Pennsylvania BUSY TIME FOR CWD SURVEILLANCE WINDING DOWN 01/29/2021
Pennsylvania BUSY TIME FOR CWD SURVEILLANCE WINDING DOWN 01/29/2021
BUSY TIME FOR CWD SURVEILLANCE WINDING DOWN 01/29/2021
HARRISBURG, PA - The Pennsylvania Game Commission monitors the effects of chronic wasting disease (CWD) year-round, but the most intense surveillance efforts coincide with Pennsylvania’s deer hunting seasons. With those seasons now closed, the public can begin to view the results of these efforts on the CWD Surveillance Dashboard, which is available online at https://pgcdatacollection.pa.gov/CWDResultsLookup.
The CWD Surveillance Dashboard is updated weekly and features an all-new way to view past and current information related to the disease. This includes data organized by season, species (white-tailed deer or elk), age, collection method, sex and collection site (down to the township level). It also allows hunters who submitted their deer for CWD testing to directly access results online.
A tutorialOpens In A New Window on how to navigate the Dashboard is available at the Game Commission’s YouTube channelOpens In A New Window.
Since July 1, 2020, the Game Commission has collected more than 11,000 CWD samples from white-tailed deer. Hunters across three Disease Management Areas (DMAs) submitted almost 5,700 of those samples. Additionally, more than 3,100 CWD samples were collected statewide from processors. Given the volume of samples, several thousand are still pending analysis.
“As part of the Game Commission’s CWD Response Plan, we asked hunters to assist with CWD surveillance efforts by submitting their harvested deer’s head for testing,” said Game Commission CWD Biologist Andrea Korman. “Thousands of hunters participated in this effort and we are thankful for their help.”
The Game Commission’s CWD Response Plan was adopted by the Pennsylvania Board of Game Commissioners last summer and was developed in collaboration with Pennsylvania stakeholders, CWD experts from state and federal wildlife agencies and non-government organizations from across the country. It is available to view online at www.pgc.pa.gov/cwd.
One of the agency’s goals, as outlined in the CWD Response Plan, is to determine the extent of CWD infection in areas around a new detection that is at the leading edge of disease expansion. There were eight specific areas where Deer Management Assistance Program (DMAP) units were strategically created, all of which surround specific locations where a deer that tested positive for CWD had recently been identified.
Hunters in those eight DMAP units were offered additional antlerless tags to help meet surveillance goals. Increasing surveillance in these areas helps to determine if the infected deer was the beginning of, or a symptom of, an established infection. Results from these efforts also guide future management actions in each of the areas, on a case-by-case basis.
In addition to the DMAP units, last fall, the Game Commission selected two specific areas as Containment Zones (CZ). These zones are small areas – about a 1-mile radius, or the average size of a deer’s home range – around the location of an outlying CWD-positive deer.
Landowners and hunters within CZs are given more opportunities to remove deer that may have been in contact with the infected deer. Special regulations and extended hunting seasons were provided to cooperating landowners and hunters. The Game Commission will continue to work with landowners to reduce the risk of CWD establishing in, and spreading from, the immediate area(s) surrounding the initial CWD detections.
Most of the deer that tested positive for CWD in the 2020-21 hunting seasons continue to be from DMA 2, located in southcentral Pennsylvania. Specifically, they have been concentrated in Bedford, Blair and Fulton counties, which the Game Commission refers to as an Established Area (EA). This area has produced nearly 90 percent of Pennsylvania’s CWD positives since it was first detected here in 2012.
“Unfortunately, CWD is well-established in DMA 2, based on the number of positive cases we continue to detect,” said Korman. “DMAP units and containment zones are management efforts the agency is employing to slow the spread of CWD and prevent new areas of the state from becoming EAs. Research has shown that once CWD sampling prevalence rates exceed 5 percent, infections can increase rapidly. This 5 percent appears to be a tipping point. Last year, almost 6 percent of the whitetails tested for CWD in the EA were found to be positive. Lessening that sample prevalence rate in the EA is a top priority.”
The Game Commission’s next steps are to take collected CWD data and use it to create a broader CWD Management Plan. This plan will determine which management actions have been most effective in the past and which ones remain most appropriate to achieve optimum results in Pennsylvania.
“The Game Commission remains focused on doing what is best for Pennsylvania’s deer herd, which in turn ensures sustainable hunting opportunities for current and future generations,” said Korman. “We appreciate the continued support of hunters and the public. We especially thank hunters for their efforts. Hunting has been a large part of our management plans and will continue to be moving forward.”
More information about CWD in Pennsylvania, including access to the new CWD Surveillance Dashboard and the CWD Response Plan, is available online at www.pgc.pa.gov/cwd.
MEDIA CONTACT: Travis Lau - 717-705-6541
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SCRAPIE PENNSYLVANIA, WHERE 3 DOCUMENTED CASES OF ATYPICAL NOR98 SCRAPIE HAVE BEEN DETECTED TO DATE, AND UPDATE ON PA SCRAPIE OUTBREAK IN 2018, SEE FURTHER DOWN...TSS
Sent: Sun, Jan 24, 2021 11:50 am
Subject: Pennsylvania CWD TSE Prion 2021
Pennsylvania WILDLIFE AGENCY 2019 ANNUAL REPORT
Managing the Spread and Prevalence of Chronic Wasting Disease
As part of the agency’s ongoing Chronic Wasting Disease surveillance, the Game Commission collects samples from deer harvested across the state to test for Chronic Wasting Disease (CWD). Within the state’s disease management areas (DMAs)—areas where CWD has been detected in captive or free ranging deer—intensified sampling occurs. Additional surveillance efforts include sampling road-killed deer, clinical suspects, and escaped captives.
During the 2018-19 deer hunting seasons, the Game Commission offered free CWD testing for hunters harvesting deer within DMAs. This provided the Game Commission with more samples to better understand the extent of the disease.
In 2018, the Game Commission tested 9,631 deer for CWD, of which 123 tested positive. The majority of these positives were detected within DMA 2, however, the discovery of two new cases—outside of DMA 2—in Juniata and Perry counties, resulted in a 2,101-square-mile expansion of DMA 2. In addition, one positive was detected in wild deer in DMA 3, which resulted in the expansion of DMA 3. CWD is not a new disease; it is currently detected in 26 states and three Canadian provinces. It was first detected in Pennsylvania in 2012 in a captive deer facility in Adams County. Shortly after, it was detected in three free-ranging deer in Bedford and Blair counties.
The escalating number of CWD detections and the emergence of this disease in new parts of the state should put all Pennsylvanians on guard to the threat that CWD poses, and the disease’s potential to have damaging impacts on Pennsylvania’s deer and deer-hunting tradition.
The Game Commission continues to monitor CWD throughout the Commonwealth to find and manage the disease where it exists. CWD is spread through direct or indirect contact, with prions (misfolded proteins) shed in saliva, urine, and feces of infected animals. This disease attacks the brains of infected deer and elk inevitably leading to death. There is no approved live-animal test for CWD and there is no known cure. While there is no evidence that CWD can be transmitted to humans, it is recommended humans avoid consuming meat from CWD-infected animals.
For more information on CWD, regulations pertaining to CWD, and options for hunters to get their deer tested, visit the Chronic Wasting Disease page of the Game Commission’s website, http://bit. ly/PGC-CWD or call 1-833-INFOCWD.
Boundaries of disease management areas as of December 2019 when this report went to print. Boundaries may change depending on the location of new CWD-positive deer. The locations of CWD services including cooperating processors and taxidermists, high-risk parts dumpsters, and head collections containers for testing are available at http://bit.ly/PGC-CWD.
GAME COMMISSION DELIVERS ANNUAL REPORT TO LEGISLATURE 03/03/2020
HARRISBURG, PA - Pennsylvania Game Commission Executive Director Bryan Burhans today presented the agency’s annual report to the General Assembly, and delivered testimony before the House Game and Fisheries Committee.
To view a copy of the agency’s annual legislative report, please visit the Game Commission’s website, www.pgc.pa.gov, put your cursor on “Information & Resources” in the menu bar under the banner on the homepage, then select “Media & Reports & Surveys” in the drop-down menu, then click on the 2019 Annual Legislative Report.
Burhans’ testimony before the House Game and Fisheries Committee follows:
Good morning, Chairman Gillespie, Chairman Kortz, and members of the House Game & Fisheries Committee.
I am Bryan Burhans, Executive Director for the Pennsylvania Game Commission.
It is my pleasure to appear before you today to deliver the annual report of the Pennsylvania Game Commission for the 2018 – 2019 fiscal year.
To offer you a closer look at the agency’s operations, I brought along hard-copy annual reports to acquaint you with our responsibilities and accomplishments.
I’d like to begin by discussing our law-enforcement efforts. As you know, our State Game Wardens often are “the face” of the Game Commission, serving on the front line, enforcing the laws and regulations that protect the Commonwealth’s wildlife.
During the previous fiscal year, game wardens issued approximately 9,500 warnings and 6,800 citations.
Graduating a new class of wardens in February of 2019 helped expand our coverage: the agency experienced an increase of approximately 6,000 law enforcement contacts in 2019 as a result of these newly filled warden positions.
That trend should continue. We just enrolled a new class of 34 cadets into the Ross Leffler School of Conservation and are currently testing for a class to take place next year. The reason for running back-to-back classes is to fill empty districts and projected retirements.
I would like to thank the Committee, and in particular, Chairman Gillespie, for working to pass Act 52 of 2019, which finally provided our game wardens with the same retirement benefits received by other state law-enforcement officers.
This crucial piece of legislation gives our officers more flexibility in career decisions in a line of work that is both mentally and physically challenging. They’ve earned this privilege, but it wasn’t possible without your commitment to them. Thank you.
Our state game lands system remains one of the finest networks of public hunting lands and managed wildlife habitat in the country.
Wildlife’s future is tied directly to habitat. Without it, neither wildlife nor hunters will have places to go. That’s why game lands are so important; they ensure the very existence of wildlife and provide Pennsylvanians more than 1.5 million acres of game lands to pursue hunting, trapping, and wildlife viewing.
This past fiscal year, the Commission added over 6,000 acres to the game lands system, this includes 3 indentures, 7 acquisitions to improve access to existing game lands, and 2 properties that contain areas of sensitive habitats for species of greatest conservation need.
Since the law was changed to allow for greater use of prescribed fire, the Game Commission has used this tool to better manage habitat on game lands, and last year over 8,000 acres were treated. This acreage would have been much higher, but we were hindered by wet weather during peak times when we conduct prescribed fire.
In addition, another 8,000 acres of forested habitat was harvested to make room for young forestland, which benefits countless wildlife including our state bird the ruffed grouse.
Wherever possible, the Commission leverages timber harvests to improve game land infrastructure, so our license-buyers can experience an immediate benefit. Last fiscal year we used services in lieu of payment from timber sales to generate 118 miles of improved roads, 157 new culverts, 3 new stream crossings, and 11 new or improved parking lots.
One of the biggest threats that wildlife continues to face is that of emerging diseases.
At the forefront is the continued spread of Chronic Wasting Disease, or CWD, which threatens the future of our wild deer herd, our hunting heritage, and the state’s $1.6 billion industry tied to hunting.
The Game Commission continues to monitor CWD throughout the Commonwealth to uncover and manage the disease wherever it exists.
In 2018-19, the Game Commission tested 9,631 deer for CWD, of which 123 tested positive. The majority of these positives were detected within DMA 2. However, the discovery of two new cases—outside of DMA 2—in Juniata and Perry counties, resulted in a 2,101-square-mile expansion of DMA 2. In addition, one positive was detected in wild deer in DMA 3, which resulted in the expansion of DMA 3, and deer in a captive facility in Lancaster County tested positive resulting in the creation of DMA 4.
In order to better inform hunters about CWD rules and regulations, we once again provided free copies of the Hunting and Trapping Digest to all license buyers.
In the summer of 2019, the Commission made available a draft CWD management plan for areas with CWD. The plan proposes a variety of management options, including increased tags, longer seasons, removing antler restrictions, and using targeted removals.
The plan was made available for public input, and we currently are reviewing public comments and finalizing the plan. The Board of Commissioners will then consider implementing management options in those areas where CWD exists.
To better manage CWD and other diseases affecting wildlife, during the summer of 2019 we announced the creation of a new partnership between the Game Commission and the University of Pennsylvania School of Veterinary MedicineOpens In A New Window called the Pennsylvania Wildlife Futures Program.
This program, established with $11 million in funding over five years from the Commission, charts a way forward for protecting wildlife from health threats, both current and future.
The program enables the School of Veterinary Medicine to hire new staff dedicated to wildlife health who will work with Game Commission employees to monitor disease threats, develop research, enhance communication and public engagement around wildlife health issues, and proactively respond to challenges as they arise.
With the support of the Pennsylvania Animal Diagnostic Laboratory System, the Wildlife Futures program resulted in immediate benefits to our hunters this year who submitted samples for CWD testing. This year, the wait time for results decreased dramatically and we were able to provide hunters with information on whether their deer tested positive for CWD in an average of 16 days; we hope to narrow this time frame further next year down to an average of 14 days.
While a majority of the program’s attention in the immediate future will focus on assisting the Game Commission in responding to CWD, that is far from the only challenge the Wildlife Future’s program will tackle.
White-nose syndrome, for one, has decimated the state’s bat population since it was first detected in Pennsylvania in 2008. Game Commission bat biologist Greg Turner is renowned for his years of research into the disease, and his efforts to analyze and minimize cave bat exposure to the disease. The Wildlife Futures partnership will lend even more support to those efforts.
And we are hopeful that the Wildlife Futures program can further the research of Commission biologist Lisa Williams, whose studies have identified West Nile virus as a major threat to Pennsylvania’s state bird, the ruffed grouse. Williams’ discovery has helped many other states in their efforts to identify an important contributing factor to ruffed grouse population declines. I note that grouse populations are being impacted by both West Nile virus, and the fact that much of our state’s forests are older. The Game Commission’s system of game lands only represents 5% of the state’s total land area. There is only so much the Game Commission can do to affect the state-wide grouse population through habitat management.
Other current disease threats, from mange in black bears and lead poisoning in bald eagles to rabies in raccoons and beyond could receive additional research attention and diagnostic support through the program in years to come.
