|
||||||||||||||||||
 |
From: TSS ()
New Rules to Govern Beef Exports to Japan "I think most ranchers won't bother with it this first year,'' the south-central Montana rancher said. "There are a lot of hoops to jump through.'' New requirements for doing business in Japan could keep many producers from tapping that once-lucrative market - at least initially. Selling beef to Japan will mean maintaining a paper trail from the ranch to the feedlot to the slaughterhouse, to verify cattle are killed at 20 months of age or younger. The levels of infection for mad-cow disease are believed to rise with age, and plans for resuming trade have been based on that cutoff. But birth records alone won't do, and in many cases, producers will need third-party verification of their documents and herds for corroboration, according to beef experts at Iowa State University. It will cost ranchers anywhere from 50 cents a head to $1.25 a head, by one estimate, just to put information into a database. "It seems very few people know about this kind of stuff, but the writing's been on the wall about this a long time,'' said John Lawrence, a livestock economist who directs the Iowa Beef Center at Iowa State and who has tracked and written on the issue. While the rules may seem confusing to ranchers, and a bit of a hassle, he and other industry experts say producers need to get used to them: Mad-cow disease has changed the rules necessary to participate in global trade. "This is a very tangible example of that,'' Lawrence said. "Things are different than they used to be.'' U.S. agricultural and political leaders have been pushing hard for the reopening of the Japanese market, which had previously been the biggest overseas market for American beef. Japan bought more than $1 billion worth in 2003 before the discovery of mad-cow disease in a Washington state cow in December 2003. That case, the first of two, prompted dozens of countries to ban U.S. beef; at least 70 countries have since lifted their bans, at least partially, according to the chief economist of the National Cattlemen's Beef Association. Japan also has made moves toward resuming limited trade. A final report on the safety of U.S. beef, expected at any time, could clear the way for that as early as this month, industry and government officials said. Though this has been in the works for over a year - and the subject of government negotiations and consistent Internet and breakfast table chatter - questions remain about whether producers will be prepared to take advantage of the market when trade resumes and whether there will be a sufficient supply of cattle. This time of year, many producers, like Donald, have long since sold their calves. Major meatpackers and dozens of feedlots have paperwork and plans in order, but many ranchers are still confused or in the dark about what they must do to qualify for the Japanese market, industry leaders and experts say. "I'll be honest with you. I think ranchers, as you look at them, are sitting there asking, 'What are we supposed to be doing?''' said John Paterson, an extension beef specialist at Montana State University in Bozeman, who admits to being a bit fuzzy himself on some of the finer points. Despite a framework for trade outlined by the U.S. Department of Agriculture, some cattlemen groups have been careful about advising ranchers on how best to position themselves, choosing to wait for the final word from Japan. "The devil will be in the details,'' said Steve Pilcher, executive vice president of the Montana Stockgrowers Association, "and it's a matter of me not trusting Japan totally.'' Donald, who is president of the stockgrowers' group, said he worries about setting a precedent in giving in to the demands of a country whose cutoff date for slaughter U.S. agriculture officials contend has no scientific basis. U.S. restrictions on Canadian cattle shipped into this country require that animals be slaughtered at younger than 30 months of age. Canada has reported three cases of mad-cow disease since May 2003. But James Hodges, president of the American Meat Institute Foundation in Washington, D.C., said the debate comes down to meeting the demands of the customer. Getting into the Japanese market again will be important for the United States and pressing its case for fuller trade, he and others said. "We're going to be going into a new era here,'' said Lynn Heinze, a spokesman for the U.S. Meat Export Federation. "It's a pain in the neck that will probably be good in the long run.'' That's how rancher Jim Peterson sees it. Peterson, who raises cattle near Buffalo, in central Montana, has been working the past two months to make sure he has sufficient documentation for the 300 calves he hopes to have eligible for the Japanese market. He also had auditors visit his place to go through his records and cattle herd. "I know of only just a very few producers in Montana that have taken the time to find out what is required and have actually done it,'' he said - while admitting that he is not completely sure yet the steps he's taken will give him access to the market and the potential for premium prices for his beef. Industry leaders expect the confusion to begin clearing once an official announcement is made. While initial trade will likely be slow, they believe it will build. "The first thing is, let's get the border open,'' Paterson said. "We need to start making some money again.'' -------------------------------------------------------------------------------- Iowa Beef Center: http://www.iowabeefcenter.org/ American Meat Institute Foundation: http://www.amif.org/index.htm U.S. Meat Export Federation: http://www.usmef.org/ (PROFILE (COUNTRY:Canada; ISOCOUNTRY3:CAN; UNTOP:021; APGROUP:NorthAmerica;) (COUNTRY:Japan; ISOCOUNTRY3:JPN; UNTOP:142; UN2ND:030; APGROUP:Asia;) (COUNTRY:United States; ISOCOUNTRY3:USA; UNTOP:021; APGROUP:NorthAmerica;) http://www.startribune.com/stories/484/5773618.html http://www.startribune.com/stories/484/5773618-2.html 7/29/05 (updated 8/16/05) Contacts: John Lawrence, Iowa State University, (515)294-6290, jdlaw@iastate.edu Rachel E. Martin, Iowa Beef Center, (515)294-9124, remartin@iastate.edu For Immediate Release AGE RECORDS WON’T BE ENOUGH FOR EXPORT TO JAPAN AMES, Iowa - - As the U.S. moves ever closer to re-establishing the beef trade with Japan, USDA continues to establish guidelines to ensure that beef products shipped to Japan are from cattle 20 months of age or less. Currently, the Japanese have agreed to accept A40 physiological maturity of the carcass measured in the cooler or age verification using production records. They will also accept beef from cattle with a proven age; however, records alone are not enough. Age verification must be done through a USDA approved Quality Systems Assessment (QSA) program. “To qualify for export to Japan, beef must comply with the regulations of the Beef Export Verification (BEV) program for Japan,” says John Lawrence, Iowa State University Extension economist and director of the Iowa Beef Center. “While packers can sort A40 beef from the cooler, producers can assure cattle will qualify for the Japanese market by participating in a Quality System Assessment program that has been pre-approved by the USDA’s Agricultural Marketing Service.” That is, cattle must have been raised by feedlots, backgrounders, and cowherds that are under a Quality System Assessment (QSA) program. Records documenting the age of the cattle and signed affidavits by the producer are needed, but are not enough information alone. “Think of the process as an audit pyramid,” says Lawrence. “USDA will approve and audit individual QSA programs, and each QSA program will accept responsibility for their participating producers.” The individual QSA programs may differ in the information required and claims made, but the program will have procedures to assure compliance including a written management plan explaining how records are kept. While the Japanese market is not currently open, some