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From: TSS ()
Title: Bovine Spongiform Encephalopathy: what is "Atypical BSE" and can we detect it? Richt, Juergen http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=202722 Hall, S - USDA, APHIS, VS, NVSL Technical Abstract: Bovine Spongiform Encephalopathy (BSE) surveillance has been ongoing in the USA since the early 1990¿s and initial testing was done at the USDA, National Veterinary Services Laboratories (NVSL) utilizing routine histopathology exclusively. In 1995, the immunohistochemistry (IHC) test was incorporated into surveillance testing in addition to routine histopathology. By 1999 virtually all BSE screening was performed by IHC and by 2001 the NVSL had switched to an automated IHC procedure. In 2002 and 2003 the NVSL tested about 20,000 high risk animals each year by IHC. In December, 2003 an animal was identified by IHC as positive for BSE (Case 1); this animal was determined to be imported from Canada. After this animal was identified, in June 2004 the USDA began its enhanced surveillance program as a shared effort between selected state veterinary diagnostic laboratories and NVSL, as part of the National Animal Health Laboratory Network. The plan called for testing as many targeted high risk animals as possible in a 12-18 month period. From June 1, 2004 through March 21, 2006, over 650,000 animals have been tested (Bio-Rad ELISA). Of those tested, two animals (Cases 2 and 3) have been identified as positive for BSE. While all three cases were strongly positive by Bio-Rad ELISA, Cases 2 and 3 have common features which are distinct from Case 1. Definitive spongiform changes in the obex, strong immunohistochemical reactions, and Western blot patterns similar to European BSE cases were observed in Case 1. In contrast, Cases 2 and 3 did not contain definitive histological lesions of BSE and the IHC staining was less intense than Case 1. In addition, Cases 2 (approximately 12 years) and Case 3 (approximately ten years) were older animals while Case 1 was 6.5 years old. Western blot analysis, PrP**Sc from Case 1 showed molecular features similar to typical BSE isolates, whereas PrP**Sc from Cases 2 and 3 revealed an unusual molecular PrP**Sc pattern: molecular mass of the unglycosylated and monoglycosylated isoform was higher than that of typical BSE isolates. Case 1 contained more PrP**Sc per brain tissue mg equivalent compared with Cases 2 and 3 using antibody 6H4. In Western Blot analysis, Case 2 and Case 3 were strongly positive with antibody P4, while Case 1 was negative or weakly positive with P4. http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194279 2005 Annual Report 4d.Progress report. http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpars=true&fy=2005 Research Project: Study of Atypical Bse Location: Virus and Prion Diseases of Livestock Project Number: 3625-32000-073-07 Approach: http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490 2005 Annual Report PERSPECTIVE On the Question of Sporadic or Atypical Bovine SpongiformEncephalopathy and Creutzfeldt-Jakob Disease Paul Brown,* Lisa M. McShane,† Gianluigi Zanusso,‡ and Linda Detwiler§ Strategies to investigate the possible existence of sporadic bovine spongiform encephalopathy (BSE) require systematic testing programs to identify cases in countries considered to have little or no risk for orally acquired disease, or to detect a stable occurrence of atypical cases in countries in which orally acquired disease is disappearing. To achieve 95% statistical confidence that the prevalence of sporadic BSE is no greater than 1 per million (i.e., the annual incidence of sporadic Creutzfeldt-Jakob disease [CJD] in humans) would require negative tests in 3 million randomly selected older cattle. A link between BSE and sporadic CJD has been suggested on the basis of laboratory studies but is unsupported by epidemiologic observation. Such a link might yet be established by the discovery of a specific molecular marker or of particular combinations of trends over time of typical and atypical BSE and various subtypes of sporadic CJD, as their numbers are influenced by a continuation of current public health measures that exclude high-risk bovine tissues from the animal and human food chains. ...... 