Recent comments

hi john, indeed, usda et al should have listened to you, sheldon, and everybody else that have tried to tell them for eons about TSE in the USA. but instead, USDA et al goes into cover-up mode, which is why this agent has now mutated and spread to hell and back. in essence, the USA was worse than the UK about spreading the agent via exports. now, well, i think it is too late. lets compare ; IN CONFIDENCE Perceptions of unconventional slow virus disease of animals in the USA G A H Wells REPORT OF A VISIT TO THE USA APRIL-MAY 1989 john, check out pages 13 to 17 http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf Gerald Wells: Report of the Visit to USA, April-May 1989 snip... The general opinion of those present was that BSE, as an overt disease phenomenon, _could exist in the USA, but if it did, it was very rare. The need for improved and specific surveillance methods to detect it as recognised... snip... It is clear that USDA have little information and _no_ regulatory responsibility for rendering plants in the US... snip... 3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a _very low profile indeed_. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be _avoided_ in the US _at all costs_... snip... http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988 Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle R.F. Marsh* and G.R. Hartsough .Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092 ABSTRACT Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England. INTRODUCTION Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough and Burger who demonstrated that the disease was transmissible with a long incubation period, and that affected mink had a spongiform encephalopathy similar to that found in scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity between TME and scrapie, and the subsequent finding that the two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was concluded that TME most likely resulted from feeding mink scrapie-infecied sheep. The experimental transmission of sheep scrapie to mink (Hanson et al., 1971) confirmed the close association of TME and scrapie, but at the same time provided evidence that they may be different. Epidemiologic studies on previous incidences of TME indicated that the incubation periods in field cases were between six months and one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be transmitted to mink in less than one year. To investigate the possibility that TME may be caused by a (particular strain of scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie agent, including their sheep or goat sources, were inoculated into a total of 61 mink. Only one mink developed a progressive neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent from an unidentified source. OBSERVATIONS AND RESULTS A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed. Experimental Transmission. The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months. DISCUSSION These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy. We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster- adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It will be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed. ACKNOWLEDGEMENTS These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations. REFERENCES Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420. MARSH http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf WORLD ASSOCIATION FOR BUIATRICS Edinburgh 8 -12 July 1996 http://www.bseinquiry.gov.uk/files/mb/m09/tab04.pdf Transmission Studies of BSE in Sheep http://www.bseinquiry.gov.uk/files/mb/m09/tab01.pdf J. Comp. Path. 2006, Vol. 134, 63-69 Experimental Second Passage of Chronic Wasting Disease (CWDmule deer) Agent to Cattle A. N. Hamir, R. A. Kunkle, J. M. Miller, J. J. Greenlee and J. A. Richt Agricultural Research Service, United States Department of Agriculture, National Animal Disease Center, 2300 Dayton Avenue, P.O. Box 70, Ames, IA 50010, USA Summary To compare clinicopathological findings in first and second passage chronic wasting disease (CWDmule deer) in cattle, six calves were inoculated intracerebrally with brain tissue derived froma first-passageCWD-affected calf in an earlier experiment. Two uninoculated calves served as controls. The inoculated animals began to lose both appetite and weight 10-12 months later, and five subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months, all cattle had been subjected to euthanasia because of poor prognosis. None of the animals showed microscopical lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and rapid Western blot (WB) techniques. Thus, intracerebrally inoculated cattle not only amplified CWD PrPres from mule deer but also developed clinicalCNSsigns in the absence of SElesions.This situation has also been shown to occur in cattle inoculated with the scrapie agent. The study confirmed that the diagnostic techniques currently used for diagnosis of bovine spongiformencephalopathy (BSE) in theUS would detect CWDin cattle, should it occur naturally. Furthermore, it raised the possibility of distinguishing CWDfromBSE in cattle, due to the absence of neuropathological lesions and to a distinctive multifocal distribution of PrPres, as demonstrated by IHC which, in this study, appeared to be more sensitive than the WB technique. snip... Discussion CWD, like all other TSEs, is characterized by a long incubation period, which in deer is seldom less than 18 months (Williams and Young, 1992). In an experimental study of cattle inoculated intracerebrally with CWD from mule deer (first passage), amplification of PrPres was demonstrated in only five of 13 (38%) cattle, after incubation periods that ranged from 23 to 63 months (Hamir et al., 2001a, 2005a). In contrast, all inoculated cattle in the present study were positive for PrPres within 16.5 months. This increased attack rate with shorter incubation periods probably indicates adaptation of the CWDmule deer agent to a new host. It could also be argued that the inoculum used for the primary passage (Hamir et al., 2001a, 2005a) had a lower infectivity titre than that used for the second passage. However, the former successfully transmitted CWD to each of five white tailed deer within two years of intracerebral inoculation (Kunkle et al., Unpublished). In cervids, clinical CWD is characterized by emaciation, changes in behaviour, and excessive salivation (Williams and Young, 1992). Although the latter was not observed in the CWD inoculated cattle, all animals showed anorexia and considerable weight loss. Five cattle also showed intermittent neurological signs. Although none of these animals showed histopathological changes in the brain, all were shown to be positive for PrPres by the IHC and WB methods. The presence of isolated vacuoles in the red nucleus is regarded as an incidental finding in cattle (McGill and Wells, 1993). The uniform susceptibility, relatively short incubation, and absence of microscopical lesions in cattle given CWD brain material passaged once through cattle resembled findings in cattle inoculated intracerebrally with the scrapie agent (Cutlip et al., 1997). In that experiment, 100% of cattle died 14-18 months after inoculation with material from the first cattle-passage of a US strain of the scrapie agent; none showed microscopical lesions and all were positive for PrPres. In the present experiment, the possibility that the PrPres seen in tissue sections represented residual CWD material from the inoculum was ruled out because of the multifocal distribution of PrPres throughout the brain (excluding cerebellar folia) and cervical spinal cord of most of the affected animals. Had the PrPres represented residual inoculum, it would probably have been confined to the sites of deposition in the midbrain or cerebrum. Moreover, in