calves born this spring will likely be exported to Asian markets. Cattle that are not part of a QSA will still trade in the existing market, but will not be eligible for Japan, according to Lawrence. According to Lawrence, cattle producers have three options to sell cattle for Japan: participate in a packer’s QSA, develop their own QSA and get it approved by USDA, or participate in a QSA of an independent company. Among other things, the owner of a QSA must conduct internal audits of its system and maintain a list of approved suppliers. Producers who participate in a single packer’s QSA will need to maintain records specific to that program. As a result, cattle covered under one packer’s QSA program cannot be sold to another packer. A producer who sells cattle to more than one packer and participates in each packer’s QSA program must maintain a separate set of documents for each company. “The challenge is finding qualified feeder cattle,” states Lawrence. Feedlots that buy feeder cattle must either have their own QSA and qualify the supplier under their program or buy cattle that are covered in a packer or an independent QSA. While large feedlots may chose to develop and maintain their own QSA, smaller-scale producers may choose to participate in an established independent QSA program. When evaluating ID suppliers, Lawrence suggests that producers should ask if the company has an approved QSA program for age verification to Japan. Relatively few QSA programs exist today, but the number is growing. For more information, including links to USDA guidelines and a list of approved programs, visit the Age & Source Verification page at www.iowabeefcenter.org. http://www.iowabeefcenter.org/content/2005/AgeRecordsWon%27tBeEnoughRelease.pdf Safeguarding American Agriculture Federal Relay Service APHIS is an agency of USDA’s Marketing and Regulatory Programs (Voice/TTY/ASCII/Spanish) An Equal Opportunity Provider and Employer 1-800-877-8339 Subject: Importation of Bovines (Cattle or Bison) from Canada for Feeding To: Feedlot Owners and Operators and Other Interested Parties The Animal and Plant Health Inspection Service (APHIS) published a final rule on January 4, 2005, entitled “Bovine Spongiform Encephalopathy; Minimal-Risk Regions and Importation of Commodities.” As a result of this publication, regulations are now in place to allow for the importation of bovines from Canada for feeding. Bovines must be less than 30 months of age when imported and when sent to slaughter. This rule is effective immediately. There are now specific post entry requirements on the movement of these animals from the Port of Entry (POE). If you intend to import feeder bovines from Canada, you must comply with the following conditions: (1) All bovines imported from Canada will be individually identified by an official Canadian eartag, applied before the bovine’s arrival at the United States POE. This eartag cannot be removed. You cannot alter, deface, remove, or otherwise tamper with the individual identification while the animal is at your feedlot. The bovines must also be marked with a CΛN brand on the right hip. (2) Shipments of bovines must move directly from the POE to the feedlot. When the shipment of animals arrives at the feedlot from the POE, the vehicle will be sealed by official government seals of Canada, or official seals of the United States [applied at the POE by either APHIS or U.S. Customs and Border Protection]. The shipment will be accompanied by VS Form 17-130 “Ruminants Imported to Designated/Approved Feedlots.” This form identifies the physical location of the feedlot, and the individual responsible for the movement of the animals. This form is issued at the POE. A copy of the official Canadian Health certificate will also accompany the shipment. (3) The official seals on the vehicle can be broken by a State or U.S. Department of Agriculture (USDA) representative, an accredited veterinarian, or his/her designee (i.e., an employee of the accredited veterinarian). The individual that breaks the seal must complete #13 to #18 of the VS Form 17-130 and return it to the POE within 14 days of receipt of the shipment. The appropriate return address is included on the form. (4) The bovines must remain at the feedlot that was identified on the VS Form 17-130. They cannot be sent to any other location except to slaughter. (5) The bovines must be moved directly from the feedlot to the slaughter establishment in a vehicle that must be sealed at the feedlot with U.S. Government seals by an accredited veterinarian or a State or USDA representative. The seals may be broken only at the slaughter establishment by a USDA representative. United States Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services National Center for Import/ Export 4700 River Road Unit 39 Riverdale, MD 20737 (301) 734-8364 FAX (301) 734-6402 Feedlot Owners and Operators and Other Interested Parties 2 (6) The accredited veterinarian or State or USDA representative must complete VS Form 1-27, “Permit for Movement of Restricted Animals.” This form will identify the location of the recognized slaughtering establishment, the individual responsible for the movement of the bovines, and the individual identification of each animal. A copy of the official Canadian health certificate and a copy of the VS 17-130 must be attached to this form and accompany the shipment to slaughter. (7) Canadian bovines must be moved as a group of Canadian bovines to the slaughter establishment. U.S. and Canadian bovines cannot be shipped in the same vehicle to slaughter. (8) It is the responsibility of the individual that is sending these animals to slaughter to ensure that they are less than 30 months of age when slaughtered. Failure to comply with any of these requirements may prevent you from receiving Canadian feeder bovines. You may also be subject to civil or criminal penalties under the Animal Health Protection Act. In order to avoid unnecessary delays at the POE and in receiving your feeder shipments, it is highly recommended that you contact the Area Veterinarian in Charge (AVIC) in the State of destination of your feedlot and provide him/her with the name and address of your feedlot and the designated individual(s) who will be responsible for removing the official government seals and completing and returning VS Form 17-130 to the port veterinarian. A list of AVICs can be found on the Internet at www.aphis.usda.gov/vs/area_offices.htm. Lee Ann Thomas, D.V.M., M.S. Director, Animals, Organisms and Vectors, and Select Agents National Center for Import and Export APHIS:VS:NCIE:DMalloy:EMarkese:tb:x5458:ECMS 0502-HSDETC I :VSNCIE:Animals:Malloy:Dear Feedlot 7.15.05.doc http://www.aphis.usda.gov/lpa/issues/bse/trade/Dear_Feedlot_7-15-05.pdf USDA, APHIS, Veterinary Services, National Center For Import And Export: Protocol For The Importation Of Cattle Or Bison For Feeding From Canada CAN feederC&B 6/15/2005 1 1. GENERAL REQUIREMENTS 1.1 For the purposes of this document, bovine is defined to include Bos taurus (domestic cattle), Bos indicus (Brahma or Zebu type cattle), and Bison bison (American buffalo). 