text:
Food and Drug Administration
21 CFR Part 589
[Docket No. 2002N-0273] (Formerly Docket No. 02N-0273) RIN 0910-AF46
Substances Prohibited From Use in Animal Food or Feed
AGENCY: Food and Drug Administration, HHS.
ACTION: Final rule.
SUMMARY: The Food and Drug Administration (FDA) is amending the agency's regulations to prohibit the use of certain cattle origin materials in the food or feed of all animals. These materials include the following: The entire carcass of bovine spongiform encephalopathy (BSE)-positive cattle; the brains and spinal cords from cattle 30 months of age and older; the entire carcass of cattle not inspected and passed for human consumption that are 30 months of age or older from which brains and spinal cords were not removed; tallow that is derived from BSE-positive cattle; tallow that is derived from other materials prohibited by this rule that contains more than 0.15 percent insoluble impurities; and mechanically separated beef that is derived from the materials prohibited by this rule. These measures will further strengthen existing safeguards against BSE.
DATES: This final rule is effective April 27, 2009. The Director of the Office of the Federal Register approves the incorporation by reference in accordance with 5 U.S.C. 552(a) and 1 CFR part 51 of a certain publication in new 21 CFR 589.2001 effective April 27, 2009.
FOR FURTHER INFORMATION CONTACT: Burt Pritchett, Center for Veterinary Medicine (HFV-222), Food and Drug Administration, 7519 Standish Pl., Rockville, MD 20855, 240-453-6860, e-mail: firstname.lastname@example.com.
Table of Contents
I. Introduction II. Comments on the Proposed Rule A. General Comments B. Comments on Proposed New Sec. 589.2001--Cattle Materials Prohibited in Animal Food or Feed C. Comments on Proposed Amendments to Sec. 589.2000--Animal Proteins Prohibited in Ruminant Feed III. Description of the Final Rule A. Definitions B. Requirements C. Recordkeeping and Access Requirements D. Changes to Sec. 589.2000--Animal Proteins Prohibited in Ruminant Feed IV. Analysis of Economic Impacts A. Summary of Final Regulatory Impact Analysis B. Cost Effectiveness of Final Rule and Alternatives C. Need for Regulation D. Benefits E. Costs F. Government Costs G. Sensitivity Analysis H. Regulatory Flexibility Analysis V. The Small Business Regulatory Enforcement Fairness Act of 1996 (SBREFA) VI. Paperwork Reduction Act of 1995 VII. Environmental Impact VIII. Federalism IX. References
I. Introduction
snip...see different commentors and replies back ;
(Comment 6) A few comments asked FDA to recognize that the USDA 18- month surveillance snapshot may not be an accurate indication of BSE prevalence in the United States. Specifically, because the BSE cases to date are likely clustered in time and location, USDA's surveillance results may underestimate the true risk.
(Response) FDA stated in the preamble to the proposed rule that the detection of one BSE case in over 418,000 samples analyzed under USDA's enhanced surveillance program at the time of the publication of the proposed rule indicates that the prevalence of BSE is very low in the U.S. cattle population. FDA notes that USDA has conducted surveillance for BSE since 1990. A July 20, 2006, USDA report entitled ``An Estimate of the Prevalence of BSE in the United States'' supports FDA's qualitative statement of a very low prevalence of BSE in the United States (Ref. 3). According to the report, a model developed in Europe was used to calculate U.S. BSE prevalence from two BSE cases detected in 735,213 samples collected over a 7-year period ending in March 2006. Results of this analysis support a conclusion that the prevalence of BSE in the U.S. cattle population is less than one infected animal per million adult cattle. FDA remains confident in the two models used by USDA. The most likely values calculated by these models for the estimated number of cases were 4 or 7 infected animals out of 42 million adult cattle. USDA's analysis was submitted to the scrutiny of a peer review process, and the expert panel agreed with the appropriateness of USDA's assumptions and the factors it considered, as well as with the estimate of BSE prevalence.
(Comment 7) One comment noted that the effectiveness of the feed ban, especially at the farm level, is not known.
(Response) Inspection results indicate that compliance by U.S. animal feed industry is high. However, FDA agrees that it is very difficult to assess compliance with the ruminant feed rule at the farm level. FDA believes excluding certain cattle-derived risk materials from all animal feed channels will minimize any residual risks from on- farm misfeeding.
(Comment 8) Two comments indicated that the agency's feed control measures for ensuring compliance with the 1997 ruminant feed rule have been inadequate, citing a Government Accountability Office (GAO) study as evidence.
(Response) FDA disagrees with these comments. FDA believes its enforcement activities are adequate for ensuring industry compliance with the 1997 ruminant feed rule. The agency's response to the GAO's study can be found in Appendix VI of the GAO's report (Ref. 4).
(Comment 9) One comment speculated that, in some species, atypical BSE might be more pathogenic than typical BSE.
(Response) FDA is not aware of any scientific evidence that atypical BSE is
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more pathogenic than typical BSE. Therefore, the agency believes that the controls in this final rule are appropriate.
full text ;
***2008 Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.
Pierluigi Gambetti, MD Director, National Prion Disease Pathology Surveillance Center
Stephen M. Sergay, MB, BCh President, American Academy of Neurology
Progress Report from the National Prion Disease Pathology Surveillance Center An Update from Stephen M. Sergay, MB, BCh & Pierluigi Gambetti, MD
April 3, 2008
April 25, 2008
Strengthening Beef Safety
The Food and Drug Administration (FDA) has issued a final regulation barring certain cattle materials from all animal feed, including pet food. FDA regulates animal feed and drugs. The U.S. Department of Agriculture (USDA) regulates meat. Together the agencies enforce regulations that ensure that specific risk materials are kept out of the human food supply.
Greetings again,
IS this strengthening beef safety, or dangling another carrot out in front of the consumer $$$
NOTHING but ink on paper. since the 8/4/97 partial and voluntary ruminant to ruminant feed ban was put in place, the fda has failed time and time again, with 100s of millions of pounds of banned mad cow feed going into commerce and fed out. in just one fda letter in 2007, 10,000,000 plus pounds of banned mad cow feed was fed out to commerce. REMEMBER, 1 GRAM could EXPOSE/kill many cows. ...TSS
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST REASON Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV Date: September 6, 2006 at 7:58 am PST
REASON Dairy and poultry feeds were possibly contaminated with ruminant based protein. VOLUME OF PRODUCT IN COMMERCE 477.72 tons DISTRIBUTION AL
VOLUME OF PRODUCT IN COMMERCE 1,484 tons DISTRIBUTION TN and WV
Wednesday, April 23, 2008
FDA Strengthens Safeguards for Consumers of Beef Issues Regulation on Animal Feeds with Added Safeguards Against BSE
2006 was a banner year too for mad cow protein fed out into commerce. those were just one of many ;
Specified Risk Materials
*** DO NOT forget what was originally promised years ago !!!
Press Release FOR IMMEDIATE RELEASE Monday, Jan. 26, 2004 FDA Press Office 301-827-6242
Expanded "Mad Cow" Safeguards Announced to Strengthen Existing Firewalls Against BSE Transmission HHS Secretary Tommy G. Thompson today announced several new public health measures, to be implemented by the Food and Drug Administration (FDA), to strengthen significantly the multiple existing firewalls that protect Americans from exposure to the agent thought to cause bovine spongiform encephalopathy (BSE, also known as mad cow disease) and that help prevent the spread of BSE in U.S. cattle.
The existing multiple firewalls, developed by both the U.S. Department of Agriculture (USDA) and HHS, have been extremely effective in protecting the American consumer from exposure to BSE. The first firewall is based on import controls started in 1989. A second firewall is surveillance of the U.S. cattle population for the presence of BSE, a USDA firewall that led to the finding of the BSE cow in December. The third firewall is FDA's 1997 animal feed ban, which is the critical safeguard to help prevent the spread of BSE through cattle herds by prohibiting the feeding of most mammalian protein to ruminant animals, including cattle. The fourth firewall, recently announced by USDA, makes sure that no bovine tissues known to be at high risk for carrying the agent of BSE enter the human food supply regulated by USDA. The fifth firewall is effective response planning to contain the potential for any damage from a BSE positive animal, if one is discovered. This contingency response plan, which had been developed over the past several years, was initiated immediately upon the discovery of a BSE positive cow in Washington State December 23.
The new safeguards being announced today are science-based and further bolster these already effective safeguards.
Specifically, HHS intends to ban from human food (including dietary supplements), and cosmetics a wide range of bovine-derived material so that the same safeguards that protect Americans from exposure to the agent of BSE through meat products regulated by USDA also apply to food products that FDA regulates.
FDA will also prohibit certain currently allowed feeding and manufacturing practices involving feed for cattle and other ruminant animals. These additional measures will further strengthen FDA's 1997 "animal feed" rule.
"Today's actions will make strong public health protections against BSE even stronger," Secretary Thompson said. "Although the current animal feed rule provides a strong barrier against the further spread of BSE, we must never be satisfied with the status quo where the health and safety of our animals and our population is at stake. The science and our own experience and knowledge in this area are constantly evolving. Small as the risk may already be, this is the time to make sure the public is protected to the greatest extent possible."
"Today we are bolstering our BSE firewalls to protect the public," said FDA Commissioner Mark B. McClellan, M.D., Ph.D. "We are further strengthening our animal feed rule, and we are taking additional steps to further protect the public from being exposed to any potentially risky materials from cattle. FDA's vigorous inspection and enforcement program has helped us achieve a compliance rate of more than 99 percent with the feed ban rule, and we intend to increase our enforcement efforts to assure compliance with our enhanced regulations. Finally, we are continuing to assist in the development of new technologies that will help us in the future improve even further these BSE protections. With today's actions, FDA will be doing more than ever before to protect the public against BSE by eliminating additional potential sources of BSE exposure."
To implement these new protections, FDA will publish two interim final rules that will take effect immediately upon publication, although there will be an opportunity for public comment after publication.
The first interim final rule will ban the following materials from FDA-regulated human food, (including dietary supplements) and cosmetics:
Any material from "downer" cattle. ("Downer" cattle are animals that cannot walk.) Any material from "dead" cattle. ("Dead" cattle are cattle that die on the farm (i.e. before reaching the slaughter plant); Specified Risk Materials (SRMs) that are known to harbor the highest concentrations of the infectious agent for BSE, such as the brain, skull, eyes, and spinal cord of cattle 30 months or older, and a portion of the small intestine and tonsils from all cattle, regardless of their age or health; and The product known as mechanically separated beef, a product which may contain SRMs. Meat obtained by Advanced Meat Recovery (an automated system for cutting meat from bones), may be used since USDA regulations do not allow the presence of SRMs in this product. The second interim final rule is designed to lower even further the risk that cattle will be purposefully or inadvertently fed prohibited protein. It was the feeding of such protein to cattle that was the route of disease transmission that led to the BSE epidemic in United Kingdom cattle in the 1980's and 1990's.
This interim final rule will implement four specific changes in FDA's present animal feed rule. First, the rule will eliminate the present exemption in the feed rule that allows mammalian blood and blood products to be fed to other ruminants as a protein source. Recent scientific evidence suggests that blood can carry some infectivity for BSE.
Second, the rule will also ban the use of "poultry litter" as a feed ingredient for ruminant animals. Poultry litter consists of bedding, spilled feed, feathers, and fecal matter that are collected from living quarters where poultry is raised. This material is then used in cattle feed in some areas of the country where cattle and large poultry raising operations are located near each other. Poultry feed may legally contain protein that is prohibited in ruminant feed, such as bovine meat and bone meal. The concern is that spillage of poultry feed in the chicken house occurs and that poultry feed (which may contain protein prohibited in ruminant feed) is then collected as part of the "poultry litter" and added to ruminant feed.
Third, the rule will ban the use of "plate waste" as a feed ingredient for ruminants. Plate waste consists of uneaten meat and other meat scraps that are currently collected from some large restaurant operations and rendered into meat and bone meal for animal feed. The use of "plate waste" confounds FDA's ability to analyze ruminant feeds for the presence of prohibited proteins, compromising the Agency's ability to fully enforce the animal feed rule.
Fourth, the rule will further minimize the possibility of cross-contamination of ruminant and non-ruminant animal feed by requiring equipment, facilities or production lines to be dedicated to non-ruminant animal feeds if they use protein that is prohibited in ruminant feed. Currently, some equipment, facilities and production lines process or handle prohibited and non-prohibited materials and make both ruminant and non-ruminant feed -- a practice which could lead to cross-contamination.
To accompany these new measures designed to provide a further layer of protection against BSE, FDA will in 2004 step up its inspections of feed mills and renderers. FDA will itself conduct 2,800 inspections and will make its resources go even further by continuing to work with state agencies to fund 3,100 contract inspections of feed mill and renderers and other firms that handle animal feed and feed ingredients. Through partnerships with states, FDA will also receive data on 700 additional inspections, for a total of 3,800 state contract and partnership inspections in 2004 alone, including annual inspections of 100 percent of all known renderers and feed mills that process products containing materials prohibited in ruminant feed.
"We have worked hard with the rendering and animal feed production industries to try and achieve full compliance with the animal feed rule," said Dr. McClellan, "and through strong education and a vigorous enforcement campaign, backed by additional inspections and resources, we intend to maintain a high level of compliance."
Dr. McClellan also noted that, in response to finding a BSE positive cow in Washington state December 23, FDA inspected and traced products at 22 facilities related to that positive cow or products from the cow, including feed mills, farms, dairy farms, calf feeder lots, slaughter houses, meat processors, transfer stations, and shipping terminals. Moreover, FDA has conducted inspections at the rendering facilities that handled materials from the positive cow, and they were found to be fully in compliance with FDA's feed rule.
To further strengthen protections for Americans, FDA/HHS intends to work with Congress to consider proposals to assure that these important protective measures will be implemented as effectively as possible.
FDA is also continuing its efforts to assist in the development of better BSE science, to achieve the same or greater confidence in BSE protection at a lower cost. For example, to enhance the ability of our public health system to detect prohibited materials in animal feed, FDA will continue to support the development and evaluation of diagnostic tests to identify prohibited materials. These tests would offer a quick and reliable method of testing animal feeds for prohibited materials and for testing other products for contamination with the agent thought to cause BSE.
FDA has publicly discussed many of the measures being announced today with stakeholders in workshops, videoconferences, and public meetings. In addition, FDA published an Advance Notice of Proposed Rulemaking in November 2002 (available online at http://www.fda.gov/OHRMS/DOCKETS/98fr/110602c.htm concerning possible changes to the animal feed rule.
Comprehensive information about FDA's work on BSE and links to other related websites are available at http://www.fda.gov.
For Immediate Release July 9, 2004 FSIS Press Office APHIS Press Office FDA Media Relations
(202) 720-9113 (202) 734-7799 (301) 827-6242
USDA and HHS Strengthen Safeguards Against Bovine Spongiform Encephalopathy WASHINGTON, July 9, 2004--HHS Secretary Tommy G. Thompson and Agriculture Secretary Ann M. Veneman today announced three actions being taken to further strengthen existing safeguards that protect consumers against the agent that causes bovine spongiform encephalopathy (BSE, also known as "mad cow disease").
The three documents on display today include:
A joint USDA Food Safety & Inspection Service (FSIS), USDA Animal and Plant Health Inspection Service (APHIS) and Food and Drug Administration (FDA) notice that asks for public comment on additional preventive actions that are being considered concerning BSE; An interim final FDA rule that prohibits the use of certain cattle-derived materials in human food (including dietary supplements) and cosmetics; and A proposed FDA rule on recordkeeping requirements for the interim final rule relating to this ban. "Today's actions continue our strong commitment to public health protections against BSE," Secretary Thompson said. "Although our current rules are strong, when it comes to public health and safety we cannot be content with the status quo. We must continue to make sure the public is protected to the greatest extent possible."
"This Administration is committed to science-based measures to enhance and protect public health," Veneman said. "The advance notice of proposed rulemaking will allow the public the opportunity to provide their input."
"The series of firewalls already in place offer excellent protection against BSE," said Acting Commissioner of the Food and Drug Administration, Dr. Lester M. Crawford. "With these additional measures, we will make a strong system even stronger by putting into effect the most comprehensive, science-based improvements possible."
The steps already taken have been effective in protecting the American consumer from exposure to BSE. Import controls on live cattle and certain ruminant products were put in place more than 15 years ago. In 1997, FDA finalized its animal feed ban, which has been the critical safeguard to stop the spread of BSE through the U.S. cattle population by prohibiting the feeding of most mammalian protein to cattle and other ruminant animals. USDA implemented additional measures in January to ensure that no cattle tissues known to be high risk for carrying the BSE agent are included in USDA-regulated products. Finally, as became evident last December, there is a contingency response plan, developed over the past several years, that is launched immediately to contain any potential damage after a BSE positive animal is found.
To allow interested parties and stakeholders the opportunity to comment on the additional regulatory and policy measures under consideration, USDA's APHIS and FSIS, along with the FDA, developed an advance notice of proposed rulemaking that includes several additional actions the federal government is considering regarding BSE.
The ANPR also provides the public a succinct report on the work of the international review team (IRT) convened by Secretary Veneman to review the U.S. response to the single case of BSE in the United States (in a cow imported from Canada), along with a summary of the many actions already taken by each agency on BSE.
USDA's FSIS continues to seek and address comments on actions taken in relation to the BSE mitigation measures and put in place in January 2004. FSIS is also specifically seeking comments on whether a country's BSE status should be taken into account when determining whether a country's meat inspection system is equivalent to the U.S. regulations including the provisions in the FSIS interim final rules.
USDA's APHIS is specifically seeking comments on the implementation of a national animal identification system. In April, USDA announced the availability of $18 million in Commodity Credit Corporation funding to expedite development of a national animal identification system, which is currently underway. APHIS is inviting comments on when and under what circumstances the program should move from voluntary to mandatory, and which species should be covered now and over the long term.
