Thursday, June 07, 2018

Michigan DNR to present chronic wasting disease recommendations to Natural Resources Commission Singeltary submission

June 7, 2018
Contact: Ed Golder, 517-284-5815

DNR to present chronic wasting disease recommendations to Natural Resources Commission

After months of talking with interested citizens and hunting and wildlife stakeholders and reviewing the best available science regarding chronic wasting disease, the Michigan Department of Natural Resources is set to present CWD recommendations to the Natural Resources Commission at its next monthly meeting Thursday, June 14, in Lansing. Recommendations will be presented during Committee of the Whole.
The department’s recommendations are the result of a six-month-long public engagement effort, during which DNR staff and NRC members met with people around the state, hosted 11 public meetings, and offered online survey and comment opportunities. The recommendations are being presented for information to the commission, as part of the public input process. 
The NRC will review, discuss and possibly modify recommendations before making a final decision at a future commission meeting. Comments may be submitted to the commission via email at NRC@michigan.gov.
“The DNR and the Natural Resources Commission appreciate the high level of engagement from our customers, partners and stakeholders, and the willingness to 
co-create strategies to address CWD,” said DNR Director Keith Creagh. “We look forward to continued engagement and cooperation as we move into hunting season this fall.”
CWD is a fatal neurological (brain and nervous system) disease found in cervids – deer, elk and moose. The disease attacks the brains of infected animals and produces small lesions that result in death. There is no cure; once an animal is infected, it will die. Initially, CWD was first discovered in Michigan in a free-ranging deer in May 2015. Since that time, CWD has been confirmed in deer in five Michigan counties: Clinton, Ingham, Ionia, Kent and Montcalm.
The Natural Resources Commission meeting will take place June 14 at the Lansing Community College Downtown Campus, Health and Human Services Department, 515 North Washington Square, Conference Room HHS 005-0078.
The full meeting’s draft agenda includes the following. 
8 a.m. – Committee on Finance and Administration
  • 2018 spend plans for DNR Fisheries and Wildlife divisions.
  • An update on 2017/2018 CWD spending.
  • The DNR’s 2019 budget, if completed by the meeting.
9 a.m. – Michigan State Parks Advisory Committee
  • A presentation of Belle Isle’s strategic management plan and 2017 annual report.
  • General updates on the DNR Parks and Recreation Division, the department’s camping cancellation policy and the Oakland County ORV planning process.  
12:30 p.m. – Committee on Wildlife and Fisheries 
  • A review of fall fishing regulations.
  • Deer harvest survey report for the 2017 seasons.
  • An update on antlerless license quotes and CWD regulations.
2 p.m. – Committee of the Whole
  • DNR director’s report, including updates on CWD, the 2019 budget and the Blue Ribbon Advisory Group on State Game Areas. 
  • A legislative report.
  • NRC committee reports.  
Immediately following the Committee of the Whole, the commission will receive public comments. To register for public comment, contact Cheryl Nelson, executive assistant to the commission, at 517-284-6237 or nelsonc@michigan.gov. Those registering by 5 p.m. Friday, June 8, will be allowed up to five minutes to address the commission. Those registering after June 8 or at the meeting will be allowed up to three minutes. Registration cards will be available at the meeting.
Following public comments, the commission is scheduled to vote on statewide trout, salmon, whitefish, lake herring and smelt regulations, as well as Wildlife Conservation Order amendments governing furbearer regulations, squirrel and falconry season dates, and open/closed deer management units. Director Creagh then is expected to approve the results of the May 2018 oil and gas lease auction, as well as several land transactions.
For more information about the Natural Resources Commission, including full agendas and meeting minutes, visit michigan.gov/nrc.
The Michigan Department of Natural Resources is committed to the conservation, protection, management, use and enjoyment of the state’s natural and cultural resources for current and future generations. For more information, go to www.michigan.gov/dnr.

https://content.govdelivery.com/accounts/MIDNR/bulletins/1f593fd

RICK SNYDER GOVERNOR 
STATE OF MICHIGAN DEPARTMENT OF NATURAL RESOURCES LANSING 
Image KEITH CREAGH DIRECTOR 
SUBMITTED: 
June 6, 2018 
MEMORANDUM TO THE NATURAL RESOURCES COMMISSION 
Subject: 
Chronic Wasting Disease Regulations Wildlife Conservation Order Amendment No. 12 of 2018 FOR INFORMATION ONLY 
Authority:
The Natural Resources and Environmental Protection Act, 1994 P A 451, authorizes the Director and the Commission to issue orders to manage wild animals in this state. 
Discussion and Background: 
Since the finding of chronic wasting disease (CWD) in a free-ranging white-tailed deer in Michigan on May 20,2015, CWD-positive deer have been found in Clinton, Ingham, Ionia, Kent, and Montcalm counties. As of mid-January 2018, after testing approximately 30,600 free- ranging deer, 57 were positively confirmed with CWD, with 48 occurring during the 2017 deer hunting season. In addition, two Privately-Owned Cervid (pOC) facilities in Mecosta County were positively confirmed with CWD in 2017. 
The Natural Resources Commission (NRC) and the Department are taking aggressive action based on the Michigan's Surveillance and Response Plan for Chronic Wasting Disease of Free- Ranging and Privately-Owned Cervids, herein referred to as "the Plan", and the recommendations from the Chronic Wasting Disease Working Group - a panel established by the NRC to develop recommendations on further steps and actions to substantially mitigate or eliminate CWD in Michigan - to address CWD in Michigan's deer population and to maintain healthy wildlife for current and future generations. In addition, the Department and the NRC hosted a series of public engagement meetings on CWD that provided an opportunity for the NRC and the Department to hear suggestions and observations from hunters and residents interested in the health of the state's deer herd. The Department and the NRC are focused on achieving specific CWD management goals that include slowing the spread of the disease, reducing or maintaining low prevalence rates, preventing the disease from reaching new areas, and preserving Michigan's rich hunting history for future generations to enjoy. 
Based on the current available state of the science, recommendations from the Chronic Wasting Disease Working Group, suggestions from the public engagement meetings, and the specific CWD management goals, the Department recommends amending the protocols and control measures in the Wildlife Conservation Order to address CWD in Michigan's deer population. 
7 
CONSTITUTION HALL· 525 WEST ALLEGAN STREET· P.O. BOX 30028· LANSING, MICHIGAN 48909-7528 www.michigan.gov/dnr (517) 284-MDNR(6367) 
Chronic Wasting Disease Regulations Wildlife Conservation Order Amendment No. 12 of 2018 Page 2 June 6, 2018 

Statewide Regulations: 

Restrictions on Tile Possession and Use of Natural Cervid Urine-Based Lures and Attractants 

Chronic wasting disease is a fatal disease caused by the transmission of infectious, self-mutating proteins (prions) contained in the body and fluids of infected cervids that causes degeneration of the central nervous system of those same species. Although nervous system tissue and lymphatic tissues have the highest infectivity, these prions are also found in blood, feces and urine of infected cervids. Susceptible cervids can acquire CWD by direct exposure to these fluids or from environments contaminated with these fluids. Deer urine is used by hunters and sportspersons as an attractant and cover scent, with most commercially made products originating from POC facilities. This market is unregulated, and thus to take a pro-active approach to reduce the risk of spread or introduction of CWD to a new area, the Department recommends restricting the possession and use of non-synthetic cervid urine-based lures and attractants while hunting or trapping game species. Only synthetic cervid urine-based lures or attractants or natural cervid urine-based lures or attractants that are labeled with the official ATA (Archery Trade Association) Seal of Participation will be legal. 

Issues Pros and Cons 

The ATA is the organization for manufacturers, retailers, distributors, sales representatives, and others working in the archery and bowhunting industry. The ATA developed a Deer Protection Program, which seeks to ensure that AT A -member scent manufacturers, and their product suppliers do everything possible to prevent the spread of CWD in wild deer, elk, and moose herds in the United States. Manufacturers and their product suppliers voluntarily join the program and agree to take measures to meet or exceed state and federal CWD requirements and ensure that their products come from healthy deer herds. Manufacturers guarantee through their participation in the program, that the cervid urine utilized in their products comes only from facilities that are also participating in the ATA Deer Protection Program, and that strictly comply with the following measures: 

Participate in a federally-approved CWD program 

Have documented all cervid movement in/out of herd 

Continually monitor their herd for CWD 

Allow additional facility inspections 

Physically inspect 100 percent of the herd every three years 

Commit to advancement of sound science related to CWD 

Remain aware of CWD instances within 30 miles, and maintain minimum fence requirements 

Most urine used for lures and attractants is produced and collected from captive cervid facilities at both large commercial and small-scale operations. Although Michigan POC facilities participate in the state's CWD monitoring program, products used may come from large interstate operations. There are a variety of unregulated processes used to collect urine, and they often result in the accumulation of a mixture of secretions, therefore providing concurrent contamination risks. There are currently no standard regulations to ensure that urine collected for lures and attractants are disease-free. 

Chronic Wasting Disease Regulations Wildlife Conservation Order Amendment No. 12 of 2018 Page 3 June 6, 2018 

Other States 

Alaska, Arizona, Arkansas, Pennsylvania (within CWD areas), Vermont, and Virginia have banned the use of urine-based lures or attractants. 

Biological 

Urine-based lures and attractants are used in several different ways, many which involve direct contact between the scent and the environment. Use of urine-based lures and attractants has the potential to spread CWD to areas where it has previously not been detected. Infectious prions present in urine can contaminate the environment, where the prions can bind to the soil and be taken up by plants and are likely to remain infectious for many years. For example, research studies indicate that as little as 10 milliliters of contaminated urine can contain enough infectious prions to risk lethal infection in 50 percent of exposed deer. Though urine is considered less infectious than saliva or feces, collection methods for many of these facilities are unlikely to exclude these materials from the final product. Though facilities approved through the AT A are enrolled in the United States Department of Agriculture (USDA) Herd Certification Program (HCP), 28 breeder facilities nationally have tested positive for CWD since 2012, with 15 of these facilities em-oiled in the USDA-HCP. 

Social 

Regulating the use of urine-based lures and attractants may affect the business of the captive cervid industry, however, approximately 90 to 95 percent of manufacturers are certified through the AT A Deer Protection Program. 

Economic 

It's still legal to buy and sell products with cervid urine and other bodily fluids, however some businesses may see a decrease in sales. 

Lower Peninsula Regulations: 

Baiting and Feeding Ball- Effective January 31, 2019 

Baiting is a popular practice among Michigan hunters, and its popularity has risen over the last few decades. However, research suggests that the relationships between baiting, feeding, and CWD transmission is in the risks associated with congregating animals. While natural food sources also congregate wildlife, human activities such as baiting or feeding do so at rates above natural sources, therefore the risk of transmitting CWD increases. The risks of congregating animals around bait and feed increases the probability of direct contact between infected and noninfected animals, and it also increases the risks of contaminating the food source or the surrounding environment. Therefore, the Department recommends instituting a baiting and feeding ban effective January 31, 2019, for the Lower Peninsula. A delayed implementation provides opportunity for those with economic interests to shift business models for next year.

