. Each firm’s operations during the period of time of receipt of these animals post 1997 were evaluated from a historical viewpoint and no evidence of noncompliance was detected.
In all, FDA visited nine slaughter facilities, eight rendering facilities and one broker of these materials. All facilities inspected were found to be in compliance with the BSE/ruminant feed ban rule
Following is a graphical representation of the animal product follow-up work performed.
Feed Investigation:
As information was learned about the index herd, FDA Investigators working with TAHC officials conducted multiple interviews with the producer of the animal regarding possible feeds, feed sources, animal husbandry practices, and other events which may have changed normal feeding practices over the course of the index animal’s life in the herd and any other information which may have been helpful in identifying the possible sources of feed for this animal and herd. FDA corroborated this information through interviews at the retail feed supply stores where the producer purchased feeds.
Follow-up at these retail feed supply stores identified 21 possible feed products the producer may have used during the history of the herd. Fifteen purchased feed products were identified, along with hay, native grass, rice straw, soybean meal, milk replacer/colostrum and bagged corn. These products were identified as originating from nine different manufacturers. Each of these manufacturers was inspected by FDA Dallas District and TFFCS Investigators.
Feed manufacturers were located throughout the State of Texas. An assignment was also issued to another FDA District to visit a Corporate Headquarters facility in an effort to review archived feed formulations and labels. During each of these inspections, the firm’s current compliance with the BSE/ruminant feed ban rule was evaluated and attempts were made to determine the protein sources used in feeds on the index farm. Many of the feeds investigated were manufactured and used prior to the implementation of the BSE/ruminant feed ban rule in 1997. Feed products of particular interest included any which may have contained a protein source and the primary focus was on identifying any possible mammalian protein source material in those feed products. We found that ruminant feeds that had contained mammalian meat and bone meal (MBM) prior to the BSE/ruminant feed ban rule had been discontinued or reformulated upon the implementation of these rules. There is no regulatory requirement for a feed mill to archive formulations for that length of time, so in those instances where an actual formulation could not be obtained, experienced employees of the firms were interviewed and their recollections recorded.
Of all the feeds in use by the producer since 1997, none were discovered to have contained prohibited material (mammalian protein). Since the age of the index animal was determined to be approximately 12 years, investigating and reconstructing a feed history over such a long period of time is challenging. This ranch is a beef cow-calf operation and minimal feed records were maintained. Due to the nature of this investigation, it is difficult to determine what feeds were in use at specific times and what the formulation of those feeds were at the time they were fed. A feed history was developed through interviews with the producer and other farm personnel since they did not maintain any feed history documentation. Interviews with personnel at retail establishments disclosed incomplete records and cash sales that did not always identify the purchaser. Dallas District investigated any and all feed ingredients that were identified as being fed or potentially fed over the course of the last 15 years of this herd’s operation. Feeds discovered during this investigation with potential mammalian protein sources are as below:
One feed, used prior to 1996, before the implementation of the feed ban, was suspected to contain mammalian meat and bone meal, but this could not be confirmed as no formulation records were available.
The producer recalled using a particular feed sporadically during the 1980’s and 1990’s, however, he could not remember the name or manufacturer of the feed and had no records identifying the product. It is not known whether this feed contained an animal protein source. Attempts to identify this feed through interviews with retail sources were unsuccessful.
The producer identified one feed product that has been used since the year 2000 which contains fish meal as a protein source. Further investigation revealed that this product had contained mammalian meat and bone meal prior to 1997, but that it had been reformulated at that time using fish meal to replace the MBM.
A tabular representation of the feed inspection follow-up activities is presented below:
Feed Dates of Use Protein Source Current BSE Inspection BSE Compliance History
Feed #1 - Range Meal 1980’s - 2000 Unknown - Unable to determine actual manufacturer, no records available from producer N/A N/A
Feed #2 - High Protein Starter Feed 2001 to present Feather meal BSE Compliant BSE Compliant
Feed #3 - High Protein Starter Feed ~1995 - 2001 Feather meal BSE Compliant BSE Compliant
Feed #4 - Cottonseed cake Prior to 1990 Cottonseed meal BSE Compliant BSE Compliant
Feed #5 - Cottonseed cake Early 1980’s - 1990’s Cottonseed meal BSE Compliant BSE Compliant
Feed #6 - Limiter 2001 to present Feather meal BSE Compliant BSE Compliant
Feed #7 - Creep pellets Prior to 1970 Likely feather meal - no formulation could be obtained N/A N/A
Feed #8 - Lick tub Since 2000 MBM prior to 1997 Fish Meal since 1997 BSE Compliant BSE Compliant
Feed #9 - Cottonseed meal Continuously Cottonseed meal BSE Compliant BSE Compliant
Feed #10 - Range Cubes Continuously since 1990 Feather meal BSE Compliant BSE Compliant[1]
Feed #11 - Sulfur Salt Block Continuously Minerals; calcium - all non-animal derived BSE Compliant BSE Compliant
Feed #12 - Lick tub Continuously since 1995 Feather meal BSE Compliant BSE Compliant
Feed #13 - Beef Supplement Prior to 1996 Prior to 1997, suspect MBM - Not able to confirm, no formulation available BSE Compliant Same manufacturer as Feed #10[1]
Feed #14 - Mineralized Salt Continuously since 1998 Minerals; calcium - all non-animal derived BSE Compliant BSE Compliant
Feed #15 - Soybean meal Since 2000, sparingly Soybean meal N/A N/A
Feed #16 - Corn Continuously Corn N/A N/A
Feed #17 - Rice straw 1996, during dry year Rice straw N/A N/A
Feed #18 - Hay Continuously Hay N/A N/A
Feed #19 - Milk Replacer Since 2000, Infrequent use Dehydrated colostrums, whey N/A N/A
Feed #20 - Grass Continuously Native grass N/A N/A
Feed #21 - Soybean meal Since 2000, sparingly Soybean meal N/A N/A
Dallas District previously documented one incident of the accidental addition of mammalian protein to a feed that was to be used for cattle at this facility. This incident was isolated to the manufacture of one lot of a custom cattle feed. A cross contamination error resulted in mammalian meat and bone meal being accidentally included in a feed. The error was detected soon after production. The firm acted swiftly in recalling the product and purchasing the animals that had consumed the feed. No products entered the human food or ruminant feed chain.
Dallas District Compliance History with BSE Feed Ban Rules:
Prior to 1997, feed manufacturers were not required to differentiate between protein sources used in ruminant and non-ruminant feeds. For a period of time following the implementation of the BSE/ruminant feed ban rule, some feed manufacturers continued to use both prohibited material and non-prohibited material within the same facility, employing separation and cleanout procedures to minimize cross-contamination. Although the regulations allow this practice, the potential for cross-contamination of ruminant feeds is greater. Most feed mills have found this practice to be difficult and have abandoned this practice.
Since the implementation of the BSE/ruminant feed ban rule in 1997, Dallas District and its State partners have inspected every known or registered feed manufacturer located in the states of Texas, Oklahoma and Arkansas. Further, every rendering operation and feed manufacturer actually processing with prohibited materials has been inspected annually. The compliance rate of the industry has been excellent.
Results:
In total FDA, along with TFFCS, conducted 33 inspections, investigations and interviews of the producer, retail feed establishments, feed manufacturers, corporate headquarters, slaughter facilities, renderers and a protein source broker. The FDA Dallas District follow-up to this incident resulted in the coordination of efforts of multiple Federal and State agencies. This report is the physical output of many hours of research, planning and coordination. All of the inspections conducted confirmed the feed manufacturers and rendering operations to be in compliance with the current BSE/ruminant feed ban rule.
Dallas District conducts annual inspections of all feed mills and rendering facilities who handle, use or produce PM for feed use. Inspections performed since the initiation of the BSE/ruminant feed ban rules in 1997 have confirmed a high degree of industry wide compliance with these important safeguards. The district also routinely coordinates and shares information regarding feed inspections with the TFFCS who are also responsible for the evaluating feed ban compliance in the state of Texas.
Food and Drug Administration August 30, 2005
http://www.fda.gov/cvm/texasfeedrpt.htm
FDA Statement FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
To protect the U.S. against BSE, FDA works to keep certain mammalian protein out of animal feed for cattle and other ruminant animals. FDA established its animal feed rule in 1997 after the BSE epidemic in the U.K. showed that the disease spreads by feeding infected ruminant protein to cattle.
Under the current regulation, the material from this Texas cow is not allowed in feed for cattle or other ruminant animals. FDA's action specifying that the material go only into swine feed means also that it will not be fed to poultry.
FDA is committed to protecting the U.S. from BSE and collaborates closely with the U.S. Department of Agriculture on all BSE issues. The animal feed rule provides crucial protection against the spread of BSE, but it is only one of several such firewalls. FDA will soon be improving the animal feed rule, to make this strong system even stronger.
####
ooops!
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
CATTLE ON FEED IN TEXAS
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
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Note: On Dec. 23, 2003, the U.S. Department of Agriculture reported that a cow in Washington state had tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease). As a result, information on this Web page stating that no BSE cases had been found in the United States is now incorrect. However, because other information on this page continues to have value, the page will remain available for viewing.
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.
FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary
The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
It is clear that the designing scientists must
also have shared Mr Bradley's surprise at the results because all the dose
levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s145d.pdf
2
6. It also appears to me that Mr Bradley's answer (that it would take less than say 100
grams) was probably given with the benefit of hindsight; particularly if one
considers that later in the same answer Mr Bradley expresses his surprise that it
could take as little of 1 gram of brain to cause BSE by the oral route within the
same species. This information did not become available until the "attack rate"
experiment had been completed in 1995/96. This was a titration experiment
designed to ascertain the infective dose. A range of dosages was used to ensure
that the actual result was within both a lower and an upper limit within the study
and the designing scientists would not have expected all the dose levels to trigger
infection. The dose ranges chosen by the most informed scientists at that time
ranged from 1 gram to three times one hundred grams. It is clear that the designing
scientists must have also shared Mr Bradley's surprise at the results because all the
dose levels right down to 1 gram triggered infection.
http://www.bseinquiry.gov.uk/files/ws/s147f.pdf
Re: BSE .1 GRAM LETHAL NEW STUDY SAYS via W.H.O. Dr Maura Ricketts
[BBC radio 4 FARM news]
http://www.maddeer.org/audio/BBC4farmingtoday2_1_03.ram
http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm
2) Infectious dose:
To cattle: 1 gram of infected brain material (by oral ingestion)
http://www.inspection.gc.ca/english/sci/bio/bseesbe.shtml
NEW MAD COW STRAIN CALLED BASE, VERY SIMILAR TO SPORADIC CJD IN HUMANS;
Medical Sciences Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease
Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria Caramelli *
*Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy
Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003)
Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease.
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C.C. and G.Z. contributed equally to this work.
||To whom correspondence should be addressed.
E-mail: salvatore.monaco@mail.univr.it .
www.pnas.org/cgi/doi/10.1073/pnas.0305777101
http://www.pnas.org/cgi/content/abstract/0305777101v1
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
PMID: 6997404 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui ds=6997404&dopt=Abstract
TSS
#################### https://lists.aegee.org/bse-l.html ####################
Subject: TRANSCRIPT OF JOHANNS ABOUT THE TEXAS MAD COW BSe Release No. 0339.05
August 30, 2005
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Tue, 30 Aug 2005 21:03:28 -0500 Content-Type: text/plain Parts/Attachments: text/plain (522 lines)
##################### Bovine Spongiform Encephalopathy #####################
From: TSS ()
Subject: TRANSCRIPT OF JOHANNS ABOUT THE TEXAS BSe Release No. 0339.05
Date: August 30, 2005 at 6:48 pm PST
Release No. 0339.05 Contact: USDA Press Office (202) 720-4623
TRANSCRIPT OF TECHNICAL BRIEFING WITH AGRICULTURE SECRETARY MIKE JOHANNS, USDA CHIEF VETERINARY OFFICER DR. JOHN CLIFFORD (ANIMAL AND PLANT HEALTH INSPECTION SERVICE), AND CENTER FOR VETERINARY MEDICINE DIRECTOR DR. STEVE SUNDLOF (FOOD AND DRUG ADMINISTRATION), UPDATE ON NATIONAL ANIMAL IDENTIFICATION SYSTEM AND BSE EPIDEMIOLOGY INVESTIGATION, WASHINGTON, DC -- AUGUST 30, 2005 SEC. MIKE JOHANNS: Thank you very much, and good afternoon everyone, and thank you for joining us. I will begin today with an announcement about the National Animal Identification System, and then what I'd like to do from there is ask Dr. John Clifford to report on the conclusion of the investigation related to the cow that tested positive for BSE in June of this year.
Many of you have heard me say before that I am deeply committed to the spirit of public service that involves listening, really listening, to the people whom we serve. We may not always agree with each other, but as public servants it is important that we listen. That's why I've been traveling around the country doing a Farm Bill listening tour to hear from the entire ag community about what's on their mind, what we're doing right, and what we might do better.
Well, today I'd like to tell you about some of the listening we've done on the National Animal Identification System. That's a good place for me to start. The system is one of the most important infrastructure initiatives in animal agriculture today. Our goal is to work hand-in-hand with producers and the states to enhance our collective ability to quickly identify animals that may be of concern in a disease outbreak.
When this system is fully implemented, we expect to be able to identify all potentially affected animals and premises within 48 hours of a disease detection.
You'd be hard-pressed to find anyone working in animal agriculture today who doesn't believe that's a worthy objective and an important investment for us to make. After all, the faster we identify affected animals and premises, the faster we are able to contain the disease.
But as with any major initiative touching so many segments of the industry, there are differing views on some pretty fundamental questions like whether data in the system should be publicly or privately held, how can we protect confidentiality of the data, and whether the data collection should be a voluntary system or a mandatory system.
Last year the USDA held a series of listening sessions around the country, some 16 in all as a matter of fact, to hear what folks around the country had to say. We also formed a special subcommittee under the Secretary's Advisory Committee on Foreign Animal and Poultry Diseases that has widespread producer representation.
And in May as you know we published a detailed thinking paper outlining our proposed strategy for getting a mandatory system in place and framing some additional questions for stakeholders to contemplate.
In their responses, producers expressed concern about confidentiality when it comes to animal movement information. Without question, the participation of producers is absolutely essential to the success of an animal identification system. That's why we paid attention when producers asked that animal movement data be privately held.
Based on the feedback, I'm putting forth guiding principles today that allow animal movement data to be maintained in a private system that can be readily accessed when necessary by state and federal animal health authorities. This allows the industry to continue developing databases that house animal movement information, and we envision those databases feeding a single, privately-held animal tracking repository that we can access.