The ANPRM also requests comment on the following measures related to animal feed, which is regulated by FDA:
removing specified risk materials (SRM's) from all animal feed, including pet food, to control the risks of cross contamination throughout feed manufacture and distribution and on the farm due to misfeeding; requiring dedicated equipment or facilities for handling and storing feed and ingredients during manufacturing and transportation, to prevent cross contamination; prohibiting the use of all mammalian and poultry protein in ruminant feed, to prevent cross contamination; and prohibiting materials from non-ambulatory disabled cattle and dead stock from use in all animal feed. FDA has reached a preliminary conclusion that it should propose to remove SRM's from all animal feed and is currently working on a proposal to accomplish this goal. Comments on these issues raised in the ANPRM are due to FDA next month.
FDA today also issued an interim final rule that prohibits the use of cattle-derived materials that can carry the BSE-infectious agent in human foods, including certain meat-based products and dietary supplements, and in cosmetics. These highÇrisk cattle-derived materials include SRM's that are known to harbor concentrations of the infectious agent for BSE, such as the brain, skull, eyes, and spinal cord of cattle 30 months of age or older, and a portion of the small intestine and tonsils from all cattle, regardless of their age. Prohibited high-risk bovine materials also include material from non-ambulatory disabled cattle, the small intestine of all cattle, material from cattle not inspected and passed for human consumption, and mechanically separated beef.
This action is consistent with the recent interim final rule issued by USDA declaring these materials to be inedible (unfit for human food) and prohibiting their use as human food.
FDA's interim final rule, in conjunction with interim final rules issued by FSIS in January 2004, will minimize human exposure to materials that scientific studies have demonstrated are likely to contain the BSE agent when derived from cattle that are infected with the disease. Consumption of products contaminated with the agent that causes BSE is the likely cause of a similar disease in people called variant Creutzfeldt-Jakob disease.
Although FDA's interim final rule has the full force and effect of law and takes effect immediately upon publication in the Federal Register, FDA is also asking for public comment on it.
In conjunction with the publication of the interim final rule, FDA is also proposing to require that manufacturers and processors of FDA-regulated human food and cosmetics containing cattle-derived material maintain records showing that prohibited materials are not used in their products. FDA is taking this action because records documenting the absence of such materials are important to ensure compliance with requirements of the interim final rule.
Publication of this USDA-FDA notice, as well as the two FDA documents, is scheduled for mid-July in the Federal Register. Comments should be submitted as directed in the addresses section of each document. Each document also provides information about how and where comments received may be viewed.
Note to Reporters: USDA news releases, program announcements and media advisories are available on the Internet. Go to the APHIS home page at www.aphis.usda.gov and click on the "News" button.
HHS news releases are available online at www.hhs.gov; FDA news releases can be found at www.fda.gov, which will also provide links to the documents discussed in this release.
Mr. Chairman, Members of the Committee, thank you for the opportunity to participate in today's hearing on measures taken by the Federal government to safeguard human and animal health in the United States from Bovine Spongiform Encephalopathy (BSE) and the response to the finding of a BSE-positive cow in the State of Washington. I am Dr. Lester M. Crawford, Deputy Commissioner, Food and Drug Administration (FDA or the Agency).
The mission of FDA is to protect the public health by assuring the safety and efficacy of our nation's human and veterinary drugs, human biological products, medical devices, human and animal food supply, cosmetics, and radiation emitting products. In fulfilling this mission, FDA is the Agency responsible for assuring that all FDA-regulated products remain safe and uncompromised from BSE and related diseases. Many FDA-regulated products contain bovine ingredients, for example, heart valves, ophthalmic devices, dental products, wound dressings, injectable drugs, vaccines, soups, gravies, sausage casings, and animal feeds.
FDA has long been actively involved nationally and internationally in efforts to understand and prevent the spread of BSE. FDA collaborates extensively with the Centers for Disease Control and Prevention (CDC), the National Institutes of Health (NIH), the Animal and Plant Health Inspection Service (APHIS) and the Food Safety and Inspection Service (FSIS) within the U.S. Department of Agriculture (USDA), Customs and Border Protection (CBP), the Environmental Protection Agency (EPA), other Federal agencies, state and local jurisdictions, and with affected industries and consumer groups. Many of these activities fit within the framework of the Department of Health and Human Service's (HHS or the Department) Bovine Spongiform Encephalopathy/Transmissible Spongiform Encephalopathy (BSE/TSE) Action Plan, which was released in August 2001. This collaboration over many years has enabled FDA to strengthen safeguards for FDA-regulated products and to respond quickly and effectively to the first case of BSE within the U.S.
Executive Summary
The mission of the Agency is to protect the public health by assuring the safety and efficacy of our nation's human and veterinary drugs, human biological products, medical devices, human and animal food supply, cosmetics, and radiation emitting products. In fulfilling this mission, FDA is the Agency responsible for assuring that all FDA-regulated products remain safe and uncompromised from BSE and related diseases.
BSE is a progressive neurological disorder of cattle that results from infection by an unconventional transmissible agent, and was first diagnosed in the United Kingdom (U.K.) in 1986. Many FDA-regulated products contain bovine ingredients, for example, heart valves, ophthalmic devices, dental products, wound dressings, injectable drugs, vaccines, soups, gravies, sausage casings, and animal feeds and thus must be taken into consideration as part the effort to prevent infectivity by BSE.
FDA has a longstanding commitment to protecting consumers from BSE by following multiple measures designed to safeguard FDA-regulated products from possible contamination by the BSE agent. Under the Federal Food, Drug, and Cosmetic (FD&C) Act, FDA has the authority to prevent the adulteration and misbranding of FDA-regulated products. Further, for medical products that require pre-market approval (e.g., drugs under Section 505 and medical devices under Section 513 of the FD&C Act), FDA has addressed safety concerns related to BSE through requirements of the application and approval process.
The U.S. employs a robust multi-layered approach to preventing the introduction and amplification of BSE. While the goal of this approach is to achieve an extremely high level of compliance with each preventative measure, this multi-layered approach is designed to protect the U.S. consumer from exposure to the BSE infective material, and to date this approach has been working. Since 1989, USDA has prohibited the importation of live animals and animal products from BSE-positive countries. Since 1997, FDA has prohibited the use of certain mammalian proteins in the manufacture of ruminant feed. FDA continues to implement policies to keep safe all FDA-regulated products, including food, food ingredients, dietary supplements, drugs, vaccines, and cosmetics from risk of any BSE-contaminated bovine material. As a result of these multiple regulatory safeguards, the risk of exposure to BSE through products, FDA regulates remains extremely low in the U.S.
FDA's 1997 animal feed regulation forms the basis of the Agency's efforts to prevent the spread of BSE through animal feed. This rule prohibits the use of most mammalian protein in the manufacture of animal feeds for ruminants. FDA implemented this rule to establish in our country feeding practices consistent with the best science and epidemiological knowledge known at the time to prevent the spread of BSE throughout herds of U.S. cattle. A risk assessment sponsored by USDA and conducted by the Harvard Center for Risk Analysis, released in November 2001, identified FDA's feed ban as one of the primary safeguards against the spread of BSE in U.S. cattle.
To maximize protection afforded by the feed regulation, FDA has developed and implemented a BSE/Ruminant Feed Ban Inspection compliance program and established the goal of 100 percent compliance. FDA's strategy for achieving uniform compliance with the feed rule focuses on three areas: education, inspection, and enforcement. FDA and its state counterparts conduct, at least annually, targeted BSE inspections of 100 percent of known renderers, protein blenders, and feed mills processing products containing material prohibited from use in ruminant feed. Compliance by these establishments with FDA's feed rule is estimated to be at better than 99 percent. As of December 20, 2003, FDA had received over 26,000 inspection reports (6,404 for Fiscal Year 2003). The majority of these inspections (around 70 percent) were conducted by state officials for FDA, with the remainder conducted by FDA officials. The total number of inspection reports represents 13,672 firms, 1,949 of which are active and handle materials prohibited from use in ruminant feed. The 1,949 active firms that handle prohibited material have been inspected by FDA and, as of December 31, 2003, only five were found to have significant violations, resulting in official action indicated (OAI). FDA is working with these firms to bring them into compliance.
On December 23, 2003, FDA was notified by USDA of a presumptive-positive finding of BSE in a cow in Washington State. FDA immediately initiated its BSE Emergency Response Plan. As part of the plan, FDA has been coordinately closely with USDA so that we can effectively investigate this BSE case, trace the various products involved, and take the appropriate steps to protect the public. FDA investigators and inspectors located the high risk material rendered from the infected cow, and the rendering plants placed a hold on the rendered material, which is being disposed of appropriately. I am happy to report that all of the establishments inspected by FDA during the course of the investigation were in compliance with the feed ban. In addition, to help address the concerns of foreign governments and restore confidence in American products, FDA has participated, along with USDA, in numerous meetings and consultations with foreign governments since USDA surveillance found the BSE-positive cow.
In addition to new policies and regulations, new knowledge and tools gained through applied research can greatly help us to be more effective in our regulatory mission, such as protecting the country from BSE. Several of FDA's Centers, as well as many private laboratories, academic institutions, and other Federal agencies (most notably NIH) are also involved in significant research activities relating to TSEs. Basic areas requiring research include: increasing our understanding of prions, learning how prions are transmitted within a species and potentially between species, developing diagnostic tests for humans and animals, developing detection methods for use on regulated products, developing methods to increase or eliminate infectivity, and designing new treatments. We are optimistic about the promise of new technologies, such as better methods to quickly distinguish the species of proteins and sensors to detect abnormal prions in food. Development of these technologies can contribute significantly to the effort to prevent the spread of BSE and must be considered carefully when evaluating potential regulatory changes to address BSE.
At the time that FDA implemented the feed rule in 1997, the Agency also recognized that evolving, complex scientific and public health issues, particularly regarding BSE required the Agency to continue to assess and scrutinize the rule to ensure its integrity as a firewall against the potential for spread of BSE. To further explore ways the animal feed regulation could be improved in November 2002, FDA published an advance notice of proposed rulemaking (ANPR) soliciting information and views from the affected industries and the public on some potential changes to its current feed regulation, including ways that the animal feed regulation could be strengthened. Although the risk of exposure to BSE in the U.S. remains extremely low and the measures in place are working, as a result of the recently discovered infected cow in the state of Washington, the Agency is evaluating the appropriateness of additional science-based measures to further strengthen our current protections.
Yesterday, Department Secretary Tommy Thompson and FDA Commissioner Mark McClellan announced several additional public health measures to further strengthen the current robust safeguards that help protect Americans from exposure to the agent that causes BSE and help prevent the spread of BSE in U.S. cattle. These measures relate to both protections for foods intended for human consumption as well as additional measures to strengthen FDA's 1997 final rule regulating animal feed. With respect to human foods, FDA announced that it will extend to FDA-regulated foods, dietary supplements and cosmetics, restrictions on using specified risk materials that would complement the recent USDA announcements. Concerning animal feed, the Agency announced a series of measures designed to lower even further the risk that cattle will be purposefully or inadvertently fed "ruminant" proteins, including, eliminating an exemption in the feed rule that allows mammalian blood and blood products at slaughter to be fed to ruminants as a protein source; banning the use of "poultry litter" as a feed ingredient for cattle and other ruminants; prohibiting the use of "plate waste" as a feed ingredient for ruminants, including cattle; and taking steps to further minimize the possibility of cross-contamination of animal feed via equipment, facilities or production lines.
Finally, FDA is increasing its inspections of feed mills and renderers in 2004. Our 2001 base funding for BSE-related activities was $3.8 million. We shifted resources internally in 2001 and received a substantial increase from Congress in 2002. Our funded level for 2004 is currently approximately $21.5 million, almost a five-fold increase over the 2001 base. FDA will itself conduct 2,800 inspections and will make its resources go even further by working with state agencies to fund 3,100 contract inspections of feed mills and renderers and other firms that handle animal feed and feed ingredients. Through partnerships with states, FDA will also receive data on 700 additional inspections, for a total of 3,800 state contract and partnership inspections in 2004. These inspections would include 100 percent of all known renderers and feed mills that process products containing prohibited materials.
The Agency looks forward to continuing to assist Congress as it evaluates the risks associated with BSE, identifies opportunities to promote technologies that will detect and prevent the spread of BSE, and considers science-based approaches to further strengthen regulatory protections and bolster the resources available to assist Federal, state, local and private efforts to assure that BSE does not present a threat to human or animal health in the U.S.
Background on Bovine Spongiform Encephalopathy (BSE)
BSE is a progressive neurological disorder of cattle that results from infection by an unconventional transmissible agent, and was first diagnosed in the U.K. in 1986. It belongs to a family of diseases, transmissible spongiform encephalopathies (TSEs), a group of transmissible, slowly progressive, degenerative diseases of the central nervous systems of several species of animals.
The vast majority of BSE cases have been reported in the U.K., where more than 183,000 cases in more than 35,000 herds have been reported through the end of November 2003. The U.K.-BSE epidemic peaked in January 1993 at nearly 1,000 new cases per week. The original source of the BSE outbreak is uncertain, but may have resulted from the feeding of scrapie-containing sheep meat-and-bone meal to cattle. Scrapie is an endemic spongiform encephalopathy and has been widespread in the U.K., where the rendered carcasses of livestock (including sheep) were fed to ruminants and other animals until 1988, as a protein-rich nutritional supplement. It appears likely that changes in the rendering process in the U.K. that had taken place around 1980 allowed the etiologic agent in infected carcasses to survive, contaminate the protein supplement, and infect cattle. There is strong evidence and widespread agreement that the outbreak was amplified by feeding rendered bovine meat-and-bone meal to young calves. BSE has a prolonged incubation period in cattle, ranging from two to eight years, with a mean of five to six years.
Outside of the U.K., 22 other countries, mostly in Europe, have reported cases of BSE in indigenous cattle to the World Organisation for Animal Health (known as the O.I.E.). Other countries may be considered at risk because of an inadequate surveillance program, a lack of information on which to make a risk assessment, or the potential for exposure to BSE.
Related Diseases
TSEs also include "scrapie" in sheep and goats, "chronic wasting disease" (CWD) in deer and elk, feline spongiform encephalopathy, transmissible mink encephalopathy, and, in humans, kuru, Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia, and Creutzfeldt-Jakob disease (CJD or "classical" CJD) and variant CJD, which was first reported in the U.K. in 1996. TSEs are not known to infect non-mammalian species.
Classic CJD occurs throughout the world, including the U.S., at a rate of about one case per million people. The median age at death in the U.S. of patients with classic CJD is 68. Most cases of CJD are considered sporadic, a small number are familial associated with a gene mutation, and a small number are iatrogenic, resulting from the accidental transmission of the causative agent via contaminated surgical equipment, or as a result of cornea or dura mater transplants, or the administration of human-derived pituitary growth hormones.
Variant CJD (vCJD) is a distinct variant from classic CJD and is strongly believed to have been acquired from eating food products containing the BSE agent. The absence of confirmed cases of vCJD in geographic areas free of BSE supports this conclusion, and the interval between the period for initial extended exposure of the population to potentially BSE-contaminated food and the onset of initial vCJD cases, approximately ten years, is consistent with known incubation periods for CJD. Experimental studies on monkeys and mice, as well as additional laboratory studies of infecting prions from vCJD patients and BSE-infected animals, also support such a relationship. The incubation period for vCJD in humans is unknown, but is at least five years and could extend up to 20 years or longer.
As of December 1, 2003, a total of 153 vCJD cases had been reported worldwide, 143 of the cases occurring in the U.K. The low number of vCJD cases relative to the number of cases of BSE in the U.K. indicates that a substantial species barrier protects humans from widespread illness. There are no cases of vCJD having been contracted in the U.S. The only person diagnosed with vCJD while living in the U.S. is a U.K. citizen believed to have acquired the disease while living in the U.K.
Legal and Regulatory Framework for FDA Protections
FDA has a longstanding commitment to protecting consumers from BSE by following multiple measures designed to safeguard FDA-regulated products from possible contamination by the BSE agent. Under the FD&C Act, FDA has the authority to prevent the adulteration and misbranding of FDA-regulated products. For example, FDA has used provisions in Section 402(a) (the food adulteration provisions) and Section 403(a) (the food misbranding provisions) of the FD&C Act to prohibit ruminant feed from containing certain protein derived from mammalian tissues. These same adulteration and misbranding provisions apply to human food. Further, for medical products that require pre-market approval (e.g., drugs under Section 505 and medical devices under Section 513 of the FD&C Act), FDA has addressed safety concerns related to BSE through requirements of the application and approval process. Additionally, when material from the one BSE-positive cow in the U.S. was traced to renderers, FDA advised those firms that this material could not be used as an animal feed because it was adulterated under Section 402(a)(5) of the FD&C Act because it was, in part, the product of a diseased animal. Under section 801 of the FD&C Act, FDA may refuse admission of imported food and certain other products that appear to be in violation of the FD&C Act. Furthermore, under Section 701(a), FDA may promulgate regulations for the efficient enforcement of the FD&C Act. For example, under Section 701(a) and other sections, FDA promulgated its "animal feed" rule (Title 21, Code of Federal Regulation (CFR) section 589.2000) to prohibit ruminant feed from containing certain protein derived from mammalian tissues. In addition, under the Public Health Service Act, FDA is authorized to make and enforce regulations to prevent the introduction, transmission, or spread of communicable diseases from foreign countries into the U.S. or between states.