Financially, the agency continues to do well from revenue increases from oil and gas operations on state game lands. As of the close of last fiscal year, the Game Fund’s Restricted Fund Balance was $88,666,123. This is an increase in almost $16 million over the previous year.
Also regarding finances, you may recall last summer the Auditor General released the results of a Game Commission financial audit covering July 1, 2014 through June 30, 2017.
Notably, the audit found no money was lost, nothing was stolen, and nothing was unaccounted for regarding PGC’s finances.
And even though the audit was centered on those years in question, the headlines in the days and weeks to follow focused on the amount held in our reserve fund, the details of which have always been available to the public; these numbers are published annually in Game News.
The Commission was criticized by the Auditor General for having an amount that he considered to be “too large.” However, the actual audit report stated that “the audit does not evaluate or make judgement as to whether any part of the Game Fund balance should or should not be used, or what amount of the fund balance reserve is appropriate.”
Given the volatility of market-driven revenue sources, such as oil, gas, and timber, and the fact the agency receives no general fund revenues from the state, maintaining a healthy reserve is critical for the agency to provide services expected by the public. Not only do these reserves allow us to provide public services during years when the agency is experiencing declines in revenue, these reserves allow us to make strategic investments. For example, if our Wildlife Futures program develops a new tool to help us manage CWD, these reserves allow us have funds available without reducing services.
Nonetheless the audit did shed some light on ways to improve our operations, which is the purpose of an audit.
In response to a recommendation provided by the audit, we also began reporting funds held in escrow alongside our fiscal year revenue and expenditures. Moving forward, we are working to implement other improvements related to the audit findings. In addition, we are currently developing our next strategic plan to better tie together the plan’s goals with the costs of achieving them, as recommended by the audit.
With the passage of Act 107 in November of last year, the Commission will undergo another audit later this year by the Legislative Budget and Finance Committee. We welcome this review and look forward to working with the Legislative Budget and Finance Committee.
And back to wildlife; Pennsylvania hunters continue to enjoy some of the best hunting in the agency’s history.
The effectiveness of our deer-management plan continues to translate into great deer hunting, with Pennsylvania ranking at or near the top nationally for an array of categories, including number of antlered deer harvested, number of antlered deer per square mile harvested, antlerless harvest, and antlerless harvest per square mile. Huge bucks are being taken everywhere across the state, as evidenced by the increase of entries to the Big Game Record Book.
Black bear hunting also has never been better, as demonstrated by 2019’s record black bear harvest and increased bear hunting opportunities.
The turkey population is robust, providing great opportunities for both fall and spring turkey hunters. In 2019, Pennsylvania hunters had a perfect safety record in the spring turkey season. For the first time ever, we had no hunting-related shooting incidents reported during the month-long spring season. We credit this to the effectiveness of the Hunter-Trapper Education training course and our dedicated team of Hunter-Trapper Education Instructors who volunteer their time to train new hunters.
The pheasant program continues to provide great opportunities for those who purchase a permit, as we continue to stock over 200,000 birds each fall.
The elk herd draws hundreds of thousands of visitors each year. New archery and antlerless elk seasons were added in 2019 and those lucky enough to be drawn for a tag can experience the hunt of a lifetime, pursuing bulls that consistently rank as world-class trophies.
Title 34 of the Game and Wildlife code, section 322, subsection c 13 defines one of our agency’s duties to “Serve the interest of sportsmen by preserving and promoting our special heritage of recreational hunting and furtaking by providing opportunity to hunt and trap the wildlife resources of this Commonwealth.” We are proud of the opportunities we can provide our license buyers to enjoy our wildlife resources. It’s a credit to sound wildlife management, vigorous law enforcement, and active habitat management.
Finally, I would like to add that 2020 represents an important year for the Pennsylvania Game Commission. It is the agency’s 125th anniversary as well as the 100-year anniversary of the creation of our game lands system. We will be celebrating both events throughout the year, and asking hunters, trappers, and those who care about wildlife to commemorate these milestones with us.
These occasions provide the opportunity to remember that the current conditions which we sometimes take for granted - thriving wildlife populations, world class hunting opportunities, and over 1.5 million acres of public hunting land - didn’t just happen, but rather they are the product of 125 years of foresight, planning, and hard work by Game Commission employees and our Board of Commissioners.
Working with these employees as their executive director has given me the opportunity to see the extent to which they are devoted to fulfilling the agency’s mission of managing our Commonwealth’s wildlife resources. The Game Commission is blessed to have a hard-charging workforce of full-time and part-time employees and volunteers. Compared to other Commonwealth agencies the Game Commission is small, but our impact has been substantial.
To help celebrate the work that has taken place over the last 125 years, I would like to take this opportunity to show a video that highlights the history of the Game Commission and discusses some of the challenges that we currently face.
At the conclusion of the video I will be happy to answer any questions you might have.
MEDIA CONTACT: Travis Lau - 717-705-6541
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Pennsylvania 2018 cwd
Managing the Spread and Prevalence of Chronic Wasting Disease As part of the agency’s ongoing Chronic Wasting Disease surveillance, the Game Commission collects samples from deer harvested across the state to test for Chronic Wasting Disease (CWD). Within the state’s disease management areas (DMAs) — areas where CWD has been detected in captive or free-ranging deer — intensified sampling occurs. Additional surveillance efforts include sampling road-killed deer, clinical suspects, and escaped captives.
During the 2017-18 deer hunting seasons, the Game Commission offered free CWD testing for hunters harvesting deer within disease management areas. This provided the Game Commission with more samples to better understand the extent of the disease.
In 2017, the Game Commission tested 7,911 deer for CWD, of which 79 tested positive. The majority of these positives were detected within DMA 2; however, three positives were detected in free-ranging deer in DMA 3. As of June 30, 2018, the Game Commission tested an additional 1,367 deer for CWD since the beginning of the year, of which 27 tested positive. All 27 positives were detected in DMA 2.
CWD is not a new disease; the disease is currently detected in 25 states and three Canadian provinces. It was first detected in Pennsylvania in 2012 in a captive deer facility in Adams County. Shortly after, it was detected in three freeranging deer in Bedford and Blair counties. As of June 30, 2018 a total of 157 free-ranging deer had tested positive for CWD in Pennsylvania. The Game Commission continues to monitor CWD throughout Pennsylvania to find and manage CWD where it exists. CWD is spread through direct or indirect contact, with prions (misfolded proteins) shed in saliva, urine, and feces of infected animals. This disease attacks the brains of infected deer and elk inevitably leading to death. There is no approved live-animal test for CWD and there is no known cure. While there is no evidence that CWD can be transmitted to humans, it is recommended humans avoid consuming meat from CWD-infected animals.
For more information on CWD, regulations pertaining to CWD, or options for hunters to get their deer tested, visit the Chronic Wasting Disease page of the Game Commission’s website, http://bit.ly/PGC-CWD.
Pennsylvania 2017 CWD
The Pennsylvania Game Commission collects samples from deer harvested across the state and tests them for chronic wasting disease (CWD), as part of the agency’s ongoing CWD surveillance. Within the state’s Disease Management Areas — where the disease has been detected in captive and free-ranging deer — intensified sampling occurs.
During the 2017-18 deer hunting seasons, the Game Commission offered free CWD testing for hunters harvesting deer within Disease Management Areas (DMAs). Free testing offered hunters a way to have their deer tested prior to consuming it, and it provides the Game Commission with additional samples to better pinpoint areas where the disease exists, so specific problem spots might be addressed.
Successful hunters within DMAs dropped off heads from more than 1,500 deer in head-collection containers. Game Commission staff collected more than 3,000 other samples within DMAs. In total, nearly 8,000 samples were collected statewide. Slightly more than 5,700 whitetails were tested for CWD in 2016; 25 tested positive, all were in or near DMA 2, the only area of the state where CWD has been detected in the wild.
By mid-January 2018, 51 deer from 2017 had tested positive for CWD; all have been within the DMAs. Forty-eight were within DMA 2, in southcentral Pennsylvania; and three were within DMA 3 in northcentral Pennsylvania. The majority of samples collected had yet to be analyzed at the time of this report.
The agency continues to assess test results to evaluate the best response to confront CWD where it exists. DMA boundaries regularly have been adjusted in relation to newly detected CWD-positive animals. During 2017, the Game Commission partnered with the U.S. Department of Agriculture’s APHIS’s Wildlife Services on a CWD surveillance effort where 30 deer were removed by sharpshooters, one of which tested positive for chronic wasting disease.
Attempting to control hot spots and remove animals with a greater likelihood of carrying the disease is the agency’s best chance at managing CWD on a larger scale, while minimizing the impact on the larger deer population or diminishing deer hunting opportunities. CWD is not a new disease, and other states have decades of experience dealing with CWD in the wild. It first was detected in Pennsylvania in 2012 at a captive deer facility, and it was detected in free-ranging deer soon after. By January 2018, in Pennsylvania, CWD had been detected in 98 free-ranging deer.
CWD is spread from deer to deer through direct and indirect contact. The disease attacks the brains of infected deer, elk, and moose, and will eventually result in the death of the infected animal. There is no live test for CWD and no known cure. There also is no evidence CWD can be transmitted to humans, however, it is recommended the meat of infected deer — or deer thought to be sick — not be consumed.
For more information on CWD, the rules applying within DMAs, or what hunters can do to have harvested deer tested for CWD, visit the Game Commission’s website, www.pgc.pa.gov. Information can be found by clicking on the button titled “CWD Information” near the top of the homepage.
Pennsylvania 2016 CWD
DMA 2 expansion continues as a result of new cases
Chronic wasting disease (CWD) is a fatal neurological disease of cervids that poses a serious threat to Pennsylvania’s deer and elk populations, and to the future of hunting. CWD continues to be a problem in wild deer in southcentral Pennsylvania. Sampling during the past year, has not detected CWD in any new areas of the state.
Pennsylvania’s first positive test for CWD was returned in 2012. The disease has since been identified in three areas of the state referred to as Disease Management Areas (DMAs): a captive cervid facility in Adams County during 2012 (DMA 1); multiple free-ranging deer in Blair, Bedford, and Fulton counties between 2012 and 2016 (DMA 2); and two captive facilities in Jefferson County during 2014 (DMA 3).
The Game Commission issued executive orders following the first detection to establish regulations to manage the spread of CWD and to intensify surveillance. The orders continue to be updated as new information becomes available. The CWD-positive captive cervid facilities in Adams and Jefferson counties were depopulated and remain under quarantine enforced by the Pennsylvania Department of Agriculture. Despite intensive surveillance, CWD has not been detected in wild deer in either of those counties. Unfortunately, new cases of CWD continue to be detected in wild deer in and around DMA 2.
By the end of 2016, 28 wild white-tailed deer had tested positive for CWD within DMA 2, and the boundaries of DMA 2 had been expanded four times based on the identification of new positives, leaving the DMA at 2,846 square miles and encompassing parts of Bedford, Blair, Cambria, Clearfield, Franklin, Fulton, Huntingdon, and Somerset counties. Deer continue to be sampled statewide with enhanced sampling efforts within the DMAs. About 6,000 samples were collected for CWD testing during 2016 representing the greatest number of samples collected in any single year within Pennsylvania. Final test results for 2016 are expected in March 2017. Chronic wasting disease has not been detected in wild Pennsylvania elk.
Pennsylvania 2015 CWD
DMA 2 expanded as a result of new cases
Chronic Wasting Disease (CWD) poses a serious threat to Pennsylvania’s white-tailed deer population and to the future of deer hunting and wildlife management.
CWD is an always-fatal prion disease affecting the brain and central nervous system of white-tailed deer and elk. It was first found on a captive deer farm in Adams County in 2012 (DMA 1) and on two captive deer farms in Jefferson County in 2014 (DMA 3). Since 2012, seventeen free-ranging wild deer from Bedford, Blair, and Fulton counties have tested positive for CWD (DMA 2). Seven of which were in the past year.
The Pennsylvania Game Commission has issued Executive Orders establishing boundaries and regulations for these three Disease Management Areas (DMAs) including a ban on movement of highrisk deer parts from these areas as well as an enhanced monitoring program. The Game Commission’s monitoring program continues to document new cases in wild deer. These new cases have resulted in increased concern and further expansion of DMA 2.
As a result of new cases, the Game Commission enhanced its monitoring efforts during 2015. Originally designed to assess distribution and occurrence of the disease, enhanced sampling seeks to assess prevalence within DMAs while continuing statewide surveillance. Sample collection efforts from deer that were hunter-harvested, road-killed, crop-kills, escapes, and clinical suspects resulted in 5,619 deer samples. These included 616 from DMA 1, 1,593 from DMA 2, 363 from DMA 3 and 47 clinically suspect deer, exhibiting symptoms consistent with CWD infection. Final testing results are expected in March 2016. The Game Commission is currently consulting with wildlife professionals across the country who are struggling to find solutions to this disease problem.
Pennsylvania 2014 CWD
The Game Commission rigorously monitors Chronic Wasting Disease, which remains a threat to Pennsylvania’s deer and elk. Since 1998, more than 52,000 deer have been tested for the disease, and a total of 10 free-ranging deer have tested positive. Special rules are enforced in areas where CWD has been detected, and in 2014 the Game Commission created a special hunting permit designed to keep the disease in check in the only area of the state where it has been detected in the wild.
Sent: Mon, Jul 27, 2020 10:30 am
Subject: Pennsylvania GAME COMMISSION UNVEILS NEW CWD RESPONSE PLAN
Pennsylvania GAME COMMISSION UNVEILS NEW CWD RESPONSE PLAN
07/25/2020
GAME COMMISSION UNVEILS NEW CWD RESPONSE PLAN
HARRISBURG, PA - The Pennsylvania Game Commission has a new plan for battling what many consider the biggest wildlife-management challenge of the 21st century.
And it’s counting on hunters to help put it into action.
Acting at its quarterly meeting today, the agency’s Board of Commissioners unanimously adopted a new Chronic Wasting Disease Response Plan. It focuses on prevention, surveillance and management of CWD, an always-fatal neurological disease caused by misfolded proteins – called prions – that affect white-tailed deer, elk and other cervid species.
CWD was first detected in Pennsylvania in a captive deer facility in 2012. It was found in free-ranging deer just a few months later.
In the years since, it’s expanded both geographically and in a growing percentage of the deer infected with CWD.
