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Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with Lyophilized Chronic Wasting Disease Prion Particulate

Posted May 15 2013 1:45pm
Research Article



Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with Lyophilized Chronic Wasting Disease Prion Particulate Complexed to Montmorillonite Clay




Tracy A. Nichols mail, Terry R. Spraker, Tara D. Rigg, Crystal Meyerett-Reid, Clare Hoover, Brady Michel, Jifeng Bian, Edward Hoover, Thomas Gidlewski, Aru Balachandran, Katherine O'Rourke, Glenn C. Telling, Richard Bowen, [ ... ], Kurt C. VerCauteren equal contributor




Abstract




Chronic wasting disease (CWD), the only known prion disease endemic in wildlife, is a persistent problem in both wild and captive North American cervid populations. This disease continues to spread and cases are found in new areas each year. Indirect transmission can occur via the environment and is thought to occur by the oral and/or intranasal route. Oral transmission has been experimentally demonstrated and although intranasal transmission has been postulated, it has not been tested in a natural host until recently. Prions have been shown to adsorb strongly to clay particles and upon oral inoculation the prion/clay combination exhibits increased infectivity in rodent models. Deer and elk undoubtedly and chronically inhale dust particles routinely while living in the landscape while foraging and rutting. We therefore hypothesized that dust represents a viable vehicle for intranasal CWD prion exposure. To test this hypothesis, CWD-positive brain homogenate was mixed with montmorillonite clay (Mte), lyophilized, pulverized and inoculated intranasally into white-tailed deer once a week for 6 weeks. Deer were euthanized at 95, 105, 120 and 175 days post final inoculation and tissues examined for CWD-associated prion proteins by immunohistochemistry. Our results demonstrate that CWD can be efficiently transmitted utilizing Mte particles as a prion carrier and intranasal exposure.



snip...



The results of this study confirm that CWD can be successfully transmitted IN as a lyophilized prion particulate adsorbed to Mte and that genotype at codon 96 affects the lymphoid distribution of CWD within the body. Additionally, two novel intranasal tracking methods were employed that provided insight into CWD translocation within the nasal cavity. The data collected in this study may also shed light on why there is a higher prevalence of CWD in males, as males participate in more behaviors that generate dust. We propose chronic, long-term exposure to CWD prions adsorbed to dust particles to be a natural CWD infection route in addition to chronic oral and nasal contact exposure.




Citation: Nichols TA, Spraker TR, Rigg TD, Meyerett-Reid C, Hoover C, et al. (2013) Intranasal Inoculation of White-Tailed Deer (Odocoileus virginianus) with Lyophilized Chronic Wasting Disease Prion Particulate Complexed to Montmorillonite Clay. PLoS ONE 8(5): e62455. doi:10.1371/journal.pone.0062455



Editor: Anthony E. Kincaid, Creighton University, United States of America



Received: November 30, 2012; Accepted: March 21, 2013; Published: May 9, 2013



This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.



Funding: Funding was provided by U.S. Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services (VS). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.



Competing interests: The authors have declared that no competing interests exist.





see full text ;









Thanks again to PLOS et al for full text access to this scientific research on the CWD TSE prion disease...tss





April/May/June 2012; © 2012 Landes Bioscience



PO-033: Replication efficiency of soil-bound prions varies with soil type



Shannon Bartelt-Hunt,1 Samuel Saunders,1 Ronald Shikiya,2 Katie Langenfeld,2 Jason Bartz2 1University of Nebraska-Lincoln; Omaha, NE USA; 2Creighton University; Omaha, NE USA


Prion sorption to soil is thought to play an important role in the transmission of scrapie and chronic wasting disease (CWD) via the environment. Sorption of PrP to soil and soil minerals is influenced by the strain and species of PrPSc and by soil characteristics. However, the ability of soil-bound prions to convert PrPc to PrPSc under these wide-ranging conditions remains poorly understood. We developed a semiquantitative protein misfolding cyclic amplification (PMCA) protocol to evaluate replication efficiency of soil-bound prions. Binding of the hyper (HY) strain of transmissible mink encephalopathy (TME) (hamster) prions to a silty clay loam soil yielded a greater-than-1-log decrease in PMCA replication efficiency with a corresponding 1.3-log reduction in titer. The increased binding of PrPSc to soil over time corresponded with a decrease in PMCA replication efficiency. The PMCA efficiency of bound prions varied with soil type, where prions bound to clay and organic surfaces exhibited significantly lower replication efficiencies while prions bound to sand exhibited no apparent difference in replication efficiency compared to unbound controls. PMCA results from hamster and CWD agent-infected elk prions yielded similar findings. Given that PrPSc adsorption affinity varies with soil type, the overall balance between prion adsorption affinity and replication efficiency for the dominant soil types of an area may be a significant determinant in the environmental transmission of prion diseases.