Preventing the Spread of BSE: FDA Protections
FDA and other Federal agencies have had preventive measures in place to reduce the U.S. consumer's risk of exposure to any BSE-contaminated meat and food products for a considerable time. Since 1989, USDA has prohibited the importation of live animals and animal products from BSE-at risk countries. Since 1997, FDA has prohibited the use of certain mammalian proteins in the manufacture of ruminant feed. FDA continues to implement policies to keep safe all FDA-regulated products, including food, food ingredients, dietary supplements, drugs, vaccines, and cosmetics from risk of any BSE-contaminated bovine material. As a result of these multiple regulatory safeguards, the risk of exposure to the BSE agent through products FDA regulates remains extremely low in the U.S. In 1998, USDA commissioned the Harvard Center for Risk Analysis to conduct an analysis and evaluation of the U.S. regulatory measures to prevent the spread of BSE in the U.S. and to reduce the potential exposure of U.S. consumers to BSE. The Harvard study concluded, among other things, that even if introduced in the U.S., due to the preventive measures currently in place in the U.S., BSE is extremely unlikely to become established in the U.S.
The U.S. employs a robust approach to preventing the introduction and amplification of BSE, and the prevention of introduction and amplification of BSE has been described as consisting of five separate firewalls. Our existing firewalls are based on a four-pronged regulatory strategy:
Our first firewall is formed through regulations and enforcement to protect U.S. borders from potentially infective materials utilizing a regime of import controls. USDA, beginning in 1989, enacted major restrictions on imports, and more restrictive import controls have been introduced as we have learned more about the science of BSE and as the worldwide epidemiology has changed. FDA remains a committed partner with USDA and CBP in protecting our borders. The second firewall is surveillance of the U.S. cattle population for the presence of BSE. Surveillance of the cattle population is the primary responsibility of USDA, and USDA has recently announced steps to increase surveillance. The third firewall is prevention of the amplification of BSE through feed provided to cattle and other ruminants, and this responsibility falls primarily on FDA. FDA's animal feed ban regulations form the basis of this third firewall and have been cited as one of the most significant elements needed to prevent the spread of BSE in the U.S. We have taken intensive steps to get an extremely high level of compliance with this feed ban. As a result, we have been able to work with the animal feed industry to achieve more than a 99% compliance rate – and we intend to continue to work for full compliance. The fourth firewall is making sure that no bovine materials that can transmit BSE be consumed by people. So even if a BSE-positive cow made it through all of the previous firewalls, which is extremely unlikely, it would not pose any risk to people. USDA and FDA have long had steps in place to help prevent any possible exposure to BSE in bovine products, and recently USDA announced additional major steps to prevent any of the tissues known to carry BSE from entering the beef supply, as well as to restrict use of certain "downer" cows that might be at higher risk of carrying BSE. FDA will be taking comparable measures to prevent human exposure to the FDA-regulated bovine products that might potentially harbor BSE. A fifth firewall is effective response planning to contain the potential for any damage from a BSE positive animal, if one is discovered at some point in the system. This urgent response plan went into place immediately upon the discovery of a BSE-positive cow in Washington State on December 23, 2003. We have inspected and traced products at 22 facilities, including feed mills, farms, dairy farms, calf feeder lots, slaughterhouses, meat processors, transfer stations, and shipping terminals. We have accounted for all the products related to the BSE-positive cow that FDA regulates, and none have gone into human or animal consumption. Moreover, FDA has conducted inspections at all the rendering facilities involved, and found they were fully in compliance with our feed rule. The goal of our firewall after firewall approach is to provide full protection of the public against BSE without adding unnecessary costs or restricting the consumption of safe beef products. FDA and USDA intend to maintain an extremely high level of compliance with each firewall. In addition, our multi-layered approach makes sure that even if each firewall doesn't function perfectly, the U.S. consumer is, nonetheless, protected from exposure to the BSE infective material.
FDA's Feed Rule: Substances Prohibited From Use in Animal Feed
Rendered feed ingredients contaminated with the BSE agent are believed to be the principal means by which BSE is amplified in cattle populations. To help prevent the establishment and spread of BSE through feed in the U.S., FDA implemented a final rule that prohibits the use of most mammalian protein in the manufacture of animal feeds for ruminants. This rule, 21 CFR 589.200, became effective on August 4, 1997. Mammalian proteins exempted from the rule are blood and blood products, gelatin, inspected meat products that have been cooked and offered for human food and further heat processed for feed (such as plate waste and used cellulosic food casings), milk products (milk and milk proteins), and any product whose only mammalian protein consists entirely of porcine or equine protein. Fats and oils, such as tallow, do not fall within the current feed rule because they are not protein.
FDA implemented this rule to establish in our country feeding practices consistent with the best science and epidemiological knowledge known at the time to prevent the spread of BSE throughout herds of U.S. cattle. A risk assessment sponsored by USDA and conducted by the Harvard Center for Risk Analysis, released in November 2001, identified FDA's feed ban as one of the primary safeguards against the spread of BSE in U.S. cattle.
To maximize protection afforded by the feed regulation, FDA has developed and implemented a BSE/Ruminant Feed Ban Inspection compliance program and established the goal of 100 percent compliance. FDA's strategy for achieving uniform compliance with the feed rule focuses on three areas: education, inspection, and enforcement.
A strong inspection presence can be considered the backbone of FDA's strategy for achieving compliance with the feed rule. FDA and its state counterparts conduct, at least annually, targeted BSE inspections of 100 percent of known renderers, protein blenders, and feed mills processing products containing material prohibited from use in ruminant feed. Compliance by these establishments with FDA's 1997 feed rule is over 99 percent. FDA has prioritized the inspection process so that any firms found to be out of compliance in their last inspection will be promptly re-inspected. In addition, FDA will conduct for-cause inspections where evidence dictates, e.g., as a result of a sampling assignment. FDA and the states also conduct inspections of selected processors that are not using prohibited material to ensure compliance with the regulation by this segment of the industry.
Inspections conducted by FDA or state investigators are classified to reflect the compliance status at the time of the inspection based upon the objectionable conditions documented. These inspection decisions are reported as OAI, Voluntary Action Indicated (VAI), or No Action Indicated (NAI).
An OAI inspection classification occurs when significant objectionable conditions or practices were found and regulatory sanctions are warranted in order to address the establishment's lack of compliance with the regulation. An example of an OAI inspection classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspections classified with OAI violations will be promptly re-inspected following the regulatory sanctions to determine whether adequate corrective actions have been implemented. A VAI inspection classification occurs when objectionable conditions or practices were found that do not meet the threshold of regulatory significance, but do warrant advisory actions to inform the establishment of findings that should be voluntarily corrected. Inspections classified with VAI violations are more technical violations of the ruminant feed rule such as minor record-keeping lapses and conditions involving non-ruminant feeds. A NAI inspection classification occurs when no objectionable conditions or practices were found during the inspection or the significance of the documented objectionable conditions found does not justify further actions. As of December 20, 2003, FDA had received over 26,000 inspection reports (6,404 for fiscal year 2003). The majority of these inspections (around 70 percent) were conducted by state officials for FDA, with the remainder conducted by FDA officials. The total number of inspection reports represents 13,672 firms, 1,949 of which are active and handle materials prohibited from use in ruminant feed. These firms, which may be in more than one category, include renderers, licensed feed mills, feed mills not licensed by FDA, protein blenders, and others (such as ruminant feeders, on-farm mixers, pet food manufacturers, animal feed salvagers, distributors, retailers, and animal feed transporters). The 1,949 active firms that handle prohibited material have been inspected by FDA and, as of December 31, 2003, only five were found to have significant violations, resulting in OAI. FDA is working with these firms to bring them into compliance.
To be transparent about inspection results, FDA has recorded inspectional findings in a newly designed FDA BSE/Ruminant Feed Inspection Database available on FDA's website. The database is dynamic, with new information being entered on a continual basis. Each entry in the database represents the results of the most recent inspection.
FDA also conducts sampling of feed and feed ingredients in the marketplace as an additional tool to target firms for inspection. This type of sample analysis is being done using feed microscopy as the method for detecting prohibited materials. Other methods, such as polymerase chain reaction (PCR), are being validated for additional analytical use.
Enforcement is an important component of the compliance strategy. FDA pursues enforcement actions when we find knowing or intentional non-compliance, or if repeated inspection and educational efforts are ineffective in assuring compliance. Our first action of choice will ordinarily be a Warning Letter, which notifies responsible parties of a violation or violations and asks for a response within a certain time frame explaining corrective actions taken. When it is consistent with the public protection responsibilities of FDA and the nature of the violation, it is our practice to afford individuals and firms an opportunity voluntarily to take appropriate and prompt corrective action. The Agency has additional, more stringent enforcement tools available when our notification to the company of documented violations does not lead to compliance with the FD&C Act, including product seizure, injunction, and prosecution.
As of January 1, 2004, FDA has issued 63 Warning Letters and has one court ordered Permanent Injunction since the BSE feed rule went into effect. Also, 47 firms recalled 280 products during the same time period; 12 of the recalls were in 2003.
Education has been, and continues to be, a critical component of our compliance strategy. Providing clear guidance and information on FDA's requirements and regulations is vital to help assure compliance. FDA has provided and sponsored many educational services and forums, including nationwide seminars, CD-ROM training, teleconferences, guidances targeted for different segments of the animal feed industry, guidance for Federal and state inspectors, and a variety of published articles. The Agency has met with many industry trade groups to discuss coordination of educational efforts with affected parties, and we expect to continue an open dialogue, seeking suggestions for types of educational approaches, sharing resources, and keeping the industry updated on new developments or problem areas that arise.
Import Controls
To minimize the risk of the introduction or spread of BSE we also must have strong enforcement measures to protect our borders. FDA's Import Program is responsible for coordinating the import of products potentially infected with or at high risk of infection with the agent associated with BSE. Operationally, FDA's Import Program provides for the review of information about FDA-regulated products offered for entry into the U.S. and the opportunity for physical examination of the products. FDA uses this information to determine whether a product is subject to refusal of admission.
In protecting the borders from potentially unsafe products, FDA works closely with USDA and CBP to ensure a coordinated and efficient BSE import control strategy. This tri-agency cooperative effort has led to a multi-layer review process whereby each agency utilizes the strengths of its particular entry procedures to produce a composite system that is considerably more robust than any one component. BSE import activities are reviewed and coordinated by an inter-agency workgroup composed of representatives from FDA, CBP, and USDA/APHIS. In fact, on February 5, 2002, with APHIS, FSIS, Canadian Food Inspection Agency (CFIA), Health Canada, and state participation, FDA conducted a simulation exercise involving the importation of potentially BSE-contaminated product and subsequent regulatory follow-up.
FDA uses Import Alerts to disseminate information regarding problems or potential problems with imported products. Import Alerts recommend that field offices examine, sample, or detain and, if warranted, refuse admission of the product in question. These Import Alerts are made available on FDA's website. With respect to its import alerts on BSE, FDA coordinates closely with APHIS and its prohibitions on the importation of products related to BSE concerns. An alert may cover an individual manufacturer, supplier, or a particular product from an entire country. Import Alerts also may be issued as a follow-up to an inspection, when it is determined that a manufacturer is in violation of good manufacturing practice requirements.
FDA has in place several import alerts targeting BSE. Import Alert 17-04, first issued in October 1994, allows detention, without physical examination, of bulk shipments of high-risk bovine tissues and tissue-derived ingredients from BSE-at-risk countries. Import Alert 99-25, first issued in January 2001, allows detention without physical examination of animal feed, animal feed ingredients, and other products for animal use from countries identified by USDA as BSE-positive or BSE-at-risk when processed animal protein is declared in the ingredients or when FDA sampling and analysis finds the presence of undeclared animal protein. Import Alert 71-02, issued in October 2003, calls for detention without physical examination of products of specific firms located in USDA-listed BSE-positive or BSE-at-risk countries, which have been identified through FDA sampling and analysis, as importing products containing animal protein. These import alerts are continuously updated as new countries are listed by USDA as either BSE-positive or BSE-at-risk, or to make other appropriate changes.
FDA's Response to the Identification of a BSE-Positive Cow in Washington State
On December 23, 2003, at approximately 3:00 pm, the Agency's Office of Crisis Management (OCM) was notified by USDA's APHIS of a presumptive-positive finding of bovine spongiform encephalopathy (BSE) in a "downer" cow slaughtered on December 9, 2003, at a USDA-inspected slaughter facility in Washington State.
FDA had in place its Bovine Spongiform Encephalopathy Emergency Response Plan that describes the roles and activities of each of the Agency components involved in managing this kind of emergency. This plan had been tested several times in tabletop and simulated incidents that actively involved state, Federal, and Canadian counterparts. The plan has been in place since 2001 and has been revised in response to the incident exercises conducted by FDA.
As provided in the Emergency Response Plan, OCM's Emergency Operations Center (EOC) is the single point of coordination for FDA's response to a BSE emergency. FDA's EOC maintains contact with HHS Secretary's Command Center (SCC), CDC's EOC, USDA/FSIS Office of Food Security and Emergency Preparedness, and other EOCs, as appropriate.
At the time of notification by USDA of the presumptive case of BSE, FDA's OCM initiated its BSE Emergency Response Plan and activated FDA's EOC. Various FDA headquarters and FDA center offices were immediately notified in accordance with the plan, as well as the FDA Seattle District Office (SEA-DO).
FDA responsibilities include conducting inspections and investigations to determine where any animal by-products went and ensuring that they did not enter commerce contrary to provisions of the FD&C Act and other statutes enforced by FDA.
On the same day FDA was notified of the presumptive case of BSE by USDA, FDA's SEA-DO dispatched five investigative teams to investigate various facilities suspected of being either a source or recipient of affected material.
An aggressive schedule of inspections and investigations was pursued by FDA which enabled FDA to announce in December 27, 2003, that its investigators and inspectors from the states of Washington and Oregon had located the high risk material rendered from the one cow that had tested positive for BSE in Washington State and that the rendering plants that processed this material had placed a hold on the rendered material. The firms, located in Washington State and Oregon, assisted and cooperated fully with FDA's investigation.
FDA advised the involved renderers on acceptable methods of disposing of material, such as landfill (coordinating with state and local officials and EPA), incineration, digestion, or conversion to a fuel/industrial source. Disposal of the meat and bone meal on hold has begun.
Communications, of course, have played a critical role in many aspects of the incident response. Late on December 23, 2003, FDA's headquarters and district staff participated in a teleconference with APHIS and Washington State officials to ensure a coordinated response to the incident. FDA, CDC, Department of Defense, and FSIS continued to participate in APHIS-initiated interagency calls throughout the response to the incident.
FDA also has kept affected industries and State counterparts informed and up-to-date. On December 23, 2003, FDA's Center for Food Safety and Applied Nutrition (CFSAN) advised Washington State milk cooperatives that there was no known risk of BSE transmission from milk. The scientific data indicate that milk from BSE cows does not transmit BSE.
In responding to the BSE incident, FDA inspected and traced products at many different facilities, including renderers, feed mills, farms, dairy farms, calf feeder lots, slaughterhouses, meat processors, transfer stations, and shipping terminals. Notably, inspectors found no deviations from FDA's feed rule.
Working with Foreign Governments
FDA officials regularly meet with representatives of foreign governments and international organizations on many levels and on many issues of common interest, including BSE. Immediately after the announcement on December 23, 2003, of a BSE-positive cow in the U.S., various foreign governments closed their markets to U.S. beef. Since that time, FDA officials, working closely with USDA officials, have been involved in numerous meetings and consultations with representatives of foreign governments to help address concerns and restore confidence in American products. For example:
FDA representatives met with Japanese officials from the Ministry of Agriculture, Forestry, and Fisheries, the Ministry of Health, Labor, and Welfare, the Food Safety Commission and the Japanese Embassy on January 9, 2004, to discuss BSE control measures in animal feed and food additives. FDA representatives met with numerous foreign attaches at USDA on January 12, 2004, to discuss FDA's Center for Veterinary Medicine measures to prevent BSE in animal feeds. FDA representatives met in separate meetings on January 13, 2004, with officials from the CFIA and from Mexico's Secretaría de Agricultura, Ganadería, Desarrollo Rural, Pesca y Alimentación to discuss current feed safety measures to prevent BSE in the U.S. The Ministers of Agriculture of the U.S., Mexico and Canada met on January 16, 2004, to coordinate ongoing interagency efforts towards expediting increased harmonization through a consultative process among the countries. I accompanied Secretary of Health and Human Services Tommy G. Thompson, at this meeting that resulted in a proposal to establish a Coordinating Committee on BSE to facilitate collaborative effort. Additionally, last week I visited with Japanese and Korean officials, as part of the U.S. Government's delegation to discuss scientific and trade implications of the U.S. BSE case. The delegation also included senior scientific, regulatory, and trade officials from USDA, and the U.S. Trade Representative. Research
Several of FDA's Centers, as well as many private laboratories, academic institutions, and other Federal Agencies (most notably NIH) are involved in significant research activities relating to TSEs. Basic areas requiring research include: increasing our understanding of prions; learning how prions are transmitted within a species and potentially between species; developing diagnostic tests for humans and animals; developing detection methods for use on regulated products; developing methods to increase or eliminate infectivity; and designing new treatments.
Most people envision research as being applied by medical practitioners to diagnose and treat disease. Applied research also is critical in a regulatory environment, where knowledge and tools gained through applied research can help us to achieve our mission more effectively and more efficiently.
Taking one example pertinent to BSE, current rendering processes do not completely inactivate the BSE agent. Advances in technology that could distinguish between BSE-infected and non-infected cattle, or that could completely inactivate the BSE agent in feed components may allow for exemptions to the feed regulations for those renderers and feed manufactures who apply these technologies.