This initiative, or innovative approach, addresses producers' concerns while at the same time enabling federal and state officials to access information that we may need for disease control purposes.
There are a number of concepts being discussed in the private sector about how this should work and how it should be funded. USDA is not favoring any one of them over the other. USDA will be scheduling a stakeholder meeting this fall to clarify expectations for the private tracking system and discuss user requirements in system specifications.
In the meantime, USDA will be finalizing and releasing the program standards that were presented in the thinking paper. Beyond that, we will be looking to industry to come together to drive this leg of the journey.
I believe strongly this is the right approach. This system has always been about government and private partnership. USDA has invested a great deal, nearly $19 million in 2004, to get the infrastructure started. Most of that went to cooperative agreements with states and with tribes. For Fiscal Year 2005, we've invested another $33 million with about half of that going to additional cooperative agreements. And there's another $33 million in the President's 2006 Budget for additional infrastructure building.
We are making great progress in the area of premise registration with 100,000 premises now registered and plans to begin later this year allocating blocks of animal identification numbers to tag manufacturers.
With today's announcement, we begin work on the next step in developing the animal identification system, tracking animal movements. The only way the system will work is if stakeholders have a role in designing it, if all are truly, fully invested. The piece of the system that is the most producer-dependent is this piece dealing with tracking animal movements, and so it simply makes good sense for producers to design and to maintain that piece of the system.
Ultimately we know we will end up with a system that embodies the best that the private system and government have to offer.
I would be happy to answer your questions about the National Animal Identification System in just a moment.
But just briefly while we're speaking of tracing animals, I did want to mention that we've completed our epidemiological investigation related to the BSE animal identified in June. This very thorough investigation has been a tremendous example of partnership at the federal, state, and, I might add, the industry level. And we appreciate that.
It's worth nothing that this investigation would have taken far less than two months if we had the National Animal Identification System in place. That delay is not significant in terms of human or animal health because BSE is not a contagious disease. But the time it has taken to identify, locate, and test animals of interest is significant to our efforts to reopen export markets, because a number of trading partners have been reluctant to make decisions until the investigation is complete.
I am pleased that we are now in a position to close the investigation, communicate this information to our trading partners, and then move forward. I have with me today Dr. John Clifford, our chief veterinarian, along with Dr. Steve Sundlof of the Food and Drug Administration, to provide you with information about their conclusions. So I'll now turn the microphone to Dr. Clifford.
DR. JOHN CLIFFORD: Thank you, Mr. Secretary. As you said, the announcement of the guiding principles for the future of a public/private partnership for animal ID is a giant step forward for a national animal identification system. Because it was developed through the integration of premises registration, animal registration, and animal tracking, the NAIS has always been viewed as a government/industry partnership. Today's announcement affirms our commitment and eagerness to work with the industry to achieve the goals of the NAIS.
Now I want to turn to the completion of the epidemiological investigation that was conducted following the BSE detection in Texas in June. Many people worked very hard on the investigation, and I'd like to thank the Veterinary Services employees involved, our colleagues from the Food and Drug Administration, the owners of the animals, along with the Texas Animal Health Commission and the Texas Feed and Fertilizer Control Service for their outstanding work.
This investigation is another great example of federal, state, and local partners cooperating to help protect livestock health in this country.
I'll now summarize our findings. Our results indicate that the positive animal, called the "index animal." was born and raised on a ranch, termed the "index farm," in Texas. It was a cream-colored Brahma cross, approximately 12 years of age at the time of its death. It was born prior to the implementation of FDA's mandatory ruminant-to-ruminant feed ban in the U.S., and that ban was implemented in August 1997.
The animal was sold through a livestock sale in November of 2004 and transported to a packing plant. The animal was dead upon arrival. The animal was therefore refused by the packing plant. This refusal was consistent with USDA's safeguards to protect the meat supply from BSE.
The animal was then shipped to a pet food plant where it was sampled for BSE. The plant did not use the animal in its product, and the carcass was destroyed.
APHIS's epidemiological investigation attempted to trace all adult animals that left the index farm after 1990. The investigation also attempted to trace all progeny born within two years of the index animal's death.
Together these animals are called "animals of interest." These steps are consistent with the guidance for epidemiological investigations and to detections of BSE issued by the International Animal Health governing body or the OIE.
During the course of this investigation, USDA removed and tested a total of 67 animals of interest from the farm where the index animal's herd originated. All of these animals tested negative for BSE.
A total of 200 additional adult animals of interest were determined to have left the index farm. Of these 200, APHIS determined that 143 animals were slaughtered, 2 animals were found alive but one was determined not to be of interest because of its age, and the other tested negative for BSE. 34 animals were presumed dead, 1 is known dead, and the remaining 20 are classified as "untraceable."
In addition to the adult animals, we also looked for two calves born to the index animal. Due to record-keeping and identification issues, we had to trace 213 calves. Of these 213, 208 entered feeding and slaughter channels, 4 are presumed to have entered feeding and slaughter channels, and 1 calf was untraceable.
As you know, BSE is not a contagious animal disease. This disease is spread through contaminated feed. To determine whether contaminated feed could have played a role in the index animal's infection, FDA and the Texas Feed and Fertilizer Control Service conducted a thorough feed investigation.
For a summary of the findings of the feed investigation, we have Dr. Steve Sundlof here from the FDA.
Before I turn things over, though, I will say that we are extremely pleased with the results of the epidemiological investigation. It shows there was no widespread problem associated with the index herd, and as you will hear more about in a moment, that the ruminant feed ban in the United States is solid. It also affirms that USDA's interlocking system of safeguards to prevent BSE from entering the food chain is working as it should.
We remain vigilant, as well, as in our efforts to determine the prevalence of BSE in the United States. To date there have been only 2 BSE-positive animals found in this country in more than 452,000 animals tested in the last 14 months.
All evidence is that the prevalence is extremely low and continues to decline given the length of time the ruminant feed ban has been in effect.
With that, I will turn things over to Dr. Steve Sundlof from the Food and Drug Administration.
DR. STEVE SUNDLOF: Thank you, Dr. Clifford. I will read an opening statement as well.
On June 24, 2005, the USDA informed the FDA that a cow in Texas tested positive for bovine spongiform encephalopathy. The animal was disposed of by incineration and did not enter the human food or animal feed chains. Although the animal posed no risk to the animal feed supply, FDA, along with USDA's Animal and Plant Health Inspection Service, the Texas Animal Health Commission, and the Texas Feed and Fertilizer Control Service conducted a feed investigation with two main objectives.
The first objective was to identify all protein sources in the animal's feed history that could potentially have been the source of the BSE agent.
The second objective was to verify that cattle of interest leaving the herd after 1997 were rendered at facilities that were in compliance with the 1997 regulation that prohibits most mammalian protein in the feed for ruminants, which hereafter we will call the BSE Ruminant Feed Rule.
The feed history investigation identified 21 products that had been used on the farm since 1990. These feed products were purchased from three retail feedstores and had been manufactured at nine different feed mills.
The investigators visited these establishments to collect information on formulation, shipping invoices, and the use of ruminant meat and bonemeal on the premises, both before the 1997 feed ban and after the 1997 feed ban.
This investigation found no feed products used on the farm since 1997 had been formulated to contain prohibited mammalian protein. The investigation identified one feed which contained an animal protein source that could not be identified and the investigation also found one feed mill that supplied feed to the farm and that used ruminant meat and bonemeal in feed formulations for nonruminant species after the BSE ruminant feed rule went into effect, and this was permitted under the rule.
And there were several feed mills that had used ruminant meat and bonemeal prior to the 1997 feed ban but had ceased to use that material after the 1997 feed ban.
The investigation into the disposition of herd-mates from this farm involved visits to nine slaughter plants and eight rendering plants. The investigation found that all rendering plants were operating in compliance with the BSE ruminant feed rule. A review of the inspection history of each of these rendering firms found no violation.
And those are my prepared comments.
SEC. JOHANNS: Very good. Thank you, both of you. And with that I think we're ready to open it up to some questions.
OPERATOR: Thank you. If you have a question you can do so by pressing *1 on your touchtone phone. Anytime you wish to cancel your question you can do so by pressing *2. Please be mindful to record your name as well as your affiliation when announced.
First question comes from Libby Quaid.
REPORTER: Hi. Thank you. A question for Dr. Sundlof with FDA. Your agency promised more than a year and a half ago to close loopholes in the feed ban. When will FDA act on that promise, and what will FDA do to close the loopholes?
DR. SUNDLOF: Thank you. Yes, we have been working on the proposed rule. We announced July 14 of 2004, in an advanced notice of proposed rulemaking, that we intended to move forward with a modification of the feed rule that would prohibit specified risk materials in all animal feeds. I can report that there's been quite a great deal of progress on that, and that we hope that a rule will be forthcoming within the next month or two.
REPORTER: Can you say what that rule will entail? Will it be different from what the ANPR was?
DR. SUNDLOF: It will -- well, the ANPR dealt with a whole lot of issues. And so I can't say it will be different, but I think you'll find it's consistent with what we announced in the ANPR.
MR. JIM ROGERS: Next question, please?
OPERATOR: Next question comes from Daniel Goldstein of Bloomberg News.
REPORTER: Yeah, hi. This question is for the Secretary. Last month or earlier this month the USDA released about 1,000 incidents where there was a case of meat plants not following the rules or violations for specified risk materials. And you spoke of some reluctance on the part of trading partners to reopen trade while there was a BSE investigation happening.
Has there been any reluctance on the part of these trading partners to reopen because of some of these violations?
SEC. JOHANNS: There hasn't been. They've asked for information. We supply that information, we answer whatever questions they have. There's an interest in it, I can say that, but I haven't had any trading partner say, 'We're not going to open the border,' or 'We're considering closing the border if they've opened it already.'
So at least at this stage it's been more of a situation where they were interested and we provided the information.
MR. ROGERS: Next question, please?
OPERATOR: Next question comes from Ron Hays of Clear Channel.
REPORTER: Yes. I guess my question is regards to some of the comments that have been made by the Japanese in recent days, Japanese Food Safety Commission. Seemingly some of their panel members questioning our feed ban and saying they're fearful that we might have as "bad of a situation as they had in Britain" is one quote we saw from the Japanese media. You know. Can anybody address-- what assurances can we make to them and to folks in this country that we are effective on our feed ban and right across the board?
SEC. JOHANNS: I'll ask Dr. Sundlof to address that in just a second, but I would just offer a thought.
That's just simply not the case. I mean, it just simply is not, not the case. We've worked very intensely, as you know, with the Japanese over many, many months now to deal with their questions and to address whatever concerns they raised. With the Japanese we've even gone beyond what international rules require. We agreed that we would start trading with animals at 20 months and under, and even the international standards don't require that.
In 452,000 animals tested in the last 14 months we've had two BSE-positive animals. So again, we'll respectfully address their question, but quite honestly I don't see any scientific basis for the issue they're raising.
Doctor, you can offer a thought if you would.
DR. SUNDLOF: Thank you, Mr. Secretary.
Well, let me just say that we've had a very effective feed ban in place since 1997. It's been over eight years now this month. And we have really focused our efforts on enforcing the ban and making sure that compliance with the feed ban was high.
And we reported on several occasions that compliance when we go out and investigate -- we did over 6,800 inspections in the last year and are projecting to do even more in the upcoming years -- that their physical inspections, where inspectors go out and do a physical examination of the feed plants or the renderers, in all cases we find the compliance by the industries affected is greater than 99 percent. So it's an extremely high compliance rate. It's hard to get any better than that.
The fact that both of these cattle that were BSE-positive in the United States were born at or before the feed ban and probably very likely consumed contaminated feed well before 1997-- there's just no indication the feed rule is not effective.
MR. ROGERS: Our next question, please?
OPERATOR: Next question comes from Steve Kay of Cattle Buyers Weekly.
REPORTER: Gentlemen, I want to go back to the proposed rule by AFDA because the question of Ron Hayes mentioned what members of Japan's Prion Subcommittee were referring to in part, and one of their concerns that we were still, we the U.S. are still allowing meat and bonemeal to be fed to nonruminants.
Now the advanced notice by FDA Dr. Sundlof suggests or proposes a ban on SRMs from all animal feed. Can you tell me, if you proceed with that, is that going to satisfy Japan, do you think? How is USDA going to convey to Japan that we might be moving in this way, because if this rule becomes a final rule but doesn't take effect for another year or more is Japan going to say, Well, we'll reopen our border in a year when this takes effect? I mean, how is all this going to play out?
SEC. JOHANNS: Well, I'll offer another thought and then Dr. Sundlof, I'd ask you to offer your thoughts.
Japan would not be justified under any science, any view of the world, to adopt that viewpoint. Again I point out with Japan we at the USDA, actually before I arrived, but made a decision to agree with Japan that we would start with the trade of animals 20 months and under.
In the history of the world we haven't found an animal that tested positive for BSE 20 months and under. They just simply have no risk here. So that approach would not be justified by international standards, it would not be justified by scientific standards. It really is time for Japan, in my opinion, to step up here and go through a science-based process and reopen the border, and hopefully we're nearing the end of that very kind of process.
Doctor, any thoughts?
DR. SUNDLOF: Thank you again, Mr. Secretary. I don't have the insight to know what the Japanese government is going to do, based on what the feed rule or the proposed feed rule will convey. But the rule is very much risk-based. It uses the Harvard Risk Assessment to actually quantitate the risk and the risk reduction of the proposed measures that we will be publishing soon. And so I would agree with the Secretary that on the basis of science, the science is clearly laid out in the proposed rule and under a risk assessment that has undergone significant peer review by the scientific community.
So I think if the decisions are going to be based in science then I think we will have a very defensible position.
MR. ROGERS: Next question, please.
OPERATOR: Next question comes come from Kerry Young of Bloomberg.
REPORTER: Hi. I just had a question on why it's taking so long to get the revised feed ban out there.
SEC. JOHANNS: Dr. Sundlof, if you could address that?
DR. SUNDLOF: Okay, thank you again. Well, one of the reasons was -- there's actually a number of reasons. Back in January 2004 when, within a month after the first case in the U.S. was reported, the Secretary of Health and Human Services at that point made a statement that the FDA would propose modifications to the feed rule that would eliminate plate waste, poultry litter, cattle blood and require that all facilities that manufacture with ruminant meat and bonemeal be dedicated to non-ruminants and not prepare any ruminant feed in those mills.
Within a week after the Secretary's announcement, the International Review Team that was advisory to the Secretary of Agriculture made recommendations that were very much different than that which the Secretary had announced the week prior. Based on that, we decided at that point to go through an advanced notice of proposed rulemaking to get all the information out, all the recommendations that the International Review Team has made, and discuss those from a risk basis.