Chronic Wasting Disease Regulations Wildlife Conservation Order Amendment No. 12 of 201 8 Page 4 June 6, 2018

Issues Pros and Cons

With the presence of CWD in the Southwest Lower Peninsula and Bovine Tuberculosis (TB) in the Northeast Lower Peninsula, the range of these two diseases now covers much of the Lower Peninsula. A proactive approach by banning baiting and feeding, with the uncertainty of the distribution of these diseases, is warranted to reduce the risk on the landscape. In addition, given that CWD is often present in areas long before it is discovered, elimination of baiting and feeding may be a strategy to lessen the spread of the disease should it be introduced in new areas.

There are both biological and social considerations to make regarding baiting and feeding. Baiting is a highly popular activity among Michigan hunters. Baiting and feeding also have economic value as a market for agricultural products. Studies suggest there may be public support for baiting regulations if they are perceived to effectively reduce transmission of a disease and if the public has been involved in the decision—making process, however studies also suggest that hunter activity may shift in response to those regulations.

Other States and Provinces

The Department sent out a survey to CWD—positive states and received responses from Alberta, Arkansas, Illinois, Iowa, Kansas, Maryland, Missouri, Mississippi, New York, North Dakota, Utah, Virginia, West Virginia, and Wisconsin. The results were the following:

Alberta: Baiting and feeding is illegal throughout the province.

Arkansas: It is illegal to feed deer within CWD affected areas, however there are certain baiting restrictions within CWD affected areas.

Illinois: Baiting and feeding is illegal statewide.

Iowa: Baiting is illegal, but feeding is allowed statewide.

Kansas: Baiting and feeding is legal statewide.

Maryland: Baiting and feeding is legal statewide.

Missouri: Baiting and feeding is illegal in the CWD affected areas.

Mississippi: Baiting and feeding is illegal in the CWD affected areas.

New York: Baiting and feeding is illegal statewide.

North Dakota: Baiting and feeding is illegal in the CWD affected areas.

Utah: Baiting and feeding is legal statewide.

Virginia: Baiting is legal, and feeding is allowed only in areas other than CWD affected areas.

West Virginia: Baiting and feeding is illegal in the CWD affected areas.

Wisconsin: Baiting and feeding is legal in counties 36 months since the last CWD confirmation or 24 months in an adjacent county; currently 48 of 72 “affected” counties remain under a baiting and feeding ban.

Biological

Chronic wasting disease can be transmitted directly (e.g., saliva, urine, and feces) and indirectly (contaminated environment) among deer. Evidence suggests that baiting and feeding increases both the congregation of deer and the risk of disease transmission through increasing the probability of contact, food source contamination, and environmental contamination. In a review

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Chronic Wasting Disease Regulations Wildlife Conservation Order Amendment No. 12 of 2018 Page 5 June 6, 2018

of 29 studies investigating the relationship between supplemental feeding and disease transmitted through close or direct contact of animals, 95 percent reported that supplemental feeding increased the risk of disease transmission. In addition, the longer the food is on the landscape, the greater the likelihood of increasing disease transmission.

Social

In Michigan, while approval (71 percent) of baiting as a practice among hunters has steadily risen since the mid-19805, most hunters do support baiting restrictions when the health of the deer herd is in jeopardy. Studies have found that hunter support for management actions to address CWD, including baiting bans, is based on the perceived efficacy of those actions. Studies have also found that hunter acceptance of management activities increases as prevalence increases and as perception of risk increases. In addition, studies have also examined hunter behavior changes in response to baiting bans. In Michigan, after the implementation of baiting regulations in the northeast Lower Peninsula due to Bovine Tuberculosis (TB), 50 percent of bowhunters and 31 percent of firearm hunters in the area reported hunting less because of the baiting ban, and 22 percent stopped hunting in the area all together. However, declines in antlerless harvest and firearm season participation in the northeast Lower Peninsula following the ban were very similar to declines statewide.

Economic

Baiting and feeding have economic value as a market for agricultural products. Instituting a baiting and feeding ban effective for 2019 will allow time for those with economic interests to shift business models for next year.

Baiting Exception for Hunters with Disabilities

According to the Michigan Deer Hawest Survey Report, hunters with disabilities are, generally, some of the least satisfied hunters in Michigan. Although efforts have been made over the last decade to establish special hunt dates, equipment permits, and accessibility provisions, the success rate for hunters with disabilities continues to remain low compared to other hunters. The NRC and the Department received public input from hunters with disabilities regarding the use of bait. Hunters with disabilities rely on bait for the purposes of successfully harvesting a deer. The Department recommends granting a baiting exception for qualified hunters with disabilities outside of the 13-County CWD Management Zone and Bovine Tuberculosis (TB) Management Zone (Alcona, Alpena, Montmorency, and Oscoda counties) during the Liberty and Independence Hunts. Baiting would be limited to current regulations, allowing only two gallons of bait per site, distributed across a 10’x10’ area, and baiting may only occur from the first day of the season to the last day of the season. All bait must be removed from the area prior to any additional hunting during the rest of the season.

Issues Pros and Cons

The Liberty Hunt is a two—day season in mid—September that takes place on private or public lands. The Independence Hunt is a four-day season in mid—October that takes place on private lands. During these hunts, individuals with qualifying disabilities may participate and may hunt antlered (antler point restrictions do not apply) or antlerless deer with a firearm. These hunts

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Chronic Wasting Disease Regulations Wildlife Conservation Order Amendment No. 12 of 2018 Page 6 June 6, 2018

provide hunters with disabilities the opportunity to deer hunt under less crowded conditions when weather conditions are more likely to be favorable.

Even though granting a baiting exception during these two hunts for individuals with qualifying disabilities will offer a service to some of our constituents, baiting causes unnatural concentrations of deer and this activity increases the risk of disease infection and spread, and repeated use of baiting areas poses a long-term risk of disease transmission. Allowing this exception may not help reduce risk of disease spread and transmission.

Other States

The Department is not aware of other CWD—positive states granting a baiting exception for hunters with disabilities.

Biological

Chronic wasting disease transmission occurs when disease prions are shed by infected animals through saliva, urine and feces, and through contact between deer and contaminated environments. Research suggests that the relationships between baiting, feeding, and CWD transmission is in the risks associated with congregating animals. While natural food sources also congregate wildlife, human activities such as baiting or feeding do so at rates above natural sources, therefore the risk of transmitting CWD increases.

Social

Granting a baiting exception for qualified hunters during these hunts may result in some social conflict. The Liberty Hunt is for both qualified hunters with disabilities and youths 16 years of age and younger. In addition, the Liberty Hunt coincides with the early antlerless firearm season, which may result in conflicts between hunters during the concurring seasons. The proposed regulations are to allow those individuals with disabilities who are eligible to hunt during the Liberty Hunt the opportunity to use bait, not youth hunters without qualifying disabilities who are hunting during the Liberty hunt or those hunting during the early antlerless season. The Independence Hunt has limited participation statewide; there were approximately 1,900 hunters in 2016 with a harvest of approximately 400 deer. The Liberty Hunt (both hunters with disabilities and youth hunters) has higher participation statewide, with approximately 22,000 hunters participating in 2016 with a harvest of approximately 6,400 deer.

Economic

There may be some local benefit to surrounding businesses that sell bait.

CWD Management Zone

Define 13-County CWD Management Zone

Chronic wasting disease has been found in a total of 57 free-ranging deer within Clinton, Ingharn, Ionia, Kent, and Montcalm counties. One of the control measures outlined in the Plan is to establish a CWD Management Zone that includes, at a minimum, any county with a boundary

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Chronic Wasting Disease Regulations Wildlife Conservation Order Amendment No. 12 of 2018 Page 7 June 6, 2018

that is intersected by a 10—mile radius around each of the documented cases where the infected animals were located. In addition, the Plan states that if results of a local population survey or credible scientific evidence suggests that cervids from within the radius are likely to move beyond these Management Zone boundaries, those boundaries should be expanded. Accordingly, the Department recommends establishing a 13-County CWD Management Zone that includes Clinton, Eaton, Gratiot, Ingharn, Ionia, Isabella, Kent, Mecosta, Montcalm, Muskegon, Newaygo, Ottawa, and Shiawassee counties.

In addition, the Department recommends eliminating the CWD Management Zone defined as Clinton, Eaton, Ingham, Ionia, and Shiawassee counties, also known as Deer Management Unit (DMU) 419. These counties will be included in the newly defined CWD Management Zone.

Issues Pros and Cons

The newly defined 13-County CWD Management Zone will allow the Department and the NRC to establish impactful regulations related to CWD and emphasizes those areas that will be impacted by CWD. In addition, it allows for continued management and surveillance as the development of the current state of the science related to CWD control continues. The Department and the NRC continue to support an aggressive approach and an adaptive management strategy. The Department will need continued support from the hunters and public related to CWD management. The Department will continue effective communications and customer service related to the regulatory changes.

Biological

The Department has tested approximately 31,000 free-ranging deer for CWD since May of 2015. Ten have tested positive for CWD in Clinton, Ingham, and Ionia counties and 47 have tested positive for CWD in Kent and Montcalm counties. Establishing the CWD Management Zone will allow the Department to continue aggressive surveillance and management outlined in the Plan.

Social

There has been expressed support for the CWD Plan and the Department’s implementation of the plan measures and protocols.

Economic

The Department does not expect an economic impact.

Baiting and Fceding Ban Effective Immediately

Of the 57 free-ranging deer that have been positively confirmed with CWD, 36 have been found in Montcalm County. Chronic wasting disease appears to be widespread in Montcalm county, and sampling in the surrounding areas (Kent, Mecosta, Gratiot, Isabella, and Newaygo) has been generally poor to identify the true scope of the disease. With CWD also identified in Clinton, Kent, Ionia, and Ingham counties, a response that bans baiting and feeding in the immediate area is a responsible endeavor to reduce the immediate risk of transmission in and near affected areas. Currently, there are baiting bans in Clinton, Eaton, Ingham, Tonia, and Shiawassee counties, and

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Chronic Wasting Disease Regulations Wildlife Conservation Order Amendment No. 12 of 201 8 Page 8 June 6, 2018

there was a baiting ban in Mecosta and Kent counties through an Interim Order of the Director that expired on March 29, 2018. The Department recommends instituting a baiting and feeding ban effective immediately for the 13-County CWD Management Zone defined as Clinton, Eaton, Gratiot, Ingham, Ionia, Isabella, Kent, Mecosta, Montcalm, Muskegon, Newaygo, Ottawa, and Shiawassee counties.

See above for the Issues Pros and Cons, Other States, Biological, Social, and Economic matters regarding baiting and feeding.

New Private Land License at a Reduced Cost; Expires First Sunday in November

snip...see full text 40 pages here;

https://www.michigan.gov/documents/dnr/12WCO2018_CWD_Regs_INFO_624924_7.pdf


I kindly submit for your info.......kind regards, terry
 
 
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
 
========================
 
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
 
 
P.141: Abundant prion shedding in CWD-infected deer revealed by Realtime conversion
 
Edward A Hoover,1 Davin M Henderson,1 Nathaniel D Denkers,1 Candace K Mathiason,1 Matteo Manca,2,3 and Byron Caughey2 1Prion Research Center, Colorado State University; Fort Collins, CO USA; 2Laboratory of Persistent Viral Diseases, NI AID; Hamilton, MT USA; 3Department of Biomedical Sciences, University of Cagliari; Monserrato, Italy
 
Background/Introduction. Chronic wasting disease (CWD) is unique among prion diseases in its efficient lateral transmission in nature. While the presence of infectious prions in body fluids and excreta of infected cervids has been demonstrated by bioassay, the dynamics, magnitude, and consequences of prion shedding remain unknown. The present studies were undertaken to determine the kinetics, duration, and magnitude of prion shedding in infected white-tailed deer.
 
