Saturday, March 10, 2012

Enhanced Surveillance Strategies for Detecting and Monitoring Chronic Wasting Disease in Free-Ranging Cervids Open-File Report 2012–1036

National Wildlife Health Center


Open-File Report 2012–1036

U.S.

Enhanced Surveillance Strategies for Detecting and Monitoring Chronic Wasting Disease in Free-Ranging Cervids

snip...

In addition to locations of known CWD-positive individuals, other spatial risk factors related to CWD exposure should be considered. For example, the risk of free-ranging animals being exposed to CWD is likely greater in areas where captive cervid facilities have or had CWD-positive animals. Current evidence indicates that CWD infection rates are much higher in captive facilities than in wild populations (Keane and others, 2008), and perhaps this is driven by environmental contamination (Miller and others, 2006). This higher rate of infection in captive animals can increase the risk of disease exposure to surrounding wild populations. Furthermore, movement of infectious animals, carcasses, or other materials across the landscape, naturally or with human assistance, likely increases the risk to uninfected populations. The frequent movement of farmed elk (Cervus elaphus) and deer between production facilities, the concentration of infected animals on some facilities, and the possibility of their escape into the wild increases the risk of spreading CWD to uninfected populations of free-ranging animals. Because the infectious prions may persist in the environment for long periods, the introduction of either captive or free-ranging uninfected animals into a contaminated environment could increase their risk of infection. For example, locations from which sheep have been removed may remain contaminated with scrapie agent for more than 15 years (Georgsson and others, 2006). In a similar manner, translocation of cervids from areas that have not been documented to be CWD-free could pose a risk of disease introduction. In this situation, the risk of introduction is likely related to the probability of infected animals being moved and their ability to spread CWD to other susceptible animals or into the environment. Thus, surveillance on and around cervid farms or free-ranging populations that have received animals from known CWD areas and bordering jurisdictions with CWD-positive animals can increase the likelihood of disease spread. Additional risk factors, such as the presence of scrapie in sheep populations that are sympatric with deer and elk (Greenlee and others, 2011), feeding of animal protein to cervids (Johnson, McKenzie, and others, 2011), baiting and feeding programs (Thompson and others, 2008), or other environmental factors also may be considered, although their roles in CWD epidemiology has not been clearly established.

The soil composition of a region may also play an important role in the occurrence and maintenance of CWD and other TSEs (Smith and others, 2011). Recently, it has been shown that certain soil types can chemically bind and increase infectivity of prion protein (PrP), creating the potential for the protein to be maintained at the soil surface for uptake by foraging animals (Johnson and others, 2006; Johnson and others, 2007; Polano and others, 2008; Imrie, 2009); however, the fate of prions may be highly dependent on source of deposition into the soil (for example, fluid or tissue; Saunders and others 2009). In addition, organic soil components (humic acids) appear to enhance the adsorption of PrP to clay minerals and show a great affinity for the protein as well; however, it is unclear whether the effect of the organic matter increases or decreases infectivity (Polano and others, 2008). The importance of soil in CWD epidemiology was reaffirmed by Walter and others (2011) who demonstrated an 8.9-percent increase in an individual’s deer’s odds of CWD infection with each 1-percent increase in soil clay content within its approximate home range in north-central Colorado. These results suggest that some regions may have a greater probability of maintaining and spreading CWD based solely on their geologic and chemical attributes. Thus, the soil characteristics within an animal’s range represent a potentially important spatial risk factor for CWD occurrence and maintenance.

snip...

Lastly, other confounding risk factors may exist that play a role in CWD spatial dynamics. Sources of potential CWD exposure not related to natural movements of live, free-ranging animals could confound interpretation of spatial distribution and changes therein. Consequently, the occurrence and distribution of other potential risk factors (for example, game farms, taxidermy operations, wildlife rehabilitation activities, artificial baiting or feeding sites, depots for carcasses of vehicle-killed cervids) should be taken into account when designing monitoring plans.

snip...