PO-248: TSE infectivity survives burial for five years with little reduction in titer



Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and R(D)SVS; University of Edinburgh; Edinburgh, UK


BSE infected animals, BSE-contaminated materials and other sources of TSE (prion) infection, such as carcasses from scrapie infected sheep, CWD infected deer and cadavers of individuals infected with CJD may all end up in the environment through burial or other methods of disposal. They may continue to act as a reservoir of TSE infectivity if cattle or other susceptible animals were to be exposed to these sources in the future. In order to address these concerns, we performed two large scale demonstration experiments under field conditions which were designed to mimic some of the ways by which TSE infected materials may have been disposed of. The project examined the fate of TSE infectivity over a period of five years in two scenarios; when the infectivity was contained within bovine heads and when the infectivity was buried without any containment. Two soil types were compared: a sandy loam and a clay loam. We used the 301V TSE strain which was derived by serial passage of BSE in VM mice.


TSE infectivity was recovered from all the heads exhumed annually for five years from both types of soil, with little reduction in the amount of infectivity throughout the period of the experiment. Small amounts of infectivity were found in the soil immediately surrounding the heads, but not in samples remote from them. Similarly there was no evidence of significant lateral movement of infectivity from the buried bolus. However large amounts of TSE infectivity were recovered at the site of burial of both boluses. There was limited vertical upward movement of infectivity from the bolus buried in clay soil and downward movement from the bolus buried in sandy soil.


Now that these experiments are completed we conclude that TSE infectivity is likely to survive burial for long periods of time with minimal loss of infectivity and restricted movement from the site of burial. These experiments emphasize that the environment is a viable reservoir for retaining large quantities of TSE infectivity, and reinforce the importance of risk assessment when disposing of this type of infectious material.








PRION 2011



Envt.16: Soil Properties as a Factor in CWD Spread in Western Canada



Alsu Kuznetsova,† Tariq Siddique and Judd Aiken


University of Alberta; Edmonton, AB Canada†Presenting author; Email: alsu@ualberta.ca


Soil can serve as a stable reservoir for infectious prion proteins (PrPSc). Soils are diverse and complex, varying in clay, silt, sand and organic components. We have shown that PrPSc binds clay minerals avidly, an interaction that considerably enhances prion infectivity. Conversely quartz sand bound PrPSc less avidly. These studies would suggest that soils with lower clay and higher sand content bind prions less avidly and do not enhance infectivity to the same level as clay-rich soils. We hypothesize that clay content of a soil plays an integral role in the spread of CWD. In this study, we present the soil properties in the western Canada. Soils of the CWD-region generally are similar in texture, clay mineralogy and soil organic matter content. In total these soils can be characterized as clay loamy, montmorillonite (smectite) with 6–10 % organic carbon. The major soils in the CWD-region are Chernozems, present in 60% of total area. These soils have a humic horizon in which organic matter has accumulated (1–17% organic C). Solonetzic soils are also common to Alberta and Saskatchewan. We suggest that the greatest risk of CWD spread in western Canada is restricted to clay loamy, montmorillonite soils with humus horizon. Such soils are predominant in the southern region of Alberta, Saskatchewan and Manitoba, but are less common in northern regions of the provinces.




Envt.28:



High Survival Rates of TSE Infectivity Buried in Two Soil



Types Allister J. Smith The Roslin Insitute; Roslin, UK Email: allister.smith@roslin.ed.ac.uk



