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From: TSS ()
CWD Annual Report – 2005 To date, we have developed a reliable, non-lethal method for detecting chronic wasting disease in mule deer that represented a significant breakthrough in improving the ability to monitor prevalence of the disease over time and space. We also have demonstrated that chronic wasting disease can be transmitted indirectly, and that fecal shedding and fecal-oral transmission is likely. We also have developed epidemic models for chronic wasting disease in captive mule deer that align well with the independent empirical findings on transmission processes, underscoring the likely importance of indirect transmission in the ecology of chronic wasting disease in natural populations. full text ; http://www.nrel.colostate.edu/projects/cwd/papers/CWD_ann_rpt_2005_w_figs.pdf Vet Pathol 42:530–549 (2005) REVIEW ARTICLE Chronic Wasting Disease E. S. WILLIAMS1 Department of Veterinary Sciences, University of Wyoming, Laramie, WY Abstract. Chronic wasting disease (CWD) is a unique transmissible spongiform encephalopathy (TSE) of mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), and Rocky Mountain elk (Cervus elaphus nelsoni). The natural history of CWD is incompletely understood, but it differs from scrapie and bovine spongiform encephalopathy (BSE) by virtue of its occurrence in nondomestic and free-ranging species. CWD has many features in common with scrapie, including early widespread distribution of disease-associated prion protein (PrPd) in lymphoid tissues, with later involvement of central nervous system (CNS) and peripheral tissues. This distribution likely contributes to apparent efficiency of horizontal transmission and, in this, is similar to scrapie and differs from BSE. Clinical features and lesions of CWD are qualitatively similar to the other animal TSEs. Microscopically, marked spongiform lesions occur in the central nervous system (CNS) after a prolonged incubation period and variable course of clinical disease. During incubation, PrPd can be identified in tissues by antibody-based detection systems. Although CWD can be transmitted by intracerebral inoculation to cattle, sheep, and goats, ongoing studies have not demonstrated that domestic livestock are susceptible via oral exposure, the presumed natural route of exposure to TSEs. Surveillance efforts for CWD in captive and free-ranging cervids will continue in concert with similar activities for scrapie and BSE. Eradication of CWD in farmed cervids is the goal of state, federal, and industry programs, but eradication of CWD from free-ranging populations of cervids is unlikely with currently available management techniques. snip... Transmission Although the exact method of transmission of CWD is not known, horizontal and indirect transmission appear to be the most important routes of spread.99 Epidemiologic observations suggest that in addition to transmission within species, CWD can be transmitted from elk to mule deer and white-tailed deer, from mule deer to elk, and from mule deer to white-tailed deer.156 Maternal transmission, if it occurs, does not appear to play a significant role in the epidemiology of the disease. 99 To date, PrPd and infectivity have not been identified in placentas of deer and elk. This is in contrast to scrapie, in which high levels of infectivity reside in the placenta,5,122,143,144 and epidemiologic investigations have found that transmission at the time of lambing appears to be important in maintaining scrapie in flocks. Results of a series of studies investigating CWD transmission have recently been published.102 Direct transmission of CWD between animals occurred, although the exact mechanism was not determined. The role of environmental contamination in maintaining infectivity is not entirely understood; however, controlled studies showed infectivity remained on pastures in which CWD-affected deer resided approximately 2 years previously. These studies were conducted in pastures presumed to be highly contaminated. Thus, extrapolation to field situations should be done with care, but these data suggest caution in managing pastures or paddocks that have housed CWD-affected cervids. In addition, mule deer were infected by contact with skeletal remains of CWD-affected deer and surrounding ground and vegetation. This information bolsters the need for caution when moving portions of harvested cervids that contain the highest amount of infectivity, such as the head and the spine, to areas where CWD does not exist. snip...end full text ; http://www.vetpathology.org/cgi/reprint/42/5/530.pdf DRAFT WYOMING GAME AND FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN February 17, 2006 6. Epidemiology of CWD: detection, shedding, and environmental contamination. http://gf.state.wy.us/downloads/pdf/CWD2005reviseddraft.pdf Experimental CWD Infection and Bioassay in the Ferret Based on the work of Bartz et al., we have developed the ferret model of CWD infection and employed this system to: (1) compare brain lesions and PrPcwd distribution in brain and lymphoid tissues in ferrets with those in deer, and (2) assay secretions/excretions from deer for CWD prion infectivity. Groups of ferrets were inoculated via the oral or intracerebral (i.c.) route with CWD + vs. CWD- deer brain homogenates, white blood cells, or saliva. Inoculated ferrets were monitored clinically and either sacrificed at pre-determined intervals from 3 to 24 months post inoculation (pi) or when terminal symptoms developed. Ferrets inoculated ic with CWD+ brain developed clinical neurologic disease and were euthanized between 14 and 19 months. Tissues were examined by histopathology, and by immunohistochemical staining, ELISA, and western blotting for Histopathologic lesions indicative of TSE included spongiform vacuolation and neuronal necrosis. PrPcwd was demonstrated in ferret brain by ELISA and western blot assays. In addition, dual immunofluorescent staining revealed PrPcwd localized at astrocyte surface membranes and within neurons. Results to date from ferret bioassay of saliva and blood cells from CWD+ deer will be reported. These studies confirm the susceptibility of the ferret to CWD infection and pose the potential that CWD infectivity can be assayed in this small animal model. ============================================= is evidence that the disease is transmitted horizontally from infected to susceptible cervids (Miller and Williams, 2003). Maternal transmission may also occur but seems to play a subordinate role. Accumulation of PrPres in gut-associated lymphoid tissues during the disease course suggests agent shedding in faeces and/or saliva as plausible transmission routes (Sigurdson et al., 1999). Residual infectivity in contaminated environments, either from excreta or from decomposed carcasses of infected animals, may also be important in sustaining epidemics. http://www.efsa.europa.eu/etc/medialib/efsa/science/biohaz/biohaz_opinions/opinion_annexes/500.Par.0001.File.dat/opinion_biohaz12_ch_wast_dis_ef70_report_en1.pdf CWD 3.4.2 Evidence for lateral transmission see Annexe 1 on distribution of tissue infectivity (old data)...tss http://72.14.209.104/search?q=cache:s7mfafLPBrYJ:ec.europa.eu/food/fs/sc/ssc/out324_en.pdf+REPORT+ON+CHRONIC+WASTING+DISEASE+AND+TISSUE&hl=en&gl=us&ct=clnk&cd=11 http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf Observations of deer and elk in captivity indicate that CWD is contagious though the exact mechanism(s) of transmission are not yet known. Based on pathogenesis of the disease it is plausible that the CWD agent exits the body in saliva and feces. The contribution of 82 environmental contamination to the epidemiology of CWD is not specifically known but observations of cohorts of elk and deer in captivity strongly suggest it is important in areas of high CWD prevalence and high densities of susceptible species. This is an area of considerable ongoing research. http://www.blackwellpublishing.com/products/journals/suppmat/nan/nan477/NAN477sm.pdf Review of research published since November 2004 SNIP... 7) EPIDEMIOLOGY AND TRANSMISSION From enclosures previously used by infected animals 28. Research reviewed in the WIN report showed that healthy cervids could be infected with CWD by grazing on pastures contaminated with excreta from infected cervids or with the carcases of diseased cervids. This provided evidence for environmental transmission of CWD. 29. A more recent experimental study examined the potential for soil to serve as a reservoir for TSEs by examining the interaction of PrPSc (from an adapted transmissible mink encephalopathy agent) with common soil minerals (Johnson et al, 2006). It was demonstrated that substantial PrPSc could be adsorbed by the clay minerals, kaolinite and montmorillonite as well as quartz. In addition, significant adsorption to whole soil samples was found. Furthermore, there was a strong interaction between PrPSc and montmorillonite. To determine whether prions remained infectious in soil, clay samples experimentally contaminated with an inoculum were ic inoculated into hamsters. Symptoms developed in these animals at approximately the same time as those injected with directly with the inoculum. The study suggests that TSE infectivity released into