Several factors need to be considered when proposing to discontinue disease surveillance in addition to assumptions of the above model. First, what is the risk of an infected individual entering the study area through immigration of free-ranging animals from known or unknown positive jurisdictions or movement of captive cervids? If this risk is greater than zero, decisions on whether or not to continue to conduct surveillance should carefully weigh the level of this risk, because ultimately some chance exists of introduction of the disease. Secondly, agencies need to consider if they have adequate spatial coverage of sampling units across the jurisdiction to ensure all potential pockets of disease are sampled, and if they have effectively sampled individual animals within sampling units. Third, agencies need to consider the social and political repercussions of stopping surveillance activities. Lastly, availability of resources will play perhaps the most important role in determining whether surveillance should proceed or not. A cautionary tale against stopping surveillance too soon is provided by past CWD developments in Michigan. CWD surveillance in Michigan had continued since 1998 with 23,739 white-tailed deer, 887 elk, and 46 moose tested as of October 21, 2008 (Daniel O’Brien, Michigan Department of Natural Resources, oral commun). In addition, 8,452 captive cervids have been tested by the Michigan Department of Agriculture. Even with 10 years of surveillance effort, the first positive case was discovered in a captive animal in fall of 2008. Thus, even with a reasonable level of surveillance effort for a considerable period of time, a new case may be detected where a jurisdiction was previously believed to be CWD-free when the probability of introduction is greater than zero.

http://pubs.usgs.gov/of/2012/1036/pdf/ofr2012_1036.pdf





*** 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.




(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)




http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf






2011



Wednesday, October 12, 2011


White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation


It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that 17 white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that 1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and 2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.

Author: Justin GreenleeJodi SmithRobert Kunkle Credits/Source: Veterinary Research 2011, 42:107



http://www.veterinaryresearch.org/content/pdf/1297-9716-42-107.pdf




http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html






PPo3-22:

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK

Key words: scrapie, evironmental persistence, sPMCA

Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.



http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099






Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html






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

http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf






Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

http://scrapie-usa.blogspot.com/2011/02/environmental-sources-of-scrapie-prions.html





Thursday, June 09, 2011


Detection of CWD prions in salivary, urinary, and intestinal tissues of deer: potential mechanisms of prion shedding and transmission


http://chronic-wasting-disease.blogspot.com/2011/06/detection-of-cwd-prions-in-salivary.html






Chemosphere. 2012 Jan 20. [Epub ahead of print]

Soil-mediated prion transmission: Is local soil-type a key determinant of prion disease incidence?

Saunders SE, Bartz JC, Bartelt-Hunt SL.

Source

Department of Civil Engineering, University of Nebraska-Lincoln, Peter Kiewit Institute, Omaha, NE 68182, USA.

Abstract

Prion diseases, including chronic wasting disease (CWD) and scrapie, can be transmitted via indirect environmental routes. Animals habitually ingest soil, and results from laboratory experiments demonstrate prions can bind to a wide range of soils and soil minerals, retain the ability to replicate, and remain infectious, indicating soil could serve as a reservoir for natural prion transmission and a potential prion exposure route for humans. Preliminary epidemiological modeling suggests soil texture may influence the incidence of prion disease. These results are supported by experimental work demonstrating variance in prion interactions with soil, including variance in prion soil adsorption and soil-bound prion replication with respect to soil type. Thus, local soil type may be a key determinant of prion incidence. Further experimental and epidemiological work is required to fully elucidate the dynamics of soil-mediated prion transmission, an effort that should lead to effective disease management and mitigation strategies.

Copyright © 2012 Elsevier Ltd. All rights reserved.


http://www.sciencedirect.com/science/article/pii/S0045653512000057




see much more on soil here ;




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.





PPo8-13:




Degradation of Pathogenic Prion Protein and Prion Infectivity by Lichens




Christopher J. Johnson,1 James P. Bennett,1 Steven M. Biro,1,2 Cynthia M. Rodriguez,1,2 Richard A. Bessen3 and Tonie E. Rocke1 1USGS National Wildlife Health Center; 2Department of Bacteriology; University of Wisconsin, Madison; 3Department of Veterinary Molecular Biology; Montana State University; Bozeman, MT USA