Materials and Methods. Longitudinal samples were collected from white-tailed deer over a 2-year span after either oral (n=11)] aerosol (n = 6) CWD exposure. The assay protocol employed phosphotungstic acid precipitation of either whole saliva or the pelleted fraction of urine to seed recombinant Syrian hamster prion PrP substrate in RT-QuIC reactions. Prion seeding activity was assayed in 8 replicates of each sample employing thioflavin T detection in a 96-well plate-based fluorometer. Prion seeding reaction rate was determined by taking the inverse of the time at which samples exceeded a threshold of 5 standard deviations above the mean fluorescence of negative controls (1/time to threshold). Seeding activity was quantitated by comparing the realtime conversion reaction rate to a standard curve derived from a reference bioassayed brain pool homogenate from deer with terminal CWD.
 
Results. We analyzed >200 longitudinally collected, blinded, then randomized saliva and urine samples from 17 CWDinfected and 3 uninfected white-tailed deer. We detected prion shedding as early as 3 months post exposure and sustained thereafter throughout the disease course in both aerosol and orally exposed deer. The incidence of non-specific false positive results from > 500 saliva and urine samples from negative control deer was 0.8%. By comparing real-time reaction rates for these body fluids to a bioassayed serially diluted brain control, we estimated that ≤1 ml of saliva or urine from pre-symptomatic infected deer constitutes a lethal infectious prion dose.
 
Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.
 
Acknowledgments. Support: NIH-RO1-NS-061902; Morris Animal Foundation D12ZO-045
 
P.154: Urinary shedding of prions in Chronic Wasting Disease infected white-tailed deer
 
Nathaniel D Denkers,1 Davin M Henderson, 1 Candace K Mathiason,1 and Edward A Hoover1 1Prion Research Center, Department of Microbiology, Immunology, and Pathology, Colorado State University; Fort Collins, CO USA
 
Background/Introduction. Chronic wasting disease (CWD) is unique among prion diseases in its efficient lateral transmission in nature, yet the dynamics and magnitude of shedding and its immediate and long term consequences remain unknown. The present study was designed to determine the frequency and time span in which CWD prions are shed in urine from infected white-tailed deer using adapted real-time quaking-induced conversion (RT-QuIC) methodology.
 
Materials and Methods. Longitudinal urine samples were collected by free catch or catheterization over a 2-year period from oral-route infected [CWD+ (n = 11)] and aerosol-route-infected [CWD+ (n = 6); CWD- (n = 3)] white-tailed deer. High speed centrifugation pelleted material from 500 µl of urine was treated with sodium phosphotungstic acid (Na-PTA), resuspended in 0.05% SDS buffer, and used as seed in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Eight (8) replicates of each sample were run and prion seeding activity was recorded as thioflavin T binding fluorescence (480 nm emission) using a fluorimeter-shaker. Samples were considered positive if they crossed an established threshold (5 standard deviations above the negative mean fluorescence).
 
Results. In our oral-route inoculation studies, prion seeding activity has been demonstrated in urine collected at 6 months post-inoculation in 6 of 10 deer (11 of 80 replicates; 14%), and intermittently at later time points in all 11 CWD+ exposed deer. Our aerosol-route inoculation studies also showed prion seeding activity in urine collected at 6 months post-inoculation in 1 of 2 deer (3 of 16 replicates; 19%), and intermittently at later time points in 4 of 6 CWD+ exposed deer. Urine from sham-inoculated control deer and all baseline samples yielded 3 false-positive prion seeding activities (3 of 352 replicates; 0.8%).
 
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.
 
Acknowledgments. Support: NIH: RO1-NS-061902 and Morris Animal Foundation: D12ZO-045 P.178: Longitudinal quantitative analysis of CWD prions shed in saliva of deer
 
Davin M Henderson, Nina Garbino, Nathaniel D Denkers, Amy V Nalls, Candace K Mathiason, and Edward A Hoover Prion Research Center, College of Veterinary Medicine and Biomedical Sciences, Colorado State University; Fort Collins, CO USA
 
Background/Introduction. Chronic Wasting Disease (CWD) is an emergent rapidly spreading fatal prion disease of cervids (deer, elk and moose). CWD has now been identified in 22 States (including two new states within the last year), 2 Canadian provinces, and South Korea. Shedding of infectious prions in excreta (saliva, urine, feces) may be an important factor in CWD transmission. Here we apply an adapted version of a rapid in vitro assay [real-time quaking-induced conversion (RT-QuIC)] to determine the time of onset, length, pattern, and magnitude of prion shedding in saliva of infected deer.
 
Materials and Methods. The RT-QuIC assay was performed as previously described in Henderson et al. PLoS-One (2013). Saliva samples were quantitated by comparison to a RT-QuIC reaction rate standard curve of a bioassayed obex sample from a terminally ill cervid.
 
Results. To better understand the onset and length of CWD prion shedding we analyzed >150 longitudinally collected, blinded, then randomized saliva samples from 17 CWD-infected and 3 uninfected white-tailed deer. We observed prion shedding, as detected by the RT-QuIC assay, as early as 3 months from inoculation and sustained shedding throughout the disease course in both aerosol and orally exposed deer. We estimated the infectious lethal dose of prions shed in saliva from infected deer by comparing real-time reaction rates of saliva samples to a bioassayed serially diluted brain control. Our results indicate that as little as 1 ml of saliva from pre-symptomatic infected deer constitutes a lethal CWD prion dose.
 
Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.
 
Acknowledgments. Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal Foundation.
 

Temporal patterns of chronic wasting disease prion excretion in three cervid species

Authors: Ian H. Plummer1​, Scott D. Wright2​,†​, Chad J. Johnson3​, Joel A. Pedersen3​, Michael D. Samuel4​ 

VIEW AFFILIATIONS 

*Correspondence: Michael D. Samuel, mdsamuel@wisc.edu 

First Published Online: 15 July 2017, Journal of General Virology doi: 10.1099/jgv.0.000845 Subject: Research Article - TSE Agents Received: 07/12/2016 Accepted: 22/05/2017 Cover date: 15/07/2017

Chronic wasting disease (CWD) is the only naturally occurring transmissible spongiform encephalopathy affecting free-ranging wildlife populations. Transmission of CWD occurs by direct contact or through contaminated environments; however, little is known about the temporal patterns of CWD prion excretion and shedding in wild cervids. We tested the urine and faeces of three species of captive cervids (elk, mule and white-tailed deer) at 6, 12, 18 and 24 months after oral inoculation to evaluate the temporal, species- and genotype-specific factors affecting the excretion of CWD prions. Although none of the animals exhibited clinical signs of CWD during the study, we determined that all three cervid species were excreting CWD prions by 6 months post-inoculation. Faecal samples were consistently positive for CWD prions for all three cervid species (88 %), and were more likely to be positive than urine samples (28 %). Cervids with genotypes encoding for the prion protein (PRNP) that were considered to be more susceptible to CWD were more likely to excrete CWD prions (94 %) than cervids with genotypes considered to be less susceptible (64 %). All cervids with CWD prions in their urine also had positive faeces (n=5), but the converse was not true. Our study is the first to demonstrate CWD prion excretion in urine by asymptomatic elk and mule deer. Our results indicate that the excretion of CWD prions in faeces and, to a lesser extent, urine may provide an important avenue for depositing prions in the environment.

Keyword(s): cervids, prions, PMCA, excretion, shedding, chronic wasting disease


P144 Environmental Contamination Assessment of CWD Shed in Excreta by RT-QuIC 

Dr. Davin Henderson1, Ms. Joanne Tennant1, Dr. Nicholas Haley2, Dr. Nathaniel Denkers1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Prion Research Center. Department of Microbiology, Immunology and Pathology. Colorado State University, Fort Collins, United States, 2Midwestern State University, Glendale , United States 

Chronic wasting disease affects free-ranging or captive populations of deer, elk and moose in the United States, Canada, Korea, and most recently Norwegian caribou and moose. CWD is unique in its ability to spread in wild populations, which likely occurs through environmental dissemination or direct contact with prions shed into bodily fluids or excreta. We have made progress to rapidly and cost-effectively detect CWD in urine and feces, which contribute substantially to environmental contamination. 

Aims: 1) Using real-time quaking induced conversion (RT-QuIC) we will estimate environmental contamination via urine and feces by CWD positive animals throughout the disease course. 2) We will apply RT-QuIC to estimate CWD incidence in populations without animal capture and assess the persistence of prion seeding activity in feces under environmental conditions in the native range of cervid species. 

Methods: CWD prions in fecal and urine samples will be concentrated via iron oxide mediated extraction (IOME) and assayed by RT-QuIC using temperature adjustment modifications to select increase to preserve sensitivity while minimizing specificity. Results: We assayed longitudinal cohorts of whitetailed deer for prion shedding in feces and urine during the CWD disease course and determined shedding kinetics and consistency. We applied a quantitative approach to these data using a reference brain sample to determine the levels of CWD prions shed in feces and urine during the disease course. 

Conclusions: In deer experimentally inoculated with CWD approximately 100 (Tg5037) cervid PrP mouse LD50 doses are shed in urine and ~90 (TG5037) mouse LD50 doses are shed in feces per day. The relationship between cerPrP transgenic mouse and cerivd LD50 doses remains to be determined. In the future, we will apply RT-QuIC detection of CWD in feces to estimate CWD incidence in populations without animal capture and to determine how long prion seeding activity remains active in fecal samples under potentially harsh environment conditions that exist in the native range of cervid species.

=====

P155 Sensitive detection of PrPCWD in soil from CWD infected farm by PMCAb 

Hyun Joo Sohn1, Kyung Je Park1, In Soon Roh1, Hyo Jin Kim1, Hoo Chang Park1, Director of division Hae Eun Kang1 1Foreign animal disease division, Animal And Plant Quarantine Agency(QIA), Gimcheon, South Korea 

Aims: Chronic wasting disease (CWD) is the prion disease that is known spread horizontally. CWD has confirmed last in Republic of Korea in 2016 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and feces of TSE-infected animals. Using serial protein misfolding cyclic amplification with beads (sPMCAb), we developed a detection method for CWD PrPCWD in soil from CWD affected farm in 2010. We found to detect PrPCWD in soil from CWD infected farm, but not detect PrPCWD in soil of normal cervid farm in Korea. Our method appears to be a very useful technique for monitoring PrPCWD levels in environmental conditions. 

