Chronic Wasting Disease CWD TSE Prion Cervid State by State and Global Update November 2020
Chronic Wasting Disease CWD TSE Prion Cervid Update November 2020 BY STATE
*** Alabama CWD TSE Prion
Alabama, to date, has detected NO cases of CWD TSE Prion...tss
WFF Reports No CWD Positives in Alabama; Testing Continues
Amy Silvano and Jerremy Ferguson of the Alabama Wildlife and Freshwater Fisheries Division take samples from a deer in north Alabama to test for CWD. Photo by Billy Pope
November 5, 2020
By DAVID RAINER, Alabama Department of Conservation and Natural Resources
With the nation focused on the coronavirus, very little has been heard about the status of chronic wasting disease (CWD) in Alabama.
Chuck Sykes, Director of the Alabama Wildlife and Freshwater Fisheries (WFF) Division, has some cautious good news about the spread of CWD in the South.
“Despite what you read on Facebook, just because COVID-19 hit, CWD didn’t go away,” Sykes said. “We just haven’t been talking about it as much. We’re still taking samples. We had a target of about 1,630 samples last year, and I think we took nearly 1,700, covering all counties, with no positives.”
Last year, Mississippi and Tennessee reported new positive CWD tests. That cautious good news is the infections are not spreading toward Alabama.
“Right now, we’re staying basically status quo from last year,” Sykes said. “It looks like the cases in Tennessee and Mississippi are moving northwest. We have no new zones, nothing any closer than what we had last year. And nothing has tested positive in Alabama, so we’re on the same protocol as we were on last year.”
Visit www.outdooralabama.com/CWD-Info and scroll down the page to view the Alabama CWD Strategic Surveillance and Response Plan, which establishes a CWD Management Zone around the location of a CWD positive deer and implements specific response protocols dependent on the distance from the CWD positive. Positive deer in Pontotoc County, Mississippi, and Hardeman County, Tennessee, have prompted a response affecting Alabama’s surveillance activities. Portions of five counties in Alabama – Colbert, Franklin, Lamar, Lauderdale and Marion – are within 50 miles of those positives. Sampling and testing for CWD have been increased substantially in those counties.
CWD has only been shown to affect members of the deer family, including whitetails, mule deer, elk, moose and caribou. CWD is a fatal neurological disease, a form of transmissible spongiform encephalopathy (TSE), which causes lesions on the brain. As the disease progresses, the affected animal will develop holes in the brain and eventually die. Infected animals may be infected for 5 years or longer before they exhibit symptoms.
The first case of CWD was discovered in Colorado in 1967. The disease spread very slowly, only taking in a 15- to 20-county region on the Colorado, Nebraska and Wyoming borders in the next 30 years. In the late 90s, CWD was detected in Saskatchewan. That incident was traced to captive elk from South Dakota that were transported to Canada. CWD continues to spread and now has been found in 26 states and three Canadian provinces. South Korea, Finland, Norway and Sweden also have detected CWD. South Korea’s CWD-positive animals can be traced back to the live transport of captive deer from infected facilities in Saskatchewan. Over the past 20-plus years, the movement of live cervids or infected carcasses by humans has contributed significantly to the increased spread of the disease.
Regulations that banned the importation of live deer into Alabama have been in effect for many years. The regulations were amended a couple of years ago to prohibit the importation of deer carcasses from all states and countries. Visit www.outdooralabama.com/cwd for regulations about importing deer parts from out-of-state.
WFF officials have placed CWD Sample Collection Stations all around the state to encourage the public to aid in the monitoring of the deer herd. Photo by Billy Pope.
Regulations allow for the importation of certain parts of the deer but not whole carcasses. Permitted parts include:
Meat from the family Cervidae (white-tailed deer, mule deer, elk, moose, fallow deer, red deer, sika deer, caribou, reindeer, etc.) that has been completely deboned Cleaned skull plates with bare attached antlers, if no visible brain or spinal cord tissue is present Unattached bare antlers or sheds Raw capes, if no visible brain or spinal cord tissue is present Upper canine teeth, if no root structure or other soft tissue is present Finished taxidermy products or tanned hides The WFF Enforcement Section has also implemented procedures to intercept the potential illegal importation of deer carcasses into the state with surveillance along state borders in an effort to keep CWD out of the state. The “Don’t Bring It Home” campaign highlights the ban on the importation of deer carcasses.
The disease is primarily spread by body fluids such as saliva, urine and feces. The infectious agent, called a prion, can even survive outside the animal’s body.
No evidence exists at this time that CWD can be transmitted to humans. However, caution is recommended when consuming deer. The prion that causes CWD cannot be eradicated by cooking.
The CDC recommends that hunters who harvest deer in areas with CWD should have the deer tested for the disease before consuming the meat. If the test comes back as CWD detected, the CDC recommends the proper disposal of the venison. That venison should not be thrown out by the individual; rather, contact a WFF official or enforcement officer who will ensure its proper disposal.
Last year, WFF set up self-service stations with freezers for hunters to drop off deer heads for sampling and testing. At the self-service locations, hunters must first remove the deer’s head with 4-6 inches of neck attached. For bucks, antlers can be removed at the base of each antler or by removing the skull plate before bagging the head. Hunters will then place the head in the provided plastic bag and tie it closed. They will need to complete all sections of the Biological Sample Tag and attach the tag to the bag with a zip tie. Hunters should remove and keep the Biological Sample Receipt located at the bottom of the Biological Sample Tag before placing the bagged head in the freezer. All materials needed to drop off a sample are provided at each freezer location. Hunters can check the results of their test by visiting www.outdooralabama.com/cwd-sampling-results and entering the six-digit number found on the Biological Sample Receipt.
Visit www.outdooralabama.com/cwd-sampling for an interactive map of self-service locations throughout the state.
“We were a little disappointed about the number of samples dropped off at the self-service freezers last year,” Sykes said. “Hopefully this year it will be better. We’ve got good relationships with a lot of hunting clubs, processors and taxidermists that are helping us. A lot of our DMAP (Deer Management Assistance Program) participants are helping us. But it would be nice to get more random samples from the public.”
In 2018, WFF provided funds for the Alabama Department of Agriculture and Industries (ADAI) to purchase equipment to perform CWD testing. The equipment is housed at ADAI’s Thompson Bishop Sparks Diagnostic Laboratory in Auburn. The equipment and technician have been certified to test for CWD by the U.S. Department of Agriculture and can test up to 90 samples per day.
To assist with these efforts, WFF recently created the Sick Deer Report. The public can report deer acting abnormally or a deer that has died for no apparent reason at www.outdooralabama.com/wildlife-related-diseases/report-sick-deer or by calling one of WFF’s district offices. Reports should include contact information for the person making the report, location of the deer and the symptoms observed. A member of the WFF staff will follow up to determine what may have caused the illness or strange behavior and see if the deer should be tested for CWD. Visit www.outdooralabama.com/hunter-resources/law-enforcement-contacts for information on the five WFF district offices.
Research into CWD received a significant boost recently when the U.S. Congress passed America’s Conservation Enhancement Act. Included in that legislation is the creation of the National Chronic Wasting Disease Task Force within the U.S. Fish and Wildlife Service.
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WFF Reports No CWD Positives; Testing Continues
Alabama Department of Conservation & Natural Resources sent this bulletin at 11/06/2020 09:53 AM CST
Outdoor Alabama Weekly WFF Reports No CWD Positives; Testing Continues By DAVID RAINER
Alabama Department of Conservation and Natural Resources
THURSDAY, OCTOBER 03, 2019
ALABAMA PREPARES FOR THE STORM Fall 2019 CWD TSE PRION Public Information Meeting Schedule
TUESDAY, MARCH 29, 2016
ALABAMA CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM?
*** Alaska CWD TSE Prion
Alaska, to date, has detected NO cases of CWD TSE Prion...tss
Chronic Wasting Disease and Alaska
THE ALASKA BOARD OF GAME 2020/2021 Proposed Changes to Regulations • Central & Southwest Region • Statewide Regulations
The title to this proposal was clarified 9/21/20 to indicate the proposed change prohibits use or urine from any species of the deer family and is not limited to deer or elk urine. PROPOSAL 130 5 AAC 92.080. Unlawful methods of taking game; exceptions. Prohibit use of urine from any species of the deer family as bait or scent lures as follows: The following methods of taking game are prohibited: …
(15) with the use of [DEER OR ELK] urine from any species of the deer (Cervidae) family, and while in immediate personal possession of [DEER OR ELK] urine from any species of the deer (Cervidae) family, including scent lures; …
(18) repealed; 7/1/2021. [WITH THE USE OF MOOSE, CARIBOU, AND REINDEER URINE AS SCENT LURES, AND WHILE IN IMMEDIATE PERSONAL POSSESSION OF MOOSE, CARIBOU, OR REINDEER URINE, INCLUDING SCENT LURES, IN UNITS 12, 19, 20, 21, 24, 25, 26(B), AND 26(C).]
What is the issue you would like the board to address and why? Chronic Wasting Disease (CWD) can be transmitted by urine, and more types (species) of urine are becoming available to hunters to use as bait or scent lures. In 2012, the Board of Game (board) prohibited the use of deer or elk urine for hunting statewide, and in March of 2020 the board prohibited the use of moose, caribou, and reindeer urine for hunting in the Interior and Eastern Arctic Region. At that meeting, the department recommended the board adopt the proposal statewide. Due to the legal meeting notice not covering statewide topics, and not wanting to delay taking action on the proposal, the board adopted the proposal for the Interior and Eastern Arctic Region only. The department is now proposing a broader prohibition on the use of natural urine as bait or scent lures, in order to further protect Alaska’s game populations.
PROPOSED BY: Alaska Department of Fish and Game (HQ-F20-043)
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2020-2021 Alaska Hunting Regulations
•Chronic Wasting Disease (CWD) - No risk to humans, high risk to deer, elk, and moose. To date, CWD has NOT been detected in free ranging Alaska wildlife. Elsewhere, infected deer species show signs including extreme weight loss, excessive salivation, stumbling, and tremors. Report these signs to ADF&G.
CHRONIC WASTING DISEASE
To date, CWD has NOT been detected in any Alaskan wildlife. However, Alaska currently maintains a general targeted diseae surveillance program that will test for CWD in clinical, suspect cases in moose, caribou, deer or elk.
Update: The Alaska Board of Game adopted Prop 104 (PDF 537 kB) during the statewide meeting — January 13–18, 2012, which prohibits the use of deer or elk urine for use in taking game.
*** Arizona CWD TSE Prion
Arizona, to date, has detected NO cases of CWD TSE Prion...tss
Q: Has the disease been detected in Arizona? A: No.
The Arizona Game and Fish Department has been testing for the presence of CWD in Arizona since 1998. While CWD has been found in the neighboring states of Utah, New Mexico and Colorado, the disease has not been detected here.
ARIZONA GAME AND FISH DEPARTMENT
CHRONIC WASTING DISEASE FY2019/2020 REPORT
EXECUTIVE SUMMARY
The Arizona Game and Fish Department (AGFD) has been surveying for chronic wasting disease (CWD) for the past 24 years. The Department continues monitoring efforts to detect the introduction of CWD in the state. During the 2019/2020 collection season, a total of 1,248 samples were tested. To date, CWD has not been detected in Arizona populations. Over the past several years, the Department has focused on increasing sample size in areas of highest concern and placed less focus on the centralized units in the state. The areas of highest concern include the game management units (GMUs) on the northern (high risk) and eastern (high and medium risk) portions of the state, as well as samples from animals harvested outside of Arizona that are brought into the state. This year, program personnel made efforts to increase sample sizes in these areas by recruiting new businesses in AGFD regions with high risk units and setting up a voluntary check station on the eastern side of the state. Despite these efforts, during 2019/2020, samples collected in high risk units accounted for only 37.4% (n=453) of samples collected from Department GMUs; this is down from 2018/2019 (55.3 %) and well below the average for the previous 5 sampling years (52.6%). We also fell short of the sampling quotas for medium risk units set forth at the beginning of the 2019/2020 season by 16.3% (49 samples). However, we exceeded our quota for sampling efforts in low risk units. The number of samples collected from medium risk GMUs (n = 251) fell short of the sampling quota of 300 by 49 samples. The number of samples collected from the low risk GMUs (n = 508) was the most since the 2011/2012 sampling season. Samples tested from out of state harvests accounted for 1.4% (n = 18), down from 4.8% (n = 63) in 2018/2019.
The Department will continue to conduct surveillance for CWD because of the impact of the disease on deer and elk populations where it currently occurs and the need to rapidly identify introduction of the disease in Arizona’s elk and deer. In the event CWD is detected in Arizona, a response plan and subsequent management options are in place.
INTRODUCTION
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*** Arkansas CWD TSE Prion
SATURDAY, NOVEMBER 21, 2020
Arkansas CWD TSE Prion positive deer confirmed in Logan County
***> To date, 891 deer and 30 elk have tested positive for the disease in Arkansas.
THURSDAY, SEPTEMBER 24, 2020
ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE 845 Cases Positive To Date
FRIDAY, JANUARY 24, 2020
Arkansas Chronic Wasting Disease CWD TSE Prion FY2020 211 Positive Cases as of January 17, 2020
SUNDAY, JANUARY 05, 2020
Arkansas Chronic Wasting Disease CWD TSE Prion 2019 to 2020 Totals As Of December 3, 2019 399 Confirmed with more pending results
*** California CWD TSE Prion
California, to date, has detected NO cases of CWD TSE Prion...tss
Since Chronic Wasting Disease (CWD) was first identified in wild deer, it has been detected in 26 states, 4 Canadian provinces, South Korea, Norway, and Finland. To date CWD has not been detected in California. This is a disease of major concern for cervids and may negatively impact these prey populations where it occurs. Through legislation and geography, California is at relatively low risk for CWD; however, it has the potential to spread to California’s deer and elk populations, and surveillance for the disease will remain a priority for CDFW. See the Q&A below to find out more about this devastating disease and what you can do to help.
CDFW - 2020 Chronic Wasting Disease Surveillance and Deer Hunter Check Stations
2020 California
BIG GAME HUNTING DIGEST
CHRONIC WASTING DISEASE
INCREASED SURVEILLANCE
Since 1999, California has tested approximately 4,500 deer and elk for CWD. To date, no CWD has been found in California deer or elk. However, the potential for CWD to spread to California’s deer and elk populations still exists and surveillance for the disease remains important. The CDFW will be increasing CWD surveillance efforts throughout the state over the next few years. Hunters are a vital partner in these surveillance efforts and voluntary CWD check stations will be set-up to facilitate surveillance throughout the state. For additional information on surveillance in CA visit www.wildlife.ca.gov/cwd or contact The Wildlife Investigations Laboratory at 916- 358-2790 or WILab@wildlife.ca.gov.
*** Colorado CWD TSE PRION
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)
SATURDAY, FEBRUARY 01, 2020
Colorado confirmed CWD TSE Prion in 24 game management units in the state where it previously hadn’t been found
*** Connecticut CWD TSE PRION
Connecticut to date, has detected NO cases of CWD TSE Prion...tss
CWD has been documented in 25 states and 4 Canadian provinces; the disease has not been found in Connecticut or New England.
What is being done about CWD in Connecticut?
Connecticut and all other northeastern states have taken measures to prevent the spread of CWD. The Connecticut Department of Energy and Environmental Protection (DEEP) has taken the following CWD management actions:
Connecticut, along with many other states, has banned the importation of live cervids (species in the deer/elk family) across state lines. An emergency regulation that was adopted in October 2005 to address concerns about CWD became permanent in September 2007. This regulation prohibits hunters from transporting into Connecticut any deer or elk carcasses or part thereof from any state where CWD has been documented, unless the meat has been de-boned. Specific wording of the regulation follows:
“Section 26-55-4: No person shall import or possess whole carcasses or parts thereof of any deer, moose, or elk from wild or captive herds from other states or Canadian Provinces where chronic wasting disease has been confirmed, including, but not limited to, Colorado, Wyoming, Utah, New Mexico, Montana, South Dakota, Kansas, Minnesota, Wisconsin, Illinois, Nebraska, Oklahoma, New York, West Virginia, Alberta and Saskatchewan. Any additional states* and provinces where chronic wasting disease is confirmed will be published in the Department's annual Hunting and Trapping Guide and on the Department's website. This provision shall not apply to meat that's de-boned, cleaned skullcaps, hides or taxidermy mounts.”
*See list above of additional states and Canadian provinces were CWD has been documented since this regulation was passed.
In fall 2003, the DEEP, in cooperation with the UCONN Wildlife Conservation Research Center, initiated a surveillance program to determine if CWD existed in Connecticut. The program included testing deer using random surveillance of hunter-harvested and road-killed deer, and targeted surveillance of suspect animals (exhibited some symptoms consistent with CWD). Through random surveillance, over 230 samples were collected statewide and all tested negative for CWD. Deer were sampled from every county and deer management zone in the state. The extent of random sampling conducted in 2003 provides a high degree of confidence that CWD is not present in Connecticut. Through targeted surveillance, 4 suspect wild deer were collected and all tested negative for CWD (3 were hit by a vehicle and initially survived; 1 was an abandoned fawn being rehabilitated at a captive facility).
In 2004, 298 randomly collected deer were tested for CWD from Deer Management Zone (DMZ) 11. Sampling efforts were focused in DMZ 11 because of the density of deer, relatively high number of captive deer facilities (6), and its close proximity to New York (New York has over 400 captive deer facilities with almost 10,000 deer and elk). Additionally, 6 suspect animals were collected and tested for CWD. All samples tested negative for CWD.
From 2005-2011, a CWD surveillance program approved by USDA-APHIS was designed to focus sampling efforts in areas that were considered high and moderate risk. During this 7-year period, a total of 4,384 testable samples were collected from deer harvested during the archery, shotgun/rifle, or crop damage season and from deer found on roadways throughout the state.
Funding provided by the U.S. Department of Agriculture, Animal and Plant Health Inspection Service (USDA-APHIS) was eliminated from the federal budget in 2012, so no CWD testing was conducted in 2012 or 2013. However, a joint partnership between Connecticut DEEP and the Stewart B. McKinney National Wildlife Refuge, with financial assistance from the U.S. Fish and Wildlife Service, National Wildlife Refuge System (USFWS-NWRS), allowed for testing to be conducted in 2014 through 2016. With the testing of over 32,000 deer in New York with no additional CWD cases being documented, the DEEP Wildlife Division no longer considers deer management zones 1, 6, and 11 to be high risk. Therefore, sampling will be stratified across all zones based on deer density. Since 2014, about 350 samples were collected each year. Since sampling efforts began in 2003, no cases of CWD have been detected in Connecticut or New England. Although additional funding sources for testing were lost in 2017, the Wildlife Division continues to collect samples to test for CWD. Hunters interested in donating deer heads for testing should keep the heads cool (not frozen) and arrange for them to be picked up by contacting Andrew.labonte@ct.gov (860-418-5921).
NEW REGULATION (effective in 2020): For the safety of Connecticut's deer herd, no person shall possess or use, for the purposes of taking or attempting to take or attract deer or for the surveillance or scouting of deer, any product bought or sold that is manufactured or refined that contains or purports to contain deer urine. Products labeled as "synthetic" may still be used. Products with vague descriptions about their contents are not recommended for use. CWD can spread through exposure to infected deer urine.