And as a result of that, we are now into rulemaking.
One other thing that was a reason for the delay is that during this time USDA was in the middle of their intense surveillance activity to try and determine the prevalence of BSE in U.S. cattle. And that was done, the questions that were before us were--the International Review Team based their recommendations on assumptions that there was significant infectivity in the U.S. cattle herd. The results of the USDA surveillance tend to cast doubt on that assumption, and so it had a major effect on which was the correct regulation or what were the correct measures that would be commensurate with the real risk?
So those are some of the reasons it has been delayed. It's a complicated regulation. It involves a lot of material that will have to be disposed of in some environmentally friendly way, and so we have to be very thoughtful about how we propose a rule that has minimal environmental impacts but yet does the greatest amount to reduce the actual risk to BSE in cattle.
SEC. JOHANNS: If I could just add something that obviously is very, very relevant and very important. Again, that's to point out that in the last 14 months we've tested 452,000 high-risk animals. These are the animals, that present themselves for testing, that experience would show from other countries would have the highest chance of being a BSE situation. We've had two out of that identify as positive. And both of those animals were born before the feed ban.
So it's obviously the decision, some years ago now, to impose the first generation of feed ban was the right decision.
MR. ROGERS: Next question, please.
OPERATOR: Next question comes from Sally Schuff from Feedstuffs.
REPORTER: Yes. This is Sally Schuff at Feedstuffs. Thank you for taking the question.
The question is a two-part question for Dr. Clifford and Dr. Sundlof. Dr. Clifford, you said when the second case was announced the test results were more similar to the Western blot test, was more similar to results found in France than in the United Kingdom, leading to some question about what strain of BSE she might have. My question to you is, has that been resolved yet? Do you have any more positive identification on the strain?
My question for Dr. Sundlof is, have you identified the source of the meat and bonemeal that was fed prior to the feed ban? Was it domestic or imported?
DR. CLIFFORD: This is John Clifford. I'll answer the first part. From a regulatory standpoint, this is a case of BSE. Looking from a molecular standpoint, there's further work that's being done internationally on some of these cases. And--but from our standpoint, this is a case of traditional BSE that we would find. So that's the way we're approaching this.
OPERATOR: Next question comes from Karen Robinson of Dallas Morning News.
REPORTER: Hello, this is Karen Robinson Jacobs with the Dallas Morning News. I wanted to go back to the Texas cow, and if you could tell us maybe a little more slowly how much cattle or meat from this particular index ranch got into the human food chain, how much got into the pet food chain, and how concerned should consumers be that they may have eaten something already before the test even began?
DR. CLIFFORD: This is John Clifford. I'd begin by saying if you look at what we know internationally, it's not very common at all. In fact it's rare to have more than one single case of BSE found within a herd. So from that standpoint alone, the risk is extremely small. In addition you have other safeguards in place. We have had a feed ban in place since 1997. It's been in place for 8 years, and then there's other cross-cutting protections as well from the food safety side that Dr. Ken Peterson's on if he wants to address as well.
But as far as actual poundage, I don't think it's possible for us to give you that actual number. There was two calves of interest that we traced. Due to the lack of appropriate records at the time, we actually traced 213 calves. Of those, it's estimated that 212 of those animals went into the feeding and slaughter channels. Those animals would have been slaughtered likely prior to 30 months of age, which we know that it's extremely small risk of having BSE prior to 30 months of age.
And also internationally and in the research community, while it's never been proven that offspring can get this disease through maternal transmission -- it's never been proven or disproven actually -- but it's thought very much from the international experts and the research it is extremely rare if it does happen.
Both of these calves were born very well prior to this animal being slaughtered. This animal did not show any clinical signs typical of BSE -- sampled and destroyed. This animal did not show any clinical signs or evidence of BSE which would make it even more unlikely that these two offspring would have any risk of having BSE.
The other 200 head that were traced were retraced as a result also of a lack of records. We were looking at cattle of interest over a five-year period of time of which this animal was born. Her approximate age was 12. We expanded one year of that and made her 11 to 13, and then we'd go another year beyond that. So we looked at animals basically in the age range of 10 to 15 years of age to remove those from the herd. And we traced every adult animal that we could from 1990.
Many of those animals would not even be of concern because they would not have received any feed at the time that she was in the herd or would have not been a birth cohort and born at the same time that she was.
So of those, 143 were reported as slaughtered, and we confirmed that 131 were definitely slaughtered; 34 were presumed dead, and 20 of those were untraceable. So again, we feel that the risk is extremely small. We do not feel that the public or our pet food industry should have any concerns relative to this issue.
MR. ROGERS: Next question, please.
OPERATOR: Next question comes from Chuck Abbott of Reuters.
REPORTER: Good afternoon. I'm curious -- what, Mr. Secretary, what you're going to do about the downer ban which is still now a preliminary rather than a permanent rule. When will you decide on the downer ban? How sweeping will it be? And what's going to happen to the surveillance testing program? It has run some months beyond its originally envisioned lifetime. I'll stop there.
SEC. JOHANNS: The surveillance program, as you know, was really open-ended. So I might debate with you a little bit on your last thought there. But here's what I would say. I am not prepared to bring the surveillance program to a conclusion, have not made a final decision on the downer ban. As you know, we've started now with the testing of the 20,000 healthy animals. We hope to have that done in the next 60 days.
Dating from the time of my confirmation hearing really until now, my view was to get the surveillance program in the kind of shape that we wanted, make sure that we'd touched all the bases. And then, in addition to that, do the additional testing of the 20,000 healthy animals and then, once we have all the information together, make a decision on some of those pending issues.
So that's where it's at.
MR. ROGERS: All right. I'd like to thank everyone for calling today. If you have further questions for the U.S. Department of Agriculture, you can call me, Jim Rogers, at 202-690-4755. If you have questions for the Food and Drug Administration, please contact my counterpart Ray Jones at 301-827-6246. This concludes the call for today, and I thank you all for participating.
Last Modified: 08/30/2005
http://www.usda.gov/wps/portal/usdahome?contentidonly=true&contentid=2005/08/0339.xml
HOW much longer can this buffoonery go on???
I only pray that the world does not buy into this phony BSE MRR policy and June 2004 Enhanced BSE surveillance program. none of it was based on sound science. THE June 2004 Enhanced BSE/TSE surveillance program was a terrible failure, other than to prove just how bad the situation is in the USA, and how out of control the Federal Government is in trying to cover it up. THE OIG should hold an inquiry into this program. THE BSE MRR policy should be dismantled, and the USA BSE GBR risk assessment should be immediately raised to BSE GBR IV. THE International guidelines for trade in animal and animal products which are developed by the World Organization for Animal Health (formerly known as the Office International des Epizooties (OIE)), is and has been terrible flawed. ALL one has to do is to look at the countries that have gone by there very minimal guidelines, most all went on to develop BSE. IT would be nice if the OIE et al would define “controlled BSE-risk country” or “effectively enforced ban”. The USA and North America have neither. THIS has been proven time and time again via the GAO, OIG and the European EFSA BSE-risk assessments of North American countries. Many Countries have not even reported there first case of BSE yet, and many countries have not even produced a risk analysis for BSE. A fine example is Mexico, which is also a BSE GBR III country. IN Mexico, they are NOT even required to remove SRM;
Working Group Report on
the Assessment of the Geographical BSE-Risk (GBR) of
MEXICO
2004
Specified Risk Material (SRM) and fallen stock
There is no SRM-ban. SRM is normally destined for human consumption. According
to the CD, fallen stock from pasture and diseased animals are incinerated and not
rendered.
Conclusion on the ability to avoid recycling
In light of the above information, it has to be assumed that the BSE agent, should it
have entered Mexico, could have been recycled and potentially amplified.
snip...
In view of the above - described consideration the combination of the very / extremely
high external challenges with a very unstable system makes the occurrence of an
internal challenge likely in Mexico from approximately 1993 onwards.
4.2 Risk that BSE infectivity entered processing
It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’
MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late
1990’s). The high level of external challenge is maintained throughout the reference
period, and the system has not been made stable, leading to increased internal
4.3 Risk that BSE infectivity was recycled and propagated
It is likely that BSE infectivity was recycled and propagated from approximately
1993. The risk has since grown consistently due to a maintained internal and external
challenge and lack of a stable system.
5. CONCLUSION ON THE GEOGRAPHICAL BSE - RISK
5.1 The current GBR as function of the past stability and challenge
The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed
that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent.
snip...end
http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/scr_annexes/566/sr04_biohaz02_mexico_report_annex_en1.pdf
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA) Publication date: 20 August 2004 Adopted July 2004 (Question N° EFSA-Q-2003-083)
Report
Summary Summary of the Scientific Report
The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.
The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.
A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.
EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
http://www.efsa.eu.int/science/efsa_scientific_reports/gbr_assessments/573_en.html
From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Tuesday, July 29, 2003 1:03 PM
To: fdadockets@oc.fda.gov
Cc: ggraber@cvm.fda.gov; Linda.Grassie@fda.gov; BSE-L
Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]
Greetings FDA,
snip...
PLUS, if the USA continues to flagrantly ignore the _documented_ science to date about the known TSEs in the USA (let alone the undocumented TSEs in cattle), it is my opinion, every other Country that is dealing with BSE/TSE should boycott the USA and demand that the SSC reclassify the USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the SSC to _flounder_ any longer on this issue, should also be regarded with great suspicion as well. NOT to leave out the OIE and it's terribly flawed system of disease surveillance. the OIE should make a move on CWD in the USA, and make a risk assessment on this as a threat to human health. the OIE should also change the mathematical formula for testing of disease. this (in my opinion and others) is terribly flawed as well. to think that a sample survey of 400 or so cattle in a population of 100 million, to think this will find anything, especially after seeing how many TSE tests it took Italy and other Countries to find 1 case of BSE (1 million rapid TSE test in less than 2 years, to find 102 BSE cases), should be proof enough to make drastic changes of this system. the OIE criteria for BSE Country classification and it's interpretation is very problematic. a text that is suppose to give guidelines, but is not understandable, cannot be considered satisfactory. the OIE told me 2 years ago that they were concerned with CWD, but said any changes might take years. well, two years have come and gone, and no change in relations with CWD as a human health risk. if we wait for politics and science to finally make this connection, we very well may die before any decisions or changes are made. this is not acceptable. we must take the politics and the industry out of any final decisions of the Scientific community. this has been the problem from day one with this environmental man made death sentence. some of you may think i am exaggerating, but you only have to see it once, you only have to watch a loved one die from this one time, and you will never forget, OR forgive...yes, i am still very angry... but the transmission studies DO NOT lie, only the politicians and the industry do... and they are still lying to this day...TSS
http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt
Gerald Wells: Report of the Visit to USA, April-May 1989
snip...
The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised...
snip...
It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US...
snip...
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_...
snip...
http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
R.F. Marsh* and G.R. Hartsough
•Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092
ABSTRACT Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England.
INTRODUCTION
Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough and Burger who demonstrated that the disease was transmissible with a long incubation period, and that affected mink had a spongiform encephalopathy similar to that found in scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity between TME and scrapie, and the subsequent finding that the two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was concluded that TME most likely resulted from feeding mink scrapie-infecied sheep. The experimental transmission of sheep scrapie to mink (Hanson et al., 1971) confirmed the close association of TME and scrapie, but at the same time provided evidence that they may be different. Epidemiologic studies on previous incidences of TME indicated that the incubation periods in field cases were between six months and one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be transmitted to mink in less than one year. To investigate the possibility that TME may be caused by a (particular strain of scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie agent, including their sheep or goat sources, were inoculated into a total of 61 mink. Only one mink developed a progressive neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent from an unidentified source.
OBSERVATIONS AND RESULTS
A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed.
Experimental Transmission. The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months.
DISCUSSION These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy. We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster- adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It will be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed.
ACKNOWLEDGEMENTS
These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations.
REFERENCES
Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420.
MARSH
http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
JAPAN AND EVERY OTHER COUNTRY IN THE WORLD HAVE EVERY RIGHT AND SCIENTIFIC REASON TO BAN USA BEEF, just for BSE/TSE, antibiotics and hormones reasons alone...
TSS
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Subject: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 1)
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Wed, 31 Aug 2005 13:19:28 -0500 Content-Type: text/plain Parts/Attachments: text/plain (878 lines)
##################### Bovine Spongiform Encephalopathy #####################
From: TSS ()
Subject: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 1)
Date: August 31, 2005 at 11:08 am PST
Texas BSE Investigation
Final Epidemiology Report
August 2005
2
Table of Contents
Executive Summary............................................................................................................. 3
Background of the Investigation......................................................................................... 3
BSE Response Plan .............................................................................................................. 3
Definition of At-Risk Cattle.................................................................................................... 3
Definition of Cattle of Interest ............................................................................................... 4
Definition of Feed Cohort...................................................................................................... 4
Definition of Birth Cohort...................................................................................................... 4
Definition of At-Risk Progeny................................................................................................ 4
Epidemiology Investigation of Index Herd: Farm A....................................................... 5
Background........................................................................................................................... 5
Progeny................................................................................................................................. 6
Birth Cohort ........................................................................................................................... 6
Feed Cohort ........................................................................................................................... 6
Removal of Cattle from the Index Farm............................................................................ 7
Tracing of Progeny .............................................................................................................. 7
Tracing of Birth Cohorts..................................................................................................... 8
Tracing of Cattle of Interest................................................................................................ 9
Calculation of Minimum Estimated Ages .............................................................................. 9
Trace Herds ........................................................................................................................ 10
Trace Herd 1........................................................................................................................ 10
Trace Herd 2........................................................................................................................ 10
Trace Herd 4........................................................................................................................ 11
Trace Herd 5........................................................................................................................ 11
Trace Herd 6........................................................................................................................ 11
Trace Herd 7........................................................................................................................ 12
Trace Herd 8........................................................................................................................ 12
Analysis of Data on Presumed Dead and Untraceable Animals.................................... 12
Appendix 1 – Final Trace-Out Diagram.............................................................................. 13
3
Executive Summary
In June 2005, an inconclusive bovine spongiform encephalopathy (BSE) sample from
November 2004, that had originally been classified as negative on the
immunohistochemistry test, was confirmed positive on SAF immunoblot (Western blot).
The U.S. Department of Agriculture (USDA) identified the herd of origin for the index cow
in Texas; that identification was confirmed by DNA analysis. USDA, in close cooperation
with the Texas Animal Health Commission (TAHC), established an incident command post
(ICP) and began response activities according to USDA’s BSE Response Plan of
September 2004. Response personnel removed at-risk cattle and cattle of interest (COI)
from the index herd, euthanized them, and tested them for BSE; all were negative. USDA
and the State extensively traced all at-risk cattle and COI that left the index herd. The
majority of these animals entered rendering and/or slaughter channels well before the
investigation began. USDA’s response to the Texas finding was thorough and effective.