6:30 Close of Day One SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM He estimates that it may be up to 14 or 15 persons which display selectively http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf THE SEVEN SCIENTIST REPORT *** http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf SEROLOGICALS CORPORATION http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf Embassy of Japan Dockets Entered on December 22, 2005 03-025IFA 03-025IFA-6 Jason Frost [PDF] http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-589.pdf Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama http://www.neurology.org/cgi/eletters/60/2/176#535 your only fooling yourselves with this stupid ukbsenvcjd only theory, and BSE methology of the OIE. most any coutnry that went by those same OIE BSE guidelines all went down with BSE. makes some political hay about trade protocol, commodities and futures. IF should do everyone a favor and dissolve there organization. ... http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf the rest i.e (the next two documented TSE cows) became atypical, of which USDA now wants us to believe are of a spontaneous nature, that feed did not cause this? r i g h t ............ STUDIES in Mission Texas of USA sheep scrapie to USA produced a TSE unlike BSE. THE USA has been rendering and feeding that same TSE back into feed for animals for human and animal consumption for decades. WHY would we have not documented these supposedly 'spontaneous' BASE cases previously ??? spontaneous TSE in any species is a myth. ... 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/ 1: J Infect Dis. 1994 Apr;169(4):814-20. Intracerebral transmission of scrapie to cattle. Cutlip RC, Miller JM, Race RE, Jenny AL, Katz JB, Lehmkuhl HD, DeBey BM, Robinson MM. USDA, Agriculture Research Service, National Animal Disease Center, Ames, IA 50010. To determine if sheep scrapie agent(s) in the United States would induce a disease in cattle resembling bovine spongiform encephalopathy, 18 newborn calves were inoculated intracerebrally with a pooled suspension of brain from 9 sheep with scrapie. Half of the calves were euthanatized 1 year after inoculation. All calves kept longer than 1 year became severely lethargic and demonstrated clinical signs of motor neuron dysfunction that were manifest as progressive stiffness, posterior paresis, general weakness, and permanent recumbency. The incubation period was 14-18 months, and the clinical course was 1-5 months. The brain from each calf was examined for lesions and for protease-resistant prion protein. Lesions were subtle, but a disease-specific isoform of the prion protein was present in the brain of all calves. Neither signs nor lesions were characteristic of those for bovine spongiform encephalopathy. MeSH Terms: Animals Brain/microbiology* Brain/pathology Cattle Cattle Diseases/etiology* Cattle Diseases/pathology Encephalopathy, Bovine Spongiform/etiology* Encephalopathy, Bovine Spongiform/pathology Immunoblotting/veterinary Immunohistochemistry Male Motor Neurons/physiology Prions/analysis Scrapie/pathology Scrapie/transmission* Sheep Sleep Stages Time Factors Substances: Prions http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8133096&dopt=Citation 9/13/2005 Intracerebral transmission of scrapie to cattle FULL TEXT PDF; SNIP... Discussion WE conclude that American sources of sheep scrapie are transmissible to cattle by direct intracerebral inoculation but the disease induced is NOT identical to BSE as seen in the United Kingdom. While there were similarities in clinical signs between this experimental disease and BSE, there was no evidence of aggressiveness, hyperexcitability, hyperesthesia (tactile or auditory), or hyperemetria of limbs as has been reported for BSE (9). Neither were there extensive neurologic lesions, which are primary for BSE, such as severe vacuolation of neurons and neuropil or neuronal necrosis and gliosis. Although some vacuolation of neuropil, chromotolysis in neurons, and gliosis were seen in the brains of some affected calves, these were industinguishable from those of controls. Vacuolated neurons in the red nucleus of both challenged and normal calves were considered normal for the bovines as previously described (50). PrP-res was found in ALL CHALLENGED CALVES REGARDLESS OF CLINCIAL SIGNS, and the amount of PrP-res positively related to the length of the incubation. ... snip... WE also conclude from these studies that scrapie in cattle MIGHT NOT BE RECOGNIZED BY ROUTINE HISTOPATHOLOGICAL EXAMINATION OF THE BRAIN AND SUGGEST THAT DETECTION OF PrP-res by immunohistochemistry or immunoblotting is necessary to make a definitive diagnosis. THUS, undiagnosed scrapie infection could contribute to the ''DOWNER-COW'' syndrome and could be responsible for some outbreaks of transmissible mink encephalopathy proposed by Burger and Hartsough (8) and Marsh and harsough (52). ... snip... Multiple sources of sheep affected with scrapie and two breeds of cattle from several sources were used inthe current study in an effort to avoid a single strain of either agent or host. Preliminary results from mouse inoculations indicate multiple strains of the agent were present in the pooled inoculum (unpublished data). ... Transmission of the sheep scrapie to cattle was attempted