That’s not good for anyone. Too much remains unknown about CWD and how it may impact humans, agriculture, and Pennsylvania’s deer and elk populations.
But what’s clear is the Game Commission’s mission, which is to “manage Pennsylvania’s wild birds, wild mammals, and their habitats for current and future generations.” So it’s taking additional steps to mitigate the effects of the disease.
The resulting response plan is not the Game Commission’s creation alone, though.
The Game Commission sought public input on the plan over a five-month period from September 2019 through February 2020. It received 447 comments. Scientific experts from other agencies and organizations also contributed.
Those comments led to substantial changes to the plan. Accordingly, the Game Commission put a revised version of the plan out for a second round of public review in the spring.
The public, agencies, and organizations submitted an additional 438 comments. Those were incorporated into the final version of the plan ultimately accepted by the Board of Commissioners.
“Development of this plan was truly a collaborative effort,” said Pennsylvania Game Commission Executive Director Bryan Burhans. “Our wildlife-management staff consulted with many of the nation’s leading CWD experts from both the public and private sectors. Agency staff also took into account the many, many comments we received from passionate deer hunters all across the state over a months-long public comment process.
“The result is a plan that’s based on the very best available science and puts our hunters first in line when it comes to opportunities to manage this disease.”
National sportsmen’s groups focused on deer and deer hunting praised the document for melding science with the passion of hunters.
“The PGC has gone the extra mile when it comes to informing people about CWD and why it’s so important that the disease is managed to protect the future of Pennsylvania’s precious wild deer resource,” said Nick Pinizzotto, President and CEO of the National Deer Alliance
“In addition, the agency made it a priority to get input on the plan from experts across the country who have various experiences dealing with the issue, which is a sign of strong leadership. We fully endorse the agency’s effort to manage CWD, working closely with hunters, who will be critical to the plans successful implementation.”
“CWD will require a stronger working relationship between the Game Commission, hunters and landowners than any other deer-related issue has previously or likely will in the future,” agreed Kip Adams, Director of Conservation for the Quality Deer Management Association.
“There haven’t been a lot of victories with CWD, but the agency’s plan to make hunters the key part of the solution is critical to its success. We fully support that the plan is science driven and complemented with enhanced public engagement.”
While there’s a lot that remains uncertain about CWD, containing the disease where it already exists and keeping prevalence rates low is critical. And right now, the best available science suggests that the only practical way to reach those dual goals and address CWD on the landscape is by reducing deer abundance.
Hunters can contribute by participating in Enhanced Surveillance Units. They are areas around certain high priority CWD-positive animals. Samples collected within an ESU will determine the extent of infection in areas at the leading edge of disease expansion.
Hunters will have increased opportunities to harvest deer in ESUs. That doesn’t equate to eliminating deer herds. The response plan calls for reducing deer numbers in ESUs by only one additional deer per square mile. That’s one deer for every 640 acres – or 485 football fields worth – of landscape.
The commission will also manage CWD within Containment Zones, small areas immediately surrounding a new, isolated CWD detection. Harvests there will be carried out with landowner cooperation in an effort to remove deer that may have come in contact with that newly discovered CWD positive deer.
Together, the samples collected in Enhanced Surveillance Units and Containment Zones will allow the Game Commission to assess CWD and adequately monitor the effects of management actions, with the goal of slowing and hopefully stopping the spread of CWD.
“Samples are key to the success of this program,” said Dr. Lisa Murphy, Co-director of the Wildlife Futures Program and Resident Director of the PADLS New Bolton Center. “A top priority of the Wildlife Futures Program, a collaborative program between the Game Commission and Penn Vet, is providing fast and accurate CWD test results.
“One of our primary goals is to prepare our staff, laboratory space and equipment so that we can provide hunters and the Game Commission with quick turn-around times on testing so decisions can be made in a timely manner.”
The response plan outlines some additional strategies meant to control CWD.
For example, it proposes a ban on the movement of high-risk parts – brains, spinal cords and spleens – from what’s called the state’s CWD “Established Area.” That’s where the disease is established on the landscape and where CWD is unlikely to be eradicated.
The intent is to reduce the movement of CWD prions from higher-prevalence areas to lower-prevalence areas within Disease Management Area 2.
No one strategy will solve the state’s CWD problem in a short time period. Effectively mitigating the disease’s effects will require a consistent long-term effort.
“Chronic wasting disease is a serious threat to Pennsylvania’s hunting heritage, the biggest we’ve faced in our lifetimes,” said Pennsylvania Game Commission President Charles Fox. “The fight ahead of us will be a challenging one.
“We’re committed as an agency to doing everything we can to win this battle for the whitetails we hold so dear. But we can’t do it alone. We need the help of all Pennsylvanians, and especially our deer hunters, to help manage our deer herd as well as this disease.”
Fighting CWD is not a lost cause, experts agree. But it will require collaboration between wildlife managers and stakeholders to sustain the state’s hunting heritage and protect Pennsylvania’s deer and elk for current and future generations.
“The Game Commission’s CWD Response Plan represents new hope for Pennsylvania to contain this disease where it already exists and minimize new outbreaks,” said Krysten Schuler, wildlife disease ecologist at the Cornell Wildlife Health Lab. “We’ve seen what happens in other states choosing the ‘do nothing’ approach. CWD not only expands geographically, but disease prevalence rates within deer herds climbs exponentially.
“That doesn’t have to be Pennsylvania’s future. If the commission and hunters partner now to support disease response actions, deer and deer hunting can both continue to thrive in Pennsylvania for the long term.”
MEDIA CONTACT: Bob Frye - 814-706-5071
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WEDNESDAY, MARCH 04, 2020
Pennsylvania YOUR STATE WILDLIFE AGENCY 2019 ANNUAL REPORT CWD TSE Prion 123 tested positive
FRIDAY, JUNE 26, 2020
Pennsylvania CWD TSE Prion AREAS EXPAND
FRIDAY, JUNE 26, 2020
Long-Term Incubation PrP CWD With Soils Affects Prion Recovery but Not Infectivity
SUNDAY, APRIL 12, 2020
PENNSYLVANIA REVISED CWD RESPONSE PLAN DRAFT AVAILABLE FOR REVIEW
SATURDAY, JANUARY 04, 2020
Pennsylvania 2020 CWD Response Plan Proposal
My submission to Pennsylvania Draft CWD Response Plan: Public Comment will be the same as my recent submission to Texas and other states, with a few additions, and is as follows;
SUNDAY, DECEMBER 22, 2019
Subject: Pennsylvania Scrapie Outbreak August 2018
Pennsylvania Steady Climb of CWD TSE Prion Confirms 250 Positive To Date In Wild Cervid As At September 12, 2019
Pennsylvania Captive Cervid Industry Total CWD TSE Prion ??? anyone's guess...
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
MONDAY, FEBRUARY 12, 2018
Pennsylvania Deer found near Jefferson County elementary school tests positive for CWD TSE Prion
***> Pennsylvania Department of Agriculture Chronic Wasting Disease CWD TSE Prion Game Farms Captive Cervid Surveillance
LAUGH OUT LOUD! LOL!
PENNSYLVANIA TOTAL CWD TSE PRION CAPTIVE CERVID INDUSTRY TO DATE... LMAO, your guess good as mine...
THURSDAY, OCTOBER 24, 2019
Pennsylvania NEWLY DETECTED CWD-POSITIVE DEER CAPTIVE-RAISED WILL EXPAND DMA 4 IN 2020
SATURDAY, NOVEMBER 10, 2018
***> Pennsylvania Thirty-Eight Deer Test Positive for Chronic Wasting Disease on Fulton and Bedford County Deer Farms
MONDAY, FEBRUARY 12, 2018
Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties
SATURDAY, AUGUST 12, 2017
*** Pennsylvania 27 deer from Bedford County farm test positive for chronic wasting disease ***
THURSDAY, JUNE 01, 2017
PENNSYLVANIA Third Case of CWD Discovered in a Captive Deer Farm in Four Months
MONDAY, MAY 15, 2017
Pennsylvania 25 more deer test positive for CWD TSE PRION in the wild
WEDNESDAY, MARCH 01, 2017
South central Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease
FRIDAY, JANUARY 13, 2017
Pennsylvania Deer Tests Positive for Chronic Wasting Disease four-year-old white-tailed deer Franklin County Hunting Preserve
Wednesday, May 11, 2016
PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL CONTROL MEASURES
Sunday, October 18, 2015
*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans Singeltary 2002 from speaking A smelly situation UPDATED 2015
Saturday, November 07, 2015
PENNSYLVANIA CHRONIC WASTING DISEASE CWD TSE PRION RULES EXPAND
Saturday, November 07, 2015
Pennsylvania 2015 September Minutes CWD Urine Scents
Tuesday, May 05, 2015
Pennsylvania CWD DETECTED IN SIX MORE FREE-RANGING DEER Disease Management Area 2 again expanded due to new cases Release #030-15
Sunday, July 13, 2014
Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Tuesday, June 11, 2013
*** CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.
ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;
''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
Wednesday, November 14, 2012
PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO LOUISIANA and INDIANA
Tuesday, October 23, 2012
PA Captive deer from CWD-positive farm roaming free
Thursday, October 11, 2012
Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests Positive
FRIDAY, MARCH 06, 2020
Pennsylvania CWD TSE Prion deer and State Rep. David Maloney, R-Berks
WEDNESDAY, MARCH 04, 2020
Politicians State Rep. David Maloney, R-Berks Helping to Spread Chronic Wasting Disease CWD TSE Prion
THURSDAY, MARCH 05, 2020
PGC Audit Reeks of Politics Research Representative Maloney Wants To Gut wildlife management and hunting and help spread CWD in Pennsylvania
MONDAY, NOVEMBER 04, 2019
Legislators legislating, or throwing away your money for battling cwd tse prion, State Rep. Steve Green, R-Fosston more money to deer farms for antibiotics?
Pennsylvania Has Confirmed 3 Cases Of Atypical Nor-98 TSE Prion To Date
THURSDAY, JANUARY 7, 2021
Atypical Nor-98 Scrapie TSE Prion USA State by State Update January 2021
Subject: Pennsylvania Scrapie Outbreak August 2018
Ag Secretary, State Veterinarian: New Animal ID Rules Help Track Disease, Prevent Outbreaks
09/18/2020
Harrisburg, PA - Agriculture Secretary Russell Redding and State Veterinarian Dr. Kevin Brightbill today reminded small-ruminant producers that new requirements for scrapie tags and premises IDs will help ensure better, faster disease tracing and control. Adhering to new federal requirements will help keep scrapie instances from becoming full-blown outbreaks, ultimately saving producers from devastating livestock and financial losses.
“We have made significant progress in eradicating this costly and fatal disease,” said Redding. “Our commonwealth must continue efforts to ensure the protection of our herds and flocks from scrapie as it threatens Pennsylvania agriculture. Establish a premises identification number for your herd or flock.”
Scrapie is known to be transmissible from infected to uninfected sheep and goats through exposure from birthing fluids and tissues. Clinical signs may be noticed 18 months to 5 years after exposure and include progressive weight loss despite no decrease in appetite, difficulty walking, fine tremors/shaking of ears and head and, most notably, extreme itching. At this time, there is no vaccine to protect animals against scrapie, and there is no known cure or treatment for the disease.
“Scrapie is a fatal infectious and progressive disease affecting the brain and spinal cord of sheep and goats and belongs to a group of diseases called transmissible spongiform encephalopathies (TSEs),” said Brightbill. “There is no evidence humans have ever been infected with scrapie.”
In August 2018, a Pennsylvania goat sampled at slaughter in July 2018, was confirmed positive for classical scrapie. The goat was traced to a Pennsylvania herd that has both sheep and goats. The herd was designated as a source flock by the United States Department of Agriculture (USDA). An additional five sheep and one goat were confirmed positive for classical scrapie within that herd at the time of partial herd depopulation. Only sheep and goats shown to be genetically susceptible to scrapie were depopulated.
To establish a premises identification number (PIN) for your herd or flock please visit the Pennsylvania Department of Agriculture Premises Registration Form to enroll your premises.
After a PIN has been established, dial USDA’s toll-free tag line at (866) 873-2824 to order scrapie tags for your herd or flock. The Pennsylvania Veterinary Diagnostic Laboratory (PVL) is offering genetic screening for owners interested in identifying scrapie resistant animals in their flocks. To find out more ask your veterinarian or call PVL at (717) 787-8808. Additionally, USDA APHIS offers free scrapie testing for deceased animals over the age of 14 months.
All sheep and goats born in Pennsylvania must be identified with a PDA-approved form of official individual identification, prior to being transported live off the birth premises. No sheep or goat, of any age, shall be imported or shipped into the Commonwealth of Pennsylvania without a department-approved form of individual identification. Additionally, per the Final Rule of the National Scrapie Eradication ProgramOpens In A New Window, all sheep and goats must be accompanied in transit by either a valid Interstate Health Certificate or owner shipper statement if the animals are moving in slaughter channels.
Up until January 1, 2021 the department will offer educational outreach and written notices of violation to gently prompt compliance. After January 1, 2021, entities failing to comply will be subject to enforcement and penalties as are allowed under the provisions of Pennsylvania’s Domestic Animal Law, including revocation of license, criminal prosecution and/or civil penalties of up to $10,000 per violation and injunctive.
Additional questions may be addressed by calling the Bureau of Animal Health and Diagnostic Services at 717-772-2852 or RA-ahds@pa.gov. Questions directed toward USDA APHIS may be addressed by calling Dr. Stephanie Ringler at 717-599-9957.
MEDIA CONTACT: Shannon Powers - 717.783.2628
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https://d1cqrq366w3ike.cloudfront.net/http/DOCUMENT/SheepUSA/March%202019%20Scrapie%20Newsletter.pdf
NOTICES DEPARTMENT OF AGRICULTURE General Quarantine Order; Scrapie [50 Pa.B. 675] [Saturday, February 1, 2020]
Positive Scrapie Cases:
• As of September 30, 2010, 72 cases of classical scrapie and 5 cases of Nor98-like scrapie were confirmed by the National Veterinary Services Laboratories (NVSL); 53 were field cases and 24 were RSSS cases collected between October 1, 2009 and September 30, 2010 and confirmed by November 8, 2010. Of the five Nor98-like scrapie cases, four were RSSS cases that originated from flocks in Ohio, Pennsylvania, Oregon, and Idaho and one was a field case form Maine. This brings the total number of Nor98-like cases detected in the United States to 11. Field cases are positive animals tested as part of a disease investigation including potentially exposed, exposed, and suspect animals or tested as part of on farm surveillance.