Two field experiments nearing completion are investigating the migration and/or persistence of TSE infectivity in the soil environment, either buried within bovine heads or buried without containment. In the first experiment five pairs of bovine heads, spiked with mouse-passaged BSE (301V) macerate, were buried within lysimeters containing either clay or sandy soil. A pair of unspiked bovine heads was also buried to act as controls. Pairs of heads have been exhumed annually during which a corer is used to take soil samples above, surrounding and below the head. Any brain material within the head is recovered during dissection. The soil samples have undergone protein extraction, and the extracts along with the brain material have been assayed for infectivity by bioassay in VM mice. Bioassay results from the first experiment show that for all four years most of the intracranial brain samples have been positive for TSE infectivity in both the clay and sandy soil. There is little change in the survival curves between years 1 and 4 indicating little reduction in the amounts of infectivity over time. There has been very limited infectivity found in samples surrounding the heads buried in the sandy soil, but infectivity has been found in the soil samples surrounding the clay heads and the levels increase slightly from years one to four, presumably as the heads have decomposed. In a parallel experiment a bolus of infectivity (301V) was placed in the centre of two large lysimeters, containing either clay or sandy soil. Over the course of four years, core samples have been taken at eight time points, on the vertical and at 3 distances from the centre. These samples have been assayed for infectivity and to date only one sample from the sandy soil has produced pathological evidence of TSE disease in one mouse. In order to ascertain whether any of the bolus remained at the end of the experiment, we collected a much larger central core (d = 16 cm) and extracted samples for bioassay, concentrating on the core portions that correlated to the original bolus location. The samples from these core portions caused disease in a high proportion of mice (bioassay still in progress), with apparently higher infectivity levels in the clay soil, so far. This result indicates that there has been very little migration of TSE infectivity without containment in either clay or sandy soil and that there has been little reduction in titre with time.





Envt.29:



Time-Dependent Decline in PrPTSE Desorption from Soil



Particles Christen B. Smith,1,† Clarissa J. Booth,2 Kartik Kumar2 and Joel A. Pedersen1–3 1Environmental Chemistry and Technology Program; 2Molecular and Environmental Toxicology Center; 3Department of Soil Science, University of Wisconsin; Madison, WI USA †Presenting author, Email: cmbell@wisc.edu



Environmental routes of transmission are implicated in epizootics of sheep scrapie and chronic wasting disease in deer, elk, and moose. Strong evidence suggests that soil may serve as an environmental reservoir of prions, which can persist in the environment for years. The disease-associated form of the prion protein (PrPTSE) readily attaches to soil particle surfaces. Prior studies reported reduced PrPTSE recovery from experimentally spiked soils after longer contact times, which in some cases has been interpreted as degradation of PrPTSE. Here, we investigate PrPTSE desorption from sterilized and untreated soil particles as a function of protein-soil contact time. Soil particles were sterilized by autoclaving or g-irradiation. Desorption of PrPTSE from whole soils, montmorillonite clay, and quartz sand was analyzed by immunoblotting following 1-, 7-, and 14-day contact times. We found that PrPTSE recovery from both sterile and untreated soil samples declined significantly with contact time suggesting the strengthening of protein-particle interactions over time. Recovery of PrPTSE from whole soils declined to a larger extent than did that from montmorillonite and quartz sand possibly reflecting t he contribution of particle-associated natural organic matter to the mechanisms of PrPTSE attachment. The influence of PrPTSE-soil particle attachment on oral disease transmission warrants investigation.











Soil clay content underlies prion infection odds



W. David Walter 1 , * , Daniel P. Walsh 2 , * , Matthew L. Farnsworth 3 , Dana L. Winkelman 1 & Michael W. Miller 2


1 United States Department of the Interior, United States Geological Survey, Colorado Cooperative Fish and Wildlife Research Unit , Fort Collins , Colorado


80523-1484, USA. 2 Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, Colorado 80526-2097, USA. 3 United States Department


of Agriculture, Animal and Plant Health Inspection Services, Veterinary Services, Centers for Epidemiology and Animal Health , Fort Collins , Colorado


80526-8117 , USA . * These authors contributed equally to this work. Correspondence and requests for materials should be addressed to M.W.M.


(email: mike.miller@state.co.us ) .


Received 6 Sep 2010 | Accepted 19 Jan 2011 | Published 15 Feb 2011 DOI: 10.1038/ncomms1203



Environmental factors — especially soil properties — have been suggested as potentially important in the transmission of infectious prion diseases. Because binding to montmorillonite (an aluminosilicate clay mineral) or clay-enriched soils had been shown to enhance experimental prion transmissibility, we hypothesized that prion transmission among mule deer might also be enhanced in ranges with relatively high soil clay content. In this study, we report apparent influences of soil clay content on the odds of prion infection in free-ranging deer. Analysis of data from prion-infected deer herds in northern Colorado, USA, revealed that a 1 % increase in the clay-sized particle content in soils within the approximate home range of an individual deer increased its odds of infection by up to 8.9 % . Our findings suggest that soil clay content and related environmental properties deserve greater attention in assessing risks of prion disease outbreaks and prospects for their control in both natural and production settings.