Background of the Investigation
On June 10, 2005, USDA announced that the November 2004 inconclusive BSE sample
tested positive on SAF immunoblot. The SAF immunoblot was run at USDA’s National
Animal Disease Center (NADC) upon the recommendation of USDA’s Office of the
Inspector General. Samples were sent to a World Organization for Animal Health (OIE)
reference laboratory for BSE in Weybridge, England, for confirmatory tests. Farm A,
located in Texas, was the suspected farm of origin for the index cow and was placed under
hold order on June 20, 2005 pending confirmation of the positive results and DNA analysis
of the herd. Weybridge confirmed the BSE positive on June 24, 2005. The carcass of the
index cow had been disposed of by incineration in November 2004. Cattle from several
units on Farm A were bled for DNA testing (a unit is a part of the business entity of a farm.
For example, a pasture on which a group resides may be a unit). Farm A was confirmed as
the farm of origin for the index cow on June 29, 2005, and an ICP was established in Texas
to coordinate the response. Removal of at-risk cattle from the index herd, and tracing of atrisk
cattle and COI that had left the index herd, commenced immediately.
BSE Response Plan
The September 2004 BSE Response Plan outlines the necessary tracing and removal of atrisk
cattle and, in some cases, COI, in response to the identification of a BSE-positive
animal. Response personnel removed at-risk animals from the index farm and traced atrisk
animals and COI in accordance with the response plan.
Definition of At-Risk Cattle
At-risk cattle were cattle that were confirmed to be: part of the birth cohort; part of the feed
cohort; or progeny of the positive cow born within 2 years prior to the positive test.
Response personnel removed at-risk cattle from the herd, euthanized them, and tested them
for BSE; all were negative.
4
Definition of Cattle of Interest
In many cases, at-risk cattle could not be definitively identified. Response personnel then
analyzed herd inventories and herd records to identify a group of cattle that include all
potential at-risk cattle and any other cattle that could not be distinguished from at-risk
cattle. All of these cattle (at-risk cattle and any additional cattle as necessary) were defined
as COI. COI that fell into the appropriate age range and could be part of the birth or feed
cohort were removed from the herd, euthanized, and tested for BSE; all were negative.
Definition of Feed Cohort
The feed cohort consisted of all cattle which, during their first year of life, were reared with
the positive animal during its first year of life and consumed the same feed during that
period. In the index herd, this definition applied to cattle in any unit that were weaned and
fed with calves from the other units for a short period of time and then later returned to
their respective units of origin from 1991-1995 (the range of years that could have
coincided with the first year of life of the index cow).
Definition of Birth Cohort
In most cases, it was impractical or impossible to definitively determine which cattle were
exposed to a feed source. Accordingly, response personnel used a birth cohort to determine
which cattle to consider at-risk. The birth cohort included all cattle born on the positive
animal’s birth premises within 1 year before or after the BSE-positive animal’s date of
birth.
Since the index cow was approximately 12 years of age, but an exact date of birth did not
appear in the herd records, response personnel used a potential age range of 12 years with 1
year added to each end of that age (age 11 to 13) to sufficiently cover the most likely age
range of the animal. In addition, if the positive animal moved from the birth premises to
any other premises during its first year of life, all cattle of less than 1 year of age that were
present on such additional premises were also considered to be at-risk. Using the age range
of the index animal, all cattle born on the index premises from 1990-1995 were part of the
birth cohort of the index animal.
Definition of At-Risk Progeny
Since the index cow was not confirmed to have been exhibiting clinical signs of BSE prior
to her positive test results, the at-risk progeny as defined by the OIE were those offspring
that were born within the 2 years prior to the positive test result. Those 2 years prior to the
positive test result would have included her calves from 2002, 2003, and 2004. According
to the owner, the index cow produced her last calf either in Fall 2003 or Spring 2004, and
the calf prior to that was born either in Fall 2002 or Spring 2003. Tracing activities
focused on these two calves as at-risk progeny.
5
Epidemiology Investigation of Index Herd: Farm A
Background
The index cow was an approximately 12-year-old yellow or cream-colored Brahma cross
that originated from Farm A located in Texas. The cow was sold through a livestock sale
on 11/11/04, purchased by an order buyer, and was transported to a packing plant on
Monday, 11/15/04. When the truck arrived at the packing plant during the late afternoon of
11/15/04, the index cow and one other were found dead on the truck and were transported
to a pet food plant later that day where they were sampled for BSE testing as part of the
enhanced BSE surveillance.
DNA analysis of blood samples taken from five of the six units of cattle that comprise
Farm A yielded four animals from two different units that were genetically related to the
index cow and confirmed Farm A as her herd of origin.
The herd on Farm A consisted of mixed breed beef cattle that are traditionally not used as
seedstock replacement animals. Market records and preliminary tracing indicated that most
animals that left the index herd either went to slaughter within a few days of sale or, in the
case of younger animals, entered into known rendering and slaughter channels immediately
following sale. There were only 11 cows identified during the investigation that were
traced from Farm A into other herds where they had been used as replacement cows.
The owner of Farm A raised this cow from birth and stated that the cow had never been off
the premises prior to its sale. She was marketed because of poor body condition (the
animal’s condition had not improved despite the early weaning of her 2003/2004 calf). The
owner stated that the cow had always been excitable and had fallen while she was being
loaded to go to the market, but that this was not unusual behavior for her in his opinion. In
addition there was a report of this cow being down in the alley at the livestock market on
11/11/04, but she apparently got up again and was able to be loaded onto the truck to go to
the packing plant. When questioned about any previous history of neurological signs in
cattle on the farm, the owner reported that no cattle on the farm had ever shown any
neurological signs, nor had there been any cases of rabies on the index farm.
Index Herd Census
Farm A consisted of 6 units (Units A through F) containing a total of about 217 adult cattle
and approximately 100 to 120 calves. Early in the investigation, response personnel
discovered that an additional unit belonging to the owner’s son and located adjacent to Unit
F could also contain COI. This group, Unit G, contained 16 adult cattle and made a
seventh unit that became included in the investigation.
On 6/22/05, the first three of the original six units were sampled for DNA testing to
confirm the herd of origin of the index cow. Those first three units consisted of: Unit A
contained 62 head with some older cattle (more likely than the other units to provide a
DNA match); Unit B with 28 head (3-year-old unit); and Unit C with 25 head (2-year-old
unit). Two additional units were sampled for DNA on 6/23/05; Unit D with 31 head and
Unit E with 30 head, both of which contained older animals.
6
The sixth unit, Unit F, containing 41 head, was purchased in 1993 from another source.
Because it did not have animals that were genetically related to the other 5 units, this unit
was not sampled for DNA testing. Unit F, and adjacent Unit G, contained COI because the
weaned heifers from those units were commingled and fed with weaned heifers from the
other units for a short period of time before they were returned to their respective units of
origin. This practice of weaning and feeding together fit the definition of a feed cohort.
Progeny
The owner did keep some replacement heifers and, although he was relatively sure that he
had not kept any offspring from the yellow cow because of her excitable demeanor, DNA
analysis of the herd revealed several animals in the herd that may have been older offspring
of the index cow. While the owner sold 12 calves at the sale with the index cow on
11/11/04, her last calf was not in that group. According to the owner, the index cow’s last
calf was born either in Fall 2003 or Spring 2004, weaned early, and sold through the
livestock market some time between February and October 2004. The calf prior to that
would have been born either in Fall 2002 or Spring 2003 and was sold at the livestock
market sometime between January and December 2003.
Birth Cohort
The owner of Farm A kept very few herd records; this made finding documentation on this
cow’s birth cohort difficult. The birth cohort, by definition, included all cattle born on the
positive animal’s birth premises within 1 year, before or after, the positive animal’s date of
birth. The index cow was approximately 12 years of age in November 2004, but there was
no exact birth date in the herd records. A potential age range of 11 to 13 years was used to
sufficiently cover the animal’s most likely age. Using this range, all cattle born on the
index premises between 1990 and 1995 were considered part of the birth cohort.
In lieu of the owner’s records, herd records from Veterinary Services’ Generic Database
(GDB) were used to compile a list of brucellosis calfhood vaccination (CV) tag numbers
from the index herd that corresponded to animals to be included in the birth cohort. There
were 121 animals identified through GDB as having been calfhood vaccinated on the index
farm between 1991 and 1994. The owner of Farm A did not calfhood vaccinate after 1994.
Moreover, calfhood vaccinates include only heifers. Therefore, the list of 121 animals was
not a complete list of all birth cohorts. However the tracing that response personnel
conducted on other COI was designed to account for the remainder of the birth cohorts.
Feed Cohort
Animals in Units A, D, and E, that were weaned and fed with the positive cow between
1991-1995, were already considered at-risk as part of the defined birth cohort. Animals in
Units B and C were 3-year-olds and 2-year-olds, respectively, and were too young to be
either birth or feed cohorts. Although Unit F was purchased separately and did not contain
animals genetically related to the other units, calves from Unit F were weaned and fed for a
short period of time with weaned calves from other units and all calves were later returned
to their respective units of origin. Since Unit F was not purchased until 1993, the feed
cohort consisted of those animals in Unit F that could have been weaned and fed with the
index cow in 1993 or 1994. Additionally, Unit G contained possible feed cohorts that
could have been weaned and fed with the index cow between the years of 1991 and 1995.
7
Feed
The feeding regimen for the cattle in this herd consisted of natural pasture, hay, mineral
supplement, syrup tubs occasionally, and a breeder’s supplement (predominantly a name
brand manufactured breeder’s cube). The Food and Drug Administration (FDA)
investigated all sources of feed and supplements used on Farm A. In-depth investigations
and site visits were conducted by FDA involving retail feed stores, feed manufacturers,
slaughter plants, renderers, and brokers. A more detailed account of the investigation is
contained in FDA’s final report.
Removal of Cattle from the Index Farm
Any animal still present within the index herd that could have been a possible birth cohort
or feed cohort of the index cow was targeted for removal as an at-risk animal. Units A, D,
E, F, and G, all of which were known to contain older animals, were inventoried.
Identification tags, tattoos, and brands were recorded, and all animals were aged based on
their dentition and any man-made identification. Cattle whose estimated age indicated that
they could have been part of the index cow’s birth or feed cohort were removed from the
herd, euthanized, and tested for BSE; all were negative.
Units B and C were exempt from the cohort removal process because they contained only
3-year-old and 2-year-old animals respectively. Although the DNA analysis of animals in
Units A through E determined that there were 2 animals present that could have been
offspring of the index cow, their estimated age by dentition revealed that they were not of
the appropriate age to be at-risk progeny. This verified the owner’s claim that he had sold
the index cow’s last two calves at the livestock market and they were not currently present
in the index herd.
After sorting by age, response personnel identified and removed the following numbers of
cows from the herd on 7/6/05: Unit A, 11 cows; Unit D, 11 cows; Unit E, 7 cows. The
same process was applied to Units F and G and the following numbers of cows were
identified and removed from the herd on 7/7/05: Unit F, 28 cows; Unit G, 10 cows.
Of the 67 animals removed from the herd as possible birth cohorts and/or feed cohorts of
the index cow, 42 were definitively identified as belonging to the birth cohort due to the
presence of a calfhood vaccination tag or tattoo that corresponded to the appropriate birth
cohort years. All 67 animals were euthanized on 7/6/05 and 7/7/05 and samples were
subsequently sent to USDA’s National Veterinary Services Laboratories (NVSL) for BSE
testing. All samples were run on the ELISA test and confirmed negative on 7/8/05 and
7/9/05. Upon confirmation of negative results, disposal of carcasses was completed by
burial in an approved landfill facility. The index farm was released from hold order on
7/11/05.
Tracing of Progeny
The 2003/2004 progeny of the index cow was known to have left the farm through a
specific livestock market sometime between February and October 2004. The 2002/2003
progeny of the index cow left the farm through the same market sometime between January
8
and December 2003. Response personnel learned early in the investigation that animals
from the index farm were sold not only under the index farm owner’s name and that of his
wife, but also by other members of the owner’s immediate family. Additionally, there were
no herd records to indicate the gender of the two at-risk progeny. Therefore, market
records for February through October 2004 and January through December 2003 were
obtained for all calves sold both by Farm A’s owner and by members of his immediate
family; response personnel traced all such calves to determine their disposition.
With the index herd being composed of mixed breed beef cattle, the calves that left the
farm were genetically unsuitable for use as replacement animals or for sale as breeding
stock, a fact that was confirmed by the trace work and the documentation of the final
disposition of the calves of interest.
Response personnel ultimately identified 213 calves of interest to be traced. Of these, 208
were confirmed to have entered known rendering/slaughter channels, 4 were presumed to
have entered rendering/slaughter channels, and 1 was purchased in cash through a livestock
market with no buyer name or contact information (this animal was classified as
untraceable. See Appendix 1). A calf was categorized as presumed to have entered
rendering/slaughter channels if it passed through at least one livestock market subsequent
to its original sale and could not be individually traced due to unknown resale date and new
backtag, but all calves resold matching that description during an appropriate date range
were purchased by known rendering/slaughter order buyers.
It was not possible to DNA test the calves that entered known rendering and slaughter
channels – most were of an age in which they were likely to have been slaughtered prior to
the time of the investigation. There were no calves traced to farms outside of rendering and
slaughter channels.
Tracing of Birth Cohorts
Since there were essentially no records maintained on the index farm, it was necessary to
compile the list of known birth cohorts using brucellosis CV tag numbers for this herd from
the period 1991 to 1994. The calves vaccinated during that time period were part of the
index cow’s birth cohort and tracing activities centered on finding those animals.
There were 121 animals whose CV tag number and/or tattoo included them as part of the
birth cohort. Of those 121 animals, 67 animals were definitively accounted for (42 were
found in the index herd, removed, and tested BSE negative; 25 were identified as having
left Farm A through the market system and were traced, 11 of those were reported
slaughtered, 13 were classified as presumed dead, and 1 was found alive, euthanized, and
tested BSE negative). Of the remaining 54 animals from the birth cohort, there may have
been several that died within the index herd, but the majority likely left the herd without
identification and would have been either re-tagged at the livestock market or consigned
directly to slaughter without identification. To account for these remaining birth cohorts,
all adult cattle that left the index farm since 1990 were traced as COI.
9
Tracing of Cattle of Interest
The investigation revealed that many animals left Farm A, arrived at markets without any
identification tags, and were subsequently re-tagged at the market. Due to lack of farm
records, it is unknown which of these re-tagged animals may have belonged to the birth
cohort. As a result, all animals that may have left Farm A since 1990 were traced as COI.