Discussed below some examples of research on BSE and vCJD that could have significant regulatory implications and benefit:
FDA's CFSAN is in the final year of funding a two-year project to develop sensors to detect abnormal prion protein in food. Work on the project should be completed in early 2004, and will result in a report on the usefulness of the sensors for detecting TSE agents in finished food products. No tests for the rapid diagnosis of vCJD have been validated as either sufficiently specific or sensitive to be used to screen the blood supply. A reliable blood-screening test for vCJD is an extremely important goal and is currently the object of considerable research activity. FDA has conducted and supported research efforts in the process of validating a rapid-DNA based method for detection of animal derived materials in animal feed and feed ingredients. As a part of this research effort, FDA has developed a Polymerase Chain Reaction probe to determine the animal species of origin from which feed ingredients were derived. FDA remains firmly committed to bringing better science to the public, to provide better public health protection at a lower cost. That's why a key part of our BSE strategy involves fostering the development of better technologies to deal with BSE. To enhance the ability of our public health system to detect prohibited materials in animal feed, FDA will continue to support the development and testing of diagnostic tests to identify prohibited materials. As these tests are developed FDA will evaluate the utility of such tests promptly and thoroughly, so that there will be a quick and reliable method of testing animal feeds for prohibited materials.
Additional Measures to Bolster Protections Against BSE
FDA implemented the feed rule in 1997 based on the best information obtainable on the science and epidemiology of BSE at the time. The Agency also recognized that evolving, complex scientific and public health issues, particularly regarding BSE and vCJD, required the Agency to continue to assess and scrutinize the rule to ensure its integrity as a firewall against the potential for spread of BSE.
The Agency held a public hearing in October 2001 to solicit information and views on its present animal feed regulation. FDA requested information and views from individuals and organizations on the present rule and whether changes in the rule or other additional measures were necessary. The Agency was particularly interested in soliciting comments and views from individuals, industry, consumer groups, health professionals, and researchers with expertise in BSE and related animal and human diseases. The Agency specifically invited comments, both oral and written, on 17 questions about ways the rule and its enforcement might be improved to achieve its original objectives of preventing the establishment and amplification of BSE in the U.S. Transcripts of the hearing were then made publicly available with access through FDA's website.
Soon after the public hearing, the USDA released the Harvard Center for Risk Analysis's findings on the impact of various risks and potential pathways for exposure of U.S. cattle and U.S. citizens to the BSE agent. This assessment of the situation in the United States concluded that, due to control measures already in place, the risk to U.S. cattle and to U.S. consumers from BSE is very low. The model also demonstrated that certain new control measures could reduce the small risk even further.
To further explore ways the animal feed regulation could be improved in November 2002, FDA published an ANPR soliciting information and views from the affected industries and the public on some potential changes to its current feed regulation, including ways that the animal feed regulation could be strengthened. Information and comments were sought on the following five aspects of the BSE feed regulation: feasibility and impacts of excluding high risk materials, such as brain and spinal cord, from rendered animal products; use of poultry litter in cattle feed and impacts of banning such use; impacts of introducing new labeling requirements for pet food; methods to prevent cross-contamination between prohibited and non-prohibited material; use of plate waste in ruminant feed and impacts of eliminating such use.
Yesterday, we announced that we will be taking several additional steps to further strengthen the current robust safeguards that help protect Americans from exposure to the agent that causes BSE and help prevent the spread of BSE in U.S. cattle. These measures relate to both protections for foods intended for human consumption as well as additional measures to strengthen FDA's 1997 final rule regulating animal feed. Many of these steps were raised in the November 2002, ANPR, as well as at the public meeting. With respect to human foods the Agency announced it will be extending to FDA-regulated foods, dietary supplements and cosmetics, restrictions on using specified risk materials that would complement the recent USDA announcements. Concerning animal feed, the Agency announced a series of measures designed to lower even further the risk that cattle will be purposefully or inadvertently fed "ruminant" proteins, including, eliminating the existing exemption in the feed rule that allows mammalian blood and blood products at slaughter to be fed to ruminants as a protein source; prohibiting the use of "poultry litter" as a feed ingredient for cattle and other ruminants; banning the use of "plate waste" as a feed ingredient for ruminants, including cattle; taking further steps to minimize the possibility of cross-contamination of animal feed via equipment, facilities or production lines; and evaluating additional mechanisms to enhance the ability of our public health system to detect prohibited materials in animal feed utilizing diagnostic tests.
In addition, FDA intends step up its inspections of feed mills and renderers in 2004. FDA is increasing its inspections of feed mills and renderers in 2004. Our 2001 base funding for BSE-related activities was $3.8 million. We shifted resources internally in 2001 and received a substantial increase from Congress in 2002. Our funded level for 2004 is currently approximately $21.5 million, almost a five-fold increase over the 2001 base. FDA will itself conduct 2,800 inspections and will make its resources go even further by working with state agencies to fund 3,100 contract inspections of feed mills and renderers and other firms that handle animal feed and feed ingredients. Through partnerships with states, FDA will also receive data on 700 additional inspections, for a total of 3,800 state contract and partnership inspections in 2004. These inspections would include 100 percent of all known renderers and feed mills that process products containing prohibited materials.
FDA has an enormous responsibility in assuring that the products the Agency regulates which contain bovine materials are safe and uncompromised by BSE or other TSEs. FDA's principal line of defense in meeting this responsibility is to cut-off all avenues for the possible spread of BSE through U.S. cattle herds. Our most powerful tool in preventing the spread of BSE in U.S. cattle herds is effective enforcement of the Agency's feed ban restrictions as part of a multi-layered set of firewalls put in place as part of the U.S. Government's comprehensive BSE prevention program.
To date, a rigorous program of education, inspections, and enforcement education have enabled us to fulfill our responsibilities as part of the U.S. plan for preventing the spread of BSE. Although the risk of exposure to BSE in the United States remains extremely low and the measures in place are working, as a result of the recently discovered infected cow in the state of Washington, the Agency will be taking additional science-based steps to further strengthen our current protections.
FDA looks forward to continuing to assist Congress as it evaluates the risks associated with BSE, identifies opportunities to promote technologies that will detect and prevent the spread of BSE, and considers science-based approaches to further strengthen regulatory protections and bolster the resources available to assure that BSE does not present a threat to human or animal health in the U.S.
Thank you for the opportunity to testify today.
OH, that's right, old lester sold out to the highest bidder $$$
Ex-FDA Chief Faces Fines in Stock Case By ANDREW BRIDGES, Associated Press Writer 1:55 PM PST, January 19, 2007
WASHINGTON -- Former FDA Commissioner Lester Crawford would face a $50,000 fine and probation but no jail time as punishment for lying about ownership of illegally held stocks, according to a deal worked out between his attorney and federal prosecutors.
Crawford and the government both have agreed to the fine and some form of probation, though his ultimate sentence will be at the discretion of Magistrate Judge Deborah A. Robinson, according to sentencing memoranda filed with the U.S. District Court in Washington.
His sentencing is set for Tuesday.
Crawford pleaded guilty in October to charges of having a conflict of interest and false reporting of information about stocks he and his wife owned in food, beverage and medical device companies he regulated while head of the Food and Drug Administration.
The U.S. Attorney's office recommended the $50,000 fine, saying it would exceed the roughly $39,000 Crawford and his wife, Cathy, made from exercising options and in dividends from the forbidden stocks they held in the FDA-regulated companies.
The government also recommended Crawford be sentenced to probation and community service but skip any jail time, according to its sentencing memo filed with the court. Crawford could face up to six months in jail under sentencing guidelines.
"Given his early acceptance of responsibility, the defendant's actions merit the stigma of criminal convictions, a fine, and probation, but not incarceration," according to the government memo, signed by assistant U.S. attorneys Howard R. Sklamberg and Timothy G. Lynch. Sklamberg declined to comment Friday.
Crawford's attorney, Barbara Van Gelder, said her client agreed to pay the fine, according to her memo to the court. However, Van Gelder specifically requested unsupervised probation, which would allow Crawford to travel overseas for work. Van Gelder did not mention community service in her memo. She did not immediately return a message seeking comment.
In October, Crawford admitted to falsely reporting that he had sold or did not own stock when he continued holding shares in the firms governed by rules of the FDA, which is illegal. Beginning in 2002, Crawford filed seven incorrect financial reports with a government ethics office and Congress, leading to the misdemeanor charges.
Although Crawford lied about ownership of the stocks -- including under oath before the Senate -- government attorneys acknowledged there is no evidence he was "engaged in a concerted scheme to use his high office for personal gain."
Van Gelder, meanwhile, suggested Crawford's wife, secretary and financial adviser prepared and handled the inaccurate financial statements Crawford filed with the government. She acknowledged, however, that Crawford remained ultimately responsible for their accuracy.
Crawford, a veterinarian and food-safety expert, abruptly resigned from the FDA in September 2005 but gave no reason for leaving. He had held the job for two months, following his confirmation by the Senate.
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On the Net:
Food and Drug Administration: http://www.fda.gov
Date: October 18, 2006 at 7:44 am PST
Former FDA Commissioner Pleads Guilty to Conflict of Interest and Making False Financial Disclosures
WASHINGTON, Oct. 17, 2006 - Lester M. Crawford, a former Commissioner of the Food and Drug Administration (FDA), has pled guilty to a Conflict of Interest charge and Making False Financial Disclosures to the U.S. Senate and the Executive Branch, announced U.S. Attorney Jeffrey A. Taylor and Inspector General Daniel Levinson, U.S. Department of Health and Human Services.
Crawford entered his guilty plea to the two misdemeanor charges this afternoon in the U.S. District Court for the District of Columbia before U.S. Magistrate Judge Deborah Robinson. Crawford is scheduled to be sentenced on January 22, 2007. He faces a sentence of up to one year in prison on each charge.
"One of the most important principles of our ethics laws is that public officials cannot have a financial interest in any decision that they make," stated U.S. Attorney Taylor. "Lester Crawford, who held one of the most important jobs in government, blatantly violated these principles. Today, he is being held accountable for his actions."
Inspector General Levinson stated, "Any Government official's disregard of the conflict of interest laws undermines the integrity of the rules of conduct established for all those in Government. Taxpayers must have confidence that administrators of Government programs will be objective and free from improper influences in carrying out their official duties."
Crawford, 68, of Chevy Chase, Maryland, held some of the most senior positions in the FDA. He served as Deputy Commissioner between February 25, 2002 and March 26, 2004, when he became Acting Commissioner. On February 15, 2005, Crawford was nominated to become Commissioner. On July 18, 2005, the U.S. Senate confirmed Crawford, who remained Commissioner until September 30, 2005.
As a senior FDA employee, Crawford was required to file regular Public Financial Disclosure Reports, known as Standard Form SF 278s. Schedule A of the SF 278 required the filer to list all investment assets having a value exceeding $1,000 that were held by the filer or the filer's spouse, as well as sources of income exceeding $200 earned by the filer during the applicable reporting period.
Each year, ethics officials at the Department of Health and Human Services reviewed Crawford's SF 278s to ensure that he and his wife were not holding stocks or stock options of companies that were "significantly regulated organizations," which federal regulations defined as organizations for which the sales of products regulated by the FDA constitute ten percent or more of annual gross sales in the organization's previous fiscal year. Any FDA employee who was required to file an SF 278 could not hold a "financial interest," such as stock or stock options, in a significantly regulated organization.
Crawford's nomination as Commissioner required confirmation by the U.S. Senate and was considered by the Senate Committee on Health, Education, Labor, and Pensions. As a nominee, Crawford was required to submit two financial disclosure documents to the Committee: an SF 278 and a Statement for Completion by Presidential Nominees. Crawford filed both forms in February 2005.
Crawford's plea to Making False Writings is based on his failure to disclose his and his wife's ownership of stock in "significantly regulated organizations" to the Senate Committee and to the Executive Branch.
During the relevant time periods, Crawford and/or his wife owned forbidden stocks in the following "significantly regulated organizations": Pepsico, Sysco, Kimberly-Clark, and Embrex.
Crawford filed a number of disclosure forms and other false writings in which he did not declare his and his wife's ownership of forbidden stocks and stock options. Specifically,
•July 1, 2004. In this SF 278, Crawford disclosed ownership of Sysco and Kimberly-Clark stock. When an HHS ethics official inquired about Crawford's ownership of this stock, Crawford responded in a December 28, 2004 email that the stocks in "Sysco and Kimberly-Clark have in fact been sold." That statement was false.
• February 23, 2005. Crawford did not disclose on this SF 278 his income from a November 17, 2004 exercise of Embrex stock options or the Crawfords' ownership of Kimberly-Clark or Sysco stock.
• February 25, 2005. Crawford failed to disclose in his nominee Statement to the Senate Committee his income from the exercise of Embrex stock options in October 2003 and November 2004. Crawford also did not disclose his remaining Embrex stock options.
Crawford's ownership of Sysco and Pepsico stock and his role as Chairman of the FDA's Obesity Working Group ("OWG") gave rise to the Conflict of Interest charge, to which he has also pled guilty. On February 11, 2004, Crawford and the OWG's Vice Chairman submitted the OWG's final report and recommendations, entitled "Calories Count: Report of the Working Group on Obesity," to then-FDA Commissioner Mark McClellan. The report contained many recommendations, including encouraging manufacturers to re-label serving sizes, noting as an example that "a 20 oz bottle of soda that currently states 110 calories per serving and 2.5 servings per bottle could be labeled as 275 calories per bottle." The FDA publicly released "Calories Count" on March 12, 2004.
On June 3, 2004, Crawford testified before the House of Representatives Committee on Government Reform about the government's role in combating obesity. In his testimony, Crawford outlined the OWG's recommendations and again stressed the importance of re-labeling serving sizes for sodas.
During the entire period from the formation of the OWG to the date of Crawford's congressional testimony, Crawford and his wife owned 1,400 shares of Pepsico stock, worth a minimum of about $62,000, and 2,500 shares of Sysco stock, worth a minimum of about $78,000. Pepsico, a leading manufacturer of soft drinks and snack foods, and its shareholders had a financial interest in the OWG's conclusions and recommendations. Sysco, a leading manufacturer of food products, and its shareholders had a financial interest in the OWG's conclusions and recommendations.
There is no evidence that the OWG's conclusions were altered because of the Crawfords' ownership of Pepsico or Sysco stock.
Following the announcement of Crawford's departure from office, Senators Mike Enzi and Edward Kennedy and Representatives Maurice Hinchey, Marcy Kaptur, Lynn Woolsey, Raúl Grijalva, and Sam Farr asked that the Inspector General investigate this matter.
In announcing today's guilty plea, U.S. Attorney Taylor and Inspector General Levinson commended Inspector Thomas Sowinski of the Inspector General's office for his outstanding investigation of this case. They also thanked the Senate Legal Counsel's Office for the help that it provided in the investigation. Finally, they commended Assistant U.S. Attorneys Howard Sklamberg and Timothy Lynch, who prosecuted the case, and intern Vi Do, who assisted in the investigation.
For Information, Contact Public Affairs Channing Phillips (202) 514-6
SO, in essence, the fda simply hung a carrot out in front of the public, and the public bit. i ain't biting. it's all about money, to hell with human health ;
reminds me of ;
To minimise the risk of farmers' claims for compensation from feed compounders.
To minimise the potential damage to compound feed markets through adverse publicity.
To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.
MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.
5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.
6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...
SEE full text ;
Sunday, March 16, 2008
MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE
Sunday, April 20, 2008
Progress Report from the National Prion Disease Pathology Surveillance Center April 3, 2008
Creutzfeldt-Jakob Disease (Variant) and Bovine Spongiform Encephalopathy (Prion Diseases) Description Since 1996, strong evidence has accumulated for a causal relationship between ongoing outbreaks, primarily in Europe, of a disease in cattle called bovine spongiform encephalopathy (BSE, or "mad cow disease") and a disease in humans called variant Creutzfeldt-Jakob disease (vCJD). Both disorders, which are caused by an unconventional transmissible agent, are invariably fatal brain diseases with incubation periods typically measured in years (1). Transmission of the BSE agent to humans, leading to vCJD, is believed to occur via ingestion of cattle products contaminated with the BSE agent; the specific foods associated with this transmission are unknown. However, a recently published case-control study involving 132 vCJD cases in the United Kingdom (UK) showed evidence of an increased risk for vCJD associated with the frequency of consuming beef products likely to contain mechanically recovered meat and head meat (such as burgers, meat pies, and sausages) (2). Bioassays and molecular tests have enabled identification of what World Health Organization consultants have classified as "high-infectivity" and "lower infectivity" tissues of cattle with BSE (3). The high-infectivity tissues include the brain, spinal cord, retina, optic nerve, and dorsal root and trigeminal ganglia, suggesting that these tissues can pose a relatively high risk of transmission. The lower infectivity tissues include peripheral nerves (e.g., sciatic and facial nerves), tonsils, nictitating membrane (third eye lid), distal ileum, bone marrow, and possibly thigh muscle. The latter tissue from one cow with BSE transmitted disease to highly BSE-sensitive transgenic mice at a rate indicative of trace levels of infectivity.
Another Young Suspect Vcjd Case In Usa (3rd In Recent Weeks), TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY
THESE cases that have come about recently in the very young are most disturbing.
a 22 year old last week died, she is suspect nvCJD. never left US. PORTSMOUTH, Va. -- A 22-year-old Portsmouth woman is close to dying, and family says doctors believe the human equivalent of Mad Cow Disease could be the reason.
another young female suspect nvCJD that is 26 years old in Alabama, She is in the final stages of CJD. She is at home in a hospital bed...very skinny...and at times in the past month has had some eating and swallowing issues. Sometimes she rallies and starts eating again. She stopped walking at Christmas. they do not expect her to live much longer than May, since that would be 14 months since her first major symptom of CJD (personal communication).