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The capacity of clay minerals and clay-laden soils to capture and enhance infectivity of shed or deposited prions 19,20,25 – 27 and the common tendency of ruminants to ingest soil both deliberately and incidentally in the course of foraging and grooming 12,44,45 provide an elegantly simple hypothetical mechanism for indirect prion transmission, as follows: infected individuals propagate infectious prions in mucosa-associated lymphoid tissues and shed prions into ingesta and saliva; ingested and environmental soil microparticles with a high phyllosilicate (especially smectite) content bind to, sequester and enhance infectivity of prions both before and after leaving the host; microparticle-bound prions are incorporated into surface soil; susceptible individuals consume contaminated soil and some become infected. (Also see Supplementary Figure S1 .) This mechanism may underlie the apparent importance of indirect transmission in explaining observed patterns of prion infection among captive mule deer 10,11 , and perhaps among sheep 3,4,6,7 . In light of these and others ’ findings, soil clay content and related environmental properties deserve greater attention in assessing local and regional risks of prion disease outbreaks and prospects for their control in natural and production settings.







Friday, February 25, 2011


Soil clay content underlies prion infection odds






Thursday, February 17, 2011


Environmental Sources of Scrapie Prions







PRION 2010



International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria



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PPo4-4:



Survival and Limited Spread of TSE Infectivity after Burial



Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK


Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.


The authors gratefully acknowledge funding from DEFRA.








Wednesday, September 08, 2010


CWD PRION CONGRESS SEPTEMBER 8-11 2010






ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD







2009 CWD SYMPOSIUM UTAH








Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area


65


Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area


Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- tracy.a.nichols@aphis.usda.gov


Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.


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The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.



snip...end...full text at ;

















PO-248: TSE infectivity survives burial for five years with little reduction in titer



Allister Smith, Robert Somerville, Karen Fernie The Roslin Institute and R(D)SVS; University of Edinburgh; Edinburgh, UK



BSE infected animals, BSE-contaminated materials and other sources of TSE (prion) infection, such as carcasses from scrapie infected sheep, CWD infected deer and cadavers of individuals infected with CJD may all end up in the environment through burial or other methods of disposal. They may continue to act as a reservoir of TSE infectivity if cattle or other susceptible animals were to be exposed to these sources in the future. In order to address these concerns, we performed two large scale demonstration experiments under field conditions which were designed to mimic some of the ways by which TSE infected materials may have been disposed of. The project examined the fate of TSE infectivity over a period of five years in two scenarios; when the infectivity was contained within bovine heads and when the infectivity was buried without any containment. Two soil types were compared: a sandy loam and a clay loam. We used the 301V TSE strain which was derived by serial passage of BSE in VM mice.



TSE infectivity was recovered from all the heads exhumed annually for five years from both types of soil, with little reduction in the amount of infectivity throughout the period of the experiment. Small amounts of infectivity were found in the soil immediately surrounding the heads, but not in samples remote from them. Similarly there was no evidence of significant lateral movement of infectivity from the buried bolus. However large amounts of TSE infectivity were recovered at the site of burial of both boluses. There was limited vertical upward movement of infectivity from the bolus buried in clay soil and downward movement from the bolus buried in sandy soil. Now that these experiments are completed we conclude that TSE infectivity is likely to survive burial for long periods of time with minimal loss of infectivity and restricted movement from the site of burial. These experiments emphasize that the environment is a viable reservoir for retaining large quantities of TSE infectivity, and reinforce the importance of risk assessment when disposing of this type of infectious material.







Monday, November 26, 2012


Aerosol Transmission of Chronic Wasting Disease in White-tailed Deer







Thursday, May 31, 2012


CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more







Thursday, December 29, 2011


Aerosols An underestimated vehicle for transmission of prion diseases? PRION www.landesbioscience.com


please see more on Aerosols and TSE prion disease here ;







Friday, February 25, 2011


Soil clay content underlies prion infection odds







Monday, January 17, 2011


Aerosols Transmit Prions to Immunocompetent and Immunodeficient Mice






Wednesday, January 07, 2009


CWD to tighten taxidermy rules Hunters need to understand regulations







Friday, February 08, 2013


*** Behavior of Prions in the Environment: Implications for Prion Biology








Friday, December 14, 2012


*** DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012








Friday, November 09, 2012


*** Chronic Wasting Disease CWD in cervidae and transmission to other species







Sunday, November 11, 2012


*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012







Friday, December 14, 2012


*** Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012







Saturday, March 09, 2013


Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest Incubation Time Model for Prion Diseases








pens, pens, PENS ??