Additionally, animals from the index farm were sold not only under the index farm owner’s
name and that of his wife, but also by other members of the owner’s immediate family;
therefore, cattle sold from the index farm by all pertinent family members were traced.
There were some older animals that left the index farm but were able to be excluded from
further trace work because they were known not to have been part of the birth cohort or
feed cohort of the index cow despite their being of the appropriate age. The index farm
owner’s late father had maintained a herd of cattle separate from the index farm but which
was added to the index farm in 1997. Complete herd test data and CV data from the GDB
was obtained for the father’s herd and those animals were excluded from the tracing
activities.
There were a total of 200 COI traced: 143 were reported to have been slaughtered (131 of
those were confirmed as having been slaughtered), 1 is known to have died previously and
was buried, 2 were found alive (1 was a known birth cohort that tested negative, 1 was
determined not to be one of the cattle of interest due to her young age), 34 were classified
as presumed dead, 20 were classified as untraceable. (See Appendix 1). Animals were
confirmed at slaughter using GDB slaughter testing data or the hard copies of slaughter
testing Form 4-54.
An animal was classified as presumed dead if records that could be used to advance the
tracing of the animal were exhausted or did not exist, and the age of the animal at the time
of the investigation was estimated to be at least 11 years old or older. Since the index herd
was not a purebred or seedstock operation, and animals leaving the herd were unlikely to
be purchased as replacement cattle, standard industry practices indicated that most adult
animals that had left the herd would have been culled and slaughtered by the time they
were in this age group. Additionally, this age cutoff was arrived at through review of
market records and the specific years in which Farm A sold cattle through the market. An
animal was classified as untraceable if all records to advance the tracing of the animal were
exhausted or did not exist, and the age of the animal at the time of the investigation was
estimated to be less than 11 years of age (the animal, therefore, could not be presumed
dead).
Calculation of Minimum Estimated Ages
Throughout the tracing process, personnel used minimum estimated ages of the 200 COI to
evaluate whether those individuals could be old enough to be part of the birth or feed
cohort of the index cow. Since Farm A’s owner maintained no records on the ages of
animals, GDB data assisted in assigning minimum estimated ages. Animals that were
wearing brucellosis CV eartags could be aged quite accurately because the exact CV date
was recorded in the GDB and those animals would have been vaccinated between 4 to 12
months of age. The GDB also contained lists of individual eartags for all animals on the
10
index farm that were included in complete herd brucellosis testing in 1991, 1993, and 1994.
Cattle included in those herd tests would have been at least 18 months of age at the time of
the test and their minimum age today could be extrapolated from that data. Finally, the
GDB also contained livestock market testing data that could also be used to assign a
minimum age because the animal would have been at least 18 months of age on date the
earliest brucellosis market test was conducted. The minimum ages calculated for the cattle
of interest were used later in an analysis by USDA’s Centers for Epidemiology and Animal
Health (CEAH) to determine the probable disposition of untraceable and presumed dead
animals based on their age.
Trace Herds
Response personnel made every attempt to trace COI to their final dispositions (which, in
most cases, was slaughter). If an animal was traced to a herd owner and the owner could
not provide information that indicated that the animal of interest was not currently present
within his/her herd, the owner’s herds were placed under hold order pending a herd
inventory to determine whether or not the animal of interest had been retained. There were
eight herds identified as the last traceable location of the animal of interest and were,
therefore, subjected to herd inventories in an attempt to locate the animal.
When an animal of interest was located within a herd, the age of the animal was estimated
using dentition and any man-made identification. If the animal fell into the appropriate age
range to be a possible birth cohort or feed cohort of the index cow, the animal was removed
from the herd and tested. If an animal of interest was located within the herd and fell into
the appropriate age range to be a possible at-risk progeny of the index cow, the animal was
sampled for DNA testing.
Trace Herd 1
The owner of Trace Herd 1 was identified as having received one of the adult COI from the
index herd. Trace Herd 1 contained 909 head of cattle in multiple pastures and was placed
under hold order on 7/21/05. Upon completion of herd inventory, the animal of interest
was not found within the herd. A GDB search of all recorded herd tests conducted on
Trace Herd 1 and all market sales by the owner failed to locate the identification tag of the
animal of interest and she was subsequently classified as untraceable. The hold order on
Trace Herd 1 was released on 8/8/05.
Trace Herd 2
Trace Herd 2 was identified as having received one of the adult COI from the index herd.
Trace Herd 2 contained 19 head of cattle on one pasture and was placed under hold order
on 7/25/05. The owner of Trace Herd 2 identified the animal of interest by her eartag while
he was feeding his cattle out of a bucket and individually penned her for inspection by field
personnel. While the cow was identified as one of the animals that had left the index farm,
her age by dentition was estimated to be only 5 years old, which was too young to have
placed her as part of the birth or feed cohort of the index animal. She was classified as
found alive but determined not to be one of the COI; the hold order on Trace Herd 2 was
released on 7/26/05.
11
Trace Herd 3
The owner of Trace Herd 3 was identified as possibly having received an animal of
interest. The herd was placed under hold order on 7/27/05. The herd inventory was
conducted on 7/28/05. The animal of interest was not present within the herd, and the hold
order was released on 7/28/05. The person who thought he sold the animal to the owner of
Trace Herd 3 had no records and could not remember who else he might have sold the cow
to. Additionally, a search of GDB for all cattle sold through the markets by that individual
did not result in a match to the animal of interest. The animal of interest traced to this herd
was classified as untraceable because all leads were exhausted.
Trace Herd 4
The owner of Trace Herd 4 was identified as having received one of the COI through an
order buyer. Trace Herd 4 was placed under hold order on 7/29/05. A complete herd
inventory was conducted on 8/22/05 and 8/23/05. There were 233 head of cattle that were
examined individually by both State and Federal personnel for all man-made identification
and brands. The animal of interest was not present within the herd. Several animals were
reported to have died in the herd sometime after they arrived on the premises in April 2005.
A final search of GDB records yielded no further results on the eartag of interest at either
subsequent market sale or slaughter. With all leads having been exhausted, this animal of
interest has been classified as untraceable. The hold order on Trace Herd 4 was released on
8/23/05.
Trace Herd 5
The owner of Trace Herd 5 was identified as having received two COI and was placed
under hold order on 8/1/05. Trace Herd 5 is made up of 67 head of cattle in multiple
pastures. During the course of the herd inventory, the owner located records that indicated
that one of the COI, a known birth cohort, had been sold to Trace Herd 8 where she was
subsequently found alive. Upon completion of the herd inventory, the other animal of
interest was not found within the herd. A GDB search of all recorded herd tests conducted
on Trace Herd 5 and all market sales by the owner failed to locate the identification tag of
the animal of interest and she was subsequently classified as untraceable due to all leads
having been exhausted. The hold order on Trace Herd 5 was released on 8/8/05.
Trace Herd 6
The owner of Trace Herd 6 was identified as possibly having received an animal of interest
and was placed under hold order on 8/1/05. This herd is made up of 58 head of cattle on
two pastures. A herd inventory was conducted and the animal of interest was not present
within the herd. The owner of Trace Herd 6 had very limited records and was unable to
provide further information on where the cow might have gone after he purchased her from
the livestock market. A search of GDB for all cattle sold through the markets by that
individual did not result in a match to the animal of interest. Additionally, many of the
animals presented for sale by the owner of the herd had been re-tagged at the market
effectually losing the traceability of the history of that animal prior to re-tagging. The
animal of interest traced to this herd was classified as untraceable due to all leads having
been exhausted. The hold order on Trace Herd 6 was released on 8/3/05.
12
Trace Herd 7
The owner of Trace Herd 7 was identified as having received an animal of interest and was
placed under hold order on 8/1/05. Trace Herd 7 contains 487 head of cattle on multiple
pastures in multiple parts of the State, including a unit kept on an island. The island
location is a particularly rough place to keep cattle and the owner claimed to have lost 22
head on the island in 2004 due to liver flukes. Upon completion of the herd inventory, the
animal of interest was not found present within Trace Herd 7. A GDB search of all
recorded herd tests conducted on Trace Herd 7 and all market sales by the owner failed to
locate the identification tag of the animal of interest. The cow was subsequently classified
as untraceable. It is quite possible though that she may have died within the herd,
especially if she belonged to the island unit. The hold order on Trace Herd 7 was released
on 8/8/05.
Trace Herd 8
Trace Herd 8 received an animal of interest, which happened to be a known birth cohort of
the index cow, from Trace Herd 5. Trace Herd 8 consists of 146 head of cattle that were
placed under hold order on 8/4/05. A herd inventory was conducted, the birth cohort was
found alive in the herd, and she was purchased and euthanized. The hold order on Trace
Herd 8 was released on 8/4/05. The cow was sampled on 8/5/05 and BSE tested by ELISA
at NVSL. Results were negative (as reported on 8/6/05); carcass disposal was completed
by alkaline digestion.
Analysis of Data on Presumed Dead and Untraceable Animals
CEAH performed an analysis of the minimum estimated ages of those COI that were
classified as either presumed dead or untraceable to determine the likely disposition of
those animals based on their ages. Moreover, CEAH performed an analysis of the likely
disposition of the one calf that was classified as untraceable during the investigation.
13
Appendix 1 – Final Trace-Out Diagram
http://www.aphis.usda.gov/lpa/issues/bse/epi-updates/bse_final_epidemiology_report.pdf
TSS
#################### https://lists.aegee.org/bse-l.html ####################
Subject: Re: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 2)
From: "Terry S. Singeltary Sr." <flounder9@VERIZON.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@LISTS.AEGEE.ORG>
Date: Wed, 31 Aug 2005 16:29:31 -0500 Content-Type: text/plain Parts/Attachments: text/plain (13499 lines)
##################### Bovine Spongiform Encephalopathy #####################
From: TSS () Subject:
Re: Texas BSE Investigation Final Epidemiology Report August 2005 (PART 1)
Date: August 31, 2005 at 2:16 pm PST
Greetings,
I must say, i was much to angry yesterday to put forth a good sound based scientific approach to a thorough critic of the facts. the reporting by the media of this blunder and the transcripts and remarks from officials at USDA et al, was just too much BSe. so i thought i might put forth a few more facts below, for whatever scientific facts on TSEs are worth with this administration. sadly, i think they are starting to believe what they are saying and have said in the past about mad cow in the USA 'no problem', 'triple firewalls', and 'sealed borders' etc.
>>>Now I want to turn to the completion of the epidemiological investigation that was conducted following the BSE detection in Texas in June. Many people worked very hard on the investigation, and I'd like to thank the Veterinary Services employees involved, our colleagues from the Food and Drug Administration, the owners of the animals, along with the Texas Animal Health Commission and the Texas Feed and Fertilizer Control Service for their outstanding work.
This investigation is another great example of federal, state, and local partners cooperating to help protect livestock health in this country. <<<
= = =
>>>But as far as actual poundage, I don't think it's possible for us to give you that actual number. There was two calves of interest that we traced. Due to the lack of appropriate records at the time, we actually traced 213 calves. Of those, it's estimated that 212 of those animals went into the feeding and slaughter channels. Those animals would have been slaughtered likely prior to 30 months of age, which we know that it's extremely small risk of having BSE prior to 30 months of age.
And also internationally and in the research community, while it's never been proven that offspring can get this disease through maternal transmission -- it's never been proven or disproven actually -- but it's thought very much from the international experts and the research it is extremely rare if it does happen.
Both of these calves were born very well prior to this animal being slaughtered. This animal did not show any clinical signs typical of BSE -- sampled and destroyed. This animal did not show any clinical signs or evidence of BSE which would make it even more unlikely that these two offspring would have any risk of having BSE.
The other 200 head that were traced were retraced as a result also of a lack of records. We were looking at cattle of interest over a five-year period of time of which this animal was born. Her approximate age was 12. We expanded one year of that and made her 11 to 13, and then we'd go another year beyond that. So we looked at animals basically in the age range of 10 to 15 years of age to remove those from the herd. And we traced every adult animal that we could from 1990.
Many of those animals would not even be of concern because they would not have received any feed at the time that she was in the herd or would have not been a birth cohort and born at the same time that she was.
So of those, 143 were reported as slaughtered, and we confirmed that 131 were definitely slaughtered; 34 were presumed dead, and 20 of those were untraceable. So again, we feel that the risk is extremely small. We do not feel that the public or our pet food industry should have any concerns relative to this issue. <<<
FACTS;
Maternal transmission
7. There is evidence from animal studies for low level maternal transmission of prions in cattle and sheep. This transmission may occur in utero, via milk and/or perinatally. However, the possibility that this putative maternal transmission might have been due to another mode of transmission, for example through a contaminated environment or feed, cannot be ruled out.
http://www.seac.gov.uk/statements/cjdtransmissionfinal.pdf
A BSE case born in September 2001
BSE has been diagnosed in a Holstein cow, born on 28 September 2001. The case was identified under the current compulsory testing programme for all animals born after 31 July 1996 slaughtered as cohorts of confirmed BSE cases. This animal was included in the cohort of the BSE case born on 3 October 2001 on the same farm and confirmed on 1 March 2005. This case born on 28 September 2001 was born on the same farm in Dyfed and it remained on this farm until it was submitted for slaughter on 12 May 2005. Disease was officially confirmed on 27 May 2005. The animal was aged 43 months at slaughter.
Another case born on the same farm on 1 May 2002 has been confirmed on 27 May 2005 in the same cohort. This is the first time that the UK has confirmed three cases born after July 1996 with the same farm of origin. Defra will be following up detailed epidemiological analysis of this case. This case is being drawn to the attention of SEAC and Professor William Hill.
Professor Hill is currently carrying out an independent assessment of the possible causes of BSE cases born after the reinforced feed ban of August 1996 (BARBs) at the request of Defra.
http://www.defra.gov.uk/animalh/bse/controls-eradication/barbinfo/28-09-2001 .pdf
A BSE case born in May 2002
BSE has been diagnosed in a Holstein Friesian cross cow, born on 1 May 2002. The case was identified under the current compulsory testing programme for all animals born after 31 July 1996 slaughtered as cohorts of confirmed BSE cases. This animal was included in the cohort of the BSE case born on 3 October 2001 on the same farm and confirmed on 1 March 2005. This case born on 1 May 2002 was born on the same farm in Dyfed and it remained on this farm until it was submitted for slaughter on 12 May 2005. Disease was officially confirmed on 27 May 2005. The animal was aged 36 months at slaughter.