• Twenty one cases of scrapie in goats have been confirmed by NVSL since implementation of the regulatory changes in FY 2002. The last infected goat herd was identified in FY 2008.
Scrapie is a dangerous transmissible disease of animals, and is so designated in § 2321(a)(36) of the Domestic Animal Law (3 Pa.C.S. § 2321(a)(36)).
Scrapie has been present in various sheep and goat herds in this Commonwealth for several years. The Department is launching an effort to identify, contain and eradicate this disease in accordance with the duty and authority imparted it under the Domestic Animal Law.
J Vet Diagn Invest 13:89–91 (2001)
Immunohistochemical detection of scrapie prion proteins in clinically normal sheep in Pennsylvania
Hyun Kim, Katherine I. O’Rourke, Mark Walter, H. Graham Purchase, John Enck, Tae Kyun Shin
Abstract. Following diagnosis of scrapie in a clinically suspect Suffolk sheep, 7 clinically normal flockmates were purchased by the Pennsylvania Department of Agriculture to determine their scrapie status using an immunohistochemical procedure. Two of the 7 euthanized healthy sheep had positive immunohistochemical staining of the prion protein of scrapie (PrP-Sc) in their brains, nictitating membranes, and tonsils. The PrP-Sc was localized in the areas of the brain where, histopathologically, there was neurodegeneration and astrocytosis. The PrP-Sc occurred within germinal centers of the affected nictitating membranes and tonsils and was located in the cytoplasm of the dendrite-like cells, lymphoid cells, and macrophages. These results confirm that immunohistochemical examination of the nictitating membrane can be used as a screen for the presence of scrapie infection in clinically normal sheep at a capable veterinary diagnostic laboratory. In sheep with a PrP-Sc–positive nictitating membrane, the diagnosis of scrapie should be confirmed by histopathology and immunohistochemical examination of the brain following necropsy. Following full validation, immunohistochemistry assays for detection of PrP-Sc in nictitating membrane lymphoid tissues can improve the effectiveness of the scrapie control and eradication program by allowing diagnosis of the disease in sheep before the appearance of clinical signs.
Scrapie is the prototype of a heterogenous group of transmissible spongiform ecnephalopathies that occur in sheep, humans, cattle, cats, mink, and cervids and are characterized by the deposition of altered prion proteins in the central nervous system of affected individuals.11 Scrapie in sheep has become a target of control measures and eradication programs. Crucial for the effectiveness of these measures is the detection of infected sheep. After infection, the disease has a particularly long incubation period during which the infected sheep may be able to transmit the disease to noninfected sheep.3 Scrapie infectivity has been detected in the lymphoreticular system of sheep well before symptoms occur.4,8,9 Detection of scrapie prion protein (PrP-Sc) in nictitating membrane or tonsil has been proposed as a diagnostic test for scrapie infection.5,11,13 In this study at the Pennsylvania Veterinary Laboratory (PVL), an immunohistochemical procedure was applied to detection of PrP-Sc in clinically normal euthanized Suffolk sheep.
A farm had 10 sheep in a flock that had been in existence since October 1991. A 7-year-old ewe from the farm was submitted to the PVL for necropsy on April 15, 1998. The ewe had shown signs of pruritis for a few months and had recently developed neurologic signs, including staggering, stumbling, and falling. The ewe was diagnosed as having scrapie by routine histopathology conducted at PVL and immunohistochemistry (IHC) of brain tissue conducted at the National Veterinary Services Laboratory (Ames, IA). On August 11, 1998, the Pennsylvania Department of Agriculture purchased the last 7 sheep in the flock to determine their scrapie status; they were 4-year-old, clinically normal Suffolk sheep. The 7 sheep were euthanized and necropsied. Gross examination revealed no scrapie-specific lesions, and the sheep had abundant fat reserves. Representative samples of the brain, nictitating membrane, and tonsil from each of the 7 animals were collected in 10% buffered formalin for histopathologic and IHC examination. All tissues were routinely processed for paraffin embedment, sectioned at 4–5 mm, and stained with either hematoxylin and eosin (HE) or the IHC procedure.
Commercially available kitsa and an automated immunostainera were used for IHC. Tissue sections of brain stem, nictitating membrane, and tonsil were mounted on positively charged slides. These sections were heated in a flame until the wax had melted, deparaffinized with solvents, and placed in a steam bath for 10 minutes. The last step is considered heat-mediated antigen retrieval. Formalin fixation eliminates the immunoreactivity of the epitope for the anti-prion protein antibody used in this study in ovine lymphoid tissues. Heat retrieval is necessary for unmasking the epitope on PrP-Sc. The primary antibody was a monoclonal mouse anti-prion protein antibody, F89/ 160.1.5,b which recognizes a conserved epitope on the PrP-Sc of cattle, sheep, mule deer, and elk.8 The primary antibody was used at a dilution of 1:400 for 2 hours at room temperature. The secondary antibody was biotinylated goat anti-mouse IgGa and was applied to tissue sections for 30 minutes at room temperature. A commercially available avidin–biotin–horseradish peroxidase complexa was used according to the manufacturer’s instructions. The chromagen/substrate was aminoethylcarbazole. All slides were counterstained with hematoxylin. Appropriate positive and negative controls were run with every test. These were tissues from sheep diagnosed with scrapie, tissues from sheep with no exposure to scrapie, and a primary antibody of the same isotype as the primary antibody used for staining the PrP-Sc but against another disease. A commercially available rabbit anti-glial fibrillary acidic protein (GFAP) primary antibodyc was also used in sequential sections at a dilution of 1:500 for 1 hour at room temperature to detect astrocytes.
Two of the 7 euthanized healthy ewes were diagnosed as scrapie positive, based on the presence of histologic lesions and the detection of the PrP-Sc antigens in the lesions by IHC with anti-scrapie antiserum as previously described.8,10
Histologic examination revealed focal, intracytoplasmic neuronal vacuolation and mild spongiform changes in the midbrain. A mild increase in astrocyte numbers (astrocytosis) was also observed in the lesions. Neuronal vacuolation ranged from a single large vacuole to a few smaller vacuoles. These vacuoles were empty and were not stained with HE. The neuropathologic changes were mainly found in the midbrain and not in the cerebrum and cerebellum. No histopathologic changes were found in the tonsils and nictitating membranes of the 2 scrapie-affected animals.
IHC detected PrP-Sc in the brain, tonsil, and nictitating membrane of the 2 sheep with histopathologic changes of scrapie. In positive brains, the PrP-Sc antigen accumulated in the outer rim of intraneuronal vacuoles (Fig. 1) of the midbrain, whereas in negative control brains the neurons had no such staining. The immunoreactivity was comprised of densely stained granules and globules around the periphery of intraneuronal vacuoles. GFAP-immunoreactive hypertrophic astrocytes surrounded the intracytoplasmic vacuolated neurons. The nictitating membrane of the affected sheep had distinct foci of PrP-Sc staining within lymphoid cells of the germinal centers (Fig. 2). The tonsilar lymphoid tissues also had a similar deposition of granules within cells of the germinal centers. Most immunoreactivity within germinal centers was located in the cytoplasm of the dendrite-like cells, lymphoid cells, and macrophages.
Scrapie of sheep and goats was recognized in Europe at least 200 years ago, although the disease was not diagnosed in the United States until 1947.7 The most widely accepted histologic lesion is astrocytosis and vacuolation in neuronal cells, leading to the classification of the disease as a spongiform encephalopathy. An astroglial reaction is a common histologic feature in natural1,2,6 and in experimental12 scrapie. Astrocytes are a target for the scrapie agent in the early pathogenesis of the disease.6 Astrocytes, upon stimulation by PrP-Sc, are thought to respond by releasing a variety of active molecules, including nitric oxide. GFAP-immunoreactive hypertrophic astrocytes were readily identified in brain specimens from scrapie-infected hamsters, particularly in those areas where the tissue damage was the most extensive.7 In scrapie infection of the brain, PrP-Sc was localized in areas where there was neurodegeneration and astrocytosis. PrP-Sc is thought to be toxic to neurons and trophic for astrocytes.12
These IHC studies support the histopathologic observations; PrP-Sc antigen was found in animals with intracytoplasmic vacuolation of neurons (spongiform changes) and astrocytosis. The IHC assay of the nictitating membrane and tonsil provides a practical method for early detection of PrPSc in live affected sheep before clinical signs appear.
IHC examination of the nictitating membrane can be used as a screen for the presence of scrapie infection in live sheep. In sheep with a PrP-Sc–positive nictitating membrane, the diagnosis of scrapie can be confirmed by histopathology and IHC examination of the brain following necropsy at a capable veterinary diagnostic laboratory in sheep .3 years of age. In younger sheep or those infected with the scrapie agent as adults, immunostaining of the lymphoid tissue may be positive in lymphoid tissue but negative in brain tissue for 1–2 years following infection. A large-scale validation study to determine the specificity and sensitivity of PrP-Sc detection in nictitating membrane lymphoid tissue as a live animal test for scrapie is underway. Use of this test can improve the effectiveness of the scrapie control and eradication program by allowing diagnosis of the disease in sheep before the appearance of clinical signs.
PROCEEDINGS ONE HUNDRED AND Nineteenth ANNUAL MEETING of the UNITED STATES ANIMAL HEALTH ASSOCIATION
Rhode Island Convention Center Providence, Rhode Island October 22 28, 2015
CWD in Farmed and Wild Cervids
Retrospective Epidemiology of CWD in Farmed Cervids In response to a 2014 USAHA Resolution, VS asked States to include a retrospective summary of the epidemiology of all positive herds with their annual HCP reports for FY2015. Unfortunately, the response to HPAI delayed completion of this summary. Five States reported information to date. A few States indicated that they did not have the resources to devote to this request. VS will continue to gather this data and to collect more comprehensive data in the future.
Summary of CWD detections
As of September 30, 2015, CWD has been confirmed in wild deer and elk in 21 US States, and in farmed cervids in 16 States. In total, 23 States have identified CWD in wild and/or farmed cervids. CWD has been reported in 70 farmed cervid herds in the United States. Confirmation of the disease in three free-ranging, wild white-tailed deer in Michigan in 2015 marked the first report of CWD in the wild cervid population in this State.
FY2015 CWD Detections in Farmed Cervids
In FY2015, CWD was identified in eight farmed cervid herds: one whitetailed deer breeding herd in Pennsylvania, one elk breeding herd in Utah (traced back from a hunting facility in Utah), one white-tailed deer (WTD) breeding herd and one WTD hunting preserve in Ohio (owned by the same producer), two WTD breeding herds in Wisconsin, one WTD and elk herd in Texas, and a second WTD herd in Texas (traced from the first positive herd in Texas). The positive animals in Utah, Ohio, and Texas represented the first reported cases of CWD in captive cervids in all three of these States.
White-Tailed Deer Breeding Herd, Pennsylvania
On October 6, 2014, the National Veterinary Services Laboratories (NVSL) confirmed CWD in a 6-year-old doe from a captive WTD breeding facility in Reynoldsville, Pennsylvania. The doe was euthanized and tested because she was classified as a CWD-exposed animal that had previously resided in two trace back exposed herds. This herd was assembled in 2013 through the purchase of 16 animals from other HCP-certified herds in Pennsylvania, and had been under quarantine for receiving exposed animals from a trace back exposed herd. The remaining herd of eight WTD was depopulated with Federal indemnity on February 18, 2015, and no additional positive animals were detected. USDA collected samples for research purposes.
Elk Breeding Herd, Utah
On December 23, 2014, NVSL confirmed CWD in 3-year-old captive elk. The elk had been at a hunting park located in northern Utah, where he had resided for approximately 3 weeks prior to being hunter killed. All hunter-killed animals at the hunt park are required to be tested for CWD, and this animal
CAPTIVE WILDLIFE AND ALTERNATIVE LIVESTOCK 139
was sampled through routine surveillance. The elk was traced back to its herd of origin, and that facility was quarantined. The herd was assembled in 1999 with bulls, and later elk cows, that originated from Colorado. Historical testing records for the herd were unavailable. The remaining 70 elk were depopulated using Federal indemnity funds on March 3, 2015, and an additional 25 elk were confirmed as CWD-positive. USDA collected samples for research purposes.
White-Tailed Deer Hunting Preserve, Ohio
On October 22, 2014, NVSL confirmed CWD in a buck taken from a captive WTD deer hunting preserve in Ohio. This was the first time that CWD had been detected in Ohio. The preserve was tested as part of Ohio’s CWD monitoring program. The herd had been under quarantine since April 2014 because it was a trace-forward herd associated with a CWD-exposed herd in Pennsylvania. The positive animal was traced to its herd of origin, a captive WTD breeding herd in Pennsylvania, through DNA identity testing. On November 26, 2014, the Ohio State Veterinarian issued an Order of Destruction for animals on the hunting preserve. The State executed this Order on April 27-30, 2015. The herd of 224 WTD was depopulated and no other positives were detected. USDA did not provide Federal indemnity.
White-Tailed Deer Breeding Herd, Ohio
On March 31, 2015, NVSL confirmed CWD infection in a 5-year-old WTD doe from a captive breeding herd in Holmesville, Ohio. The index animal was received from a Wisconsin WTD farm in January 2013. The CWD-positive herd was owned by the same individual as the Ohio hunt preserve that was found to be CWD positive in October 2014. On May 22, 2015, NVSL confirmed a second positive case in the same herd - a yearling WTD doe that was a natural addition in the same breeding herd. The herd had been under quarantine since April 1, 2014 due to epidemiological linkages with two WTD herds in Pennsylvania – one a positive herd and the other a traceback exposed herd. USDA provided Federal indemnity and depopulated this herd on June 15 and 16, 2015. USDA collected samples for research purposes. NVSL confirmed CWD in 16 additional animals in the herd. Of the 16 positives, one was natural addition and the rest were purchased additions. The positive animals were purchased from February 26, 2013 through September 24, 2013, except for one purchased in 2012. Eleven purchased additions traced-back to three herds in Pennsylvania and four purchased additions traced to three other herds in Ohio.