*** Delaware CWD TSE PRION
Delaware, to date, has detected NO cases of CWD TSE Prion...tss
Chronic Wasting Disease (CWD) is a naturally occurring disease of the brain and nervous system in deer, elk, and moose. CWD attacks the brain of these animals producing small lesions that eventually result in death. The body condition of animals that contract CWD tends to deteriorate before death. Currently there is no treatment for deer that contract CWD and is invariably fatal to the animal. No cases of human infection have been associated with CWD. Since 2002, the Division has collected over 9,000 CWD samples from deer harvested in Delaware and none have been positive for the disease.
Delaware Deer Management Plan 2010 – 2019
A Guide to How and Why Deer are Managed in The First State
To be better prepared if CWD is detected in Delaware, the Division of Fish & Wildlife is currently working on a response plan. Currently, this response plan has been written but has not yet been finalized. Final preparations will be made in the near future. Detailed information on HD, CWD, and other common diseases and ailments that afflict whitetailed deer can be found in Appendix 6.
Chronic Wasting Disease - Chronic Wasting Disease (CWD) is not currently found in Delaware.
*** Florida CWD TSE Prion
Florida, to date, has detected NO cases of CWD TSE Prion...tss
Florida Fish and Wildlife Conservation Commission
CWD Monitoring Program
The Florida Fish and Wildlife Conservation Commission (FWC) has an ongoing monitoring program to detect Chronic Wasting Disease (CWD). It has not been found in Florida; however, continued surveillance is necessary to confirm Florida remains free of CWD. Hunters can support the FWC’s surveillance efforts by voluntarily submitting their deer heads for testing (skull cap and antlers can be removed and kept by the hunter). Learn more by calling the CWD hotline at 866-293-9282.
CWD has not been found in Florida. The FWC is working with the Florida Department of Agriculture and Consumer Services, hunters, captive cervid owners, landowners, and the public to help keep Florida CWD free.
MONDAY, AUGUST 01, 2016
Florida Fish and Wildlife Conservation Commission CWD TSE Prion Surveillance Monitoring Programs and Testing
*** Georgia CWD TSE Prion
Georgia, to date, has detected NO cases of CWD TSE Prion...tss
How can it be prevented from coming to Georgia?
The movement of live animals is the greatest risk factor for introducing CWD. Because there is no reliable live test available to check for CWD in deer, deer movements pose a high risk for moving animals that may be shedding prions but not yet showing symptoms of the disease. As such, the live importation of all deer species from other states has been prohibited since 2005. Additionally, Georgia hunters hunting in CWD positive states may only bring home boned out meat, hides, cleaned skull plate with antlers attached, elk ivories, and finished taxidermy mounts. All other carcass parts must be left behind. While the requirement applies only to CWD positive states, this is a good practice to follow no matter what state you’re hunting. Actions that increase the transfer of saliva among deer, such as supplemental feeding, should also be discouraged or minimized.
Although we have not detected the disease in Georgia, it is possible that it could exist and has not been found yet.
Feeding deer increases the possibility of direct contact with an infected individual or the body fluids of that animal, particularly saliva. Feeders that spread feed, such as spin feeders pose less risk of saliva transfer than trough style or gravitational feeders. Although CWD prions can be found in the urine of infected animals there has been no documented spread of the disease through use of natural deer urine attractants. However, to minimize the potential risk of spreading the disease in this manner, only natural urine products bearing the Archery Trade Association Deer Protection Program Checkmark or synthetic urine products may be used. Read more about the prevention of CWD.
Keep CWD out of Georgia.
Georgia Surveillance and Response Strategies for Chronic Wasting Disease of Free-Ranging and Captive Cervids
Revised September 2018
Charlie Killmaster, State Deer Biologist
Kristina Johannsen, Programs Operations Manager
Appendix:
History of CWD Sampling Efforts in Georgia
Prior to the federally funded project in 2002, GA DNR-WRD did not have in place any active surveillance program for the white-tailed deer herd. All prior year sampling efforts were related only to collection and submittal of target animals and any illegal animals removed from private ownership. During 2002, GA DNR-WRD conducted CWD surveillance sampling under a Federal Aid Agreement with the US Fish and Wildlife Service. This surveillance plan was premised with the following assumptions: that CWD was not endemic in the State at any level; that CWD was not endemic in any surrounding state at any level; that introduction into Georgia would therefore likely occur through importation of infected animals from areas where CWD is present; and that such importation would likely be done in conjunction with a high-fence enclosure. Following from these assumptions, GA DNRWRD proceeded to identify such enclosures where significant animal movement was documented or where very little documentation of activities was available. From this, GA DNR-WRD circumscribed sampling plots with four-mile radii around suspect facilities (i.e. high-fence enclosures). GA DNR-WRD collected samples during this year of the project. All results found that CWD was not detected. During 2003, GA DNR-WRD began sampling through the USDA national CWD program. The USDA protocol did not allow for those (casual) assumptions made during the 2002 sampling program. The sampling protocol was therefore changed to provide a more statistically defensible sampling regime in the absence of the above listed assumptions. During the 2003 program, GA DNR-WRD identified the State’s white-tailed deer herd as a single population and sampled accordingly. During the 2003 program samples were collected statewide. All results found that CWD was not detected. From that point until 2011, all sampling was conducted under the USDA protocol when Federal project funding ceased. From 2012 to present, sampling has focused on roadkilled deer, sick deer, and hunter-killed deer within elevated risk counties.
SATURDAY, SEPTEMBER 07, 2013
Georgia House Bill 1043 and Chronic Wasting Disease CWD
*** Hawaii CWD TSE Prion ???
Hawaii nothing about cwd tse prion, no cwd tse prion response plan, no cwd tse prion testing history, nothing i could find, i did find this;
*** Idaho CWD TSE Prion
Idaho, to date, has detected NO cases of CWD TSE Prion...tss
Chronic Wasting Disease Status in Idaho
Idaho Fish and Game has not detected Chronic Wasting Disease (CWD) in Idaho. CWD is a contagious and always-fatal neurological disease that affects deer, elk, and moose.
Montana, Utah and Wyoming have confirmed cases of CWD in animals close to the Idaho border. There is no cure for this fatal disease and CWD could impact Idaho’s elk, deer and moose populations. The threat of CWD is a serious concern and Fish and Game is taking all practical steps to minimize the risk.
CWD Status in Idaho: Not detected
SATURDAY, JULY 21, 2018
Idaho Fish and Game Commission Quarterly Meeting July 25 26, 2018 Chronic Wasting Disease CWD TSE Prion
*** Illinois CWD TSE Prion
Illinois, to date, has detected 1002 cases of CWD TSE Prion...tss
Illinois Chronic Wasting Disease (CWD): 2019-2020 Surveillance and Management Report (Project Period: July 1, 2019 - June 30, 2020)
Doug Dufford and Patrick McDonald
Wildlife Disease Program, Illinois Department of Natural Resources
September 28, 2020
Executive Summary
Table 1. Number of CWD positive deer by fiscal year (July 1 through June 30).
TOTAL 1002
SEE CHART;
Table 1. Number of CWD positive deer by fiscal year (July 1 through June 30).
03 04 05 06 07 08 09 10 11 12 13 14 15 16 17 18 19 20 Total
Boone 9 25 13 15 13 11 9 14 7 5 4 5 6 11 7 3 6 10 173
Carroll – – – – – – – – – – – – – – 2 2 1 4 9
Cook – – – – – – – – – – – – – – – – – 1 1
DeKalb – 4 1 5 6 8 4 3 7 5 7 8 8 3 3 1 3 1 77
DuPage – – – – – – – – – – 1 – – – – – – 1 2
Grundy – – – – – – – – 2 5 3 3 5 3 7 2 10 17 57
Jo Daviess – – – – – – – – 1 – 1 4 7 9 10 8 12 25 77
Kane – – – – – – – – 4 7 4 5 7 8 5 2 3 2 47
Kankakee – – – – – – – – – – – – 1 1 2 – 2 3 9
Kendall – – – – – – – – – – 1 4 6 6 6 1 5 11 40
Lake – – – – – – – – – – – 1 – – – – – – 1
LaSalle – – – – 1 – – – 3 – 1 2 6 5 4 5 6 20 53
Livingston – – – – – – – – – – – – 2 – 2 – 1 7 12
McHenry 2 2 4 4 4 – 4 3 3 3 3 7 6 8 8 8 14 30 113
Ogle – – – 2 – – 1 – 4 2 3 1 2 6 2 3 10 7 43
Stephenson – – – – – 1 – 1 1 2 3 4 6 10 11 12 8 26 85
Will – – – – – – – – – – – 2 1 1 – – – 4 8
Winnebago 3 20 13 25 18 18 12 16 10 7 5 13 8 1 6 4 9 7 195
Total 14 51 31 51 42 38 30 37 42 36 36 59 71 72 75 51 90 176 1002
SNIP...SEE FULL REPORT;
Illinois Chronic Wasting Disease (CWD): 2019-2020 Surveillance and Management Report (Project Period: July 1, 2019 - June 30, 2020)
SUNDAY, DECEMBER 22, 2019
Illinois CWD TSE Prion 90 CWD-positive deer with 826 confirmed positive Total positives through June 30, 2019
*** Indiana CWD TSE Prion
Indiana, to date, has detected no cases of CWD TSE Prion...tss
2019 INDIANA WHITE-TAILED DEER REPORT
A total of 772 hunter-harvested deer, 28 road-killed deer, and 32 targeted deer were tested for CWD statewide in 2019. Our ability to detect the disease in the targeted surveillance areas ranged from 1.53% to 5.10% in the northwest targeted area, and from 1.50% to 2.06% in the northeast targeted area (Table 6-2). To date, no wild deer from Indiana have tested positive for CWD.
2020-2021 CWD Surveillance
Indiana DNR is conducting targeted CWD surveillance in northwest and northeast Indiana during the 2020-2021 deer hunting season. The DNR requests voluntary assistance from hunters in this effort. Participants will receive a metal tag reminiscent of historic confirmation tags as tokens of appreciation.
Biologists are collecting samples (lymph nodes at the junction of the head and neck) from deer harvested within the surveillance area during three weekends:
Nov. 7 and 8, 2020
Nov. 14 and 15, 2020
Nov. 21 and 22, 2020
FRIDAY, OCTOBER 04, 2019
Indiana CWD TSE Prion Surveillance 2019 and before?
TUESDAY, FEBRUARY 14, 2012
Oppose Indiana House Bill 1265 game farming cervids
*** Iowa CWD TSE Prion
Iowa, to date, has detected 89 cases of CWD TSE Prion...tss
Iowa, wild and captive cwd tse prion total ???
Public meeting on fatal deer disease set for March 10 in Leon
Leon, Iowa - Deer hunters who hunt in Decatur County take note– chronic wasting disease has shown up in your area. A hunter harvested wild deer taken during the first shotgun season in Decatur County has tested positive for chronic wasting disease.
The Iowa Department of Natural Resources (DNR) has scheduled a meeting on March 10, at 7 p.m., in the Central Decatur CSD, 1201 NE Poplar, in Leon, to discuss the status of chronic wasting disease in Iowa and how deer hunters can help stop or slow the spread of this disease.
Tyler Harms, wildlife biologist for the Iowa DNR, will coordinate the meeting. He said there are several things hunters can do today to help monitor for the disease.
“The first and most important is to allow sampling of hunter harvested deer,” he said. “Second, is to remove any mineral blocks and feeders that unnaturally concentrates deer and increases the chance of spreading any disease and finally report any sick or emaciated deer to the DNR.
“We want people to come to this meeting, ask their questions, hear the concerns from other hunters,” Harms said. “Deer hunting is an important tradition and, for some, a large part of their identity. It is also important to us and we need to work together to combat this disease. Our goal is to provide quality deer hunting today, tomorrow, and for future generations.”
The Iowa DNR has tested nearly 74,000 deer tissue samples for chronic wasting disease since monitoring began in 2002. The disease first appeared in Iowa’s wild deer herd in 2013. So far, there have been 89 positive tests.
The Iowa DNR sets an annual goal of collecting 6,900 deer tissue samples. The effort has focused on portions of northeast and eastern Iowa near Wisconsin, Illinois, and south-central Iowa near Missouri, where the disease has been detected. Additional testing has been conducted in Pottawattamie, Cerro Gordo and Davis counties, following positive tests from captive facilities. All counties have at least 15 samples collected annually. The disease has been found in every state around Iowa.
Chronic wasting disease is a neurological disease belonging to the family of diseases known as transmissible spongiform encephalopathies, or prion diseases. It attacks the brain of infected deer and elk causing the animals to lose weight, display abnormal behavior, lose body functions and die. It is always fatal to the infected animal.
“Deer hunting is one of Iowa’s great traditions. We want to educate and work with our hunters so we continue to have the best deer herd in the country for generations to come,” he said.
The Iowa DNR has more information about chronic wasting disease and other infectious disease online at www.iowadnr.gov/cwd. ;
Media Contact: Andy Kellner, Wildlife Biologist, Iowa Department of Natural Resources, 515-975-8318.
DNR News Releases
Test results are in, chronic wasting disease has been found in four new counties 2/11/2020 1:49:00 PM
Chronic wasting disease has been confirmed in wild deer from Woodbury, Winneshiek, Fayette and Decatur counties this year, bringing the total number of counties in Iowa where wild deer have tested positive to eight.
“We will schedule meetings in these areas in the next few months to discuss chronic wasting disease, our response and the role hunters play in helping us to manage for this disease,” said Tyler Harms, wildlife biologist with the Iowa DNR.
In the past, the DNR has set up a surveillance zone around where the positive deer was taken, then works with hunters to increase the number of samples collected within the zone to get a better idea of the extent to which the disease is on the ground.
“Early detection is key,” Harms said. “We want to increase the surveillance in close proximity to the positive deer to hopefully catch any other positives in the area. In these surveillance zones, we want to manage our deer herd toward the lower end of our population goal to help slow disease transmission.”
The Iowa DNR submitted nearly 7,000 deer tissue samples for testing from hunter harvested or road killed deer collected statewide in the 2019-2020 season that resulted in 43 positive wild deer.
“While the number of positives this year jumps out, it’s not out of the realm of what we would expect,” Harms said.
The Iowa DNR contacted all hunters with a positive deer and offered the opportunity to come collect the deer meat, hide and other animal parts or were provided other options for carcass disposal. The Centers for Disease Control advises against consuming animals that have tested positive for disease.
Hunters play an important role in preventing the spread of this disease by not using feed or salt-mineral licks that increase the concentration of deer, which can spread disease.
Hunters who harvest a deer in a county known to have chronic wasting disease but who live in a county where the disease has not been found, should bone out their deer and either leave the carcass on the land where it was harvested or disposed of within that county. Contact the local landfill for requirements. Make absolutely sure not to transport and dump carcasses outside of the area where the deer were shot as this will spread the disease to new areas.
The Iowa DNR samples deer from every county with increased sample quotas set in areas where the disease has been confirmed or where it has been confirmed across the border in neighboring states.
The Iowa DNR has been testing deer for chronic wasting disease since 2002. The first positive was in 2013 near Harpers Ferry in Allamakee County. To date, there have been 89 positive wild deer. More information is available online athttp:// www.iowadnr.gov/cwd.
Iowa's Voluntary
Chronic Wasting Disease Surveillance Program
What Is The Iowa Department of Agriculture and Land Stewardship, Bureau of Animal Industry Doing About CWD?
The Iowa Department of Agriculture has initiated the voluntary CWD Surveillance Inventory Program which requires CWD surveillance, reporting, and testing of those farmed cervidae 12 months of age and older that dies
Elk
from any cause. Before any cervidae is imported into the state it must have a Certificate of Veterinary Inspection (CVI - health certificate), permit issued by our Department, meet Iowa’s import requirements (http://www.iowaagriculture.gov/animalIndustry/animalAdmissionRegs.asp), and a review of the herd history.
Since the start of the CWD surveillance program in 2000, the farmed cervid producers have submitted over 5,556 brain samples for CWD testing. If CWD is diagnosed in a farmed cervid, the farm would be quarantined and the disease eradicated using recommended disease control strategies. The threat of CWD is a serious concern to Iowa and the cervidae industry. All practical steps to minimize the spreading of the disease are taken. Requirements for the Iowa CWD Program include annual inventory reconciliation recorded by a State District Veterinarian within 90 days of the CWD anniversary date. Inventory requirements are:
1) Records shall be kept to document the history/accountability of all animals in the herd. This includes identification, date of birth and sex of all animals born or received on the premise.
2) All animals must have two forms of official identification which are outlined in the Rules under 64.104 Definitions “Official Cervid Identification”.
3) A copy of a health certificate (CVI) properly filled out and signed by an accredited veterinarian shall be kept to document movement in or out of the herd. Owners need to retain their health certificates for at least five years.
4) Surveillance will be maintained by collecting and submitting appropriate samples from all cases of mortality, including slaughter, in animals 12 months of age and older, keeping copies of the laboratory reports.
The CWD Program herd producers upon satisfactory completion of their annual inventories will receive a letter of status verification, and a billfold size certificate card with their herd’s status, CWD herd number, anniversary date, and expiration date.
Triennial Physical Herd Inventory Inspections: Physical Inventories can be performed as part of an official herd test for tuberculosis or brucellosis. Physical Herd Inventories are separate and different from Annual Inventories conducted by our State District Veterinarians and the Physical Herd Inventories are to be conducted triennially.
Physical Herd Inventories will be required for advancement in the program. Physical Herd Inventory completions are allowed during the 90 days before or the 90 days after your herd’s expiration date.
A complete Physical Herd Inventory must provide verification to reconcile all deer and verification of two approved individual identifications (one must be a USDA official identification tag) with the records maintained by the owner. All Cervid animals must have official identification tags before 12 months of age. The owner must present the entire herd for the Physical Herd Inventory inspection where the department, a state authorized veterinarian (accredited veterinarian – their herd veterinarian) or authorized federal personnel can safely read all identifications on the animals and be able to record all identification devices. Attached Instructions for the CWD HCP Physical Herd Inventory/Inspection and Chronic Wasting Disease Herd Certification Program Agreement to be reviewed and completed by an accredited veterinarian and a farmed cervid producer.
A complete physical herd inventory must be performed at the time a herd enrolls in the Chronic Wasting Disease Herd Certification Program. Official Cervid Identification: All Cervid 12 months of age or older (All Animals under 12 months of age leaving the premises), shall have a minimum of two forms of animal identification.
USDA Approved with USDA shield - Information on official animal identification devices can be found on the APHIS Traceability website at the following address: http://www.aphis.usda.gov/traceability/devices.shtml
The second form of identification must be one that is approved by IDALS: Unique material tag which provides unique animal identification and CWD herd number.
Nov. 22, 2019
Two Cases of Chronic Wasting Disease Found at Deer Farms
Positive tests were confirmed on farms in Van Buren County
DES MOINES, Iowa (Nov. 22, 2019) — The Iowa Department of Agriculture and Land Stewardship has confirmed that Chronic Wasting Disease (CWD) has been found in captive white-tail deer on two separate farms in Van Buren County, Iowa. Both sites are quarantined while the Department works to trace potential exposures and contain the disease.
There is no evidence that CWD can spread to humans, pets or domestic livestock. CWD is a neurological disease that only affects deer, elk and moose. It is caused by an abnormal protein called a prion and impacts the brain of the infected animal. The prions can attach to soil and spread the disease among deer. Symptoms of the disease include excessive salivation, thirst and urination, loss of appetite, progressive weight loss, listlessness as well as drooping ears and head.
The disease was detected as part of the Department’s voluntary CWD monitoring program. Participating producers test deceased farm-raised deer and elk over 12 months of age. Positive test results must be reported to the Iowa Department of Agriculture.