AND now, a 3rd young female, 23 years old. hmmm, i am pondering about just how long all those downers were in the school lunch program, and IS the incubation period catching up now ??? is this a first of many more to come ???
see full text ;
Thursday, April 24, 2008
RE-FOIA OF DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E. OF FOREIGN ORIGIN IN THE UNITED STATES [Docket No. 00-072-1]
Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (TSS comment submission) P.S.2008 i see they have killed access to my submission. here was the original ;
-------- Original Message --------
Subject: Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission) Date: Sun, 11 Jul 2004 21:34:22 -0500 From: "Terry S. Singeltary Sr." To: email@example.com CC: email@example.com, email@example.com
No. 04-047-l
No. 04-021ANPR
No. 2004N-0264
Federal Measures to Mitigate BSE Risks: Considerations for Further Action
Greetings FDA, USDA and APHIS et al,
I would kindly like to comment on the continued delay of the regulations that have been proposed for years to reduce the risk of BSE/TSE in the USA. Each day that is wasted debating this issue allows this agent to spread, and many many more humans and animals become needlessly exposed to this agent via a multitude of potential routes and sources right here in the USA. TO continue to ignore the new findings from several scientists about the fact that BSE is not the only strain of TSE in cattle, the fact that new atypical strains of TSE are showing up in not only cattle, but sheep and the fact that the new strain of TSE in cattle seems to be more similar to sporadic CJD as opposed to the nv/v CJD, to continue to ignore these findings will only further spread this agent.
CWD and Scrapie have been running rampant in the USA for decades. BOTH of which have been rendered and fed back to animals for human/animal consumption for decades. All of which transmits to primates by the natural and non-forced oral consumption of TSE scrapie, CJD, Kuru agent (and CWD by inoculation).
Strong Scientific evidence discovered back in the 80s support the fact that a TSE has been prevalent in the USA bovine for decades, either undetected or ignored. IF you consider the recent stumbling and staggering TEXAS cow that was showing all signs of a CNS/TSE disorder that was ordered to be rendered without BSE/TSE test, brains, spinal cord, head and all (as to no possible evidence left of TSE), I would think the 'ignored' or 'covered up' to be the better terminology. Then you have the Downer in Washington state that was actually a good walker and then all the banned Canadian products that some how found it's way across the border into the USA, considering all this, it is very difficult for me to believe that the FDA/USDA/APHIS et al are doing everything possible to protect the 'consumer'. Hardly the case;
Congressman Henry Waxmans Letter to the Honorable Ann Veneman http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf
-------- Original Message -------- Subject: Re: Congressman Henry Waxmans Letter to the Honorable Ann Veneman on failure by USDA/APHIS TO TEST TEXAS MAD COW Date: Wed, 9 Jun 2004 16:48:31 -0500 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: firstname.lastname@example.com References: <email@example.com>
######## Bovine Spongiform Encephalopathy #########
October 1998
BSE Red Book 2.1-36
188.8.131.52 Laboratory Coordination--The Laboratory Coordination Officer will advise the READE(3 Director concerning laboratory capabilities and appropriate laboratory examinations to be conducted to provide needed results as rapidly as possible. This individual will assist with interpretation of results.
seems that if the 'enhanced BSE/TSE testing program' is to test some 400,000+ animals in 1 1/2 years, they better hurry up, times a wasting.
BSE Red Book 2.1-39
7.6 Depopulation Procedures
Under no circumstances may BSE suspects be sent fo slaughhter or rendering.
BSE Red Book 2.1-40
7.7 Disposal Under no circumstances may BSE suspects be sent to slaughter or rendering. Notify FDA, CVM if you suspect that the carcass of a BSE-confirmed animal has moved to rendering or animal feed manufacturing. Field personel should arrange for the carcass to be transported to and examined by a qualified veterinary pathologist or field veterinary medical officer. After the pathologic examination has been completed and the necessary diagnostic specimens have been obtained, field personnel should arrange for disposal of the carcass. Before a method of disposal is selected, there are many factors that must be considered, and often other State and Federal agencies must be consulted. The environmental and legal impacts of the operation must be considered. Upon recommendation of the State or Federal agencies, VS may consider other disposal methods.
7.7.3 Rendering Because BSE is spread by rendered animal protein, BSE-suspect and confirmed carcasses must not be rendered, unless the rendered material is incinerated. Notify FDA, CVM if you suspect that dead BSE animals or carcasses have moved to rendering or animal feed manufacturing.
7.10.11 Prevention--Suspects and animals confirmed to have BSE must not be rendered. Producers, feed mills, and rendering establishments should adhere to U.S. State and local rendering policies and FDA regulations concerning the feeding of rendered animal protein to ruminants.
Terry S. Singeltary Sr. wrote:
######## Bovine Spongiform Encephalopathy #########
May 13, 2004
The Honorable Ann M. Veneman Secretary of Agriculture Department of Agriculture 1400 Independence Avenue, SW Washington, DC 20250
Dear Madam Secretary:
1 am writing to express concern that the recent failure of the U.S. Department of Agriculture (USDA) to test a Texas cow with neurological symptoms for bovine spongiform encephalopathy (BSE) may reflect wider problems in the surveillance program. USDA apparently does not keep track of how many cows condemned for central nervous system symptoms are tested for BSE nor does it require that suspect carcasses be held pending testing. Effective surveillance and control of BSE in the United States require a reliable system for ensuring that potentially infected cows are tested and that no infected materials enter the animal or human food supply.
Under USDA regulations, any cow that exhibits signs of central nervous system (CNS) problems must be condemned by Food Safety Inspection Service (FSIS) personnel at the plant.1 According to a 1997 Animal and Plant Health Inspection Service (APHIS) Memorandum, brain samples all of such animals should be sent for BSE testing.2 The memorandum notes that "[i]t is essential that brain specimens be collected from adult cattle condemned for CNS signs as part of our national surveillance of BSE."3
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
2 USDA APHIS, Veterinary Services Memorandum No. 580.16. Procedures/or Investigation of Adult Cattle With Clinical Signs of Central Nervous System (CNS) Disease and Procedures for Surveillance of Downer Cows for Bovine Spongiform Encephalopathy (BSE) (June 11,1997).
3 Id.
4 U.S. Confirms a Failure to Use Mad Cow Test, Wall Street Journal (May 4, 2004).
The Honorable Ann M. Veneman May 13,2004 Page 2
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:
Based on information provided by the Food Safety and Inspection Service (FSIS), the number of adult cattle (2 years of age or greater) condemned at slaughter due to CNS signs is much greater than the number whose brains have been collected for testing.6
Despite recognizing the problem more than six years ago, however, USDA apparently did not adopt procedures to ensure that these samples would be collected. In March 2004, the Government Reform Committee asked USDA to provide, for each of the last five years, the number of BSE tests performed on cattle condemned by FSIS inspectors on the basis of CNS symptoms.7 In response, USDA provided information on the numbers of cattle condemned for CNS symptoms by FSIS, but replied that "[i]t is not possible to determine, from the data we currently collect, how many of these cattle were tested by APHIS for BSE."8 It thus appears that not only does USDA not routinely track the gap between the number of condemned and tested cattle, but that USDA could not even calculate this gap when requested to do so by Congress.
There also appears to be a lack of clarity regarding the disposition of cattle with CNS symptoms while BSE tests are pending. In the past, companies could send cattle awaiting BSE testing results for rendering, which would allow their remains to be used in feed for animals other than ruminants, such as pigs and chickens. After this incident, both FDA and USDA policy appear to have changed in different ways.
USDA policy has apparently shifted to requesting that companies not send cattle to rendering while awaiting test results. A May 5, 2004 memo from APHIS states, "it is requested though not required that [the cattle] not go to inedible rendering until the sample comes
USDA's San Angelo Vets and Techs Ordered Not to Test Suspect Cow, Meating Place (May 5, 2004).
6 USDA APHIS, supra note 2.
7 Letter from Rep. Tom Davis and Rep. Henry A- Waxman to Secretary of Agriculture Ann M. Veneman (Mar. 8, 2004).
8 Letter from Ronald F. Hicks, Assistant Administrator, Office of Program Evaluation, Enforcement, and Review- FSIS. to Reo. Henrv A. Waxman- Attachment 1 (Mar. 22- 2004).
The Honorable Ann M. Veneman May 13,2004 Page 3
back negative."9 There is no explanation of why this course of action is requested, but not required.
FDA policy also appears to have shifted towards prohibiting the use of carcasses of cattle with CNS symptoms and indeterminate BSE status in certain types of animal feed. On April 30, FDA requested that the rendering company holding the remains of the Texas cow either destroy them or use them exclusively in swine feed. m the case that the remains are included in swine feed, 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."10
Any confusion over what to do with cattle condemned for CNS symptoms awaiting testing for BSE seems unnecessary. The obvious approach is to require companies either to destroy the carcasses or hold them until test results become available. Such a policy would avoid any need for complicated traceback procedures after the discovery of a positive result. According to the information provided to the Committee by USDA, the FSIS has condemned only 200 to 250 cows per year because of signs of central nervous system damage." Mandating the destruction or holding of their carcasses would have minimal economic impact.
The experience with the BSE-infected cow in Washington State illustrates the prudence of waiting for the results of BSE tests. Prior to December 2003, USDA permitted cattle that were sampled as part of the BSE surveillance program to enter commerce even while BSE tests were pending. As a result, when the BSE-infected cow was discovered, it had already entered the food supply. This led to a complicated and partially successful traceback procedure in which hundreds of thousands of pounds of beef had to be destroyed. Because of this debacle, USDA quickly developed a new policy to require holding all carcasses from the human food chain during BSE testing.
I appreciate that you have taken steps to enhance the safety of the U.S. food supply since the discovery of BSE in the United States. I urge you to consider the lessons of this latest
9 Memo from John R. Clifford, Acting Deputy Administrator, Veterinary Services, and William Smith, Assistant Administrator, Office of Field Operations, Food Safety and Inspection Service, to VSMT, Regional Directors, Area Veterinarians in Charge, and Veterinary Services, Subject: Policy Statement Regarding BSE Sampling of Condemned Cattle at Slaughter Plants - for Immediate Implementation (May 5, 2004) (online at http://www.aphis.usda.gov/lpa/issues/bse/BSE_APHIS-FSIS.pdf).
10 FDA, Statement on Cow -with Central Nervous System Symptoms (Apr. 20, 2004) (online at http://www.fda.gov/bbs/topics/news/2004/NEW01061.html).
11 The yearly totals of FSIS antemortem CNS condemnation for all adult cattle were 233 (1999), 220 (2000), 201 (2001), 249 (2002), and 247 (2003). The database for 2003 had not yet closed.
The Honorable Ann M. Veneman May 13,2004 Page 4
incident. USDA should develop a process that ensures the tracking of cattle condemned for CNS signs and should institute a policy requiring all carcasses with pending BSE tests to be destroyed or held. If there are any statutory barriers to these steps, please do not hesitate to let me know.
Henry A. Waxman Ranking Minority Member
Congressman Henry Waxmans's Letter to the Honorable Ann Veneman http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_may_13_let.pdf
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NOW, after being told that last year that strict TSE guidelines would be put into place to plug any leaks in the triple TSE fire walls that have been leaking, we see again the same old industry backed rhetoric 'protect the industry at all cost', and again, measures to protect the American consumer from a horrible disease has been set back due to corporate greed. OF course it was said long ago;
It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US...
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_...
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.
DUE to the new 'atypical' TSEs showing up in different species, it is paramount that removing specified risk materials (SRMs) from all animal feed, including pet food, in order to control the risks of cross contamination throughout feed manufacture and distribution and on the farm due to misfeeding is a no brainer. FAILING to do this will only continue to spread this agent.
AGAIN, due to the findings of new 'atypical' TSEs showing up in different species, we must require dedicated equipment or facilities for handling and storing feed and ingredients during manufacturing and transportation, to prevent cross contamination. WE must not let the industry and politics dictate science.
BASE in cattle in Italy of Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease
Identification of possible animal origins of prion disease in human beings
A further comparison6 of BASE with sCJD in people revealed that, at least in terms of PrPSc characteristics, BASE was similar to a particular type of sCJD sCJD(MV2) (figure). These researchers conclude not only that BASE is a new strain of BSE, but also that characteristics of human and animal PrPSc could help to identify potential risk factors for disease in individuals with sCJD of unknown origin.
THE LANCET " Vol 363 " June 19, 2004 " www.thelancet.com 2013
Characterization of two distinct prion strains derived from bovine spongiform encephalopathy transmissions to inbred mice S. E. Lloyd, J. M. Linehan, M. Desbruslais, S. Joiner, J. Buckell, S. Brandner, J. D. F. Wadsworth and J. Collinge J Gen Virol 2004 85 (8): p. 2471-2478
J Gen Virol -- Future Table of Contents Alert (not yet published...TSS)
Journal of Virological Methods 117 (2004) 2736 Atypical scrapie cases in Germany and France are identified by discrepant reaction patterns in BSE rapid tests A. Buschmanna, A.-G. Biacabe b, U. Ziegler a, A. Bencsik b, J.-Y. Madecb, G. Erhardt c, G. Lühken c, T. Baron b, M.H. Groschup a,? a Federal Research Centre for Virus Diseases of Animals, Institute for Novel and Emerging Infectious Diseases, Boddenblick 5a, 17493 Greifswald-Insel Riems, Germany b AFSSA-Lyon Unité Virologie-ATNC, 31 Avenue Tony Garnier, 69364 Lyon Cedex 07, France c Department of Animal Breeding and Genetics, Justus-Liebig University Giessen, Ludwigstr. 21B, 35390 Giessen, Germany Received 27 August 2003; received in revised form 13 November 2003; accepted 18 November 2003 Abstract The intensified surveillance of scrapie in small ruminants in the European Union (EU) has resulted in a substantial increase of the number of diagnosed cases. Four rapid tests which have passed the EU evaluation for BSE testing of cattle are also recommended currently and used for the testing of small ruminants by the EU authorities. These tests include an indirect ELISA (cELISA), a colorimetric sandwich ELISA (sELISA I), a chemiluminescent sandwich ELISA (sELISA II), and a Western blot (WB). To this point, the majority of samples have been screened by using either sELISA I (predominantly in Germany) or WB (predominantly in France). In this study, it is shown that a number of the German and French scrapie cases show inconsistent results using rapid and confirmatory test methods. Forty-eight German sheep, 209 French sheep and 19 French goat transmissible spongiform encephalopathy (TSE) cases were tested. All cases were recognised by the sELISA I and either one of the confirmatory methods (scrapie-associated fibrils (SAF)-immunoblot or immunohistochemistry). Surprisingly, three rapid tests failed to detect a significant number of scrapie cases (29 in France and 24 in Germany). The possible reasons for these inconsistent reaction patterns of scrapie cases are discussed. Similar discrepancies have not been observed during rapid testing of cattle for BSE, the disease for which all diagnostic methods applied have been evaluated. © 2003 Elsevier B.V. All rights reserved. Keywords: Scrapie; Prion protein; Rapid test; Confirmatory method 1. Introduction
4. Discussion Since the spring of 2002, rapid tests are being used for active surveillance of scrapie in the national sheep herds of the EU member states. These tests have been approved by the European commission and they include a colorimetric sandwich ELISA, a luminescence sandwich ELISA, an indirect ELISA using chemiluminescence as well as a rapid Western blotting assay. According to EU legislation (EC regulation 999/2001 and amendments), rapid tests are only approved for screening brain samples. In case of a reactive result, the sample has to be examined in the national reference laboratory using one of the OIE approved confirmatory methods which are SAF-immunoblotting and immunohistochemistry. The introduction of this active surveillance programme in the EU using BSE rapid tests demonstrated that scrapie in small ruminants is much more prevalent than had been previously estimated. Moreover, we found that not all scrapie cases are detected equally well by the four applied rapid tests as a significant portion of the samples were found positive with the sELISA I test but were not reactive with the rapid WB and sELISA II. The cELISA could only be used on a rather small number of samples, however, it must be assumed from the available results that it shows a performance similar to that of the rapid WB and sELISA II. Although some of the sELISA I results were weak positive, all cases that were initially detected using this method were confirmed by using OIE-recommended methods. It is therefore concluded that the sELISA I results are true positive, whereas the rapid WB, sELISA II and cELISA results of the same samples must be considered as false negative. This of course presupposes that the currently applied con- firmatory methods do not produce any false positive results. All samples that were first detected by using the rapid WB also gave positive results using the other rapid test methods. This observation supports the hypothesis that the rapid WB fails to detect certain positive sheep. Regrettably, it was not feasible during this study to retest small ruminant field samples that had initially been negative in the rapid WB with the sELISA I test in order to check if any positive samples had been ignored during the first screening. Non-uniform rapid test results were reproducible when selected coded samples were exchanged between the German and French national TSE reference laboratories and the samples were repeatedly positive in the sELISA I. Furthermore, it should be emphasised that the reactivity using this test was generally high (more than four times the cut-off level in most cases), showing that negative results obtained with other methods cannot be explained by threshold levels of protease resistant prion protein in these particular samples alone. Brainstem samples collected in abattoirs and rendering plants do not always fulfill the desired diagnostic quality standards in terms of freshness and in sampling localisation. In the beginning, we therefore could not exclude the possibility that single incongruent test results were due to varying PrPSc concentrations in the brainstems. However, the large number of such samples and the variety of the sample histories argue against such artefacts. However, such effects may explain why a few cases were negative by immunohistochemistry, but positive by SAF-immunoblotting, a diagnostic method where PrPSc is concentrated from larger brain areas. These 53 atypical scrapie cases in France and Germany out of a set of 276 may represent a novel strain of this disease in the field. Similar observations have also been made by the Norwegian National TSE Reference Laboratory, where some sheep scrapie samples were not reactive using the rapid WB (Benestad et al., 2003). However, not all characteristics described for those Nor98 designated cases match the atypical scrapie cases reported here. In particular, all Nor98 cases display a strong signal at 12 kDa that seems to be absent in a number of the German and French cases. We therefore postulate that at least three different scrapie phenotypes A. Buschmann et al. / Journal of Virological Methods 117 (2004) 2736 35 (typical scrapie and two atypical strains) exist within the European sheep flock. To determine critical factors affecting the rapid WB detection of PrPSc, we undertook a series of exchange experiments. The detection of atypical cases was improved after replacing the rapid WB homogenisation buffer supplied within the testkit of which the composition is undisclosed by an in-house homogenisation buffer containing desoxycholate and NP40 as detergents. Attempts were also made to replace the proteinase K solution, the detection antibody (by mab L42 that is directed to the same epitope as mab 6H4), and the conjugate antibody. Although no single critical step was revealed that alone enabled the detection of samples, these modifications altogether led to positive results for almost all atypical samples. It became also evident that minor changes in the sample treatment may have major effects when the modified SAF-immunoblotting technique was applied: while some of the atypical samples were negative with this method in which the first ultracentrifugation step is omitted and PK digestion is performed prior to SAF preparation, the same samples became clearly positive when the other SAF preparation protocol was applied. However, the physiochemical characteristics of ovine PrPSc derived from different scrapie isolates that are the basis for the observed effects still need further research efforts. PrP molecules derived from animals affected with different TSE strains vary in their cleavage sites for proteinase K digestion and therefore display different molecular weights when analysed in immunoblot (Hill et al., 1998; Baron et al., 2000; Stack et al., 2002). For example, the N-terminus of PrP derived from BSE-affected sheep is digested further by proteinase K than PrP derived from scrapie-affected sheep and therefore leads to a residual PrP of a lower molecular mass. This effect has been proposed as a possible diagnostic marker to differentiate between BSE and scrapie infections in sheep. Our experiments showed that this variation in the PK cleavage site between scrapie and BSE in sheep has no impact on the performance of the rapid tests on ovine BSE PrPSc since all commercial rapid tests detect PrPSc derived from experimentally BSE infected sheep of the PrPARQ/ARQ genotype (data not shown). Moreover, WB and sELISA II use the same monoclonal antibody (mab 6H4; Korth et al., 1997) which binds to an epitope far away from the PK cleavage site (aa 144148) and would therefore not be expected to react differently with scrapie- and BSE-derived PrPSc. The same is the case with the French immunoblot test that uses mab SAF 84 (Demart et al., 1999), binding to an epitope in the same region of the protein (aa 125163). No information is available on the PrP epitopes that are targeted in the sELISA I and cELISA. TSE infectivity can only be confined reliably, to date, by transmission experiments to an appropriate host. As it cannot be ruled out completely at this stage that non-infectious PrPC may also form intracellular aggregates with increased protease resistance and hydrophobicity that may lead to false positive results in diagnostic tests, the level of infectivity of such atypical cases is currently being examined by inoculation into RIII, C57B1 and VM95 mice. In case of a transmission to these mouse strains, the lesion profile scores will be determined and PrPSc will be analysed concerning its glycotype and PK resistance. The use of rapid tests for small ruminants was introduced by the EU Commission on the basis of their successful evaluation for BSE testing in cattle (Moynagh and Schimmel, 1999) in order to achieve an overview of the scrapie prevalence in the EU. Unfortunately, no independent evaluation has been performed in the EU to date to reveal the individual rapid tests performance on small ruminant scrapie cases. Therefore, their specificity and sensitivity for this use can only be estimated by the results of samples selected randomly that have been tested individually by the manufacturers. Inconsistencies in the ability of rapid tests to identify positive cases would question the current efforts to intensify and standardise the scrapie surveillance in the EU member states. Our data show that the actual numbers of scrapie cases and the prevalence of scrapie may be seriously underestimated in countries where rapid tests that may produce false-negative results are used. In the German epidemiosurveillance scheme for scrapie, the sELISA I is applied for testing of more than 80% of the samples, while in France 60% of the samples are tested with the rapid WB. Therefore, it must be accepted that the current EU-wide epidemiosurveillance programme can only give a general impression of the scrapie situation but may miss on average up to 12% of the true number of German scrapie cases and up to 16% of the French cases (estimated numbers take into account the applied test methods and the numbers of atypical cases since 2002). This must be kept in mind when scrapie prevalence data obtained by BSE rapid testing are interpreted. Acknowledgements We wish to acknowledge Matthias Kramer and Sandra Göbel (FRCVDA-Wusterhausen, Germany) and Didier Calavas (AFSSA-Lyon, France) for epidemiological data, Bertrand Bedhom (LABOGENA, France) for genotype analysis of French scrapie cases and J. Grassi (C.E.A.-Saclay, France) for supply of SAF 70 and SAF 84 antibody. This work was partly funded by the German Ministry of Consumer Protection, Nutrition and Agriculture (BMVEL). References
Vet Pathol -- Ersdal et al. 40 (2): 164
... up PrP rapidly at a young age, as Heggebø et al. ... Ersdal, MJ Ulvund) and 133449/111 (SL Benestad) from the ... Vet Rec 147:439-441, 2000[ISI][Medline]; Bendheim PE ... http://www.vetpathology.org/cgi/content/full/40/2/164 -
[PDF] Accumulation of Pathogenic Prion Protein (PrP ) in Nervous and ...
