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From: TSS (216-119-132-86.ipset12.wt.net)
In Reply to: Neuroinvasion by Scrapie following Inoculation via the Skin Is Independent of Migratory Langerhans Cells posted by TSS on January 13, 2005 at 1:38 pm:
WHAT does the fda say, everything is ok, but what about before July 14, 2004 ??? WHAT about all that cream and eye make-up my mother used for decades and she Similarly, FDA has prohibited the use of the cattle materials that carry the highest risk of BSE in human food, including dietary supplements, and in cosmetics. FDA's rule prohibits use of the following cattle material in human food and cosmetics: * cattle material from non-ambulatory, disabled cattle, FDA's rule also requires that food and cosmetics manufacturers and processors make available to FDA any existing records relevant to their compliance with these prohibitions. FDA has also published a proposal requiring manufacturers and processors of food and cosmetics made with cattle material to establish and maintain records demonstrating that their products do not contain prohibited cattle material. 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. Since 1989, USDA has prohibited the importation of live animals and an imal products from BSE-positive countries. Subsequently, USDA expanded the ban to include both countries with BSE and countries at risk for BSE. Since 1997, FDA has prohibited the use of most mammalian protein in the manufacture of ruminant feed. In 2004, FDA issued a rule prohibiting the use of certain cattle materials in human food and cosmetics, and USDA issued a rule prohibiting certain cattle materials from use as human food. This document was issued in January 2004 and updated in July 2004. July 9, 2004 I. FDA'S New Interim Final Rule Prohibiting Use of Certain Cattle Materials that May Carry the Risk of Bovine Spongiform Encephalopathy in Human Foods and Cosmetics II. FDA's Proposed Rule on Recordkeeping Requirements for Human Food and Cosmetics Manufactured From, Processed With, or Otherwise Containing Material From Cattle In response to the finding of an adult cow that tested positive for BSE in the State of Washington, FDA is taking action to minimize human exposure to materials that scientific studies have demonstrated to contain the BSE agent when they come from cattle infected with the disease. This action is consistent with the interim final rule issued by the U.S. Department of Agriculture (USDA) prohibiting certain cattle materials from use as human food. It is widely accepted that consumption of products contaminated with the agent that causes BSE results in the human illness, variant Creutzfeldt-Jakob disease (vCJD). In conjunction with the interim final rule (IFR), FDA is issuing a proposed rule to require that manufacturers and processors of human food and cosmetics that are manufactured from, processed with, or otherwise contain material from cattle, establish and maintain records sufficient to demonstrate that the food and cosmetics are in compliance with the IFR. * specified risk materials The interim final rule also requires that FDA-regulated food and cosmetic manufacturers and processors make available to FDA any existing records that may be relevant to their compliance with the prohibitions in the rule. What are specified risk materials? Specified risk materials, from cattle 30 months and older, are the: * brain Specified risk materials from cattle of any age are the * tonsils and Prohibited cattle materials do not include tallow that contains no more than 0.15 percent hexane-insoluble impurities and tallow derivatives. What products are covered by the interim final rule? All FDA-regulated human food and cosmetics, including: * Dietary supplements and dietary ingredients How can food manufacturers and processors comply? Manufacturers and processors who currently use prohibited cattle materials will need to switch to alternative ingredients. In addition, the rule requires that manufacturers and processors make existing records related to compliance with the rule available to FDA for inspection and copying. When does the rule take effect? This rule is in effect as of July 14, 2004, the date of its publication in the Federal Register, however, FDA is providing a 90-day comment period on this interim final rule. The rule applies to human food and cosmetics manufactured from, processed with, or that otherwise contain material, from cattle slaughtered on or after the interim final rule's effective date. How to comment on this interim final regulation: Comments on this interim final regulation, (Docket Number 2004N-0081), will be accepted until October 12, 2004. Written comments can be sent to the Dockets Management Branch (HFA-305), Food and Drug Administration, 5630 Fishers Lane, Room 1061, Rockville, MD 20852. Comments can be sent electronically to www.fda.gov/dockets/ecomments