1.2 No import permit is required if the bovines are offered for entry at a land border port listed in 9 CFR 93.403(b) and meet one of the following conditions: a) are born in the United States or Canada and have been in no other region, or b) are legally imported into Canada from a bovine spongiform encephalopathy (BSE)-free region and have been unconditionally released and eligible to move freely within Canada for at least 60 days prior to importation into the United States. In any other case, the importer must obtain an import permit from: U.S. Department of Agriculture (USDA) Animal and Plant Health Inspection Service (APHIS) Veterinary Services (VS) National Center for Import-Export (NCIE) 4700 River Road, Unit 39 Riverdale, Maryland 20737-1231 The web site to obtain the import permit application (VS 17-129) is: http://www.aphis.usda.gov/vs/ncie. 1.3 An original and two copies of the official Canadian health certificate are required for each vehicle. The official health certificate must be issued by a veterinarian designated or accredited by the Canadian Food Inspection Agency (CFIA), and must be endorsed by a full-time salaried veterinarian employed by CFIA attesting to the certifications required in this protocol. The health certificate is valid for 30 days from the issue date. 1.4 The official health certificate must include: a) name and address of the importer; b) species, breed, and number of bovines to be imported; c) purpose of the importation; d) individual bovine identification, which includes the eartag number, and any other identification present on the animal, including registration number (if any); e) description of the bovines, including age in months, color, and markings (if any) USDA, APHIS, Veterinary Services, National Center For Import And Export: Protocol For The Importation Of Cattle Or Bison For Feeding From Canada CAN feederC&B 6/15/2005 2 f) region/country of origin (Note: this part should read Canada. If the animals originated in the United States, then the certificate can indicate “U.S.” in this part); g) address or other means of identifying the premises of origin and any other premises where the bovine resided immediately prior to export; h) specific physical location of the feedlot where the bovines are to be moved after importation; i) name and address of the exporter; j) port of embarkation in Canada, the mode of transportation, route of travel, and port of entry in the United States; and k) identification numbers of the Canadian seals that have been applied to the vehicle. 1.5 Each animal must be individually identified by an official Canadian eartag, applied before the animal’s arrival at the port of entry into the United States. All tags must be clean and readable and preferably in the right ear to expedite inspection at the port of entry. Complete ear tag numbers must be recorded on the health certificate. 1.6 USDA considers all Canadian provinces to be free of bovine brucellosis. 1.7 Currently, USDA considers all Canadian provinces, except for the province of Manitoba, to have a bovine tuberculosis (TB) accredited free status. The province of Manitoba has a TB modified accredited advanced (MAA) TB status. Feeder cattle or bison from Manitoba are not required to have a TB test. 2. HEALTH CERTIFICATIONS 2.1 The bovines have been kept in Canada during the last 60 days immediately preceding the date of shipment to the United States, and during this time, Canada has been free from foot-and-mouth disease, rinderpest, and contagious bovine pleuropneumonia. [Ref: 9CFR 93.405(a)(1)] 2.2 The bovines are not in quarantine in Canada. [Ref: 9CFR 93.405(a)(2)] 2.3 The bovines have been inspected and found to be free from any evidence of communicable disease and that, as far as can be determined, they have not been exposed to any such disease during the preceding 60 days. [Ref: 9CFR 93.418(a)] 2.4 The bovines are from a brucellosis free province. [Ref: 9CFR 93.418(c)] 2.5 The bovines have continuously resided in a TB accredited free or MAA Canadian province or U.S. State. 2.6 In regard to BSE: USDA, APHIS, Veterinary Services, National Center For Import And Export: Protocol For The Importation Of Cattle Or Bison For Feeding From Canada CAN feederC&B 6/15/2005 3 2.6(a) the bovines are less than 30 months of age when imported into the United States [Ref: 9CFR 93.436]; 2.6(b) the bovines are subject to a ruminant feed ban equivalent to the requirements established by the U.S. Food and Drug Administration [Ref: 9CFR 93.436] [Ref: 21CFR 589.2000]; 2.6(c) the bovines have been permanently and humanely identified before arrival at the port of entry with a distinct and legible CΛN mark that has been properly applied with a freeze brand, hot iron, or other permanent method, and is easily visible on the live animal. This mark must also be visible on the carcass before skinning, be not less than 2 inches, and must be applied to each animal’s right hip, high on the tail-head (over the junction of the sacral and first coccygeal vertebrae) [Ref: 9CFR 93.436]; and 2.6(d) the bovines are not pregnant. 2.7 Other means of permanent identification may be used if requested in writing and approved by NCIE prior to import. 3. TESTING 3.1 No tests are required for feeder bovines. 4. PORT OF ENTRY INSPECTION 4.1 Bovines must be presented by appointment to a U.S. port of entry listed in 9 CFR 93.403(b). The VS Form 17-29 “Declaration of Importation” must be completed by the customs broker and must be presented to the port veterinarian along with the official health certificate. 4.2 Bovines must arrive at the port of entry in a vehicle that has been sealed in Canada with seals of the national government of Canada. (In the event that Customs and Border Protection [CBP] inspected the vehicle, CBP will reseal the vehicle with official seals.) The Canadian seal numbers must be included on the health certificate. If the vehicle arrives at the port of entry and the seals are broken, missing, or do not match the seal numbers on the health certificate, the vehicle will be refused entry. In the event that the shipment does not comply with protocol requirements, the port veterinarian will document the number of animals in the shipments that are rejected. The port veterinarian will also contact the appropriate officials with CBP and CFIA port authorities to inform them of the refusal of the shipment. 4.3 The port veterinarian shall inspect the animals and examine the health certificate and verify that the requirements of this protocol have been met. The port veterinarian will then issue VS Form 17-130 “Ruminants Imported to Designated/Approved USDA, APHIS, Veterinary Services, National Center For Import And Export: Protocol For The Importation Of Cattle Or Bison For Feeding From Canada CAN feederC&B 6/15/2005 4 Feedlots” and VS Form 17-30, “Report of Animals, Poultry or Eggs offered for Importation.” 4.4 If the Canadian seals are broken by the APHIS port veterinarian at the port of entry, official seals of the U.S. Government will be applied by the port veterinarian and noted on the VS Form 17-130 along with any Canadian or CBP seals that remain intact on the vehicle. 5. POST ENTRY REQUIREMENTS 5.1 The sealed shipment must be moved directly from the port of entry as a group to the feedlot identified on the VS Form 17-130. 5.2 The seals can only be broken at the feedlot by a State or U.S. Department of Agriculture (USDA) representative, an accredited veterinarian, or his/her designee (i.e., an employee of the accredited veterinarian). It is the responsibility of the State or U.S. Department of Agriculture (USDA) representative, an accredited veterinarian, or his/her designee (i.e., an employee of the accredited veterinarian) to complete #13 to 18 on VS Form 17-130 and return it to the port veterinarian within 14 days of receipt of the shipment. If the seals are broken, missing, or do not match the seal numbers listed on VS Form 17-130, the individual receiving the shipment must immediately notify the port veterinarian and the AVIC. 5.3 No person may alter, deface, remove, or otherwise tamper with the individual official animal identification while the animal is in the United States or moving into or through the United States. Official animal identification may be removed only at the time of slaughter. 5.4 The bovines must remain at the feedlot identified on APHIS Form VS 17-130 until transported from the feedlot to a recognized slaughtering establishment for slaughter. 5.5 Canadian bovines must be moved directly from the feedlot as a group of Canadian bovines to a recognized slaughter establishment in vehicles that are sealed by an accredited veterinarian or a State or USDA representative with seals of the U.S. Government. The seals may be broken only at the recognized slaughtering establishment by a USDA representative. 