*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.







now, decades later ;





2012



PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer



Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA



Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. The purpose of these experiments was to determine susceptibility of white-tailed deer (WTD) to scrapie and to compare the resultant clinical signs, lesions, and molecular profiles of PrPSc to those of chronic wasting disease (CWD). We inoculated WTD intracranially (IC; n = 5) and by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate. All deer were inoculated with a 10% (wt/vol) brain homogenate from sheep with scrapie (1ml IC, 1 ml IN, 30 ml oral). All deer inoculated by the intracranial route had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues as early as 7 months-post-inoculation (PI) and a single deer that was necropsied at 15.6 months had widespread distribution of PrPSc highlighting that PrPSc is widely distributed in the CNS and lymphoid tissues prior to the onset of clinical signs. IC inoculated deer necropsied after 20 months PI (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of WTD were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.









2011


*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.







Scrapie in Deer: Comparisons and Contrasts to Chronic Wasting Disease (CWD)


Justin J. Greenlee of the Virus and Prion Diseases Research Unit, National Animal Disease Center, ARS, USDA, Ames, IA provided a presentation on scrapie and CWD in inoculated deer. Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. We inoculated white-tailed deer intracranially (IC) and by a natural route of exposure (concurrent oral and intranasal inoculation) with a US scrapie isolate. All deer inoculated by the intracranial route had evidence of PrPSc accumulation and those necropsied after 20 months post-inoculation (PI) (3/5) had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. A single deer that was necropsied at 15.6 months PI did not have clinical signs, but had widespread distribution of PrPSc. This highlights the facts that 1) prior to the onset of clinical signs PrPSc is widely distributed in the CNS and lymphoid tissues and 2) currently used diagnostic methods are sufficient to detect PrPSc prior to the onset of clinical signs. The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in white-tailed deer after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile consistent with CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie. Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. While two WB patterns have been detected in brain regions of deer inoculated by the natural route, unlike the IC inoculated deer, the pattern similar to the scrapie inoculum predominates.


Committee Business:


The Committee discussed and approved three resolutions regarding CWD. They can be found in the report of the Reswolutions Committee. Essentially the resolutions urged USDA-APHIS-VS to:


Continue to provide funding for CWD testing of captive cervids


Finalize and publish the national CWD rule for Herd Certification and Interstate Movement


Evaluate live animal test, including rectal mucosal biopsy, for CWD in cervids








2011 Annual Report


Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit


2011 Annual Report


In Objective 1, Assess cross-species transmissibility of transmissible spongiform encephalopathies (TSEs) in livestock and wildlife, numerous experiments assessing the susceptibility of various TSEs in different host species were conducted. Most notable is deer inoculated with scrapie, which exhibits similarities to chronic wasting disease (CWD) in deer suggestive of sheep scrapie as an origin of CWD.


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4.Accomplishments 1. Deer inoculated with domestic isolates of sheep scrapie. Scrapie-affected deer exhibit 2 different patterns of disease associated prion protein. In some regions of the brain the pattern is much like that observed for scrapie, while in others it is more like chronic wasting disease (CWD), the transmissible spongiform encephalopathy typically associated with deer. This work conducted by ARS scientists at the National Animal Disease Center, Ames, IA suggests that an interspecies transmission of sheep scrapie to deer may have been the origin of CWD. This is important for husbandry practices with both captive deer, elk and sheep for farmers and ranchers attempting to keep their herds and flocks free of CWD and scrapie.







White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection


Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS


Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.


see full text ;







how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ??



? game farms in a state X $465,000., do all these game farms have insurance to pay for this risk of infected the wild cervid herds, in each state ??



how many game farms, are too many game farms ?



when you have states handing out shooting pen permits like candy on halloween, just to advance their coffers, then other states wanting to do the same thing, with most all of them ignoring the science on shooting pens and cwd, what do you expect is going to happen.



when is enough, enough ?





Tuesday, December 20, 2011


CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011


The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.


RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.


Form 1100-001


(R 2/11)


NATURAL RESOURCES BOARD AGENDA ITEM


SUBJECT: Information Item: Almond Deer Farm Update


FOR: DECEMBER 2011 BOARD MEETING


TUESDAY


TO BE PRESENTED BY TITLE: Tami Ryan, Wildlife Health Section Chief



SUMMARY:










SEE MORE USAHA REPORTS HERE, 2012 NOT PUBLISHED YET...TSS

















Wednesday, November 14, 2012


PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO LOUISIANA and INDIANA







Pennsylvania CWD number of deer exposed and farms there from much greater than first thought


Published: Wednesday, October 17, 2012, 10:44 PM Updated: Wednesday, October 17, 2012, 11:33 PM







Tuesday, October 23, 2012


PA Captive deer from CWD-positive farm roaming free







HERE, we see why these shooting pen owners some much like the USDA oversight of these game farms ;


USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”


problem solved $$$...TSS




Sunday, January 06, 2013


USDA TO PGC ONCE CAPTIVES ESCAPE "it‘s no longer its business.”






what happened to the PA deer from the CWD index heard that went to Louisiana ??