This is the most recently born case of BSE confirmed in the UK. The previous most recent case was the related case born on 3 October 2001. Another case born on the same farm on 28 September 2001 has been confirmed on 27 May 2005 in the same cohort. This is the first time that the UK has confirmed three cases born after July 1996 with the same farm of origin. Defra will be following up detailed epidemiological analysis of this case. This case is being drawn to the attention of SEAC and Professor William Hill. Professor Hill is currently carrying out an independent assessment of the possible causes of BSE cases born after the reinforced feed ban of August 1996 (BARBs) at the request of Defra.
http://www.defra.gov.uk/animalh/bse/controls-eradication/barbinfo/01-05-2002 .pdf
>>>I'll now summarize our findings. Our results indicate that the positive animal, called the "index animal." was born and raised on a ranch, termed the "index farm," in Texas. It was a cream-colored Brahma cross, approximately 12 years of age at the time of its death. It was born prior to the implementation of FDA's mandatory ruminant-to-ruminant feed ban in the U.S., and that ban was implemented in August 1997. <<<
FACTS, THE AUGUST 4, 1997 RUMINANT TO RUMINANT FEED BAN WAS ONLY PARTIAL AND VOLUNTARY, it was nothing more than ink on paper. THE USA cattle have been fed ruminant protein in high concentrations, as proven in TEXAS, where we not only render the falling, stumbling and staggering highly suspect mad cows, we also feed them up documented 5.5 grams each of ruminant protein at the Purina mill, where the FDA again ignores proven and sound science that shows indeed less than a gram, up to one tenth of a gram is lethal. THIS sound science was documented at the time of the Purina feed mill mad cow blunder ;
CATTLE ON FEED IN TEXAS
FOR IMMEDIATE RELEASE P01-05 January 30, 2001 Print Media: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
---------------------------------------------------------------------------- ----
Note: On Dec. 23, 2003, the U.S. Department of Agriculture reported that a cow in Washington state had tested positive for bovine spongiform encephalopathy (BSE, or mad cow disease). As a result, information on this Web page stating that no BSE cases had been found in the United States is now incorrect. However, because other information on this page continues to have value, the page will remain available for viewing.
FDA ANNOUNCES TEST RESULTS FROM TEXAS FEED LOT
Today the Food and Drug Administration announced the results of tests taken on feed used at a Texas feedlot that was suspected of containing meat and bone meal from other domestic cattle -- a violation of FDA's 1997 prohibition on using ruminant material in feed for other ruminants. Results indicate that a very low level of prohibited material was found in the feed fed to cattle.
FDA has determined that each animal could have consumed, at most and in total, five-and-one-half grams - approximately a quarter ounce -- of prohibited material. These animals weigh approximately 600 pounds.
It is important to note that the prohibited material was domestic in origin (therefore not likely to contain infected material because there is no evidence of BSE in U.S. cattle), fed at a very low level, and fed only once. The potential risk of BSE to such cattle is therefore exceedingly low, even if the feed were contaminated.
According to Dr. Bernard Schwetz, FDA's Acting Principal Deputy Commissioner, "The challenge to regulators and industry is to keep this disease out of the United States. One important defense is to prohibit the use of any ruminant animal materials in feed for other ruminant animals. Combined with other steps, like U.S. Department of Agriculture's (USDA) ban on the importation of live ruminant animals from affected countries, these steps represent a series of protections, to keep American cattle free of BSE."
Despite this negligible risk, Purina Mills, Inc., is nonetheless announcing that it is voluntarily purchasing all 1,222 of the animals held in Texas and mistakenly fed the animal feed containing the prohibited material. Therefore, meat from those animals will not enter the human food supply. FDA believes any cattle that did not consume feed containing the prohibited material are unaffected by this incident, and should be handled in the beef supply clearance process as usual.
FDA believes that Purina Mills has behaved responsibly by first reporting the human error that resulted in the misformulation of the animal feed supplement and then by working closely with State and Federal authorities.
This episode indicates that the multi-layered safeguard system put into place is essential for protecting the food supply and that continued vigilance needs to be taken, by all concerned, to ensure these rules are followed routinely.
FDA will continue working with USDA as well as State and local officials to ensure that companies and individuals comply with all laws and regulations designed to protect the U.S. food supply.
http://www.fda.gov/bbs/topics/NEWS/2001/NEW00752.html
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys
Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
Published online January 27, 2005
http://www.thelancet.com/journal/journal.isa
For personal use. Only reproduce with permission from Elsevier Ltd Research Letters
Up to 400 000 cows with undiagnosed bovine spongiform encephalopathy (BSE) infection are estimated to have been slaughtered for food before brain and spinal cord were banned from human consumption in 1989. More restricted exposure to BSE could have continued through 1995 from consumption of processed meat products containing mechanically recovered meat contaminated with central nervous system (CNS) tissue and spinal ganglia.1 The discovery of BSE in Canada and the USA, where consumption of brain and other viscera was allowed until 2003, and of secondary cases of variant Creutzfeldt-Jakob disease (vCJD) in the UK, possibly attributable to contaminated blood donated by people with pre-clinical primary infection, reinforces the need for an experimental assessment of the risk of oral exposure to BSE. We therefore investigated oral transmission of BSE to non-human primates. We chose cynomolgus macaques for the study because these old-world monkeys have a digestive physiology similar to that of human beings, are methionine homozygous at codon 129 of the PRNP gene, and have a BSE neuropathology similar to that of vCJD.2,3 We gave two 4-year-old adult macaques a 5 g oral dose of brain homogenate from a BSE-affected cow. We tested for proteinase-resistant prion protein (PrPres) in this homogenate with a commercial BSE-testing ELISA kit (Bio-Rad, Marnes-la-Coquette, France). A sample of the 100% homogenate brain paste inoculum that was fed to the primates was rehomogenised at 20% weight-pervolume in the kit buffer. Serial dilutions were made with a pool of 20% weight-per-volume BSE-negative brain homogenate in the same buffer. Testing was done according to the manufacturer’s instructions and results were confirmed by a western blot test (Bio-Rad) with a similar process of PrPres dilution. With both methods, dilutions of up to 1 in 300 provided a positive signal (figure A). One macaque developed neurological disease 60 months after exposure and was killed at 63 months because of recumbency. Histopathological examination of the brain of this animal showed the typical pathology of vCJD (figure B) and an accumulation of PrPres associated with the follicular dendritic cells in tonsils (figure C), spleen, and intestine. A western blot showed similar patterns of PrPres in a brain sample from the macaque and the BSE-infected bovine inoculum (figure D). The other macaque remained free of clinical signs 76 months after exposure, and a tonsil biopsy done at 72 months was negative (figure E). In a previous study, two macaques orally dosed with 5 g of brain from a macaque with terminal clinical BSE became ill after 44 and 47 months.4 The results of the present study suggest that the incubation period for interspecies transmission of BSE can be considerably
Published online January 27, 2005
http://image.thelancet.com/ extras/05let1056web.pdf
snip...end...tss
8 hr BSE confirmation turnaround took 7+ months to confirm this case, so the BSE MRR policy could be put into place. ...TSS
-------- Original Message --------
Subject: re-USDA's surveillance plan for BSE aka mad cow disease
Date: Mon, 02 May 2005 16:59:07 -0500
From: "Terry S. Singeltary Sr."
Greetings Honorable Paul Feeney, Keith Arnold, and William Busbyet al at OIG, ...............
snip...
There will be several more emails of my research to follow. I respectfully request a full inquiry into the cover-up of TSEs in the United States of America over the past 30 years. I would be happy to testify...
Thank you, I am sincerely, Terry S. Singeltary Sr. P.O. Box , Bacliff, Texas USA 77518 xxx xxx xxxx
Date: June 14, 2005 at 1:46 pm PST
In Reply to:
Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results
posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced. June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns. Three days later same mad cow found in November turns out to be positive. Both resignation are unexpected. just pondering... TSS
Date: June 14, 2005 at 1:46 pm PST In
Reply to: Re: Transcript Ag. Secretary Mike Johanns and Dr. John Clifford, Regarding further analysis of BSE Inconclusive Test Results posted by TSS on June 13, 2005 at 7:33 pm:
Secretary of Agriculture Ann M. Veneman resigns Nov 15 2004, three days later inclusive Mad Cow is announced.
June 7th 2005 Bill Hawks Under Secretary for Marketing and Regulatory Programs resigns.
Three days later same mad cow found in November turns out to be positive.
Both resignation are unexpected.
just pondering... TSS
MAD COW IN TEXAS NOVEMBER 2004. ...TSS
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update?
I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
terry
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Fri, 19 Nov 2004 11:38:21 –0600
From: Carla Everett
To: "Terry S. Singeltary Sr." References: <[log in to unmask]>
The USDA has made a statement, and we are referring all callers to the USDA web site. We have no information about the animal being in Texas.
Carla At 09:44 AM 11/19/2004, you wrote:
>Greetings Carla,
>>i am getting unsubstantiated claims of this BSE 'inconclusive' cow is from
>TEXAS. can you comment on this either way please?
>>thank you,
>Terry S. Singeltary Sr.
>>
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 18:33:20 -0600 From: Carla Everett
To: "Terry S. Singeltary Sr."
References: ...sniptss
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something. At 06:05 PM 11/22/2004,
you wrote:
>why was the announcement on your TAHC site removed?
>>Bovine Spongiform Encephalopathy:
>November 22: Press Release title here
>>star image More BSE information
>>>>terry
>>Carla Everett wrote:
>>>no confirmation on the U.S.' inconclusive test...
>>no confirmation on location of animal.>>>>>>
==========================
-------- Original Message --------
Director, Public Information Carla Everett ceverett@tahc.state.tx.us
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 17:12:15 –0600
From: "Terry S. Singeltary Sr."
To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>
Greetings Carla,still hear a rumor;
Texas single beef cow not born in Canada no beef entered the food chain?
and i see the TEXAS department of animal health is ramping up for something, but they forgot a url for update? I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???
terry
==============================
Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 21:07:51 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett
References: <419E14E2.5040104@wt.net> <6.0.0.22.2.20041119113601.02682730@tahc.state.tx.us> <41A2724F.3000901@wt.net> <6.0.0.22.2.20041122174504.02796d38@tahc.state.tx.us> <41A27EBC.4050700@wt.net> <6.0.0.22.2.20041122183204.02801d88@tahc.state.tx.us>
ok, thank you Carla. i hate rumors and 'inconclusive' announcements. kind regards, terry Carla Everett wrote:
> our computer department was working on a place holder we could post
> USDA's announcement of any results. There are no results to be
> announced tonight
> by NVSL, so we are back in a waiting mode and will post the USDA
> announcement
> when we hear something.
> > > At 06:05 PM 11/22/2004, you wrote:
> >> why was the announcement on your TAHC site removed?
>> >> Bovine Spongiform Encephalopathy:
>> November 22: Press Release title here
>> >> star image More BSE information
>> >> >> >> terry
>> >> Carla Everett wrote: no confirmation on the U.S.' inconclusive test...
>>> no confirmation on location of animal.
I still want my Texas mad cows confirmed BY WB! TSS
-------- Original Message --------
Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???
Date: Mon, 22 Nov 2004 21:07:51 -0600
From: "Terry S. Singeltary Sr."
To: Carla Everett
References: <419E14E2.5040104@wt.net> <6.0.0.22.2.20041119113601.02682730@tahc.state.tx.us> <41A2724F.3000901@wt.net> <6.0.0.22.2.20041122174504.02796d38@tahc.state.tx.us> <41A27EBC.4050700@wt.net> <6.0.0.22.2.20041122183204.02801d88@tahc.state.tx.us>
ok, thank you Carla. i hate rumors and 'inconclusive' announcements.
kind regards, terry
Carla Everett wrote:
our computer department was working on a place holder we could post USDA's announcement of any results. There are no results to be announced tonight by NVSL, so we are back in a waiting mode and will post the USDA announcement when we hear something.
At 06:05 PM 11/22/2004, you wrote:
why was the announcement on your TAHC site removed?
Bovine Spongiform Encephalopathy: November 22: Press Release title here star image More BSE information
terry
Carla Everett wrote:
no confirmation on the U.S.' inconclusive test... no confirmation on location of animal.
I still want my Texas mad cows confirmed BY WB!
TSS
48 HOUR BSE TEST TURN AROUND TURNS INTO ALMOST A YEAR, from Nov. 2004 when Texas TAHC first announced BSE postive, then took it back, and then almost one year later, Nov. 2005, a final BSE positive confirmation was announced, after only scientist around the globe, and literally an act of Congress took place by the Honorable Fong order the sample retested. ...Thank YOU!
ONE YEAR LATER, finally confirmed $$$
Release No. 0233.05 Contact: USDA Press Office (202) 720-4623
Printable version Email this page
TRANSCRIPT OF MEDIA CONFERENCE WITH REMARKS MADE BY AGRICULTURE SECRETARY MIKE JOHANNS, DR. JOHN CLIFFORD, CHIEF VETERINARY OFFICER, ANIMAL PLANT HEALTH INSPECTION SERVICE, AND DR. DANNY MATTHEWS, TSE PROGRAM MANAGER, VETERINARY LABORATORIES AGENCY, WEYBRIDGE, ENGLAND - WASHINGTON D.C. - JUNE 24, 2005
SNIP...
"So let me start first with the test results. As you are aware, last November we had an inconclusive report from a rapid screening test. USDA then conducted two IHC confirmatory tests, and both came out negative. A few weeks ago an additional confirmatory test was conducted, and that test is referred to as the Western blot test.
"On June 10 I learned that test was reactive and shared those results at that time.
"We now have the test results from the lab in Weybridge, England, as well as the results from additional testing in our own lab, and again I am here today to share those results with you.
"The results confirm the presence of BSE in this animal, an animal that was blocked from entering the food supply thanks to the firewalls that are in place. It is critically important to note that this animal was identified as a high risk animal. A sample was taken, and the carcass was incinerated.
Tuesday, July 14, 2009
U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red Book Date: February 14, 2000 at 8:56 am PST
WHERE did we go wrong $$$
TSS
2004, highly suspect stumbling and staggering mad cow reported, however, NO TESTING DONE, ON ORDERS FROM AUSTIN $
May 4, 2004
Statement on Texas Cow With Central Nervous System Symptoms
On Friday, April 30th, the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison)...
USDA regulations, any cow that exhibits signs of central nervous system (CNS)
According to a 1997 Animal and Plant Health Inspection Service (NHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "it is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
May 13,2004
Page 2
snip...
The cow slaughtered at the Lone Star Beef slaughterhouse last week staggered and fell, and was condemned ante mortem by FSIS personnel.4 Despite a request from APHIS personnel at the plant to conduct BSE testing, however, an APHIS supervisor in Austin reportedly refused the test and instructed the plant to send the carcass for rendering.5
This sequence of events is troubling, and it raises the question of whether this is an isolated incident. In 1997, USDA noted a major gap between the number of cattle condemned for CNS symptoms and the number of these cows actually tested for mad cow disease. The Department found:
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.