5.6 The shipment must also be accompanied to the slaughter establishment by VS 17-130 and VS Form 1-27 completed by an accredited veterinarian or a State or USDA representative. VS Form 1-27 must identify the physical location of the recognized slaughtering establishment, the individual responsible for the movement of the animals, and the individual identification of each animal, which includes the USDA, APHIS, Veterinary Services, National Center For Import And Export: Protocol For The Importation Of Cattle Or Bison For Feeding From Canada CAN feederC&B 6/15/2005 5 official eartag and any other identification present on the animal. A copy of the official Canadian health certificate must also accompany the shipment. 5.7 The bovines must be less than 30 months of age when slaughtered. 6. BREEDING ANIMALS 6.1 Breeding cattle or bison cannot be imported from Canada at this time. http://www.aphis.usda.gov/lpa/issues/bse/trade/CAN%20feeder_c-b_7-15.pdf TSS ----- Original Message ----- Thank you for taking this submission via email. i have had trouble submitting via the comment page due to the length of my submission. I was not sure that my file attachment that i submitted via the ; EDOCKET: Go to http://www.epa.gov/feddocket I submitted yesterday, just did not know if the file reached anyone. so to make sure, I am sending to you to submit for me. many thanks, Terry From: TSS () August 24, 2005 Importation of Whole Cuts of Boneless Beef from Japan [Docket No. 05-004-1] RIN 0579-AB93 TSS SUBMISSION My name is Terry S. Singeltary Sr. ======================================================================== This section of the FEDERAL REGISTER contains notices to the public of ======================================================================== Animal and Plant Health Inspection Service 9 CFR Part 94 [Docket No. 05-004-1] AGENCY: Animal and Plant Health Inspection Service, USDA. ACTION: Proposed rule. ----------------------------------------------------------------------- SUMMARY: We are proposing to amend the regulations governing the DATES: We will consider all comments that we receive on or before ADDRESSES: You may submit comments by any of the following methods: snip... International guidelines for trade in animal and animal products Chapter 2.3.13 of the Code and supplemented by Appendix 3.8.4 of the Greetings again APHIS ET AL, Muscle tissue has recently been detected with PrPSc Yoshifumi Iwamaru, Yuka Okubo, Tamako Ikeda, Hiroko Hayashi, Mori- Priori Disease Research Center, National Institute of Animal Health, 3-1-5 Abstract Bovine spongiform encephalopathy (BSE) is a disease of cattle that causes The specified risk materials (SRM) are tissues potentially carrying BSE The 11th BSE case in Japan was detected in fallen stock surveillance. PrPSc was detected in brain, spinal cord, dorsal root ganglia, trigeminal Our results suggest that the currently accepted definitions of SRM in 179 T. Kitamoto (Ed.) International Symposium of Prion Diseases held in Sendai, October 31, to The hardback book title is 'PRIONS' Food and Drug Safety 107 Vet Pathol 42:107–108 (2005) Letters to the Editor Editor: Absence of evidence is not always evidence of absence. In the article ‘‘Failure to detect prion protein (PrPres) by immunohistochemistry in striated muscle tissues of animals experimentally inoculated with agents of transmissible spongiform encephalopathy,’’ recently published in Veterinary Pathology (41:78–81, 2004), PrPres was not detected in striated muscle of experimentally infected elk, cattle, sheep, and raccoons by immunohistochemistry (IHC). Negative IHC, however, does not exclude the presence of PrPSc. For example, PrPres was detected in skeletal muscle in 8 of 32 humans with the prion disease, sporadic Creutzfeldt-Jakob disease (CJD), using sodium phosphotungstic acid (NaPTA) precipitation and western blot.1 The NaPTA precipitation, described by Wadsworth et al.,3 concentrates the abnormal isoform of the prion, PrPres, from a large tissue homogenate volume before western blotting. This technique has increased the sensitivity of the western blot up to three orders of magnitude and could be included in assays to detect PrPres. Extremely conspicuous deposits of PrPres in muscle were detected by IHC in a recent case report of an individual with inclusion body myositis and CJD.2 Here, PrPres was detected in the muscle by immunoblotting, IHC, and paraf- fin-embedded tissue blot. We would therefore caution that, in addition to IHC, highly sensitive biochemical assays and bioassays of muscle are needed to assess the presence or absence of prions from muscle in experimental and natural TSE cases. Christina Sigurdson, Markus Glatzel, and Adriano Aguzzi Institute of Neuropathology University Hospital of Zurich Zurich, Switzerland References 1 Glatzel M, Abela E, et al: Extraneural pathologic prion protein in sporadic Creutzfeldt-Jakob disease. N Engl J Med 349(19):1812–1820, 2003 2 Kovacs GG, Lindeck-Pozza E, et al: Creutzfeldt-Jakob disease and inclusion body myositis: abundant diseaseassociated prion protein in muscle. Ann Neurol 55(1): 121–125, 2004 3 Wadsworth JDF, Joiner S, et al: Tissue distribution of protease resistant prion protein in variant CJD using a highly sensitive immuno-blotting assay. Lancet 358:171–180, 2001 Diagnosis of prions in patients should utilize novel strategy, team says A technique for detecting prions in tissue, developed in recent years by The finding indicates that the diagnostic technique, known as the The finding suggests that reliance on the current methods for detecting In the study, the team compared the ability of the CDI and the two "In about 80 percent of the different brain regions examined, prions "These findings indicate that histology and immunohistochemistry should "If the traditional techniques are used at autopsy, they must be applied Moreover, while the study examined the efficacy of the CDI in comparison "The studies reported here are likely to change profoundly the approach More broadly, the scientists say, the high sensitivity of the CDI "Whether immunohistochemistry underestimates the incidence of one or The finding will be printed on-line and in print on March 1, 2005 in The study brings into high relief the different detection strategies of Standard immunohistochemistry, developed in the DeArmond lab 20 years The limitation of this technique is that scientists have since learned The CDI addresses this limitation by revealing the region of PrPSc that Detractors would say that it is not necessary to detect the minute level Prusiner won the 1997 Nobel Prize in Physiology or Medicine for The CDI was developed by members of the Prusiner lab. The CDI Prusiner, Safar, DeArmond and other members of the Institute for Other co-authors of the study were Michael D. Geschwind, Camille The study was funded by the National Institutes of Health, the John The UCSF Institute for Neurodegenerative Diseases: FURTHER COMPARISON OF THE CDI TO THE STANDARD DIAGNOSTIC PROCEDURES, Explanation as to why the CDI is more sensitive than Western blot DeArmond cites additional evidence about Western blot analysis from a Explanation as to why IHC for prions is less sensitive than the CDI: IHC ### http://pub.ucsf.edu/newsservices/releases/200502147/ NEUROSCIENCE Diagnosis of human prion disease Jiri G. Safar *, , Michael D. Geschwind , , Camille Deering *Institute for Neurodegenerative Diseases, Memory and Aging Contributed by Stanley B. Prusiner, December 22, 2004 Abstract With the discovery of the prion protein (PrP), The clinical diagnosis of human prion disease is often Recently, the role of IHC in the diagnosis of scrapie in the The CDI was developed to quantify PrPSc in tissue samples The CDI detected HuPrPSc with a sensitivity comparable to Our studies show that only the CDI detected PrPSc in all Histologic changes in prion disease have been shown to Studies of the white matter in CJD brains were particularly Most immunoassays that detect HuPrPSc do so only after Gerstmann–Sträussler–Scheinker, an inherited human prion The studies