Chronic Wasting Disease was first identified in captive mule deer at a research facility in Colorado in 1967. The disease was then found in Wisconsin in 2002. Since 2002, Iowa has tested for CWD in 7,447 captive deer and elk as part of its surveillance program. The last confirmed case in Iowa was in Buchanan County in 2016.
To learn more about CWD, visit https://iowaagriculture.gov/animal-industry-bureau/chronic-wasting-disease.
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED
79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
-30-
For Immediate Release Tuesday, December 20, 2016
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov
CHRONIC WASTING DISEASE FOUND AT A DEER FARM IN BUCHANAN COUNTY
DES MOINES – Chronic Wasting Disease (CWD) has been confirmed in one captive white-tail at a deer farm in Buchanan County, Iowa. The Iowa Department of Agriculture and Land Stewardship has quarantined the site.
The disease was detected as part of the Department’s voluntary CWD monitoring program. The farm where the disease was found participates in the program which requires CWD surveillance and testing of all farmed deer and elk 12 months of age and older that dies. Test results must be shared with the Department.
CWD was found in neighboring Wisconsin in 2002. Since then, Iowa has tested for CWD in 57,765 wild deer and 10,157 captive deer and elk as part of its surveillance program.
The Iowa Department of Natural Resources will increase testing of wild deer in the Buchanan County area. DNR staff will work with hunters and landowners to collect samples from hunter-harvested deer, roadkills and targeted deer displaying symptoms of CWD.
There is no evidence that CWD can spread to humans, pets or domestic livestock.
CWD is a neurological disease that only affects deer, elk and moose. It is caused by an abnormal protein, called a prion, which affects the brains of infected animals, causing them to lose weight, display abnormal behavior and lose bodily functions. The prions can attach to soil and spread the disease among deer.
Symptoms of the disease include excessive salivation, thirst and urination, loss of appetite, progressive weight loss, listlessness as well as drooping ears and head.
Chronic wasting disease was first identified in captive mule deer at a research facility in Colorado in 1967.
TUESDAY, FEBRUARY 25, 2020
Iowa Chronic Wasting Disease CWD TSE Prion Cases Climb To 89 positive To Date in Wild Cervid
MONDAY, FEBRUARY 10, 2020
Iowa CWD TSE Prion 2019/20 (confirmed or suspect) 43 cases to date Wild Cervid
Iowa CWD TSE Prion 2019/20 (confirmed or suspect) 43 cases to date Wild Cervid
Captive Population Positives (5)
Map Date February 4, 2020
SUNDAY, NOVEMBER 24, 2019
Iowa Two Cases of Chronic Wasting Disease Found at Deer Farms
THURSDAY, FEBRUARY 08, 2018
Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season
***Kansas CWD TSE Prion
Kansas, As of 30 June 2020, CWD has been detected in 363 cervids - two captive elk and 361 wild, free-ranging deer in Deer Management Units 1, 2, 3, 4, 5, 7, 15, 16, 17, 18.
These include 82 mule deer, 274 white-tailed deer, 2 captive elk, and 5 unknown deer species.
2020-2021 CWD Sampling Information
The first case of CWD was found in a captive bull elk in Harper County in 2001.
As of 30 June 2020, CWD has been detected in 363 cervids - two captive elk and 361 wild, free-ranging deer in Deer Management Units 1, 2, 3, 4, 5, 7, 15, 16, 17, 18.
These include 82 mule deer, 274 white-tailed deer, 2 captive elk, and 5 unknown deer species.
Surveillance efforts began in 1996 and, to date, 27,863 cervids have been sampled and tested for CWD.
Hunters and other wildlife enthusiasts can avoid the human-assisted spread of CWD by not transporting a live or dead deer or elk from areas where CWD occurs. HUNTERS ARE ENCOURAGED TO USE ELECTRONIC DEER CHECK-IN OR LEAVE EVIDENCE OF SEX ATTACHED TO THE CARCASS.
BONE-OUT DEER, AND LEAVE CARCASSES IN THE COUNTIES WHERE DEER ARE TAKEN. MOVING CARCASSES MOVES PRIONS AND CWD TO NEW LOCATIONS!
There is currently no known treatment or eradication method for CWD, so preventing the introduction of the the disease into new areas is of utmost importance to the health of local deer herds. Baiting and feeding deer tend to concentrate deer at small point on the landscape, often with the trails leading to the feeding sites resembling the wheel spokes of a bicycle. Anytime animals are concentrated at this type of "hub," the likelihood of disease transmission increases in a deer herd. More alarming, the transferring of CWD prions to healthy deer is not the only concern. Diseases such as bovine tuberculosis, foot rot, and fungal infections; and a host of detrimental parasites, including exotic lice, flukes, mange mites, lungworms, and barberpole worms are transmitted more efficiently when deer are concentrated in a small area, especially around feeding stations. Think of future generations of hunters and do your best to lower wildlife disease transmission risk.
2020-2021 CWD Test Results (Results Added As Tests Are Completed)
Animal ID Test Result K031197 Negative
After the 2015-2016 seasons, prevalence was calculated to be between 10-20% with 95% confidence in bucks 2.5 years-old and older in the Northwest Zone. After 2019-2020 CWD surveillance, prevalence in the Northwest Zone was calculated to be 34.1 - 49.5% with 95% confidence in bucks 2.5 years-old and older. Currently, the overall trend is increasing prevalence and eastward spread.
Another major concern is the potential of CWD spreading from captive cervid farms into the wild cervid population. Once a disease gets into a wild population, it is virtually impossible eradicate. KDWPT recommends that every captive cervid operator enroll in the voluntary CWD monitoring program administered by the Kansas Department of Agriculture's Animal Health Division. The sooner diseases such as CWD can be detected in captives, the sooner control efforts can begin and possibly prevent disease from spreading to wild populations of the state. CWD is only one of many diseases that could go undetected in an unmonitored captive cervid herd. Bovine tuberculosis and Foot and Mouth Disease (FMD), for example, are serious diseases that could seriously damage not only populations of deer and an annual 350 million-dollar hunting economy, but could also threaten the 6 billion-dollar Kansas cattle industry via quarantines, loss of accreditation, and loss of global export.
2020-2021 CWD SAMPLING INFORMATION
IMPORTANT: Help Control the Spread of CWD and CWD Prions in Kansas!!
1. Use Electronic Deer Check-In or Leave Evidence of Sex Attached to the Carcass.
2. Remove the musculature (deboning) from the carcass and leave the carcass at the kill site. Make sure to complete Step 1 first.
3. If at all possible, do not transport a carcass from counties known to have CWD (see map above) to other counties. Use electronic deer check-in: https://programs.ksoutdoors.com/Programs/Electronic-Deer-Check-in
4. If you have to transport a whole carcass away from the kill site, take or send the deboned carcass, spinal column and head to your county landfill for disposal, once you have deboned the carcass at your place of processing. Don't carelessly discard this material where other deer and scavengers can contact it. Careless discarding of a cervid skeleton could potentially start a CWD hotspot in your area.
5. Keep the permit with the meat.
For more information about CWD, visit the CWD Alliance website at http://cwd-info.org/.
CWD Regulations for Kansas and Other States Click HERE for information concerning CWD Regulations for Resident and Non-Resident Hunters
Links to more information about Chronic Wasting Disease: National Wildlife Health Center (USGS) has links to current research and popular articles such as “The Quiet Spread of CWD” which appeared in Field & Stream.
Centers for Disease Control and Prevention has information about CWD and humans.
Chronic Wasting Disease Alliance has links to state regulations regarding CWD carcass
American Veterinary Medical Association has information about precautions hunters and anyone who spends time outdoors should take to protect themselves from potential risks.
Chronic Wasting Disease In Kansas Deer: 2018-2019 Update
PRATT – In a continuing effort to monitor the prevalence and spread of chronic wasting disease (CWD) in Kansas deer, the Kansas Department of Wildlife, Parks and Tourism (KDWPT) has collected and tested samples from 360 deer so far this year. Thirty-seven of those samples were confirmed positive. The targeted region for sampling deer taken by hunters this year was southwestern Kansas. However, sick or suspect deer observed in other parts of the state were also tested, and KDWPT recommends that hunters who take deer in counties where CWD is known to occur have their deer tested, as well.
The 37 confirmed positives came from deer taken in Cheyenne, Rawlins, Decatur, Norton, Phillips, Smith, Thomas, Sheridan, Gove, Rooks, Osborne, Scott, Lane, Hamilton, Haskell, Hodgeman, Ford, Edwards, Stafford, Reno, and Pratt counties. While most positives are still coming from northwest Kansas, new counties were added to the list this year, including several that show the disease’s spread to the south and east – Haskell, Edwards, Pratt, Osborne, and Reno.
Testing History
CWD infects members of the deer family, including whitetail and mule deer, elk and moose. CWD testing in Kansas began in 1996 to help track the occurrence of the disease in the state’s wild deer, and more than 28,000 tissue samples have undergone lab analysis since. The first CWD occurrence documented in a wild Kansas deer was a whitetail doe killed by a hunter in 2005 in Cheyenne County. To date, 216 deer have tested positive, and most have occurred in a region that includes Decatur, Rawlins, Sheridan and Norton counties.
snip...
WEDNESDAY, OCTOBER 16, 2019
Kansas Chronic Wasting Disease CWD TSE Prion Update With 216 cervids Positive To Date
SUNDAY, OCTOBER 07, 2018
Kansas Chronic Wasting Disease CWD TSE Prion Update 143 Confirmed Cases To Date
***Kentucky CWD TSE Prion
Kentucky, to date, CWD has not been found in the State of Kentucky...
Kentucky CWD TSE Prion response plan
Kentucky Department of Fish & Wildlife Resources Commission Meeting Live Teleconference - Web link posted at fw.ky.gov
December 4, 2020
#1 Sportsman’s Lane Frankfort, KY 8:30 AM (ET)
Establish a fee-based test for deer hunters seeking Chronic Wasting Disease (CWD) testing
o Make available voluntary CWD testing outside standard surveillance protocols
Attachment NB-3
***Louisiana CWD TSE Prion
Louisiana, to date, CWD has not been found in the State of Louisiana...
LDWF CWD has not yet been found in Louisiana, but Texas, Arkansas, and Mississippi have documented it in their deer populations.
TUESDAY, JULY 12, 2016
Louisiana Notice of Intent Cervid Carcass Importation (LAC XIX.V.1.119) CWD TSE PRION
THURSDAY, APRIL 14, 2016
Louisiana Chronic Wasting Disease CWD TSE Prion Surveillance and Testing Program?
***Maine CWD TSE Prion
Maine, to date, CWD has not been detected...tss
Maine has actively monitored for CWD each year since 1999, and since that time screened approximately 9,000 wild deer. Thus far, Maine proudly remains CWD free.
Current through Register Vol. 2020-42, October 14, 2020
Section 001-203-3 - DEFINITIONS:
1.Captive: Cervids that are privately or publicly maintained or held for economic or other purposes within a perimeter fence or confined space.
2.Case Definition: A deer 12 months of age or older having chronic weight loss and exhibiting any or all of the following symptoms: isolates self from herd, listlessness, blank facial expression, head drooping, loss of muscle control, repetitive walking in pen, hyperexciteability, nervousness, interest in grain, but no interest in hay, hypersalivation, teeth grinding, increased urination and drinking of water.
3.Cervids: All members of the cervid family and hybrids including but not limited to elk, reindeer and related species.
4.Herd Inventory: A physical herd census with third party validation. The current animal census must be reconciled with the records from the previous annual herd inventory by state or federal personnel, or a specifically authorized accredited veterinarian.
5.Certificate of Veterinary Inspection: A legible certificate or form issued by an accredited veterinarian, issued within 30 days preceding importation, and approved by the chief livestock official of the state or country of origin. The Certificate of Veterinary Inspection must contain the following information:
a) Names and full addresses (and physical addresses if different) of Consignor and Consignee.
b) Official identification for each animal
c) Age, sex and breed for each animal
d) All required test results
e) Signature of accredited veterinarian attesting to the health of the animals
f) The following statement:
"To the best of my knowledge, these cervids have not been exposed to Brucellosis, Tuberculosis or Bluetongue for one year prior to the date of entry. In addition, these cervids originate from a herd that has participated in a state or USDA sanctioned CWD Surveillance program for a minimum of 60-months and do not demonstrate clinical signs compatible with CWD or have not been exposed to CWD positive cervids or cervids demonstrating clinical signs of CWD for the previous five years."
6.CWD Certified Herd: A cervid herd that has successfully completed 60-months of participation in the monitoring program and has had no CWD positive cervids nor have any cervids been exposed to a positive CWD cervid.
7.Chronic Wasting Disease (CWD): A transmissible spongiform encephalopathy (TSE) of cervids.
8.CWD Program: A program of surveillance, monitoring, testing and related actions designed to provide a status of Chronic Wasting Disease.
9.CWD Exposed Cervid: A cervid that is or has been in the last 60-months part of a CWD positive herd.
10.CWD Positive Cervid: A cervid that has had a diagnosis of CWD confirmed by means of an official CWD test conducted by a laboratory certified by US Department of Agriculture.
11.CWD Negative Cervid: A cervid that has had an official CWD test conducted by a laboratory certified by the US Department of Agriculture and that has test results in a "not detected" or negative classification.
12.CWD Suspect Cervid: A cervid for which inconclusive laboratory evidence suggests a diagnosis of CWD.
13.CWD Infected Zone. A defined geographic area, as defined by the Commissioner of the Maine Department of Agriculture, Conservation and Forestry, and in consultation with the Commissioner of Inland Fisheries and Wildlife, respective of state boundaries, in which CWD is present, whether in wild or captive herds.
14.Department: The Maine Department of Agriculture, Conservation and Forestry.
15.Department of Inland Fisheries and Wildlife: The Maine Department of Inland Fisheries and Wildlife (IF&W).
16.Enrollment Date: The day, month and year in which the State officially enrolls an owner's herd in the CWD Surveillance Program and initial enrollment requirements are met.
17.Herd: One or more cervids that are under common ownership or supervision and are grouped on one or more parts of any single premises, and all cervids under common ownership or supervision on two or more premises, which are geographically separated, but on which cervids have been commingled or had direct or indirect contact with one another.
18.Importation Permit: A document issued by the Department prior to the time of entry that authorizes the importation of cervids into the State.
19.License: A license issued by the Division of Animal and Plant Health, Department of Agriculture, Conservation and Forestry entitling the holder to propagate, possess, purchase and/or sell cervids.
20.Mandatory Reporting: The requirement that all cervids meeting the CWD case definition be evaluated by an accredited veterinarian and reported to the Department immediately.
21.Monitored Herd: A program of surveillance, monitoring, testing and related actions designed to identify CWD infection in special purpose herds or in those herds not participating in the CWD Certified Herd program.
22.Owner: An individual, partnership, company, corporation or other legal entity that has legal or rightful title to an animal or herd of animals.
23.Permit Application for State Entry: An application, which must be submitted to the Department prior to the issuance of an importation permit.
24.Special Purpose Herd: A captive herd managed and maintained in such a manner that no live cervid is removed or allowed to be removed from the designated premises, such as a Maine licensed commercial large game shooting area.
25.USDA: The United States Department of Agriculture, Animal and Plant Health Inspection Service.
26.Official Identification. The identification ofcervids with a minimum of two state and federally approved identifiers. The identification must enable the trace-back of cervids to herd of origin.
a) Identification shall include at least one of the following: permanent tattoo; microchip; or official state ear tag;
b) Identification may include one of the following: herd ear tag; leg tag; collar tag; or other identification approved by the Department.
27.Official Test: A CWD test approved by the U.S. Department of Agriculture and performed at a U.S. Department of Agriculture approved laboratory.
28.Premises: The ground, area, buildings, water sources and equipment commonly shared by a herd of animals.
29. Quarantine: An order issued by a State or Federal official prohibiting the movement of animals to and from a designated premises.
01-001 C.M.R. ch. 203, § 3
CHAPTER 305
ERADICATION OF DISEASES
§1801. Reportable diseases
The commissioner shall, by rule adopted in a manner consistent with the Maine Administrative Procedure Act, determine which diseases or pathogens must be classified as "reportable." The form of transmissible spongiform encephalopathy known as chronic wasting disease is reportable. It is a
MRS Title 7. AGRICULTURE AND ANIMALS Generated 10.14.2020 Title 7. AGRICULTURE AND ANIMALS | 241
violation of this chapter for any owner, agent of any owner, veterinarian or other person having knowledge of the existence of such disease or pathogen or the exposure of domestic animals to such disease or pathogen not to properly report the existence of such disease or pathogen or exposure of domestic animals to the department immediately after knowledge of such disease or pathogen or exposure of domestic animals to such disease or pathogen. [PL 2001, c. 572, §32 (RPR).] It is a violation of this chapter for any person to cause a domestic animal to be driven, trucked or otherwise moved intrastate or interstate when that person has knowledge that the animal is infected with or has been exposed to a reportable disease or pathogen. It is a violation of this chapter for any person to cause a domestic animal to be driven, trucked or otherwise moved intrastate or interstate when that person has knowledge that the animal has been treated with a vaccine or other substance that might make that animal capable of spreading a reportable disease or pathogen among susceptible domestic animals. A domestic animal infected with or exposed to a reportable disease or pathogen may be moved only under the direction of the commissioner. [PL 2001, c. 572, §32 (RPR).]
SECTION HISTORY
PL 1971, c. 594, §7 (AMD). PL 1977, c. 694, §122 (AMD). PL 1999, c. 765, §6 (AMD). PL 2001, c. 572, §32 (RPR).
§1802. Condemnation of diseased animals
The commissioner may, when he deems it necessary, condemn and take possession of diseased or exposed domestic animals, or domestic animals suspected of being diseased or exposed, for diagnostic purposes, and may pay the owner for the same, health, condition and market value being considered. This condemnation shall not be considered licensing or an adjudicatory proceeding, as defined by the Maine Administrative Procedure Act. [PL 1977, c. 694, §123 (NEW).]
SECTION HISTORY
PL 1977, c. 694, §123 (AMD).
§1803. Transportation of diseased animals
It is a violation of this chapter for a person to cause a domestic animal to be driven, trucked or otherwise moved into the State when that person has knowledge that the animal is infected with or has been exposed to any contagious disease or to a pathogen that is classified as a reportable pathogen under section 1801. [PL 2001, c. 572, §33 (RPR).]
SECTION HISTORY
PL 2001, c. 572, §33 (RPR).
We were concerned about the enforcement of the herd certification program nationwide. There had been some serious lapses, the majority of new cases of CWD in terms of facilities or states in the last year had come from certified facilities and noncompliance. The state vet was very committed to a program of testing and following up. They tested every animal that died in a captive deer facility in Maine. From an IFW standpoint, we were monitoring deer across the state. We were sampling in towns where there were deer farms and sampling wild deer adjacent to that. The idea of a total ban on moving live deer across the country was being discussed. There were some states that were prohibiting any wild deer from being brought into their state. Most everyone was looking at a ban on the movement of carcasses. Ours had been strengthened in the proposed rule.
*** Maryland CWD TSE Prion
Maryland, to date, 80 confirmed cases to date from CWD TSE Prion...tss
Maryland detects additional 28 positives from last year's CWD TSE Prion sampling, total stands at 80 confirmed cases to date...