soil may be preserved in a bioavailable form which may contribute to disease transmission. The authors suggest this study adds to the evidence for environmental transmission of CWD. http://www.seac.gov.uk/papers/CWD-review.pdf 1 Program in Cellular and Molecular Biology, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 2 Department of Animal Health and Biomedical Sciences, School of Veterinary Medicine, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 3 Molecular and Environmental Toxicology Center, University of Wisconsin Madison, Madison, Wisconsin, United States of America, 4 Department of Soil Science, University of Wisconsin Madison, Madison, Wisconsin, United States of America An unidentified environmental reservoir of infectivity contributes to the natural transmission of prion diseases (transmissible spongiform encephalopathies [TSEs]) in sheep, deer, and elk. Prion infectivity may enter soil environments via shedding from diseased animals and decomposition of infected carcasses. Burial of TSE-infected cattle, sheep, and deer as a means of disposal has resulted in unintentional introduction of prions into subsurface environments. We examined the potential for soil to serve as a TSE reservoir by studying the interaction of the disease-associated prion protein (PrPSc) with common soil minerals. In this study, we demonstrated substantial PrPSc adsorption to two clay minerals, quartz, and four whole soil samples. We quantified the PrPSc-binding capacities of each mineral. Furthermore, we observed that PrPSc desorbed from montmorillonite clay was cleaved at an N-terminal site and the interaction between PrPSc and Mte was strong, making desorption of the protein difficult. Despite cleavage and avid binding, PrPSc bound to Mte remained infectious. Results from our study suggest that PrPSc released into soil environments may be preserved in a bioavailable form, perpetuating prion disease epizootics and exposing other species to the infectious agent. Funding. This work was supported by USEPA grant 4C-R070-NAEX (JAP) and DOD grant DAMD17–03–1–0369 (JMA). Competing interests. The authors have declared that no competing interests exist. Editor: David Westaway, University of Toronto, Canada Received: December 20, 2005; Accepted: March 8, 2006; Published: April 14, 2006 DOI: 10.1371/journal.ppat.0020032 Copyright: © 2006 Johnson et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abbreviations: BH, brain homogenate; BSE, bovine spongiform encephalopathy; CWD, chronic wasting disease; dpi, days postinoculation; Kte, kaolinite; Mte, montmorillonite; PK, proteinase K; PrPC, normal cellular isoform of the prion protein; PrPSc, disease-associated prion protein; TSE, transmissible spongiform encephalopathy * To whom correspondence should be addressed. E-mail: joelpedersen@wisc.edu Citation: Johnson CJ, Phillips KE, Schramm PT, McKenzie D, Aiken JM, et al. (2006) Prions Adhere to Soil Minerals and Remain Infectious. PLoS Pathog 2(4): e32 snip... Discussion snip... In conclusion, soil and soil minerals have the potential to bind PrPSc and maintain infectivity. These findings will serve as the basis for further study on the interaction of PrPSc with other soil components (humic substances, quartz, and other minerals), the stability of soil-bound PrPSc under typical environmental conditions (UV light, freeze-thaw cycles) and the effect of soil microorganisms and extracellular enzymes on protein integrity. Our current results suggest that sorption of PrPSc to clay minerals may limit its migration through the soil column. Maintenance of prion infectivity at the soil surface may contribute to the propagation of CWD and scrapie epizootics and enhance the likelihood of interspecies transmission of these diseases. snip...full text ; http://pathogens.plosjournals.org/archive/1553-7374/2/4/pdf/10.1371_journal.ppat.0020032-S.pdf Copyright © 2006 American Chemical Society Delphine Rapp, Patrick Potier, Lucile Jocteur-Monrozier, and Agnès Richaume* Ecologie Microbienne, Université Claude Bernard Lyon 1 - UMR CNRS 5557 - USC INRA 1193, bat. G. Mendel, 43 Bd du 11 Novembre 1918, 69 622 Villeurbanne Cedex, France Received for review April 19, 2006 Revised manuscript received July 21, 2006 Accepted July 27, 2006 Abstract: This study is part of a European project focused on understanding the biotic and abiotic mechanisms involved in the retention and dissemination of transmissible spongiform encephalopathies (TSE) infectivity in soil in order to propose practical recommendations to limit environmental contamination. A 1-year field experiment was conducted with lamb carcasses buried in a pasture soil at