or as an e-mail to fdadockets@oc.fda.gov. Please ensure that you include in your submission the docket number that applies to your comment: Prohibited Cattle Materials--Docket No. 2004N-0081. What would be required in the companion recordkeeping proposal? Manufacturers and processors of FDA-regulated human food and cosmetics that use cattle material in their products would be required to keep records demonstrating that these materials do not contain prohibited cattle materials. The proposal also would require that manufacturers and processors make these records available to FDA for inspection and copying. What types of records would be required? Generally, FDA would expect a manufacturer or processor to have a signed and dated affirmation, including contact information, from the slaughter establishment stating that cattle material supplied by the establishment in a particular shipment does not contain prohibited cattle materials. For human food and cosmetics containing tallow, a manufacturer or processor would need to maintain records (signed, and dated, with contact information) either from the slaughter establishment affirming that the tallow was produced from material containing no prohibited cattle materials, or from the tallow supplier affirming that the tallow contains no more than 0.15 percent insoluble impurities. How long would the records have to be retained? FDA is proposing that these records be retained for two years. Where would the records have to be maintained? Records would have to be maintained at the manufacturing or processing establishment or at a reasonably accessible location. Electronic records would be acceptable and are considered to be reasonably accessible if they are accessible from an onsite location. What about imported human food and cosmetic products containing cattle materials? Importers would be required to electronically affirm their compliance with these recordkeeping requirements at the time the products enter the U.S. and would have to provide the required records to FDA within a reasonable time, if requested. How to comment on proposed regulations: FDA invites comments on this proposal, e.g., suggestions to make the proposal more effective or less burdensome, questions regarding the agency's data or assumptions, submission of information the agency may not have. The agency is especially interested in comments on other ways in which the proposed recordkeeping requirements might be satisfied, as well as comments on whether existing recordkeeping practices include the required information and, if not, what changes the proposal would necessitate. Comments on this proposed regulation, Recordkeeping Requirements for Human Food and Cosmetics Manufactured From, Processed With, or Otherwise Containing Material from Cattle, Docket Number 2004N-0257, will be accepted until August 13, 2004. Written comments on the proposal can be sent to the Dockets Management Branch (HFA-305), Food and Drug Administration, 5630 Fishers Lane, Room 1061, Rockville, MD 20852. Comments can be sent electronically to www.fda.gov/dockets/ecomments or as an e-mail to fdadockets@oc.fda.gov. Please ensure that you include in your submission the docket number that applies to your comment: Recordkeeping - Docket No. 2004N-0257. 14 July 2004 ----------------------------------------------------------------------- [Federal Register: July 14, 2004 (Volume 69, Number 134)] ----------------------------------------------------------------------- DEPARTMENT OF HEALTH AND HUMAN SERVICES Food and Drug Administration [Docket No. 2004N-0291] AGENCY: Food and Drug Administration, HHS. ACTION: Notice. ----------------------------------------------------------------------- SUMMARY: The Food and Drug Administration (FDA) is announcing the ADDRESSES: Submit written requests for single copies of the risk FOR FURTHER INFORMATION CONTACT: Morris Potter, Center for Food Safety SUPPLEMENTARY INFORMATION: I. Background Cosmetics may be made from a variety of cattle-derived ingredients. [[Page 42192]] There are several routes through which cosmetics contaminated with II. Risk Assessment for Cosmetics and Potential Contamination With the The risk assessment presents scientific evidence on the risk of III. Electronic Access The risk assessment is available electronically at http://www.cfsan.fda.gov Dated: July 9, 2004. BILLING CODE 4160-01-S http://cryptome.org/fda071404.txt July 14, 2004 The discovery of a cow with bovine spongiform encephalopathy (BSE) in Washington State in December 2003 triggered action to put in place additional safeguards against BSE. Even though the cow was born in Canada, the fact that the cow was discovered in the U.S. and had been sent to slaughter and rendering before it was identified as positive indicates a vulnerability in the U.S. BSE protective net. While BSE is usually identified with either food safety