Methods: There are total of three steps with two washing steps for PrPCWD extraction and one amplification step for PrPCWD detection from soils of natural CWD farms which have confirmed horizontal spread of CWD in 2010 and 2016. The first washing step consists of slow rotating to remove large impurities. The second washing step was detached PrPCWD from abnormal prion contaminated soil by strong vortex. The last step was PrPCWD amplification step using sPMCAb. Sonication was performed with a Misonix 4000 sonicator with amplitude set to level 70, generating an average output of 160W during each cycle. One round consisted of 56 cycles of 30 sec of sonication followed 10min of 37℃ incubation. The samples(20uL) after each round of amplification were mixed with proteinase K (200ug/ml) and incubated 37℃ for 1hr. Samples were separated by SDS-PAGE and transferred onto PVDF membrane. After blocking, the membrane was incubated for 1h with 1st antibody S1 anti rabbit serum (QIA, 1:3000) and developed with enhanced chemiluminescent detection system 

Results: We had collected 35 soil samples from the four farms which were confirmed CWD and five trace farm in 2016. After three rounds of sPMCAb, we detected PrPCWD in 10 samples from areas which were positive animals habitat but not detect PrPCWD in soil of wild cervids habitat and normal cervid farm in Korea. These results suggest that our method can be a very useful tool for monitoring PrPCWD contamination in environments 

Conclusions: This sPMCAb method using soil washing solution by slow rotating and vortex is effective extraction method of PrPCWD from CWD contaminated soils. The method developed in this study will be useful for assessment of PrPCWD levels in the contaminated soils.

=====

P52 NaPTA/RT-QUIC detection of PrPCWD in saliva and urine of CWD-infected cervids and TgElk mice 

Hyun Joo Sohn1, Kyung Je Park1, Gordon Mitchell2, In Soon Roh1, Hyo Jin Kim1, Hae Eun Kang1 1Foreign Animal Disease Division Animal And Plant Quarantine Agency(QIA), Gimcheon, South Korea, 2Canadian Food Inspection Agency, Ottawa, Canada 

Aims: Chronic wasting disease(CWD) is the only prion disease affecting free-ranging animals, reported in North America, South Korea and Norway. CWD agents are shed in saliva, urine and feces which most likely contribute to the horizontal transmission between cervid species.The development of amplification-based seeding assays have been instrumental in the detection of low levels of prions in clinical samples. Using NaPTA precipitation and real-time quaking-induced conversion(NaPTA/RT-QUIC), we established a ultrasensitive detection method for PrPCWD in the saliva and urine of CWD affected cervids. Also we performed the longitudinal study to detect PrPCWD from ,in the CWD-infected, sequentially sampled transgenic mice overexpressing elk prion protein(TgElk mice). 

Methods: Five saliva and two urine samples from CWD-infected cervids at the terminal stage of disease, and 28 urine samples from sequentially sampled CWD-infected TgElk mice (TgElk CWD) were stored at -80℃. 100uL of each sample was mixed with 10uL 2.8% sodium phosphotungustic acid (NaPTA) and incubated for 1hr at 37℃ with shaking at 1,350 rpm. Samples were centrifuged for 30min at 16,100 g. The pellet was resuspended in 10uL of 0.1% SDS/PBS for 30min at 55℃. RT-QUIC reactions were set up in 96-well clear bottom optic plates and consisted of 98uL RT-QUIC buffer [final concentrations of 1XPBS, 1mM EDTA, 10uM Thioflavin, 300mM NaCl buffer and 0.1mg/ml recombinant hamster recombinant protein(23-231) and 2uL of sample. The RT-QUIC assay was performed on a FLUOstar Omega fluorescence plate reader that was preheated to 55℃ for 60hr with 1min shaking at 700rpm followed by 1min incubation. 

Results: NaPTA/RT-QUIC was applied to measure PrPCWD in urine samples collected on every 15days from 30dpi to 120dpi when CWD infected TgElk mice reached terminal stage. . and dpi typicallyCWD in PrPCWD in the urine in TgElk CWD was detectable in early stages(30 and 45dpi), disappeared during the intermediate stages of infection(60 and 75dpi) and reached the highest levels at 90dpi. PrPCWD was also detectable in late and terminal stages(120dpi). In addition, PrPCWD was detected in terminal urine samples from two sika deer(experimental cases) and terminal saliva samples from five cervids were also observed to consistently yield positive results by the NaPTA/RT-QUIC assay. 

Conclusions: We demonstrate that CWD prions can be detected by NaPTA/RT-QUIC in the saliva and urine of TgElk mice, red deer and sika deer at the early and terminal stages of disease. Our method appears to be a very useful technique for both diagnosis and surveillance of CWD

=====

PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 

 Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO

PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS

PRION 2017 CONFERENCE VIDEO


 
urine, feces, and chronic wasting disease cwd tse prion risk factors, loading up the environment
 

From: Terry S. Singeltary Sr. 

Sent: Saturday, November 07, 2015 11:54 AM 

To: David.Putnam@pa.gov ; D.Putnam@pa.gov ; Putnam@pa.gov Cc: pgc-swregion@pa.gov ; pgc-ncregion@pa.gov ; pgccomments@pa.gov 

Subject: re-Pennsylvania 2015 September Minutes CWD Urine Scents


MONDAY, JUNE 17, 2013

Early detection of chronic wasting disease prions in urine of pre-symptomatic deer by real-time quaking-induced conversion assay

 
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
 
Date: Sat, 20 Jul 2002 09:43:10 -0700
 
From: "Terry S. Singeltary Sr."
 
Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
 
Date: Sat, 25 May 2002 18:41:46 -0700
 
From: "Terry S. Singeltary Sr."
 
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de
 
######## Bovine Spongiform Encephalopathy #########
 
MAD DEER/ELK DISEASE AND POTENTIAL SOURCES
 
snip...
 
now, what about those 'deer scents' of 100% urine', and the prion that is found in urine, why not just pass the prion with the urine to other deer...
 
Mrs. Doe Pee Doe in Estrus Model FDE1 Mrs. Doe Pee's Doe in Estrus is made from Estrus urine collected at the peak of the rut, blended with Fresh Doe Urine for an extremely effective buck enticer. Use pre-rut before the does come into heat. Use during full rut when bucks are most active. Use during post-rut when bucks are still actively looking for does. 1 oz.
 
http://www.gamecalls.net/huntingproducts/deerlures.html
 
ELK SCENT/SPRAY BOTTLE
 
Works anytime of the year *
 
100 % Cow Elk-in-Heat urine (2oz.) *
 
Economical - mix with water in spray mist bottle *
 
Use wind to your advantage
 
Product Code WP-ESB $9.95
 
http://www.elkinc.com/Scent.asp
 
prions in urine?
 
[PDF] A URINE TEST FOR THE IN-VIVO DIAGNOSIS OF PRION DISEASES
 
 
Terry S. Singeltary Sr.
 
Thank You For Your Comments Thank you for submitting your comments on the Draft Deer Management Plan.
 
https://www3.dgif.virginia.gov/web/wildlife/deer/management-plan/draft/comment/thanks/
 
DRAFT Virginia Deer Management Plan 2015-2024 (bans urine scents do to CWD 2015)
 

Saturday, November 07, 2015
 
Pennsylvania 2015 September Minutes CWD Urine Scents
 


i would kindly like to applaud Michigan DNR efforts now to help contain and or stop CWD TSE Prion. please note, i got banned from michigan-sportsman.com for these very warnings, to help prevent the spread of cwd in Micigan, after being there for 16 years helping bring this very same information to the table. they lay claim that i was passing unsubstantiated cwd information. seems it's just the opposite at Micjhigan-sportsman.com, seems to me, these days, that is sole purpose of that forum now, is to pass junk science to the public, thanks to the pro shooting pens and outfitters et al. i believe now imo, that michigan-sportsman.com has now become part of the cwd problem in Michigan. so sad, to have a select few totally screw up a good forum.

I wish to submit the following to Michigan Natural Resources Commission.


what is Michigan feeding their cervid ???


2017 Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed

Subject: MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017


MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017


FDA BSE/Ruminant Feed Inspections Firms Inventory 


11998 DET-DO MI 48846-847 OPR 4/4/2017 OAI 


http://www.accessdata.fda.gov/scripts/BSEInspect/bseinspections.csv 


NAI = NO ACTION INDICATED


OAI = OFFICIAL ACTION INDICATED


VAI = VOLUNTARY ACTION INDICATED


RTS = REFERRED TO STATE


OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions...end...TSS


V. Use in animal feed of material from deer and elk NOT considered at high risk for CWD 

FDA continues to consider materials from deer and elk NOT considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal feeds in accordance with current agency regulations, 21 CFR 589.2000. 

Deer and elk not considered at high risk include: 

(1) deer and elk from areas not declared by State officials to be endemic for CWD and/or to be CWD eradication zones; and 

(2) deer and elk that were not at some time during the 60-month period immediately before the time of slaughter in a captive herd that contained a CWD-positive animal.




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

snip...

In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

Animals considered at high risk for CWD include:

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

snip...

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).

The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).

Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

snip...

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

snip...

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

snip...

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

snip...

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

snip...



TUESDAY, APRIL 18, 2017 

*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***



TUESDAY, JANUARY 17, 2017 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION



THIS April, 4, 2017 violation of the mad cow 21 CFR 589.2000 OAI is very serious for the great state of Michigan, some 20 years post FDA mad cow feed of August 1997. if would most likely take a FOIA request and a decade of wrangling to find out more. 

TUESDAY, JANUARY 17, 2017

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION 

I would kindly like to comment on this FDA BSE/Ruminant Feed Inspections Firms Inventory (excel format)4 format, for reporting these breaches of BSE TSE prion protocols, from the extensive mad cow feed ban warning letters the fda use to put out for each violations. simply put, this excel format sucks, and the FDA et al intentionally made it this difficult to follow the usda fda mad cow follies. this is an intentional format to make it as difficult as possible to follow these breaches of the mad cow TSE prion safety feed protocols. to have absolutely no chronological or numerical order, and to format such violations in a way that they are almost impossible to find, says a lot about just how far the FDA and our fine federal friends will go through to hide these continued violations of the BSE TSE prion mad cow feed ban, and any breaches of protocols there from. once again, the wolf guarding the henhouse $$$

NAI = NO ACTION INDICATED

OAI = OFFICIAL ACTION INDICATED

VAI = VOLUNTARY ACTION INDICATED

RTS = REFERRED TO STATE

OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions. 

2016


ONE more thing, please remember, the label does not have to say ''deer ration'' for cervid to be pumped up with. you can get the same ''high protein'' from many sources of high protein feed for animals other than cattle, and feed them to cervid...

Saturday, August 29, 2009

FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009


Friday, September 4, 2009

FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009


 RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II 

___________________________________

PRODUCT

Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007

CODE

Cattle feed delivered between 01/12/2007 and 01/26/2007

RECALLING FIRM/MANUFACTURER

Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007. Firm initiated recall is ongoing.

REASON

Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

42,090 lbs.

DISTRIBUTION

WI ___________________________________

PRODUCT

Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007

CODE

The firm does not utilize a code - only shipping documentation with commodity and weights identified.

RECALLING FIRM/MANUFACTURER

Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.

REASON

Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

VOLUME OF PRODUCT IN COMMERCE

9,997,976 lbs.