Status of CWD in Maryland
The Department of Natural Resources has tested 10,882 deer for CWD since 1999. The disease was detected for the first time in Maryland from a deer taken by a hunter in November 2010. To date, 80 infected deer have been documented in the state. Forty-six of the deer originated in Allegany County Harvest Management Unit 233, including three on Billmeyer Wildlife Management Area, fifteen on Green Ridge State Forest, and one on Sideling Hill Wildlife Management Area. Twelve positive deer have been detected in Allegany County Harvest Management Unit 231 near Cumberland, and three have been detected in Harvest Management Unit 232. In Washington County, fourteen positive deer have been detected in Harvest Management Unit 250, including one on Woodmont Natural Resources Management Area. Four positive deer have been found in Washington County Harvest Management Unit 251, and one has now been found in Harvest Management Unit 252.
Number of White-tailed Deer that have Tested Positive for Chronic Wasting Disease by Harvest Management Unit (HMU) in Maryland, 2010 – 2019. County HMU Number Positive
Allegany 230 0
231 12
232 3
233 46
234 0
Washington 250 14
251 4
252 1
Total 80
* White-tailed deer harvested on public lands are included in the appropriate private land HMU code.
The department has been testing deer for CWD with increasing intensity since 1999. Initially, only deer that appeared to have classic CWD symptoms were tested. Beginning in 2002, the department began more intensive sampling and collected samples from deer in all counties of the state. In 2010, sampling efforts were focused on Allegany and western Washington counties due to the presence of positive cases in nearby West Virginia and Virginia. West Virginia first detected CWD in Hampshire County in 2005 and it was found in Frederick County, Virginia in early 2010. Pennsylvania documented a deer positive for CWD in 2012.
Sampling is conducted on road-kills and deer brought by hunters to cooperating deer processors. Staff remove the brain stem and certain lymph nodes and those tissues are sent to a laboratory for testing. Any samples that test positive by the first lab are then sent to the USDA National Veterinary Services Laboratories for confirmation. This testing takes several months to complete. Positive samples are traced back to the hunter that harvested the deer and the department works with that hunter to determine the exact location where the animal was taken.
The Maryland Department of Agriculture, Maryland Department of Health & Mental Hygiene, the Southeastern Cooperative Wildlife Disease Study, and the United States Department of Agriculture are integral partners in all CWD surveillance plans to assist in monitoring wild deer populations, protect domestic animals and preserve human health.
Deer Hunters and CWD
Concerns over CWD should not stop hunters from enjoying the hunting season or any venison they may acquire. CWD has not been shown to be transmissible to humans. However, it is recommended that hunters field-dressing or butchering deer should take the same precautions as they would to protect against other pathogens or diseases. It is also recommended to not consume venison from infected deer.
The following common-sense precautionary measures are recommended for the safe handling, field-dressing and home processing of venison:
Avoid shooting or handling a deer that appears sick.
Wear latex or rubber gloves when field-dressing or butchering deer.
Remove all internal organs.
Remove the meat from the bones and spinal column if home processing a deer
Do not use household knives or utensils when field-dressing or home processing a deer.
Avoid cutting through bones or the spinal column (backbone).
If you saw off antlers or through a bone, or if you sever the spinal column with a knife, be sure to disinfect these tools prior to using them for the butchering or removal of meat.
Always wash hands and instruments thoroughly after dressing and processing game meat.
Use a 50/50 solution of household chlorine bleach and water to disinfect tools and work surfaces. Wipe down counters and let them dry; soak knives for one hour.
Deer Urine Lures and CWD
Recent research has shown that deer urine can contain infected prions. Until more is known about whether commercial deer lures pose a realistic risk of spreading CWD, we recommend that hunters use caution when placing natural urine-based lures in the environment and suggest the following:
Whenever possible, avoid using natural urine lures and instead use synthetic lures. Research has shown synthetic lures to be as effective as natural lures. Hunters should avoid placing deer lures on the ground or on vegetation where deer can come into contact with them. Deer lures can be safely placed above deer height, yet still allow air currents to disperse the scent and attract deer. Hunters should not place urine-based lures on their skin or clothing.
CWD Management
Due to the detection of CWD in Allegany and Washington counties, the department has created a Chronic Wasting Disease Management Area (CWDMA) to help slow the spread of the disease. The current CWDMA (see map below) consists of all public and private lands in Allegany and Washington counties. Currently, whole deer carcasses cannot be transported out of the CWDMA unless they are transported to an approved processor or taxidermist (see below).
Whole deer carcasses or deer parts cannot be transported out of the CWDMA, except for:
Meat with no part of the spinal column, backbone, or head attached, Hind quarters and front shoulders with no spinal column or backbone attached, (hunters MUST have checked in their deer and obtained a confirmation number in order to transport a quartered deer) Cleaned hide with no head attached, Skull plate cleaned of all meat and brain tissue, Antlers with no meat or soft tissue attached, Finished taxidermy mounts or tanned hides, Whole deer carcasses or parts being transported directly to the meat processors or taxidermists listed below, or to the landfill located within Allegany or Washington County.
Currently, the following taxidermists and meat processors are approved to prepare or process deer carcasses or deer parts taken from within Maryland’s CWDMA. This provision provides an opportunity for hunters harvesting deer within Maryland’s CWDMA to transport carcasses or other deer parts directly to one of these approved businesses for meat processing, taxidermy services or for preparation for transport to another taxidermist.
If you choose to quarter your deer in the field, it is permissible to leave the carcass remains at the kill site when hunting on Department of Natural Resources public lands. Hunters should obtain permission when hunting on private lands. Whenever possible, the department encourages hunters to bag the remains and dispose of them in a landfill. It is not permissible to leave or dispose of carcass remains in public parking areas, along roadways or near other public use areas.
Meat Processors
Allegany County
- B&B Country Meats, Frostburg, MD, 301-689-6225
- B&B Butchering, Orleans, MD, 301-478-2558
Washington County
- Banzhoff’s Custom Butchering, Williamsport, 301-223-9326
- Ernst Market, Clear Spring, MD, 301-842-2292
- Holsinger's Meats and Deli, Maugansville, MD, 301-733-9263
- Leitersburg Butcher Shop, Hagerstown, MD, 301-491-9911
- Sunnyland/Ray Burger's Meats, Williamsport, MD, 301-223-9637
- Wolford’s Meat Shop, Big Pool, 301-842-3156
Frederick County - Clint’s Cuts, Mt. Airy, 301-865-5120
- Pry's Deer Processing, Knoxville, 301-834-8752
- Rob’s Deer Shop, Rocky Ridge, 301-271-7780
- Wolfe's Deer Shop, Thurmont, MD, 240-549-2613
Taxidermists Allegany County - Brian McKinley, Cumberland, 240-580-4148
- Donnie Burley, Cumberland, 301-707-6272
- Richard Kroll, Barton, 301-359-5010
- Robert Friend, Westernport, 301-359-9784
- Steven Fairgrieve, Barton, 301-707-9261
Washington County - Draper's Taxidermy, Fairplay, 301-582-3173
- Fairview Wildlife Studio, Hagerstown, 301-791-1568
- Kaetzel's Taxidermy, Smithsburg, 301-667-2495
- Kline’s Taxidermy, Smithsburg, 301-416-0201
- Martin's Taxidermy Studio, Boonsboro, 301-432-5909
- Millstone Taxidermy, Hancock, 240-520-7226
- Mountin' Man Taxidermy, Knoxville, MD, 301-834-5197
- Quirauk Mountain Skull Works, Cascade, 301-331-6916
- South Mountain Taxidermy, Boonsboro, 301-432-6006
Frederick County - Baker Taxidermy, Frederick, 240-674-2752
- Brian Keane Taxidermy, Frederick, 301-682-9210
- Carder's Taxidermy, Ijamsville, 240-674-9146
- Geisinger Taxidermy, Thurmont, 301-271-0501
- Natalie's Taxidermy, Myersville, 240-315-3471
- Roger's Taxidermy, Thurmont, 301-606-7015
- Whitetail Studios, Thurmont, 301-271-4858
Please note: Due to the significant enlargement of the CWDMA, dumpsters will no longer be furnished for carcass disposal. Carcasses can either be quartered in the field, taken to an approved processor or taxidermist listed above, or disposed of at the Allegany or Washington County landfill for a fee. Whole carcasses are still permitted to be transported freely about within the CWDMA to private residences, hunting camps, etc.
Please also check the department website for updates on CWD surveillance and management in Maryland. Hunter assistance and cooperation is essential to the department’s efforts to monitor and manage CWD in Maryland.
2020 Chronic Wasting Disease Management Area Map
2020 Chronic Wasting Disease Map for Maryland
Carcass Importation Ban The primary objective in the management of CWD is to prevent or slow its spread into new areas. One possible mode of disease transmission is by the movement and disposal of infected carcasses. In an effort to minimize the risk for disease spread, Maryland, along with many other states, has adopted regulations that prohibit the importation of whole carcasses and certain carcass parts of deer, moose and elk harvested from states that have CWD.
A person may bring only the following parts of a dead deer, elk, or moose into Maryland from another state or province’s designated CWD containment, surveillance, or management area: (1) meat with no part of the spinal column or head attached; (2) hind quarters and front shoulders with no spinal column or backbone attached; (3) meat without backbone; (4) cleaned hide with no head attached; (5) skull plate cleaned of all meat and brain tissue; (6) antlers with no meat or soft tissue attached; (7) upper canine teeth, also known as buglers, whistlers, or ivories; and (8) finished taxidermy mounts or tanned hides.
Importation of whole deer, elk, moose or other cervid carcasses is prohibited from CWD positive areas identified within the states and provinces listed in the link below. To get the latest information on CWD positive areas in any of these states or provinces call the number listed or go to www.cwd-info.org
Any person who imports or possesses a cervid carcass or part of a cervid that was tested for chronic wasting disease in another state or province and is notified that the cervid tested positive, must report the test results to the Maryland Department of Natural Resources within 24 hours of receiving such notification- by telephone at 301-842-0332; or by FAX 301-842-1026; or by email to brian.eyler@maryland.gov
Travelers may pass through Maryland with cervid carcasses, provided that no parts are disposed of or remain in the state.
If you hunt deer, elk, moose or other cervids in other states and/or provinces, particularly those in which CWD has been detected, check with the respective fish and wildlife agencies regarding special regulations or specific advice for hunters. Also check with your home state fish and wildlife agency to ensure that animals lawfully killed elsewhere may be imported and possessed in your state. Additional information can be found at the CWD Alliance website www.cwd-info.org
Taking Deer Carcasses out of Maryland
Because Maryland is considered a CWD positive state, deer hunters must follow carcass importation regulations in other states when they transport a deer carcass out of Maryland (see www.cwd-info.org).
The surrounding states of Delaware, Pennsylvania, Virginia, and West Virginia each have specific regulations as to whether they will allow whole deer carcasses or only parts of carcasses to enter from Maryland. Likewise, the regulations for each of these states vary as to whether they apply to deer from anywhere in Maryland, or just to deer taken within the CWDMA. Hunters are strongly encouraged to check state regulations before transporting deer carcasses.
Travelers may pass through Maryland with cervid carcasses, provided that no parts are disposed of or remain in the state.
How You Can Help
You can help by reporting any deer that are emaciated, unhealthy or acting abnormally to the by calling 410-260-8540. You can also help by cooperating if department staff ask permission to collect brain tissue samples from deer you harvested.
Maryland CWD response plan
FRIDAY, OCTOBER 09, 2020
Maryland detects additional 28 positives from last year's CWD TSE Prion sampling, total stands at 80 confirmed cases to date
Maryland Chronic Wasting Disease Detected in 25 Deer
WEDNESDAY, FEBRUARY 21, 2018
Maryland Chronic Wasting Disease CWD TSE Prion Found In Ten Deer Allegany and Washington Counties
SATURDAY, MARCH 04, 2017
Maryland DNR Six Deer Test Positive for Chronic Wasting Disease
TUESDAY, MARCH 29, 2016
Maryland Department of Natural Resources Five Deer Test Positive for Chronic Wasting Disease ONE OUTSIDE CWD MANAGEMENT ZONE
SUNDAY, NOVEMBER 27, 2011
Chronic Wasting Disease Found In A White-Tailed Deer In Maryland
Thursday, February 10, 2011
Chronic Wasting Disease Found In A White-Tailed Deer In Maryland
*** Massachusetts CWD TSE Prion
Massachusetts, to date, no cases of CWD TSE Prion has been detected...tss
2020
2019
Mr. Stainbrook stressed the following important points: CWD has not been detected in Massachusetts and we have strong regulations in place to reduce the risks, noting that, since regulations adopted in 2005, no live deer can be brought into the state and there is a carcass ban from CWD-positive areas. He also stressed that Massachusetts has had no documented cases of CWD in humans or livestock. In other states with CWD, there is evidence of decreased hunter interest and corresponding loss of license sales, as well as deer population decreases in areas with an incidence rate greater than 20%.
Mr. Stainbrook also reviewed the history of funding of CWD research, the places where CWD is found, the spread of the disease over time, recent research, steps to reduce the risks to Massachusetts deer, and the outreach efforts that are being undertaken in Massachusetts to publicize the issue and educate hunters. Please refer to Page 73 in the Wildlife Section of this Annual Report for a recently updated map of the incidence of CWD in the U.S. and Canada.
***Michigan CWD TSE Prion
Michigan, to date, CWD TSE Prion has been detected in 192 cervid...tss
Michigan CWD TSE Prion POSTIVIES captive vs wild ???
Feb. 27, 2020
Contact: Chad Stewart, 517-282-4810
Broad CWD surveillance, hunter assistance during Michigan’s 2019 deer seasons help identify 65 CWD-positive deer
In all, 65 CWD-positive deer were identified from the 2019 hunting seasons – and all were from counties with a known CWD presence.
CWD MAP
SUNDAY, OCTOBER 11, 2020
Michigan Chronic Wasting Disease CWD TSE Prion increases to 191 positive to date
TUESDAY, SEPTEMBER 22, 2020
Michigan CWD TSE Prion 189 Positive To Date UPDATE September 2020
WEDNESDAY, MARCH 25, 2020
Michigan CWD TSE Prion Total Suspect Positive Deer Moves Up To 188 with total deer tested 80,687 to date
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
TUESDAY, JANUARY 07, 2020
Michigan Total CWD TSE Prion Positive Suspect-Positive Deer Jump To 174 confirmed to date
*** Minnesota CWD TSE Prion
Minnesota, to date, CWD has 95 wild deer have tested positive...tss
Minnesota Deer testing finds additional cases of chronic wasting disease
November 19, 2020
A wild deer harvested in Dakota County on Nov. 7 and a vehicle-killed deer in Olmsted County on Nov. 4 were confirmed positive for chronic wasting disease. To date, 95 wild deer have tested positive for CWD in Minnesota.
cwd response plan
THURSDAY, NOVEMBER 19, 2020
Minnesota Deer testing finds additional cases of chronic wasting disease, to date, 95 wild deer have tested positive for CWD in Minnesota
FRIDAY, OCTOBER 16, 2020
Minnesota CWD TSE Prion confirmed in Houston County farmed deer herd
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
***Mississippi CWD TSE Prion
Mississippi, to date, As of August 2020, Mississippi has detected 56 CWD-positive deer...tss
Tackling CWD: There are multiple reasons why CWD needs to be managed in Mississippi.
11/2/2020 9:32:27 AM
By William T. McKinley and Kamen Campell
snip...
Mississippi initially discovered CWD in February 2018.
This first detection was an adult buck in Issaquena County.
Samplings in the following deer season uncovered CWD in Pontotoc County (October 2018), Marshall County (November 2018), Benton County (December 2018), Panola County (February 2019), and Tallahatchie County (February 2019).
As of August 2020, Mississippi has detected 56 CWD-positive deer.
The most recent positives were two sick deer reported in July and August by a landowner in Benton County. A total of 35 deer tested positive during the 2019-2020 hunting season, all of which were harvested in Benton and Marshall counties. One in seven bucks 2.5 years and older sampled in the 2019-2020 season in Benton County tested positive for CWD (see table below).
Prevalence ranges from less than 1% (in four counties) to 13% (Benton County). MDWFP reports prevalence as the percentage of hunter-harvested bucks 2.5 years and older that are CWD-positive. Tennessee has detected 687 CWD-positive deer since the discovery in December 2018, most of which were harvested in counties that border Mississippi. The disease could likely be present but not detected in other counties. CWD has been detected within six miles of Alcorn, Desoto, Leflore, Sharkey, Tate, Tippah, Union, and Warren counties.
MDWFP will operate a minimum of 46 CWD drop-off freezers for hunters across Mississippi to acquire samples in the upcoming season. Hunters drop off the head of a harvested deer, provide contact information, and remove the receipt from the submission card. Additionally, MDWFP will be working with numerous taxidermists across the state. Hunters can view their test results online. MDWFP will personally contact any hunter submitting a positive animal.
Mississippi is participating in multiple research projects, in-state and nationwide, to further our efforts in managing CWD. Examples include CWD strain typing, white-tailed deer genotyping, CWD control methods, and deer movement studies within CWD-endemic areas.
MDWFP would like to thank hunters for submitting more than 6,000 samples last season; however, Mississippi’s deer herd needs hunters’ continued help to battle this insidious disease. Hunters are urged to stay updated on CWD, report sick deer, and submit deer heads for sampling. Visit MDWFP’s CWD page at mdwfp.com to learn more about CWD and to read the 2019-2020 CWD Annual Report.
Chronic Wasting Disease
Mississippi Department of Wildlife, Fisheries, and Parks
Surveillance and Management Report
2019 - 2020
TUESDAY, JANUARY 28, 2020
Mississippi MDWFP North MS CWD Management Zone Since October 2019, 25 CWD-positive deer have been detected from this zone
SATURDAY, JANUARY 04, 2020
Mississippi CWD TOTALS JUST ABOUT DOUBLE Since October 1, 2019 To Date Statewide Total is 37 Confirmed
***Missouri CWD TSE Prion
Missouri, to date, CWD has been detected in 162 cervid...tss
WEDNESDAY, MAY 06, 2020
Missouri 46 new cases Chronic Wasting Disease found, total to date at 162 documented CWD
MDC REPORTS FINAL CWD RESULTS FOR 2019-2020 SEASON
News from the region: Statewide Joe JerekMay 06, 2020 JEFFERSON CITY, Mo. – The Missouri Department of Conservation (MDC) reports it has completed its monitoring and testing efforts for the 2019-2020 chronic wasting disease (CWD) surveillance year. From those efforts, MDC reports it has confirmed 46 new cases of the deadly deer disease.
These new findings bring the total number of CWD cases in the state to 162. MDC has tested more than 137,000 deer since the first cases of CWD were found in free-ranging deer in Missouri in 2012. https://mdc.mo.gov/newsroom/mdc-reports-final-cwd-results-2019-2020-season
Missouri 2019 - 2020 CWD
WEDNESDAY, MAY 06, 2020
Missouri 46 new cases Chronic Wasting Disease found, total to date at 162 documented CWD
TUESDAY, FEBRUARY 11, 2020
Missouri MDC 2019-2020 SAMPLING RESULTS CWD TSE PRION TO DATE 28 Positive
SUNDAY, JANUARY 19, 2020
Missouri CWD TSE Prion 2019-2020 SAMPLING RESULTS TO DATE 25 Positive
THURSDAY, JANUARY 02, 2020
Missouri MDC officially reports more than 20 new cases of Chronic Wasting Disease CWD TSE Prion
***Montana CWD TSE Prion
Montana, to date, CWD has been detected in 275 cervid...tss
MONTANA DEPARTMENT OF LIVESTOCK REPORTS CHRONIC WASTING DISEASE (CWD) DETECTION IN FLATHEAD COUNTY GAME FARM
Friday, November 20, 2020/Categories: Department of Livestock/Tags:
FOR IMMEDIATE RELEASE:
November 20, 2020
CONTACT: Dr. Tahnee Szymanski, MT Dept. of Livestock, (406) 444–5214, tszymanski@mt.gov Dr. Marty Zaluski, MT Dept. of Livestock, (406) 444 –2043, mzaluski@mt.gov
The Department of Livestock Reports Chronic Wasting Disease (CWD) Detection in Flathead County Game Farm
Helena, Mont.—On November 19 the Montana Department of Livestock received notification that a single game farm animal in Flathead County was confirmed positive for Chronic Wasting Disease (CWD). This is the second detection of CWD in domestic cervids in Montana this year.