or animal health, cosmetics, because of the ways they are used, provide another route for BSE infectivity to enter the human system. Cosmetics may contain a wide range of cattle-derived ingredients, many of which may carry the BSE agent. FDA prepared this assessment of the risks to public health if cattle-derived ingredients are used in cosmetics. This qualitative risk assessment follows the generally accepted framework for risk assessments endorsed by the Codex Alimentarious Commission, the U.S. National Academy of Sciences, and other authoritative bodies. The framework divides risk assessment into four components: (1) hazard identification, (2) exposure assessment, (3) hazard characterization (or dose-response assessment), and (4) risk characterization. The risk assessment uses scientific evidence to the extent that it exists. The agency has determined that this qualitative risk assessment is appropriate to the circumstances. In April 1996, British scientists reported a previously undetected new variant of Creutzfeldt-Jakob disease (vCJD) in young patients, with symptoms somewhat different from sporadic CJD (Refs. 1 and 2). All cases of vCJD had histopathologic evidence of spongiform changes in the brain, but also showed formation of "florid" plaques (a core of amyloid protein with surrounding halos of vacuoles) not typically seen in other forms of CJD (Ref. 3). Clinically, vCJD usually begins with a psychiatric presentation, such as depression, anxiety, nightmares or hallucinations. These symptoms are followed by memory impairment, then dementia in the late stages. The clinical course may last up to two years before death occurs (Ref. 4). Because scientific evidence suggests that the presence and infectivity of abnormal prion proteins in vCJD share characteristics with abnormal prion proteins found in cattle with BSE, scientists have concluded that exposure to the BSE agent is the most plausible explanation for the occurrence of vCJD (Refs. 5 - 8). Monkeys (genetically the closest animal model to humans) inoculated with samples of brain from BSE-infected cattle have been found to develop a TSE that is histopathologically similar to vCJD (Ref. 9), as have mice inoculated or fed with BSE-infected tissue (Ref. 10). In addition, studies have shown that abnormal prion proteins from vCJD patients are molecularly similar to abnormal prion proteins from BSE-infected cattle and different from abnormal prion proteins from patients with CJD and other spongiform encephalopathies (Ref. 4). Prions are predominantly found in the central nervous system, portions of the intestine, and tonsils of cattle with BSE. Cosmetic ingredients can be derived from some of these tissues. Although large prion doses are known to have a shorter incubation period before the disease develops, even low doses may cause vCJD if infectious prions survive digestion and the host survives long enough to complete a longer incubation period. Although most scientists believe that vCJD in humans is caused by consumption of cattle-derived food products contaminated with the agent that causes BSE (Refs. 11-14), exposure from cosmetics derived from cattle protein is another potential route of exposure. BSE in the United States Use of Cattle Protein in Cosmetics Absorption of Prions from Cosmetics It is well-documented that central nervous system tissue, including the optic nerve, carries infectivity in animals with TSEs and humans with vCJD, and serves as an efficient route of transmission. In mice, intraocular injection of scrapie caused infection along the optic nerve, which eventually spread into non-neural tissue via the lymphatic system (Ref. 15). In addition to intraocular injection, infectivity has been transmitted to animals via the conjunctiva of the eye (mucosal tissue). Scott et al. (Ref. 16) found that scrapie was induced in 42 percent of rodents by dropping a high concentration of infectivity onto the conjunctiva. Klitzman et al. (Ref. 17) suggested that kuru, a human TSE disease found only among the Fore people of New Guinea, might have been transmitted by rubbing infected human brain into eyes or cut skin, while handling and consuming infected brain during funeral rituals. Cut or abraded skin also has been proposed as a route for contracting TSE diseases. The transmission of kuru through cut skin has been suggested and was mentioned previously. Taylor et al. (Ref. 18) and Ingrosso et al. (Ref. 19) demonstrated increased transmission of scrapie via oral mucosal tissue. In one study, 100 percent of mice with experimentally damaged oral mucosal tissue developed scrapie through ingestion of infected material, while only 71 percent of mice with intact mucosa developed the disease (Ref. 18). In addition, Pammer et al. (Ref. 20) and Sugaya et al. (Ref. 21) noted that epithelial cells, dendritic cells, and keratinocytes (the primary cell types found in the