in 1979 by using intracerebral, intramuscular, subcutaneous, and oral routes of inoculation of 5, 8- to 11-month old cattlw with a homologous mixture of brain from 1 affected sheep (61, 62). ONE of the 5 cattle develped neurologic signs 48 months after inoculation. Signs were disorientation, incoordination, a stiff-legged stilted gait, progressive difficulty in rising, and finally in terminal recumbency. The clinical course was 2.5 months. TWO of the 5 cattle similarly inoculated with brain tissue from a goat with scrapie exhibited similar signs 27 and 36 months after incoluation. Clinical courses were 43 an 44 days. Brain lesions of mild gliosis and vacuolation and mouse inoculation data were insufficient to confirm a diagnosis of scrapie. This work remained controversial until recent examination of the brains detected PrP-res in all 3 cattle with neurologic disease but in none of the unaffected cattle (62). Results of these studies are similar to ours and underscore the necessity of methods other than histopathology to diagnose scrapie infection in cattle. We believe that immunologic techniques for detecting PrP-res currently provide the most sensitive and reliable way to make a definitive diagnosis... http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf Visit to USA ... info on BSE and Scrapie http://www.bseinquiry.gov.uk/files/yb/1988/10/00001001.pdf snip... http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf Title: Experimental Transmission of Transmissible Mink Encephalopathy (Tme) to Cattle by Intracerebral Inoculation Technical Abstract: To compare clinicopathological findings of transmissible mink encephalopathy (TME) with other transmissible spongiform encephalopathies (TSE, prion diseases) that have been shown to be experimentally transmissible to cattle (sheep scrapie, and chronic wasting disease, CWD), 2 groups of calves (n = 4 each) were intracerebrally inoculated with TME agents from 2 different sources (mink with TME and a bovine with TME). Two uninoculated calves served as controls. Within 15.3 months post inoculation (PI), all animals from both inoculated groups developed clinical signs of central nervous system (CNS) abnormality; their CNS tissues had microscopic spongiform encephalopathy (SE); and PrP**res was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify TME PrP**res but also develop clinical CNS signs and extensive lesions of SE. The latter has not been shown with other TSE agents (scrapie and CWD) similarly inoculated into cattle. The findings also suggest that the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) would detect TME in cattle should it occur naturally. However, it would be a diagnostic challenge to differentiate TME in cattle from BSE. Our recent preliminary results indicate that WB may be able to differentiate between bovine TME and BSE. Pelt Production Up 3 Percent Mink pelt production in the United States in 2005 totaled The number of pelts by color class as a percent of the total U.S. Value of Pelt Production Up 33 Percent Mink pelts produced during the 2005 crop year were valued at http://usda.mannlib.cornell.edu/reports/nassr/other/zmi-bb/mink0706.pdf http://www.aphis.usda.gov/lpa/pubs/fsheet_faq_notice/fs_ahtme.html Mink offal is now rendered with other species and will decline in value under the first four regulatory options. Mink are raised for their pelts and oil. Most mink farmers kill and pelt their own animals once a year near the end of November or in early December. Once the pelts are removed, the fat is then scrapped from the hide. This fat is used to manufacture mink oil that is sought for cosmetic uses because of its hypoallergenic qualities and in leather treatments. The total value of mink production in 1995 was $143 million, an increase of 72 percent from 1994. In 1995, 446 mink farms produced a total of 2.69 million pelts (NASS, 1996b). Mink producers vary in size but most are small operations. Mink farming is concentrated in Utah (130 2-11 farms), Wisconsin (77 farms), and Minnesota (52 farms). There has been recent consolidation within the industry, with the number of farms decreasing by 8 percent from 1993 to 1994 and 3 percent from 1994 to 1995. The market price for mink pelts is subject to wide demand fluctuations based on fashion and weather. Once the pelt and fat are removed, the entire carcass is then rendered. Mink carcasses sent to rendering (minus the pelt and fat) weigh an average of 2.5 pounds, so the total estimated offal produced per year is 6.7 million pounds. Mink farmers are reported to have difficulty with getting renderers to pick-up their material because of its low volume and the infrequency of offal generation. DO they test for TSE in Mink and what are these figures if so ???
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