White-Tailed Deer Breeding Herd, Wisconsin
On October 6, 2014, NVSL confirmed CWD in a 2-year-old doe born in June of 2012 that died on a Richland County farm. The facility is within the CWD management zone in Wisconsin. The remaining 51 deer were euthanized on November 20, 2014, and seven additional positives (all males born in 2012) were found. Two of these seven were purchased additions with the last added to the herd in January 2013. All sales from this herd were to shooting preserves. This premise was double fenced and had been compliant in a herd certification program for over ten years.
White-Tailed Deer Breeding Herd, Wisconsin REPORT OF THE COMMITTEE
140
On June 19, 2015, NVSL confirmed CWD in a seven-year-old female WTD from a breeding facility in Eau Claire County. The doe was a natural addition to this breeding herd. This is the first positive CWD case, captive or wild, in this county. The doe was found dead and was showing no clinical signs of CWD at the time of death. Since 2003, this herd has tested 391 animals for CWD and all had “not detected” results. In addition, 317 animals have tested “not detected” from the associated hunting preserve over the same time period. A second positive natural addition doe from this herd was confirmed positive by NVSL on September 10, 2015. Several escape episodes have occurred from this herd. The herd is currently under quarantine and plans are underway for depopulation with State indemnity.
White-Tailed Deer and Elk Breeding Herd, Texas
On June 30, 2015, NVSL confirmed CWD in a 2-year-old WTD buck from a captive WTD and elk breeding herd in Medina County, Texas, approximately 500 miles from previously reported positive free-ranging mule deer in far West Texas. This was the first time that the disease had been detected in farmed cervids in the State. The index buck was born on the premises and found dead on June 18, 2015. Over 40 high-risk deer (i.e., pen mates, dam, others) were euthanized and tested after the index case was found. The NVSL confirmed CWD infection in two of those deer. Interestingly, all three of the positive deer identified to date on this premises have the same AI sire. However, the significance of this finding is unclear. In the past five years, records indicate that 130 WTD from 33 facilities moved into the positive herd and 838 WTD moved out of the positive herd to 147 different herds. One positive WTD was found in one of these trace-out herds (see herd description below). Additionally, 23 elk were also moved from this herd to another herd in TX in 2014. All trace-outs have been intrastate except for movements to two premises in Mexico. Premises that have received deer from the index herd are under movement restrictions. VS is collaborating with animal health authorities in Mexico. VS paid indemnity and depopulated this herd on September 30, 2015, and no additional positive animals were detected. USDA collected samples for research purposes.
White-Tailed Deer Herd, Texas
On September 14, 2015 NVSL confirmed CWD from tissues from a WTD in Lavaca County, Texas. This animal was a traceout from the first CWD positive herd from June 30, 2015. Additional epidemiology is ongoing.
WEDNESDAY, MARCH 04, 2020
Pennsylvania YOUR STATE WILDLIFE AGENCY 2019 ANNUAL REPORT CWD TSE Prion 123 tested positive
FRIDAY, JUNE 26, 2020
Pennsylvania CWD TSE Prion AREAS EXPAND
SUNDAY, FEBRUARY 16, 2020
Jerking for Dollars, Are Texas Politicians and Legislators Masturbating Deer For Money, and likely spreading CWD TSE Prion?
TUESDAY, DECEMBER 31, 2019
In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus
SUNDAY, AUGUST 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
SUNDAY, AUGUST 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
WEDNESDAY, MARCH 13, 2019
CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood
SATURDAY, DECEMBER 02, 2017
TEXAS TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play
SUNDAY, JANUARY 22, 2017
Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry
FRIDAY, DECEMBER 20, 2019
Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission
TEXAS CWD TSE PRION STRAIN UNLIKE ANYTHING EVER SEEN
“Wow,” he said. “Unlike anything we've seen before.”
The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.
snip...
THURSDAY, SEPTEMBER 05, 2019
Unique Profile of The Texas CWD TSE Prion isolates, the TSE Prion CWD, Scrapie, BSE in Livestock, and CJD in Humans
FRIDAY, OCTOBER 18, 2019
TAHC Exotic CWD Susceptible Species Rules, Regulations, TSE PRION, WHEAT, GRAINS, HAY, STRAY, GLOBAL CONCERNS GROW, UPDATE, October 17, 2019
THURSDAY, FEBRUARY 27, 2020
Texas Chronic Wasting Disease Discovered at Deer Breeding Facility in Kimble County AND TO DATE, 169 postive cases detected white-tailed deer, red deer and mule deer
TUESDAY, FEBRUARY 04, 2020
TEXAS REPORTS 20 NEW CWD TSE PRION CASES 3 WILD 17 BREEDER 166 POSITIVE TO DATE
Colorado Chronic Wasting Disease Response Plan December 2018
I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds.
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IMPORTANT PUBLIC HEALTH MESSAGE
Disease in humans resulting from CWD exposure has not been reported to date. However, public health officials cannot determine there is no risk from eating meat from infected animals. Consequently, officials recommend that people avoid exposure to CWD-infected animals. Please see the Colorado Department of Public Health and Environment website
for the most current recommendations on carcass testing and other preventive measures.
To minimize exposure to CWD and other diseases of potential concern, Colorado Parks and Wildlife (CPW) and state public health officials advise hunters not to shoot, handle or consume any deer, elk or moose that is acting abnormally or appears to be sick. When fielddressing game, wear rubber gloves and minimize the use of a bone saw to cut through the brain or spinal cord (backbone). Minimize contact with brain or spinal cord tissues, eyes, spleen or lymph nodes. Always wash hands and utensils thoroughly after dressing and processing game meat. (the map on page 71, cwd marked in red, is shocking...tss)
TUESDAY, SEPTEMBER 17, 2019
Michigan House Bill 4687 State Legislators Turn To Draft Dodger Ted Nugent To Make Scientific Decisions over DNR on CWD TSE Prion
SUNDAY, FEBRUARY 09, 2020
Management of chronic wasting disease in ranched elk: conclusions from a longitudinal three-year study
Although the herd owners were presented with additional management directives, including culling of CWD positive bulls and those animals positive by an amplification assay (RT-QuIC), they were not implemented due to concern regarding its potential impact on hunting revenue.
PAYING TO PLAY CWD TSE PRION IN INDIANA
JUNK SCIENCE POLITICS AND LEGISLATION THERE FROM $$$
*** Indiana Politicians and contributions from the Game Farm Industry, and whom is taking the bait $$$ will this buy their vote in support of the cervid game farming industry ???
MONDAY, NOVEMBER 04, 2019
Legislators legislating, or throwing away your money for battling cwd tse prion, State Rep. Steve Green, R-Fosston more money to deer farms for antibiotics?
TUESDAY, FEBRUARY 25, 2020
***> Novel Strain of the Chronic Wasting Disease Agent Isolated From Experimentally Inoculated Elk With LL132 Prion Protein
CWD WEBINAR CWD YESTERDAY! December 11, 2019
Dr. Mckenzie and CIDRAP on CWD TSE Prion
122: Prions and Chronic Wasting Disease with Jason Bartz
Texas CWD Symposium: Transmission by Saliva, Feces, Urine & Blood
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
''On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis. ''
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO
cwd update on Wisconsin from Tammy Ryan...
Wyoming CWD Dr. Mary Wood
''first step is admitting you have a problem''
''Wyoming was behind the curve''
wyoming has a problem...
TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?
OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?
apparently, no ID though. tell me it ain't so please...
23:00 minute mark
''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''
Wyoming CWD Dr. Mary Wood
''first step is admitting you have a problem''
''Wyoming was behind the curve''
wyoming has a problem...
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
SATURDAY, JANUARY 19, 2019
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission
Greetings TAHC et al,
Thank You Kindly for letting me comment again on cwd tse prion.
My comments 1-8 with updated science in references to back all my concerns up with...
1. ALL CWD TSE PRION RULES MUST BE MADE MANDATORY, voluntary does not work.
2. TAHC MUST BAN THE MOVEMENT OF ALL CERVID BY GAME FARMS, BREEDERS, SPERM MILLS, URINE MILLS, HORN MILLS, VELVET MILLS, HIGH/LOW FENCE, WITH ALL VEHICLES AND FARM EQUIPMENT BEING LIMITED TO ONLY THOSE SITES.
3. ALL CAPTIVE FARMING PUT ON HOLD WITH NO MORE PERMITTED
4. ALL CAPTIVE FARMING CERVID MUST BE TESTED ANNUALLY LIVE AND DEAD AND VERIFIED, THAT OLD BSe of ''just another escapee' does not cut it anymore, see why here;
WEDNESDAY, FEBRUARY 10, 2016
Wisconsin Two deer that escaped farm had chronic wasting disease CWD
436 Deer Have Escaped From Farms to Wild
Tuesday, 18 March 2003 00:00
As the DNR prepared to hand over authority for overseeing game farms to the agriculture department, it sent 209 conservation wardens to 550 farms to collect information, attempt to pinpoint the source of the disease and to learn whether other deer had been exposed to it. The audit found that most farms were in compliance, but the DNR found many violations and instances of poor record keeping. Also in numerous instances, fences did not stop wild and captive deer from intermingling. see;
436 Deer Have Escaped From Farms to Wild
Tuesday, 18 March 2003 00:00
TUESDAY, JULY 14, 2015
TWO Escaped Captive Deer on the loose in Eau Claire County Wisconsin CWD postive farm Yellow ear tag
5. ALL CAPTIVE FARMING CERVID ON ANY FARM MUST BE KILLED AND INCINERATED, COMPLETE ERADICATION OF ANY CWD POSITIVE HERD
6. ALL CAPTIVE FARMING CERVID OPERATIONS MUST BE INSURED TO PAY FOR ANY CLEAN UP OF CWD AND QUARANTINE THERE FROM FOR THE STATE, NO MORE ENTITLEMENT PROGRAM FOR CERVID GAME FARMING PAY TO PLAY FOR CWD TSE PRION OFF THE TAX PAYERS BACK, QUARANTINE MUST BE FOR AT LEAST 16 YEARS WITH NO MOVEMENT IN OR OUT OF THAT PREMISES
7. TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
***> PLEASE SEE HISTORY OF TEXAS TRUCKING CWD TSE PRION DISEASE AT THE BOTTOM OF MY SUBMISSION, TOO LONG TO POST HERE.
8.CONSIDERING RECENT SCIENCE THAT CWD TSE PRION WILL TRANSMIT ORALLY TO PIGS AND ALSO SCRAPIE TO PIGS BY ORAL ROUTES, CONSIDERING CWD TRANSMIT EASILY TO CERVID BY ORAL ROUTE, CONSIDERING A NEW TSE PRION OUTBREAK IN A NEW LIVESTOCK SPECIES, THE CAMEL, CONSIDERING THE FACT THE USA THAT THE 1997 BSE feed regulation at 589.2000, which remains in effect but which applies only to feed for cattle and other ruminants, and specifically, the new section 589.2001, WAS AND STILL IS A TOTAL AND COLOSSAL FAILURE, AND PROVEN TO BE SO BY RECENT COMMENTS COMING FROM THE FDA, BUT FIRST, COMMENTS FROM DEFRA;
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.....
***> cattle, pigs, sheep, cwd, tse, prion, oh my!
***> 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).
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). 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 suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> 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 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 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.
***> In summary, our results establish aerosols as a surprisingly efficient modality of prion transmission. This novel pathway of prion transmission is not only conceptually relevant for the field of prion research, but also highlights a hitherto unappreciated risk factor for laboratory personnel and personnel of the meat processing industry. In the light of these findings, it may be appropriate to revise current prion-related biosafety guidelines and health standards in diagnostic and scientific laboratories being potentially confronted with prion infected materials. While we did not investigate whether production of prion aerosols in nature suffices to cause horizontal prion transmission, the finding of prions in biological fluids such as saliva, urine and blood suggests that it may be worth testing this possibility in future studies.
Adriano Aguzzi ''We even showed that a prion AEROSOL will infect 100% of mice within 10 seconds of exposure''
WOW!...tss
Rabbits are not resistant to prion infection
Francesca Chianinia,1, Natalia Fernández-Borgesb,c,1, Enric Vidald , Louise Gibbarda , Belén Pintadoe , Jorge de Castroc , Suzette A. Priolaf , Scott Hamiltona , Samantha L. Eatona , Jeanie Finlaysona , Yvonne Panga , Philip Steelea , Hugh W. Reida , Mark P. Dagleisha , and Joaquín Castillab,c,g,2 a
Moredun Research Institute, Penicuik, Near Edinburgh EH26 0PZ, Scotland, United Kingdom; b CIC bioGUNE, Derio 48160, Bizkaia, Spain; g IKERBASQUE, Basque Foundation for Science, Bilbao 48011, Bizkaia, Spain; c Department of Infectology, Scripps Florida, Jupiter, FL 33458; f Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840; d Centre de Recerca en Sanitat Animal (CReSA), UAB-IRTA, Universitat Autònoma de Barcelona, 08193 Bellaterra, Barcelona, Spain; and e Centro Nacional de Biotecnología (CNB), 28049 Cantoblanco, Madrid, Spain
Edited by Reed B. Wickner, National Institutes of Health, Bethesda, MD, and approved February 16, 2012 (received for review December 6, 2011)
The ability of prions to infect some species and not others is determined by the transmission barrier. This unexplained phenomenon has led to the belief that certain species were not susceptible to transmissible spongiform encephalopathies (TSEs) and therefore represented negligible risk to human health if consumed. Using the protein misfolding cyclic amplification (PMCA) technique, we were able to overcome the species barrier in rabbits, which have been classified as TSE resistant for four decades. Rabbit brain homogenate, either unseeded or seeded in vitro with disease-related prions obtained from different species, was subjected to serial rounds of PMCA. De novo rabbit prions produced in vitro from unseeded material were tested for infectivity in rabbits, with one of three intracerebrally challenged animals succumbing to disease at 766 d and displaying all of the characteristics of a TSE, thereby demonstrating that leporids are not resistant to prion infection. Material from the brain of the clinically affected rabbit containing abnormal prion protein resulted in a 100% attack rate after its inoculation in transgenic mice overexpressing rabbit PrP. Transmissibility to rabbits (>470 d) has been confirmed in 2 of 10 rabbits after intracerebral challenge. Despite rabbits no longer being able to be classified as resistant to TSEs, an outbreak of “mad rabbit disease” is unlikely.