Monday, April 15, 2013


Deer farmers in the state of Louisiana are under a quarantine due to Chronic Wasting Disease CWD






Friday, September 28, 2012


Stray elk renews concerns about deer farm security Minnesota






Monday, June 11, 2012


OHIO Captive deer escapees and non-reporting






Friday, October 12, 2012


Texas Animal Health Commission (TAHC) is Now Accepting Comments on Rule Proposals for “Chronic Wasting Disease (CWD)”


TO: comments@tahc.state.tx.us;


Texas Animal Health Commission (TAHC)







please note, I do not know how much of this 125 TONS of banned mad cow protein was part of the ;




e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;


bbbut, this was about 10 years post mad cow feed ban from 1997. 10 years later, and still feeding banned mad cow protein to cervids??


considering that .005 gram is lethal to several bovines, and we know that the oral consumption of CWD tainted products is very efficient mode of transmission of CWD.


Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS Products manufactured from 02/01/2005 until 06/06/2006


Date: August 6, 2006 at 6:16 pm PST


PRODUCT


a) CO-OP 32% Sinking Catfish, Recall # V-100-6;


b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;


c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;


d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;


***e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;


f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;


g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;


h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;


i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;


j) CO-OP LAYING CRUMBLES, Recall # V-109-6;


k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;


l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;


m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6


CODE


Product manufactured from 02/01/2005 until 06/06/2006


RECALLING FIRM/MANUFACTURER


Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.


REASON


Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".


VOLUME OF PRODUCT IN COMMERCE


125 tons


DISTRIBUTION


AL and FL


END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006


###






10,000,000 lbs banned blood laced meat and bone meal mbm 2007







-------- Original Message --------


Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability


Date: Fri, 16 May 2003 11:47:37 –0500


From: "Terry S. Singeltary Sr."


To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000096/!x-usc:mailto:fdadockets@oc.fda.gov


Greetings FDA,


i would kindly like to comment on; Docket 03D-0186FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;


snip...


Oral transmission and early lymphoid tropism of chronic wasting diseasePrPres in mule deer fawns (Odocoileus hemionus ) These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.


snip...






now, just what is in that deer feed? _ANIMAL PROTEIN_



Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES


Date: Sat, 25 May 2002 18:41:46 -0700 From: "Terry S. Singeltary Sr." Reply-To: BSE-LTo: BSE-L


8420-20.5% Antler DeveloperFor Deer and Game in the wildGuaranteed Analysis Ingredients / Products Feeding Directions


snip...


_animal protein_




snip...


DEPARTMENT OF HEALTH & HUMAN SERVICESPUBLIC HEALTH SERVICEFOOD AND DRUG ADMINISTRATIONApril 9, 2001 WARNING LETTER01-PHI-12CERTIFIED MAILRETURN RECEIPT REQUESTED


Brian J. Raymond, Owner Sandy Lake Mills 26 Mill Street P.O. Box 117 Sandy Lake, PA 16145


PHILADELPHIA DISTRICT


Tel: 215-597-4390


Dear Mr. Raymond:Food and Drug Administration Investigator Gregory E. Beichner conducted an inspection of your animal feed manufacturing operation, located in Sandy Lake, Pennsylvania, on March 23,2001, and determined that your firm manufactures animal feeds including feeds containing prohibited materials. The inspection found significant deviations from the requirements set forth in Title 21, code of Federal Regulations, part 589.2000 - Animal Proteins Prohibited in Ruminant Feed. The regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE) . Such deviations cause products being manufactured at this facility to be misbranded within the meaning of Section 403(f), of the Federal Food, Drug, and Cosmetic Act (the Act).Our investigation found failure to label your swine feed with the required cautionary statement "Do Not Feed to cattleor other Ruminants" The FDA suggests that the statement be distinguished by different type-size or color or other means of highlighting the statement so that it is easily noticed by a purchaser.