reported here are likely to change profoundly Our results suggest that using the CDI to test large numbers Acknowledgements Methods We used a highly sensitive method of detection — involving the concentration of PrPSc by differential precipitation with sodium phosphotungstic acid, which increased the sensitivity of Western blot analysis by up to three orders of magnitude — to search for PrPSc in extraneural organs of 36 patients with sporadic Creutzfeldt–Jakob disease who died between 1996 and 2002. Results PrPSc was present in the brain tissue of all patients. In addition, we found PrPSc in 10 of 28 spleen specimens and in 8 of 32 skeletal-muscle samples. Three patients had PrPSc in both spleen and muscle specimens. Patients with extraneural PrPSc had a significantly longer duration of disease and were more likely to have uncommon molecular variants of sporadic Creutzfeldt–Jakob disease than were patients without extraneural PrPSc. Conclusions Using sensitive techniques, we identified extraneural deposition of PrPSc in spleen and muscle samples from approximately one third of patients who died with sporadic Creutzfeldt–Jakob disease. Extraneural PrPSc appears to correlate with a long duration of disease. From the Institute of Neuropathology and National Reference Center for Prion Diseases, University Hospital of Zurich, Zurich, Switzerland. Dr. Glatzel and Mr. Abela contributed equally to the article. Address reprint requests to Dr. Aguzzi at the Institute of Neuropathology, University Hospital of Zurich, Schmelzbergstr. 12, CH-8091 Zurich, Switzerland, or at adriano@pathol.unizh.ch . Gabor G. Kovacs, MD PhD 1 2, Elisabeth Lindeck-Pozza, MD 1, Leila Chimelli, MD, PhD 3, Abelardo Q. C. Araújo, MD, PhD 4, Alberto A. Gabbai, MD, PhD 5, Thomas Ströbel, PhD 1, Markus Glatzel, MD 6, Adriano Aguzzi, MD, PhD 6, Herbert Budka, MD 1 * *Correspondence to Herbert Budka, Institute of Neurology, AKH 4J, Wühringer Gürtel 18-20, POB 48, A-1097 Vienna, Austria Funded by: Abstract Pathologicalprion protein (PrPSc) is the hallmark of prion diseases affecting primarily the central nervous system. Using immunohistochemistry, paraffin-embedded tissue blot, and Western blot, we demonstrated abundant PrPSc in the muscle of a patient with sporadic Creutzfeldt-Jakob disease and inclusion body myositis. Extraneural PrPC-PrPSc conversion in Creutzfeldt-Jakob disease appears to become prominent when PrPC is abundantly available as substrate, as in inclusion body myositis muscle. -------------- Received: 16 June 2003; Revised: 11 September 2003; Accepted: 11 September 2003 http://www3.interscience.wiley.com/ AS Professor Aguzzi kindly put it most recently ; 107 Christina Sigurdson, Markus Glatzel, and Adriano Aguzzi http://www.emboreports.org/ http://www.bseinquiry.gov.uk/files/yb/1990/01/19009001.pdf Recall Release CLASS II RECALL Congressional and Public Affairs WASHINGTON, Aug. 19, 2005 - Green Bay Dressed Beef, a Green Bay, Wis., establishment, is voluntarily recalling approximately 1,856 pounds of beef products that may contain portions of the backbone from a cow just over 30 months old, the U.S. Department of Agriculture's Food Safety and Inspection Service announced today. The product was from a cow imported directly for slaughter from Canada. Based on information provided by Canada, the products subject to this Class II recall are from a cow that is approximately one month older than the 30-month age limit. Both ante-mortem and post-mortem inspection were done on the cow in question. FSIS inspection program personnel determined the cow to be healthy and fit for human food. FSIS' designation of this recall as Class II is because it is a situation where there is a remote probability of adverse health consequences from the use of the product. FSIS learned about this as a result of a Canadian audit of their health certificate that accompanied the imported cow. Prior to slaughter, the health certificate accompanying the cow was presented to the establishment, and it appeared complete and accurate. However, a subsequent audit of information related to the health certificate by Canadian officials found that it was not accurate. Action has been taken by Canadian Food Inspection Agency officials in response to findings from the audit. The products subject to recall are: Each box bears the establishment number "410" inside the USDA seal of inspection. The products were produced on August 4, and were distributed to wholesale distributors in Pennsylvania, Florida, Illinois, Maryland, Minnesota and Wisconsin. Under the interim final rules FSIS implemented on January 12, 2004, certain specified risk materials must be removed from all cattle depending on the age of the animal. On this animal all specified risk materials for cattle 30 months and over were removed, with the exception of the vertebral column. At the time of slaughter, the animal was certified to be under 30 months of age and removal of the vertebral column was not required. A subsequent audit determined the animal was just over 30 months of age; therefore, the vertebral column is required to be removed. This is the reason for the recall of the selected products. Consumers with questions about the recall may contact Sally VandeHei, Executive Assistant at 1-877-894-3927. National media with questions may contact Jim Mulhern at (202) 496-2468. Local media with questions may contact Susan Finco at (920) 965-7750 ext.158. Consumers with other food safety questions can phone the toll-free USDA Meat and Poultry Hotline at 1-888-MPHotline (1-888-674-6854). The hotline is available in English and Spanish and can be reached from 10 a.m. to 4 p.m. (Eastern Time), Monday through Friday. Recorded food safety messages are available 24 hours a day. # : Docket No. 03-080-1 -- USDA ISSUES PROPOSED RULE TO ALLOW LIVE ANIMAL IMPORTS FROM CANADA EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA) Report Summary The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003. The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties. A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90’s when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries. EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases. From: Terry S. Singeltary Sr. [flounder@wt.net] Greetings FDA, snip... PLUS, if the USA continues to flagrantly ignore the _documented_ science to date about the known TSEs in the USA (let alone the undocumented TSEs in cattle), it is my opinion, every other Country that is dealing with BSE/TSE should boycott the USA and demand that the SSC reclassify the USA BSE GBR II risk assessment to BSE/TSE GBR III 'IMMEDIATELY'. for the SSC to _flounder_ any longer on this issue, should also be regarded with great suspicion as well. NOT to leave out the OIE and it's terribly flawed system of disease surveillance. the OIE should make a move on CWD in the USA, and make a risk assessment on this as a threat to human health. the OIE should also change the mathematical formula for testing of disease. this (in my opinion and others) is terribly flawed as well. to think that a sample survey of 400 or so cattle in a population of 100 million, to think this will find anything, especially after seeing how many TSE tests it took Italy and other Countries to find 1 case of BSE (1 million rapid TSE test in less than 2 years, to find 102 BSE cases), should be proof enough to make drastic changes of this system. the OIE criteria for BSE Country classification and it's interpretation is very problematic. a text that is suppose to give guidelines, but is not understandable, cannot be considered satisfactory. the OIE told me 2 years ago that they were concerned with CWD, but said any changes might take years. well, two years have come and gone, and no change in relations with CWD as a human health risk. if we wait for politics and science to finally make this connection, we very well may die before any decisions Development on Human and Animal Health Aspects of Transmissible Spongiform Encephalopathies 2005-2008 3.2.1 The species barrier and the carrier state 3.2.1.1 The possibility of ‘carrier’ states in animals and humans, and our present inability to identify them, pose a potential threat to public and animal health. The susceptibility of humans to BSE infection, and the ability of the disease to remain clinically silent for many years, is of major concern to DH. Although the death of a UK blood donor from vCJD in 1999 three years after making the donation and the subsequent death from vCJD of the recipient in 2003 have not been causally linked, transmission of infection through blood transfusion is the most likely explanation327. The case heightens concerns that ‘carriers’ could be transmitting the disease through blood, tissue and organ donation or by contaminating surgical instruments when undergoing surgery. DH will continue to support research to detect infectious prions in human tissue, to investigate the decontamination of surgical instruments and to develop measures to protect blood supplies. 