The CWD positive animal was found as a result of mandatory surveillance of all age eligible animal mortalities in game farm animals in Montana. Montana’s CWD Herd Certification Program requires all animals greater than 12 months of age to be tested. The CWD positive animal was not exhibiting any clinical signs of CWD but was found dead on the affected premises. The infection was confirmed by the National Veterinary Services Laboratories in Ames, Iowa through the identification of the prion in tissue samples collected from the animal.
The Department has placed the herd under quarantine and is conducting an epidemiological investigation. Montana law requires CWD positive game farm herds to undergo complete depopulation and post-mortem testing of the herd, or quarantine of the entire herd for a period of five years from the last CWD positive case.
State Veterinarian Dr. Marty Zaluski stated, “An epidemiologic investigation will be conducted, but at this time, the source of the disease is unknown.” Zaluski added, “We will look at historical animal movements associated with this captive herd and proximity to infected wildlife to try to determine the source of exposure.”
Montana Fish Wildlife and Parks (FWP) has documented CWD in wild cervids across much of Montana through surveillance that began in 2017. In 2019, approximately 7,000 wild deer, elk, and moose were sampled statewide, with 140 of them testing positive for CWD.
CWD is a progressive, fatal disease that affects the nervous system of white-tailed deer, mule deer, elk, and moose. Transmission can occur through direct contact between animals, through
urine, feces, saliva, blood and antler velvet. Infected carcasses may serve as a source of environmental contamination and can infect other animals. Infected animals may carry the disease for years without showing signs of illness, but in later stages, signs may include progressive weight loss, lack of coordination and physical debilitation.
There is no known transmission of CWD to humans. However, the Centers for Disease Control and Prevention (CDC) recommends that hunters harvesting an animal in areas known for the presence of CWD, have their animal tested. If the animal tests positive, the CDC advises against eating the meat.
The mission of the Montana Department of Livestock is to control and eradicate animal diseases, prevent the transmission of animal diseases to humans, and to protect the livestock industry from theft and predatory animals. For more information on the Montana Department of Livestock, visit www.liv.mt.gov.
Positive CWD Samples: 275 Total since CWD testing began in 2017
Montana CWD management plan
In October 2017, CWD was first detected in free-ranging deer in Montana. It was detected in captive game farms in Montana in 1999 and again in 2020.
Montana CWD Map
http://fwp.mt.gov/fishAndWildlife/diseasesAndResearch/diseases/chronicWastingDisease/management.html
WEDNESDAY, OCTOBER 21, 2020
Montana 18 deer test positive for chronic wasting disease CWD TSE Prion
CWD positives from across the state, no new areas
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
FRIDAY, FEBRUARY 07, 2020
Montana 142 animals tested positive for CWD thus far during 2019/20 sampling
FRIDAY, JANUARY 17, 2020
Montana Moose Tests Positive for Chronic Wasting Disease CWD TSE PRION in Libby Area
Montana Fish, Wildlife & Parks 2019 CWD Surveillance Hunter Test Results CWD TSE PRION LOOKS LIKE 136 POSITIVE SO FAR, count them up...
WEDNESDAY, DECEMBER 25, 2019
Montana 16 more deer positive for CWD first time positive hunting district 705 in southeast
Nebraska CWD TSE Prion
Nebraska, to date, 815 deer and 14 elk have been detected with CWD...tss
The Nebraska Game & Parks Commission has tested over 55,000 deer and over 280 elk, with 815 deer and 14 elk testing positive overall. 49 counties have detected CWD in free ranging herds. NGPC sent in 1,804 deer samples and 124 elk samples in 2019 with 171 deer and 6 elk (see map below), but no population declines attributable to the disease have yet occurred.
Nebraska Chronic wasting disease testing paused, will resume in 2021
FOR IMMEDIATE RELEASE
Chronic wasting disease testing paused, will resume in 2021
LINCOLN, Neb. — With the move to online deer checking for the November firearm season, the Nebraska Game and Parks Commission will not collect samples to test for chronic wasting disease.
Hunters wishing to have their deer tested for chronic wasting disease can do so, for a fee, through the Nebraska Veterinary Diagnostic Laboratory at the University of Nebraska-Lincoln. Learn more at vbms.unl.edu/tse-test.
The agency typically collects approximately 1,200 samples from older age-class bucks in specific management units during the nine-day firearm season. Check stations are the primary way staff collects a scientifically robust number of lymph nodes to test for the disease. The results aid in future deer management decisions.
Testing will take place in targeted regions of the state over the next several years, and Game and Parks plans to resume chronic wasting disease testing for the 2021 November firearm season.
Chronic wasting disease is prion disease that attacks the brain of infected deer and elk, eventually causing emaciation, listlessness, excessive salivation and death. According to the Centers for Disease Control and Prevention, no person is known to have contracted chronic wasting disease; however, hunters should cautiously handle and process deer and avoid consuming animals that test positive or look sick. Livestock and other animals not in the deer family do not appear susceptible to chronic wasting disease.
Hunters can help prevent the spread of chronic wasting disease by using proper carcass disposal methods. Chronic wasting disease prions, the infectious proteins that transmit the disease, can remain viable for months or even years in the soil. Hunters should field dress animals at the place of kill, avoid spreading spinal cord or brain tissue to meat, and dispose of the head (brain), spinal column and other bones at a licensed landfill. Learn more about chronic wasting disease at http://OutdoorNebraska.gov/cwd.
-30-
2019 Final CWD testing results
Elk and deer season testing results from the Nebraska Veterinary Diagnostic Laboratory (NVDL) can be viewed below. Only positive results are shown for deer. The CWD# column on the results corresponds to the hunter’s seal number.
Download final 2019 CWD positive deer results
Download 2019 elk results
Download 2020 elk results
FRIDAY, JANUARY 03, 2020
Nebraska November 2019 firearm season CWD TSE Prion 169 positives from 1,803 deer sampled in the Pine Ridge, Plains, Missouri, Elkhorn, Calamus East and Loup East management units
MONDAY, DECEMBER 17, 2018
Nebraska Confirms 131 Cases of CWD detected for first time in Valley, Keya Paha counties
see history Nebraska cwd Singeltary
***Nevada CWD TSE Prion
Nevada, to date, has not detected CWD TSE Prion...tss
NEVADA 2019–2020 BIG GAME Help Prevent the Spread of C.W.D. Page 53 HUNTING GUIDE
To date, CWD has not been detected in Nevada, however, cases have been identified in eastern and central Utah. Nevada and Utah share migratory deer and elk herds; for these reasons, NDOW focuses annual surveillance efforts primarily in the eastern half of the state. Surveillance consists of collecting the brain stem and adjacent lymph nodes from hunter harvested adult deer and elk. We also collect samples from animals killed on the road or sick animals displaying symptoms consistent with CWD infection.
***New Hampshire CWD TSE PRION
New Hampshire, to date, CWD is not known to be present in New Hampshire...tss
***New Jersey CWD TSE Prion
New Jersey, to date, Surveys of New Jersey deer harvested in several deer seasons have found no evidence of the disease...tss
NJDEP Division of Fish and Wildlife
Office of Fish and Wildlife Health and Forensics
2019-2020 CWD Survey
Retropharyngeal lymph node samples were collected from 1,091 hunter-killed deer from 6 participating butchers as part of the 2019-2020 statewide CWD surveillance effort. Of the hunter harvested deer 54% were female, 46% were male, 3 were not recorded (Table 1; Figures 3 and 4). In addition to hunter killed deer, 8 wild white-tailed deer, 6 males and 2 females, with clinical signs were opportunistically tested for CWD throughout the year (July 1, 2019 – June 30, 2020). In total 1,099 wild white-tailed deer were sampled in this survey bringing the current total of wild deer sampled in New Jersey from 1997-2020 to 9,129.
The top three DMZ’s sampled this year included Zone 12 with 191 samples, Zone 8 with 125 samples, and Zone 14 with 65 samples (Table 2). Of the 21 counties, Hunterdon with 298, Somerset with 158 and Burlington with 111, had the largest sample sizes (Figure 2). Hudson County was the only county not represented. Figure 2 shows the number of deer sampled this season based on county and DMZ. The age of deer is an important consideration for CWD surveillance since older individuals more are more likely to be infected due to the long incubation period of the CWD prion. Fawns, or deer less than 1.5 years old, were not sampled. In order to consider age in the survey, deer were given scores from 1 to 3 for age groups 1.5, 2.5, and 3.5 respectively. In this year’s survey 27% had an age-weighted score of 1, 38% had an age-weighted score of 2, 35% had an age-weighted score of 3, and 16 were not recorded. These age-weighted scores are shown by county in Figure 1. The top 3 counties with the most deer with scores of 3 included Hunterdon with 109, Somerset with 69, and Burlington with 34.
A total of 2 captive deer, including a male Sika deer and a female elk, were collected for CWD testing statewide. This brings the total number of captive deer tested in NJ since 1997 to 151 white-tailed deer, 7 elk, 2 reindeer, 4 red deer, 1 sika deer and 3 axis deer, all of which tested negative. This year, no deer harvested out of state were tested.
Table 1: Breakdown of Total Deer Sampled by County and Sex
***New Mexico CWD TSE Prion
New Mexico, to date, has detected 58 cases of CWD, and imo that figure might be low, considering...tss
FRIDAY, FEBRUARY 08, 2019
New Mexico Chronic Wasting Disease CWD TSE Prion Update 2018-2019?
WEDNESDAY, FEBRUARY 07, 2018
New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.
THURSDAY, NOVEMBER 02, 2017
New Mexico Chronic Wasting Disease CWD Figures 2016 - 2017 Update ???
From: TSS
Subject: CWD TWO NEW CASES NEAR WHITE SANDS MISSLE RANGE NEW MEXICO
Date: June 27, 2005 at 4:43 pm PST
New Mexico Department of Game and Fish
Contact: Dan Williams, (505) 476-8004
dan.williams@state.nm.us
FOR IMMEDIATE RELEASE, JUNE 24, 2005:
TWO MULE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
ANGLER LANDS STATE RECORD BLUE CATFISH AT ELEPHANT BUTTE LAKE
TWO MULE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
SANTA FE – Two mule deer captured in the Organ Mountains as part of an ongoing research project near White
Sands Missile Range have tested positive for chronic wasting disease (CWD), a fatal neurological disease that
attacks the brains of infected deer and elk, the Department of Game and Fish announced.
The number of confirmed CWD cases in New Mexico now stands at 11 since 2002, when the disease was first
confirmed in a deer found near the eastern foothills of the Organ Mountains. All 11 CWD-infected deer were found
in the same general area of southern New Mexico. The origin of the disease in New Mexico remains unknown.
The carcasses of the infected deer will be incinerated, said Kerry Mower, the Department’s lead wildlife disease
biologist.
Chronic wasting disease causes animals to become emaciated, display abnormal behavior, lose bodily functions
and die. The disease has been found in wild deer and elk, and in captive deer and elk, in eight states and two
Canadian provinces. There currently is no evidence of CWD being transmitted to humans or livestock.
Mower said the most recent CWD-positive deer showed no obvious physical signs of having the disease. They
were captured in April 2005 and tested as part of a 3-year-old research project studying deer population dynamics
in southern New Mexico. More than 140 deer have been captured alive and tested for the study, in which
researchers hope to find the cause of a 10-year decline in the area deer population. Study participants include the
Department of Game and Fish, the U.S. Army at White Sands Missile Range and Fort Bliss, Bureau of Land
Management, U.S. Geological Survey at New Mexico State University, and San Andres National Wildlife Refuge.
Hunters can assist the Department in its CWD research and prevention efforts by bringing their fresh, legally
harvested deer or elk head to an area office, where officers will remove the brain stem for testing. Participants will
be eligible for drawings for an oryx hunt on White Sands Missile Range and a trophy elk hunt on the Valle Vidal.
For more information about the drawing and chronic wasting disease, visit the Department web site at
www.wildlife.state.nm.us.
SEE MAP ;
Greetings list members,
I am deeply concerned with these CWD mad deer so close to the Texas border. WHAT keeps them from crossing the border to Texas ??? IF these illegal aliens can so easily cross our borders, why not these infected deer? maybe we should get these minute men to start watching for mad deer coming in to Texas from New Mexico.
I mentioned my concerns several other times before;
-------- Original Message --------
Subject: Current status of CWD testing in Texas
Date: Tue, 10 May 2005 09:09:47 -0500
From: "kschwaus"
To:
Mr. Singeltary,
I was asked to provide you with the following information. If you have any other questions regarding CWD sampling in Texas, please do not hesitate to give me a call. My office number is below.
Below I have included a chart showing CWD samples that have been tested since the fall of 2002 through the present at the eco-region level. The second chart shows the totals on a given year. The unknown location samples come from private individuals sending in samples directly to the Texas Veterinary Medical Diagnostic Lab (TVMDL). Due to the confidentiality laws that the TVMDL operates under, they are unable to provide TPWD with the location of those samples.
Region Population Estimate
Sampling from Fall 2002 to Present
Pineywoods
502,521
975
Gulf Prairie
90,664
441
Post Oak Savannah
291,119
1146
Black Land Prairies
54,505
153
Cross Timbers
441,031
1015
Edwards Plateau
1,608,390
1618
South Texas Plains
500,183
1253
Rolling Plains
231,358
352
High Plains
49,981
81
Trans Pecos
148,174
173
Unknown Location
1,896
Total
3,917,926
9,103
Samples Collected By
2002-03
2003-04
2004-Present
TPWD
1,722
2,955
2,540
Private (unknown location)
326
608
952
Total
2,048
3,563
3,492
Thank you,
Kevin Schwausch
Big Game Program Specialist
Texas Parks & Wildlife Department
PO Box 1394
Burnet, TX 78611
512-756-4476
===============================
I would like to thank Kevin and TPWD for there prompt reply with updated data.
I am still concerned about the Texas, New Mexico border and New Mexico's apparent lack of CWD testing updates. Makes one wonder about there CWD testing program. NO report/reply back from New Mexico about there CWD testing update yet. ...
TSS
===================
THURSDAY, SEPTEMBER 22, 2016
New Mexico CWD confirmed in 5 McGregor Range deer during the 2015-16 hunting season
WEDNESDAY, MARCH 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015
MONDAY, SEPTEMBER 17, 2012
New Mexico DGF EXPANDS CHRONIC WASTING DISEASE CONTROL AREAS, while Texas flounder
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
SUNDAY, OCTOBER 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009
***New York CWD TSE Prion
New York, to date, CWD TSE Prion has been detected in 5 captive cervid and 2 wild cervid...tss
In spring 2005, CWD was first detected in New York in a captive deer herd in Oneida County. A second infected deer was discovered in a nearby captive herd within days of the index case. Deer had been exchanged between the two herds. Both herds were depopulated and indemnification was paid by DEC. Five captive deer tested positive for CWD. The index herd also had a taxidermy studio and engaged in the rehabilitation of white-tailed deer; deer may have been exposed to CWD via improperly handled taxidermy waste (salt). Immediate intensive sampling efforts began in a 10-mile radius “containment area” around those herds. Two wild deer tested positive for CWD during that sampling effort. Emergency regulations were subsequently enacted, which included: ...snip...see full report;
New York State Interagency CWD Risk Minimization Plan
New York State Department of Environmental Conservation Division of Fish and Wildlife
Prepared February 2018
SECOND CASE OF CWD FOUND IN ONEIDA COUNTY DEER
State's Trace Back Finds Second Positive CWD in Herd Directly Linked to Index Herd
*** NOTE TO REPORTERS: There will be an 11:00 am press conference call with State officials from the Departments of Agriculture & Markets and Environmental Conservation to answer any questions regarding today’s announcement. To participate in the call, reporters should call 1-866-814-1918. Please be prepared to provide the operator with the conference ID# – 682688 and conference name – CWD.
A second positive case of chronic wasting disease (CWD) in New York State has been confirmed in a white-tailed deer from a captive herd in Oneida County that is directly linked to the herd where a white-tailed doe was found positive for CWD earlier this week.
CWD is a transmissible disease that affects the brain and central nervous system of deer and elk. There is no evidence that CWD is linked to disease in humans or domestic livestock other than deer and elk.
During the investigation of the State’s first case of CWD this week, the New York State Department of Agriculture and Markets found that one of the herds associated with the index animal had recently sent a sample to the State’s Veterinary Diagnostic Laboratory to be tested for CWD. The sample was collected and sent for testing as part of the State’s mandatory CWD surveillance and testing protocols.
The positive sample was from a two and a half year old white-tailed deer that died from aspiration pneumonia, which is often but not exclusively associated with CWD. Due to the direct association with the index herd, the Department expedited the testing procedure by re-routing the sample to the National Veterinary Services Laboratory in Ames, Iowa, which late yesterday found the sample to be positive for CWD.
Two days ago, the New York State Departments of Agriculture and Markets, and Environmental Conservation announced the State’s first case of CWD, found in a six-year old white-tailed doe from a captive herd in Oneida County. The deer was sampled as part of the State’s Enhanced CWD Surveillance and Monitoring Program.
Currently, the index herd and the six other associated herds including the second positive herd are under quarantine. All animals remaining in the index herd and the herd with the second confirmed positive herd will be depopulated and tested for CWD. The investigation to determine the source of the infection is ongoing.
The New York State Department of Agriculture and Markets will continue to seek any susceptible deer that came into contact with either herd and to assess the health and environmental risks associated with such establishments.
The New York State Department of Environmental Conservation will continue to conduct intensive monitoring of the wild deer population surrounding the two positive herds to determine if CWD has spread to wild deer.
CWD is a transmissible spongiform encephalopathy (TSE) of deer and elk. Scientific and epidemiological research into CWD is ongoing. To date, research shows that the disease is typified by chronic weight loss, is always fatal, and is transmissible between susceptible species. CWD has only been found in members of the deer family in North America, which include white-tailed deer, mule deer, elk and moose.
More information and the transcript of Thursday’s press conference regarding the first positive case of CWD in New York State can be found at the Department of Agriculture and Markets’ website at www.agmkt.state.ny.us or at the Department of Environmental Conservation’s website at www.dec.state.ny.us .
###
DEC began CWD monitoring efforts in 2002, but intensified the effort in 2005 after CWD was confirmed in both captive and wild deer in Oneida County – the first incidents of the disease in New York State. Since that time, DEC has tested over 40,000 deer statewide with no additional cases being discovered, until now.
New York State Interagency
Chronic Wasting Disease
Response Plan 2015-2025
New York State Interagency CWD Risk Minimization Plan
snip...
The Oneida County CWD outbreak in 2005 was at a captive deer facility where the owner mixed taxidermy and deer rehabilitation activities together so NY has taken steps to limit co-occurrence of these activities. This captive facility was designated as Special Purpose (Monitored) and conducted required testing. The subsequent epidemiological investigation revealed CWD-positive animals in the facility and in the wild.
snip...
*From publication of the new rule (Oct. 15, 2013) forward, all new CWD-certified herds will be required to have a restraint system.
Why are deer carcasses and parts a risk for CWD entry?