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In summary, after 3 y postchallenge with three different rabbitderived inocula, we have obtained one positive clinical case, one possible preclinical case, two intercurrent deaths, and six animals that have remained healthy. Although the incubation periods do not directly correlate with the degree of susceptibility, these data might indicate that rabbits are poorly susceptible to prion infection. Although the rabbits used in this study were not inbred, they all had identical full-length PrP sequences and, to date, no difference has been detected in the ORF PrP sequence in any other published rabbit PrP sequence placed in GenBank. To further investigate this, two types of second passage experiment were performed; three raPrPTg mice and 10 rabbits were all intracerebrally inoculated using brain homogenate from the clinically affected rabbit. In contrast to 100% of the de novo RaPrPSc-inoculated transgenic mice having succumbed to a standard clinical prion disease and thereby demonstrating a high rate of transmissibility in vivo, two of 10 rabbits developed a TSE (477 and 540 dpi, respectively) to date. A plausible explanation for the evident differences between these two transmission studies would be the high level of rabbit PrPC expression (4- to 6-fold) in the murine model. In addition, it is well known that even if overexpression does not increase susceptibility, it can significantly reduce the incubation time of disease (2). However, the two positive TSE cases in the second rabbit passage, even though 8 rabbits remained clinically normal at 560 dpi, have led us to conclude that rabbits can no longer be considered a prionresistant species. The long incubation times, even after a second passage, might be due to the presence of some unknown, and probably rare, susceptibility factor in rabbits, which may also be present, for example, in equids and canids.
To critically evaluate this risk, several experiments are currently underway to characterize this new prion disease in rabbits and other species to examine its ability to cross the species barrier. In addition, supplementary experiments have been initiated in rabbits and also in transgenic mice that overexpress rabbit PrPC, to evaluate their susceptibilities to other important prion diseases including CWD and BSE. There are several factors that any potential new TSE epidemic would require: (i) the new prion should be efficiently transmitted through the homologous species; (ii) animals should be edible by humans and should be slaughtered at an age at which the disease has developed, thereby increasing the chance that prions have replicated (especially for those prions that require long incubation times); and (iii) the meat and bone meal should be recycled and fed to new members of the same species. In the light of these data and taking into account the previous three factors, it is unlikely there will be an outbreak of “mad rabbit disease,” and consumers of rabbit meat face much less of a risk than consumers of cattle or sheep products.
THURSDAY, AUGUST 08, 2019
Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie
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).
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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.
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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.
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***> READ THIS VERY, VERY, CAREFULLY, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are;
BSE TESTING (failed terribly and proven to be a sham)
BSE SURVEILLANCE (failed terribly and proven to be a sham)
BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham)
these are facts folks. trump et al just admitted it with the feed ban.
see;
FDA Reports on VFD Compliance
John Maday
August 30, 2019 09:46 AM VFD-Form 007 (640x427)
Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.
SUNDAY, SEPTEMBER 1, 2019
***> FDA Reports on VFD Compliance
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
I STRENUOUSLY URGE TEXAS FDA MODIFY THESE FEED BANS ASAP!
SEE;
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary
View Attachment:View as format pdf
Journal of Wildlife Diseases, 56(3), 2020, pp. 000–000
Wildlife Disease Association 2020
EFFECT OF ORAL COPPER SUPPLEMENTATION ON SUSCEPTIBILITY IN WHITE-TAILED DEER (ODOCOILEUS VIRGINIANUS) TO CHRONIC WASTING DISEASE
Oral Cu supplementation increased liver Cu concentrations compared to controls but did not affect susceptibility to CWD or survival after natural exposure in the captive white-tailed deer we studied.
SATURDAY, JANUARY 18, 2020
United States wildlife and wildlife product imports from 2000–2014 and TSE PRION aka Mad Cow Type Disease
***> HUMAN TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE 1 IN 5,000 NOT ONE IN A MILLION!
***> I urge every Country around the Globe to Declare an Extraordinary Emergency Due To A Foreign Animal Disease Chronic Wasting Disease CWD TSE Prion from the USA, Canada, and Mexico (they have no clue), all of North America should have this Declaration of Emergency against them, just like the one called way back when the shoe was on the other foot with the mad sheep of mad river valley, except this time, it's not a wag the dog false flag, this is for real...terry
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.
snip...see full text submission;
FRIDAY, DECEMBER 20, 2019
Texas TAHC, Administrative Code, Title 4, Part 2, Chapter 40, Chronic Wasting Disease Amendments Open For Comment beginning December 20, 2019 thru January 20, 2020 Terry Singeltary Comments Submission
*** TEXAS TAHC OLD STATISTICS BELOW FOR PAST CWD TESTING ***
CWD TEXAS TAHC OLD FILE HISTORY
updated from some of my old files, some of the links will not work.
*** Subject: CWD testing in Texas ***
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
To: flounder@wt.net
snip...see ;
MONDAY, AUGUST 14, 2017
*** Texas Chronic Wasting Disease CWD TSE Prion History ***
THURSDAY, JULY 09, 2020
Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date
Research Paper
Management of chronic wasting disease in ranched elk: conclusions from a longitudinal three-year study
N.J. Haley,D.M. Henderson,R. Donner,S. Wyckoff,K. Merrett,J Tennant,
Pages 76-87 | Received 09 Oct 2019, Accepted 28 Jan 2020, Published online: 07 Feb 2020
Download citation https://doi.org/10.1080/19336896.2020.1724754
ABSTRACT
Chronic wasting disease is a fatal, horizontally transmissible prion disease of cervid species that has been reported in free-ranging and farmed animals in North America, Scandinavia, and Korea. Like other prion diseases, CWD susceptibility is partly dependent on the sequence of the prion protein encoded by the host’s PRNP gene; it is unknown if variations in PRNP have any meaningful effects on other aspects of health. Conventional diagnosis of CWD relies on ELISA or IHC testing of samples collected post-mortem, with recent efforts focused on antemortem testing approaches. We report on the conclusions of a study evaluating the role of antemortem testing of rectal biopsies collected from over 570 elk in a privately managed herd, and the results of both an amplification assay (RT-QuIC) and conventional IHC among animals with a several PRNP genotypes. Links between PRNP genotype and potential markers of evolutionary fitness, including pregnancy rates, body condition, and annual return rates were also examined. We found that the RT-QuIC assay identified significantly more CWD positive animals than conventional IHC across the course of the study, and was less affected by factors known to influence IHC sensitivity – including follicle count and PRNP genotype. We also found that several evolutionary markers of fitness were not adversely correlated with specific PRNP genotypes. While the financial burden of the disease in this herd was ultimately unsustainable for the herd owners, our scientific findings and the hurdles encountered will assist future CWD management strategies in both wild and farmed elk and deer.
KEYWORDS: Prion, elk, RAMALT, RT-QuIC, antemortem
snip...
This manuscript describes one such property, a herd of over 570 elk maintained on 3500 acres of fenced habitat in northwestern Colorado.
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Return rate of CWD positive animals In the 2017 sampling period, 315 animals were tested for CWD antemortem. Of those, 71 tested positive by IHC, RT-QuIC, or both. Thirty-four infected animals (thirty-three cows and one bull) were euthanized and confirmed CWD positive post-mortem, with the remaining thirty-seven animals (Twenty-six bulls and eleven cows) released back onto the property. Of those animals which were released, four were harvested in the fall of 2017 and were found to be CWD positive post-mortem. Three of the remaining thirty (10%) returned for the 2018 sampling period, the remainder were lost in the field and went untested. All three were 132ML heterozygous animals, each positive again on antemortem testing in year three. In contrast, 120 of the 329 animals negative by antemortem testing were harvested in the fall of 2017, with 26 found to be CWD positive (21.7%). Of the remaining 209 animals, 141 returned for the 2018 sampling period (67.5%), with the remaining animals presumed lost in the field, untested. (Table 1 and Figure 1)
Over the course of the entire study, four of forty-nine CWD positive 132MM animals released back onto the property (8.2%) returned for a second year of sampling. Nine of thirty-three 132ML animals positive for CWD returned for a second year of sampling (27%), a return rate that was significantly greater than that of CWD positive 132MM animals (risk ratio: 3.34, p = 0.03). The lone 132LL cow identified during the course of antemortem testing in year two did not return for sampling in year three. Cumulatively, just 13 of 82 animals identified as CWD positive and released onto the property returned the following year (15.9%). These low rates of yearly return are in stark contrast to the cumulative return rate for CWD negative animals. For animals homozygous for the 132M allele, 107/144 returned in year two, and 28/69 returned in year three (63% overall). For 132ML heterozygous animals, 170/221 returned in year two, with 62/181 returning in year three (58% overall). Twenty-five of thirty-five animals homozygous for the 132L allele returned in year two, with fifteen of thirty-five returning in year three (57% overall). Cumulatively, 60% of animals negative for CWD returned the following year – a yearly return rate nearly over 3.5 times that of CWD positive animals (risk ratio: 3.62, p < 0.001; 95% confidence interval 1.96–6.69).
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Discussion
While reports on the management of chronic wasting disease in wild deer and elk are many and varied [33–43], rare is the case presented for managing the disease in farmed cervids. Almost without exception, farmed cervids are immediately placed under quarantine and eventually depopulated when CWD is discovered on site [12]. This manuscript reports our efforts to manage CWD in a large elk herd, in a controlled setting with endemic CWD, through the use of annual live animal testing and targeted culling of CWD positive cows. Although the herd owners were presented with additional management directives, including culling of CWD positive bulls and those animals positive by an amplification assay (RT-QuIC), they were not implemented due to concern regarding its potential impact on hunting revenue. Ultimately, we could not completely evaluate our management practices, as the herd was slowly depopulated after the final sampling period due to the financial burden brought by the disease.
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***> at present, no PrPC allele conferring absolute resistance in cervids has been identified.
J Gen Virol. 2017 Nov; 98(11): 2882–2892.
Published online 2017 Oct 23. doi: 10.1099/jgv.0.000952
PMCID: PMC5845664
PMID: 29058651
Estimating chronic wasting disease susceptibility in cervids using real-time quaking-induced conversion
Chronic wasting disease (CWD) resistance in cervids is often characterized as decreased prevalence and/or protracted disease progression in individuals with specific alleles; at present, no PrPC allele conferring absolute resistance in cervids has been identified.
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In summary, evaluating the amplification rates and efficiencies of recombinant PrPC substrates by RT-QuIC could be a useful tool for estimating the susceptibility of rare or newly discovered PRNP alleles, allowing researchers to target specific alleles for downstream evaluation in challenge studies. In the face of an ever-expanding CWD-endemic area, it is increasingly important to characterize the natural susceptibility of these alleles, as well as their geographical distribution and the evolutionary basis for their rarity. Do the QGAK, 225F and 225Y alleles represent recent, random anomalies, or are they more primitive mutations that adversely affect reproductive fitness? Perhaps they are an indication that cervids with these rare alleles were themselves once the target of a primordial prion strain. While some evidence has been presented for distinct strains of CWD, little is known about their geographical distribution or virulence in cervid hosts of diverse PRNP backgrounds. It is possible that, with the appropriate framework, RT-QuIC could allow for the discrimination of known and novel prion strains. Without further research into disease management and prevention, including resistance, the only certainty seems to be that CWD will continue its insidious spread, with further discoveries in new hosts and geographical locations.
P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1
Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWO
In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible. ***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
PRION 2016 CONFERENCE TOKYO
***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
ADOPTED: 26 September 2019 doi: 10.2903/j.efsa.2019.5863 Update on chronic wasting disease (CWD) III
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3.2.1.2. Non-cervid domestic species
The remarkably high rate of natural CWD transmission in the ongoing NA epidemics raises the question of the risk to livestock grazing on CWD-contaminated shared rangeland and subsequently developing a novel CWD-related prion disease. This issue has been investigated by transmitting CWD via experimental challenge to cattle, sheep and pigs and to tg mouse lines expressing the relevant species PrP.
For cattle challenged with CWD, PrPSc was detected in approximately 40% of intracerebrally inoculated animals (Hamir et al., 2005, 2006a, 2007). Tg mice expressing bovine PrP have also been challenged with CWD and while published studies have negative outcomes (Tamguney et al., 2009b), unpublished data provided for the purposes of this Opinion indicate that some transmission of individual isolates to bovinised mice is possible (Table 1).
In small ruminant recipients, a low rate of transmission was reported between 35 and 72 months post-infection (mpi) in ARQ/ARQ and ARQ/VRQ sheep intracerebrally challenged with mule deer CWD (Hamir et al., 2006b), while two out of two ARQ/ARQ sheep intracerebrally inoculated with elk CWD developed clinical disease after 28 mpi (Madsen-Bouterse et al., 2016). However, tg mice expressing ARQ sheep PrP were resistant (Tamguney et al., 2006) and tg mice expressing the VRQ PrP allele were poorly susceptible to clinical disease (Beringue et al., 2012; Madsen-Bouterse et al., 2016). In contrast, tg mice expressing VRQ sheep PrP challenged with CWD have resulted in highly efficient, life-long asymptomatic replication of these prions in the spleen tissue (Beringue et al., 2012).
A recent study investigated the potential for swine to serve as hosts of the CWD agent(s) by intracerebral or oral challenge of crossbred piglets (Moore et al., 2016b, 2017). Pigs sacrificed at 6 mpi, approximately the age at which pigs reach market weight, were clinically healthy and negative by diagnostic tests, although low-level CWD agent replication could be detected in the CNS by bioassay in tg cervinised mice. Among pigs that were incubated for up to 73 mpi, some gave diagnostic evidence of CWD replication in the brain between 42 and 72 mpi. Importantly, this was observed also in one orally challenged pig at 64 mpi and the presence of low-level CWD replication was confirmed by mouse bioassay. The authors of this study argued that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high and that the detection of infectivity in orally inoculated pigs with a mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.
3.2.1.3. Other species
Studies have demonstrated that the CWD agent(s) can be transmitted by the IC route in several species of rodents, such as voles (Subfamily Arvicolinae), deer mice (Peromyscus maniculatus), mice and hamsters (Subfamily Cricetinae). The susceptibility was, however, variable, being high in voles and deer mice but lower in mice and hamsters (Raymond et al., 2007; Heisey et al., 2010; Kurt et al., 2011; Di et al., 2013; Lee et al., 2013). Mink (subfamily Mustelinae) (Harrington et al., 2008), ferrets (Mustela putorius) (Bartz et al., 1998; Sigurdson et al., 2008) and cats (Mathiason et al., 2013) were susceptible to IC challenge with NA CWD sources, while CWD transmitted poorly to raccoons (Procyon lotor) by the IC route (Moore et al., 2019).
