CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
NATURAL RESOURCES BOARD AGENDA ITEM
SUBJECT: Inf01mation Item: Almond Deer Fatm Update
FOR: DECEIVIBER 2011 BOARD MEETING
TO BE PRESENTED BY I TITLE: Tami Ryan, Wildlife Health Section Chief
In April 20 II, the Natural Resources Board approved the Department purchase of a former deer farm known as Buckhorn Flats in Portage County. Following acquisition the property officially became a Bureau of Wildlife Management program property. Staff in the Bureau's Wildlife Health Section, the West Central District, and Northeast District have taken steps towards public outreach with the local community, developed a property managment plan and biosecurity protocols, are working towards the installation of a secondary fence, and are awaiting research proposals that will advance the scientific understanding of Chronic Wasing Disease.
DATE: November 21, 20 ll FILE REF: 2300
TO: Natural Resources Board
FROM: Cathy Stepp
SUBJECT: Almond Deer Farm Update
The first case of Chronic Wasting Disease (CWD) among Wisconsin's farm-raised deer occurred in a white-tailed deer buck shot by a hunter at the property (formerly known as Buckhorn Flats) in September 2002. This situation prompted the eventual depopulation of the entire farm. The deer, a mix of does and yearlings, were destroyed on January 17, 2006- 4 years later- by U.S. Department of Agriculture shooters under a USDA agreement with the farm owner. Sixty of the 76 animals tested positive for CWO. The 76 deer constituted the breeding herd in the breeding facility on the farm. The prope1ty also had a hunting preserve until2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWO was not detected in those animals. The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The nearly 80% prevalence rate discovered on Buckhorn Flats is the highest prevalence recorded in any captive cervid operation in North America.
The DNR acquired the property on April 13, 20 ll. After extensive consideration and pursuit of several options, it was decided that purchasing the property and subsequent management of the property is the only realistic option to keep the fences intact. Wisconsin's wild white-tailed deer herd is one of the state's most valuable natural resources, and those deer are a valuable resource of recreational, economic, and ecological significance to all citizens of the state. CWO is a serious long-term threat to Wisconsin's deer herd and the future of Wisconsin's hunting traditions. Over 1,200 free-ranging deer have been tested since 2002 in Portage County with no detections of CWD. We have ve~y high levels of confidence that CWO does not occur in the free-ranging herd in this area. This is of pmticular significance considering this farm is located 60 miles nmih of any known occurrence of CWO in wild deer.
The Hall farm is the most concerning of the depopulated game farms in Wisconsin because of its potential high level of soil contamination. Similar concerns exist to some degree for all nine positive farms and any future farms in which CWD positive cervids are found. However, Buckhorn Flats is a unique situation due to the nearly 80% prevalence rate that occurred there, which is the highest infection rate in a captive cervid farm in North America and perhaps the world. The property has undergone cleaning and disinfection per USDA guidelines. Under the established premise plan, no species of cervids could be brought onto the property for five years, and fences were to be maintained to keep free-ranging deer from entering the property. The premise plan expired on May 24, 20 ll. Despite this five year premise plan and site decontamination, the department had serious concerns over the bioavailability of infectious prions at this site to free-ranging white-tailed deer should the fences be removed or otherwise compromised.
Based on current scientific knowledge, CWD prions are known to persist in the environment for at least 3 years and potentially much longer. Evidence of environmental transmission was documented in a Colorado research facility where mule deer became infected with CWD. Furthermore, the likely transmission of CWD via soil is corroborated by recent studies that show that prions bind to soil components with high affinity and are not easily removed by water. These findings suggest that soil may contribute more significantly to TSE transmission than previously recognized.
Department Actions to Date
The DNR has taken steps to inform the public regarding the background of the Almond Farm as well as future plans for the property. A secondary fence, research, and occupancy of the house are all topics of interest. A description of each topic is identified below:
A. A Property Management Plan was developed to provide a background and future plans for the property. Chapters within the plan include a description of the property, research opportunities, facilities, public communications, and biosecurity protocols (see attachment).