studies on sheep scrapie, Hamir et al. (2002) showed that intracerebrally inoculated brain material containing PrPres was present for only a few days in sufficient quantity to be detectable immunohistochemically. The present work confirms previous observations that PrPres IHC labelling in cattle inoculated with the mule deer CWD agent is multifocal and glial cell-associated. This unusual pattern was first reported in descriptions of the primary CWD transmission to cattle (Hamir et al., 2001a, 2005a), and the study described here showed that it was maintained through the second passage in cattle. Further studies now in progress will determine whether this feature also characterizes CWD transmission to cattle fromother cervid species other than mule deer, namely, white tailed deer and elk. In this and an earlier study of CWD in cattle (Hamir et al., 2001a), IHC labelling differed from that seen in cattle with BSE or experimental transmissible mink encephalopathy (TME), both of which are associated with widespread diffuse labelling of grey matter neuropil, with labelled particles that are not obviously cell-associated except occasionally at neuronal cell membranes (Wells and Willsmith, 1995; Hamir et al., 2005a). The IHC pattern in bovine CWD also contrasts markedly with that seen in scrapie-inoculated cattle, in which intracytoplasmic labelling of neurons is a prominent feature (Cutlip et al., 1994, 1997). When brainstems of CWD-infected cattle were analysed by WB for the presence of PrPres, only three of six samples were found to be positive (Table 1). In contrast, all samples from the midbrain area were positive by this technique (Table 1; Fig. 5). It was noteworthy, however, that both brainstem and midbrain sections of all animals infected with CWD gave positive IHC results (Table 1) and a positive WB was associated with strong IHC labelling. This may indicate that the IHC procedure is more sensitive than the WB method for cattle-passaged CWD. However, given the multifocal nature of PrPres distribution in the CNS of CWD-infected cattle, this result is not surprising. WB analysis requires a small sample of brain tissue (e.g. 0.2 g, as in the present study) to produce a 10% homogenate; approximately 10 ml (1 mg brain tissue equivalent) of this homogenate are loaded on to an SDS-PAGE gel for further analysis. Bearing in mind the multifocal pattern of PrPres distribution, the brain tissue used for the preparation of WB homogenate, unlike the large amount examined in the IHC procedure, might well contain few if any foci of PrPres deposition, whereas the larger piece of tissue section used for IHC may contain detectable PrPres. In this respect, therefore, the IHC method would seem preferable to the WB procedure and to other procedures (e.g. ELISA-based tests) in which only small amounts of tissue are used for analysis. In comparison with experimental TME in cattle (Hamir et al., 2005b), the experimental bovine CWD in this study was associated with less extensive IHC labelling in non-CNS (i.e. other than brain and spinal cord) neural tissues. Whereas the retina was positive in all cattle inoculated with TME, none of the CWD-infected cattle in this experiment had any retinal labelling. Similarly, in the present study there was no labelling in the pituitary gland, a tissue sometimes positive in TME-infected cattle. Because the incubation time for second passage CWD transmission (mean of 468 days) was only slightly longer than for TME (mean of 430 days), it seems likely that these different tissue affinities reflect a biological difference between these two TSE agents. PrPres IHC labelling was not observed in striated muscles (heart, tongue, masseter, diaphragm) of the experimental animals. This observation accorded with our previous findings (Hamir et al., 2004a) in which striated muscle tissues from 20 animals (cattle, sheep, elk and raccoons) were examined for PrPres. In these animals, all of which had developed a TSE after experimental inoculation, PrPres was found by IHC examination in the brains, but not in muscle tissues. However, recent investigations with an enriched WB technique (Mulcahy et al., 2004) have enabled us to detect PrPres in the tongues of some sheep and elk experimentally inoculated with scrapie and CWD, respectively. This technique failed, however, to detect PrPres in cattle inoculated with CWD or TME (Bessen et al., unpublished). This study is still in progress, and the tongues of TSE-infected animals are currently being tested after careful removal from the carcasses to ensure non-contamination with infected brain material. The present study and a previous experiment (Hamir et al., 2005a) have established the biological characteristics of the CWDmule deer agent in cattle. However, isolates of CWD from other cervids (e.g. CWDwhite-tailed and CWDelk) may differ. Transmission experiments with different CWD isolates are therefore needed to examine the possibility of variation in the CWD agent in wild cervids. Such experiments have recently been initiated at the National Animal Disease Center (NADC).............snip...END...TSS ALSO, I THINK THE DOWNER COW FIGURE IS UNDERESTIMATED; Released May 5, 2005, by the National Agricultural Statistics Service (NASS), Agricultural Statistics Board, U.S. Department of Agriculture. For information on Non-ambulatory Cattle and Calves call Mike Miller at 720-3040, office hours 7:30 a.m. to 4:30 p.m. ET. Non-Ambulatory Cattle and Calves Non-ambulatory cattle and calves in the United States totaled 465,000 head during 2003 and 450,000 head during 2004. The number of non-ambulatory cattle 500 pounds or greater totaled 280,000 head in 2003 and 270,000 head in 2004. The number of calves under 500 pounds reported as non-ambulatory totaled 185,000 head in 2003 and 180,000 head in 2004. The number of operations that reported non-ambulatory cattle and calves was 103,000 in 2003 and 81,000 in 2004. In 2003, there were 66,800 beef cow operations reporting non-ambulatory cattle and calves compared to 49,700 in 2004. There were 22,800 dairy operations reporting nonambulatory cattle and calves in 2003 compared to 23,000 in 2004. This report is released as a cooperative effort between the National Agricultural Statistics Service and Animal and Plant Health Inspection Service - Veterinary Services. Data for this report were collected on the January 1, 2004 and 2005 Cattle Surveys. .......END....TSS From: TSS () Subject: Interspecies Transmission of Chronic Wasting Disease Prions to Squirrel Monkeys (Saimiri sciureus) Date: October 19, 2005 at 8:33 am PST 0022-538X/05/$08.00+0 doi:10.1128/JVI.79.21.13794-13796.2005 Copyright © 2005, American Society for Microbiology. All Rights Reserved. Interspecies Transmission of Chronic Wasting Disease Prions to Squirrel Monkeys (Saimiri sciureus) Richard F. Marsh,1, Anthony E. Kincaid,2 Richard A. Bessen,3 and Jason C. Bartz4* Department of Animal Health and Biomedical Sciences, University of Wisconsin, Madison 53706,1 Department of Physical Therapy,2 Department of Medical Microbiology and Immunology, Creighton University, Omaha, Nebraska 68178,4 Department of Veterinary Molecular Biology, Montana State University, Bozeman, Montana 597183 Received 3 May 2005/ Accepted 10 August 2005 Chronic wasting disease (CWD) is an emerging prion disease of deer and elk. The risk of CWD transmission to humans following exposure to CWD-infected tissues is unknown. To assess the susceptibility of nonhuman primates to CWD, two squirrel monkeys were inoculated with brain tissue from a CWD-infected mule deer. The CWD-inoculated squirrel monkeys developed a progressive neurodegenerative disease and were euthanized at 31 and 34 months postinfection. Brain tissue from the CWD-infected squirrel monkeys contained the abnormal isoform of the prion protein, PrP-res, and displayed spongiform degeneration. This is the first reported transmission of CWD to primates. ---------------------------------------------------------------------------- ---- * Corresponding author. Mailing address: Department of Medical Microbiology and Immunology, Creighton University, 2500 California Plaza, Omaha, NE 68178. Phone: (402) 280-1811. Fax: (402) 280-1875. E-mail: jbartz@creighton.edu . Deceased. ---------------------------------------------------------------------------- ---- Journal of Virology, November 2005, p. 13794-13796, Vol. 79, No. 21 0022-538X/05/$08.00+0 doi:10.1128/JVI.79.21.13794-13796.2005 Copyright © 2005, American Society for Microbiology. All Rights Reserved. http://jvi.asm.org/cgi/content/abstract/79/21/13794?