epidermis) have been found to contain infectious prion protein, indicating that these cells are potential targets for peripheral infection with a TSE disease. Use of BSE-contaminated cosmetics could provide a means of human infection via several routes discussed above. Many cosmetics are typically applied in the area of the eye (mascara, eye brow pencil, eyeliner, eye lotion, and eye makeup remover) and almost any cosmetic, including shampoo, can get into the eye via eye rubbing or incorrect application. Any cosmetic product, but particularly shaving creams and gels and lotions, may be applied to cut or abraded skin. Cosmetics that are ingested, such as lipstick, dentifrices, mouthwash, and breath fresheners, would have an oral route of infection, and the ingested fraction would have the same risk as prion-contaminated meat and other food products derived form cattle. Furthermore, the presence of cattle derived ingredients is not generally obvious to the consumer, since the source of the ingredient (i.e. cattle derived) does not need to be placed on the label. Prions with a particular abnormal tertiary structure are apparently able to generate a similar misconformation in normal proteins, which can in turn cause further misconformations. This allows propagation of the disease and is also important for understanding the relationship between dose, response, and the incubation required for the disease to develop. Once the prions have entered the brain, the prion concentration grows with a relationship that has been described as exponential (Ref. 14). In cattle, there is a minimal incubation period of six months to a year required for the development of the disease, regardless of the size of the initial dose, although incubation periods of 4 or more years appear to be more common (Refs. 11 and 12). The lag period may reflect the fact that transmission from food to brain may be preceded by symptomless amplification of infectious prions in the intestine and lymphoreticular tissues. While cattle at this stage would be clinically normal and may have negative BSE test results, various tissues could be infectious (Refs. 11 and 12). Despite widespread exposure in the U.K. to BSE-contaminated meat products, only a very small percentage of the exposed population has been diagnosed with vCJD to date. However, ongoing experiments indicate that the infectious dose for cattle is very low. One gram of affected bovine brain homogenate is sufficient to cause BSE in more than 50 percent of calves exposed by mouth. Five years after oral consumption of lower doses of brain material, 2 of 15 calves fed 0.1 gram had onset of BSE, and 1 of 15 fed 0.01 gram had developed the disease. This experiment is ongoing (Ref. 22). There is thought to be a 10- to 10,000-fold increase in the amount of infectious material needed to cause illness in humans as compared with cattle, because of the species barrier (Ref. 23). This is not a quantitative risk assessment. However, it does sketch out the logical structure that a quantitative model could use if one were constructed. Some conclusions can be drawn without a quantitative analysis. Since there is considerable uncertainty associated with the premises outlined in the present analysis, it follows that there will also be considerable uncertainty associated with the risk estimate. In the exposure assessment, there are considerable uncertainties associated with the origin of protein used in making cosmetics, the effect of processing on prion concentration, and the transmission rates for dermal and ocular exposure. Particularly large uncertainties associated with the dose response assessment include the magnitude of the species barrier and the length of the incubation period. With exception of the uncertainty associated with estimates of the dermal and ocular transmission rates, most of the uncertainties associated with a risk assessment of BSE prions in cosmetics are also associated with the risk from food consumption. For example, the number of BSE-affected cattle and the variability in human susceptibility will impact the risk of both food- and cosmetic-associated vCJD. Some of these uncertainties may concomitantly affect both sides of a cost-benefit analysis. In particular, if there is not substantial use of cattle-derived protein in making cosmetics, then there will be little exposure, and also little economic consequence from regulating use. Conversely, high use would require substantial substitution and alternative means of animal-by-product disposal. A form of spongiform encephalopathy that occurs in humans (vCJD) is thought to result from the same protein (a prion) that causes BSE in cattle. Although the primary source of exposure is likely to be due to the ingestion of beef and other food derived from cattle, other routes of exposure may also be important. Although small doses require longer incubation