File Format: PDF/Adobe Acrobat ... 166 Vet Pathol 40:2, 2003 Ersdal, Ulvund, Benestad, and Tranulis ... RPLN Ileum Lambs RPLN DJLN Ileum Spleen F89/160.1.5 L42 R521 R505 ORourke et al. ... http://www.vetpathology.org/cgi/reprint/40/2/164.pdf -
[PDF] SCIENTIFIC PAPERS File Format: PDF/Adobe Acrobat ... 2003 Mar- 2003 Mar 31; 34(2):185-92. SEAC/SCI/79/17 Ersdal C, Ulvund MJ, Benestad SL, Tranulis MA. ... Vet Rec. ... SEAC/SCI/79/25 He L, Lu XY, Jolly AF et al. ... http://www.seac.gov.uk/papers/SEAC-SCI-79.pdf -
SCRAPIE - NORWAY: NEW PHENOTYPE ***************************************** A ProMED-mail post
ProMED-mail, a program of the International Society for Infectious Diseases
Date: 16 Nov 2003 From: Terry Singletary Source: The Veterinary Record, 16 Aug 2003 [edited]
[With new information, it appears there is potentially a new phenotype of atypical' BSE/TSE in animals in Japan and France. The article below indicates a new strain of Scrapie, the 'Nor98', which also has negative IHC and histology. Although this article does not suggest a link to the atypical forms seen in cattle, it does seem more than coincidence that there are also appearing different strains, or perhaps atypical strains of scrapie as well. It has been believed for years that there is a link between BSE and scrapie; perhaps this is another bit of research that should be carefully examined. Mod.TG]
Cases of scrapie with unusual features in Norway and designation of a new type, Nor98. The Veterinary Record, 16 August 2003, vol. 153, no. 7, pp. 202-208(7) Benestad S.L.; Sarradin P.; Thu B.; Schonheit J.; Tranulis M.A.; Bratberg B.
Abstract: 5 cases of scrapie with unusual features have been diagnosed in Norway since 1998. The affected sheep showed neurological signs dominated by ataxia, and had the PrP genotypes homozygous A136 H154 Q171/ A136H154Q171 or heterozygous A136H154Q171/A136R154Q171, which are rarely associated with scrapie. Brain histopathology revealed neuropil vacuolisation essentially in the cerebellar and cerebral cortices; vacuolation was less prominent in the brainstem, and no lesions were observed at the level of the obex. The deposits of PrPSc were mainly in the cortex of the cerebellum and cerebrum, and no PrPSc was detectable by immunohistochemistry or ELISA in the lymphoid tissues investigated.
Western blot analysis showed that the glycotype was different from other known scrapie strains and from the BSE strain. From a diagnostic point of view, these features indicate that this type of scrapie, designated Nor98, could have been overlooked and may be of significance for sampling in scrapie surveillance programmes.
Document Type: Research article ISSN: 0042-4900
DOI (article): NO_DOI SICI (online): 0042-4900(20030816)153:7L.202;1- Publisher: BVA Publications
-- ProMED-mail
NOT to forget the 'atypical' VERMONT USA' sheep scrapie/BSE/TSE? back in 2000 with the testing conveniently ignored and put off once again with animal TSEs. Why I ask?
IN the year 2000, some sheep in Vermont were confiscated due to what the USDA/APHIS said was an 'atypical TSE'.
WE were told there would be additional testing to confirm exactly what TSE we were dealing with;
Release No. 0141.02
Ed Curlett (301) 734-3256 Jerry Redding (202) 720-6959
WASHINGTON, April 11, 2002 -- The U.S. Department of Agriculture today announced that tests conducted on a flock of sheep confiscated last year from a farm in Vermont confirm that two of the 125 sheep tested positive for an atypical undifferentiated transmissible spongiform encephalopathy (TSE) of foreign origin. The flock of 125 sheep was confiscated in March 2001 after four animals from an associated flock tested positive for TSE in July 2000. USDA will continue to conduct additional tests to determine the type of TSE in these sheep.
"These results confirm our previous conclusions were correct and that we took the appropriate preventative actions in confiscating these animals," said Bobby Acord, administrator of USDAs Animal and Plant Health Inspection Service. "USDAs actions to confiscate, sample and destroy these sheep were on target. As a result of our vigilance, none of these confiscated animals entered the animal or human food supply."
The sheep, imported from Belgium and the Netherlands in 1996, were placed under certain federal restrictions when they entered the country as part of USDA's scrapie control efforts. In 1998, USDA learned that it was likely that sheep from Europe were exposed to feed contaminated with bovine spongiform encephalopathy. At that time, the state of Vermont, at the request of USDA, imposed a quarantine on these flocks, which prohibited slaughter or sale for breeding purposes.
On July 10, 2000, several sheep from the flock tested positive for a TSE, a class of degenerative neurological diseases that is characterized by a very long incubation period and a 100 percent mortality rate in infected sheep. Two of the better known varieties of TSE are scrapie in sheep and BSE in cattle. There is no evidence that scrapie poses a risk to human health.
On July 14, 2000, USDA issued a declaration of extraordinary emergency to acquire the sheep. This action was contested by the flock owners. A federal district court judge ruled in favor of USDA based on the merits of the case. The flock owners appealed to the Second Circuit Court requesting a stay, which was denied. The sheep were confiscated by USDA in March 2001 and transported to USDA's National Veterinary Services Laboratories in Ames, Iowa, where they were humanely euthanized. Tissue samples were collected from the sheep for diagnostic testing and USDA will continue with additional tests which could take up to 2 - 3 years to complete. In all, USDA has acquired 380 sheep from a total of three flocks. All of the animals were humanely euthanized, sampled and disposed and did not enter the animal or human food supply.
Our goal continues to be to prevent, detect and eradicate foreign animal diseases to protect American agriculture, natural resources and consumers," said Acord. "We will continue to utilize the scientific results of these and other tests conducted during the last several years to strengthen our extensive surveillance, monitoring and prevention efforts."
For more information about USDAs ongoing surveillance, monitoring and prevention efforts as it relates to this situation, please visit www.aphis.usda.gov/oa/tse/index.html
NOW, June 2004 those same test that we were told would start in 2002, have yet to be started. THE TSE those VERMONT sheep was supposedly to have had, has yet to be confirmed.
IGNORING the fact Scrapie does transmit to primates by their non forced consumption of known infectious scrapie tissues.
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.
IGNORING the fact Scrapie transmission studies have never been done on man.
IGNORING the fact surveillance for TSE in man in the USA and other places around the globe is terribly under funded and lacking in guidance. to date some 25 states make it reportable, with some states having an age bracket only documenting the younger victims. leaving the door open to spread the agent through the medical and surgical arena.
With the recent announcement of the UK contingency plan for the emergence of naturally occurring BSE in sheep June 2004, and the terrible implications for human health this would cause, full text some 31 pages;
you would have thought that this would have been at the top of someone's priority list. However, it does not look that way.
I ask again, WHY?
I wish to submit the following;
-------- Original Message --------
Subject: Re: AW: [BSE-L] USDA did not test possible mad cows - Dr. Detwiler, what about those sheep? Date: Sun, 13 Jun 2004 11:27:24 -0500 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To: firstname.lastname@example.com References: <email@example.com> <firstname.lastname@example.com>
######## Bovine Spongiform Encephalopathy #########
Greetings list members,
Thought I should let the list know that Dr. Detwiler kindly replied to my question about the delayed 'atypical' TSE testing in the Vermont sheep and tried to explain what caused the delay. If I interpreted it correctly, seems it was the fault of the U.K. ;
-------- Original Message -------- Subject: Sheep Date: Sat, 12 Jun 2004 14:26:04 EDT From: firstname.lastname@example.com To: email@example.com
Mr. Singeltary.
I hope this finds you well. As you are aware I left the USDA last year. I can only update you on the sheep before that time. Contact was established with the UK on doing the bioassay studies. They agreed. However, we were prioritized after their own needs, hence the delay. I am aware that there are now additional labs in Europe running the mouse bioassay strain typing. You will have to contact USDA for further word.
Linda Detwiler =========
My reply to Dr. Detwiler;
-------- Original Message -------- Subject: Re: Sheep Date: Sat, 12 Jun 2004 13:53:57 -0500 From: "Terry S. Singeltary Sr." To: email@example.com References: <firstname.lastname@example.com>
hello Dr. Detwiler,
thanks for your kind reply.
However, we were prioritized after their own needs, hence the delay.
not sure i understand that?
You will have to contact USDA for further word.
already done that, and there answer was;
Dear Mr. Singeltary,
The Western blot tests on these animals were completed in April of this year. That means that we can begin the mouse inoculations. To get the results of the Western blot tests, you will need to submit a Freedom of Information Act request through our FOIA office. The FAX number there is 301-734-5941.
Have a nice day,
Jim Rogers APHIS LPA
and with my previous attempts for information via the FOIA through this administration (as you are probably very well aware of) they have all been ignored/refused. so any further attempts would be fruitless i am sure.
thanks anyway...
kindest regards, Terry
firstname.lastname@example.com wrote:
Mr. Singeltary.
Terry S. Singeltary Sr. wrote:
######## Bovine Spongiform Encephalopathy #########
Greetings Dr. Detwiler,
glad to see you are still with us, you had become very silent lately. hope you are enjoying semi retirement.
recently, i inquired through the BSE-L and via USDA official about those Vermont sheep via belgium which there was an Extraordinary Declaration of Emergency declared here in the USA due to atypical scrapie. The thread is;
Confiscation of Sheep in Vermont and testing results ? Thu, 20 May 2004 12:10:03 -0500 "Terry S. Singeltary Sr." Bovine Spongiform Encephalopathy BSE-L
Imported Belgium/Netherlands Sheep Test Results Background Factsheet Veterinary Services April 2002 APHIS
Additional tests will be conducted to determine exactly what TSE the animals haveBSE or scrapie. These tests involve the use of bioassays that consist of injecting mice with tissue from the infected animals and waiting for them to develop disease. This testing may take at least 2 to 3 years to complete.
or if those old urls dont work, go here;
DECLARATION OF EXTRAORDINARY EMERGENCY BECAUSE OF AN ATYPICAL T.S.E (PRION DISEASE) OF FOREIGN ORIGIN IN THE UNITED STATES - Terry S. Singeltary Sr. 7/20/00 (0)
[Federal Register: July 20, 2000 (Volume 65, Number 140)] [Notices] [Page 45018] >From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr20jy00-32]
Office of the Secretary
[Docket No. 00-072-1]
Declaration of Extraordinary Emergency Because of an Atypical Transmissible Spongiform Encephalopathy (Prion Disease) of Foreign Origin
A transmissible spongiform encephalopathy (TSE) (prion disease) of foreign origin has been detected in the United States. It is different from TSE's previously diagnosed in the United States. The TSE was detected in the progeny of imported sheep. The imported sheep and their progeny are under quarantine in Vermont. Transmissible spongiform encephalopathies are degenerative fatal diseases that can affect livestock. TSE's are caused by similar, as yet uncharacterized, agents that usually produce spongiform changes in the brain. Post-mortem analysis has indicated positive results for an atypical TSE of foreign origin in four sheep in Vermont. Because of the potentially serious consequences of allowing the disease to spread to other livestock in the United States, it is necessary to seize and dispose of those flocks of sheep in Vermont that are affected with or exposed to the disease, and their germ plasm. The existence of the atypical TSE of foreign origin represents a threat to U.S. livestock. It constitutes a real danger to the national economy and a potential serious burden on interstate and foreign commerce. The Department has reviewed the measures being taken by Vermont to quarantine and regulate the flocks in question and has consulted with appropriate officials in the State of Vermont. Based on such review and consultation, the Department has determined that Vermont does not have the funds to compensate flock owners for the seizure and disposal of flocks affected with or exposed to the disease, and their germ plasm. Without such funds, it will be unlikely to achieve expeditious disposal of the flocks and germ plasm. Therefore, the Department has determined that an extraordinary emergency exists because of the existence of the atypical TSE in Vermont. This declaration of extraordinary emergency authorizes the Secretary to seize, quarantine, and dispose of, in such manner as he deems necessary, any animals that he finds are affected with or exposed to the disease in question, and their germ plasm, and otherwise to carry out the provisions and purposes of the Act of July 2, 1962 (21 U.S.C. 134-134h). The State of Vermont has been informed of these facts.