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=cwd&searchid=1129736446553_4280&stored_search=&FIRSTINDEX=0&volume=79&issue=21&journalcode=jvi =================================== Intra- & Inter-species Transmission of Chronic Wasting Disease (Show All REXs) Description: This research is intended to investigate the intra- and inter-species transmissibility of the causative agent of chronic wasting disease (CWD), believed to be a structurally modified form of the prion protein (PrPCWD), of white-tailed deer (Odocoileus virginianus). Our lab has identified five alleles in the PrP-coding region of white-tailed deer from the CWD-affected region of southern Wisconsin. Combinations of the alleles represent variability within the population and may result in differences in incubation period, levels of susceptibility, variable clinical symptoms and/or pathology within deer. We will test these ideas by inoculating white-tailed deer of known genotype with known-genotype PrPCWD and by conducting cell-free conversion experiments with the possible combinations of PrPCWD. We believe environment may be a reservoir of CWD, which opens possibilities of transmission to wildlife that share habitat with white-tailed deer. We will identify the species that consume deer carrion, as they are the most likely to encounter PrPCWD, collect 100 of each species from the CWD-affected region of southern Wisconsin and evaluate them for lesion profiles indicative of prion disease. We believe the primary carrion consumers will include coyote (Canis latrans), red fox (Vulpes vulpes), gray fox (Urocyon cinereoargenteus), raccoon (Procyon lotor), striped skunk (Mephitis mephitis), Virginia opossum (Didelphis virginiana), and mink (Mustela vison). Since species barriers are difficult to cross we dont expect to find a large prevalence of prion disease in this population of wildlife. To address the possibility of transmission to these species, we will inoculate raccoons, striped skunks, Virginia opossums and Eastern cottontails (Sylvilagus floridanus) with PrPCWD. We will test transmission to other species by cell-free conversion with as many species as possible, starting with those whose life history are most likely to expose them to PrPCWD. The species that we are collecting from the CWD-affected region of southern Wisconsin for prion disease assessment are a significant collection that we will use to survey a range of other wildlife diseases. This is a five-year project with publications anticipated in the third through fifth year. Students that would join me for work could experience lab or field work. We will be placing dead deer on the landscape, setting remote-triggered cameras on the deer and checking the cameras every other day. We will collect raccoons, skunks, opossums, coyotes and foxes from trappers and conduct necropsies on them at the WVDL. We will be running Western blots for TSE testing on the brains of the animals we necropsy. We will do PCR/Sequencing on the prion-coding region of each species, clone it into an expression vector and conduct cell-free conversions on the resulting protein. Date: Feb 20 Week: Week 1 (Week of Feb 20) Location (where students meet host): Room 237 Animal Health & Biomedical Sciences Building, 1656 Linden Drive Meets From: 3:30 pm until 5:30 pm Pre-REX Reading: None Laboratory: Lab Address: 237 Animal Health & Biomedical Sciences Bldg, 1656 Linden Drive Lab Phone: 262-7362 Lab Website: http://www.ahabs.wisc.edu/Faculty/Aiken-j/index.html Department or Institute: Animal Health & Biomedical Sciences College or School: School of Veterinary Medicine Host: Dr. Judd Aiken Host Email: jma@ahabs.wisc.edu Host Phone: 262-7362 Co-Host: Chad Johnson Co-Host Email: cjjohns3@students.wisc.edu Co-Host Phone: Total Number of Students Allowed: 5 Number of Openings: 0 ================================ USA EXPORTS 2006 http://www.ers.usda.gov/Briefing/Cattle/Data/AnnualLivestockTable.xls TOP FIVE COUNTRIES IMPORTING USDA MAD COW PRODUCTS The Economic Impact of BSE on the U.S. Beef Industry: Product Value Losses, Regulatory Costs, and Consumer Reactions 3.4 U.S. Beef Export Customers Table 3.4 provides a dollar value ranking, by country, of beef export shipments during 2003. Five countries, Japan, Mexico, South Korea, Canada, and Hong Kong, were the recipients of 90 percent of U.S .beef exports during 2003, based on value. Japan, historically the largest U.S. beef export customer, represented 35 percent of U.S. beef exports during 2003. http://www.ksda.gov/Default.aspx?tabid=349&mid=2252&ctl=Download&method=attachment&EntryId=479 WHOS EATING THOSE USDA MAD COW BRAINS OF AN ATYPICAL STRAIN ? 0206.29.0010: HEARTS OF BOVINE ANIMALS, EDIBLE, FROZEN Skip this table U.S. Domestic Exports: December 2003 and 2003 Year-to-Date, not Seasonally Adjusted (FAS Value, in Thousands of Dollars) (Units of Quantity: Kilograms) December 2003 2003, through December Quantity Value Quantity Value WORLD TOTAL 1,180,635 1,038 17,267,397 12,630 Angola 0 0 47,849 31 China 0 0 97,868 41 Colombia 0 0 355,787 379 Costa Rica 0 0 4,816 4 El Salvador 4,545 4 4,545 4 Greece 0 0 15,000 6 Guatemala 0 0 19,051 18 Honduras 0 0 9,780 8 Hong Kong 45,347 110 454,574 862 Indonesia 597,243 459 8,098,035 4,681 Ivory Coast 0 0 27,216 8 Japan 0 0 19,835 20 Korea, South 49,890 50 213,036 213 Lithuania 0 0 55,194 31 Mexico 280,421 234 2,664,118 2,384 Netherlands 0 0 108,698 61 Peru 0 0 452,116 458 Russia 203,189 181 4,528,474 3,280 Saudi Arabia 0 0 3,293 6 Singapore 0 0 44,906 21 Switzerland 0 0 8,010 8 United Arab Emirates 0 0 135 3 United Kingdom 0 0 35,061 105 0206.29.0020: KIDNEYS OF BOVINE ANIMALS, EDIBLE, FROZEN Skip this table U.S. Domestic Exports: December 2003 and 2003 Year-to-Date, not Seasonally Adjusted (FAS Value, in Thousands of Dollars) (Units of Quantity: Kilograms) December 2003 2003, through December Quantity Value Quantity Value WORLD TOTAL 330,004 231 3,566,918 1,818 China 49,424 26 141,576 64 Gabon 0 0 49,437 28 Greece 0 0 966 6 Indonesia 0 0 23,610 15 Ivory Coast 49,891 25 1,699,427 704 Jamaica 115,626 67 875,874 436 Mexico 115,063 113 521,638 465 Russia 0 0 115,377 70 Saudi Arabia 0 0 1,660 3 South Africa 0 0 111,960 18 Thailand 0 0 25,393 10 0206.29.0030: BRAINS OF BOVINE ANIMALS, EDIBLE, FROZEN Skip this table U.S. Domestic Exports: December 2003 and 2003 Year-to-Date, not Seasonally Adjusted (FAS Value, in Thousands of Dollars) (Units of Quantity: Kilograms) December 2003 2003, through December Quantity Value Quantity Value WORLD TOTAL 57,279 56 192,198 225 Ivory Coast 0 0 24,971 8 Mexico 57,279 56 161,158 211 Sweden 0 0 6,069 6 0206.29.0040: SWEATBREADS OF BOVINE ANIMALS, EDIBLE, FROZEN Skip this table U.S. Domestic Exports: December 2003 and 2003 Year-to-Date, not Seasonally Adjusted (FAS Value, in Thousands of Dollars) (Units of Quantity: Kilograms) December 2003 2003, through December Quantity Value Quantity Value WORLD TOTAL 48,735 69 581,306 689 Bahamas 0 0 4,551 5 Hong Kong 0 0 48,988 15 Japan 0 0 18,629 51 Mexico 48,735 69 507,453 611 Switzerland 0 0 1,685 6 0206.29.0050: LIPS OF BOVINE ANIMALS, EDIBLE, FROZEN Skip this table U.S. Domestic