periods for clinical signs to develop, small doses of infectious prions can potentially cause disease. Cosmetics that contain protein derived from bovine sources are a potential source of exposure. It has been demonstrated experimentally that TSEs may result from ocular absorption of protein, and systemic absorption of protein may also occur when cosmetics are applied to lacerated or abraded skin. As a result, it may be concluded that there is some risk of occurrence of vCJD from the use of cattle-derived protein in cosmetics. However, since there are large uncertainties associated with the quantitative estimates of many of the important variables, any quantitative estimate of the risk or rate at which the disease may be expected to occur would be correspondingly imprecise. The risk of BSE from cosmetics may be reduced through the control of exposure. Aside from the derivation processes used on tallow, the effectiveness of cosmetic manufacturing processes for inactivating BSE prions is unknown. The surest way to prevent transmission of BSE-prion through cosmetics is to avoid the use of high-risk cattle-derived protein in the manufacture of cosmetics. 1. Will, R.G., J.W. Ironside, M. Zeidler, S.N. Cousens, K. Estibeiro, A. Alperovitch, S. Poser, M. Pocchiari, A. Hofman, and P.G. Smith. 1996. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet 347: 921-25. Chazot, G., E. Broussolle, C.I. Lapras, T. Blattler, A. Aguzzi, and N. Kopp. 1996. New variant of Creutzfeldt-Jakob disease in a 26-year-old French man. Lancet 347: 1181. Prusiner, S.B. 2001. Shattuck Lecture--Neurodegenerative diseases and prions. N Engl J Med 344 (20): 1516-1526. Collinge, J. 2001. Prion diseases of humans and animals: Their causes and molecular basis. Annu. Rev. Neurosci. 24: 519-50. Almond, J. and J. Pattison. 1997. Human BSE. Nature 389: 437-38. Scott, M.R., R. Will, J. Ironside, H-O.B Nguyen, P. Tremblay, S.J. DeArmond, and S.B. Prusiner. 1999. Compelling transgenetic evidence for transmission of bovine spongiform encephalopathy prions to humans. Proc. Natl. Acad. Sci. 96 (26): 15137-142. Hill, A.F., M. Desbruslais, S. Joiner, K.C.L. Sidle, I. Gowland, J. Collinge L.J. Doey, and P. Lantos. 1997. The same prion strain causes vCJD and BSE. Nature 389: 448-450. Collinge, J. 1999. Variant Creutzfeldt-Jakob disease. Lancet 354: 317-323. Lasmezas, C.I., J-G. Fournier, V. Nouvel, H. Boe, D. Marce, F. Lamoury, N. Kopp, J-J. Hauw, J. Ironside, M. Bruce, D. Dormont and J-P. Deslys. 2001. Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt-Jakob disease: Implications for human health. Proc. Natl. Acad. Sci. 98 (7): 4142-4147. Bruce, M.E., R.G. Will, J. W. Ironside, I. McConnell, D. Drummond, A. Suttie, L. McCardle, A. Chree, J. Hope, C. Birkett, S. Cousens, H. Fraser, and C.J. Bostock. 1997. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature 389: 498-501. Brown, P. 1997. The risk of bovine spongiform encephalopathy ('mad cow disease') to human health. J. Am. Med. Assn. 278 (12): 1008-1011. Brown, P., R.G. Will, R. Bradley, D.M. Asher, and L. Detwiler. 2001. Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease: Background, evolution, and current concerns. Emerging Infect. Dis. 7 (1): 6-16. Scientific Steering Committee, European Commission. 1999. Opinion of the Scientific Steering Committee on the Human Exposure Risk (HER) via food with respect to BSE. Accessed online at http://europa.eu.int/comm/food/fs/bse/scientific_advice08_en.html. Harvard Center for Risk Analysis, Harvard School of Public Health. 2003. Evaluation of the potential for bovine spongiform encephalopathy in the United States. Accessed online at http://www.hcra.harvard.edu/pdf/madcow.pdf. Fraser, J.R. 1996. Infectivity in extraneural tissues following intraocular scrapie infection. J. Gen. Virol. 77: 2663-68. Scott, J.R., J. D. Foster and H. Fraser. 1993. Conjunctival instillation of scrapie in mice can produce disease. Vet Microbiol 34 (4): 305-309. Klitzman R.L., M.P. Alpers, and D.C. Gajdusek. 1984. The natural incubation period of kuru and the episodes of transmission in three clusters of patients. Neuroepidemiology 3 (1): 3-20. Taylor, D.M., I. McConnell, and H. Fraser. 1996. Scrapie infection can be established readily through skin scarification in immunocompetent but not immunodeficient mice. J. Gen. Virol. 77: 1595-99. Ingrosso, L., F. Pisani, and M. Pocchiari. 1999. Transmission of the 263K scrapie strain by the dental route. J. Gen. Virol. 80: 3043-47. Pammer, J., W. Weninger, and E. Tschachler. 1998. Human keratinocytes express cellular prion-related protein in vitro and during inflammatory skin diseases. Am. J. Pathol. 153: 1353-58. Sugaya, M., K. Nakamura, T. Watanabe, A. Asahina, N. Yasaka, Y. Koyama, M. Kusubata, Y. Ushiki, K. Kimura, A. Morooka, S. Irie, T. Yokoyama, K. Inoue, S. Itohara, and K. Tamaki. 