three depths (25, 45, and 105 cm). Microbial community response to carcasses was monitored through the potential proteolytic activity and substrate induced respiration (SIR). Soil above carcasses and control soil exhibited low proteolytic capacity, whatever the depth of burial. Contrastingly, in soil beneath the carcasses, proteolysis was stimulated. Decomposing carcasses also stimulated SIR, i.e., microbial biomass, suggesting that proteolytic populations specifically developed on lixiviates from animal tissues. Decomposition of soft tissues occurred within 2 months at subsurface while it lasted at least 1 year at deeper depth where proteolytic activities were season-dependent. The ability of soil proteases to degrade the form of prion protein was shown in vitro and conditions of burial relevant to minimize the risk of prion protein dissemination are discussed. http://pubs.acs.org/cgi-bin/abstract.cgi/esthag/asap/abs/es060943h.html 70. A member considered that, since the TSE agent is a protein, it was likely to decay quickly due to the pH of, and bacteria present in, soil. However, a member pointed out good evidence suggesting that the Chronic Wasting Disease agent persisted in the environment. Dr Matthews informed members that a VLA project on infectivity in sheep exposed to the farm environment indicated that material on pasture is infectious for at least 2 months. Members agreed that in view of the resistance of PrPsc to degradation, evidence from CWD and the VLA studies, it was safer to assume survival of the agent in soil for a significant amount of time. 71. In response to members’ questions about the field spreading of fertiliser, Alan Brewer (Defra) informed the committee that some dust can arise from the activity, both from the fertiliser distribution process (that depends on the type of spreading mechanism) and from tractor wheels kicking up soil in arable situations. But it was not possible to indicate whether there was any likelihood of dust particles containing fertiliser drifting onto adjoining fields. He added that it was recognised as good practice for farmers not to spread fertiliser into hedges and watercourses. http://www.seac.gov.uk/minutes/final87.pdf Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies Title: PRION INFECTION OF MUCOSAL TISSUE Bessen, Richard - MONTANA STATE UNIVERSITY Technical Abstract: To investigate the site(s) of prion agent shedding in chronic wasting disease (CWD), we examined the distribution of the prion agent in mucosal tissue from ruminants and rodents with experimental prion disease. We chose the tongue as a peripheral target of prion infection since is a densely innervated tissue at the oral mucosa that we postulate can be a site of CWD agent shedding. The prion agent, PrP**Sc, was present in tongues from elk infected with the CWD agent and sheep infected with the scrapie agent. In hamsters infected with the prion agent, PrP**Sc was found in nerve fibers and skeletal muscle cells as well as in taste cells. In fungiform papillae on the tongue, the distribution of PrP**Sc was consistent with deposition in the taste bud and the surrounding stratified squamous epithelium. These findings suggest that the prion agent can spread from the brain to the tongue along sensory and motor fibers. The presence of the prion agent in the tongue of ruminants and rodents indicates that 1) ingestion of tongue or tongue derived food products can pose a risk to human and animal health, and 2) the localization of the prion agent at the mucosal surface of the tongue could provide a site for prion agent shedding and subsequent transmission to naive hosts. Title: ABNORMAL PRION PROTEIN IN ECTOPIC LYMPHOID TISSUE IN A KIDNEY OF AN ASYMPTOMATIC WHITE-TAILED DEER EXPERIMENTALLY INOCULATED WITH THE AGENT OF CHRONIC WASTING DISEASE Hamir, Amirali Interpretive Summary: Chronic wasting disease (CWD) is a fatal disease of brain and spinal cord of deer and elk. It belongs to a group of transmissible spongiform encephalopathy (TSE) diseases which includes bovine spongiform encephalopathy or "mad cow disease". Infection by the CWD agent induces accumulations of an abnormal form of protein (called prion or PrP**res) in tissues of nervous and lymphoid systems. This report documents presence of PrP**res within kidney of a white tailed deer that was experimentally inoculated by intracerebral route with CWD. The deer was euthanized and examined at 10 months post inoculation. At that age it did not show any clinical signs of the disease but lesions of TSE were detected in the tissues. These findings confirm early involvement of tissues in white tailed deer. Also, it corroborates