DISTRIBUTION

ID and NV

END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

###



ALSO, PLEASE NOTE OUTBREAK OF MAD GOAT DISEASE IN MICHIGAN ??? 
i have been very concerned about this for years and years...terry

SUNDAY, JUNE 3, 2018 

Clinical, pathological, and molecular features of classical and L-type atypical-BSE in goats



***> PLEASE WATCH THIS VIDEO, AND BE SURE TO SEE AROUND THE 8 MINUTE MARK, VERY, VERY, DISTURBING...terry



***> LISTEN TO THIS CWD BLUES DIDDY ABOUT WISCONSIN CWD TSE PRION...terry

LISTEN TO THIS NICE LITTLE CWD BLUES DIDDY BY TAMI ABOUT WISCONSIN CWD TSE PRION. WOW, ANNUAL UPDATES NOW, FROM HERE ON OUT, ABOUT CWD...200,000 CWD TESTS, WITH OVER 3500 CWD POSITIVE CASES, SEEING INCREASING TRENDS IN PREVALENCE AND DISTRIBUTION...CARCASS DISPOSAL SIGNIFICANT CHALLENGE...CWD SAMPLING EFFORTS GONE DONE, WHILE CWD POSITIVES HAVE GONE UP...ALSO, 40 SELF SERVING KIOSKS ACROSS STATE AND FREE HUNTER SERVICE CWD TESTING AND SICK DEER POLICY REPORTING AND TESTING ACROSS STATE!


CWD National Perspective: Captive Herd Certification Program - Dr. Tracy Nichols





WEDNESDAY, MARCH 07, 2018 

Michigan DNR CWD National Perspective: Captive Herd Certification Program - Dr. Tracy Nichols

CURRENT STATUS OF CWD IN CAPTIVE CERVID HERDS IN 16 STATES AS OF MAY 2017

43 ELK HERDS

37 WTD HERDS

1 RED DEER HERD

6 MIX SPECIES HERDS

85 CWD-POSITIVE CAPTIVE HERDS 

snip...see


January 14, 2018

Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases

http://www.michigan.gov/emergingdiseases/0,4579,7-186-81018_25806-357110--,00.html

http://chronic-wasting-disease.blogspot.com/2018/01/michigans-chronic-wasting-disease.html

MONDAY, APRIL 16, 2018 

Rumor has it, Dr. Kroll to speak for Michigan DNR about Chronic Wasting Disease CWD TSE Prion, God Help Michigan 



michigan-sportsman.com and chronic wasting disease science and or your 1st amendment?


michigan-sportsman.com removes thread urls from cwd sound science;





Deer Scents Banned Due To Cwd Transmission

Discussion in 'Wildlife Diseases' started by terry, Apr 26, 2007.
  1. Apr 26, 2007 #1
    terry

    terry

    Messages:
    1,446
    Likes Received:
    51
    Location:
    Bacliff, TEXAS USA
    Subject: DEER SCENTS BANNED DUE TO CWD TRANSMISSION
    Date: April 25, 2007 at 7:18 am PST


    Last updated at 4:42 PM on 24/04/07


    Deer scents banned
    Wildlife Act amended to avoid chronic wasting disease


    BY BETH JOHNSTON
    The Daily News

    Nova Scotian hunters will have to leave their deer pee at home.

    In an effort to stop the contagious, lethal Chronic Wasting Disease from hitting Nova Scotian deer and elk, the Department of Natural Resources is banning the use of deer scents which contain deer bodily fluid.

    The disease has been diagnosed in commercial game farms in several states and provinces where the products originate. There are no regulations on the imported scents, which hunters can purchase at WalMart and Canadian Tire.

    Hunters often soak cotton balls in the urine from a doe in heat to attract bucks.

    Chronic wasting disease – a transmissible neurological disease of deer and elk – is a very serious problem in Western Canada and parts of the United States, said Natural Resources wildlife director Barry Sabean.

    “We don’t have it and we don’t want it,” he said.

    (For full story, see Wednesday's edition of The Daily News)


    http://www.hfxnews.ca/index.cfm?sid=24902&sc=89


    BETTER LATE THAN NEVER......TSS











TUESDAY, APRIL 17, 2018 

***> Chronic wasting disease: Bambi vs. the prion <***

Research Project: Immunodiagnostics to Detect Prions and Other Important Animal Pathogens 

Location: Produce Safety and Microbiology Research


FRIDAY, APRIL 20, 2018 

***> Scrapie Transmits To Pigs By Oral Route

what about the terribly flawed USA tse prion feed ban? 

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies


***> CWD TO PIGS <***

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

Location: Virus and Prion Research

Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin

Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:

Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.

Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.

Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:

This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.

CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.

Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.


CONFIDENTIAL

EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...


we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.

 
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....


snip...see much more here ;

WEDNESDAY, APRIL 05, 2017

Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease


WEDNESDAY, APRIL 05, 2017

*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***

 

***> CATTLE ARE HIGHLY SUSCEPTIBLE TO WHITE-TAILED DEER CWD AND MULE DEER CWD <***


***> cattle are highly susceptible to white-tailed deer CWD and mule deer CWD

***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.

SNIP...


price of prion poker goes up for cwd to cattle;

Monday, April 04, 2016

*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***


 i believe i would be more concerned with Czub Canadian study, the cwd oral transmission study to Macaque, than this other recent study here...

TUESDAY, MAY 15, 2018 

CATTLE (BOS TAURUS) RESIST CHRONIC WASTING DISEASE FOLLOWING ORAL INOCULATION CHALLENGE OR TEN YEARS’ NATURAL EXPOSURE IN CONTAMINATED ENVIRONMENTS?


THURSDAY, MARCH 08, 2018 

Cervid, Wild Hogs, Coyotes, Wolves, Cats, Rodents, Gut Piles and Scavengers, A Potential Risk as Regards Disease Transmission CWD TSE Prion



May 4, 2018

 ***Mineral licks as environmental reservoirs of chronic wasting disease prions



-----Original Message-----
From: Terry Singeltary <flounder9@verizon.net>
To: Tracy.A.Nichols <Tracy.A.Nichols@aphis.usda.gov>
Sent: Fri, Mar 30, 2018 12:51 pm
Subject: Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018

Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018

Greetings APHIS, USDA, Dr. Tracy Nichols, et al, 

I wish to kindly submit my comments on the Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards please. i have submitted online and sent a hard copy to Dr. Nichols via email. i know that my concern may not be the same concern as others, but ramifications from cwd tse prion can be long lasting, and science is still emerging. however, the science today warrants immediate and further actions be taken. my comments, with reference materials, are as follows, and will be formatted in such a way, i will address issues by numbers 1-10, and under each one of my comments by each number, i will reference my comments with science to back up what i am stating/asking...thank you kindly, terry

1. I believe that immediately, there should be a 'DECLARATION OF EXTRAORDINARY EMERGENCY FOR FOREIGN ANIMAL DISEASE OF THE United States of America USA' due to Chronic Wasting Disease CWD Transmissible Spongiform Encephalopathy TSE Prion disease. All Intercontinental, International, Interstate movements of cervid should be banned immediately from the USA, and documented CWD TSE Prion Countries. There was a 'DECLARATION OF EXTRAORDINARY EMERGENCY FOR FOREIGN ANIMAL DISEASE' declared in the USA way back On July 10, 2000, several sheep from the flock tested positive for a TSE, a class of degenerative neurological diseases that is characterized by a very long incubation period and a 100 percent mortality rate in infected sheep. Two of the better known varieties of TSE are scrapie in sheep and BSE in cattle. On July 14, 2000, USDA issued a declaration of extraordinary emergency to acquire the sheep. but those test were wrong, and a decade later after FOIA request after request, turns out those sheep from Belgium never had any TSE Prion disease. long story, but what is the difference here, especially since we are dealing with Chronic Wasting Disease CWD TSE Prion, and the fact now that not only has CWD been exported from North America to South Korea, and to Norway, but now Finland has confirmed it's first case of Chronic Wasting Disease CWD TSE Prion. So, where does the 'BUCK' stop? why has this 'DECLARATION OF EXTRAORDINARY EMERGENCY FOR FOREIGN ANIMAL DISEASE OF THE United States of America USA' due to Chronic Wasting Disease CWD Transmissible Spongiform Encephalopathy TSE Prion disease, not already been declared, and why has not a Intercontinental, International, Interstate movements of cervid BAN not already been put in place, especially since the recent findings of oral transmission studies with the Macaque, in relations with oral transmission of muscle meat with cwd, and oral transmission of cwd to the pig? do we just continue to truck, ship, or fly this CWD TSE Prion all around the globe, just to save the industry? see; August 15, 2000 OIG case # NY-3399-56 REDACTED, VT ''Enclosed is OIG's notification that they have scheduled an investigation of the following individual. REDACTED is alleged to have provided possibly inaccurate test results involving diseased sheep. However, because the results were determined to be inconclusive, no actual violation was actually committed.''

http://foiamadsheepmadrivervalley.blogspot.com/

2. Voluntary Chronic Wasting Disease Herd Certification Program should be made MANDATORY immediately, OR NO PERMIT TO FARM DEER OR ELK, PERIOD! you don't want to join, then fine, you don't farm cervid and or any product there from.

3. INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose? 

4. QUARANTINE OF ALL CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 years
Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3Correspondence Gudmundur Georgsson ggeorgs@hi.is1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland3 Bethesda, Maryland, USAReceived 7 March 2006Accepted 6 August 2006In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.

http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pdf?expires=1521907990&id=id&accname=guest&checksum=51DB085BD612A0603240F09E29D4AADD

Survival of Scrapie virus after 3 years interment

Paul Brown, D. Carleton Gajdusek

https://web.archive.org/web/20090505211734/http://www.bseinquiry.gov.uk/files/sc/Seac07/tab03.pdf

Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;

Some unofficial information from a source on the inside looking out -

Confidential!!!!

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!!!

---end personal email---end...tss

5. DESCRIBING APHIS' intent to amend the regulations to define susceptible species based on scientific evidence of natural infection or experimental infections through natural routes and adding the genera Rangifer and Muntiacus to the list of susceptible species...

snip...see full text;

*** APHIS USDA CFIA CWD TSE Prion Herd Certifications Update ***

FRIDAY, MARCH 30, 2018 

Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018

Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon.net Attachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary View Attachment:View as format pdf 






BSE, TYPICAL AND ATYPICAL, AKA MAD COW DISEASE, Scrapie, and CWD, have all now been linked to sporadic creutzfeldt jakob disease tse prion...


O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), 

***is the third potentially zoonotic PD (with BSE and L-type BSE), 

***thus questioning the origin of human sporadic cases. 

We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. 

=============== 

***thus questioning the origin of human sporadic cases*** 

=============== 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. 

============== 


***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 


PRION 2016 TOKYO

Saturday, April 23, 2016

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis

Prion 2016 Animal Prion Disease Workshop Abstracts

WS-01: Prion diseases in animals and zoonotic potential

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 


why do we not want to do TSE transmission studies on chimpanzees $

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

snip...

R. BRADLEY


Title: Transmission of scrapie prions to primate after an extended silent incubation period) 

*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. 


ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION 

10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question... 

''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)

EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors 

First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132 ;

also, see; 

8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available. 

snip... 

The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure. 


zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm 

***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116*** 


To date there is no direct evidence that CWD has been or can be transmitted from animals to humans. 

However, initial findings from a laboratory research project funded by the Alberta Prion Research Institute (APRI) and Alberta Livestock Meat Agency (ALMA), and led by a Canadian Food Inspection Agency (CFIA) scientist indicate that CWD has been transmitted to cynomolgus macaques (the non-human primate species most closely related to humans that may be used in research), through both the intracranial and oral routes of exposure. 