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
""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.
http://www.usda.gov/wps/portal/!ut/p/_s.7_0_A/7_0_1OB?contentidonly=true&contentid=2005/08/0336.xml
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.
http://www.aphis.usda.gov/lpa/issues/bse/epi-updates/bse_final_epidemiology_report.pdf
-------- Original Message --------
Subject: RE: Greetings again Professor Aguzzi ... TSS
Date: Fri, 11 Mar 2005 09:19:49 +0100
From: "Adriano Aguzzi"
T o: "'Terry S. Singeltary Sr.'"
Dear Mr. Singeltary
I sympathize with your wish to have the most sensitive assay implemented. However, the situation is not as simple as one might think. In the case of homogeneously distributed agent, biochemical detection of PrPSc is indeed likely to be more sensitive than immunohistochemistry. In the case of variegated, punctate distribution of the agent, morphological methods may indeed be an asset.
There are also issues of feasibility. In my laboratory, we routinely run phosphotungstic acid precipitation followed by Western blotting. However, this is an extraordinarily cumbersome procedure. The sensitivity is increased vastly, but the amount of work needed is also amazing. There is no way I could see our own procedure implemented for mass screening of millions of cows - unless one would draft a veritable army of laboratory technicians.
For all these reasons, while I see all your points, I feel unable to offer a strong public opinion in favor or against any specific methods. The final decision needs to take into account a variety of complex factors, and that is why I believe that it is best left to a panel of experts rather than to a public discussion.
Best regards Adriano Aguzzi
____________________________
Prof. Adriano Aguzzi (MD PhD hc FRCP FRCPath) Institute of Neuropathology, University Hospital of Zürich Schmelzbergstrasse 12, CH-8091 Zürich, Switzerland Tel. ++41-1-255 2107 Tel. (direct line): 2869 Fax: ++41-1-255 4402, cellular: +41-79-320 1516 http://www.unizh.ch/pathol/neuropathologie/
-----Original Message-----
From: Terry S. Singeltary Sr. [mailto:flounder@wt.net] ;
Sent: Thursday, March 10, 2005 20:18
Subject: Greetings again Professor Aguzzi ... TSS
Greetings again Professor Aguzzi,
A kind greetings from Texas. I hope you do not mind, but I must ask you several questions that will put you in the hot seat. Someone with credibility must come forward, such as yourself and speak out about the fact of the non scientific approach that USDA et al has take after the first diagnosis of BSE in the USA. This being, the refusal to use Western Blot on any suspicious or inconclusive BSE/TSE test. IHC is like a brain biopsy on trying to diagnose a CJD case. IF you take the sample from a part of the brain that is not that tainted, you will not get a reading. WB is much more sensitive, especially now with the Phospohtugstic acid precipitation step. IF Prusiners CDI was validated, who knows, that might even be more sensitive. Bottom line, we need you to come forward and state publicly ''the facts'' about USDA et al decision not to use WB on not only questionable samples, but on ALL samples. would you be willing to comment on this, to me or someone from the media (under the understanding it will be for the public)? I have several questions for you??? This is very very important in terms of human health (i.e. that nov. pos. pos. incl. neg cow).
P.S. there is one other top TSE scientist that has come forward and said what the USDA et al did with that cow was ''not logical''. (this will not be published for another 3 or 4 weeks). ONE other TOP TSE scientist saying the same thing would be much better for the public to hear and understand. anyway, does not hurt to ask, and i hope you come through here for us. I know this is a very loaded question, but times a wasting, and human health is at risk here...
thank you, with kindest regards,
I am sincerely,
Terry S. Singeltary Sr.
##################### Bovine Spongiform Encephalopathy #####################
I would like to add to the first paragraph of Adriano Aguzzis comments. We have seen cases in Europe, where a positive result obtained with our Western blot rapid test(Prionics-Check WESTERN)could not be confirmed with IHC, but with the OIE-Western blot procedure, and we have also seen cases where the result could be confirmed by IHC but not by OIE-Western blot. As Adrino Aguzzi pointed out both IHC and OIE-Western have their limitations, but when combined and when performed well they pick up BSE reliably. In case of doubt, i.e. if a rapid test comes out consistently positive but an initial attempt of confirmation with IHC (or OIE-Western) fails, we recommend to routinely do a second test with the respective alternative method. This is the procedure most national reference centers, which are responsible for final confirmation of BSE cases, are following. Regards Markus Moser Prionics
-------- Original Message --------
Subject: Q&A Dr. Jean-Philippe Deslys USDA REFUSAL TO USE WB ON TEXAS COW WITH BSE SYMPTOMS (FULL TEXT)
Date: Fri, 22 Apr 2005 11:53:47 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@LISTS.UNI-KARLSRUHE.DE
##################### Bovine Spongiform Encephalopathy #####################
Q&A Dr. Jean-Philippe Deslys
1. What is the standard regime for testing of suspect animals in the EU?
The regime is an initial screening by a high-output test, the Bio-Rad test. If a result raises suspicion, a confirmatory test is conducted with the Western blot test.
2. How long has this been the case?
Its a fairly recent development. Only recently has the Western blot test become sensitive enough, with the addition of phospohtungstic acid precipitation step. The Bio-Rad test (which Deslys helped develop) is extremely sensitive, and the standard Western blot is extremely reliable with high-signal test results. However, it had to be made more sensitive for low-signal (samples with low density of malformed prions) samples. It has been made more sensitive.
Reproducibility is the problem with the IHC test. It is not standardized; depending on the lab and its protocols, or even on the technician involved in the test, one can get conflicting results.
3. Is there a way to measure the three tests in sensitivity, accuracy and objectivity?
Historically, yes. The IHC was the gold standard at one point, but we have shifted to the Western blot. It requires less work, it is more sensitive and its results are reproducible. IHC relies on localization. If you have a weak signal case, you may get lucky and test a spot with a high concentration of prions. But the opposite it true too; you can miss an infection by testing a sample with low concentrations. Western blot is much better for low signal situations.
4. The USDA in 2003 used the Western blot to confirm the BSE case in Washington state, and it sent samples to the U.K. for independent testing. In the case this November, which it announced was negative, it instead used the IHC test and did not send samples to the U.K. Is this good science?
Its not logical. If you have two consecutive questionable screenings, you do another test. I can only advise, its managements duty at USDA to make the decisions. But when you have a discrepancy between the rapid test and the IHC, it is only logical to confirm it with another test.
5. We are hearing now about a new strain of BSE, atypical BSE or aBSE. Or BaSE. We have heard that IHC, the so-called gold standard, cannot detect the variant. Is this true?
Yes. There have been a few cases, one in Italy, one in Belgium, one here in France. It seems to only affect very old animals. The distribution in the brain is very different than we see with BSE, it looks very different. The IHC test will come back negative.
This his a very recent phenomenon. I have no opinion on its virulence. We do not know where it comes from. It could be a version of sporadic infection. Western blot caught them, but we would not even know it existed if we werent running systematic testing in the EU.
BSE was around for a long time before we caught it and by then, it was everywhere. It had become highly infectious. It probably amplified due to low-temperature rendering. The disease was recycled through the food chain, and was given time to amplify. By the time it was identified, even good cooking couldnt eliminate it.
I cant stress enough that systematic testing is necessary. Withdrawing all positives from the food chain is the best way to break the cycle.
What can happen with testing of only cattle that are clearly at risk is that several can remain undetected. Canada has tested about 30,000 head of cattle and has three positives. That would indicate that there are probably undiscovered cases. And what happens then is that the disease is allowed to amplify. You have to maintain testing.
When people choose to protect their economic interests over public health, it can have a boomerang effect. It happened all through Europe. They always deny; its not OUR problem, it is our neighbors problem. And then a single case is discovered and the public reacts. The economic results are devastating. It would be better to just assume BSE is present and use systematic testing as protection. That way, the public is reassured that it is not entering the food supply.
By systematic testing, I mean doing as we do in the EU, which is to test every animal over 30 months of age when it is slaughtered. In Europe, three times as many cases of BSE have been caught by systematic testing as by clinical testing (of clearly sick animals). In 2004, eight clinical cases were discovered, 29 were discovered at rendering plants, and 17 at slaughter. We should be using these tests as a weapon to protect the public and to give them assurance that the food supply is being protected.
6. USDAs list of specified risk materials excludes some products, like blood and bone meal, that are banned in the EU and UK. Is our feed supply safe?
With SRMs, where do you stop? Tests have found prions in meat, nerves travel through meat, and so on. The main infectivity is in the brain and the spinal cord. A blood and bone meal ban in animal feed is not really necessary, because except in cases of highly infective animals, it is unlikely that they are dangerous in themselves. If you combine systematic testing and targeted SRM removal, the brain and the spinal column in cattle over 30 months, you can have a compromise that is both safer and less costly than expanded feed bans.
Certainly, you can stop the spread of BSE with a total ban on offal. But it has to be a total ban. It cant be given to sheep or swine or poultry. It would be very expensive and virtually impossible to accomplish. You can have farmers using the wrong feed or transportation errors.
Systematic testing makes far more sense. I think of it as a thermometer. It not only allows us to catch the disease, it also allows us to monitor its progress. We can watch the levels of infectivity and if they start going up instead of down, we can take measures.
To an extent, our environment is contaminated. About 10 percent of wild animals test positive for TSEs. If you recycle these agents, they can evolve and get more dangerous. This is probably what happened with BSE. It wasnt very dangerous until it evolved to the disease we know today.
People complain that testing is very expensive. It is much more expensive to kill and test whole herds.
7. In your opinion, is infected feed the sole method of transmission of BSE, apart from the very rare maternal transmission?
Feed is the main problem. However, we are seeing some other possibilities, including through fat and greases. Calves are fed milk extracts, with the cream removed. To make it nutritious, they are using fat and grease from cattle.
(FOLLOW QUESTION: Would that allow BSE to develop into an infective level in cattle younger than 30 months, assuming they might be getting infected at a younger age?)
8. You were involved in a study that tested two primates who were fed infected brain tissue. One eventually died of TSE; the other survived. The press reported that the main finding was that it would take something on the order of 1.5 kilograms of infected matter to create an infection, but that seems to be an oversimplification. Could you explain it further?
The findings suggest that as little as five grams is enough to infect. The 1.5 kilo figure is the amount of infected tissue that would have to be ingested from an animal that would be below the threshold of infection, and would test negative. In other words, even though a younger animal may be developing the disease, it would take a considerable amount of tissue to transmit the disease.
An animal could be just below the testing level, and not be particularly dangerous. But that is why you have to keep testing. Once it reaches the threshold, it can become highly infective.
9. BSE is a pretty horrifying disease, but overall, it has killed less than 200 humans, and only a handful in recent years. Listeria, by comparison, kills thousands every year. Overall, how do you rate the threat from BSE?
The overall risk is not particularly high. Over two million infected animals went into the food chain in Europe, 400,000 of them before the SRMs, the brains and spinal column, were removed from the carcass. Less than 200 died, and less than 4,000 are at risk of developing the disease. What we know now is that one particle is not going to kill you. There has to be condensation of the prions to be truly dangerous.
This is not a sterile world. But the danger is that now that the crisis appears to be over, attention will turn elsewhere and that will allow the disease to amplify again. Just as we stopped paying attention to AIDS when medication seemed to control it, then were surprised when a new and more infectious and aggressive strain appeared, we could be surprised by a more serious strain of BSE. That is why I support systematic testing for the long term. The object is to keep levels of BSE low, and to recognize the danger if it suddenly pops back up. ...END
TSS
######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
-------- Original Message --------
Subject: US CHOICE OF MAD COW TEST QUESTIONED
Date: Wed, 24 Mar 2004 16:12:06 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
######## Bovine Spongiform Encephalopathy #########
US CHOICE OF MAD COW TEST QUESTIONED
The US plans to measure the incidence of mad cow disease in its cattle with a test that its own officials have said gives too many false positives. Some experts fear the choice reflects an official desire to downplay the impact of the first positive BSE tests that emerge, when they turn out not to be confirmed.
Last week the US Department of Agriculture (USDA) approved two tests, including one made by the Californian firm BioRad, for screening up to 300,000 cattle for BSE, starting in July. No more tests will be licensed for months. Announcing the testing plan, chief veterinary officer Ron DeHaven cautioned that "there will be positive results", many of them false.
BioRad's antibody-based test for the prion protein that causes BSE has given numerous false positives in Belgium and Germany. And in Japan only 8 of 113 cattle that repeatedly tested positive with BioRad were confirmed by slower tests that do not give false positives.
The USDA even wrote last May that "it is well known" that tests like BioRad's give false positives. It states that other kinds of quick tests are more suitable for testing for very low levels of BSE, which are expected in the US.
The second quick test approved by the USDA, made by Maine-based IDEXX, could also in theory give false positives. It remains unclear how reliable it is, because there has been little practical experience with the test so far. It is not yet approved for use in Europe, where the vast majority of BSE tests are done.
Debora MacKenzie, Brussels correspondent, New Scientist. tel +32-2-245-0412 fax +32-2-245-0552 mobile +32-49-754-0444
=====================
Greetings,
odd that the USDA et al approves two US-OWNED tests that are _known_ to give false positives, when they know other rapid TSE test are much more reliable. IT's like they purposely do not want to find any TSE in the USA bovine, so they pick the worst test available. The USDA own experts think BioRad is not suitable for supposedly BSE/TSE free and low incidence areas, so why did they choose this test and or the IDEXX, which i dont think has even been submitted to the EU for evaluation and has no commercial experiance to my knowledge. You could almost get the feeling they are deliberately skipping over Prionics for the least supperior TSE rapid test. I believe the Canadians finally did choose prionics. maybe paul or marcus might comment? seems if North America is going to be a consolidated BEEF trading market amongst themselves and expect to export there tainted products everywhere, they could at least come up with the same TSE rapid Test. how can one use a less reliable test and the other use a more reliable test, and it all be the same? i know there is a word Dehaven used, but it slips my mind now, (consolidated markets) that's not it, but you get the just of my thoughts, i think;-)...TSS
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
-------- Original Message --------
Subject: Re: US CHOICE OF MAD COW TEST QUESTIONED
Date: Thu, 25 Mar 2004 00:53:39 +0100
From: Moser Markus
Reply-To: Bovine Spongiform Encephalopathy
######## Bovine Spongiform Encephalopathy #########
Regarding your question about Canada's BSE-test choice for their official BSE surveillance, I can confirm that they chose the Prionics-Check Western rapid test. Regards Markus
CONTINUED
-------- Original Message --------
Subject: Re: US CHOICE OF MAD COW TEST QUESTIONED
Date: Thu, 25 Mar 2004 01:11:04 +0100
From: Roland Heynkes
Reply-To: Bovine Spongiform Encephalopathy
######## Bovine Spongiform Encephalopathy #########
Dear Terry,
odd that the USDA et al approves two US-OWNED tests that are _known_ to give false positives, when they know other rapid TSE test are much more reliable.
the BioRad-test seems to be the most sensitive rapid BSE test and it is clear that you "get" false positive results when you try to confirm its results with a less sensitive method like immune histochemistry. Poorly trained technicians of course may produce some false positives with the BioRad-test, but immune histochemistry produces many false negatives especially in the hands of not very experienced people. Generally the false negative and not the much fewer false positive results are the problem of all actually available BSE tests.