B. The DNR held a public meeting the evening of July 28th at the Almond-Bancroft School to discuss the recent acquisition of the deer farm formerly known as Buckhorn Flats. Twenty-nine people signed in and stayed for the 2-hour duration including local deer farmers, conservation congress delegates, etc. Following 45 minutes of presentation, the meeting focused on the question and answer period. The DNR also asked for public input regarding how they could help in varying capacities at the Almond Farm (see attachment).
C. The DNR will begin timber removal from outside the fence this winter. Timber removal from inside the fence has begun with hazardous trees removed. The construction of a second fence 10 – 12 feet outside the present fence will begin in the spring. This will add an additional level of security for keeping wild deer from entering the farm and maintain the integrity of the perimeter (see attachment).
D. The DNR plans to use the Almond Farm as a CWD research facility. Because the question of how long a contaminated site is a risk to deer is of national and international interest, there may be opportunities for research and funding at this facility. One way to potentially assess whether there is a risk to deer from the Almond Farm is to conduct bioassays focusing on prions persisting in soil and what role environmental contamination plays in disease transmission. A proposal is pending from the University of Wisconsin – Stevens Point that concerns prion degradation via composting. The group is seeking additional funding from the University of Wisconsin – Madison and representatives in Canada. USGS is also contemplating a proposal contingent on funding from their pending federal budget. Any proposed research that includes bringing captive cervids onto the property will be thoroughly reviewed by the CWD Research Committee consisting of the Wildlife Health Team, the Wildlife Policy Team, and Department administration as well as external CWD experts prior to permission being granted to ensure that the health of the wild deer herd will not be endangered. The double fencing described above will be critical to minimize the risk of ingress of free-ranging and egress of any experimental captive cervids. E. The house is rented and currently occupied by a Northeast district wildlife employee. The Lessee agrees to perform weekly fence inspections to insure that the fence integrity has not been compromised. The Lessee also pays for all utilities, and will provide lawn care, snow removal, gutter cleaning, and other miscellaneous maintenance as needed. In exchange for these services the monthly rental fee has been waived. It is agreed that the Lessor and the Lessee shall review said waiver of the monthly rental charge at the end of every twelve months that this lease is in effect (see attachment).
Almond Farm Property Management Plan
Questions/Comments from Almond Farm Public Meeting (07-28-2011)
DNR News Release – Almond Farm Public Meeting Announcement (07/18/2011)
External Fence Aerial Photo
Natural Resources Board Agenda Item – Land Acquisition of the Almond Farm
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BACKGROUND ; SUPPORTING
The first case of CWD among Wisconsin’s farm-raised deer occurred in a white-tailed deer buck shot by a hunter at Buckhorn Flats in September 2002. This situation prompted the eventual depopulation of the entire farm. The deer, a mix of does and yearlings, were destroyed on January 17, 2006 by U.S. Department of Agriculture shooters under a USDA agreement with the farm owner, Stan Hall. Tissue samples were sent to the Wisconsin Veterinary Diagnostic Laboratory for initial screening tests and to the USDA National Veterinary Services Laboratories in Ames, Iowa, for confirmation.
These laboratory results show that 60 of the 76 animals tested positive for chronic wasting disease. The 76 deer constituted the breeding herd on Hall’s farm. He also operated a hunting preserve on the property until 2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWD was not detected in those animals. The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.
The property has undergone cleaning and disinfection as per USDA guidelines. Under an established premise plan, no species of cervids could be brought onto the property for five years, and fences must be maintained to keep wild deer from entering the property so long as the property remained under current ownership. The premise plan expired on May 24, 2011.
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. Evidence of environmental transmission also was documented in a Colorado research facility where mule deer became infected with CWD in two of three paddocks where infected deer carcasses had decomposed on site 1.8 years earlier, and in one of three paddocks where infected deer had last resided 2.2 years earlier (Miller et al. 2004).