Both infected brain and muscle tissues were found to transmit disease. 

Health Canada’s Health Products and Food Branch (HPFB) was asked to consider the impact of these findings on the Branch’s current position on CWD in health products and foods. 

Summary and Recommendation: 

snip...

Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle. 

These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle. 


*** WDA 2016 NEW YORK *** 

We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. 

In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. 

***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. 

Student Presentations Session 2 

The species barriers and public health threat of CWD and BSE prions 

Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University 

Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. 

These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. 

The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. 

We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. 

We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. 

***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders


CDC CWD 2018 TRANSMISSION


Transmissible Spongiform Encephalopathies

Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY


BSE INQUIRY

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.


*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

snip...

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

snip...

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

snip...

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;


TUESDAY, SEPTEMBER 12, 2017 

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 


SATURDAY, JANUARY 27, 2018 

CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018


Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018

CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE. 

THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$

BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.

SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.

SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.

SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***


CDC CWD TSE PRION UPDATE USA JANUARY 2018

As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk. CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast.. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand. Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd. As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids. 

Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018 

snip.... 



*** 2017-2018 CWD TSE Prion UPDATE

Prion 2017 Conference Abstracts CWD

 2017 PRION CONFERENCE 

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 

Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 

University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 

This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 

Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 

At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 


PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 

Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO 

PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS 

*** PRION 2017 CONFERENCE VIDEO 




TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT 

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress



SATURDAY, JULY 29, 2017 

Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC 


*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. 


Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}...TSS

resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.

snip...



Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ 

Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations

In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.


Prions in Skeletal Muscles of Deer with Chronic Wasting Disease 

Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.


 *** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.

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)

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


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 ;


> However, to date, no CWD infections have been reported in people. 

key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** 




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

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.


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.


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


I urge everyone to watch this video closely...terry 

*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***


> However, to date, no CWD infections have been reported in people. 

key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** 






P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum

Justin Greenlee1, S JO Moore1, Jodi Smith1, M Heather WestGreenlee2 and Robert Kunkle1

1National Animal Disease Center; Ames, IA USA

2Iowa State University; Ames, IA USA

The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n = 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. 

***In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.


*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

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

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

snip...

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 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.



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

snip...

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.




the tse prion aka mad cow type disease is not your normal pathogen. 

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. 

you cannot cook the TSE prion disease out of meat. 

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. 

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. 

the TSE prion agent also survives Simulated Wastewater Treatment Processes. 

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. 

you can bury it and it will not go away. 

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. 

it’s not your ordinary pathogen you can just cook it out and be done with. 

that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. 

Laboratory of Central Nervous System Studies, National Institute of 

Neurological Disorders and Stroke, National Institutes of Health, 

Bethesda, MD 20892. 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. 

PMID: 8006664 [PubMed - indexed for MEDLINE] 


TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 


 *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 


*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years *** 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 


Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. 

Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. 

Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.

=========================

***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

========================

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. 


New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication 


Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production 


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


A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing 


Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals 


PPo4-4: 

Survival and Limited Spread of TSE Infectivity after Burial 




Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

imageTimm Konold1*,  imageStephen A. C. Hawkins2,  imageLisa C. Thurston3,  imageBen C. Maddison4,  imageKevin C. Gough5,  imageAnthony Duarte1 and  imageHugh A. Simmons1

1Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK
2Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK
3Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK
4ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
5School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK

Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie-affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.

snip...

Discussion
 
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
 
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
 
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
 
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
 
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
 
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
 
 
Wednesday, December 16, 2015
 
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
 

Singeltary submission ;

Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose

*** DOCUMENT ID: APHIS-2006-0118-0411



THURSDAY, APRIL 05, 2018 

Boone and Crocket Club B&C News Release CHRONIC WASTING DISEASE TSE Prion


THURSDAY, APRIL 19, 2018

Theodore Roosevelt Conservation Partnership Chronic Wasting Disease CWD What You Can Do!


SUNDAY, APRIL 8, 2018 

Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018


SATURDAY, MARCH 10, 2018

Chronic Wasting Disease CWD TSE Prion Goes Global Finland Falls, Behind Norway and S. Korea

FINLAND REPORTS FIRST CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN A moose or European elk (Alces alces)


WEDNESDAY, MARCH 28, 2018 

The executioner in Nordfjella and Chronic Wasting Disease CWD TSE Prion Skrantesjuke


TUESDAY, FEBRUARY 27, 2018 

NORWAY CWD TSE PRION Skrantesjuke Nordfjella zone 1 Complete Eradication Complete


FRIDAY, NOVEMBER 24, 2017 

Norwegian Food Safety Authority makes changes to measures to limit the spread of disease Skrantesjuke (CWD) in deer wildlife


WEDNESDAY, MARCH 21, 2018 

World Animal Organization (OIE) Appoints Veterinary Institute as first European reference laboratory for land animal health field of CWD or skrantesjuke scratch disease



NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES

"Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health," the article states.

NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES

Subject: Prion Disease in Dromedary Camels, Algeria

Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.




***> IMPORTS AND EXPORTS <***

SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN



2017 USAHA RESOLUTION

RESOLUTION NUMBER: 1 Combined with 6, 13, 16, and 22 APPROVED

SOURCE: COMMITTEE ON ANIMAL EMERGENCY MANAGEMENT

COMMITTEE ON FOREIGN AND EMERGING DISEASES

 COMMITTEE ON SWINE

 COMMITTEE ON CATTLE AND BISON

 COMMITTEE ON SHEEP, GOATS AND CAMELIDS

SUBJECT MATTER: Adequate Funding for Prevention, Diagnosis, and Response for Foreign Animal Disease Outbreaks 


Tuesday, April 17, 2018 

Genetic variation of the prion protein gene (PRNP) in alpaca (Vicugna pacos)


Wednesday, May 30, 2018 

Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago



SUNDAY, JUNE 3, 2018 

Clinical, pathological, and molecular features of classical and L-type atypical-BSE in goats



ONE DECADE POST MAD COW FEED BAN OF AUGUST 1997...2007
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.
 
*** This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.
 
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
 
see page 176 of 201 pages...tss
 
 
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply;
 
 
Wednesday, July 15, 2015
 
Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?
 
 
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
 
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
 
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
 
Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT
 

Tuesday, March 20, 2018 

Variably protease-sensitive prionopathy (VPSPr), sporadic creutzfeldt jakob disease sCJD, the same disease, what if?



This was not simply another farmer but the third farmer......
 
 
suspect case of CJD in a farmer who has had a case of BSE in his beef suckler herd.
 
 
cover-up of 4th farm worker ???
 
 
 
CONFIRMATION OF CJD IN FOURTH FARMER
 
 
now story changes from;
 
SEAC concluded that, if the fourth case were confirmed, it would be worrying, especially as all four farmers with CJD would have had BSE cases on their farms.
 
to;
 
This is not unexpected...
 
was another farmer expected?
 
 
4th farmer, and 1st teenager
 
 
2. snip...
 
Over a 5 year period, which is the time period on which the advice from Professor Smith and Dr. Gore was based, and assuming a population of 120,000 dairy farm workers, and an annual incidence of 1 per million cases of CJD in the general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an individual in the general population to develop CJD. Using the actual current annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5 TIMES.
 
3. You will recall that the advice provided by Professor Smith in 1993 and by Dr. Gore this month used the sub-population of dairy farm workers who had had a case of BSE on their farms - 63,000, which is approximately half the number of dairy farm workers - as a denominator. If the above sums are repeated using this denominator population, taking an annual incidence in the general population of 1 per million the observed rate in this sub-population is 10 TIMES, and taking an annual incidence of 0.7 per million, IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than that in the general population...
 
 
CJD FARMERS WIFE 1989


 
20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A 19 year old died from sCJD in France in 1985. There is no evidence of an iatrogenic cause for those cases....
 
 
THE COVER UP OF MAD COW DISEASE IN FARMERS, FARMERS WIVES, AND VICKY RIMMER, THE DAY MAD COW SCIENCE CHANGED $$$
 
Monday, May 19, 2008
 
*** SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS ***
 
 
DOES ANYONE BESIDES ME SEE A PATTERN YET ???
 
Vickey Rimmer, 16, DID NOT DIE FROM nvCJD, she died from a form of sporadic CJD, whatever the hell that is. and there have been 16 year old die from sporadic CJD in the USA as well.
 
SIMPLY PUT, the ukbsenvcjd only theory was wrong from day one. the elderly are expendable, pets and kids are not.
 
Science was dictated by 'big buisness' after the Vickey Rimmer case with the ukbsenvcjd only myth.
 
and there have been 16 year old die from sporadic CJD in the USA as well.
 
snip...
 
I have interviewed Mrs Rimmer at my constituency surgery
 
IF there is nothing to hide, why is there so much SECRECY? WHY is the Government and other Bodies trying to stop any CHANCE OF PEOPLE CONNECTING THE TWO DISEASES. The B.S.E. problem is obvious, but if the correct measures are taken, surely the problem could be contained, however, as it stands the lack of investigation and interest of the possibility of B.S.E. and C.J.D. being linked is open for speculation and surely someone has to account for peoples lives! WHY is so much trouble being taken to convice people that B.S.E. and C.J.D. are not linked? Guilty Conscience perhaps ? - or cover up?
 
HOUSE OF COMMONS
 
FROM BARRY JONES, M.P.
 
22 FEBRUARY 1994
 
 
Alleged Case of Creutzfeld Jakob Disease: Victoria Rimmer.
 
(now story changes that biopsy shows she does not have CJD...tss)
 
 
now story changes to ;
 
Advice
 
7. The Parliamentary Secretary is invited to note the recent statements made on __________ and the present position which remains that CJD cannot be confirmed, in this case at this stage.
 
 
3. The Medical Director at ___________________ Hospital advised the Department on 6 June that the results of ___________________ brain biopsy had been received and that it showed NO EVIDENCE OF CJD. ______________ Hospital subsequently issued a statement to the press to this effect and this was publicised widely in the press (doc 1). News coverage which followed suggested that the statement made by ________________ Hospital had been misleading (doc 2). Enquires have been made of the Medical Director at _______________ Hospital who has CONFIRMED THAT THE STATEMENT ISSUED BY THE HOSPITAL WAS ISSUED IN ERROR. The facts are that two pathology reports on the same piece of brain tissue were recieved. The first report indicated that CJD was unlikely, The second report indicated that CJD was possible, PERHAPS EVEN LIKELY, but that no definitive diagnosis could be made before a post mortem was undertaken.
 
 
MAD COW MEAL DESTROYED MY DAUGHTERS LIFE
 
A TEENAGE GIRL may have caught the human form of MAD COW DISEASE by eating a contaminated burger it was claimed last night.
 
VICKY RIMMER, 16, has the killer Creutzfeldt-Jakob disease (CJD).
 
 
GIVE ME BACK MY LIFE
 
THEY BEGGED ME TO HUSH IT UP – GRAN’S AGONY
 
 
HUSH UP! GOVERNMENT TOLD GRAN: ''YOU MUST THINK OF THE ECONOMY''
 
 
WHY IS MY GIRL DYING ? '' IT WAS LIKE SOMEBODY OLD INSIDE A YOUNG PERSON'S BODY
 

see Professor Aguzzi on scjd and bse in Switzerland. 