Exports: December 2003 and 2003 Year-to-Date, not Seasonally Adjusted (FAS Value, in Thousands of Dollars) (Units of Quantity: Kilograms) December 2003 2003, through December Quantity Value Quantity Value WORLD TOTAL 620,626 1,393 16,539,594 23,262 Hong Kong 0 0 23,587 8 Mexico 620,626 1,393 16,513,038 23,245 Taiwan 0 0 2,969 10 0206.29.0090: OFFAL OF BOVINE ANIMALS, EDIBLE, NESOI, FROZEN Skip this table U.S. Domestic Exports: December 2003 and 2003 Year-to-Date, not Seasonally Adjusted (FAS Value, in Thousands of Dollars) (Units of Quantity: Kilograms) December 2003 2003, through December Quantity Value Quantity Value WORLD TOTAL 8,464,956 16,117 118,262,413 197,532 Argentina 1,497 9 1,497 9 Australia 6,103 6 72,627 71 Bahamas 0 0 25,367 55 Barbados 0 0 1,282 6 Belgium 0 0 718,837 142 Bulgaria 0 0 328,698 261 Burkina 0 0 23,496 21 Canada 304,064 276 8,137,388 6,048 China 734,212 1,750 7,554,286 16,429 Colombia 0 0 109,398 141 Costa Rica 0 0 53,911 37 Denmark 0 0 8,327 33 Dominican Republic 19,578 168 112,192 767 Egypt 0 0 167,000 96 Federal Rep. of Germany 104,016 21 2,266,317 583 Gabon 24,494 16 339,168 177 Greece 23,610 26 47,220 51 Guatemala 0 0 200,509 233 Guyana 0 0 11,555 12 Hong Kong 339,453 704 4,490,896 7,651 Indonesia 104,013 108 1,231,976 666 Israel 0 0 119,230 121 Ivory Coast 0 0 1,429,316 876 Jamaica 79,203 73 780,910 696 Japan 2,614,703 7,006 29,370,030 78,245 Jordan 0 0 72,709 390 Korea, South 1,084,495 2,217 19,825,887 37,280 Macedonia (Skopje) 0 0 143,699 51 Malaysia 0 0 24,776 10 Mexico 2,463,516 2,922 30,710,290 37,936 Netherlands 0 0 38,512 65 Nicaragua 0 0 9,411 11 Panama 0 0 480,391 472 Peru 0 0 47,135 29 Philippines 37,875 15 216,218 116 Poland 47,175 36 954,552 532 Romania 0 0 991,737 765 Russia 368,385 325 3,490,349 2,441 Singapore 0 0 5,307 15 St Lucia 2,442 3 10,896 14 Sweden 0 0 46,200 45 Taiwan 106,122 436 1,601,333 3,327 Turks and Caicos Islands 0 0 8,536 14 United Arab Emirates 0 0 27,439 130 United Kingdom 0 0 1,842,710 369 Uruguay 0 0 112,893 95 Top of page http://www.ita.doc.gov/td/industry/otea/Trade-Detail/Latest-December/Exports/02/020629.html 0206.21.0000: TONGUES OF BOVINE ANIMALS, EDIBLE, FROZEN Skip this table U.S. Domestic Exports: December 2003 and 2003 Year-to-Date, not Seasonally Adjusted (FAS Value, in Thousands of Dollars) (Units of Quantity: Kilograms) December 2003 2003, through December Quantity Value Quantity Value WORLD TOTAL 1,377,073 7,372 27,349,941 105,661 Canada 0 0 5,159 7 China 66,968 208 675,449 1,382 Costa Rica 0 0 6,567 18 Hong Kong 121,237 431 2,176,415 3,917 Indonesia 24,957 13 39,957 17 Japan 920,049 5,943 17,255,240 83,562 Korea, South 89,412 404 2,435,561 8,129 Malaysia 0 0 23,596 10 Mexico 45,264 126 1,258,740 3,282 Poland 0 0 23,596 14 Russia 51,472 49 3,083,619 3,942 Taiwan 57,714 198 354,691 1,260 Vietnam 0 0 11,351 121 Top of page Source: Foreign Trade Division , U.S. Census Bureau. Presented by: Office of Trade and Economic Analysis (OTEA), International Trade Administration, U.S. Department of Commerce. http://www.ita.doc.gov/td/industry/otea/Trade-Detail/Latest-December/Exports/02/020621.html ##################### Bovine Spongiform Encephalopathy ##################### Subject: USDA, SPONTANEOUS MAD COW DISEASE, THE TOOTH FAIRY AND SANTA CLAUS Date: June 12, 2006 at 5:18 am PST IF we all believe the BSe that the USDA is trying to put out now about atypical BSE in USA cattle just arising spontaneously, then we all should believe in the tooth fairy and santa claus as well. IF USA scrapie transmitted to USA cattle long ago in experiments in a lab in Mission Texas did not produce UK BSE, but something very different, then why would USA TSE cattle produce the UK human version of mad cow i.e. nvCJD? IT wouldn't. USA sporadic cjd is increasing, the USA also has atypical human cases of unknown origin as well? THERE are over 20 strains of scrapie, plus the atypical in sheep, and these strains are increasing in numbers. SCRAPIE, CWD, AND TSE IN CATTLE i.e. ANIMAL TSE RAMPANT IN USA FOR DECADES, and amplified via rendering and feeding practices, where USDA triple firewalls against BSE were nothing more than a mere smoke screen. NO test tube TSE by either Prusiner or Soto, to date, have ever produced a TSE identical to the sporadic CJD. IN fact, no test tube TSE has ever been produced that resembles _any_ natural field TSE. IF you feed BSE tainted materials to cattle and primate, you have BSE and nvCJD. IF you feed USA sheep strain to USA cattle, you get USA TSE. IF you feed USA tainted cattle to humans, you get USA mad cow disease. IF you feed sporadic CJD to primate you get a CJD infected primate. NOTHING spontaneous about it at all. USA is in a very unique situation. there are more documented TSE in different species than any other country, all of which have been rendered and fed back to animals for human and animal consumption, for decades. Millions exposed, and of these Millions, how many surgical and dental procedures have been done on these exposed, to pass on to others, via the 'friendly fire' mode of transmission? IF, the spontaneous TSE was true, then this would be Prusiner and everyone else that is trying to cash in on this agent with there TSE rapid test, this would be there dream come true. IT would require mandatory BSE/TSE testing of all species, due to the fact you could not ever eradicate it through any intervention. BUT, then again, the spontaneous TSE is like believing in the tooth fairy or santa clause will be arriving at your house this year. How long can this sharade continue $ How many more will become exposed and have to die $ Medical Sciences Identification of a second bovine amyloidotic spongiform encephalopathy: Molecular similarities with sporadic Creutzfeldt-Jakob disease Cristina Casalone *, Gianluigi Zanusso , Pierluigi Acutis *, Sergio Ferrari , Lorenzo Capucci , Fabrizio Tagliavini ¶, Salvatore Monaco ||, and Maria Caramelli * *Centro di Referenza Nazionale per le Encefalopatie Animali, Istituto Zooprofilattico Sperimentale del Piemonte, Liguria e Valle d'Aosta, Via Bologna, 148, 10195 Turin, Italy; Department of Neurological and Visual Science, Section of Clinical Neurology, Policlinico G.B. Rossi, Piazzale L.A. Scuro, 10, 37134 Verona, Italy; Istituto Zooprofilattico Sperimentale della Lombardia ed Emilia Romagna, Via Bianchi, 9, 25124 Brescia, Italy; and ¶Istituto Nazionale Neurologico "Carlo Besta," Via Celoria 11, 20133 Milan, Italy Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved December 23, 2003 (received for review September 9, 2003) Transmissible spongiform encephalopathies (TSEs), or prion diseases, are mammalian neurodegenerative disorders characterized by a posttranslational conversion and brain accumulation of an insoluble, protease-resistant isoform (PrPSc) of the host-encoded cellular prion protein (PrPC). Human and animal TSE agents exist as different phenotypes that can be biochemically differentiated on the basis of the molecular mass of the protease-resistant PrPSc fragments and the degree of glycosylation. Epidemiological, molecular, and transmission studies strongly suggest that the single strain of agent responsible for bovine spongiform encephalopathy (BSE) has infected humans, causing variant Creutzfeldt-Jakob disease. The unprecedented biological properties of the BSE agent, which circumvents the so-called "species barrier" between cattle and humans and adapts to different mammalian species, has raised considerable concern for human health. To date, it is unknown whether more than one strain might be responsible for cattle TSE or whether the BSE agent undergoes phenotypic variation after natural transmission. Here we provide evidence of a second cattle TSE. The disorder was pathologically characterized by the presence of PrP-immunopositive amyloid plaques, as opposed to the lack of amyloid deposition in typical BSE cases, and by a different pattern of regional distribution and topology of brain PrPSc accumulation. In addition, Western blot analysis showed a PrPSc type with predominance of the low molecular mass glycoform and a protease-resistant fragment of lower molecular mass than BSE-PrPSc. Strikingly, the molecular signature of this previously undescribed bovine PrPSc was similar to that encountered in a distinct subtype of sporadic Creutzfeldt-Jakob disease. -------------------------------------------------------------------------------- C.C. and G.Z. contributed equally to this work. ||To whom correspondence should be addressed. E-mail: salvatore.monaco@mail.univr.it. www.pnas.org/cgi/doi/10.1073/pnas.0305777101 http://www.pnas.org/cgi/content/abstract/0305777101v1 : J Infect Dis 1980 Aug;142(2):205-8 Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates. Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC. Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation. PMID: 6997404 http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract Atypical cases of TSE in cases of TSE in cattle and sheep cattle and sheep H. De H. De Bosschere Bosschere CODA/CERVA CODA/CERVA Nat. Ref. Lab. Vet. Nat. Ref. Lab. Vet. TSEs TSEs Belgium http://www.var.fgov.be/pdf/1100_TSEDAY.pdf USDA 2004 ENHANCED BSE SURVEILLANCE PROGRAM AND HOW NOT TO FIND BSE CASES (OFFICIAL DRAFT OIG REPORT) snip... CATTLE With CNS Symptoms Were NOT Always Tested snip... Between FYs 2002 and 2004, FSIS condemned 680 cattle of all ages due to CNS symptoms. About 357 of these could be classified as adult. We could validate that ONLY 162 were tested for BSE (per APHIS records. ... snip... WE interviewed officials at five laboratories that test for rabies. Those officials CONFIRMED THEY ARE NOT REQUIRED TO SUBMIT RABIES-NEGATIVE SAMPLES TO APHIS FOR BSE TESTING. A South Dakota laboratory official said they were not aware they could submit rabies-negative samples to APHIS for BSE testing. A laboratory official in another State said all rabies-negative cases were not submitted to APHIS because BSE was ''NOT ON THEIR RADAR SCREEN." Officials from New York, Wisconsin, TEXAS, and Iowa advised they would NOT submit samples from animals they consider too young. Four of the five States contacted defined this age as 24 months; Wisconsin defined it as 30 months. TEXAS officials also advised that they do not always have sufficient tissue remaining to submit a BSE sample. ... snip... FULL TEXT 54 PAGES OF HOW NOT TO FIND BSE IN USA ; http://www.house.gov/reform/min/pdfs_108_2/pdfs_inves/pdf_food_usda_mad_cow_july_13_ig_rep.pdf HUMAN TSE USA 2005 Animal Prion Diseases Relevant to Humans (unknown types?) Thu Oct 27, 2005 12:05 71.248.128.109 About Human Prion Diseases / Animal Prion Diseases Relevant to Humans Bovine Spongiform Encephalopathy (BSE) is a prion disease of cattle. Since 1986, when BSE was recognized, over 180,000 cattle in the UK have developed the disease, and approximately one to three million are likely to have been infected with the BSE agent, most of which were slaughtered for human consumption before developing signs of the disease. The origin of the first case of BSE is unknown, but the epidemic was caused by the recycling of processed waste parts of cattle, some of which were infected with the BSE agent and given to other cattle in feed. Control measures have resulted in the consistent decline of the epidemic in the UK since 1992. Infected cattle and feed exported from the UK have resulted in smaller epidemics in other European countries, where control measures were applied later. Compelling evidence indicates that BSE can be transmitted to humans through the consumption of prion contaminated meat. BSE-infected individuals eventually develop vCJD with an incubation time believed to be on average 10 years. As of November 2004, three cases of BSE have been reported in North America. One had been imported to Canada from the UK, one was grown in Canada, and one discovered in the USA but of Canadian origin. There has been only one case of vCJD reported in the USA, but the patient most likely acquired the disease in the United Kingdom. If current control measures intended to protect public and animal health are well enforced, the cattle epidemic should be largely under control and any remaining risk to humans through beef consumption should be very small. (For more details see Smith et al. British Medical Bulletin, 66: 185. 2003.) Chronic Wasting Disease (CWD) is a prion disease of elk and deer, both free range and in captivity. CWD is endemic in areas of Colorado, Wyoming, and Nebraska, but new foci of this disease have been detected in Nebraska, South Dakota, New Mexico, Wisconsin, Mississippi Kansas, Oklahoma, Minnesota, Montana, and Canada. Since there are an estimated 22 million elk and deer in the USA and a large number of hunters who consume elk and deer meat, there is the possibility that CWD can be transmitted from elk and deer to humans. As of November 2004, the NPDPSC has examined 26 hunters with a suspected prion disease. However, all of them appeared to have either typical sporadic or familial forms of the disease. The NPDPSC coordinates with the Centers for Disease Control and state health departments to monitor cases from CWD-endemic areas. Furthermore, it is doing experimental research on CWD transmissibility using animal models. (For details see Sigurdson et al. British Medical Bulletin. 66: 199. 2003 and Belay et al. Emerging Infectious Diseases. 10(6): 977. 2004.) http://www.cjdsurveillance.com/abouthpd-animal.html SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is with a human TSE surveillance system that is terrible flawed. in 1997 cases of the _reported_ cases of cjd were at 54, to 163 _reported_ cases in 2004. see stats here; p.s. please note the 47 PENDING CASES to Sept. 2005 p.s. please note the 2005 Prion D. total 120(8) 8=includes 51 type pending, 1 TYPE UNKNOWN ??? p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN??? p.s. please note 2004 prion disease (6) 6=7 TYPE UNKNOWN??? http://www.cjdsurveillance.com/resources-casereport.html CWD TO HUMANS = sCJD ??? AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease. snip... http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf snip...end full text ; http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf VERY VERY IMPORTANT THING TO REMEMBER >> Differences in tissue distribution could require new regulations >> regarding specific risk material (SRM) removal. Research Project: Study of Atypical Bse Location: Virus and Prion Diseases of Livestock Project Number: 3625-32000-073-07 Project Type: Specific C/A Start Date: Sep 15, 2004 End Date: Sep 14, 2007 Objective: The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species. Approach: This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal. http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490 3.57 The experiment which might have determined whether BSE and scrapie were caused by the same agent (ie, the feeding of natural scrapie to cattle) was never undertaken in the UK. It was, however, performed in the USA in 1979, when it was shown that cattle inoculated with the scrapie agent endemic in the flock of Suffolk sheep at the United States Department of Agriculture in Mission, Texas, developed a TSE quite unlike BSE. 32 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE. http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820543 The findings of the initial transmission, though not of the clinical or neurohistological examination, were communicated in October 1988 to Dr Watson, Director of the CVL, following a visit by Dr Wrathall, one of the project leaders in the Pathology Department of the CVL, to the United States Department of Agriculture. 