In addition, we note that you are using approximately 140 pounds of cracked corn to flush your mixer used in the manufacture of animal feeds containing prohibited material. This flushed material is fed to wild game including deer, a ruminant animal.Feed material which may potentially contain prohibited material should not be fed to ruminant animals which may become part of the food chain.The above is not intended to be an all-inclusive list of deviations fromthe regulations. As a manufacturer of materials intended for animalfeed use, you are responsible for assuring that your overall operation and the products you manufacture and distribute are in compliance withthe law. We have enclosed a copy of FDA's Small Entity Compliance Guideto assist you with complying with the regulation... blah, blah, blah...




snip...end...full text ;


2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed


EMC 1 Terry S. Singeltary Sr. Vol #: 1









see my full text submission here ;







Sunday, April 21, 2013


Politicians ignore alarming CWD spike in Wyoming valley Wisconsin






Tuesday, April 16, 2013


Cervid Industry Unites To Set Direction for CWD Reform and seem to ignore their ignorance and denial in their role in spreading Chronic Wasting Disease






Thursday, May 02, 2013


Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING







what about human exposure to CWD and friendly fire (iatrogenic) pass it forward mode of transmission i.e. 2nd hand exposure via surgical, medical, blood, tissue, dental, to humans ??




Monday, May 23, 2011


CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning


Public release date: 23-May-2011


Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences


CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or "Mad Cow Disease"), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.


"While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases," commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta."But it's also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents."


Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.


CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.


Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.


The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.


The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.


According to Abrams, "The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health."


###


The article is "Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey" by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.


In an accompanying podcast CDC's Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast .








Thursday, May 26, 2011


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.


Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey


Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD


Accepted 15 November 2010. Abstract Full Text PDF References .


Abstract


The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.







CDC


Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012


SNIP...


Interspecies transmission of CWD to noncervids has not been observed under natural conditions. CWD infection of carcass scavengers such as raccoons, opossums, and coyotes was not observed in a recent study in Wisconsin (22). In addition, natural transmission of CWD to cattle has not been observed in experimentally controlled natural exposure studies or targeted surveillance (2). However, CWD has been experimentally transmitted to cattle, sheep, goats, mink, ferrets, voles, and mice by intracerebral inoculation (2,29,33).


CWD is likely transmitted among mule, white-tailed deer, and elk without a major species barrier (1), and other members of the cervid family, including reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD infection. Black-tailed deer (a subspecies of mule deer) and European red deer (Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34). Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation (35). Continued study of CWD susceptibility in other cervids is of considerable interest.


Reasons for Caution There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD.


Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation.


Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified, CWD will likely continue to emerge in North America. ...



SNIP...










Generation of a new form of human PrPSc in vitro by inter-species transmission from cervids prions


Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man.






Our results also have profound implications for understanding the mechanisms of the prion species barrier and indicate that the transmission barrier is a dynamic process that depends on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans and that this ability progressively increases with CWD spreading.









P35


ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD


Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5


The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.








PPo3-7:



Prion Transmission from Cervids to Humans is Strain-dependent


Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA


Key words: CWD, strain, human transmission


Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.


Acknowledgement Supported by NINDS NS052319 and NIA AG14359.




PPo2-27:


Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions


Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA


Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.




PPo2-7:


Biochemical and Biophysical Characterization of Different CWD Isolates


Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany


Key words: CWD, strains, FT-IR, AFM


Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.









2012


Envt.06:


Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates


Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Aru Balachandran,2 Jürgen Richt,3 Vincent Beringue,4 Juan-Maria Torres,5 Paul Brown,1 Bob Hills6 and Jean-Philippe Deslys1


1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Canadian Food Inspection Agency; Ottawa, ON Canada; 3Kansas State University; Manhattan, KS USA; 4INRA; Jouy-en-Josas, France; 5INIA; Madrid, Spain; 6Health Canada; Ottawa, ON Canada


†Presenting author; Email: emmanuel.comoy@cea.fr


The constant increase of chronic wasting disease (CWD) incidence in North America raises a question about their zoonotic potential. A recent publication showed their transmissibility to new-world monkeys, but no transmission to old-world monkeys, which are phylogenetically closer to humans, has so far been reported. Moreover, several studies have failed to transmit CWD to transgenic mice overexpressing human PrP. Bovine spongiform encephalopathy (BSE) is the only animal prion disease for which a zoonotic potential has been proven. We described the transmission of the atypical BSE-L strain of BSE to cynomolgus monkeys, suggesting a weak cattle-to-primate species barrier. We observed the same phenomenon with a cattleadapted strain of TME (Transmissible Mink Encephalopathy). Since cattle experimentally exposed to CWD strains have also developed spongiform encephalopathies, we inoculated brain tissue from CWD-infected cattle to three cynomolgus macaques as well as to transgenic mice overexpressing bovine or human PrP. Since CWD prion strains are highly lymphotropic, suggesting an adaptation of these agents after peripheral exposure, a parallel set of four monkeys was inoculated with CWD-infected cervid brains using the oral route. Nearly four years post-exposure, monkeys exposed to CWD-related prion strains remain asymptomatic. In contrast, bovinized and humanized transgenic mice showed signs of infection, suggesting that CWD-related prion strains may be capable of crossing the cattle-to-primate species barrier. Comparisons with transmission results and incubation periods obtained after exposure to other cattle prion strains (c-BSE, BSE-L, BSE-H and cattle-adapted TME) will also be presented, in order to evaluate the respective risks of each strain.