2002. Expression of cellular prion-related protein by murine Langerhans cells and keratinocytes. J. Dermato. Sci. 28: 126-134. Vossen, P., J. Kreysa, and M. Goll. 2003. Overview of the BSE risk assessment of the European Commission's Scientific Steering Committee (SSC) and it TSE/BSE ad hoc group. Accessed online at http://europa.eu.int/comm/food/fs/sc/ssc/out364_en.pdf. Scientific Steering Committee, European Commission. 2000. Oral exposure of humans to the BSE agent: Infective dose and species barrier. Accessed online at http://europa.eu.int/comm/food/fs/sc/ssc/out79_en.pdf. http://www.cfsan.fda.gov/%7Ecomm/bse-ra.html -------- Original Message -------- COMMENT SUBMISSION Greetings FDA, I would kindly like to comment on the potential for TSE transmission from What is Kuru? snip... PLEASE NOTE the later ''or by contact with open sores or wounds.'' > and the disease was transmitted either through eating or by contact > the Fore women would scoop the brains of their dead relatives out of Sydney Morning Herald, Saturday, August 28, 1999 The transmission of KURU into animals supported the belief that the Masters, C.J., Gajdusek, D.C. and Gibbs, C.J., (1980). The spongiform SCCNFP/0724/03, final snip...FULL TEXT; http://www.vegsource.com/talk/madcow/messages/92820.html THE following was posted the next day by FDA; July 14, 2004 horizontal rule The discovery of a cow with bovine spongiform encephalopathy (BSE) in While BSE is usually identified with either food safety or animal This qualitative risk assessment follows the generally accepted In April 1996, British scientists reported a previously undetected new Prions are predominantly found in the central nervous system, portions BSE in the United States Use of Cattle Protein in Cosmetics Absorption of Prions from Cosmetics It is well-documented that central nervous system tissue, including the Cut or abraded skin also has been proposed as a route for contracting Use of BSE-contaminated cosmetics could provide a means of human Prions with a particular abnormal tertiary structure are apparently able In cattle, there is a minimal incubation period of six months to a year Despite widespread exposure in the U.K. to BSE-contaminated meat This is not a quantitative risk assessment. However, it does sketch out With exception of the uncertainty associated with estimates of the Some of these uncertainties may concomitantly affect both sides of a A form of spongiform encephalopathy that occurs in humans (vCJD) is The risk of BSE from cosmetics may be reduced through the control of 1. Will, R.G., J.W. Ironside, M. Zeidler, S.N. Cousens, K. Estibeiro, 2. Chazot, G., E. Broussolle, C.I. Lapras, T. Blattler, A. Aguzzi, 3. Prusiner, S.B. 2001. Shattuck Lecture--Neurodegenerative diseases 4. Collinge, J. 2001. Prion diseases of humans and animals: Their 5. Almond, J. and J. Pattison. 1997. Human BSE. Nature 389: 437-38. 6. Scott, M.R., R. Will, J. Ironside, H-O.B Nguyen, P. Tremblay, S.J. 7. Hill, A.F., M. Desbruslais, S. Joiner, K.C.L. Sidle, I. Gowland, 8. Collinge, J. 1999. Variant Creutzfeldt-Jakob disease. Lancet 354: 9. Lasmezas, C.I., J-G. Fournier, V. Nouvel, H. Boe, D. Marce, F. 10. Bruce, M.E., R.G. Will, J. W. Ironside, I. McConnell, D. Drummond, 11. Brown, P. 1997. The risk of bovine spongiform encephalopathy ('mad 12. Brown, P., R.G. Will, R. Bradley, D.M. Asher, and L. Detwiler. 13. Scientific Steering Committee, European Commission. 1999. Opinion 14. Harvard Center for Risk Analysis, Harvard School of Public Health. 15. Fraser, J.R. 1996. Infectivity in extraneural tissues following 16. Scott, J.R., J. D. Foster and H. Fraser. 1993. Conjunctival 17. Klitzman R.L., M.P. Alpers, and D.C. Gajdusek. 1984. The natural 18. Taylor, D.M., I. McConnell, and H. Fraser. 1996. Scrapie infection 19. Ingrosso, L., F. Pisani, and M. Pocchiari. 1999. Transmission of 20. Pammer, J., W. Weninger, and E. Tschachler. 1998. Human 21. Sugaya, M., K. Nakamura, T. Watanabe, A. Asahina, N. Yasaka, Y. 22. Vossen, P., J. Kreysa, and M. Goll. 2003. Overview of the BSE risk 23. Scientific Steering Committee, European Commission. 2000. Oral THIS was just published ; Scrapie transmission following exposure through the skin is Joanne Mohan, Karen L. Brown, Christine F. Farquhar, Moira E. Bruce and E-mail The Corresponding Author Institute for Animal Health, Ogston Building, West Mains Road, Edinburgh Received 9 March 2004; Revised 22 April 2004; accepted 12 May 2004. Background: Transmissible spongiform encephalopathies (TSEs) are chronic Author Keywords: Transmissible spongiform encephalopathy; Scrapie; Skin; author. Tel.: +44 131 667 5204; fax: +44 131 668 3872. http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T87-4CTD13F-3&_coverDate=08%2F31%2F2004&_alid=189125137&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=5079&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=8878b345dd3743a8fe239a820e6aea0b
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