33 http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820546 The results were not published at this point, since the attempted transmission to mice from the experimental cow brain had been inconclusive. The results of the clinical and histological differences between scrapie-affected sheep and cattle were published in 1995. Similar studies in which cattle were inoculated intracerebrally with scrapie inocula derived from a number of scrapie-affected sheep of different breeds and from different States, were carried out at the US National Animal Disease Centre. 34 The results, published in 1994, showed that this source of scrapie agent, though pathogenic for cattle, did not produce the same clinical signs of brain lesions characteristic of BSE. 3.58 There are several possible reasons why the experiment was not performed in the UK. It had been recommended by Sir Richard Southwood (Chairman of the Working Party on Bovine Spongiform Encephalopathy) in his letter to the Permanent Secretary of MAFF, Mr (now Sir) Derek Andrews, on 21 June 1988, 35 though it was not specifically recommended in the Working Party Report or indeed in the Tyrrell Committee Report (details of the Southwood Working Party and the Tyrell Committee can be found in vol. 4: The Southwood Working Party, 1988-89 and vol. 11: Scientists after Southwood respectively). The direct inoculation of scrapie into calves was given low priority, because of its high cost and because it was known that it had already taken place in the USA. 36 It was also felt that the results of such an experiment would be hard to interpret. While a negative result would be informative, a positive result would need to demonstrate that when scrapie was transmitted to cattle, the disease which developed in cattle was the same as BSE. 37 Given the large number of strains of scrapie and the possibility that BSE was one of them, it would be necessary to transmit every scrapie strain to cattle separately, to test the hypothesis properly. Such an experiment would be expensive. Secondly, as measures to control the epidemic took hold, the need for the experiment from the policy viewpoint was not considered so urgent. It was felt that the results would be mainly of academic interest. 38 http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm#820550 http://www.bseinquiry.gov.uk/report/volume2/chaptea3.htm REPORT OF THE COMMITTEE ON SCRAPIE Chair: Dr. Jim Logan, Cheyenne, WY Vice Chair: Dr. Joe D. Ross, Sonora, TX Dr. Deborah L. Brennan, MS; Dr. Beth Carlson, ND; Dr. John R. Clifford, DC; Dr. Thomas F. Conner, OH; Dr. Walter E. Cook, WY; Dr. Wayne E. Cunningham, CO; Dr. Jerry W. Diemer, TX; Dr. Anita J. Edmondson, CA; Dr. Dee Ellis, TX; Dr. Lisa A. Ferguson, MD; Dr. Keith R. Forbes, NY; Dr. R. David Glauer, OH; Dr. James R. Grady, CO; Dr. William L. Hartmann, MN; Dr. Carolyn Inch, CAN; Dr. Susan J. Keller, ND; Dr. Allen M. Knowles, TN; Dr. Thomas F. Linfield, MT; Dr. Michael R. Marshall, UT; Dr. Cheryl A. Miller, In; Dr. Brian V. Noland, CO; Dr. Charles Palmer, CA; Dr. Kristine R. Petrini, MN; Mr. Stan Potratz, IA; Mr. Paul E. Rodgers, CO; Dr. Joan D. Rowe, CA; Dr. Pamela L. Smith, IA; Dr. Diane L. Sutton, MD; Dr. Lynn Anne Tesar, SD; Dr. Delwin D. Wilmot, NE; Dr. Nora E. Wineland, CO; Dr. Cindy B. Wolf, MN. The Committee met on November 9, 2005, from 8:00am until 11:55am, Hershey Lodge and Convention Center, Hershey, Pennsylvania. The meeting was called to order by Dr. Jim Logan, chair, with vice chairman Dr. Joe D. Ross attending. There were 74 people in attendance. The Scrapie Program Update was provided by Dr. Diane Sutton, National Scrapie Program Coordinator, United States Department of Agriculture (USDA), Animal and Plant Health Inspection Services (APHIS), Veterinary Services (VS). The complete text of the Status Report is included in these Proceedings. Dr. Patricia Meinhardt, USDA-APHIS-VS-National Veterinary Services Laboratory (NVSL) gave the Update on Genotyping Labs and Discrepancies in Results. NVSL conducts investigations into discrepancies on genotype testing results associated with the Scrapie Eradication Program. It is the policy of the Program to conduct a second genotype test at a second laboratory on certain individual animals. Occasionally, there are discrepancies in those results. The NVSL conducts follow-up on these situations through additional testing on additional samples from the field and archive samples from the testing laboratories. For the period of time from January 1, 2005, until October 15, 2005, there were 23 instances of discrepancies in results from 35 flocks. Of those 23 instances, 14 were caused by laboratory error (paperwork or sample mix-up), 3 results from field error, 5 were not completely resolved, and 1 originated from the use of a non-approved laboratory for the first test. As a result of inconsistencies, one laboratory’s certification was revoked by APHIS-VS. snip... Infected and Source Flocks As of September 30, 2005, there were 105 scrapie infected and source flocks. There were a total of 165** new infected and source flocks reported for FY 2005. The total infected and source flocks that have been released in FY 2005 was 128. The ratio of infected and source flocks cleaned up or placed on clean up plans vs. new infected and source flocks discovered in FY 2005 was 1.03 : 1*. In addition 622 scrapie cases were confirmed and reported by the National Veterinary Services Laboratories (NVSL) in FY 2005, of which 130 were RSSS cases. Fifteen cases of scrapie in goats have been reported since 1990. The last goat case was reported in May 2005. Approximately 5,626 animals were indemnified comprised of 49% non-registered sheep, 45% registered sheep, 1.4% non-registered goats and 4.6% registered goats. Regulatory Scrapie Slaughter Surveillance (RSSS) RSSS was designed to utilize the findings of the Center for Epidemiology and Animal Health (CEAH) Scrapie: Ovine Slaughter Surveillance (SOSS) study. The results of SOSS can be found at http://www.aphis.usda.gov/vs/ceah/cahm/Sheep/sheep.htm . RSSS started April 1, 2003. It is a targeted slaughter surveillance program which is designed to identify infected flocks for clean-up. During FY 2005 collections increased by 32% overall and by 90% for black and mottled faced sheep improving overall program effectiveness and efficiency as demonstrated by the 26% decrease in percent positive black faced sheep compared to FY 2004. Samples have been collected from 62,864 sheep since April 1, 2003, of which results have been reported for 59,105 of which 209 were confirmed positive. During FY 2005, 33,137 samples were collected from 81 plants. There have been 130 NVSL confirmed positive cases (30 collected in FY 2004 and confirmed in FY 2005 and 100 collected and confirmed in FY 2005) in FY 2005. Face colors of these positives were 114 black, 14 mottled, 1 white and 1 unknown. The percent positive by face color is shown in the chart below. Scrapie Testing In FY 2005, 35,845 animals have been tested for scrapie: 30,192 RSSS; 4,742 regulatory field cases; 772 regulatory third eyelid biopsies; 10 third eyelid validations; and 129 necropsy validations (chart 9). Animal ID As of October 04, 2005, 103,580 sheep and goat premises have been assigned identification numbers in the Scrapie National Generic Database. Official eartags have been issued to 73,807 of these premises. *This number based on an adjusted 12 month interval to accommodate the 60 day period for setting up flock plans. http://www.usaha.org/committees/reports/2005/report-scr-2005.pdf Date: April 30, 2006 at 4:49 pm PST SCRAPIE USA UPDATE AS of March 31, 2006 2 NEW CASES IN GOAT, 82 INFECTED SOURCE FLOCKS, WITH 4 NEW INFECTED SOURCE FLOCKS IN MARCH, WITH 19 SCRAPIE INFECTED RSSS REPORTED BY NVSL http://www.aphis.usda.gov/vs/nahps/scrapie/monthly_report/monthly-report.html Published online before print October 20, 2005 Proc. Natl. Acad. Sci. USA, 10.1073/pnas.0502296102 Medical Sciences A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes ( sheep prion | transgenic mice ) Annick Le Dur *, Vincent Béringue *, Olivier Andréoletti , Fabienne Reine *, Thanh Lan Laï *, Thierry Baron , Bjørn Bratberg ¶, Jean-Luc Vilotte ||, Pierre Sarradin **, Sylvie L. Benestad ¶, and Hubert Laude * *Virologie Immunologie Moléculaires and ||Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway Edited by Stanley B. Prusiner, University of California, San Francisco, CA, and approved September 12, 2005 (received for review March 21, 2005) Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health. -------------------------------------------------------------------------------- Author contributions: H.L. designed research; A.L.D., V.B., O.A., F.R., T.L.L., J.