Key words: prion, lichen, bioassay, protease, degradation




Few biological systems have been identified that degrade the transmissible spongiform encephalopathy (TSE)-associated form of the prion protein (PrPTSE) and TSE infectivity. Stability of the TSE agent allows scrapie and chronic wasting disease agents to persist in the environment and cause disease for years. Naturally-occurring or engineered processes that reduce infectivity in the environment could aid in limiting environmental TSE transmission. We have previously identified that species of at least three lichens, unusual, symbiotic organisms formed from a fungus and photosynthetic partner, contain a serine protease capable of degrading PrPTSE under gentle conditions. We tested the hypothesis that lichen extracts from these three species reduce TSE infectivity by treating infected brain homogenate with extracts and examining infectivity in mice. We found lichen extracts diminished TSE infectious titer by factors of 100 to 1,000 and that reductions in infectivity were not well-correlated with the extent of PrPTSE degradation observed by immunoblotting. For example, treatment of brain homogenate with Cladonia rangiferina extract caused <100-fold reduction in PrP immunoreactivity but ~1,000-fold decrease in infectivity, suggesting that some PrPTSE remaining after extract treatment was rendered uninfectious or that the lichen protease favors more infectious forms of PrPTSE. Our data also indicate that lichen species closely related to those with prion-degrading protease activity do not necessarily degrade PrPTSE. Characterization of the lichen species-specificity of PrPTSE degradation within the genera Cladonia and Usnea and comparison with known lichen phylogeny has yielded clusters of species on which to focus searches for anti-prion agents.





PPo8-14: Enzymatic Digestion of Chronic Wasting Disease Prions Bound to Soil




Samuel E. Saunders,1 Jason C. Bartz,2 Kurt C. Vercauteren3 and Shannon L. Bartelt-Hunt1 1Department of Civil Engineering; University of Nebraska-Lincoln; Peter Kiewit Institute; Omaha, Nebraska USA; 2Department of Medical Microbiology and Immunology; Creighton University; Omaha, Nebraska USA; 3USDA; Animal and Plant Health Inspection Service; Wildlife Services; National Wildlife Research Center; Fort Collins, CO USA




Chronic wasting disease (CWD) and sheep scrapie can be transmitted via indirect environmental routes, and it is known that soil can serve as a reservoir of prion infectivity. Given the strong interaction between the prion protein (PrP) and soil, we hypothesized that binding to soil enhances prion resistance to enzymatic digestion, thereby facilitating prion longevity in the environment and providing protection from host degradation. We characterized the performance of a commercially available subtilisin enzyme, the Prionzyme, to degrade soil-bound and unbound CWD and HY TME PrP as a function of pH, temperature, and treatment time. The subtilisin enzyme effectively degraded PrP adsorbed to a wide range of soils and soil minerals below the limits of detection. Signal loss occurred rapidly at high pH (12.5) and within 7 d under conditions representative of the natural environment (pH 7.4, 22°C). Serial PMCA of treated soil samples suggests a greater than 6-log decrease in infectious titer compared with controls. We observed no apparent difference in enzyme effectiveness between bound and unbound CWD PrP. Our results show that although adsorbed prions do retain relative resistance to enzymatic digestion compared with other brain homogenate proteins, they can be effectively degraded when bound to soil. Our results also suggest a topical application of a subtilisin enzyme solution may be an effective decontamination method to limit disease transmission via environmental ‘hot spots’ of prion infectivity.





PPo8-21:




Detection of PrPCWD in Rocky Mountain Elk Feces Using Protein Misfolding Cyclic Amplification




Bruce E Pulford,1 Terry Spraker,1 Jenny Powers,2 Margaret Wild2 and Mark D. Zabel1 1Department of Microbiology; Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; 2Biological Resource Management Division; United States National Park Service; CO, USA




Key words: CWD, feces, PMCA, elk




Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy affecting cervids, including mule and white-tailed deer (Odocoileus hemionus and virginianus), elk (Cervus elaphus nelsoni) and moose (Alces alces shirasi). The method of CWD transmission between hosts is unclear, though there is evidence that feces excreted by infected animals may play a role. Recently, CWD prions was detected in feces using bioassays in cervidized mice, which took many months to produce results. In this study, we use a more rapid procedure, protein misfolding cyclic amplification (PMCA), to test elk feces for the presence of PK-resistant cervid PrP (PrPCWD). Feces were collected from symptomatic and asymptomatic elk in several northern Colorado locations, homogenized, mixed with normal brain homogenate from Tg5037 mice (expressing cervid PrP) and subjected to up to 9 rounds of PMCA (1 round = 40 secs sonication/30 mins at 70% maximum power, 24 hours). Western blots were used to detect PrPCWD using BAR-224 anti-PrP antibody. Rectal and CNS tissue from the elk were IHC-labeled and examined for the presence of PrPCWD. Fecal samples from symptomatic and asymptomatic elk that tested positive by IHC showed characteristic PrPCWD bands on western blots following PMCA. In addition, PMCA detected PrPCWD in 25% of fecal samples from IHC-negative animals. These data suggest that PMCA may (1) prove useful as a non-invasive method to supplement or even replace IHC testing of cervids for CWD, and (2) identify additional asymptomatic carriers of CWD, the prevalence of which may be underestimated using IHC.