the recently published finding of presence of PrP**res in organs other than brain and lymphoid systems in laboratory animals with TSE (scrapie) by demonstration of the same phenomenon in a natural host species. Title: TRANSMISSION OF CHRONIC WASTING DISEASE AGENT OF MULE DEER (CWD**MD) TO SUFFOLK SHEEP BY INTRACEREBRAL ROUTE Hamir, Amirali Technical Abstract: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) that has been identified in captive and free-ranging cervids in the U.S. since 1967. To determine the transmissibility of CWD to sheep, 8 Suffolk lambs [4 QQ and 4 QR at codon 171 of prion protein (PRNP) gene] were inoculated intracerebrally with a pooled brain suspension from 28 mule deer naturally affected with CWD (CWD**md). Two other lambs (1 QQ and 1 QR at codon 171 of the PRNP gene) were kept as non-inoculated controls. Within 36 months post inoculation (MPI), 2 animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in the sheep with the clinical signs of TSE and its tissues were positive for the abnormal prion protein (PrP**res) by immunohistochemistry and Western blot. Between 36 and 60 MPI, 3 other sheep were euthanized because of conditions unrelated to TSE. The remaining 3 sheep remained non-clinical at the termination of the study (72 MPI) and were euthanized at that time. One of the 3 animals revealed SE and its tissues were positive for PrP**res. Both sheep positive for PrP**res were homozygous QQ at codon 171. Retrospective examination of the PRNP genotype of the 2 TSE-positive animals revealed that the sheep with clinical prion disease (euthanized at 35 MPI) was heterozygous (AV) and the sheep with the sub-clinical disease (euthanized at 72 MPI) was homozygous (AA) at codon 136 of the PRNP. These findings demonstrate that transmission of the CWD**md agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a significant part in successful transmission and incubation period of CWD**md. Title: EXPERIMENTAL SECOND PASSAGE OF CHRONIC WASTING DISEASE (CWD(MULE DEER)) AGENT TO CATTLE Hamir, Amirali Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB. ==================================================== http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html Transmission Baier, M., S. Norley, J. Schultz, M. Burwinkel, A. Schwarz and C. Riemer. 2003. Prion diseases: infectious and lethal doses following oral challenge. J. of General Virology 84:1927-1929. Hamir, A.N., J.M. Miller, R.C. Cutlip, M.J. Stack, M.J. Chaplin, and A.L. Jenny. 2003. Preliminary Observations on the Experimental Transmission of Scrapie to Elk (Cervus elaphus nelsoni) by Intracerebral Inoculation. Vet Pathol. 40:81-85. Hamir, A.N., J.M. Miller, R.C. Cutlip, M.J. Stack, M.J. Chaplin, A.L. Jenny and E.S. Williams. 2003. Experimental inoculation of scrapie and chronic wasting disease agents in raccoons (Procyon lotor). The Veterinary Record 153:121-123. Lupi, O., 2003. Could ectoparasites act as vectors for prion disease?. International J. of Dermatology. 42:425-429. Miller, M.W. and E.S. Williams. 2003. Prion disease: Horizontal prion transmission in mule deer. Nature 425:35-36. Race, R.; Raines, A.; Baron, T.; Miller, M.; Jenny, A.; Williams, E. 2002. Comparison of Abnormal Prion Protein Glycoform Patterns from Transmissible Spongiform Encephalopathy Agent-Infected Deer, Elk, Sheep, and Cattle. Journal of Virology 76(23):12365-12368. Gould, D.; Voss, J.; Miller, M.; Bachand, A.; Cummings, B.; Frank, A. 2003. Brief Communcations; Survey of cattle in northeast Colorado for evidence of chronic wasting disease: geographical and high-risk targeted sample. Journal Vet. Diagn. Invest. 15: 274-277. Hunter, N.; Foster, J.; Chong, A.; McCutcheon, S.; Parnham, D.; Eaton, S.; MacKenzie, C.; Houston, F. 2002. Transmission of prion diseases by blood transfusion. Journal of General Virology 83:2897-2905. Belay, E.D., P. Gambetti, L.B. Schonberger, P. Parchi, D.R. Lyon, S. Capellari, J.H. McQuiston, K. Bradley, G. Dowdle, M. Crutcher and C.R. Nichols. 2001. Creutzfeldt-Jakob disease in unusually young patients who consumed venison. Arch. Neurol. 58(10): 1673-1678. Hamir, A.N., R.C. Cutlip, J.M. Miller, E.S. Williams, M.J. Stack, M.W. Miller, K.I. O'Rourke and M.J. Chaplin. 2001. Preliminary findings on the experimental transmission of chronic wasting disease agent of mule deer to cattle. J. Vet. Diagn. Invest. 13(1): 91-96. Hill, A.F., S. Joiner, J. Lineham, M. Desbruslais, P.L Lantos and J. Collinge. 2000. Species-barrier-independent prion replication in apparently resistant species. Proc. Natl. Acad. Sci. 97(18): 10248-10253. Raymond, G.J., A. Bossers, L.D. Raymond, K.I. O'Rourke, L.E. McHolland, P.K. Bryant III, M.W. Miller, E.S. Williams, M. Smits and B. Caughey. 