Prions are found throughout the body, but are in higher concentrations in specific tissues, such as the brain, spinal cord, tonsils, lymph nodes, spleen, and intestinal tract (Williams 2005). Disposal of deer carcasses by hunters is not easily regulated in New York. A deer carcass that is disposed of on the landscape where it is available to scavengers and wild deer presents a risk because prions are not easily degraded and can remain viable for an undetermined amount of time [>16 years for scrapie prions (Georgsson et al. 2006)]. Prions bind to soil particles and remain infectious and prions can be taken up by plants (Pritzkow et al. 2015). Scavengers may transport prions in feces (VerCauteren et al. 2012, Nichols et al. 2015). A minimum of 54,000 deer are taken to taxidermists and processors each year in New York and of those, an estimated 3-5% (>2000) are deer harvested from outside the state. When conducting a 2012 survey of deer hunting businesses in the state, DEC biologists found that many deer processors and taxidermists were unaware that DEC’s solid waste regulations applied to their businesses for waste disposal (Appendix V). For disposal, 50% of businesses used a landfill, 25% used rendering services exclusively, and 15% indicated they composted, used a pit, or otherwise left carcasses on the landscape where they could be encountered by wild deer and present a risk of disease transmission to wild deer. The remaining 10% used a variety of methods, with <1% choosing incineration. Our concern is that 25% of businesses (those not using landfills or rendering) were disposing of waste with a method that made prions directly available to wild deer.
Is CWD in New York State? CWD was discovered in two captive deer facilities in New York in 2005 and subsequently in two wild whitetailed deer nearby. Intensive annual surveillance has not identified any additional cases in that area or in the rest of the state. Keeping CWD out of New York is a priority for the NYS Department of Environmental Conservation (DEC) and the NYS Department of Agriculture and Markets (DAM).
SATURDAY, MARCH 24, 2018
New York Status Chronic Wasting Disease CWD TSE Prion History To Date
SATURDAY, AUGUST 05, 2017
CWD PLAN Singeltary Submission Comment New York State DEC
Greetings New York State DEC, and Honorable Team Members et al,
i wish to kindly submit comments on your CWD Plan. my comments will follow a snip of your request for comments page CWD Risk Minimization Plan. please take my submission very seriously, and please read over the most updated science on the CWD TSE Prion, and i have included the most recent data on Prion 2017 Conference with video url link. i only wish, ...
***North Carolina CWD TSE Prion
North Carolina, to date, At the time of this printing, CWD has NOT been confirmed in North Carolina
SATURDAY, SEPTEMBER 20, 2014
North Carolina Captive cervid licenses and permits Senate Bill 744 Singeltary Submission
***North Dakota CWD TSE Prion
North Dakota, to date, CWD has been detected in 26 cervid (personal communication Dr. Charlie Bahnson, wildlife veterinarian for the North Dakota Game and Fish Department...November 23, 2020).
FEBRUARY 2020 • NUMBER 7 • VOLUME LXXXII
Eight deer taken during the 2019 North Dakota deer gun season tested positive for chronic wasting disease, according to Dr. Charlie Bahnson, wildlife veterinarian for the North Dakota Game and Fish Department.
All were antlered deer taken from areas previously known to have CWD – six from unit 3F2 and two from 3A1. Bahnson said six of the eight were mule deer, with two whitetails from unit 3F2. CWD was not detected in any deer harvested in the eastern portion of the state where hunterharvested surveillance was conducted last fall. In addition, no elk or moose tested positive.
“Only about 15% of hunters submit heads for testing in units where CWD has been found, so the infection rate is more meaningful than the raw number of positive animals found,” Bahnson said. “Approximately 3% of harvested mule deer were infected with CWD in unit 3F2, and roughly 2% in unit 3A1. Our infection rate in whitetails in 3F2 was about 1%.
“Overall,” he continued, “we could probably live with these current infection rates long-term, but they suggest an upward trend and we’ve certainly seen an expansion in the known distribution of the disease. We need to continue to try to limit the spread within our herds as best as we can.”
CWD is a fatal disease of deer, moose and elk that can cause long-term population declines if left unchecked.
Bahnson said the eight positive deer put the total at 11 detected since September 1. As previously reported, two mule deer taken in September tested positive for CWD – one was harvested during the archery season from deer gun unit 4B, and one during the youth season in unit 3A1. CWD was also detected in a whitetailed deer from unit 3F2 that was euthanized in December following a report from the public that it appeared sick and was displaying erratic behavior.
Game and Fish will use its 2019 surveillance data to guide its CWD management strategy moving forward. More information about CWD is available on the Game and Fish Department’s website, gf.nd.gov/cwd.
Taking aim at chronic wasting disease: Fatal deer disease a focus as rifle hunting season approaches
Written By: Brad Dokken | Nov 4th 2019 - 8am.
To date, 17 deer – all wild – have tested positive for CWD in North Dakota, Bahnson said. First detected in 2009 in south-central North Dakota, CWD in the past year has been found in northwest North Dakota and, most recently, McKenzie County in the North Dakota Badlands, where a mule deer buck shot with a bow in September in hunting Unit 4B tested positive.
The deer in 4B was tested as part of a routine sampling effort. A second mule deer buck taken during the September youth season in Unit 3A1 in Divide County also tested positive.
Both deer appeared perfectly healthy, Bahnson said. That’s been the case with most of the nearly 30,000 deer Game and Fish has tested since it began sampling for the disease in 2002, he said.
Deer found near Williston tests positive for CWD
Written By: Forum staff reports | Mar 19th 2019 - 2pm.
BISMARCK — A white-tailed deer found dead just south of Williston in late February has been confirmed positive for chronic wasting disease (CWD), according to Dr. Charlie Bahnson, wildlife veterinarian for the North Dakota Game and Fish Department.
The find means CWD is much farther south than previously thought, officials said.
CWD is a fatal disease of deer, moose and elk that can cause long-term population declines if left unchecked. Since 2009, 14 other deer have tested positive for CWD in North Dakota; 13 from Grant and Sioux counties in hunting unit 3F2 in the southwest, and the other taken last fall from the northwest in Divide County.
The deer found near Williston is the first documented case of a mortality due to CWD in North Dakota. Previous deer found with CWD were hunter harvested before they became sick. This latest deer was severely emaciated and had an empty digestive tract, officials said.
The Game and Fish Department will collect additional samples for testing through targeted removal over the next week or so. In addition to the targeted removal and testing, Game and Fish will review the need to amend the current CWD proclamation to reflect the new CWD positive.
Chronic Wasting Disease Detected in McKenzie County
Two mule deer taken in September tested positive for chronic wasting disease, including one during the archery season from deer gun unit 4B in McKenzie County, where CWD had not previously been found. The other deer was harvested during the youth season in unit 3A1 in Divide County where CWD was first detected last fall.
North Dakota Game and Fish Department wildlife veterinarian Dr. Charlie Bahnson said the finding in 4B marks the first detection of CWD in the badlands.
“This is an iconic place to hunt big game where people travel to from across the state,” Bahnson said. “By no means does this first detection spell doom for hunting in this area, as long as we are proactive in trying to keep infection rates from climbing. We also need to reduce the chance of CWD spreading to new areas.”
Game and Fish will review its CWD management strategy after the deer rifle season and will consider making revisions for next season. While unit 4B does not have carcass transportation restrictions in place for 2019, Bahnson does recommend that hunters in 4B submit their deer for testing, and avoid transporting high-risk carcass parts, such as the brain and spinal column, outside of the hunting unit.
North Dakota CWD 2020
TUESDAY, MARCH 03, 2020
North Dakota Eight deer taken during the 2019 deer gun season tested positive for chronic wasting disease CWD TSE Prion
FRIDAY, JANUARY 17, 2020
North Dakota 11 Positive Chronic Wasting Disease CWD TSE Prion detected since Sept 1, 2019
***Ohio CWD TSE Prion
Ohio, to date, cwd tse prion has been detected in 24 CWD POSITIVES IN CAPTIVE CERVID ZERO IN WILD...tss
THURSDAY, JULY 30, 2020
Ohio Deer Summary 2019 - 2020 CWD TSE Prion 24 Confirmed To Date All Captive Cervid
Please note, to date, 24 CASES OF CWD TSE PRION POSITIVE HAVE BEEN DETECTED IN _CAPTIVE_ Cervid in Ohio, with the latest being announced May 16, 2020 in Wayne County farm. ''Subsequent to that announcement, another doe tested positive on the same farm, bringing the total number of CWD+ deer (all captive) to 24''.
personal communication Michael J. Tonkovich, Ph.D. Deer Program Administrator Ohio DNR Division of Wildlife, July 30, 2020.
Sent: Sat, May 16, 2020 10:18 am
Subject: Ohio Chronic Wasting Disease Detected on Wayne County Farm
Chronic Wasting Disease Detected on Wayne County Farm
May 15, 2020 | Animal Health
Chronic Wasting Disease Detected on Wayne County Farm
REYNOLDSBURG, Ohio (May 15, 2020) – Chronic Wasting Disease (CWD) has been detected at a farm in Wayne County. CWD is a degenerative brain disease that affects elk, mule deer and white-tailed deer. Investigators with the Ohio Department of Agriculture (ODA) detected CWD in a doe in the herd. ODA is conducting an epidemiological investigation on the farm and developing a herd plan. ODA has applied for an indemnity plan with the United States Department of Agriculture for depopulation of the herd. This is necessary in order to stop the transmission and spread of CWD. Once approved, ODA officials will depopulate the affected herd.
CWD has occurred in Ohio in the past but has been eradicated through depopulation. It has never been found in Ohio’s wild deer herd population. If you have questions or concerns regarding CWD, please contact the Division of Animal Health at 614-728-6220 or by email, animal@agri.ohio.gov. https://agri.ohio.gov/wps/portal/gov/oda/divisions/animal-health/news-and-events/cwd-detected-on-wayne-co-farm A captive white-tailed deer breeding facility in Holmes County was confirmed CWD-positive in January 2018 and depopulated in February 2018. Two of the 93 deer euthanized were CWD-positive as well. A disease surveillance area (DSA) has been established around the facility and will remain in effect for at least three years.
SUNDAY, JANUARY 14, 2018
Ohio ODA confirms CWD TSE Prion in another captive deer Ohio detects CWD in captive deer again
Chronic Wasting Disease found in Ohio captive deer
The Ohio Department of Agriculture (ODA) confirmed a positive case of Chronic Wasting Disease (CWD) in a captive deer. The state is taking quarantine action to control the further spread of the disease and there is no evidence that CWD has affected the wild deer population in the state.
The positive sample was taken from a single buck on a hunting preserve in Guernsey County and tested as part of Ohio’s CWD monitoring program for captive white-tailed deer operations. The animal was transferred from a captive breeding facility in Holmes County just days before it was harvested. Both the hunting preserve and the breeding farm are under quarantine and are subject to intensive monitoring and sampling protocols. The quarantine will remain enforced until the state is satisfied that disease transference can no longer occur between captive operations.
“While the confirmed case is unfortunate, this proves the necessity of testing and monitoring the health of captive deer populations in Ohio in order to monitor the health of the animals and to manage exposure to diseases,” said State Veterinarian Dr. Tony Forshey. “ODA will work with our state partners and continue to take whatever steps necessary in order to manage CWD and prevent exposure to Ohio’s wild deer population.”
ODA regulates Ohio’s captive white-tailed deer facilities and monitors the health of animals through regular testing of deer at both farms and hunting preserves. The Ohio Department of Natural Resources, Division of Wildlife conducts regular surveillance throughout Ohio to monitor the health of the state’s wild deer population. Acting in an abundance of caution, increased surveillance of wild deer will occur around the quarantined facilities associated with the recent CWD positive test. Again, no CWD has ever been confirmed in Ohio’s wild deer population.
Snip...
CWD confirmed in captive Ohio deer
January 12, 2018 Ohio DNR Reports
REYNOLDSBURG, Ohio – The Ohio Department of Agriculture (ODA) confirmed a positive case of chronic wasting disease (CWD) in a captive deer, the ODA and Ohio DNR announced in a shared news release Friday, Jan. 12.
The state is taking quarantine action to control the further spread of the disease and there is no evidence that CWD has affected the wild deer population in the state, the release said.
The positive sample was taken from a single buck on a hunting preserve in Guernsey County and tested as part of Ohio’s CWD monitoring program for captive white-tailed deer operations. The animal was transferred from a captive breeding facility in Holmes County just days before it was harvested. Both the hunting preserve and the breeding farm are under quarantine and are subject to intensive monitoring and sampling protocols. The quarantine will remain enforced until the state is satisfied that disease transference can no longer occur between captive operations.
“While the confirmed case is unfortunate, this proves the necessity of testing and monitoring the health of captive deer populations in Ohio in order to monitor the health of the animals and to manage exposure to diseases,” said State Veterinarian Dr. Tony Forshey. “ODA will work with our state partners and continue to take whatever steps necessary in order to manage CWD and prevent exposure to Ohio’s wild deer population.”
ODA regulates Ohio’s captive white-tailed deer facilities and monitors the health of animals through regular testing of deer at both farms and hunting preserves. The Ohio DNR, Division of Wildlife conducts regular surveillance throughout Ohio to monitor the health of the state’s wild deer population. Acting in an abundance of caution, increased surveillance of wild deer will occur around the quarantined facilities associated with the recent CWD positive test. Again, no CWD has ever been confirmed in Ohio’s wild deer population, the DNR added in the release.
SUNDAY, NOVEMBER 08, 2020
OHIO CHRONIC WASTING DISEASE TSE PRION UPDATE TO DATE 24 CWD POSITIVES IN CAPTIVE CERVID ZERO IN WILD
WEDNESDAY, AUGUST 05, 2015
Ohio confirms to me Chronic Wasting Disease
CWD Spreads 19 confirmed cases to date Just got off the phone with Christy Clevenger of Ohio
Ohio Department of Agriculture March 2012 – Present (3 years 6 months) Reynoldsburg, Ohio CWD program
Ms. Clevenger confirmed, to date, from the Yoder debacle, 1 confirmed case of CWD from the Hunting Preserve, 2 confirmed cases from the Breeding Farm, and 16 confirmed cases of CWD from the Breeder Depopulation, with a total to date of 19 cases of CWD in Ohio...with sad regards, Terry
***Oklahoma CWD TSE Prion
Oklahoma, to date, CWD has been detected in 6 cases of CWD TSE Prion documented to date in Captive Cervid...tss
1st cwd positive captive 1998, 2nd cwd positive captive 2019, 3 cwd positives from that herd depopulation, with 1 additional Trace Out CWD Trace Out Positive, equal to date 6 captive CWD positives in Oklahoma to date, and since my confirming these figures the last time via phone, i am told now i will have to fill out a FOIA request for any further reports of CWD TSE Prion in captive herds in Oklahoma.
THURSDAY, NOVEMBER 19, 2020
Oklahoma Proper Carcass Disposal Cervid Importation with 6 cases of CWD TSE Prion documented to date in Captive Cervid
TUESDAY, JANUARY 07, 2020
Oklahoma Farmed Elk Lincoln County CWD Depopulation 3 Positive Elk with 1 Additional Dead Trace Out Confirmed Positive
***Oregon CWD TSE Prion
Oregon, to date, CWD has not been detected in Oregon...tss
***Pennsylvania CWD TSE Prion
Pennsylvania, to date, CWD has been detected in 481 wild cervid as of August, 8, 2020, and captive positives is anyones guess...tss
Wild Positives as of 08.08.2020
County #
Bedford 230
Blair 71
Fulton 132
Total for CCMZ 433
Total for PA 481
MAP
Current Status:
Following the detection of CWD in both captive and free-ranging deer in Pennsylvania, an executive order (PDF) was issued by the Game Commission to establish Disease Management Areas (DMAs). Within DMAs, rehabilitation of cervids (deer, elk and moose); the use or possession of cervid urine-based attractants in an outdoor setting; the removal of high-risk cervid parts; and the feeding of wild, free-ranging cervids are prohibited. Increased testing continues in these areas to determine the distribution of the disease. Newly confirmed cases alter the boundaries of DMAs as the Game Commission continues to manage the disease and minimize its effect on free ranging cervids.
As a result of discovering CWD in both captive and free-ranging deer, the Pennsylvania Game Commission expanded DMAs 2, 3 and 4 for 2020. Of course, CWD has been detected in wild or captive deer and/or elk in many other states and provinces. So for the most up-to-date maps and descriptions of DMA boundaries, visit the interactive map.
DMA 1 was established after CWD was discovered on a captive deer farm in Adams County in 2012 (DMA 1 has since been eliminated).
DMA 2 was established in 2012 and now covers approximately 7,470 square miles, an expansion of 755 square miles over last year. For 2020 biologists expanded it west into Westmoreland County as the result of a CWD-positive adult female roadkill deer, northwest into Cambria and Indiana counties as the result of CWD-positive captive deer facilities and north into Centre County and Mifflin, Union, and Snyder counties as the result of two CWD-positive adult male roadkill deer. DMA 2 currently includes all or parts of Indiana, Cambria, Clearfield, Centre, Union, Snyder, Blair, Huntingdon, Mifflin, Juniata, Perry, Cumberland, Westmoreland, Somerset, Bedford, Fulton, Franklin, and Adams counties.
DMA 3 was established in 2014 and now covers approximately 1,233 square miles, an expansion of 114 square miles over last year. For 2020 biologists expanded it southwest into Jefferson, Indiana, and Armstrong counties because of a CWD-positive yearling male roadkill deer. DMA 3 now covers portions of Jefferson, Clearfield, Indiana, Armstrong, and Clarion counties.
DMA 4 was established in 2018 and now covers approximately 746 square miles, an increase of 397 square miles over last year. For 2020 biologists expanded it further south into Lancaster County after detection of a captive deer with CWD. It now covers portions of Berks, Lancaster, and Lebanon counties.
https://www.pgc.pa.gov/Wildlife/Wildlife-RelatedDiseases/Pages/ChronicWastingDisease.aspx
Agriculture Department Revises Chronic Wasting Disease Quarantine Requirements For Deer Farms In Bedford, Blair, Fulton Counties
08/28/2020
Harrisburg, PA - The Pennsylvania Department of Agriculture today announced changes to quarantine requirements for deer farms in Blair, Bedford and Fulton Counties to control Chronic Wasting Disease (CWD). The department established a CWD Core Captive Management Zone, to control the disease in the area of the state where it is most prevalent, while allowing deer farms to stay in business.
“Pennsylvania has taken CWD very seriously, taking aggressive steps to contain the disease, using a scientific, fact-based approach,” State Veterinarian Dr. Kevin Brightbill said. “Despite aggressive measures, we have seen a rapid increase in the number of deer testing positive over the past two years.
“The goal of implementing such a zone is to slow the spread of CWD across Pennsylvania while scientists race toward establishing long-term solutions. This order provides a path forward for deer farmers to maintain their livelihoods and continue to offer goods and services. A key component of the order is providing incentive for deer farms to implement management techniques, such as herd density and age management, genetic selection and other rapidly evolving scientific advancements that make their operations and their herds less susceptible to CWD.”
CWD is a highly contagious disease that develops very slowly in the lymph nodes, spinal tissue and brains of deer and similar animals like reindeer and elk. It does not affect other livestock. To date there is no evidence that it can be spread to humans.
The PA Department of Agriculture oversees the state’s deer farming industry. Pennsylvania’s 760 breeding farms, hunting preserves and hobby farms provide breeding does, breeder and trophy bucks, semen, embryos, antlers and urine products to Pennsylvania and states across the nation.