It is therefore not so easy to say, if the BioRad-test produced a false positive or if the confirming test produced a false negative result and which of them is more reliable. I for sure would not eat the meat of a cow which was seemingly false positive tested with the BioRad-test.
IT's like they purposely do not want to find any TSE in the USA bovine, so they pick the worst test available.
The BioRad-test is definitively not the worst test available (have a look on the EU results) and when a government does not want to get positive results, it uses immune histochemistry instead.
The USDA own experts think BioRad is not suitable for supposedly BSE/TSE free and low incidence areas, so why did they choose this test and or the IDEXX, which i dont think has even been submitted to the EU for evaluation and has no commercial experiance to my knowledge.
Are you sure that USDA has experts for BSE testing?
You could almost get the feeling they are deliberately skipping over Prionics for the least supperior TSE rapid test. I believe the Canadians finally did choose prionics. maybe paul or marcus might comment?
The Prionics western blot test is also a good rapid test which of course does not produce false positive results. In addition this test allows to see new variants of BSE, which would not be seen with the BioRad. But at least in Europe its positive results become confirmed by the OIE Western blot exactly as the BioRad results. Because of this control step the BioRad test cannot produce significantly more problems.
seems if North America is going to be a consolidated BEEF trading market amongst themselves and expect to export there tainted products everywhere, they could at least come up with the same TSE rapid Test. how can one use a less reliable test and the other use a more reliable test, and it all be the same? i know there is a word Dehaven used, but it slips my mind now, (consolidated markets) that's not it, but you get the just of my thoughts, i think;-)...TSS
Not the minor differences between the rapid tests are the problem, but the much to low testing numbers and the prefered IHC-testing in the USA. In Germany we test every month as many as the USA is going to test per year (mostly with BioRad) - and we have only 13 million cattle.
kind regards
Roland
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
-------- Original Message --------
Subject: Re: US CHOICE OF MAD COW TEST QUESTIONED
Date: Thu, 25 Mar 2004 02:51:09 +0100
From: Moser Markus
Reply-To: Bovine Spongiform Encephalopathy
######## Bovine Spongiform Encephalopathy #########
Dear Roland
Immunohistochemistry, correctly executed, is the gold standard, together with the OIE Western blotting method. It allows detection of infection even in cases where prion aggregates can only be detected in few individual cells. It is certainly not less sensitive than either Bio-Rad or Prionics. In fact, the abundant data on all three methods indicate equal diagnostic sensitivity (if sampling is done appropriate: note that immunohistochemistry has to be conducted on different tissue samples, since the tissue has to be formalin fixed). In case a BSE case obtained with a rapid test cannot be confirmed in a first approach with one of the gold standard methods, the second method will be used. I agree, that the sensitivity of immunohistochemistry can be negatively influenced e.g. by only looking at a limited number of slides or by not carefully examining the slides for prion aggregates. However, if a rapid test is not confirmed by immunohistochemistry due to a sloppy analysis, it will still show up in the OIE Western blot. Nevertheless, it is of course possible, that a true positive result cannot be confirmed e.g. if only the tissue sample used for the initial testing contained prion aggregates, which is theoretically possible, since the aggregates are not evenly distributed in the tissue. This is why it is not formally possible to disproof with 100% certainty an initial positive diagnosis (and you are right: it's certainly wise to rather not eat any suspicious animals). Nevertheless, false positives cannot in general be attributed to faulty confirmatory tests, but to the fact that the ELISA method simply produces a certain rate of false positives, which is why we offer rapid BSE tests on both platforms, the ELISA and the Western technology. And we make it clear to our customers, that when choosing the Prionics-Check LIA (the ELISA based test) coping with occasional false positive results will be inevitable. The LIA is therefore mostly used in European countries, with well established levels of BSE, while the Prionics-Check Western is also used in BSE-free countries (where a maximum positive predictive value is important to support the conclusion of low frequency or absence of BSE, which would otherwise be difficult for the reason you indicated and I mentioned above, i.e. due to the reason that it is hard to formally disprove an initial diagnosis with absolute certainty). Regards, Markus
-------- Original Message --------
Subject: Re: ''INCONCLUSIVE'' IS NEGATIVE or so they claim...OFFICIAL REPORT
Date: Tue, 1 Feb 2005 16:59:27 -0600
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
References: <41A3B789.6080907@wt.net> <41A4ED7C.4090501@wt.net>
##################### Bovine Spongiform Encephalopathy #####################
*** 2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006 ***
THURSDAY, FEBRUARY 23, 2012
EIGHT FORMER SECRETARIES OF AGRICULTURE SPEAKING AT USDA'S 2012 AGRICULTURE OUTLOOK FORUM INDUCTED INTO USA MAD COW HALL OF SHAME
THURSDAY, OCTOBER 22, 2015
Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened
2020 DECEMBER
WEDNESDAY, DECEMBER 9, 2020
Biden's pick Tom Vilsack Failed Terribly on Mad Cow BSE TSE Prion, why put him back as top Agriculture pick?
THURSDAY, DECEMBER 17, 2020
THE MAD COW BSE TSE PRION THAT STOLE CHRISTMAS DECEMBER 2003, WHAT REALLY HAPPENED, A REVIEW 2020
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
WEDNESDAY, FEBRUARY 03, 2021
Scrapie TSE Prion United States of America a Review February 2021 Singeltary et al
TUESDAY, JANUARY 5, 2021
Exploration of genetic factors resulting in abnormal disease in cattle experimentally challenged with bovine spongiform encephalopathy
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
June 17, 2019
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
June 17, 2019
APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission
Greetings APHIS et al,
I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.
THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.
Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.
The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.
WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.
WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.
AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...
Comment from Terry Singeltary
Posted by the Animal and Plant Health Inspection Service on Jun 19, 2019
WEDNESDAY, JANUARY 1, 2020 USDA OIE BSE TSE PRION FDA PART 589 BSE TSE PRION aka MAD COW FEED BAN Failure 2020 UPDATE
Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
THURSDAY, DECEMBER 17, 2020
THE MAD COW BSE TSE PRION THAT STOLE CHRISTMAS DECEMBER 2003, WHAT REALLY HAPPENED, A REVIEW 2020
I URGE EVERYONE TO READ IN FULL, THE OIE REPORT 2019 ABOUT ATYPICAL BSE TSE PRION, SRMs, SBOs, and feed...tss
''Experts could not rule out other causes due to the difficulty of investigating individual cases. Some constraints are the long incubation period of the disease and the lack of detailed information available from farms at the time of the trace-back investigation.''
Scientists investigate origin of isolated BSE cases
The European response to bovine spongiform encephalopathy (BSE) after the crisis of the 1980s has significantly reduced prevalence of the disease in cattle. However, isolated cases are still being reported in the EU and for this reason the European Commission asked EFSA to investigate their origin.
The key measure for controlling BSE in the EU is a ban on the use of animal proteins in livestock feed. This is because BSE can be transmitted to cattle through contaminated feed, mainly in the first year of life.
Sixty cases of classical BSE have been reported in cattle born after the EU ban was enforced in 2001. None of these animals entered the food chain. Classical BSE is the type of BSE transmissible to humans. The Commission asked EFSA to determine if these cases were caused by contaminated feed or whether they occurred spontaneously, i.e. without an apparent cause.
EFSA experts concluded that contaminated feed is the most likely source of infection. This is because the infectious agent that causes BSE has the ability to remain active for many years. Cattle may have been exposed to contaminated feed because the BSE infectious agent was present where feed was stored or handled. A second possibility is that contaminated feed ingredients may have been imported from non-EU countries.
Experts could not rule out other causes due to the difficulty of investigating individual cases. Some constraints are the long incubation period of the disease and the lack of detailed information available from farms at the time of the trace-back investigation.
EFSA experts made a series of recommendations to maintain and strengthen the EU monitoring and reporting system, and to evaluate new scientific data that become available.
The European response to BSE
The coordinated European response to BSE has succeeded in reducing the prevalence of the disease. Between 2005 and 2015 about 73,000,000 cattle were tested for BSE in the EU, out of which 60 born after the ban tested positive for classical BSE. The number of affected animals rises to 1,259 if cattle born before the ban are included. The number of classical BSE cases has dropped significantly in the EU over time, from 554 cases reported in 2005 to just two in 2015 (both animals born after the ban). Moreover the EU food safety system is designed to prevent the entry of BSE-contaminated meat into the food chain.
MONDAY, NOVEMBER 30, 2020
***> REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRION
see updated concerns with atypical BSE from feed and zoonosis...terry
WEDNESDAY, DECEMBER 23, 2020
BSE research project final report 2005 to 2008 SE1796 SID5
TUESDAY, JANUARY 5, 2021
Exploration of genetic factors resulting in abnormal disease in cattle experimentally challenged with bovine spongiform encephalopathy
THURSDAY, SEPTEMBER 26, 2019
Veterinary Biologics Guideline 3.32E: Guideline for minimising the risk of introducing transmissible spongiform encephalopathy prions and other infectious agents through veterinary biologics
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
snip...
[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
snip...see full archive and more of this;
*** 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
PLOS ONE Journal
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 ***
***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 ***
WEDNESDAY, DECEMBER 23, 2020
Idiopathic Brainstem Neuronal Chromatolysis IBNC BSE TSE Prion a Review 2020
***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.
In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.
***Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.
P-088 Transmission of experimental CH1641-like scrapie to bovine PrP overexpression mice
Kohtaro Miyazawa1, Kentaro Masujin1, Hiroyuki Okada1, Yuichi Matsuura1, Takashi Yokoyama2
1Influenza and Prion Disease Research Center, National Institute of Animal Health, NARO, Japan; 2Department of Planning and General Administration, National Institute of Animal Health, NARO
Introduction: Scrapie is a prion disease in sheep and goats. CH1641-lke scrapie is characterized by a lower molecular mass of the unglycosylated form of abnormal prion protein (PrpSc) compared to that of classical scrapie. It is worthy of attention because of the biochemical similarities of the Prpsc from CH1641-like and BSE affected sheep. We have reported that experimental CH1641-like scrapie is transmissible to bovine PrP overexpression (TgBoPrP) mice (Yokoyama et al. 2010). We report here the further details of this transmission study and compare the biological and biochemical properties to those of classical scrapie affected TgBoPrP mice.
Methods: The details of sheep brain homogenates used in this study are described in our previous report (Yokoyama et al. 2010). TgBoPrP mice were intracerebrally inoculated with a 10% brain homogenate of each scrapie strain. The brains of mice were subjected to histopathological and biochemical analyses.
Results: Prpsc banding pattern of CH1641-like scrapie affected TgBoPrP mice was similar to that of classical scrapie affected mice. Mean survival period of CH1641-like scrapie affected TgBoPrP mice was 170 days at the 3rd passage and it was significantly shorter than that of classical scrapie affected mice (439 days). Lesion profiles and Prpsc distributions in the brains also differed between CH1641-like and classical scrapie affected mice.
Conclusion: We succeeded in stable transmission of CH1641-like scrapie to TgBoPrP mice. Our transmission study demonstrates that CH 1641-like scrapie is likely to be more virulent than classical scrapie in cattle.
snip...
In the US, scrapie is reported primarily in sheep homozygous for 136A/171Q (AAQQ) and the disease phenotype is similar to that seen with experimental strain CH1641.
CH1641
SUNDAY, OCTOBER 11, 2020
Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ
WEDNESDAY, JULY 31, 2019
The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L
THURSDAY, SEPTEMBER 24, 2020
The emergence of classical BSE from atypical/ Nor98 scrapie
TUESDAY, NOVEMBER 17, 2020
The European Union summary report on surveillance for the presence of transmissible spongiform encephalopathies (TSE) in 2019 First published 17 November 2020
WEDNESDAY, OCTOBER 28, 2020
EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission
WEDNESDAY, DECEMBER 2, 2020
EFSA Evaluation of public and animal health risks in case of a delayed post-mortem inspection in ungulates EFSA Panel on Biological Hazards (BIOHAZ) ADOPTED: 21 October 2020
i wonder if a 7 month delay on a suspect BSE case in Texas is too long, on a 48 hour turnaround, asking for a friend???
SUNDAY, OCTOBER 4, 2020
Cattle Meat and Offal Imported from the United States of America, Canada and Ireland to Japan (Prions) Food Safety Commission of Japan
TUESDAY, SEPTEMBER 29, 2020
ISO's Updated 22442 Animal Tissue Standards — What Changed? TSE Prion!
THURSDAY, AUGUST 20, 2020
Why is USDA "only" BSE TSE Prion testing 25,000 samples a year?
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison. snip..... The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip.....
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion. snip..... In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip.....
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip.....
***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are;
BSE TESTING (failed terribly and proven to be a sham)
BSE SURVEILLANCE (failed terribly and proven to be a sham)
BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham)
these are facts folks. trump et al just admitted it with the feed ban.
see;
FDA Reports on VFD Compliance
John Maday
August 30, 2019 09:46 AM VFD-Form 007 (640x427)
Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.
SUNDAY, SEPTEMBER 1, 2019
***> FDA Reports on VFD Compliance
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
SUNDAY, APRIL 14, 2019
Estimation of prion infectivity in tissues of cattle infected with atypical BSE by real time-quaking induced conversion assay
WEDNESDAY, APRIL 24, 2019
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection Aug 29, 2018 A Review of Science 2019
THURSDAY, JANUARY 7, 2021
Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021
TUESDAY, SEPTEMBER 22, 2020
APHIS USDA MORE SCRAPIE ATYPICAL Nor-98 Confirmed USA September 15 2020
THURSDAY, DECEMBER 31, 2020
Autoclave treatment of the classical scrapie agent US No. 13-7 and experimental inoculation to susceptible VRQ/ARQ sheep via the oral route results in decreased transmission efficiency
WEDNESDAY, MAY 29, 2019
***> Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures
USDA HERE'S YOUR SIGN!
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
Terry S. Singeltary Sr.
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