Diagnosis and Reporting of Creutzfeldt-Jakob Disease 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease 

To the Editor: 

In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally. 

Terry S. Singeltary, Sr Bacliff, Tex 

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. 


Tracking spongiform encephalopathies in North America

Xavier Bosch

Published: August 2003


Summary;

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). "I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source."

Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

"Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited". 



26 March 2003 

Terry S. Singeltary, retired (medically) CJD WATCH 

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? 


***> U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 


***> 2001 FDA CJD TSE Prion Singeltary Submission 


2 January 2000 British Medical Journal U.S. 

Scientist should be concerned with a CJD epidemic in the U.S., as well 


15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S. 






















































































































































































































































































































































































































































































































































































Sent: Monday, January 08,2001 3:03 PM

WOW, my submission held up on the www for 17 years, and was proven to be true, and now, it has been removed from the www, the same url does not work anymore and it was just working this year. nothing like the FDA et al cleaning up any evidence of truth with their mad cow debacle and sporadic cjd cover up contineus...so sad$$$

let's review the truth about sporadic cjd shall we;



michigan-sportsman.com and chronic wasting disease science and or your 1st amendment?


michigan-sportsman.com removes thread urls from cwd sound science;





Deer Scents Banned Due To Cwd Transmission

Discussion in 'Wildlife Diseases' started by terry, Apr 26, 2007.
  1. Apr 26, 2007 #1
    terry

    terry

    Messages:
    1,446
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    Location:
    Bacliff, TEXAS USA
    Subject: DEER SCENTS BANNED DUE TO CWD TRANSMISSION
    Date: April 25, 2007 at 7:18 am PST


    Last updated at 4:42 PM on 24/04/07


    Deer scents banned
    Wildlife Act amended to avoid chronic wasting disease


    BY BETH JOHNSTON
    The Daily News

    Nova Scotian hunters will have to leave their deer pee at home.

    In an effort to stop the contagious, lethal Chronic Wasting Disease from hitting Nova Scotian deer and elk, the Department of Natural Resources is banning the use of deer scents which contain deer bodily fluid.

    The disease has been diagnosed in commercial game farms in several states and provinces where the products originate. There are no regulations on the imported scents, which hunters can purchase at WalMart and Canadian Tire.

    Hunters often soak cotton balls in the urine from a doe in heat to attract bucks.

    Chronic wasting disease – a transmissible neurological disease of deer and elk – is a very serious problem in Western Canada and parts of the United States, said Natural Resources wildlife director Barry Sabean.

    “We don’t have it and we don’t want it,” he said.

    (For full story, see Wednesday's edition of The Daily News)


    http://www.hfxnews.ca/index.cfm?sid=24902&sc=89


    BETTER LATE THAN NEVER......TSS








*** SATURDAY, MARCH 03, 2018 ***

*** Michigan-sportsman.com without warning bans terry singeltary sr. for posting peer review sound science on CWD TSE Prion after 16 years ***


you would think, that a Doctor for pete's sake, has more to bring to the table than what Dr. Jim Brauker brought to the table on Michigan-sportsman.com imo, because everything that i stated in that old article, has come to pass, and Dr. Jim Brauker et al don't even get that. now that is frightening, but thanks for posting it anyway, you will figure it out some day...








Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018

Discussion in 'Wildlife Diseases' started by terry, Feb 18, 2018.
Tags: 
Page 1 of 2
  1. Feb 18, 2018#1
    terry

    terry

    Messages:
    1,446
    Likes Received:
    51
    Location:
    Bacliff, TEXAS USA
    Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018

    FRIDAY, FEBRUARY 16, 2018

    Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion

    http://chronic-wasting-disease.blogspot.com/2018/02/wisconsin-deer-from-now-quarantined-pa.html

    FRIDAY, JANUARY 26, 2018

    WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE

    http://chronic-wasting-disease.blogspot.com/2018/01/wisconsin-reports-588-cwd-tse-prion.html

    MONDAY, FEBRUARY 12, 2018

    Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties

    http://chronic-wasting-disease.blogspot.com/2018/02/pennsylvania-cwd-tse-prion-has-been.html

    SATURDAY, FEBRUARY 17, 2018

    Montana Special Hunts 9 more cases CWD TSE Prion to date, more samples still pending

    http://chronic-wasting-disease.blogspot.com/2018/02/montana-special-hunts-9-more-cases-cwd.html

    FRIDAY, FEBRUARY 09, 2018

    Mississippi Chronic Wasting Disease confirmed in a White-tailed Deer

    http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-chronic-wasting-disease.html

    TUESDAY, FEBRUARY 13, 2018

    *** MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations ***

    http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-state-department-of-health.html

    WEDNESDAY, NOVEMBER 22, 2017

    Minnesota Chronic Wasting Disease discovered in Winona County farm

    http://chronic-wasting-disease.blogspot.com/2017/11/minnesota-chronic-wasting-disease.html

    FRIDAY, NOVEMBER 24, 2017

    Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting
    CWD TSE PRION DISEASE risk factors

    http://chronic-wasting-disease.blogspot.com/2017/11/todd-robbins-miller-president-of.html

    WEDNESDAY, JANUARY 24, 2018

    TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE

    http://chronic-wasting-disease.blogspot.com/2018/01/texas-chronic-wasting-disease-cwd-tse.html

    FRIDAY, FEBRUARY 16, 2018

    Texas Deer Breeders Continue fight against the state’s wildlife agency and its regulations trying to contain CWD TSE Prion

    http://chronic-wasting-disease.blogspot.com/2018/02/texas-deer-breeders-continue-fight.html

    WEDNESDAY, FEBRUARY 07, 2018

    New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.

    http://chronic-wasting-disease.blogspot.com/2018/02/new-mexico-bans-all-live-cervid.html

    FRIDAY, FEBRUARY 09, 2018

    Virginia 2017 Hunt Confirms 16 Cases Chronic Wasting Disease CWD TSE Prion

    http://chronic-wasting-disease.blogspot.com/2018/02/virginia-2017-hunt-confirms-16-cases.html

    MONDAY, FEBRUARY 05, 2018

    Nebraska Chronic Wasting Disease CWD TSE Prion 2017 Survey Confirms 203 Positives From 1,807
    Deer Sampled

    http://chronic-wasting-disease.blogspot.com/2018/02/nebraska-chronic-wasting-disease-cwd.html

    SATURDAY, FEBRUARY 03, 2018

    Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018

    http://chronic-wasting-disease.blogspot.com/2018/02/arkansas-reports-346-positive-cwd-tse.html

    THURSDAY, FEBRUARY 08, 2018

    Utah Chronic Wasting Disease CWD TSE Prion Update to date from 2017 Hunting Season

    http://chronic-wasting-disease.blogspot.com/2018/02/utah-chronic-wasting-disease-cwd-tse.html

    TUESDAY, JANUARY 30, 2018

    Colorado Chronic Wasting Disease CWD TSE Prion 7/2015-6/2016 Results (2017?)

    http://chronic-wasting-disease.blogspot.com/2018/01/colorado-chronic-wasting-disease-cwd.html

    THURSDAY, JANUARY 25, 2018

    Ohio Chronic Wasting Disease CWD TSE Prioin aka mad deer update 2016-2017 SEASON SUMMARY

    http://chronic-wasting-disease.blogspot.com/2018/01/ohio-chronic-wasting-disease-cwd-tse.html

    SATURDAY, JANUARY 20, 2018

    Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have
    tested positive for CWD majority of samples collected still are being analyzed

    http://chronic-wasting-disease.blogspot.com/2018/01/pennsylvania-cwd-tse-prion-cases.html

    WEDNESDAY, JANUARY 24, 2018

    Illinois Chronic Wasting Disease CWD TSE Prion cases mounting with 75 confirmed 2017 and 685 total to date

    http://chronic-wasting-disease.blogspot.com/2018/01/illinois-chronic-wasting-disease-cwd.html

    THURSDAY, FEBRUARY 08, 2018

    Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season

    http://chronic-wasting-disease.blogspot.com/2018/02/iowa-dnr-wayne-county-confirms-cwd-with.html

    SATURDAY, FEBRUARY 10, 2018
    Chronic wasting disease management in ranched elk using rectal biopsy testing Research Paper 09 Feb 2018

    http://chronic-wasting-disease.blogspot.com/2018/02/chronic-wasting-disease-management-in.html

    January 14, 2018

    Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases

    http://www.michigan.gov/emergingdiseases/0,4579,7-186-81018_25806-357110--,00.html

    http://chronic-wasting-disease.blogspot.com/2018/01/michigans-chronic-wasting-disease.html

    Michigan UPDATE, see also ;

    Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan
    Contact: Dwayne Etter (DNR), 517-284-4725 or David Williams (MSU), 517-917-0716 Agency: Natural Resources

    Jan. 30, 2018

    Michigan State University and the Michigan Department of Natural Resources will be placing location-tracking collars on white-tailed deer in south-central Michigan as part of a multiyear study of deer disease, including chronic wasting disease.

    http://www.michigan.gov/som/0,4669,7-192-47796-458819--,00.html

    January 14, 2018

    Missouri MDC REPORTS 15 NEW CASES OF CWD TSE Prion in Deer

    http://chronic-wasting-disease.blogspot.com/2018/01/missouri-mdc-reports-15-new-cases-of.html

    MONDAY, JANUARY 29, 2018

    Wyoming, Hanna, WGFD diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 161

    http://chronic-wasting-disease.blogspot.com/2018/01/wyoming-hanna-wgfd-diagnosed-chronic.html

    MONDAY, JANUARY 29, 2018

    North Dakota CWD Confirmed whitetail buck and a mule deer doe 2017 deer gun season from unit 3F2

    http://chronic-wasting-disease.blogspot.com/2018/01/north-dakota-cwd-confirmed-whitetail.html

    TUESDAY, DECEMBER 12, 2017

    *** Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017 ***

    (zoonosis and environmental risk factors towards the bottom, after state by state reports)

    http://chronic-wasting-disease.blogspot.com/2017/12/chronic-wasting-disease-cwd-tse-prion.html

    MONDAY, MARCH 13, 2017

    CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017

    http://chronic-wasting-disease.blogspot.com/2017/03/chronic-wasting-disease-cwd-tse-prion.html

    SATURDAY, JANUARY 14, 2017

    CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017

    http://chronic-wasting-disease.blogspot.com/2017/01/chronic-wasting-disease-cwd-tse-prion.html

    Terry S. Singeltary Sr.
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  3. Feb 24, 2018#2
    ezcaller

    ezcaller

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    Terry I have read only a few of these reports surrounding the Great lakes areas .Have they found any thing different and is anyone cautioning to the dangers of consuming.

  5. Feb 24, 2018#3
    terry

    terry

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    here is what i had on who is cautioning about what with relations to cwd tse prion and zoonosis potential, or has it already happened as sporadic cjd, i have put all recent science on cwd tse prion zoonosis from prion conference 2015, 2016, and 2017 in the Mississippi Health report link, and there was a recent article with a map of the GL area that might help ;

    Surveillance for the disease is ongoing, and DNR added a new nine-township Core CWD Area in Montcalm and Kent counties in late 2017.

    [​IMG]

    Deer check stations in Michigan. Image: Michigan Department of Natural Resources.