Pennsylvania deer farms must participate in one of two stringent programs – the federal Herd Certified program, or the state Herd Monitored Program. Both programs require proper IDs; record-keeping on all animals moved on or off farms; annual herd inventories; reporting of CWD suspects, animals that die, escape or are stolen; testing animals over a year old that die for any reason; maintaining a minimum 8-foot high fence; obtaining permits to import animals from out-of-state; and other measures to monitor herds for disease.
Blair, Bedford and Fulton County deer farms in the new CWD Core Captive Management Zone will be affected by the updated quarantine as follows:
Farms will not be permitted to move high risks parts out of the zone. This includes the brain, eyes, tonsils, lymph nodes, backbone, spleen and anything containing visible brain or spinal cord material where the prions that spread CWD are concentrated. Farms will be permitted to move low risk parts out of the zone including antlers, clean skull caps, capes and deboned meat. Deer farms in this zone can continue to import deer into the zone. Deer farms in this zone can continue to offer hunts. Herd Monitored farms will not be permitted to move live deer out of this zone to other parts of Pennsylvania. Herd Certified farms will continue to be permitted to sell deer out of state, with a permit. Herd Certified farms who screen their entire herd using live animal rectal lymphoid screening for prion detection through a licensed, accredited veterinarian with non-detected results will be permitted to sell live deer, embryos and semen to other parts of Pennsylvania. Deer Farms will be able to buy, sell and transfer live deer if the annual rate of CWD positive animals in their herd remains below five percent. The formula for calculating this rate is included in the quarantine order. Deer farms crossing the five percent threshold will be required to segregate females from males and may continue hunting operations as terminal male hunting facilities until the 60-month quarantine period has expired. No new premises or business with CWD-susceptible species may be established within this zone. Pre-existing establishments with CWD-susceptible species will be grandfathered at the time of publication of this quarantine order, as long as such establishments continuously maintain an active business inventory. The updated quarantine affects deer farms outside the Core Captive Management Zone as follows:
Farms will continue to be allowed to sell breeding stock, trophy bucks, embryos and semen bucks to farms within the zone. Farms are restricted from buying live deer, embryos and semen from the zone unless purchased from Herd Certified farms that in the past three years screened their entire herd using live animal rectal lymphoid testing for prion and established non-detected results. The new quarantine order can be found in the Pennsylvania Bulletin or on the department’s website. A map of locations of deer farms that have had CWD-positive deer, and locations of positive deer in the wild can be found on the department’s website.
Find CWD genetic testing through the Pennsylvania Veterinary Laboratory at padls.agriculture.pa.gov.
Find more information about Pennsylvania’s captive deer CWD programs, and the department’s broader efforts to safeguard animal health, at agriculture.pa.gov.
MEDIA CONTACT: Shannon Powers - 717.603.2056; shpowers@pa.gov
# # #
https://www.media.pa.gov/pages/Agriculture_details.aspx?newsid=958
MONDAY, JULY 27, 2020
Pennsylvania GAME COMMISSION UNVEILS NEW CWD RESPONSE PLAN
FRIDAY, JUNE 26, 2020
Pennsylvania CWD TSE Prion AREAS EXPAND
SUNDAY, APRIL 12, 2020
PENNSYLVANIA REVISED CWD RESPONSE PLAN DRAFT AVAILABLE FOR REVIEW
WEDNESDAY, MARCH 04, 2020
Pennsylvania YOUR STATE WILDLIFE AGENCY 2019 ANNUAL REPORT CWD TSE Prion 123 tested positive
WEDNESDAY, MARCH 04, 2020
Politicians State Rep. David Maloney, R-Berks Helping to Spread Chronic Wasting Disease CWD TSE Prion
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...
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?
***Rhode Island CWD TSE PRION
Rhode Island, to date, CWD has not been documented in Rhode Island...tss
***South Carolina CWD TSE Prion
South Carolina, to date, CWD has not been detected...tss
Does CWD exist in South Carolina?
To date CWD has not been found in South Carolina. To establish whether CWD occurs in South Carolina, the South Carolina Department of Natural Resources (SCDNR) initiated a CWD surveillance program in fall 2002. This program included testing deer using two different surveillance approaches. These consisted of (1) active random sampling of hunter-killed deer, (2) targeted surveillance of clinical suspect and highrisk animals. The active random surveillance was designed to detect CWD in the free-ranging deer population, even if the prevalence was very low (less than 0.5%). Deer have been sampled from every county in the state. Over the past five years, samples collected using this approach resulted in over 1,500 deer testing negative for CWD. Without sampling the entire deer population, South Carolina’s deer herd cannot be declared absolutely free of CWD. Even so, the Department’s surveillance efforts provide a high degree of confidence that CWD is not present in South Carolina’s deer herd. Compared to many other states, South Carolina lacks several significant risk factors typically associated with CWD; in particular, importation of deer has never been allowed and it appears that commercial movements of deer has played a role in the spread of CWD in other states. Also, South Carolina’s geographic location is far from any state were CWD has been diagnosed.
> South Carolina’s deer population peaked in the mid to late 1990’s at just over 1,000,000 deer.
> Currently the statewide population is estimated at about 730,000 deer.
http://www.dnr.sc.gov/wildlife/deer/2015DeerHarvest.pdf
> Over the past five years, samples collected using this approach resulted in over 1,500 deer testing negative for CWD.
> Surveillance since 2002 has included samples from all 46 South Carolina counties and over 6,000 total deer have been tested.
SO, to put this in perspective, in South Carolina, anywhere from 750,000 to 1,000,000 deer in South Carolina in any give year, and from that, in the past five years, only 1,500 deer tested for CWD tse prion, and from the year 2002, around 15 years, only 6,000 deer have been tested for CWD tse prion in South Carolina. That is not enough CWD testing folks, for anyone wanting to find CWD TSE Prion. IF you wait for CWD to find you, you have failed terribly, because it will find you, but by then it's much too late. If you think game farms are the only culprits helping to introduce CWD into your state, you are only fooling yourselves. you can't wish cwd away, you can't hope it will not find you, because it will, ask Norway, CWD knows no borders, National or International.
TUESDAY, NOVEMBER 28, 2017
South Carolina Chronic Wasting Disease CWD TSE Prion Emergency Response Plan?
***South Dakota CWD TSE Prion
South Dakota, to date, CWD has found 546 cases of CWD (311 deer and 235 elk) in free-ranging deer and elk since testing began in 1997.
South Dakota is reporting a total of 95 positive deer and elk (15 mule deer, 59 white-tailed deer and 21 elk) in the testing period of July 1, 2019 to June 30, 2020.
To date, South Dakota has found 546 cases of CWD (311 deer and 235 elk) in free-ranging deer and elk since testing began in 1997. Wind Cave National Park (WICA) accounts for 166 of these animals (154 elk, 12 deer). Thirty-two elk and 12 deer have been found in Custer State Park. A total of 29,795 wild deer and elk have been tested for CWD since 1997.
CWD was first identified in South Dakota in 7 captive cervid herds in the winter of 1997-1998. CWD was recently identified in captive cervid herds in Meade and Clark counties in 2019. CWD was first found in free-ranging wildlife in a white-tailed deer in Fall River County during the 2001 big game hunting season. In South Dakota, CWD has been detected in free-ranging wildlife in Bennett, Butte, Corson, Custer, Fall River, Haakon, Harding, Jackson, Meade, Lawrence, Pennington and Tripp counties, Custer State Park, and Wind Cave National Park. A map of the known distribution of CWD within free-ranging deer and elk can be found at the bottom of the page under "Related Maps".
The maps below illustrate where CWD has been confirmed by deer and elk hunting units (as of August 2020) .
TUESDAY, FEBRUARY 11, 2020
South Dakota Chronic Wasting Disease CWD TSE Prion Detected in New Areas
***Tennessee CWD TSE Prion
Tennessee, to date, has detected Summary of CWD Testing Results for the 2019-2020 Deer Season = 491 positives detected.
Currently, there are 11 counties affected by CWD, including high-risk counties where CWD has been detected within ten miles of the county border, and positive counties in which CWD has been detected. High-risk counties include Crocket, Gibson, Lauderdale, and McNairy counties. Positive counties include Chester, Fayette, Hardeman, Haywood, Madison, Shelby, and Tipton counties.
On December 14, 2018, TWRA was informed by its CWD diagnostic laboratory 10 hunter-harvested deer from Hardeman and Fayette Counties were suspect for CWD. These deer had been sampled in November during the opening weekend of the deer gun season. Once the CWD-suspect deer were confirmed positive, TWRA’s CWD Response Plan was enacted and the Tennessee Fish and Wildlife Commission (TFWC) established what is now known as Unit CWD, extended the deer season in the affected area to get more deer sampled, and instituted deer carcass exportation and wildlife feeding restrictions to help prevent disease spread.
The 2018-2019 Deer Season
Thanks to the cooperation of hunters and the actions of the Commission, the extended season in January 2019 was a very successful data-gathering effort and TWRA was able to learn a lot about the frequency and distribution of CWD in the affected area. With the aid of hunters, processors, and taxidermists, TWRA was able to test over 3,100 deer. Of these deer, 185 deer were confirmed positive for CWD, with 107 confirmations coming from Fayette County, 77 from Hardeman County, and one from Madison County. It was also determined, in accordance with TWRA’s CWD Management Plan; another 5 southwestern counties were affected since CWD was detected within 10 miles of their borders. These five counties include Chester, Haywood, McNairy, Shelby, and Tipton Counties and were considered high-risk status for CWD. In all counties designated high risk or positive, carcass transportation and wildlife feeding regulations are applicable.
The 2019-2020 Deer Season
The TWRA and the Tennessee Fish and Wildlife Commission (TFWC) created Unit CWD, consisting of Chester, Haywood, Fayette, Hardeman, Madison, McNairy, Shelby, and Tipton counties. Unit CWD deer bag limits and seasons were tailored to empower hunters to increase the deer harvest to keep the number of diseased deer in the affected area to a minimum, reduce disease rates where possible, and keep CWD from spreading. With incredible support and participation from hunters, processors, taxidermists, and TWRA field staff, a grand total 14, 243 samples were tested for CWD. These tests were collected by way of mandatory check station weekends, drop-offs at 27 freezer locations, 13 taxidermists, 21 processors, and from deer showing clinical symptoms. This was a remarkably commendable effort from all involved! See the 2019-2020 CWD Results table for the county by county breakdown. By the close of the season, CWD had been found in wild deer in three additional counties and three additional counties are now considered high risk. The current status of CWD affected counties:
- Positive Counties (CWD positive deer found within the county): Chester, Fayette, Hardeman, Haywood, Madison, Shelby, and Tipton
- High-Risk Counties (CWD positive deer found within 10 miles of the county border): Crocket, Gibson, Lauderdale, and McNairy
In all counties designated high risk or positive, carcass transportation and wildlife feeding regulations are applicable.
Summary of CWD Testing Results for the 2019-2020 Deer Season = 491 positives detected.
Currently, there are 11 counties affected by CWD, including high-risk counties where CWD has been detected within ten miles of the county border, and positive counties in which CWD has been detected. High-risk counties include Crocket, Gibson, Lauderdale, and McNairy counties. Positive counties include Chester, Fayette, Hardeman, Haywood, Madison, Shelby, and Tipton counties.
On December 14, 2018, TWRA was informed by its CWD diagnostic laboratory 10 hunter-harvested deer from Hardeman and Fayette Counties were suspect for CWD. These deer had been sampled in November during the opening weekend of the deer gun season. Once the CWD-suspect deer were confirmed positive, TWRA’s CWD Response Plan was enacted and the Tennessee Fish and Wildlife Commission (TFWC) established what is now known as Unit CWD, extended the deer season in the affected area to get more deer sampled, and instituted deer carcass exportation and wildlife feeding restrictions to help prevent disease spread.
The 2018-2019 Deer Season
Thanks to the cooperation of hunters and the actions of the Commission, the extended season in January 2019 was a very successful data-gathering effort and TWRA was able to learn a lot about the frequency and distribution of CWD in the affected area. With the aid of hunters, processors, and taxidermists, TWRA was able to test over 3,100 deer. Of these deer, 185 deer were confirmed positive for CWD, with 107 confirmations coming from Fayette County, 77 from Hardeman County, and one from Madison County. It was also determined, in accordance with TWRA’s CWD Management Plan; another 5 southwestern counties were affected since CWD was detected within 10 miles of their borders. These five counties include Chester, Haywood, McNairy, Shelby, and Tipton Counties and were considered high-risk status for CWD. In all counties designated high risk or positive, carcass transportation and wildlife feeding regulations are applicable.
The 2019-2020 Deer Season
The TWRA and the Tennessee Fish and Wildlife Commission (TFWC) created Unit CWD, consisting of Chester, Haywood, Fayette, Hardeman, Madison, McNairy, Shelby, and Tipton counties. Unit CWD deer bag limits and seasons were tailored to empower hunters to increase the deer harvest to keep the number of diseased deer in the affected area to a minimum, reduce disease rates where possible, and keep CWD from spreading. With incredible support and participation from hunters, processors, taxidermists, and TWRA field staff, a grand total 14, 243 samples were tested for CWD. These tests were collected by way of mandatory check station weekends, drop-offs at 27 freezer locations, 13 taxidermists, 21 processors, and from deer showing clinical symptoms. This was a remarkably commendable effort from all involved! See the 2019-2020 CWD Results table for the county by county breakdown. By the close of the season, CWD had been found in wild deer in three additional counties and three additional counties are now considered high risk. The current status of CWD affected counties:
- Positive Counties (CWD positive deer found within the county): Chester, Fayette, Hardeman, Haywood, Madison, Shelby, and Tipton
- High-Risk Counties (CWD positive deer found within 10 miles of the county border): Crocket, Gibson, Lauderdale, and McNairy
In all counties designated high risk or positive, carcass transportation and wildlife feeding regulations are applicable.
Deer Management in Tennessee 2019-2023 A Strategic Plan for the Systems, Processes, Protocols, and Programs Pertaining to the Management of White-tailed Deer in Tennessee
Chronic wasting disease (CWD) is in the family of diseases known as transmissible spongiform encephalopathies (TSE). It is caused by a prion or infectious protein particle that persists in the environment indefinitely. In Tennessee, native white-tailed deer and reintroduced wild elk, as well as several exotic captive cervid species, including captive elk, are at risk for infection with CWD. CWD is the greatest threat to the future of deer and deer hunting in Tennessee, and TWRA is proactively addressing this threat.
We have monitored deer for CWD since 2004. In November 2018, we began implementation of a new CWD surveillance strategy weighted towards counties with higher risk (Schuler et al. 2018). On December 14th, 2018 we received notification from our CWD testing facility that 10 samples collected during our CWD surveillance tested positive for CWD. The 10 positive samples occured in two counties that were considered high risk and received increased surveillance under the new strategy.
Immediate implementation of our CWD Response Plan (TWRA 2018), resulted in over 180 additional positives being confirmed in these two counties as well as one in southwest Madison County.
As this plan was being finalized, we began developing a long-term management plan for CWD in light of these findings. With the exception of minor revisions, the objectives outlined below were mostly developed prior to finding CWD in Tennessee. These objectives still apply, but more objectives, strategies, and actions will likely arise as a CWD Management Plan is further developed.
SATURDAY, JANUARY 25, 2020
Tennessee 2019-20 deer season 462 CWD TSE Prion Confirmed To Date
THURSDAY, DECEMBER 20, 2018
Tennessee Confirms Ten Plus Three More Preliminary Chronic Wasting Disease Cases Enacts CWD Response Plan
SATURDAY, DECEMBER 15, 2018
Tennessee Preliminarily Detects Ten Chronic Wasting Disease Cases; Enacts CWD Response Plan Friday, December 14, 2018
THURSDAY, DECEMBER 20, 2018
Tennessee Confirms Ten Plus Three More Preliminary Chronic Wasting Disease Cases Enacts CWD Response Plan
SATURDAY, DECEMBER 15, 2018
Tennessee Preliminarily Detects Ten Chronic Wasting Disease Cases; Enacts CWD Response Plan Friday, December 14, 2018
WEDNESDAY, NOVEMBER 22, 2017
Tennessee Four Charged with Illegal Importation of Deer Carcasses from a CWD Positive State
Saturday, January 07, 2017
Tennessee Republican representative Bud Hulsey wants to weaken CWD Carcass Ban rule and put other states at risk
SATURDAY, APRIL 13, 2013
Tennessee Launches CWD Herd Certification Program in the wake of legislation for game farms
2013
Greetings Tennessean Hunters et al, and politicians,
well, the writing is on the wall Tennessee hunters.
it’s only a matter a time for Tennessee and CWD, and the big ag and officials can’t wait for it $$$
it’s only a matter of time now Tennesseans, and your state too will be full of CWD.
sad...
Monday, November 12, 2012
Tennessee The White-tailed Deer Breeding and Farming Act pushes to legalize deer farming 2012
Tennessee dad faces fatal, untreatable illness as family hopes for cure
Alexandria Hein By Alexandria Hein | Fox News
Tony Gibson, a 32-year-old welder and ironworker, initially showed symptoms of confusion and forgetfulness earlier this year. (iStock)
A Tennessee father who was given a year to live after being diagnosed with an extremely rare degenerative illness now requires 24-hour care at a nursing facility as his family hopes for a cure for the currently untreatable condition. Tony Gibson, a 32-year-old welder and ironworker, initially showed symptoms of confusion and forgetfulness earlier this year, his wife, Danielle, told News Channel 5.
Gibson was diagnosed with Creutzfeldt-Jakob Disease (CJD), which according to the National Institute of Neurological Disorders and Stroke, is a degenerative, fatal brain disorder that strikes in about one in a million per year, worldwide. It’s estimated that 350 Americans are diagnosed each year, although it’s typically diagnosed in older patients with symptoms beginning at around 60, and death occurring within one year.
Patients may first exhibit memory issues, behavioral changes, visual disturbances and lack of coordination before it advances to mental deterioration, blindness, weakness of extremities and coma. Gibson told the news outlet doctors believe her husband’s case is sporadic, which occurs in patients with no known risk factors and accounts for about 85 percent of all CJD cases. There are two other types of CJD, with one often compared to mad cow disease.
According to NINDS, symptoms of sporadic CJD are comparable to those of Alzheimer’s and Huntington’s disease, but deterioration occurs more quickly in CJD patients. While there are studies underway, no successful treatment has been developed.
In a Facebook post honoring CJD Awareness Day on Nov. 12, Gibson wrote that her husband went from being a strong man to a 90-year-old within months.
“This is the most devastating thing I’ve ever seen,” Danielle Gibson, who is caring for the couple’s four children at-home, told New Channel 5. “I’ve seen a lot of terrible things. I’ve seen ALS, but this has to be the worst.”
***Texas CWD TSE Prion
Texas, to date, CWD has been detected in 185 Cases...tss
SUNDAY, AUGUST 30, 2020
Texas CWD TSE Prion 3 More Documented, 185 Cases To Date
Sent: Thu, Jul 9, 2020 10:00 am
Subject: Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date
Texas CWD TSE Prion Jumps To 182 Confirmed Cases
2020-06-25 Free Range El Paso N/A Mule Deer F 5.5
2020-06-16 Free Range El Paso N/A Mule Deer M 5.5
2020-06-10 Breeder Release Site Medina Facility #3 White-tailed Deer F 5.5
2020-06-10 Breeder Release Site Medina Facility #3 White-tailed Deer M 3.5
2020-06-10 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 5.5
2020-06-09 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 2.5
2020-06-09 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 4.5
2020-05-22 Free Range Hartley N/A Mule Deer M 4.5
2020-05-22 Free Range Hartley N/A Mule Deer F 5.5
2020-05-22 Free Range Hartley N/A Mule Deer M 4.5
2020-05-22 Free Range Dallam N/A Mule Deer M 2.5
2020-05-22 Free Range Hartley N/A Mule Deer M 5.5
2020-05-22 Free Range Hartley N/A Mule Deer M 5.5
SUNDAY, MARCH 08, 2020
Texas CWD TSE Prion Confirms 169 Positive To Date
THURSDAY, JULY 09, 2020
Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date
SATURDAY, JULY 04, 2020
TAHC CHAPTER 40 CHRONIC WASTING DISEASE 406th COMMISSION MEETING AGENDA June 23, 2020 8:30 A.M.