-L.V., and H.L. performed research; T.B., B.B., P.S., and S.L.B. contributed new reagents/analytic tools; V.B., O.A., and H.L. analyzed data; and H.L. wrote the paper. A.L.D. and V.B. contributed equally to this work. To whom correspondence should be addressed. Hubert Laude, E-mail: laude@jouy.inra.fr www.pnas.org/cgi/doi/10.1073/pnas.0502296102 http://www.pnas.org/cgi/content/abstract/0502296102v1 12/10/76 AGRICULTURAL RESEARCH COUNCIL REPORT OF THE ADVISORY COMMITTE ON SCRAPIE Office Note CHAIRMAN: PROFESSOR PETER WILDY snip... A The Present Position with respect to Scrapie A] The Problem Scrapie is a natural disease of sheep and goats. It is a slow and inexorably progressive degenerative disorder of the nervous system and it ia fatal. It is enzootic in the United Kingdom but not in all countries. The field problem has been reviewed by a MAFF working group (ARC 35/77). It is difficult to assess the incidence in Britain for a variety of reasons but the disease causes serious financial loss; it is estimated that it cost Swaledale breeders alone $l.7 M during the five years 1971-1975. A further inestimable loss arises from the closure of certain export markets, in particular those of the United States, to British sheep. It is clear that scrapie in sheep is important commercially and for that reason alone effective measures to control it should be devised as quickly as possible. Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias" Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously. snip... 76/10.12/4.6 http://www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf Like lambs to the slaughter 31 March 2001 Debora MacKenzie Magazine issue 2284 What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie? FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease. Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America. Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in ... The complete article is 889 words long. full text; http://www.newscientist.com/article.ns?id=mg16922840.300 Neurobiology Adaptation of the bovine spongiform encephalopathy agent to primates and comparison with Creutzfeldt- Jakob disease: Implications for human health Corinne Ida Lasmézas*,, Jean-Guy Fournier*, Virginie Nouvel*, Hermann Boe*, Domíníque Marcé*, François Lamoury*, Nicolas Kopp, Jean-Jacques Hauw§, James Ironside¶, Moira Bruce, Dominique Dormont*, and Jean-Philippe Deslys* * 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) Abstract 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. http://www.pnas.org/cgi/content/full/041490898v1 USDA CWD PROGRAM http://www.aphis.usda.gov/vs/nahps/cwd/ USDA CWD MAP (slow to update) http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html DRAFT WYOMING GAME AND FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN February 17, 2006 snip... 5. Predicted population effects on free-ranging elk based on captive elk chronically exposed to the CWD prion. Forty-three female elk calves were trapped at the National Elk Refuge and transported to Sybille in February 2002. Elk were housed in pens, assumed to be environmentally contaminated with the CWD prion. Elk will be held throughout their lifetimes. Elk dying will be examined and cause of death determined. From these data, it will should be possible to model free-ranging elk mortality and population dynamics under extreme circumstances of CWD prion exposure and transmission. As of December 2005 (46 months post capture), 11 of 43 elk have died due to CWD. This compares to 100% mortality in less than 25 months in elk orally inoculated with different dosages of the CWD prion. REVISED DRAFT http://gf.state.wy.us/downloads/pdf/CWD2005reviseddraft.pdf Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J. Sigurdson,4‡ Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§ 1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging, 3Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA. *These authors contributed equally to this work. †Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA. ‡Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland. §To whom correspondence should be addressed: E-mail: gtell2@uky.edu Prions are transmissible proteinaceous agents of mammals that cause fatal neurodegenerative diseases of the central nervous system (CNS). The presence of infectivity in skeletal muscle of experimentally infected mice raised the possibility that dietary exposure to prions might occur through meat consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious prion disease of North American cervids, is of particular concern. The emergence of CWD in an increasingly wide geographic area and the interspecies transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns about zoonotic transmission of CWD. To test whether skeletal muscle of diseased cervids contained prion infectivity, Tg(CerPrP)1536 mice (2) expressing cervid prion protein (CerPrP), were inoculated intracerebrally with extracts prepared from the semitendinosus/semimembranosus muscle group of CWD-affected mule deer or from CWD-negative deer. The availability of CNS materials also afforded direct comparisons of prion infectivity in skeletal muscle and brain. All skeletal muscle extracts from CWD-affected deer induced progressive neurological dysfunction in Tg(CerPrP)1536 mice with mean incubation times ranging between 360 and ~490 d, whereas the incubation times of prions from the CNS ranged from ~230 to 280 d (Table 1). For each inoculation group, the diagnosis of prion disease was confirmed by the presence of PrPSc in the brains of multiple infected Tg(CerPrP)1536 mice (see supporting online material for examples). In contrast, skeletal muscle and brain material from CWD-negative deer failed to induce disease in Tg(CerPrP)1536 mice (Table 1) and PrPSc was not detected in the brains of sacrificed asymptomatic mice as late as 523 d after inoculation (supporting online material). Our results show that skeletal muscle as well as CNS tissue of deer with CWD contains infectious prions. Similar analyses of skeletal muscle BSE-affected cattle did not reveal high levels of prion infectivity (3). It will be important to assess the cellular location of PrPSc in muscle. Notably, while PrPSc has been detected in muscles of scrapie-affected sheep (4), previous studies failed to detect PrPSc by immunohistochemical analysis of skeletal muscle from deer with natural or experimental CWD (5, 6). Since the time of disease onset is inversely proportional to prion dose (7), the longer incubation times of prions from skeletal muscle extracts compared to matched brain samples indicated that prion titers were lower in muscle than in CNS where infectivity titers are known to reach high levels. Although possible effects of CWD strains or strain mixtures on these incubation times cannot be excluded, the variable 360 to ~490 d incubation times suggested a range of prion titers in skeletal muscles of CWD-affected deer. Muscle prion titers at the high end of the range produced the fastest incubation times that were ~30% longer than the incubation times of prions from the CNS of the same animal. Since all mice in each inoculation group developed disease, prion titers in muscle samples producing the longest incubation times were higher than the end point of the bioassay, defined as the infectious dose at which half the inoculated mice develop disease. Studies are in progress to accurately assess prion titers. While the risk of exposure to CWD infectivity following consumption of prions in muscle is mitigated by relatively inefficient prion transmission via the oral route (8), these results show that semitendinosus/semimembranosus muscle, which is likely to be consumed by humans, is a significant source of prion infectivity. Humans consuming or handling meat from CWD-infected deer are therefore at risk to prion exposure. References and Notes 1. P. J. Bosque et al., Proc. Natl. Acad. Sci. U.S.A. 99, 3812 (2002). 