Environmental contamination has been identified as a possible cause of recurrence of CWD-infection on elk farms in Canada, when elk were reintroduced one year after depopulation, clean up and disinfection. To date, 8 CWD infected farms remain under CFIA (government of Canada) quarantine indefinitely and will not be allowed to repopulate with cervids until there is additional research on detection of prions in soils and better understanding of the duration of persistence of disease-causing prion post depopulation of CWD-infected cervid farms (Douglas, CFIA, pers. comm.).
Furthermore, the likely transmission of CWD via soil is corroborated by recent studies showing long-term persistence of prions in soil, that prion binds to soil components with high affinity and is not easily removed by water, and that oral prion disease transmission may be enhanced when bound to soil (Johnson et al. 2006, Schramm et al. 2006, Johnson et al. 2007). These findings suggest that soil may harbor more TSE infectivity and contribute more significantly to TSE transmission than previously recognized. These studies highlight the concerns about the risk of transmission via environmental contamination beyond five years and that efforts should be made to prevent freeranging deer from coming into contact with these contaminated facilities.
OBJECTIVE FOR PROPERTY
Maintain the Perimeter Deer Fence
The primary reason for DNR purchase of the property is to ensure that the deer fence remains intact, preventing wild deer from accessing the prion infected property. The DNR has an ethical and financial responsibility to maintain the fences until the science offers a solution for assessing the risk of remediating the site. The fence will be inspected frequently and repaired as needed.
It is desired to construct a second deer proof fence outside of the existing fence as further insurance for the property. The land immediately outside of the current fence will be cleared of all trees and brush to prepare of installation of the fence and allow vehicle access between the fences. It is hoped that land clearing will be completed in the fall of 2011 with the new fence being constructed as soon as conditions permit in 2012, however, the timing is contingent on funding.
The DNR plans to use the Almond Farm as a CWD research facility. Because the question of how long a contaminated site is a risk to deer is of national and international interest, there may be opportunities for research and funding at this facility. One way to potentially assess whether there is a risk to deer from the Almond Farm is to conduct bioassays, either on site or at an alternate location, to monitor for disease transmission. Any proposed research that includes bringing captive cervids onto the property will be thoroughly reviewed by the CWD Research Committee consisting of the Wildlife Health Team, the Wildlife Policy Team, and Department administration as well as external CWD experts prior to permission being granted to ensure that the health of the wild deer herd will not be endangered. The double fencing described above will be critical to minimize the risk of ingress of free-ranging and egress of any experimental captive cervids.
The “Almond Farm” owned by the Wisconsin DNR is a CWD prion contaminated facility, and specific guidelines for apparel and equipment sanitization must be followed to prevent prion contamination outside of the contaminated facility. Sanitization guidelines for equipment and surfaces are based upon recommendations from the American Association of Veterinary Laboratory Diagnosticians: Laboratory Safety and Waste disposal Committee and Pathology Committee 2004 publication, “Best Management Practices for Handling Suspect Biosafety Level 2 Animal Transmissible Spongiform Encephalopathy (TSE) Diagnostic Samples. (Scrapie, Chronic Wasting Disease and Transmissible Mink Encephalopathy) In Animal Health Laboratories” These guidelines are as follows:
General Apparel Guidelines
Facilities should have dedicated PPE (Personal Protective Equipment) that stays on site, and should not be removed under any circumstance. Examples of this are as follows: Boots/overshoes, gloves, eye and ear protection, coveralls, etc.
Anyone entering either facility that chooses to not wear dedicated reusable PPE shall be required to utilize disposable PPE that must be disposed of after each daily use. Examples of acceptable disposable PPE are: Tyvek coveralls, disposable gloves, plastic boot covers, etc.
Any personal footwear not left on site must be sanitized utilizing a 50/50 bleach/water solution*.
Upon entry into contaminated areas, personal footwear should be either removed and replaced by dedicated facility boots, or must be covered with plastic boot covers.
Personal clothing should be covered by putting on disposable Tyvek coveralls to prevent clothing contamination.
If contaminated material will be handled, hands should be covered with latex/nitrile gloves.
Prior to exiting contaminated areas of the facility, all persons must walk through a 50/50* bleach/water solution if boots are worn, or boot covers must be removed and disposed of.