2000. Evidence of a molecular barrier limiting susceptibility of humans, cattle and sheep to chronic wasting disease. The EMBO Journal 19(17): 4425-4430. Sigurdson, C.J., E.S. Williams, M.W. Miller, T.R. Spraker, K.I. O'Rourke and E.A. Hoover. 1999. Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus). J. of General Virology 80(10): 2757-2764. http://www.aphis.usda.gov/vs/nahps/cwd/cwd-research.html#Transmission 2003D-0186 -------- Original Message -------- Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability i would kindly like to comment on; Docket 03D-0186 FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Several factors on this apparent voluntary proposal disturbs me greatly, 1. MY first point is the failure of the partial ruminant-to-ruminant feed 2. WHAT about sub-clinical TSE in deer and elk? with the recent 3. WE must ban not only CNS (SRMs specified risk materials), 4. THERE are and have been for some time many TSEs in the 5. UNTIL we ban all ruminant by-products from being fed back 6. IT is paramount that CJD be made reportable in every state 7. WE must learn from our past mistakes, not continue to make REFERENCES Department of Pathology, College of Veterinary Medicine and Biomedical Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail Mule deer fawns (Odocoileus hemionus) were inoculated orally with a snip... These results indicate that mule deer fawns develop detectable PrP res snip... http://vir.sgmjournals.org/cgi/content/full/80/10/2757 8420-20.5% Antler Developer snip... _animal protein_ http://www.surefed.com/deer.htm BODE'S GAME FEED SUPPLEMENT #400 snip... _animal protein_ http://www.bodefeed.com/prod7.htm Ingredients Grain Products, Plant Protein Products, Processed Grain By-Products, http://www.bodefeed.com/prod6.htm MORE ANIMAL PROTEIN PRODUCTS FOR DEER Bode's #1 Game Pellets GUARANTEED ANALYSIS Grain Products, Plant Protein Products, Processed Grain By-Products, FEEDING DIRECTIONS http://www.bodefeed.com/prod8.htm INGREDIENTS Grain Products, Roughage Products (not more than 35%), Processed Grain DIRECTIONS FOR USE Deer Builder Pellets is designed to be fed to deer under range http://www.profilenutrition.com/Products/Specialty/deer_builder_pellets.html DEPARTMENT OF HEALTH & HUMAN SERVICES April 9, 2001 WARNING LETTER 01-PHI-12 Brian J. Raymond, Owner Tel: 215-597-4390 Dear Mr. Raymond: Food and Drug Administration Investigator Gregory E. Beichner conducted Our investigation found failure to label your In addition, we note that you are using approximately 140 pounds of The above is not intended to be an all-inclusive list of deviations from http://www.fda.gov/foi/warning_letters/g1115d.pdf http://www.fda.gov/ohrms/dockets/dailys/03/oct03/100203/100203.htm TONS Products manufactured from 02/01/2005 until 06/06/2006 ********************************* e) "Big Jim's" BBB Deer Ration, Big Buck Blend, ********************************* f) CO-OP 40% Hog Supplement Medicated Pelleted, ### ##################### Bovine Spongiform Encephalopathy ##################### Subject: SEAC Position statement - Chronic wasting disease in UK deer January 2005 (updated July 2006) SEAC Statement -------------------------------------------------------------------------------- Position statement - Chronic wasting disease in UK deer Background 3. SEAC considered a review of the published, and some unpublished, research on CWD, together with surveillance data on TSEs in European cervids and information on UK cervid populations 1. A further review of the published literature was considered together with additional surveillance data on TSEs in European cervids 2. Origins 5. Data supporting any of these possible origins of CWD are either absent or equivocal. Although CWD could have originated from scrapie, the differing properties of the two prion diseases in strain typing bioassays, whilst limited, do not support this hypothesis. Evidence for multiple strains of CWD is equivocal. It seems most likely that CWD arose from a spontaneous change of endogenous PrP resulting in a disease-associated and laterally-transmissible form of PrP, although direct data to support this hypothesis are lacking. Host range 7. There are no direct data relating to the transmissibility of CWD to UK cervid species. However, comparison of a limited number of PrP codons indicates some homology in the endogenous PrP gene of European and North American cervid species. Thus, the possibility that UK cervids may be susceptible to CWD cannot be excluded, in particular red deer (Cervus elaphus elaphus) which are closely related to Rocky Mountain elk. 8. There is no evidence to suggest that CWD is present in UK cervids. However, because surveillance in the UK is very limited, a low level prevalence of CWD cannot be ruled out. The committee endorsed the opinion of the European Food Safety Authority on CWD surveillance in the European Union (2004) 3. 