    Also, the confirmation of CWD in a free-ranging deer from Montcalm County last September led to the mandatory testing of heads for all deer harvested by hunters within 72 hours and within 5 miles of the core area.

    “We continue to test deer from portions of Montcalm and Ionia counties that were harvested during the special January deer season,” Niewoonder said. “There are at least 34 deer from Montcalm County that are either confirmed or suspected CWD-positive from this past deer season.”


    http://greatlakesecho.org/2018/02/02/michigan-cranks-up-testing-deer-for-chronic-wasting-disease/

    http://www.michigan.gov/emergingdiseases/0,4579,7-186-76711_78204-357110--,00.html


    see; *** (4) CWD transmission to humans has already occurred.


    ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE ???

    here is the latest;

    Cervid to human prion transmission

    Kong, Qingzhong

    Case Western Reserve University, Cleveland, OH, United States

    Abstract

    Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that:

    (1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;

    (2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;

    (3) Reliable essays can be established to detect CWD infection in humans;and
    *** (4) CWD transmission to humans has already occurred.

    We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.

    Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3.

    Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
    Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.

    Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
    Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
    Funding Agency Agency National Institute of Health (NIH)

    Institute National Institute of Neurological Disorders and Stroke (NINDS)
    Type Research Project (R01)
    Project # 1R01NS088604-01A1
    Application # 9037884
    Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
    Program Officer Wong, May
    Project Start 2015-09-30
    Project End 2019-07-31
    Budget Start 2015-09-30
    Budget End 2016-07-31
    Support Year 1
    Fiscal Year 2015
    Total Cost $337,507
    Indirect Cost $118,756
    Institution
    Name Case Western Reserve University
    Department Pathology
    Type Schools of Medicine
    DUNS # 077758407
    City Cleveland
    State OH
    Country United States
    Zip Code 44106

    http://grantome.com/grant/NIH/R01-NS088604-01A1 http://grantome.com/grant/NIH/R01-NS088604-01A1

    see what Mississippi Health, CDC, and Canada Health et al, and more are saying here ;

    TUESDAY, FEBRUARY 13, 2018

    MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations

    http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-state-department-of-health.html



    kind regards, terry
    357Maximum and ezcaller like this.
  6. Feb 25, 2018#4
    ezcaller

    ezcaller

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    Thank you!Ted Rize
  7. Feb 25, 2018#5
    otcarcher

    otcarcher

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    Proof positive of the lengths one will go to link sporadic CJD with CWD, when no such link exists....anywhere. Fear-mongering anti-meat agenda, pure and simple. This "Crusade" of yours started by trying to link cattle to sporadic CJD. When that failed, you moved on to deer and CWD. Your agenda-driven history is well known and well documented in multiple other states. Michigan is just next on your list, until people here wise up to your agenda as well.
    Last edited: Feb 25, 2018
  8. Feb 25, 2018#6
    terry

    terry

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    otcarcher, you are either not paying attention, or your just oblivious to science, or just another person from the industry (take your pick) that likes to pass fake news/science, either way, i don't care, the science speaks for itself, and anyone with any kind of brain can see for themselves, and make their own minds up. as i said before, go to pubmed and search the word sporadic or spontaneous, and there is a laundry list of different diseases linked to both, simply meaning they don't know. sporadic alone hits 51329 hits, see;

    https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic

    BUT now, science has shown that indeed BSE, Scrapie, and CWD, can and has been linked to sporadic spontaneous creutzfeldt jakob disease sCJD by peer review studies, by scientist. but to have a Government admit that in print has not happened yet. with nvCJD to BSE it took 10 years and the science was staring them in the face, as now CWD TSE Prion in cervid. i just posted all the latest peer review science here, no advertisements, not making any money from this, it's just science, for those that want see for themselves, all the source links are there, it's just science, don't be scared, make your own minds up for Petes sake, or, just take old otcarcher, post: 6656454, member: 103301 word for it...LMAO!

    2014

    ***Moreover, L-BSE has been transmitted more easily to transgenic mice overexpressing a human PrP [13,14] or to primates [15,16] than C-BSE.

    ***It has been suggested that some sporadic CJD subtypes in humans may result from an exposure to the L-BSE agent.

    *** Lending support to this hypothesis, pathological and biochemical similarities have been observed between L-BSE and an sCJD subtype (MV genotype at codon 129 of PRNP) [17], and between L-BSE infected non-human primate and another sCJD subtype (MM genotype) [15].

    snip...

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4213560/pdf/viruses-06-03766.pdf

    Title: Transmission of scrapie prions to primate after an extended silent incubation period)
    *** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.

    *** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
    *** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

    http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160

    Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.

    Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.

    These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

    http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

    *** WDA 2016 NEW YORK ***

    *** We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.

    Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders

    http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf

    http://bovineprp.blogspot.com/2017/12/

    http://bse-atypical.blogspot.com/2010/09/atypical-bse-strains-and-sporadic-cjd.html

    http://prionunitusaupdate.blogspot.com/2017/07/why-us-needs-to-continue-prion-disease.html

    http://bse-atypical.blogspot.com.ar/2017/07/usda-oie-alabama-atypical-l-type-base.html

    Sunday, February 25, 2018

    PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW

    http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html

    p.s., but don't forget from day one what BSE Inquiry scientist said;

    Volume 2: Science

    4. The link between BSE and vCJD

    1 Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrPSc found in vCJD. It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people.

    kind regards, terry
    357Maximum likes this.
  9. Feb 25, 2018#7
    otcarcher

    otcarcher

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    Complete nonsense, Terry. In order for CWD to cause sporadic CJD in humans, it would have to jump the species barrier. There is no evidence of such occurrence anywhere. This is simply more of your unsubstantiated cut and paste fear-mongering anti-meat agenda from a high-school dropout. I understand the science. I have a degree in it.
  10. Feb 25, 2018#8
    noshow

    noshow

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    I see that news channel 3 Iteam is running a special tomorrow night about cwd here in Michigan. It's called fear of infection. Should be interesting.
  11. Feb 25, 2018#9
    357Maximum

    357Maximum

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    Thank You for posting the info. Too bad those that would rather stick their head in the dirt and treat CWD as just a distraction to protect their almighty trophy antler obsession give you so much grief over it. If I ever shoot a deer with CWD I know exactly who I am offering the steaks to, I am sure he would gladly eat a plate full of it seeing as how it is of no concern to him. :lol: Some of us are smart enough to realize Mother Nature finds a way, some of us are blinded by the bones on a deer's head and cannot see that unfortunately. That is what it is I suppose but it is not too hard to see who has the agenda here...so again I thank you for keeping us up to date on this topic. Some of us learned early on that Mother Nature is out to kill us all....others well they would rather pretend all is right in the world if it means they get bigger antlers. I really wonder if some of the big antler guys with an agenda have ever eaten a piece of venison. :sad:
  12. Feb 25, 2018#10
    otcarcher

    otcarcher

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    I'm not sticking my head in the sand at all. I want to see the discussion to remain factual instead of anti-meat agenda driven nonsense. He's attempted to blame the meat industry by connecting cattle to sporadic CJD since the 90's when it took his mom. This discussion has nothing to do with antlers Maxi. It's about sticking with facts, not BS.
  13. Feb 25, 2018#11
    357Maximum

    357Maximum

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    I don't believe you, and I feel your intentions are not genuine, not in the least, deal with it. It is my right to feel that way going from the evidence presented to me over the last couple of years...like I said...deal with it. The possibilities for critters both big and small to morph/evolve is very real. The proof is all around us, the fact that you would rather ignore this just for a few more inches of bone tells me all I need to know. The fact you get away with constantly insulting this man is also a bit beyond belief. I do not allow that type of behavior on my forum, but I do not control this one.........lucky for you. I knew it was a mistake taking you off ignore. I will go fix that mistake now...so please feel free to type away.
  14. Feb 25, 2018#12
    otcarcher

    otcarcher

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    Who is Terry Singletary? Look for yourself. You don't have to believe me. I couldn't care less. This is but one example of hundreds Maxi. You want more?

    https://www.consumerfreedom.com/articles/138-mad-cow-scaremongers/

    I'm not making this up. It has zero to do with antlers.

    Additionally, I've already sent Steve other links to support my statements. His to choice to share or not. This agenda of Terry's started in Texas, then spread from there.
  15. Feb 26, 2018#13
    terry

    terry

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    otcarcher, post: 6656883, member: 103301, like i said before, sadly, you have nothing, you and your industry have nothing but rhetoric. everything i said back in the old article has come to pass, and you still just can't figure that out, so please, keep posting it. but for others, this link below will explain who they are.

    let's take a closer look shall we ;

    The Center for Consumer Freedom (CCF) (formerly called the "Guest Choice Network (GCN)") is a front group for the restaurant, alcohol and tobacco industries. It runs media campaigns which oppose the efforts of scientists, doctors, health advocates, environmentalists and groups like Mothers Against Drunk Driving, calling them "the Nanny Culture -- the growing fraternity of food cops, health care enforcers, anti-meat activists, and meddling bureaucrats who 'know what's best for you.'"

    CCF is registered as a tax-exempt, non-profit organization under the IRS code 501(c)(3). Its advisory board is comprised mainly of representatives from the restaurant, meat and alcoholic beverage industries.

    http://www.sourcewatch.org/index.php?title=Center_for_Consumer_Freedom

    http://en.wikipedia.org/wiki/Center_for_Consumer_Freedom

    SNIP...SEE FULL TEXT AND MORE HERE

    http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html

    http://madcowusda.blogspot.com/2014/09/mad-cow-scaremongers-consumerfreedomcom.html

    otcarcher, post: 6656883, member: 103301, you and your cervid captive farming industry buddies bring nothing but rhetoric to the table. that is why you are a big part of the problem, and will continue to be so imo. especially if they have you as a spokesperson...LOL!


    Sunday, February 25, 2018

    PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW

    http://prionconference.blogspot.com/2018/02/prion-round-table-conference-2018-may.html


    terry
  16. Feb 26, 2018#14
    otcarcher

    otcarcher

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    Yea, you said the same thing in Texas and Iowa too. Antlers had nothing to do with them calling you out either. Your anti-meat agenda has spread from Texas to the the North. It's now Michigan's turn to be exposed to your absolute nonsense. You had one goal from the start, to link meat to the death of your loved one . You couldn't link cattle, now you're moving to deer and venison. What better way to end hunting than to instill fear in hunters that meat will kill them. 

    And the fear-mongering continues in your recent ramblings trying to link sCJD with CWD. It doesn't exist. Not according to the CDC, or the WHO, or the Neurological Institutes of various states. You'll post links ad nauseum but completely ignore the 10 other studies that refute it. You aren't looking for a factual conversation, you're looking for a scapegoat.

    But hey, maybe if you cut and paste enough nonsense you know absolutely zero about, you'll succeed in blaming venison where you failed in blaming cattle.
    Last edited: Feb 26, 2018
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  17. Feb 27, 2018#15
    bioactive

    bioactiveTornado JimPremium Member

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    So this is Terry Singletary? While I feel for his loss due to CJD he has shown himself over the years to be a shrill alarmist who works tirelessly to frighten people without any sound science behind his rants.











God help the great state of Michigan with CWD TSE Prion, and all it's fair chase hunters...terry




Terry S. Singeltary Sr.


posted by Terry S. Singeltary Sr. at 3:34 PM

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