All contaminated disposable apparel must be removed prior to exiting the facility.
Trash receptacles for disposable clothing, gloves, and boot covers should be lined and emptied daily, with liners being tightly sealed and placed directly into closed dumpsters designated for waste disposal in a sanitary landfill.
All tools, instruments, surfaces, and equipment that have been used in potentially contaminated areas of the facility should be sanitized using a 50/50 bleach/water solution*.
Tools or instruments that come into contact with blood, other bodily fluids, or tissues from potentially positive animals should be soaked in a 50/50 bleach/water solution for 60 minutes to be fully disinfected.
All equipment used on site must be sanitized prior to being transferred to alternate locations (preferably, equipment used on site will be kept on-site).
Equipment that is intended to be moved from the property can only enter on frozen snow covered ground.
Equipment that may be moved between facilities (skid steer, ATV’s, etc.) must be pressure-washed on site prior to movement.
* 50/50 (1:1) Bleach/water solution is a chemically approved and proven method of sanitizing surfaces, sampling/necropsy instruments, and footwear. By using a 50/50 solution, the concentration of chlorine is @20,000 ppm, which is required to neutralize prions to an acceptable level of biosafety. For more information on recommended sanitization procedures, refer to: BEST MANAGEMENT PRACTICES FOR HANDLING SUSPECT BIOSAFETY LEVEL 2 ANIMAL TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY (TSE) DIAGNOSTIC SAMPLES (SCRAPIE, CHRONIC WASTING DISEAS E AND TRANSMISSIBLE MINK ENCEPHALOPATHY) IN ANIMAL HEALTH LABORATORIES: AAVLD BMP CWD scrapie FINAL 18 Feb 2004.pdf
SNIP...SEE FULL TEXT ;
Wednesday, November 16, 2011
Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
*** 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.
THE LANCET VOL 337: FEB 2, 1991
Survival of Scrapie virus after 3 years interment
Paul Brown D. Carleton Gajdusek
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
Some unofficial information from a source on the inside looking out -
As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
You can take that with however many grains of salt you wish, and we can debate these issues all day long, but the bottom line, this is not rocket-science, all one has to do is some experiments and case studies. But for the life of me, I don't know what they are waiting on?
Terry S. Singeltary Sr. Bacliff, Texas USA
SEE FULL TEXT ;
Thursday, February 17, 2011
Environmental Sources of Scrapie Prions
see my full posting here ;
Wednesday, October 12, 2011
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
Accelerated shedding of prions following damage to the olfactory epithelium
Richard A. Bessen1,*, Jason M. Wilham2, Diana Lowe1, Christopher P. Watschke1, Harold Shearin1, Scott Martinka1, Byron Caughey2 and James A. Wiley1
+ Author Affiliations
1Department of Immunology and Infectious Diseases, Montana State University, Bozeman, Montana, USA 2Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergies and Infectious Diseases, Hamilton, Montana, USA
In this study we investigated the role of damage to the nasal mucosa in the shedding of prions into nasal fluids as a pathway for prion transmission. Here we demonstrate that prions can replicate to high levels in the olfactory sensory epithelium (OSE) in hamsters and that induction of apoptosis in olfactory receptor neurons (ORNs) in the OSE resulted in sloughing off of the OSE from nasal turbinates into the lumen of the nasal airway. In the absence of nasotoxic treatment olfactory marker protein (OMP), which is specific for ORNs, was not detected in nasal lavages. However, after nasotoxic treatment that leads to apoptosis of ORNs both OMP and prion proteins were present in nasal lavages. The cellular debris that was released from the OSE into the lumen of the nasal airway was positive for both OMP and the disease-specific isoform of the prion protein, PrPSc. Using the real time quaking-induced conversion assay to quantify prions, a 100- to 1,000-fold increase in prion seeding activity was observed in nasal lavages following nasotoxic treatment. Since neurons replicate prions to higher levels than other cell types and ORNs are the most environmentally exposed neurons, we propose that an increase in ORN apoptosis or damage to the nasal mucosa in a host with a pre-existing prion infection of the OSE could lead to a substantial increase in the release of prion infectivity into nasal fluids. This mechanism of prion shedding from the olfactory mucosa could contribute to prion transmission.