Envt.07:


Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease


Martin L. Daus,1,† Johanna Breyer,2 Katjs Wagenfuehr,1 Wiebke Wemheuer,2 Achim Thomzig,1 Walter Schulz-Schaeffer2 and Michael Beekes1 1Robert Koch Institut; P24 TSE; Berlin, Germany; 2Department of Neuropathology, Prion and Dementia Research Unit, University Medical Center Göttingen; Göttingen, Germany †Presenting author; Email: dausm@rki.de


Chronic wasting disease (CWD) is a contagious, rapidly spreading transmissible spongiform encephalopathy (TSE) occurring in cervids in North America. Despite efficient horizontal transmission of CWD among cervids natural transmission of the disease to other species has not yet been observed. Here, we report a direct biochemical demonstration of pathological prion protein PrPTSE and of PrPTSE-associated seeding activity in skeletal muscles of CWD-infected cervids. The presence of PrPTSE was detected by Western- and postfixed frozen tissue blotting, while the seeding activity of PrPTSE was revealed by protein misfolding cyclic amplification (PMCA). The concentration of PrPTSE in skeletal muscles of CWD-infected WTD was estimated to be approximately 2000- to 10000-fold lower than in brain tissue. Tissue-blot-analyses revealed that PrPTSE was located in muscle- associated nerve fascicles but not, in detectable amounts, in myocytes. The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.






UPDATED DATA ON 2ND CWD STRAIN


Wednesday, September 08, 2010


CWD PRION CONGRESS SEPTEMBER 8-11 2010






CJD9/10022


October 1994


Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ


Dear Mr Elmhirst,


CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT


Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.


The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.


The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.


The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.


I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.







now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ??




“Our conclusion stating that we found no strong evidence of CWD transmission to humans”


From: TSS (216-119-163-189.ipset45.wt.net< http://216-119-163-189.ipset45.wt.net >)


Subject: CWD aka MAD DEER/ELK TO HUMANS ??


Date: September 30, 2002 at 7:06 am PST


From: "Belay, Ermias"


To:


Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"


Sent: Monday, September 30, 2002 9:22 AM


Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS


Dear Sir/Madam,


In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.


That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.


Ermias Belay, M.D. Centers for Disease Control and Prevention




-----Original Message-----


From:


Sent: Sunday, September 29, 2002 10:15 AM


To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV


Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS


Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS


Thursday, April 03, 2008


A prion disease of cervids: Chronic wasting disease


2008 1: Vet Res. 2008 Apr 3;39(4):41


A prion disease of cervids: Chronic wasting disease


Sigurdson CJ.



snip...


*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,


snip...



full text ;










Sunday, January 22, 2012


Chronic Wasting Disease CWD cervids interspecies transmission








Friday, November 09, 2012


*** Chronic Wasting Disease CWD in cervidae and transmission to other species







Friday, November 09, 2012


*** Chronic Wasting Disease CWD in cervidae and transmission to other species







Sunday, November 11, 2012


*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease November 2012







Friday, December 14, 2012


Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005 - December 14, 2012







*** NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;


Wednesday, March 18, 2009 Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II


___________________________________


PRODUCT


a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9;


b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9;


c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9;


d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9;


e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9;


f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9;


CODE


Elk Meats with production dates of December 29, 30, and 31


RECALLING FIRM/MANUFACTURER


Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009.


Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing.


REASON


Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD).


VOLUME OF PRODUCT IN COMMERCE


Unknown


DISTRIBUTION


NV, CA, TX, CO, NY, UT, FL, OK


___________________________________







Monday, February 09, 2009


Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have CWD


snip...


Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a new prion strain


Date: August 25, 2007 at 12:42 pm PST


our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions.







Wednesday, March 18, 2009


Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II








Tuesday, March 05, 2013


Chronic Wasting Disease Management Plan/Environmental Impact Statement, Shenandoah National Park Virginia








Monday, April 15, 2013


Dr. Stephen B. Thacker Director Centers for Disease Control and Prevention's Office of Science, Epidemiology and Laboratory Services (OSELS) dies from Creutzfeldt Jakob Disease CJD


















kind regards, terry



layperson



Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518






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