3.2.1.2 Animal models of some TSEs have detected infectivity in blood. Experiments, which have involved transfusing large volumes of blood from infected sheep to healthy recipient sheep, have demonstrated that infectivity can be transmitted by blood transfusion. A central part of DH policy in this area has been the leucodepletion of blood donations and the efficacy of this technology can now be tested in sheep. probable means by which the disease was being spread. In an attempt to prevent further infections a ban on incorporating ruminant protein in ruminant feed was introduced in July 1988. Due to the long incubation period associated with this disease the efficacy of this control measure was not immediately apparent. As time passed it became clear from the number of cases born after the ban that it was not wholly effective. 4.5.5 Epidemiological analysis of these cases showed that a high proportion of them occurred in areas where the pig population was high. This observation, coupled with research data that showed that only a very small dose of the infective material was needed to cause disease in cattle, led to the conclusion that cross-contamination of feed was occurring. 4.5.6 Since 1988, increasingly stringent feed controls have been put in place. Key amongst these have been: • the ban on the use of specified bovine offal in all animal feed (September 1990); • the ban on feeding any farmed animal, including horses and fish, with mammalian meat and bone meal. (This began in March 1996 but following this ban there was a recall scheme and the date from which the ban was considered to be fully effective is regarded as being 1 August 1996); 62 v6.1 • EU-wide controls on feed which extended the ban to include all processed animal protein, including that derived from birds and fish (implemented in the UK from 1 August 2001). 4.5.7 As illustrated in fig. [ ] these later measures have reduced the spread of BSE. However, they have not been one hundred per cent effective. As at 31st December 2003 there had been 81 cases of BSE in animals born since 1 August 1996 in the UK. full text 33 PAGES ; http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf http://www.bseinquiry.gov.uk/ Cutlip RC, Miller JM, Race RE, Jenny AL, Katz JB, Lehmkuhl HD, DeBey BM, USDA, Agriculture Research Service, National Animal Disease Center, Ames, IA To determine if sheep scrapie agent(s) in the United States would induce a MeSH Terms: Substances: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8133096&dopt=Citation http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf COMMENTING ON THE SRMs AND THE REMOVAL OF SRMs. I FIND IT DISTURBING THAT RECENTLY, WOULD it not be likely that from some of these noncompliance reports that ALL we have heard about in the last 7 years or better, well, since the SINCE some 460 of these occurred because slaughter plants did not have an WHAT about the SRM violations? Violations of rules about the removal and In 10 percent of the NRs analyzed, plants incorrectly identified the age of IN my opinion, this could have led to many feed discrepancies and should WASHINGTON - August 18 - In stark contrast to the public relations message More than half the violations (460) occurred because slaughter plants did "The fact that 60 percent of the violations were due to a failure to even The analysis also found that: The violations described in the NRs occurred from January 2004 through March In 10 percent of the NRs analyzed, plants incorrectly identified the age of Public Citizen sent the FOIA request to the USDA in December 2004 after the ### On August 19, 2005, no inconclusive test results were reported. National Veterinary Services Laboratory (NVSL) Immunohistochemistry (IHC) Testing Summary The BSE enhanced surveillance program involves the use of a rapid screening test, followed by confirmatory testing for any samples that come back "inconclusive." The weekly summary below captures all rapid tests conducted as part of the enhanced surveillance effort. It should be noted that since the enhanced surveillance program began, USDA has also conducted approximately 9,200 routine IHC tests on samples that did not first undergo rapid testing. This was done to ensure that samples inappropriate for the rapid screen test were still tested, and also to monitor and improve upon IHC testing protocols. Of those 9,200 routine tests, one test returned a non-definitive result on July 27, 2005. That sample underwent additional testing at NVSL, as well as at the Veterinary Laboratories Agency in Weybridge, England, and results were negative. We have to be careful that we don't get so set in the way we do things that Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't Dr. Keller: Tissues are routinely tested, based on which tissue provides an Dr. Detwiler: That's on the slaughter. But on the clinical cases, aren't THE International guidelines for trade in animal and animal products which are developed by the World Organization for Animal Health (formerly known as the Office International des Epizooties (OIE)), is and has been terrible flawed. ALL one has to do is to look at the countries that have gone by there very minimal guidelines, most all went on to develop BSE. IT would be nice if the OIE et al would define “controlled BSE-risk country” or “effectively enforced ban”. The USA and North America have neither. THIS has been proven time and time again via the GAO, OIG and the European EFSA BSE-risk assessments of North American countries. Many Countries have not even reported there first case of BSE yet, and many countries have not even produced a risk analysis for BSE. A fine example is Mexico and Canada. I pointed out about Canada above, but now lets look at Mexico, which is also a BSE GBR III country. IN Mexico, they are NOT even required to remove SRM; the Assessment of the Geographical BSE-Risk (GBR) of MEXICO 2004 There is no SRM-ban. SRM is normally destined for human consumption. According to the CD, fallen stock from pasture and diseased animals are incinerated and not rendered. Conclusion on the ability to avoid recycling In light of the above information, it has to be assumed that the BSE agent, should it have entered Mexico, could have been recycled and potentially amplified. high external challenges with a very unstable system makes the occurrence of an internal challenge likely in Mexico from approximately 1993 onwards. 4.2 Risk that BSE infectivity entered processing It is likely that BSE infectivity entered processing at the time of imported ‘at - risk’ MBM (1993) and at the time of slaughter of imported live ‘at - risk’ cattle (mid to late 1990’s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable, leading to increased internal 4.3 Risk that BSE infectivity was recycled and propagated It is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system. 