3.2.2. European isolates
The host range of CWD in Europe has been much less investigated so far, due to its recent identification. Among the cervid species involved in the CWD epidemics in North America, only some species (such as moose and reindeer) inhabit Europe; mule deer, white-tailed deer and elk/wapiti are American cervid species, although a few populations of white-tailed deer have been introduced into Europe. Others cervids that mainly inhabit Europe are red deer and roe deer. After the first detection in a reindeer in Norway in 2016 (Benestad et al., 2016), CWD has been detected in wild reindeer, moose and one red deer in Norway (Mysterud and Edmunds, 2019), in a moose in Finland in March 2018 and in three moose in Sweden in March, May and September 2019. CWD has not been detected
Chronic Wasting Disease (CWD) III www.efsa.europa.eu/efsajournal 14 EFSA Journal 2019;17(11):5863
so far in wild roe deer, fallow deer or white-tailed deer nor in any farmed cervid species. However, for fallow deer and white-tailed deer, the number of animals tested by the surveillance systems is still very low.
The potential host range of European CWD strains is under investigation by bioassay experiments in a range of model species; most of these studies are ongoing and there are no published data available so far. Data from the experiments that are known to be ongoing in different laboratories have been gathered for the purposes of this Opinion. Overall, reindeer CWD, moose CWD and red deer CWD brain isolates (and LRS isolates from some selected cases) are being tested for transmissibility in mice, hamsters, bank voles and in a range of tg mouse lines expressing PrP sequences from: cervids (Q226 or E226 deer PrP variants), small ruminants (ARQ, VRQ, AHQ and ARR PrP polymorphic variants), cattle, pig, vulture and human (M129 and V129 PrP polymorphic variants) (see Section 3.3.1). Importantly, in most of these animal models, the transmissibility of European CWD isolates will be directly comparable with the outcome of similar (published or ongoing) experiments with CWD isolates from North America.
While most of these studies are still ongoing, some experiments with CWD isolates from Europe have already produced evidence of transmission in some recipient species (Table 1). These include bank voles, conventional laboratory mice and tg mice expressing cervid PrP, sheep PrP and mouse PrP. The same rodent models are also susceptible to NA CWD isolates and will therefore allow comparative strain typing of NA and European CWD strains in due course. There is no strong evidence so far for rodent models being widely susceptible to NA isolates but not to European isolates or vice versa.
Table 1 summarises more than 500 ongoing, published or unpublished primary transmission experiments of NA or European CWD isolates from different cervids into various rodent models, which have been gathered following the requests described in Section 2.2. The CWD isolates are grouped according to geographical origin and cervid species, with each column summarising the results obtained with one or more CWD isolates from a given species and country. Rodent models are grouped according to the PrP species expressed. Some species have polymorphic PrP sequences, so more than one PrP sequence per species has been modelled. In these cases, each row summarises the data obtained with more than one PrP variant of a given species. Therefore, conventional mice include wt mice expressing PRNPa or PRNPb mouse PrP variants; bank voles include two genetic lines with different amino acids at codon 109 (Bv109M and Bv109I); tg-cervidPrP mice include mouse lines expressing several cervid PrP variants (the deer wt Q226, the elk wt E226, the WTD variant S96, the elk variant M132); tg-sheepPrP mice include mouse lines expressing the ARQ, VRQ, AHQ or ARR small ruminant PrP variants; finally, tg-humanPrP mice include mouse lines expressing M or V at the human PrP polymorphic codon 129. Therefore, each box in the Table 1 summarises the outcome of bioassay experiments with one or more CWD isolates (from the same species and origin) in one or more recipient rodent models (expressing PrP from a single given species).
Chronic Wasting Disease (CWD) III www.efsa.europa.eu/efsajournal 15 EFSA Journal 2019;17(11):5863
Most of the studies conducted by molecular/biochemical methods are still ongoing. The preliminary data obtained by molecular/biochemical methods were difficult to summarise and will not be reported in the present Opinion. This was mainly due to lack of detail in the results obtained by direct PrPSc analyses (PrPres typing, conformational stability, proteinase K resistance, which are intended to investigate CWD strains) and to the different methodological approaches employed in amplification assays (PMCA and RT-QuIC). The information gathered by this activity shows that experiments aimed at modelling the species barrier for NA or European CWD isolates into different animal species, including humans, are underway in different laboratories and will be of help for understanding the potential host range of CWD strains.
3.2.3 Impact of the PRNP gene on transmissibility
Polymorphisms in the PRNP gene are known to influence susceptibility/resistance to prion disease in both small ruminants and humans (for recent review, see EFSA BIOHAZ Panel 2014, EFSA BIOHAZ Panel, 2017; Diack et al., 2014). Effects of host PRNP polymorphisms on CWD susceptibility/resistance have also been described in a number of cervid species (reviewed in EFSA BIOHAZ Panel, 2017, 2018).
However, deer and elk wild-type PrP primary structures are equivalent, except at residue 226, which is glutamate in elk and glutamine in deer. The effect of this difference on CWD pathogenesis has been recently investigated using a gene-targeting approach in which the mouse PrP coding sequence was replaced with elk or deer PrP. The results obtained following experimental challenge with deer and elk CWD inocula from NA showed that the resulting GtE226 and GtQ226 mice had distinct kinetics of disease onset, with incubation times shorter in GtE226 than in GtQ226 mice, indicating that amino acid differences at PrP residue 226 dictate the selection and propagation of divergent strains in deer and elk with CWD. As prion strain properties largely dictate host range potential, these findings suggest that prion strains from elk and deer might pose distinct risks to sympatric species or humans exposed to CWD (Bian et al., 2019).
The most common cervid species in Europe (moose, red deer, reindeer and roe deer) share the same PrP primary structure, i.e. Q226. However, red deer PrP is polymorphic at residue 226 and can therefore code for either Q226 or E226. Interestingly, CWD cases detected so far in four Norwegian moose, the first Swedish moose and one Norwegian reindeer are all homozygous for Q226 (Benestad, 2019b,c,d), but the CWD case in red deer is instead homozygous for E226 (Vikøren et al., 2019). The impact of these differences in PrP genotype on the transmissibility and strain properties of European CWD isolates is currently under investigation using GtE226 and GtQ226 mice (Bian et al., 2019). PRNP genotypes of the other reindeer from Norway and of the other moose cases in Sweden and Finland are not in the public domain.
Data on the transmissibility of CWD in species with different PrP sequences obtained by in vivo or in vitro modelling allow the investigation of the structural basis of the transmission barriers for CWD. This in turn could provide hints for predicting, to some extent, the susceptibility of non-cervid species to CWD. Taken together, studies with CWD isolates from NA suggest that the 165–175 sequence similarity between cervid and host PrP is one important factor governing the susceptibility of different species to CWD (reviewed by Kurt et al., 2016). In particular, polymorphisms at N/S170 in the recipient species might be important for susceptibility, with species that have N170 being more susceptible than those with S170 (Kurt et al., 2016). However, this must not be seen as an absolute rule, as species having S170 in their PrP, such as squirrel monkeys, have also been reported to be susceptible to CWD. It is however pertinent to note that all livestock species and humans have PrP sequences with S170, so they should not be considered among the species with supposedly high susceptibility to NA CWD isolates. Ongoing experiments in rodent models seem to indicate a similar trend for European CWD isolates, as rodent models, apparently more susceptible to European CWD isolates such as bank voles and tg mice expressing deer PrP, are N170.
Little information is currently known about the genetics of either wild or farmed cervid populations in Europe. A recent published study of several deer species (mostly in Great Britain) reported that red deer showed the most PRNP gene variation, with polymorphisms at codons 98, 168, 226 and 247 and marked variability in genotype frequencies in different regions. Other deer species showed less variation, with roe and fallow deer having identical PRNP gene sequences in all the animals sampled. Based on comparison with PRNP sequences of NA cervids affected by CWD and limited experimental challenge data, the authors conclude that a high proportion of wild deer in Great Britain may be susceptible to CWD (Robinson et al., 2019). A similar conclusion was reached by a previous study of 715 genotyped cervids (red deer, roe deer and chamois) from the UK and Italy (Peletto et al., 2009).
3.2.4. Concluding remarks
• The transmission of prions between species is limited by the ‘transmission barrier’ and the amino acid sequence of the host PrP plays a very key role in the overall susceptibility to TSE. Even for prions deriving from the same species, the host range may vary according to the prion strain, implying that different CWD strains might have different host ranges and different potential for transmitting to livestock species and to humans.
• Whether the natural host range of CWD in NA extends beyond the family Cervidae is currently unclear and no natural infections have been reported so far in other wildlife species (e.g. predators and scavengers) with overlapping geographical ranges.
• NA CWD has been transmitted experimentally to cattle and sheep, but with incomplete attack rates. The species barrier appears higher for pigs, although challenged animals can support low-level prion amplification.
• Experimental transmission to tg mice and other rodent models shows some difference in the host ranges of different isolates but, particularly for the European isolates, many bioassays are still ongoing and data are not yet available.
• The number of strains, the strain diversity, the prevalence and the potential host range of disease in both NA and Europe CWD may be underestimated.
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WEDNESDAY, JULY 15, 2020
Kansas Chronic Wasting Disease Confirmed in Captive Cervid Herd
TUESDAY, JUNE 09, 2020
Wisconsin Trempealeau County Deer Farm Tests Positive for CWD Release Date: June 9, 2020
MONDAY, JUNE 01, 2020
Wisconsin CWD TSE Prion Continues to Spiral Out of Control, 6585 Cases Confirmed to Date in Wild, and it's anyone's guess for captive
TUESDAY, MAY 19, 2020
Montana White-tailed deer in Gallatin County suspected positive for CWD
MONDAY, FEBRUARY 03, 2020
Montana Chronic Wasting Disease CWD TSE Prion in Eastern Part of State Game Farm Elk
SATURDAY, MAY 16, 2020
Ohio Chronic Wasting Disease Detected on Wayne County Farm
THURSDAY, MAY 14, 2020
COLORADO As of February 2020, CWD has been detected in 33 of 54 deer herds, 14 of 43 elk herds, and 2 of 9 moose herds
Colorado Chronic Wasting Disease Response Plan December 2018
I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds.
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IMPORTANT PUBLIC HEALTH MESSAGE
Disease in humans resulting from CWD exposure has not been reported to date. However, public health officials cannot determine there is no risk from eating meat from infected animals. Consequently, officials recommend that people avoid exposure to CWD-infected animals. Please see the Colorado Department of Public Health and Environment website
for the most current recommendations on carcass testing and other preventive measures.
To minimize exposure to CWD and other diseases of potential concern, Colorado Parks and Wildlife (CPW) and state public health officials advise hunters not to shoot, handle or consume any deer, elk or moose that is acting abnormally or appears to be sick. When fielddressing game, wear rubber gloves and minimize the use of a bone saw to cut through the brain or spinal cord (backbone). Minimize contact with brain or spinal cord tissues, eyes, spleen or lymph nodes. Always wash hands and utensils thoroughly after dressing and processing game meat. (the map on page 71, cwd marked in red, is shocking...tss)
TUESDAY, JANUARY 07, 2020
Oklahoma Farmed Elk Lincoln County CWD Depopulation 3 Positive Elk with 1 Additional Dead Trace Out Confirmed Positive
FRIDAY, JUNE 26, 2020
Pennsylvania CWD TSE Prion AREAS EXPAND
WEDNESDAY, JANUARY 29, 2020
Pennsylvania CWD TSE Prion 2019-20 hunting seasons as of January 14, 148 of the samples had tested positive for CWD in Wild Deer
SUNDAY, DECEMBER 22, 2019
Pennsylvania Steady Climb of CWD TSE Prion Confirms 250 Positive To Date In Wild Cervid As At September 12, 2019
Pennsylvania Captive Cervid Industry Total CWD TSE Prion ??? anyone's guess...
THURSDAY, JANUARY 30, 2020
Michigan CWD TSE Prion Total Suspect Positive Deer Jumps To 181 to date
MONDAY, JANUARY 27, 2020
Michigan CWD TSE Prion MDARD 3 positive white-tailed deer from a Newaygo County deer farm depopulation and quarantine efforts update?
TUESDAY, JANUARY 14, 2020
Michigan MDARD has confirmed chronic wasting disease (CWD) in 3 white-tailed deer from a Newaygo County deer farm
WEDNESDAY, APRIL 29, 2020
Minnesota CWD investigation spurred by Douglas County deer farm detection concludes
SATURDAY, MARCH 14, 2020
Minnesota 4 More Farmed Deer and 1 wild positive for CWD TSE Prion
TUESDAY, JANUARY 21, 2020
Minnesota CWD update test results from deer harvested in the 2019 hunting season and the special hunts have returned 27 wild deer tested positive for CWD all from the southeast DMZ
FRIDAY, JANUARY 10, 2020
Minnesota Investigation leads to additional CWD positive deer on Pine County farm
FRIDAY, OCTOBER 04, 2019
Inactivation of chronic wasting disease prions using sodium hypochlorite
i think some hunters that don't read this carefully are going to think this is a cure all for cwd tse contamination. IT'S NOT!
first off, it would take a strong bleach type sodium hypochlorite, that is NOT your moms bleach she uses in her clothes, and store bought stuff.
Concentrated bleach is an 8.25 percent solution of sodium hypochlorite, up from the “regular bleach” concentration of 5.25 percent.Nov 1, 2013 https://waterandhealth.org/disinfect/high-strength-bleach-2/
second off, the study states plainly;
''We found that a five-minute treatment with a 40% dilution of household bleach was effective at inactivating CWD seeding activity from stainless-steel wires and CWD-infected brain homogenates. However, bleach was not able to inactivate CWD seeding activity from solid tissues in our studies.''
''We initially tested brains from two CWD-infected mice and one uninfected mouse using 40% bleach for 5 minutes. The results from these experiments showed almost no elimination of prion seeding activity (Table 4). We then increased the treatment time to 30 minutes and tested 40% and 100% bleach treatments. Again, the results were disappointing and showed less than a 10-fold decrease in CWD-seeding activity (Table 4). Clearly, bleach is not able to inactivate prions effectively from small brain pieces under the conditions tested here.''