PPo3-19:




Detection of CWD Prions in Salivary and Urinary Tissues of Deer: Potential Mechanisms of Pathogenesis and Prion Shedding




Nicholas J. Haley,1 Candace K. Mathiason,1 Glenn C. Telling2 and Edward A. Hoover1 1Department of Microbiology, Immunology and Pathology; College of Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort Collins, Colorado USA; 2Department of Molecular Biology and Genetics; University of Kentucky; Lexington, Kentucky USA




Key words: chronic wasting disease, transmission, PMCA, pathogenesis, excretion, urine, saliva, salivary gland, urinary bladder, kidney, blood




Saliva and urine are thought to play an important role in the transmission and pathogenesis of chronic wasting disease (CWD) in captive and free-ranging cervids. We have previously identified PrPCWD in a variety of excreta using serial PMCA (sPMCA) and bioassay; however the source of infectious prions in urine and saliva has yet to be identified. In the present study, we applied sPMCA to tissues associated with saliva and urine production and excretion in an effort to seek proximal sources of prion shedding. Oropharyngeal and urogenital tissues, along with blood and obex from CWD-exposed cervids (comprising over 300 individual samples) were analyzed blindly in duplicate and scored based on apparent CWD burden. PrPCWD was detected by three rounds of sPMCA in tissues associated with saliva and urine production and excretion, notably salivary gland and urinary bladder; whereas blood samples from the same animals and concurrent negative controls (n = 116 of 117) remained negative. Route of inoculation and CNS burden appeared to play an important role in terminal prion distribution, in that IV-inoculated animals and those with increasing CNS levels of PrPCWD had higher and more widely distributed accumulation in excretory tissues. PMCA identification of PrPCWD in oropharyngeal and urogenital tissues—in the absence of detection by conventional methods—may indicate the presence of protease- sensitive infectious prions in excretory tissues not revealed by assays employing PK digestion or other means to remove PrPC reactivity. Thus, evaluation of peripheral tissues via sPMCA may allow additional insights into prion transmission, trafficking and pathogenesis.






PPo3-26:




Identification of Renal Origin for CWD Urinary Prion Excretion in Deer




Davis M. Seelig,1 Nicholas J. Haley,1 Jan P. Langeveld and Edward A. Hoover1 1Colorado State University; Department of Microbiology, Immunology and Pathology; Fort Collins, CO USA; 2Central Institute for Animal Disease Control (CIDC-Lelystad); Lelystad, The Netherlands




Chronic wasting disease (CWD) is an efficiently transmitted prion disease of cervids. Although bioassays have confirmed the presence of infectious prions in urine and other body fluids of infected deer, origin and mechanisms of prion transfer to and shedding in excreta remains unknown. To address these questions, we have developed enhanced immunohistochemistry (IHC) methods employing tyramide signal amplification (TSA) on formalin-fixed, paraffin-embedded (FFPE) tissues of n = 20 CWD-infected white-tailed deer. Using these methods we have demonstrated PrPCWD present granular to clumped aggregates both within the cytoplasm of renal tubule cells and in the interstitium. Cytoplasmic PrPCWD aggregates were detected most commonly in proximal convoluted tubule epithelial cells. PrPCWD was not identified in the lower urinary tract (ureters or bladder) of any CWD-infected animal. In summary, we present evidence for PrPCWD accumulation within the renal tubule cells, which may identify a proximate tissue source and explain the manner by which infectious prions are excreted in the urine of infected deer, thereby leading to the high degree of direct and indirect horizontal transmission of chronic wasting disease.