5. CONCLUSION ON THE GEOGRAPHICAL BSE - RISK 5.1 The current GBR as function of the past stability and challenge The current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. snip...end The action means that cattle sold by the companies to Texas ranchers after Friday's announcement are subject to seizure by the federal government, said a high-ranking Treasury official who asked not to be named. "Cattle already purchased and owned before the companies were identified as tied to the drug cartels are not going to suddenly be blocked," the official said. The Treasury Department plans to inform cattle associations and other groups later this week of the action taken against the Mexican companies, officials said. The Treasury also will provide other information, such as the brands used by the cattle companies linked to the drug cartels. For now, buyers are expected to practice due diligence when purchasing cattle. Two Mexican drug cartels were named in the Treasury Department's statement, the Arriola Marquez organization and the Arellano Felix cartel based in Tijuana. The Arriola Marquez group, based in Mexico's Chihuahua state, is linked to Mexican drug kingpin Joaquin "El Chapo" Guzman, the department said. Guzman leads one of the factions fighting for control of Nuevo Laredo and its smuggling routes into Texas, officials have said. snip... It is not clear how many Mexican cattle owned by companies linked to drug cartels had been sold in Texas, said government officials and Texas cattle raisers. snip...end http://www.chron.com/cs/CDA/ssistory.mpl/topstory/3319609 TRIPLE firewalls and SEALED borders, I dont think so. MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, London WC1N 3BG, UK Distinct prion strains can be distinguished by differences in incubation period, neuropathology and biochemical properties of disease-associated prion protein (PrPSc) in inoculated mice. Reliable comparisons of mouse prion strain properties can only be achieved after passage in genetically identical mice, as host prion protein sequence and genetic background are known to modulate prion disease phenotypes. While multiple prion strains have been identified in sheep scrapie and Creutzfeldt-Jakob disease, bovine spongiform encephalopathy (BSE) is thought to be caused by a single prion strain. Primary passage of BSE prions to different lines of inbred mice resulted in the propagation of two distinct PrPSc types, suggesting that two prion strains may have been isolated. To investigate this further, these isolates were subpassaged in a single line of inbred mice (SJL) and it was confirmed that two distinct prion strains had been identified. MRC1 was characterized by a short incubation time (110±3 days), a mono-glycosylated-dominant PrPSc type and a generalized diffuse pattern of PrP-immunoreactive deposits, while MRC2 displayed a much longer incubation time (155±1 days), a di-glycosylated-dominant PrPSc type and a distinct pattern of PrP-immunoreactive deposits and neuronal loss. These data indicate a crucial involvement of the host genome in modulating prion strain selection and propagation in mice. It is possible that multiple disease phenotypes may also be possible in BSE prion infection in humans and other animals. ======================= Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria Caramelli * *Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease. -------------------------------------------------------------------------------- C.C. and G.Z. contributed equally to this work. ||To whom correspondence should be addressed. E-mail: salvatore.monaco@mail.univr.it. www.pnas.org/cgi/doi/10.1073/pnas.0305777101 * Commissariat à l'Energie Atomique, Service de Neurovirologie, Direction des Sciences du Vivant/Département de Recherche Medicale, Centre de Recherches du Service de Santé des Armées 60-68, Avenue du Général Leclerc, BP 6, 92 265 Fontenay-aux-Roses Cedex, France; Hôpital Neurologique Pierre Wertheimer, 59, Boulevard Pinel, 69003 Lyon, France; § Laboratoire de Neuropathologie, Hôpital de la Salpêtrière, 83, Boulevard de l'Hôpital, 75013 Paris, France; ¶ Creutzfeldt-Jakob Disease Surveillance Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, United Kingdom; and Institute for Animal Health, Neuropathogenesis Unit, West Mains Road, Edinburgh EH9 3JF, United Kingdom Edited by D. Carleton Gajdusek, Centre National de la Recherche Scientifique, Gif-sur-Yvette, France, and approved December 7, 2000 (received for review October 16, 2000) There is substantial scientific evidence to support the notion that bovine spongiform encephalopathy (BSE) has contaminated human beings, causing variant Creutzfeldt-Jakob disease (vCJD). This disease has raised concerns about the possibility of an iatrogenic secondary transmission to humans, because the biological properties of the primate-adapted BSE agent are unknown. We show that (i) BSE can be transmitted from primate to primate by intravenous route in 25 months, and (ii) an iatrogenic transmission of vCJD to humans could be readily recognized pathologically, whether it occurs by the central or peripheral route. Strain typing in mice demonstrates that the BSE agent adapts to macaques in the same way as it does to humans and confirms that the BSE agent is responsible for vCJD not only in the United Kingdom but also in France. The agent responsible for French iatrogenic growth hormone-linked CJD taken as a control is very different from vCJD but is similar to that found in one case of sporadic CJD and one sheep scrapie isolate. These data will be key in identifying the origin of human cases of prion disease, including accidental vCJD transmission, and could provide bases for vCJD risk assessment. Introduction IN light of Asante/Collinge et al findings that BSE transmission to the -------- Original Message -------- Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD Date: Thu, 28 Nov 2002 10:23:43 -0000 From: "Asante, Emmanuel A" To: Dear Terry, I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention. Thank you for your interest in the paper. In respect of your first question, the simple answer is, yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc. can be of any further assistance please to not hesitate to ask. Best wishes. <> ____________________________________ Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: e.asante@ic.ac.uk (until 9/12/02) New e-mail: e.asante@prion.ucl.ac.uk (active from now) ____________________________________ snip... full text ; http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm SCRAPIE USA MONTHLY REPORT 2005 AS of March 31, 2005, there were 70 scrapie infected source flocks (Figure 3). There were 11 new infected and source flocks reported in March (Figure 4) with a total of 51 flocks reported for FY 2005 (Figure 5). The total infected and source flocks that have been released in FY 2005 are 39 (Figure 6), with 1 flock released in March. The ratio of infected and source flocks released to newly infected and source flocks for FY 2005 = 0.76 : 1. IN addition, as of March 31, 2005, 225 scrapie cases have been confirmed and reported by the National Veterinary Services Laboratories (NVSL), of which 53 were RSSS cases (Figure 7). This includes 57 newly confirmed cases in March 2005 (Figure 8). Fourteen cases of scrapie in goats have been reported since 1990 (Figure 9). The last goat cases was reported in January 2005. New infected flocks, source flocks, and flocks released or put on clean-up plans for FY 2005 are depicted in Figure 10. ... FULL TEXT ; http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html http://www.aphis.usda.gov/vs/nahps/cwd/labmap.html Chronic Wasting Disease and Potential Transmission to Humans 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. Conclusions Environmental Sources of Prion Transmission in Mule Deer Suggested citation for this article: Miller MW, Williams ES, Hobbs NT, Wolfe LL. Environmental sources of prion transmission in mule deer. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm Whether transmission of the chronic wasting disease (CWD) prion among cervids requires direct interaction with infected animals has been unclear. We report that CWD can be transmitted to susceptible animals indirectly, from environments contaminated by excreta or decomposed carcasses. Under experimental conditions, mule deer (Odocoileus hemionus) became infected in two of three paddocks containing naturally infected deer, in two of three paddocks where infected deer carcasses had decomposed in situ ≈1.8 years earlier, and in one of three paddocks where infected deer had last resided 2.2 years earlier. Indirect transmission and environmental persistence of infectious prions will complicate efforts to control CWD and perhaps other animal prion diseases. Prions cannot be directly demonstrated in excreta or soil. However, CWD infection–specific protease-resistant prion protein (PrPCWD) accumulates in gut-associated lymphoid tissues (e.g., tonsils, Peyer patches, and mesenteric lymph nodes) of infected mule deer (11,17,22), which implicates alimentary shedding of the CWD agent in both feces and saliva (10,11,17). Because PrPCWD becomes progressively abundant in nervous system and lymphoid tissues through the disease course (11), carcasses of deer succumbing to CWD also likely harbor considerable infectivity and thus serve as foci of infection. We could not determine the precise mechanism for CWD transmission in excreta-contaminated paddocks, but foraging and soil consumption seemed most plausible. Deer did not actively consume decomposed carcass remains, but they did forage in the immediate vicinity of carcass sites where a likely nutrient flush (23) produced lush vegetation (Figure). Our findings show that environmental sources of infectivity may contribute to CWD epidemics and illustrate the potential complexity of such epidemics in natural populations. The relative importance of different routes of infection from the environment cannot be discerned from our experiment, but each could play a role in sustaining natural epidemics. Although confinement likely exaggerated transmission probabilities, conditions simulated by this experiment do arise in the wild. Mule deer live in established home ranges and show strong fidelity to historic home ranges (24-26). As a result of such behavior, encounters with contaminated environments will occur more frequently than if deer movements were random. Feces and carcass remains are routinely encountered on native ranges, thus representing natural opportunities for exposure. Social behavior of deer, particularly their tendency to concentrate and become sedentary on their winter range, also may increase the probability of coming into contact with sources of infection in their environment. The ability of the CWD agent to persist in contaminated environments for >2 years may further increase the probability of transmission and protract epidemic dynamics (8). Because infectivity in contaminated paddocks could not be measured, neither the initial levels nor degradation rate of the CWD agent in the environment was estimable. However, the observed persistence of the CWD agent was comparable to that of the scrapie agent, which persisted in paddocks for ≈1 to 3 years after removal of naturally infected sheep (7). Similarities between the CWD and scrapie agents suggest that environmental persistence may be a common trait of prions. Whether persistence of the BSE prion in contaminated feed production facilities or in environments where cattle reside contributed to BSE cases in the United Kingdom after feed bans were enacted (27) remains uncertain but merits further consideration. Indirect transmission and environmental persistence of prions will complicate efforts to control CWD and perhaps other animal prion diseases. Historically, control strategies for animal prion diseases have focused on infected live animals as the primary source of infection. Although live deer and elk represent the most plausible mechanism for geographic spread of CWD, our data show that environmental sources could contribute to maintaining and prolonging local epidemics, even when all infected animals are eliminated. Moreover, the efficacy of various culling strategies as control measures depends in part on the rates at which the CWD agent is added to and lost from the environment. Consequently, these dynamics and their implications for disease management need to be more completely understood. The first positive result in a wild deer was announced on April 27, 2005 and came from a yearling white-tailed deer sampled from the Town of Verona, Oneida County. The second positive result is from a 3-year-old doe, located within a mile of the location where the initial positive result was detected. The sample tissues were tested at the State's Veterinary Diagnostic Laboratory at Cornell University. These are the first known occurrences of CWD in wild deer in New York State. DEC implemented intensive monitoring efforts after CWD was found in two captive white-tailed deer herds in Oneida County – the first incidents of CWD in New York State. On April 8, 2005, the State Department of Agriculture and Markets (DAM) completed testing of the captive deer and found a total of five positive results for CWD in the two captive herds. DEC, along with the U.S. Department of Agriculture's Wildlife Services program, completed intensive monitoring on April 30, 2005. The effort resulted in 290 samples of wild deer from Oneida County, two from neighboring Madison County, and 25 wild deer from the Town of Arietta, Hamilton County. Since 2002, DEC has conducted statewide sampling of wild deer for CWD. When combined with sampling efforts in Oneida and Hamilton Counties, DEC has collected more than 3,700 samples from wild white-tailed deer. DEC and DAM will continue public outreach to interested parties in central New York to help educate citizens on CWD and to discuss next steps to be taken. The agencies will hold a public meeting on Thursday, May 12, 2005, at 7 p.m. in the Vernon-Verona-Sherrill High School Auditorium, located on State Highway 31 in the Town of Verona. In addition, DEC and DAM will conduct additional outreach and continue to aggressively pursue inspection and enforcement across the State. DAM continues to investigate, sample and test white-tailed deer from two captive herds directly associated with the two herds that were confirmed positive for CWD in Oneida County. Results for these sampling efforts will be announced when available. Statewide sampling for CWD - which has resulted in more than 1,000 tests each year - will be increased to closely monitor the distribution and prevalence of CWD in wild deer. In addition, DEC has implemented emergency regulations regarding the handling, transport and management of deer in the State. The emergency regulations are currently in effect and represent an aggressive response to the recent discovery of chronic wasting disease (CWD) in Oneida County. DEC's emergency regulations are designed to ensure the proper handling of deer and prevent further spread of CWD in the wild herd. The emergency regulations are effective for 90 days. In addition, DEC will begin the process of developing permanent regulations, which will appear in the State Register and include a 45-day public comment period. CWD is a transmissible disease that affects the brain and central nervous system of certain deer and elk. There is no evidence that CWD is linked to disease in humans or domestic livestock other than deer and elk. More information on CWD can be found at DEC's website at www.dec.state.ny.us/website/dfwmr/wildlife/deer/currentcwd.html 05-48 P.O. Box 42 Bacliff, Texas USA 77518 Please note that it may take between 24 and 72 hours for the EDOCKET staff to process your comment before it is available publicly through EDOCKET. You can use the identifier noted above to find your comment through the Quick or Advanced Search pages when it is available. http://docket.epa.gov/edkfed/do/EDKStaffAttachDownloadPDF?objectId=090007d480993808 http://docket.epa.gov/edkfed/do/EDKStaffCollectionDetailView?objectId=0b0007d48096b40d
|