''We found that both the concentration of bleach and the time of treatment are critical for inactivation of CWD prions. A 40% bleach treatment for 5 minutes successfully eliminated detectable prion seeding activity from both CWD-positive brain homogenate and stainless-steel wires bound with CWD. However, even small solid pieces of CWD-infected brain were not successfully decontaminated with the use of bleach.''
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0223659
https://chronic-wasting-disease.blogspot.com/2019/10/inactivation-of-chronic-wasting-disease.html
i think with all the fear from recent studies, and there are many, of potential, or likelihood of zoonosis, if it has not already happened as scjd, i think this study came out to help out on some of that fear, that maybe something will help, but the study plainly states it's for sure not a cure all for exposure and contamination of the cwd tse prion on surface materials. imo...terry
HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...
* 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]
Wednesday, September 11, 2019
Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion
172. Establishment of PrPCWD extraction and detection methods in the farm soil
Kyung Je Park, Hoo Chang Park, In Soon Roh, Hyo Jin Kim, Hae-Eun Kang and Hyun Joo Sohn
Foreign Animal Disease Division, Animal and Plant Quarantine Agency, Gimcheon, Gyeongsangbuk-do, Korea
ABSTRACT
Introduction: Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. 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 faeces of TSE-infected animals. Soil can serve as a stable reservoir for infectious prion proteins. We found that PrPCWD can be extracted and detected in CWD contaminated soil which has kept at room temperature until 4 years after 0.001 ~ 1% CWD exposure and natural CWD-affected farm soil through PBS washing and sPMCAb.
Materials and Methods: Procedure of serial PMCAb. CWD contaminated soil which has kept at room temperature (RT) for 1 ~ 4 year after 0.001%~1% CWD brain homogenates exposure for 4 months collected 0.14 g. The soil was collected by the same method once of year until 4 year after stop CWD exposure. We had conducted the two steps. There are two kinds of 10 times washing step and one amplification step. The washing step was detached PrPSc from contaminated soil by strong vortex with maximum rpm. We harvest supernatant every time by 10 times. As the other washing step, the Washed soil was made by washing 10 times soil using slow rotator and then harvest resuspended PBS for removing large impurity material. Last step was prion amplification step for detection of PrPCWD in soil supernatant and the washed soil by sPMCAb. Normal brain homogenate (NBH) was prepared by homogenization of brains with glass dounce in 9 volumes of cold PBS with TritonX-100, 5 mM EDTA, 150 mM NaCl and 0.05% Digitonin (sigma) plus Complete mini protease inhibitors (Roche) to a final concentration of 5%(w/v) NBHs were centrifuged at 2000 g for 1 min, and supernatant removed and frozen at −70 C for use. CWD consisted of brain from natural case in Korea and was prepared as 10%(w/v) homogenate. Positive sample was diluted to a final dilution 1:1000 in NBH, with serial 3:7 dilutions in NBH. Sonication was performed with a Misonix 4000 sonicator with amplitude set to level 70, generating an average output of 160W with two teflon beads during each cycle. One round consisted of 56 cycles of 30 s of sonication followed 9 min 30 s of 37°C incubation. Western Blotting (WB) for PrPSc detection. The samples (20 µL) after each round of amplification were mixed with proteinase K (2 mg/ml) and incubated 37°C for 1 h. Samples were separated by SDS-PAGE and transferred onto PVDF membrane. After blocking, the membrane was incubated for 1 h with 1st antibody S1 anti rabbit serum (APQA, 1:3000) and developed with enhanced chemiluminescence detection system.
Results: We excluded from first to third supernatant in view of sample contamination. It was confirmed abnormal PrP amplification in all soil supernatants from fourth to tenth. From 0.01% to 1% contaminated washed soils were identified as abnormal prions. 0.001% contaminated washed soil did not show PrP specific band (Fig 1). The soil was collected by the same method once of year until 4 year after stop CWD exposure. After sPMCAb, there were no PrPCWD band in from second to fourth year 0.001% washed soil. but It was confirmed that the abnormal prion was amplified in the washing supernatant which was not amplified in the washed soil. we have decided to use soil supernatant for soil testing (Fig. 2). After third rounds of amplification, PrPSc signals observed in three out of four sites from CWD positive farm playground. No signals were observed in all soil samples from four CWD negative farm (Fig. 3).
Conclusions: Our studies showed that PrPCWD persist in 0.001% CWD contaminated soil for at least 4 year and natural CWD-affected farm soil. When cervid reintroduced into CWD outbreak farm, the strict decontamination procedures of the infectious agent should be performed in the environment of CWD-affected cervid habitat.
===
186. Serial detection of hematogenous prions in CWD-infected deer
Amy V. Nalls, Erin E. McNulty, Nathaniel D. Denkers, Edward A. Hoover and Candace K. Mathiason
Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA
CONTACT Amy V. Nalls amy.nalls@colostate.edu
ABSTRACT
Blood contains the infectious agent associated with prion disease affecting several mammalian species, including humans, cervids, sheep, and cattle. It has been confirmed that sufficient prion agent is present in the blood of both symptomatic and asymptomatic carriers to initiate the amyloid templating and accumulation process that results in this fatal neurodegenerative disease. Yet, to date, the ability to detect blood-borne prions by in vitro methods remains difficult.
We have capitalized on blood samples collected from longitudinal chronic wasting disease (CWD) studies in the native white-tailed deer host to examine hematogenous prion load in blood collected minutes, days, weeks and months post exposure. Our work has focused on refinement of the amplification methods RT-QuIC and PMCA. We demonstrate enhanced in vitro detection of amyloid seeding activity (prions) in blood cell fractions harvested from deer orally-exposed to 300 ng CWD positive brain or saliva.
These findings permit assessment of the role hematogenous prions play in the pathogenesis of CWD and provide tools to assess the same for prion diseases of other mammalian species.
Considering the oral secretion of prions, saliva from CWD-infected deer was shown to transmit disease to other susceptible naïve deer when harvested from the animals in both the
and preclinical stages69
of infection, albeit within relatively large volumes of saliva (50 ml). In sheep with preclinical, natural scrapie infections, sPMCA facilitated the detection of PrPSc within buccal swabs throughout most of the incubation period of the disease with an apparent peak in prion secretion around the mid-term of disease progression.70
The amounts of prion present in saliva are likely to be low as indicated by CWD-infected saliva producing prolonged incubation periods and incomplete attack rates within the transgenic mouse bioassay.41
snip...
Indeed, it has also been shown that the scrapie and CWD prions are excreted in urine, feces and saliva and are likely to be excreted from skin. While levels of prion within these excreta/secreta are very low, they are produced throughout long periods of preclinical disease as well as clinical disease. Furthermore, the levels of prion in such materials are likely to be increased by concurrent inflammatory conditions affecting the relevant secretory organ or site. Such dissemination of prion into the environment is very likely to facilitate the repeat exposure of flockmates to low levels of the disease agent, possibly over years.
snip...
Given the results with scrapie-contaminated milk and CWD-contaminated saliva, it seems very likely that these low levels of prion in different secreta/excreta are capable of transmitting disease upon prolonged exposure, either through direct animal-to-animal contact or through environmental reservoirs of infectivity.
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
***>>> 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.
HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...
* 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]
Wednesday, September 11, 2019
Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion
SATURDAY, MARCH 16, 2019
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary Submission
THURSDAY, SEPTEMBER 27, 2018
***> Estimating the impact on food and edible materials of changing scrapie control measures: The scrapie control model
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]
2018 - 2019
***> This is very likely to have parallels with control efforts for CWD in cervids.
Rapid recontamination of a farm building occurs after attempted prion removal
Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2
Abstract
The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity.
Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids.
Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent.
Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA).
A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay.
Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3.
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
snip...
As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.
Funding This study was funded by DEFRA within project SE1865.
Competing interests None declared.
Saturday, January 5, 2019
Rapid recontamination of a farm building occurs after attempted prion removal
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018
P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer
Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1)
(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada.
Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer.
Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection.
Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD.
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> 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.
Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3
Correspondence
Gudmundur Georgsson ggeorgs@hi.is
1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland
2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland
3 Bethesda, Maryland, USA
Received 7 March 2006 Accepted 6 August 2006
In 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.
TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION
*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION
SEE;
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
Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).
Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
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.
source reference Prion Conference 2015 abstract book
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
Sandra Pritzkow,1 Rodrigo Morales,1 Fabio Moda,1,3 Uffaf Khan,1 Glenn C. Telling,2 Edward Hoover,2 and Claudio Soto1, * 1Mitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, 6431 Fannin Street, Houston, TX 77030, USA
2Prion Research Center, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA
3Present address: IRCCS Foundation Carlo Besta Neurological Institute, 20133 Milan, Italy *Correspondence: claudio.soto@uth.tmc.edu http://dx.doi.org/10.1016/j.celrep.2015.04.036
SUMMARY
Prions are the protein-based infectious agents responsible for prion diseases. Environmental prion contamination has been implicated in disease transmission. Here, we analyzed the binding and retention of infectious prion protein (PrPSc) to plants. Small quantities of PrPSc contained in diluted brain homogenate or in excretory materials (urine and feces) can bind to wheat grass roots and leaves. Wild-type hamsters were efficiently infected by ingestion of prion-contaminated plants. The prion-plant interaction occurs with prions from diverse origins, including chronic wasting disease. Furthermore, leaves contaminated by spraying with a prion-containing preparation retained PrPSc for several weeks in the living plant. Finally, plants can uptake prions from contaminated soil and transport them to aerial parts of the plant (stem and leaves). These findings demonstrate that plants can efficiently bind infectious prions and act as carriers of infectivity, suggesting a possible role of environmental prion contamination in the horizontal transmission of the disease.
INTRODUCTION
snip...
DISCUSSION
This study shows that plants can efficiently bind prions contained in brain extracts from diverse prion infected animals, including CWD-affected cervids. PrPSc attached to leaves and roots from wheat grass plants remains capable of seeding prion replication in vitro. Surprisingly, the small quantity of PrPSc naturally excreted in urine and feces from sick hamster or cervids was enough to efficiently contaminate plant tissue. Indeed, our results suggest that the majority of excreted PrPSc is efficiently captured by plants’ leaves and roots. Moreover, leaves can be contaminated by spraying them with a prion-containing extract, and PrPSc remains detectable in living plants for as long as the study was performed (several weeks). Remarkably, prion contaminated plants transmit prion disease to animals upon ingestion, producing a 100% attack rate and incubation periods not substantially longer than direct oral administration of sick brain homogenates.
Finally, an unexpected but exciting result was that plants were able to uptake prions from contaminated soil and transport them to aerial parts of the plant tissue. Although it may seem farfetched that plants can uptake proteins from the soil and transport it to the parts above the ground, there are already published reports of this phenomenon (McLaren et al., 1960; Jensen and McLaren, 1960;Paungfoo-Lonhienne et al., 2008). The high resistance of prions to degradation and their ability to efficiently cross biological barriers may play a role in this process. The mechanism by which plants bind, retain, uptake, and transport prions is unknown. We are currently studying the way in which prions interact with plants using purified, radioactively labeled PrPSc to determine specificity of the interaction, association constant, reversibility, saturation, movement, etc.
Epidemiological studies have shown numerous instances of scrapie or CWD recurrence upon reintroduction of animals on pastures previously exposed to prion-infected animals. Indeed, reappearance of scrapie has been documented following fallow periods of up to 16 years (Georgsson et al., 2006), and pastures were shown to retain infectious CWD prions for at least 2 years after exposure (Miller et al., 2004). It is likely that the environmentally mediated transmission of prion diseases depends upon the interaction of prions with diverse elements, including soil, water, environmental surfaces, various invertebrate animals, and plants.
However, since plants are such an important component of the environment and also a major source of food for many animal species, including humans, our results may have far-reaching implications for animal and human health. Currently, the perception of the riskfor animal-to-human prion transmission has beenmostly limited to consumption or exposure to contaminated meat; our results indicate that plants might also be an important vector of transmission that needs to be considered in risk assessment.
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
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 ***
WEDNESDAY, MARCH 13, 2019
CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood
Subject: Prion 2019 Conference
See full Prion 2019 Conference Abstracts
see scientific program and follow the cwd studies here;
Thursday, May 23, 2019
Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts
THURSDAY, DECEMBER 19, 2019
TSE surveillance statistics exotic species and domestic cats Update December 2019
MONDAY, DECEMBER 16, 2019
Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update
***> ''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) <***
What if?
> 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).***
Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
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.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Prion 2017 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
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip…
see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry
PRION 2019 ABSTRACTS
1. Interspecies transmission of the chronic wasting disease agent
Justin Greenlee
Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service
ABSTRACT
The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.
53. Evaluation of the inter-species transmission potential of different CWD isolates
Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa
aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile
ABSTRACT
Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.
56. Understanding chronic wasting disease spread potential for at-risk species
Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
CONTACT Catherine I. Cullingham cathy.cullingham@ualberta.ca
ABSTRACT
Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.
KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates
Thursday, May 23, 2019
Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts
see full Prion 2019 Conference Abstracts
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
snip…full text;
SATURDAY, FEBRUARY 09, 2019
Experts: Yes, chronic wasting disease in deer is a public health issue — for people
SATURDAY, FEBRUARY 23, 2019
Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019
TUESDAY, NOVEMBER 04, 2014
Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011
Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "
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
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.
sporadic, spontaneous CJD, 85%+ of all human TSE, just not just happen. never in scientific literature has this been proven.
if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;
sporadic = 54,983 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
spontaneous = 325,650 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous
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).***
FRIDAY, JULY 26, 2019
Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species
TUESDAY, JANUARY 21, 2020
***> 2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020
***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***
***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<***
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
***> 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.<***
***> 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) <***
FRIDAY, OCTOBER 25, 2019
Experts testify United States is underprepared for bioterrorism threats Transmissible Spongiform Encephalopathy TSE Prion disease
***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.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
https://www.nature.com/articles/srep11573
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.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***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
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.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***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
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
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
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
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
MONDAY, JULY 27, 2020
Pennsylvania GAME COMMISSION UNVEILS NEW CWD RESPONSE PLAN
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
3:27 PM
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