Friday, February 25, 2011



Soil clay content underlies prion infection odds Soil clay content underlies prion infection odds







Saturday, March 10, 2012


CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein feed CUSTOM MADE for deer and elk





Wednesday, October 14, 2009


Detection of protease-resistant cervid prion protein in water from a CWD-endemic area






AS THE CROW FLIES, SO DOES CWD



Sunday, November 01, 2009


American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases






Wednesday, January 07, 2009


CWD to tighten taxidermy rules Hunters need to understand regulations






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







Friday, December 11, 2009


CWD, FECES, ORAL LESIONS, Aerosol and intranasal transmission











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 ;







The CDC just released a paper on the concern of these game farms and CWD, and also CWD to humans risk factor update.




I kindly urge you to look at the map ;



Colorado


Captive CWD discovered 1967


Free ranging CWD discovered 1981



PLEASE STUDY THIS MAP !



SEE CWD MAP, RELATE TO DATES OF GAME FARM INFECTION, TO DATE OF INFECTION RATE IN WILD, SURROUNDING SAID INFECTED GAME FARMS. ...TSS







*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***


Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012






SNIP...



Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).



SNIP...



*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***


Saturday, February 18, 2012


Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease


CDC Volume 18, Number 3—March 2012






see much more here ;






Thursday, February 09, 2012


50 GAME FARMS IN USA INFECTED WITH CHRONIC WASTING DISEASE






Saturday, February 04, 2012


Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised






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.



Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.


However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.


Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < <








SNIP...SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html



Friday, February 03, 2012

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html






Thursday, February 09, 2012

Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/colorado-farm-raised-deer-farms-and-cwd.html





Monday, February 13, 2012

Stop White-tailed Deer Farming from Destroying Tennessee’s Priceless Wild Deer Herd oppose HB3164

http://chronic-wasting-disease.blogspot.com/2012/02/stop-white-tailed-deer-farming-from.html





Tuesday, February 14, 2012

Oppose Indiana House Bill 1265 game farming cervids

http://chronic-wasting-disease.blogspot.com/2012/02/oppose-indiana-house-bill-1265-game.html





Wednesday, February 15, 2012

West Virginia Deer Farming Bill backed by deer farmers advances, why ? BE WARNED CWD

http://chronic-wasting-disease.blogspot.com/2012/02/west-virginia-deer-farming-bill-backed.html





Monday, November 14, 2011

WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wyoming-creutzfeldt-jakob-disease-cwd.html




http://gf.state.wy.us/web2011/wildlife-1000288.aspx




http://gf.state.wy.us/services/news/pressreleases/index.asp






CWD WISCONSIN


http://dnr.wi.gov/news/




http://dnr.wi.gov/org/land/wildlife/hunt/regs/bait.htm





Chronic Wasting Disease and the Science in support of the Ban on Baiting and Feeding Deer.


Timothy R. Van Deelen Ph.D. Wisconsin DNR Research


http://dnr.wi.gov/org/land/wildlife/Whealth/issues/Cwd/doc/cwdscsu.pdf




http://search.dnr.wi.gov/search?q=cwd&btnG=DNR+Search&client=DNR_frontend&output=xml_no_dtd&proxystylesheet=DNR_frontend&getfields=*&entqr=0&oe=UTF-8&ie=UTF-8&ud=1&sort=date%3AD%3AS%3Ad1&site=default_collection







2011 Law Enforcement deer gun season report


ILLEGAL BAITING AND FEEDING OF DEER


Across the state, baiting and feeding complaints and arrests were down significantly. Hotline complaints regarding illegal baiting and feeding were down 5% from 2010 and 50% from 2009. Arrests for illegal baiting were down 15%, and arrests for illegal feeding were down 13% from 2010 numbers.


http://dnr.wi.gov/org/es/enforcement/docs/2011%20le%20deer%20season%20report%20(web%20version).pdf





Wednesday, November 16, 2011

Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wisconsin-creutzfeldt-jakob-disease-cwd.html





Sunday, November 13, 2011

COLORADO CWD CJD TSE PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/colorado-cwd-cjd-tse-prion-reporting.html





PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;



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.

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html





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


http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html






kind regards, terry

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posted by Terry S. Singeltary Sr. at 4:08 PM

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