2. S. R. Browning et al., J. Virol. 78, 13345 (2004). 3. A. Buschmann, M. H. Groschup, J. Infect. Dis. 192, 934 (2005). 4. O. Andreoletti et al., Nat. Med. 10, 591 (2004). 5. T. R. Spraker et al., Vet. Pathol. 39, 110 (2002). 6. A. N. Hamir, J. M. Miller, R. C. Cutlip, Vet. Pathol. 41, 78 (2004). 7. S. B. Prusiner et al., Biochemistry 21, 4883 (1980). 8. M. Prinz et al., Am. J. Pathol. 162, 1103 (2003). 9. This work was supported by grants from the U.S. Public Health Service 2RO1 NS040334-04 from the National Institute of Neurological Disorders and Stroke and N01-AI-25491 from the National Institute of Allergy and Infectious Diseases. Supporting Online Material www.sciencemag.org/ Materials and Methods Fig. S1 21 November 2005; accepted 13 January 2006 Published online 26 January 2006; 10.1126/science.1122864 Include this information when citing this paper. Table 1. Incubation times following inoculation of Tg(CerPrP)1536 mice with prions from skeletal muscle and brain samples of CWD-affected deer. Inocula Incubation time, mean d ± SEM (n/n0)* Skeletal muscle Brain CWD-affected deer H92 360 ± 2 d (6/6) 283 ± 7 d (6/6) 33968 367 ± 9 d (8/8) 278 ± 11 d (6/6) 5941 427 ± 18 d (7/7) D10 483 ± 8 d (8/8) 231 ± 17 d (7/7) D08 492 ± 4 d (7/7) Averages 426 d 264 d Non-diseased deer FPS 6.98 >523 d (0/6) FPS 9.98 >454 d (0/7) >454 d (0/6) None >490 d (0/6) PBS >589 d (0/5) *The number of mice developing prion disease divided by the original number of inoculated mice is shown in parentheses. Mice dying of intercurrent illnesses were excluded. http://www.sciencemag.org/ www.sciencemag.org/ Supporting Online Material for Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers, Shawn R. Browning, Tanya S. Seward, Christina J. Sigurdson, Michael W. Miller, Edward A. Hoover, Glenn C. Telling§ §To whom correspondence should be addressed: E-mail: gtell2@uky.edu Published 26 January 2006 on Science Express DOI: 10.1126/science.1122864 This PDF file includes: Materials and Methods Fig. S1 Supporting Online Materials Materials and Methods Homogenates of semitendinosus/semimembranosus muscle (10% w/v in phosphate buffered saline) were prepared from five emaciated and somnolent mule deer, naturally infected with CWD at the Colorado Division of Wildlife, Wildlife Research Center. These deer were identified as D10, D08, 33968, H92, and 5941. CWD infection was confirmed in all cases by the presence of histologic lesions in the brain including spongiform degeneration of the perikaryon, the immunohistochemical detection of disease-associated PrP in brain and tonsil, or by immunoblotting of protease-resistant, disease associated PrP (CerPrPSc). Semitendinosus/semimembranosus muscle was also obtained from two asymptomatic, mock inoculated deer, referred to as FPS 6.68 and 9.98, that originated from a CWD non-endemic area and which were held indoors at Colorado State University from ten days of age. These control deer were confirmed negative for CWD by histopathological and immunohistochemical analysis of brain tissue at autopsy. The utmost care was taken to avoid inclusion of obvious nervous tissue when muscle biopsies were prepared and to ensure that contamination of skeletal muscle samples with CNS tissue did not occur. Fresh, single-use instruments were used to collect each sample biopsy and a central piece from each sample was prepared with fresh, disposable instruments to further isolate muscle tissue for inoculum preparation. Brain samples for transmission were prepared separately from muscle as additional insurance against cross contamination. 1 Groups of anesthetized Tg(CerPrP)1536 mice were inoculated intracerebrally with 30 µl of 1 % skeletal muscle or brain extracts prepared in phosphate buffered saline (PBS). Inoculated Tg(CerPrP) mice were diagnosed with prion disease following the progressive development of at least three neurologic symptoms including truncal ataxia, ‘plastic’ tail, loss of extensor reflex, difficultly righting, and slowed movement. The time from inoculation to the onset of clinical signs is referred to as the incubation time. For PrP analysis in brain extracts of Tg(CerPrP)1536 mice, 10 % homogenates prepared in PBS were either untreated (-) or treated (+) with 40 µg/ml proteinase K (PK) for one hour at 37oC in the presence of 2% sarkosyl. Proteins were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis, analyzed by immunoblotting using anti PrP monoclonal antibody 6H4 (Prionics AG, Switzerland), incubated with appropriate secondary antibody, developed using ECL-plus detection (Amersham), and analyzed using a FLA-5000 scanner (Fuji). 2 Fig. S1 PrP in brain extracts from representative Tg(CerPrP)1536 mice receiving muscle or CNS tissue inocula from CWD-affected or CWD-negative deer. Extracts were either treated (+) or untreated (-) with proteinase K (PK) as indicated. The positions of protein molecular weight markers at 21.3, 28.7, 33.5 kDa (from bottom to top) are shown to the left of the immunoblot. 3 http://www.sciencemag.org/ Chronic Wasting Disease and Potential Transmission to Humans Ermias D. Belay,* Ryan A. Maddox,* Elizabeth S. Williams,† Michael W. Miller,‡ Pierluigi Gambetti,§ and Lawrence B. Schonberger* *Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †University of Wyoming, Laramie, Wyoming, USA; ‡Colorado Division of Wildlife, Fort Collins, Colorado, USA; and §Case Western Reserve University, Cleveland, Ohio, USA Suggested citation for this article: Belay ED, Maddox RA, Williams ES, Miller MW, Gambetti P, Schonberger LB. Chronic wasting disease and potential transmission to humans. Emerg Infect Dis [serial on the Internet]. 2004 Jun [date cited]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm http://www.cdc.gov/ncidod/EID/vol10no6/03-1082.htm Research Environmental Sources of Prion Transmission in Mule Deer Michael W. Miller,* Elizabeth S. Williams,† N. Thompson Hobbs,‡ and Lisa L. Wolfe* *Colorado Division of Wildlife, Fort Collins, Colorado, USA; †University of Wyoming, Laramie, Wyoming, USA; and ‡Colorado State University, Fort Collins, Colorado, USA 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 http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm ATYPICAL TSEs in USA CATTLE AND SHEEP ? http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf UKBSEnvCJD only theory Singeltary et al 2006 (please note, et al in this term means all victims and familes of the sporadic CJD that are still looking for answers. ...TSS) http://www.microbes.info/forums/index.php?act=Attach&type=post&id=13 http://www.microbes.info/forums/index.php?showtopic=306 NEW STRAIN OF TSE USA CATTLE OR JUST INCOMPETENCE IN TESTING??? http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf CJD WATCH http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm CJD WATCH MESSAGE BOARD http://disc.server.com/Indices/167318.html Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 #################### https://lists.aegee.org/bse-l.html ####################