9. Transmission studies using parenteral routes of administration to cattle, sheep and a single goat, together with data from in vitro PrP conversion experiments, suggest that a significant barrier to CWD transmission to these species may exist. No transmission has been evident so far in an on-going oral transmission study in cattle after seven years. However, evidence from transmission experiments in cattle using the intracerebral route suggests that should cattle ever become infected with CWD, the barrier to transmission between cattle would be appreciably lower. In addition, these experiments show that the neuropathology of CWD is very different from BSE allowing CWD to be distinguished from BSE should natural transmission of CWD ever occur. Furthermore, no signs of infection have been observed from monitoring of cattle co-habiting areas with infected cervids, or in cattle, sheep or goats in close contact with infected cervids in research facilities. Thus, although the data are limited, there is currently no evidence to suggest that CWD can be transmitted naturally to cows, sheep or goats, and it is likely that there is a strong species barrier to such transmission. Routes of transmission 11. There have also been suggestions that the lateral transmission of CWD may be influenced by environmental factors. Pathogenesis BSE in UK deer Human health implications 15. No study has examined the transmission of CWD to non-human primates by the oral route. However, CWD has been transmitted by intracranial inoculation to non-human primates. Transmission experiments using two strains of transgenic mice expressing human PrP, show that these animals do not develop CWD, suggesting a significant species barrier to the transmission of CWD to humans exists. However, these findings must be interpreted with caution as they may not accurately predict the human situation. Data from in vitro experiments on conversion of human PrP by disease-associated forms of PrP, including PrPCWD, are equivocal. 16. The committee concluded there is no evidence of transmission of CWD to humans from consumption of venison, and that there may be significant barriers to transmission. Nevertheless, as the data are extremely limited a risk cannot be ruled out should CWD enter UK herds. Conclusions 18. There is no evidence of transmission of CWD to humans from consumption of meat from infected cervids. Although epidemiological and experimental data on potential transmission of CWD are extremely limited, they suggest that there may be a significant species barrier. It would be helpful if further studies were available assessing the potential species barrier for transmission to humans. 19. Although limited, there is no evidence CWD can be transmitted to cattle, sheep or goats by natural means. 20. In summary, it appears that CWD currently poses relatively little risk to human health, or to the health of cattle, sheep or goats in the UK. Nevertheless, as a risk cannot be excluded a watching brief should be maintained. 1. The information considered by the committee in 2004 is available here. 2. The information considered by the committee in 2006 is available here. 3. http://www.efsa.eu.int/science/biohaz/biohaz_opinions/501_en.html http://www.seac.gov.uk/statements/state0706.htm 5. Data supporting any of these possible origins of CWD are either absent or equivocal. Although CWD could have originated from scrapie, the differing properties of the two prion diseases in strain typing bioassays, whilst limited, do not support this hypothesis. Evidence for multiple strains of CWD is equivocal. It seems most likely that CWD arose from a spontaneous change of endogenous PrP resulting in a disease-associated and laterally-transmissible form of PrP, although direct data to support this hypothesis are lacking. ................end this study is on going at the moment and, as yet, we have no results. All results will probably appear on the UK Food Standards Agency web pages but I’m afraid we really do not know just how long this study will take to complete as no one has undertaken this work before. Moredun Research Institute Pentlands Science Park Bush Loan, Penicuik, Near Edinburgh, EH26 0PZ Scotland, UK ============== TSS #################### https://lists.aegee.org/bse-l.html ####################
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