Dated: This declaration of extraordinary emergency shall become effective July 14, 2000. Dan Glickman, Secretary of Agriculture. [FR Doc. 00-18367 Filed 7-19-00; 8:45 am] BILLING CODE 3410-34-P
http://frwebgate.access.gpo.gov/cgi-bin/getdoc.cgi?dbname= 2000_register&docid=fr20jy00-32 ================================ [Federal Register: July 20, 2000 (Volume 65, Number 140)] [Notices] [Page 45018] >From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr20jy00-31]
======================================================================== Notices Federal Register ________________________________________________________________________
This section of the FEDERAL REGISTER contains documents other than rules or proposed rules that are applicable to the public. Notices of hearings and investigations, committee meetings, agency decisions and rulings, delegations of authority, filing of petitions and applications and agency statements of organization and functions are examples of documents appearing in this section.
[[Page 45018]]
Office of the Secretary
[Docket No. 00-072-2]
Declaration of Emergency Because of an Atypical Transmissible Spongiform Encephalopathy (Prion Disease) of Foreign Origin
A transmissible spongiform encephalopathy (TSE) (prion disease) of foreign origin has been detected in the United States. It is different from TSE's previously diagnosed in the United States. The TSE was detected in the progeny of imported sheep. The imported sheep and their progeny are under quarantine in Vermont. Transmissible spongiform encephalopathies are degenerative fatal diseases that can affect livestock. TSE's are caused by similar, as yet uncharacterized, agents that usually produce spongiform changes in the brain. Post-mortem analysis has indicated positive results for an atypical TSE of foreign origin in four sheep in Vermont. Because of the potentially serious consequences of allowing the disease to spread to other livestock in the United States, it is necessary to seize and dispose of those flocks of sheep in Vermont that are affected with or exposed to the disease, and their germ plasm. The existence of the atypical TSE of foreign origin represents a threat to U.S. livestock. It constitutes a real danger to the national economy and a potential serious burden on interstate and foreign commerce. APHIS has insufficient funds to carry out the seizure and disposal of animals and germ plasm necessary to eliminate this disease risk. These funds would be used to compensate the owners of the animals and germ plasm for their seizure and disposal in accordance with 21 U.S.C. 134a. Therefore, in accordance with the provisions of the Act of September 25, 1981, as amended (7 U.S.C. 147b), I declare that there is an emergency that threatens the livestock industry of this country and hereby authorize the transfer and use of such funds as may be necessary from appropriations or other funds available to agencies or corporations of the United States Department of Agriculture to seize and dispose of animals that are affected with or exposed to this TSE, and their germplasm, in accordance with 21 U.S.C. 134a.
Dated: This declaration of emergency shall become effective July 14, 2000. Dan Glickman, Secretary of Agriculture. [FR Doc. 00-18368 Filed 7-19-00; 8:45 am] BILLING CODE 3410-34-P
I was told that ;
-------- Original Message -------- Subject: Re: hello Dr. Sutton...question please...scrapie...TSS Date: Thu, 20 May 2004 14:36:09 -0400 From: firstname.lastname@example.com To: firstname.lastname@example.com
Dear Mr. Singeltary,
The Western blot tests on these animals were completed in April of this year. That means that we can begin the mouse inoculations. To get the results of the Western blot tests, you will need to submit a Freedom of Information Act request through our FOIA office. The FAX number there is 301-734-5941.
Have a nice day,
Jim Rogers APHIS LPA =========
Dr. Detwiler, my question is, why have these very important test been delayed for so long when we were told they were to have been started some 2+ years ago?
who made this call to delay these very important test and why ?
thank you, with kindest regards,
Linda Detwiler wrote:
######## Bovine Spongiform Encephalopathy #########
######### http://mailhost-alt.rz.uni-karlsruhe.de/warc/bse-l.html ##########
WHAT ABOUT THE POTENTIAL FOR BSE IN SHEEP AND GOATS OR ANY OF THE OTHER NEW ''ATYPICAL'' TSEs SHOWING UP?
02-Jun-04, 10:45 BSE IN SHEEP CONTINGENCY PLAN - CONSULTATION LAUNCH
Defra and the other UK Agriculture and Rural Affairs Departments today launched a consultation on the UK contingency plan on possible actions if BSE were confirmed in sheep.
The total prevalence of scrapie in the USA is really unknown.
USA SCRAPIE Infected and Source Flocks;
As of September 30, 2003, there were 50 scrapie infected and source flocks (figure 3 ). There were 73 newly infected flocks reported in FY 2003 (figure 4 ). In addition, 351 scrapie cases were also confirmed and reported by the National Veterinary Services Laboratories (NVSL) (figures 5
and 6 ). No case of scrapie in goats was reported in FY 2003. The last case was confirmed in August 2002. New infected and source flock numbers and the number of these flocks released in FY 2003 are depicted in chart 4 . Sixty flocks, which is equivalent to 82 percent of the new scrapie infected and source flocks identified in FY 2003, were released or put on clean-up plans in FY 2003.
Current Distribution of CWD among Captive Cervid Herds Map Image
Click on the Picture above to See a Larger Image
Bullet Represents captive elk herds that are currently CWD-positive. Bullet Represents captive deer herds that are currently CWD-positive.
Depopulated Captive Cervid Herds Map Image
Click on the Picture above to See a Larger Image Bullet Represents CWD-positive captive elk herds that were depopulated due to CWD. Bullet Represents CWD-positive captive deer herds that were depopulated due to CWD.
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids Map Image Click on the Picture above to See a Larger Image
Bullet Represents counties in which CWD has been identified in free-ranging cervids. Note that large counties in the western states make the CWD area appear larger than actual extent. Refer to state wildlife agencies (links on the State Information page) for more detailed information on wildlife occurrances.
DUE to the new 'atypical' TSEs showing up, prohibiting the use of all mammalian and poultry protein in ruminant feed, to prevent cross contamination, is the only way to assure that CWD, Scrapie, BSE and all new 'atypical' TSEs will not cross-contaminate.
CATTLE have gone clinical with TSE as young as 20 months, to only be concerned and to set regulations only for the 30 month and older cattle is not sufficient to prevent the spread of this agent. The age limit should be 12 months;
DEAD STOCK DOWNERS are of major concern for TSEs. DUE not ignore the sub clinical TSE population. TO change regulations and to only focus on the CNS (stumbling, staggering and twitching cow), will further help spread this agent by ignoring the younger documented cows that have been documented (as young as 20 month, see documentation of these young cattle with BSE/TSE);
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA [takes a few minutes to load]
Broken bones and such may be the first signs of a sub clinical BSE/TSE cow;
MRC-43-00 Issued: Monday, 28 August 2000
A team of researchers led by Professor John Collinge at the Medical Research Council Prion Unit1 report today in the Proceedings of the National Academy of Sciences, on new evidence for the existence of a ?sub-clinical? form of BSE in mice which was unknown until now.
The scientists took a closer look at what is known as the ?species barrier? - the main protective factor which limits the ability of prions2 to jump from one species to infect another. They found the mice had a ?sub-clinical? form of disease where they carried high levels of infectivity but did not develop the clinical disease during their normal lifespan. The idea that individuals can carry a disease and show no clinical symptoms is not new. It is commonly seen in conventional infectious diseases.
Researchers tried to infect laboratory mice with hamster prions3 called Sc237 and found that the mice showed no apparent signs of disease. However, on closer inspection they found that the mice had high levels of mouse prions in their brains. This was surprising because it has always been assumed that hamster prions could not cause the disease in mice, even when injected directly into the brain.
In addition the researchers showed that this new sub-clinical infection could be easily passed on when injected into healthy mice and hamsters.
The height of the species barrier varies widely between different combinations of animals and also varies with the type or strain of prions. While some barriers are quite small (for instance BSE easily infects mice), other combinations of strain and species show a seemingly impenetrable barrier. Traditionally, the particular barrier studied here was assumed to be robust.
Professor John Collinge said: "These results have a number of important implications. They suggest that we should re-think how we measure species barriers in the laboratory, and that we should not assume that just because one species appears resistant to a strain of prions they have been exposed to, that they do not silently carry the infection. This research raises the possibility, which has been mentioned before, that apparently healthy cattle could harbour, but never show signs of, BSE.
"This is a timely and unexpected result, increasing what we know about prion disease. These new findings have important implications for those researching prion disease, those responsible for preventing infected material getting into the food chain and for those considering how best to safeguard health and reduce the risk that theoretically, prion disease could be contracted through medical and surgical procedures."
Professor Collinge is a consultant neurologist and Director of the newly formed MRC Prion Unit based at The Imperial College School of Medicine at St Mary?s Hospital. He is also a member of the UK Government?s Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit is was set up in 1999, and its work includes molecular genetic studies of human prion disease and transgenic modelling of human prion diseases.
Prions are unique infectious agents that cause fatal brain diseases such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad cow disease) in animals. In some circumstances prions from one species of animals can infect another and it is clear that BSE has done this to cause the disease variant CJD in the UK and France. It remains unclear how large an epidemic of variant CJD will occur over the years ahead.
The strain of prion used here to infect the mice is the Sc237 strain (also known as 263K) which infects hamsters, and until now was assumed not to infect mice.
This research was funded by the Medical Research Council and Wellcome Trust.
The Medical Research Council (MRC) is a national organisation funded by the UK tax-payer. Its business is medical research aimed at improving human health; everyone stands to benefit from the outputs. The research it supports and the scientists it trains meet the needs of the health services, the pharmaceutical and other health-related industries and the academic world. MRC has funded work which has led to some of the most significant discoveries and achievements in medicine in the UK. About half of the MRC?s expenditure of £345 million is invested in over 50 of its Institutes and Units, where it employs its own research staff. The remaining half goes in the form of grant support and training awards to individuals and teams in universities and medical schools.
The Wellcome Trust is the world's largest medical research charity with a spend of some £600 million in the current financial year 1999/2000. The Wellcome Trust supports more than 5,000 researchers, at 400 locations, in 42 different countries to promote and foster research with the aim of improving human and animal health. As well as funding major initiatives in the public understanding of science, the Wellcome Trust is the country's leading supporter of research into the history of medicine.
THE recent findings of positive 'inconclusives' that turned up negative was not only a nightmare to the consumer, but also to the farmers and industry as well. Using Prionics or Bio-Rad or whatever rapid TSE test will never eliminate the potential for human error. IF we look at the recent discovery of the BSE in Switzerland in the Zoo Zebu, the testing they perform would have eliminated this mix-up;
A. Laboratory where diagnosis was made: Institute of Animal Neurology, University of Bern (OIE Reference Laboratory for bovine spongiform encephalopathy).
B. Diagnostic tests used:
- histology;
- immunohistochemistry;
- ELISA (two different kits);
- western blot.
All tests gave positive results.
ALSO, if we look at the USA BSE EMERGENCY RESPONSE PLAN, where it states;
Subject: U.S. Emergency Bovine Spongiform Encephalopathy Response Plan Summary Date: Tue, 4 May 1999 18:25:12 -0500 From: "Terry S. Singeltary Sr." Reply-To: BSEL To: BSEL snip... If additional tests do suggest a presumptive diagnosis of BSE, an NVSL pathologist will hand carry the sample to the United Kingdom for confirmation. It is at this critical point, when NVSL suggests a diagnosis of BSE and is preparing to send the sample to the United Kingdom, that this BSE Response Plan is initiated. The Plan begins the preliminary notification from NVSL to APHIS. Preliminary Notification The director of NVSL is responsible for immediately notifying the APHIS, Veterinary Services (VS) deputy administrator when tests suggest a presumptive diagnosis of BSE. Once NVSL has made a presumptive diagnosis of BSE, APHIS and FSIS field activities will also be initiated. APHIS will receive notification (either confirming or not confirming NVSL's diagnosis) from the United Kingdom anywhere between 24 and 96 hours. (The international animal health community has recognized the United Kingdom's Central Veterinary Laboratory {CVL} as the world's reference laboratory for diagnosing BSE. Other countries, including Belgium, France, Ireland, Luxembourg, the Netherlands, Portugal, and Switzerland, have all sent samples to this lab to confirm their first case of BSE). snip...end...TSS
WHY is the UK not going to verify the findings of BSE/TSE in tissue samples as the original BSE emergency response plan told them too?
I think that having several different rapid TSE test kits (Prionics, Bio-Rad etc.) along with the IHC and finally the OIE reference laboratory for confirmation is the best possible answer. Prusiner et al have a test that is some 1,000 times more sensitive and I only ponder why we are not using it? My fear is that once testing becomes more sensitive, more tissue/organ will become known to hold infectivity of some titre of the TSE agent. THEN we must ponder if _accumulation_ may play a role? With the threat from new atypical TSEs in many species and the real threat from iatrogenic CJD, the fact that we do not yet know how these new 'atypical' phenotpyes will transmit and how infectious there tissues may be, we must act now, we cannot flounder any longer.
Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA [takes a few minutes to load]
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed
Comment Number: EC -10
Accepted - Volume 2
PDF]Freas, William TSS SUBMISSION
File Format: PDF/Adobe Acrobat -
Page 1. J Freas, William From: Sent: To: Subject: Terry S. Singeltary
Sr. [email@example.com] Monday, January 08,200l 3:03 PM freas ...
Asante/Collinge et al, that BSE transmission to the 129-methionine
genotype can lead to an alternate phenotype that is indistinguishable
from type 2 PrPSc, the commonest _sporadic_ CJD;
Docket Management Docket: 96N-0417 - Current Good Manufacturing Practice in Manufacturing, Packing, or Holding Dietary Ingredients a Comment Number: EC -2 Accepted - Volume 7
[PDF] Appendices to PL107-9 Inter-agency Working Group Final Report 1-1 File Format: PDF/Adobe Acrobat - View as HTML Agent, Weapons of Mass Destruction Operations Unit Federal Bureau of those who provided comments in response to Docket No. ... Meager 8/18/01 Terry S. Singeltary Sr ...
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]
# Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0)
Docket Management
Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC-254 [TSS SUBMISSION]
Dockets Entered On October 2, 2003 Table of Contents, Docket #, Title, 1978N-0301,
OTC External Analgesic Drug Products, ... EMC 7, Terry S. Singeltary Sr. Vol #: 1, ...
Daily Dockets Entered on 02/05/03
DOCKETS ENTERED on 2/5/03. ... EMC 4 Terry S. Singeltary Sr. Vol#: 2. ... Vol#: 1.
03N-0009 Federal Preemption of State & Local Medical Device Requireme. ...
Docket Management
Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater
Comment Number: EC -1
Accepted - Volume 1
Daily Dockets - 04/10/03
... 00D-1662 Use of Xenotransplantation Products in Humans. EMC 98 Terry S. Singeltary Sr. Vol#: 3. 01F ... www.fda.gov/ohrms/dockets/dailys/03/Apr03/041003/041003.htm - 05-20-2003 - Cached
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
-------- Original Message --------
Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material >From Deer and Elk in Animal Feed; Availability Date: Fri, 16 May 2003 11:47:37 -0500 From: "Terry S. Singeltary Sr." To: email@example.com
Greetings FDA,
i would kindly like to comment on;
Docket 03D-0186
FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability
Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;
1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the _total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...
2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test to assure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthy ones as well. it this is not done, they system will fail...
3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.
4. THERE are and have been for some time many TSEs in the USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.
5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread these TSE mad cow agents in the USA. I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in the USA, but this has yet to happen...
6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)
7. WE must learn from our past mistakes, not continue to make the same mistakes...
Six white-tailed deer fawns test positive for CWD
MADISON -- Six fawns in the area of south central Wisconsin where chronic wasting disease has been found in white-tailed deer have tested positive for the disease, according to Department of Natural Resources wildlife health officials. These are the youngest wild white-tailed deer detected with chronic wasting disease (CWD) to date.
Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month. Two of the six fawns with CWD detected were 5 to 6 months old. All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.
Issued: Monday, 28 August 2000 NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE
A team of researchers led by Professor John Collinge at the Medical Research Council Prion Unit1 report today in the Proceedings of the National Academy of Sciences, on new evidence for the existence of a 'sub-clinical' form of BSE in mice which was unknown until now.
The scientists took a closer look at what is known as the 'species barrier' - the main protective factor which limits the ability of prions2 to jump from one species to infect another. They found the mice had a 'sub-clinical' form of disease where they carried high levels of infectivity but did not develop the clinical disease during their normal lifespan. The idea that individuals can carry a disease and show no clinical symptoms is not new. It is commonly seen in conventional infectious diseases.
Researchers tried to infect laboratory mice with hamster prions3 called Sc237 and found that the mice showed no apparent signs of disease. However, on closer inspection they found that the mice had high levels of mouse prions in their brains. This was surprising because it has always been assumed that hamster prions could not cause the disease in mice, even when injected directly into the brain.
In addition the researchers showed that this new sub-clinical infection could be easily passed on when injected into healthy mice and hamsters.
The height of the species barrier varies widely between different combinations of animals and also varies with the type or strain of prions. While some barriers are quite small (for instance BSE easily infects mice), other combinations of strain and species show a seemingly impenetrable barrier. Traditionally, the particular barrier studied here was assumed to be robust.
Professor John Collinge said: "These results have a number of important implications. They suggest that we should re-think how we measure species barriers in the laboratory, and that we should not assume that just because one species appears resistant to a strain of prions they have been exposed to, that they do not silently carry the infection. This research raises the possibility, which has been mentioned before, that apparently healthy cattle could harbour, but never show signs of, BSE.
"This is a timely and unexpected result, increasing what we know about prion disease. These new findings have important implications for those researching prion disease, those responsible for preventing infected material getting into the food chain and for those considering how best to safeguard health and reduce the risk that theoretically, prion disease could be contracted through medical and surgical procedures."
Professor Collinge is a consultant neurologist and Director of the newly formed MRC Prion Unit based at The Imperial College School of Medicine at St Mary's Hospital. He is also a member of the UK Government's Spongiform Encephalopathy Advisory Committee (SEAC). The MRC prion unit is was set up in 1999, and its work includes molecular genetic studies of human prion disease and transgenic modelling of human prion diseases.