Monday, January 05, 2009
CWD, GAME FARMS, BAITING, AND POLITICS
Thursday, August 28, 2008
cwd, feeding, and baiting piles
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
more concern here ;
Saturday, November 12, 2011
Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease
Fri, 22 Sep 2006 09:05:59 –0500
Monday, June 27, 2011
Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria
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
SEE MORE HERE ;
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: email@example.com
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: firstname.lastname@example.org 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: email@example.com 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 the 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.
Friday, February 20, 2009
Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease
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
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- firstname.lastname@example.org
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.
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 ;
Wednesday, January 07, 2009
CWD to tighten taxidermy rules Hunters need to understand regulations
DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)
The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why??than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!! Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....
Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!
And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...
Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"
again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.
You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)
December 2011, price of TSE Prion Poker Goes Up $$$
Saturday, December 3, 2011
Isolation of Prion with BSE Properties from Farmed Goat
Volume 17, Number 12—December 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
Sunday, June 26, 2011
Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque
Wednesday, August 24, 2011
There Is No Safe Dose of Prions
Wednesday, August 24, 2011
All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD
Thursday, August 4, 2011
Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011
Monday, February 7, 2011
FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ??
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
Saturday, October 24, 2009
SaBTO Advisory Committee on the Safety of Blood, Tissues and Organs 2nd Public Meeting 27 October 2009
Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)
Sunday, July 27, 2008
Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)
-------- Original Message --------
Subject: Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)
Date: Sun, 11 Jul 2004 21:34:22 –0500
From: "Terry S. Singeltary Sr."
To: email@example.com CC: firstname.lastname@example.org, email@example.com
Response to Public Comments
Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005
The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp). Comments on technical aspects of the risk assessment were then submitted to FSIS. Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary. This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:
Suppressed peer review of Harvard study October 31, 2002.
October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024
Sunday, February 14, 2010
[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
Thursday, April 9, 2009
Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Thursday, April 09, 2009
Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed
Greetings FDA et al,
I kindly wish to comment on the following ;
[Docket No. FDA-2002-N-0031] (formerly Docket No. 2002N-0273) RIN 0910-AF46
[Federal Register: April 9, 2009 (Volume 74, Number 67)] [Proposed Rules] [Page 16160-16161] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr09ap09-18]
From: Terry S. Singeltary Sr. [firstname.lastname@example.org]
Sent: Monday, July 24, 2006 1:09 PM To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98 8/3/2006
Greetings FSIS, I would kindly like to comment on the following ;
Terry S. Singeltary
From: Terry S. Singeltary Sr. [email@example.com]
Sent: Thursday, September 08, 2005 6:17 PM
Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle
I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle
Docket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305
Comment Number: EC –254
Accepted - Volume 11
Sources: World Trade Atlas What is the level of passenger traffic arriving in the United States from the affected country? Approximately 185,000 direct flights from Greece arrived to US airports in fiscal year 2000. Also, an unknown number of passengers from Greece arrived via indirect flights. Under APHIS-PPQ's agriculture quarantine inspection monitoring, 584 air passengers from Greece were sampled for items of agricultural interest in fiscal year 2000. Of these passengers, 14 carried meat (non-pork) items that could potentially transmit pathogens that cause BSE; most passengers carried from one to two kilograms (kg) of meat, although one passenger in November 1999 carried 23 kg of meat in a suitcase. Florida, Massachusetts, and New York were the reported destinations of these passengers. None of the passengers with meat items reported plans to visit or work on a ranch or farm while in the US. Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base
Greetings list members, i just cannot accept this;
> 23 kg of meat in a suitcase (suitcase bomb...TSS)
> The data do not provide a species of origin code for these
> products, therefore they may not contain any ruminant product.
what kind of statement is this? how stupid do they think we are? it could also very well mean that _all_ of it was ruminant based products !
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 firstname.lastname@example.org