Prions are unique infectious agents that cause fatal brain diseases such as Creutzfeldt-Jakob disease (CJD) in humans and scrapie and BSE (mad cow disease) in animals. In some circumstances prions from one species of animals can infect another and it is clear that BSE has done this to cause the disease variant CJD in the UK and France. It remains unclear how large an epidemic of variant CJD will occur over the years ahead.
The strain of prion used here to infect the mice is the Sc237 strain (also known as 263K) which infects hamsters, and until now was assumed not to infect mice.
This research was funded by the Medical Research Council and Wellcome Trust.
The Medical Research Council (MRC) is a national organisation funded by the UK tax-payer. Its business is medical research aimed at improving human health; everyone stands to benefit from the outputs. The research it supports and the scientists it trains meet the needs of the health services, the pharmaceutical and other health-related industries and the academic world. MRC has funded work which has led to some of the most significant discoveries and achievements in medicine in the UK. About half of the MRC's expenditure of £345 million is invested in over 50 of its Institutes and Units, where it employs its own research staff. The remaining half goes in the form of grant support and training awards to individuals and teams in universities and medical schools.
The Wellcome Trust is the world's largest medical research charity with a spend of some £600 million in the current financial year 1999/2000. The Wellcome Trust supports more than 5,000 researchers, at 400 locations, in 42 different countries to promote and foster research with the aim of improving human and animal health. As well as funding major initiatives in the public understanding of science, the Wellcome Trust is the country's leading supporter of research into the history of medicine.
©2002 Medical Research Council Data Protection policy Contact the MRC
Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1
Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5
Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail firstname.lastname@example.com
Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.
These results indicate that mule deer fawns develop detectable PrP res after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node. He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.
now, just what is in that deer feed? _ANIMAL PROTEIN_
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-L To: BSE-L
8420-20.5% Antler Developer For Deer and Game in the wild Guaranteed Analysis Ingredients / Products Feeding Directions
_animal protein_
_animal protein_
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage Products, Roughage Products 15%, Molasses Products, __Animal Protein Products__, Monocalcium Phosphate, Dicalcium Pyosphate, Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (source of Vitamin D3), Vitamin E Supplement, Vitamin B12 Supplement, Riboflavin Supplement, Niacin Supplement, Calcium Panothenate, Choline Chloride, Folic Acid, Menadione Soduim Bisulfite Complex, Pyridoxine Hydorchloride, Thiamine Mononitrate, d-Biotin, Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried Sacchoromyces Berevisiae Fermentation Solubles, Cellulose gum, Artificial Flavors added.
http://www.bodefeed.com/prod6.htm ===================================
Bode's #1 Game Pellets A RATION FOR DEER F3153
GUARANTEED ANALYSIS Crude Protein (Min) 16% Crude Fat (Min) 2.0% Crude Fiber (Max) 19% Calcium (Ca) (Min) 1.25% Calcium (Ca) (Max) 1.75% Phosphorus (P) (Min) 1.0% Salt (Min) .30% Salt (Max) .70%
Grain Products, Plant Protein Products, Processed Grain By-Products, Forage Products, Roughage Products, 15% Molasses Products, __Animal Protein Products__, Monocalcium Phosphate, Dicalcium Phosphate, Salt, Calcium Carbonate, Vitamin A Acetate with D-activated Animal Sterol (source of Vitamin D3) Vitamin E Supplement, Vitamin B12 Supplement, Roboflavin Supplement, Niacin Supplement, Calcium Pantothenate, Choline Chloride, Folic Acid, Menadione Sodium Bisulfite Complex, Pyridoxine Hydrochloride, Thiamine Mononitrate, e - Biotin, Manganous Oxide, Zinc Oxide, Ferrous Carbonate, Calcium Iodate, Cobalt Carbonate, Dried Saccharyomyces Cerevisiae Fermentation Solubles, Cellulose gum, Artificial Flavors added.
FEEDING DIRECTIONS Feed as Creep Feed with Normal Diet
Grain Products, Roughage Products (not more than 35%), Processed Grain By-Products, Plant Protein Products, Forage Products, __Animal Protein Products__, L-Lysine, Calcium Carbonate, Salt, Monocalcium/Dicalcium Phosphate, Yeast Culture, Magnesium Oxide, Cobalt Carbonate, Basic Copper Chloride, Manganese Sulfate, Manganous Oxide, Sodium Selenite, Zinc Sulfate, Zinc Oxide, Sodium Selenite, Potassium Iodide, Ethylenediamine Dihydriodide, Vitamin E Supplement, Vitamin A Supplement, Vitamin D3 Supplement, Mineral Oil, Mold Inhibitor, Calcium Lignin Sulfonate, Vitamin B12 Supplement, Menadione Sodium Bisulfite Complex, Calcium Pantothenate, Riboflavin, Niacin, Biotin, Folic Acid, Pyridoxine Hydrochloride, Mineral Oil, Chromium Tripicolinate
Deer Builder Pellets is designed to be fed to deer under range conditions or deer that require higher levels of protein. Feed to deer during gestation, fawning, lactation, antler growth and pre-rut, all phases which require a higher level of nutrition. Provide adequate amounts of good quality roughage and fresh water at all times.
April 9, 2001 WARNING LETTER
Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145 PHILADELPHIA DISTRICT
Tel: 215-597-4390
Dear Mr. Raymond:
Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23, 2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattle or other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.
In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal. Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.
The above is not intended to be an all-inclusive list of deviations from the regulations. As a manufacturer of materials intended for animal feed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance with the law. We have enclosed a copy of FDA's Small Entity Compliance Guide to assist you with complying with the regulation... blah, blah, blah...
posted here;
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 7 Terry S. Singeltary Sr. Vol #: 1
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed
EMC 7 Terry S. Singeltary Sr. Vol #: 1
Chronic Wasting Disease and Potential Transmission to Humans
Ermias D. Belay,*Comments Ryan A. Maddox,* Elizabeth S. Williams, Michael W. Miller,! Pierluigi Gambetti,§ and Lawrence B. Schonberger* *Centers for Disease Control and Prevention, Atlanta, Georgia, USA; University of Wyoming, Laramie, Wyoming, USA; !Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA
Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm
Chronic wasting disease (CWD) of deer and elk is endemic in a tri-corner area of Colorado, Wyoming, and Nebraska, and new foci of CWD have been detected in other parts of the United States. Although detection in some areas may be related to increased surveillance, introduction of CWD due to translocation or natural migration of animals may account for some new foci of infection. Increasing spread of CWD has raised concerns about the potential for increasing human exposure to the CWD agent. The foodborne transmission of bovine spongiform encephalopathy to humans indicates that the species barrier may not completely protect humans from animal prion diseases. Conversion of human prion protein by CWD-associated prions has been demonstrated in an in vitro cell-free experiment, but limited investigations have not identified strong evidence for CWD transmission to humans. More epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions.
Transmission to Other Animals
Concerns have been raised about the possible transmission of the CWD agent to domestic animals, such as cattle and sheep, which may come in contact with infected deer and elk or CWD-contaminated environments. If such transmissions were to occur, they would potentially increase the extent and frequency of human exposure to the CWD agent. In addition, passage of the agent through a secondary host could alter its infectious properties, increasing its potential for becoming more pathogenic to humans. This phenomenon may have occurred with BSE when a strain of scrapie, a possible original source of the BSE outbreak, changed its pathogenic properties for humans after infecting cattle. However, the exact origin of BSE remains unknown.
Although CWD does not appear to occur naturally outside the cervid family, it has been transmitted experimentally by intracerebral injection to a number of animals, including laboratory mice, ferrets, mink, squirrel monkeys, and goats (1 ,26 ). In an experimental study, the CWD agent was transmitted to 3 of 13 intracerebrally injected cattle after an incubation period of 22 to 27 months (27 ). The susceptibility of cattle intracerebrally challenged with the agent of this disease was substantially less than that observed after intracerebral scrapie challenge: nine of nine cattle succumbed to scrapie challenge after intracerebral injection (28 ). In ongoing experimental studies, after >6 years of observation, no prion disease has developed in 11 cattle orally challenged with the CWD agent or 24 cattle living with infected deer herds (E.S. Williams and M.W. Miller, unpub. data) (1 ). In addition, domestic cattle, sheep, and goat residing in research facilities in close contact with infected cervids did not develop a prion disease.
[PLEASE NOTE, THIS HAS BEEN UPDATED TO AN ADDITIONAL 2 COWS AND ONE SHEEP, making the total transmission of CWD to cattle at 5 and one transmission of CWD to one sheep, MILLER ET AL BSE-L...TSS]
The lack of evidence of a link between CWD transmission and unusual cases of CJD, despite several epidemiologic investigations, and the absence of an increase in CJD incidence in Colorado and Wyoming suggest that the risk, if any, of transmission of CWD to humans is low. Although the in vitro studies indicating inefficient conversion of human prion protein by CWD-associated prions raise the possibility of low-level transmission of CWD to humans, no human cases of prion disease with strong evidence of a link with CWD have been identified. However, the transmission of BSE to humans and the resulting vCJD indicate that, provided sufficient exposure, the species barrier may not completely protect humans from animal prion diseases. Because CWD has occurred in a limited geographic area for decades, an adequate number of people may not have been exposed to the CWD agent to result in a clinically recognizable human disease. The level and frequency of human exposure to the CWD agent may increase with the spread of CWD in the United States. Because the number of studies seeking evidence for CWD transmission to humans is limited, more epidemiologic and laboratory studies should be conducted to monitor the possibility of such transmissions. Studies involving transgenic mice expressing human and cervid prion protein are in progress to further assess the potential for the CWD agent to cause human disease. Epidemiologic studies have also been initiated to identify human cases of prion disease among persons with an increased risk for exposure to potentially CWD-infected deer or elk meat (47 ). If such cases are identified, laboratory data showing similarities of the etiologic agent to that of the CWD agent would strengthen the conclusion for a causal link. Surveillance for human prion diseases, particularly in areas where CWD has been detected, remains important to effectively monitor the possible transmission of CWD to humans. Because of the long incubation period associated with prion diseases, convincing negative results from epidemiologic and experimental laboratory studies would likely require years of follow-up. In the meantime, to minimize the risk for exposure to the CWD agent, hunters should consult with their state wildlife agencies to identify areas where CWD occurs and continue to follow advice provided by public health and wildlife agencies. Hunters should avoid eating meat from deer and elk that look sick or test positive for CWD. They should wear gloves when field-dressing carcasses, bone-out the meat from the animal, and minimize handling of brain and spinal cord tissues. As a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where CWD has been identified.
see full text ;
Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734.
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob
disease in the United States
Email Terry S. Singeltary:
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to
comment on the CDC's attempts to monitor the occurrence of emerging
forms of CJD. Asante, Collinge et al [1] have reported that BSE
transmission to the 129-methionine genotype can lead to an alternate
phenotype that is indistinguishable from type 2 PrPSc, the commonest
sporadic CJD. However, CJD and all human TSEs are not reportable
nationally. CJD and all human TSEs must be made reportable in every
state and internationally. I hope that the CDC does not continue to
expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in
the USA in both animal and man. CWD in deer/elk is spreading rapidly and
CWD does transmit to mink, ferret, cattle, and squirrel monkey by
intracerebral inoculation. With the known incubation periods in other
TSEs, oral transmission studies of CWD may take much longer. Every
victim/family of CJD/TSEs should be asked about route and source of this
agent. To prolong this will only spread the agent and needlessly expose
others. In light of the findings of Asante and Collinge et al, there
should be drastic measures to safeguard the medical and surgical arena
from sporadic CJDs and all human TSEs. I only ponder how many sporadic
CJDs in the USA are type 2 PrPSc?
IN SHORT, we have floundered to long in the regulation of human/animal TSEs. EACH day longer, more and more people will become exposed. YOU can step up to the plate and act now, forget about corporate/political interest, act in the best of public health, with the available science to date (it's all there), or you can pay later. AT what cost you ask, depends which loved one you loose to this agent. THIS goes far beyond the bad hamburger. 85%+ of all CJD (sporadic), did not just happen. sporadic CJD simply means CJD from unknown route and source of agent, and we have many of both right here in the USA. What phenotype is anyone's guess?
ALL SRM must be removed. ALL animals for human/animal consumption must be tested for TSE. ALL human TSEs must be made reportable Nationally and Internationally. with CJD/TSE questionnaire asking real questions as to route and source of agent. THIS must pertain to all ages!
CJD Watch message board
Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION] P.S. 2008 another TSS submission with url shut down recently by fda. SO, again, here is the original ;
From: Terry S. Singeltary Sr. [email@example.com] Sent: Tuesday, July 29, 2003 1:03 PM To: firstname.lastname@example.com Cc: firstname.lastname@example.com; firstname.lastname@example.com; BSE-L Subject: Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION TO DOCKET 2003N-0312]
Greetings FDA,
my name is Terry S. Singeltary Sr., i lost my mother to hvCJD (Heidenhain Variant Creutzfeldt Jakob Disease).
i would kindly like to comment on the proposed HACCP method of detecting and or preventing TSEs in the human/animal feed supply.
it seems to me by implementing something that was designed for Astronauts instead of cattle, something that the GAO has already stated is terribly flawed (HACCP), i find it very disturbing to continue to insist on refusing to use rapid TSE TESTING in sufficient numbers to find TSEs, as with other Countries that they too once thought they were BSE free. for example, it took Italy 1 MILLION rapid TSE tests since 2001 to find 102 cases of BSE. THE USA has only tested 48,000 cattle in the 14 years of surveillance. there is documented proof that indeed the USA cattle have been infected with a TSE for decades, but the FDA/USDA and other USA Gov. agencies continue to conveniently ignore these findings. YOU must not ignore what Richard Marsh found. Plus, you must not ignore Asante/Collinge new findings that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD. The USA has been feeding ruminant by-products back to cattle, deer, elk and sheep for decades, and TSEs in these species have been recycled for feed for decades in the USA. The rendering process here in the USA will not kill this agent. to implement any HACCP over massive rapid TSE testing is only prolonging the inevitable, and will only allow the agent to spread further. it is simply a band-aid approach to something that needs a tourniquet...
3. Meat and Poultry: Better USDA Oversight and Enforcement of Safety
Rules Needed to Reduce Risk of Foodborne Illnesses. GAO-02-902, August 30.
FSIS Is Not Ensuring that Plants' HACCP Plans Meet Regulatory Requirements
According to FSIS's food safety systems correlation reviews, inspectors are not consistently identifying and documenting failures of plants' HACCP plans to meet regulatory requirements. Furthermore, FSIS does not expect its inspectors to determine whether HACCP plans are based on sound science--the cornerstone of an effective plan. While in-depth verification reviews examine the scientific aspects of HACCP plans, they have been conducted in very few plants, and consumer safety officers hired to review the scientific soundness of HACCP plans may take several years to assess the plans at all plants. Moreover, inspectors in 55 percent of the 5,000 plants nationwide did not document any HACCP violations during fiscal year 2001. When we brought this information to the attention of FSIS officials, they were surprised that so many plants had no HACCP violations for an entire year.
2. USDA believes that the title of the report is misleading. We disagree. We believe the title accurately reflects the concerns detailed throughout the body of the report.
FDA acknowledges that it has not yet identified and inspected all firms subject to the ban" pg. 3 ;
The report concludes that "federal actions do not sufficiently ensure that all BSE-infected animals or products are kept out or that if BSE were found it would be detected promptly and not spread to other cattle through animal feed or enter the human food chain" italics added pg. 3 ;
and why does everybody conveniently ignore these findings;
Asante/Collinge et al, that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest _sporadic_ CJD;
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.
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.
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 alt 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 wili 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.
02N-0273 - Substances Prohibited From ... [PART 1 TSS SUBMISSION] ... compare search on 8/8/01...tss =====ANIMAL PROTEIN ... had to request to the FOIA >>for the USA madcow feed ban warning letters. ... www.fda.gov/ohrms/dockets/dailys/ 03/Jan03/012403/8004be07.html - 68k -
Docket Management Docket: 02N-0273 - Substances Prohibited From ... [PART 2 TSS SUBMISSION]
The problem is diminishing in most of the 15 EU nations, but in Britain there were 260 positive tests between January and May, compared with 156 for the same period last year.
The higher number could be explained partly by the greater number of tests carried out this year in Britain: 198,143 compared with 122,801.
The European Commission carried out about 4.1 million tests across member states - about 10% of cattle in the bloc.
It found 591 positive cases of bovine spongiform encephalopathy in the first five months of the year, down from 603 over the same period last year.
USA TEST ONLY 48,000 CATTLE IN 14 YEARS, from 100 MILLION CATTLE IN ANY GIVEN YEAR, to 2003, TOTAL TSE TEST EVER IN USA BOVINE;
As of April 30, 2003, over 48,000 brains have been examined for BSE or another form of a TSE in cattle (figure 3
For the USA to continue to _flounder_ with these TSEs, as they have done for the past 30 years or so, will only allow the agent to spread. to continue to ignore what every other Country around the globe has dealt with and is still dealing with, and to think that the USA is any different, should be taken with great suspicion $
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...
Terry S. Singeltary Neurology Online, 27 Jan 2003 [Full text]
anything less than 1 million rapid TSE test in USA cattle annually for 5 years, anything less than that, simply put, they don't want to find...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, TEXAS USA 77518
Docket Management Docket: 02N-0273 - Substances Prohibited From Use in
Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed
Comment Number: EC -10
Accepted - Volume 2
[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
APHIS-2006-0041-0006 TSE advisory committee for the meeting December 15, 2006
[Federal Register: January 9, 2007 (Volume 72, Number 5)] [Proposed Rules] [Page 1101-1129] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr09ja07-21]
BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01 Date: January 9, 2007 at 9:08 am PST
suppressed peer review of Harvard study October 31, 2002
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518