''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...
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.''
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
FRIDAY, DECEMBER 20, 2019
TEXAS ANIMAL HEALTH COMMISSION EXECUTIVE DIRECTOR ORDER DECLARING A CHRONIC WASTING DISEASE HIGH RISK AREA CONTAINMENT ZONE FOR PORTIONS OF VAL VERDE COUNTY
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, FEBRUARY 16, 2020
***> Jerking for Dollars, Are Texas Politicians and Legislators Masturbating Deer For Money, and likely spreading CWD TSE Prion?
TUESDAY, FEBRUARY 04, 2020
TEXAS REPORTS 20 NEW CWD TSE PRION CASES 3 WILD 17 BREEDER 166 POSITIVE TO DATE
FRIDAY, MAY 22, 2020
TPW Commission has adopted rules establishing Chronic Wasting Disease (CWD) management zones to further detection and response efforts among WTD
SUNDAY, MARCH 01, 2020
Texas As one CWD investigation continues, another launches...THE FULL MONTY!
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
*** 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 ***
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.
***Utah CWD TSE Prion
Utah, to date, as of October 7, 2020, 118 mule deer and two elk have tested positive for CWD TSE Prion...tss
SATURDAY, OCTOBER 10, 2020
Utah As of October 7, 2020, 118 mule deer and two elk have tested positive for CWD TSE Prion
WEDNESDAY, JANUARY 29, 2020
Utah CWD TSE Prion Since July 1, 2019, the DWR confirmed 16 positive deer statewide Six of those, including Coal, were in the La Sal Unit, 59 test pending
***Vermont CWD TSE Prion
Vermont, to date, CWD has not been detected...tss
***Virginia CWD TSE Prion
Virginia, to date, has detected 84 CWD-positive deer have been detected in Virginia in Frederick and northern Shenandoah counties...tss
HUNTING &TRAPPING IN VIRGINIA July 2020-June 2021
CWD Surveillance in Virginia
Chronic wasting disease (CWD) is an infectious, fatal, neurologic disease of deer.
Since 2009, a total of 84 CWD-positive deer have been detected in Virginia in Frederick and northern Shenandoah counties.
An additional four CWDpositive deer have been detected in Clarke (2), Culpeper (1), and Fauquier (1) counties.
The success of the Department’s CWD surveillance and management efforts hinge directly on hunter participation. DWR greatly appreciates hunters’ cooperation and assistance in this effort.
Disease Management Area Boundaries
In 2020, Disease Management Area 1 (DMA1) will include Frederick, Shenandoah, Warren, and Clarke counties. DMA2 will include Culpeper, Fauquier, Loudoun, Madison, Orange, Page, and Rappahannock counties.
HUNTING &TRAPPING IN VIRGINIA July 2020-June 2021
Chronic Wasting Disease
• Chronic wasting disease (CWD) has been found in Clarke and Fauquier counties.
• Disease Management Area 2 (DMA2) has been expanded to include Fauquier, Loudoun, Page, and Rappahannock counties, in addition to Culpeper, Madison, and Orange counties (see page 39).
• Whole deer carcasses, and parts containing brain or spinal cord tissue, originating from a Disease Management Area (DMA) cannot be transported to any county not designated as a DMA (see pages 39-40).
• Whole deer carcasses, and parts containing brain or spinal cord tissue, originating from DMA1 may be transported only within DMA1 (see pages 39-40).
• Whole deer carcasses, and parts containing brain or spinal cord tissue, originating from DMA2 may be transported anywhere within both DMA1 and DMA2 (see pages 39-40).
• All deer killed in Culpeper, Madison, and Shenandoah counties on November 14, 2020 must be brought to a designated CWD sample station to be tested for CWD (see page 39).
• Feeding of deer is now prohibited year round in Prince William County (see page 19).
Chronic Wasting Disease (CWD) was confirmed by the Virginia Department of Game and Inland Fisheries (DGIF) in 14 deer in Frederick County and two deer in Shenandoah County during the 2017 deer hunting season. Fifteen of the deer were harvested by hunters and one deer was killed by a vehicle. Approximately 1,500 deer from Frederick, Clarke, Warren, and Shenandoah counties were tested for CWD during the 2017 hunting season. Since 2009, 38 CWD-positive deer have been confirmed in Frederick (35) and Shenandoah (3) Counties.
Nine new cases of Chronic Wasting Disease (CWD) were detected in Frederick County during the 2016 deer hunting season. Seven were deer harvested by hunters and two were killed by vehicles. All of the new cases were detected in the same general areas as previous cases. In total, 22 CWD-positive deer have been detected in Virginia since CWD was first discovered in western Frederick County in fall 2009.
CWD Surveillance in Virginia Chronic Wasting Disease (CWD) is an infectious, fatal, neurologic disease of deer. Since 2009, a total of 67 CWD-positive deer have been detected in Virginia in western Frederick and northern Shenandoah counties. In fall 2018, CWD was detected for the first time in a single deer in Culpeper County.
As of April 2019, the Department has diagnosed 68 positive cases of CWD in Virginia since 2009.
In fall 2018, the Department worked with fifty permitted taxidermists across the state to enhance Virginia’s CWD surveillance. Of the more than 1,600 samples submitted by participating taxidermists, CWD was only detected in one deer harvested in Culpeper County.
WEDNESDAY, NOVEMBER 18, 2020
Virginia DWR hunter-harvested CWD positive deer was recently confirmed in Loudoun County
FRIDAY, FEBRUARY 28, 2020
Virginia DGIF say 21 new cases of CWD TSE Prion confirmed in white-tailed deer in northwest Virginia throughout 2019
TUESDAY, APRIL 23, 2019
Virginia DGIF CWD TSE Prion As April 2019 the Department has diagnosed 68 positive cases since 2009
WEDNESDAY, FEBRUARY 13, 2019
Virginia DGIF REPORTS 28 NEW CWD-POSITIVE WHITE-TAILED DEER IN NORTHWEST VIRGINIA
FRIDAY, FEBRUARY 09, 2018
Virginia 2017 Hunt Confirms 16 Cases Chronic Wasting Disease CWD TSE Prion
Sunday, July 17, 2016
Virginia Chronic Wasting Disease CWD As of March 2016 has diagnosed 13 CWD-positive white-tailed deer
***Washington CWD TSE Prion
Washington, to date, CWD has not been detected in Washington...tss
To date, CWD has not been detected in Washington.
The Washington Department of Fish and Wildlife has been testing for chronic wasting disease (CWD) since 1995. To date, CWD has not been detected in Washington. We urge hunters to help us maintain our healthy deer, elk, and moose populations. For more information on CWD, check out wdfw.wa.gov/species-habitats/diseases/chronicwasting.
***West Virginia CWD TSE Prion
West Virginia, to date, total number of confirmed CWD cases in deer in the Eastern Panhandle is 398 — 358 deer in Hampshire County, six deer in Hardy County, 21 deer in Berkeley County, seven deer in Mineral County and six deer in Morgan County.
West Virginia, In the 2018 deer seasons, CWD has now been detected in 350 deer in Hampshire County, six in Hardy County, 15 in Berkeley County, four in Mineral County and one in Morgan County.
Five deer taken in Morgan County during buck season test positive for Chronic Wasting Disease By Editor | January 15, 2020 | 0 by Kate Evans
Five deer that were hunter-harvested in Morgan County during the first two days of the 2019-2020 buck firearms season tested positive for Chronic Wasting Disease (CWD).
A deer harvested during the 2018-2019 hunting season also tested positive for the disease – the first one confirmed in the county.
West Virginia Division of Natural Resources wildlife biologist Jim Crum said that the five CWD deer were harvested in the southern portion of Morgan County.
He said it was not unexpected due to the presence of disease in surrounding states and counties and within West Virginia. Crum was pleased that the number of Morgan County positives were so few.
Last year’s deer that had Chronic Wasting Disease was found along the Berkeley County line right along the Sleepy Creek Wildlife Management Area.
Chronic Wasting Disease is a fatal neurological disease of deer, elk, and moose. Chronic Wasting Disease is caused by abnormal infectious proteins called prions. Prions can pass between deer through saliva, feces, urine, and through water or soil contaminated with prions.
Check stations
The Division of Natural Resources (DNR) ran mandatory check stations in Morgan County, Berkeley County and Mineral County for the first two days of buck season where hunters had to bring their deer, Crum said.
There were three check stations in Morgan County plus one at Cacapon State Park and a total of 13 check stations in the three counties on November 25 and November 26. There were also some walk-ins in Hampshire County at the District Office in Romney where officials did sampling, he said.
DNR specialists collected 170 deer samples in Morgan County and the
Chronic Wasting Disease agent was detected in five deer, Crum said. Every one of the five deer did not appear sick, which he said was typical when DNR officials do Chronic Wasting Disease monitoring.
Hunters who submitted deer samples were given a receipt and had the chance to check with the DNR to see if their deer tested positive for CWD.
Regional count near 400
Crum said the total Eastern Panhandle count for Chronic Wasting Disease for the 2019-2020 hunting season is 22 hunter-harvested deer
out of 716 samples. That includes five deer in Morgan County, six deer in Berkeley County, eight deer in Hampshire County and three deer in Mineral County. There were also three additional clinical deer that were shot and looked sick.
Added to figures from June 2019, the total number of confirmed CWD cases in deer in the Eastern Panhandle is 398 — 358 deer in Hampshire County, six deer in Hardy County, 21 deer in Berkeley County, seven deer in Mineral County and six deer in Morgan County.
Crum noted that CWD is a covert disease where the mortality is distributed over time.
“It doesn’t present as a mass die-off. Over the years it reduces the herd,” he said.
Containment area, feeding ban
The West Virginia Chronic Wasting Disease containment area and current regulations regarding baiting and feeding of deer and deer transport are still the same, Crum said. The Chronic Wasting Disease containment area includes all of Morgan, Berkeley, Jefferson, Hampshire, Mineral, Grant and Hardy Counties.
Morgan, Berkeley, Hampshire, Mineral and Hardy Counties have restrictions about the disposal and transport of deer carcasses and also feeding and baiting deer restrictions. Grant and Jefferson Counties only have the feeding and baiting restrictions. The restrictions are designed to combat the spread of Chronic Wasting Disease.
Dead deer or their parts may not be transported beyond the boundary
of Berkeley, Hampshire, Hardy, Mineral and Morgan Counties except for the following: meat that has been boned out, quarters or other portions of meat with no part of the spinal column or head attached, cleaned hide with no head attached, clean skull plate (no meat or tissue attached) with antlers attached, antlers with no meat or tissue attached and finished taxidermy mounts.
Chronic Wasting Disease has been found in wild free-ranging deer or
captive deer and/or elk populations in 26 states and three Canadian provinces.
Chronic Wasting Disease was first diagnosed in West Virginia in 2005, Virginia in 2009, Maryland in 2010, and Pennsylvania in 2012.
Crum said that Chronic Wasting Disease has grown here since it was first detected in 2005.
Tips
The Division of Natural Resources requests residents to contact the
Romney office at 304-822-3551 if they kill or see a very sick or emaciated deer.
Residents should not use natural deer urine-based lures in the environment and avoid placing them on the ground or on vegetation that deer can reach.
The biggest thing that people can do to reduce the spread of CWD is to stop baiting and feeding deer, Crum said. People have misplaced sympathy for the animals and think they’ll starve. They don’t realize that feeding them promotes disease transmission and introduces foreign materials into a free-ranging animal.
Crum also noted that other states have placed a moratorium on the transfer of captive live cervids into the state or within the state to prevent the spread of Chronic Wasting Disease.
Crum said the Center for Disease Control and Prevention and the World Health Organization advise hunters not to consume any known infected animals or ones that appear sick.
WVDNR 2018-2019 ANNUAL REPORT
snip...
WILDLIFE RESOURCES
White-tailed Deer
Efforts to control the spread and monitor chronic wasting disease (CWD) in free-ranging deer in West Virginia continued.
In the 2018 deer seasons, samples taken from 814 hunter harvested deer brought to WVDNR staffed stations were tested for CWD. Twenty-seven samples were found to have the abnormal protein associated with CWD. CWD has now been detected in 350 deer in Hampshire County, six in Hardy County, 15 in Berkeley County, four in Mineral County and one in Morgan County.
Elk
Radio telemetry monitoring continued for both the elk group released in 2016 and the two groups released in 2018. Eight mortalities were recorded in July and August from the elk released in June 2018 and attributed to the effects of the extended holding time in the elk soft release facility mandated by the USDA. Twenty-two additional mortalities were recorded. Seventeen of those deaths have been attributed to meningeal worm (Parelaphostrongylus tennuis), two were linked to birthing complications, two were unknown and one was a suspected poaching case. Mortalities were detected and located using telemetry and then either recovered for lab necropsies or necropsied in the field. Samples were shipped to the Southeastern Cooperative Wildlife Disease Study lab at the University of Georgia College of Veterinary Medicine for analysis. The salt block/trail camera study throughout the Elk Management Zone continued to allow for monitoring of native-born and uncollared animals and to detect elk which may move in from surrounding states. In addition, several high use areas were monitored by trail cameras to detect calving successes. Several collars were removed from maturing bulls as they had outgrown the initial collar size placed on them as young elk.
Efforts were made January-April to bait and capture individual elk that were not collared or were experiencing radio collar issues (signal, battery life, etc.). Fourteen elk were captured, including four untagged calves, and equipped with new collars. Several presentations regarding program status were given to both public and government groups including the USFS and the WV Legislature. Zero elk were imported into West Virginia.
SUNDAY, JULY 17, 2016
West Virginia Chronic Wasting Disease CWD has been found in 195 white-tailed deer As of June 2016
Sunday, June 29, 2014
Chronic wasting disease spreads in West Virginia
Friday, February 28, 2014
West Virginia Deer farming bill passes in House unanimously
***Wisconsin CWD TSE Prion
Wisconsin, to date, has detected 7,109 cases of CWD data released through November 22, 2020...tss
WILD WISCONSIN - OFF THE RECORD • EPISODE 51 CWD Updates For The 2020 Deer Season
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...
SUNDAY, SEPTEMBER 20, 2020
Wisconsin Sinks Further Into the Abyss With CWD TSE Prion 2020
Wisconsin Game Farm deer and elk
Chronic Wasting Disease Positives in Farm-raised Deer
Revised: 01/22/2020
County (Premises #) Sample Collection Date of First CWD Positive in Farm-Raised Deer Sample Collection Date of Last CWD Positive in Farm-Raised Deer Total CWD Positive in Farm-Raised Deer
Portage(1) 9/4/2002 1/18/2006 82
Walworth(1) 9/20/2002 12/13/2002 6
Manitowoc 3/5/2003 3/5/2003 1
Sauk(1) 10/3/2003 10/3/2003 1
Racine 5/1/2004 5/1/2004 1
Walworth(2) 7/28/2004 11/3/2004 3
Crawford 1/19/2005 1/25/2007 2
Portage(2) 9/22/2008 11/18/2008 2
Jefferson 12/1/2008 12/1/2008 1
Marathon 11/7/2013 10/7/2019 104
Richland(1) 9/13/2014 11/19/2014 8
Eau Claire 6/8/2015 11/24/2015 34
Oneida 11/4/2015 10/6/2019 14
Iowa(1) 1/22/2016 9/14/2019 4
Oconto 9/4/2016 10/31/2019 52
Shawano 9/18/2017 9/19/2019 27
Waupaca 9/21/2017 12/7/2017 12
Washington 2/18/2018 11/15/2018 12
Richland(2) 5/11/2018 5/11/2018 1
Dane 5/16/2018 5/16/2018 1
Iowa(2) 5/18/2018 5/18/2018 21
Marinette 5/19/2018 5/19/2018 1
Sauk(2) 6/4/2018 11/28/2018 2
Portage(3) 10/23/2018 10/23/2018 1
Portage(4) 11/16/2018 5/1/2019 8
Forest 1/8/2019 11/18/2019 3
Burnett 7/30/2019 7/30/2019 1
The Farm-Raised Deer Program provides the requirements for keeping and moving farm-raised deer in Wisconsin, including registration, recordkeeping, disease testing, movement, and permit requirements.
Wisconsin Deer Farm Statistics
The following data is updated annually during the license renewal process:
Number of registered deer premises in Wisconsin 338
Number of hunting ranches 69 of the 338
Number of premises enrolled in the CWD herd status program 145
The following data was last updated September 17, 2019:
Number of farms with a CWD positive test since 2001 27
Number of herds depopulated as a result of a CWD positive 17
Registered Deer Farms and Past/Current CWD Farms CWD Affected Counties September 2019
Burnett County Elk Tests Positive for CWD Release Date: August 26, 2019
Contact: Leeann Duwe, Public Information Officer, (608) 224-5005
Download PDF
MADISON –Based on test results from the National Veterinary Services Laboratory in Ames, IA, the Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP) confirms that an elk from a breeding farm in Burnett County has tested positive for chronic wasting disease (CWD). The 6-year old male was euthanized due to an injury and showed no symptoms of the disease. As a result of the positive finding, DATCP has quarantined the farm and the remaining 5 elk in the herd. A quarantine means no animals may move in or out of the property and restricts movement of carcasses. No elk have left the farm since the herd was formed in 2014.
The owner will continue to test all elk that die to monitor if the disease has spread to other animals in the herd. DATCP's Division of Animal Health will investigate the animal's health history and the premises to determine if any other herds may have been exposed to the CWD-positive elk.
CWD is a fatal, neurological disease of deer, elk, and moose caused by an infectious protein called a prion that affects the animal's brain. Testing for CWD can only be performed after the animal's death. More information about CWD is available at https://datcp.wi.gov/Pages/Programs_Services/ChronicWastingDi sease.aspx. DATCP regulates deer farms for registration, recordkeeping, disease testing, movement, and permit requirements. To learn more about deer farm regulations in Wisconsin, visit DATCP's farm-raised deer program at https://datcp.wi.gov/Pages/Programs_Services/FarmRaisedDeer.aspx. The Department of Natural Resources monitors the state's wild whitetail deer for CWD and has resources available at https://dnr.wi.gov/topic/wildlifehabitat/regulations.html. ;
###
''The owner will continue to test all elk that die to monitor if the disease has spread to other animals in the herd. DATCP's Division of Animal Health will investigate the animal's health history and the premises to determine if any other herds may have been exposed to the CWD-positive elk.''
the decision and policy NOT to depopulate positive cwd tse prion infected captive herds in Wisconsin or anywhere else, at this time,
is a grave mistake, and also, a 5 year quarantine is not near long enough for the cwd tse prion, science shows this...terry
WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO
cwd update on Wisconsin from Tammy Ryan...
WEDNESDAY, FEBRUARY 05, 2020
Wisconsin CWD TSE Prion 2019 to date wild deer 1317 positive and Captive Farmed Livestock Cervid CWD update
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
WEDNESDAY, FEBRUARY 10, 2016
Wisconsin Two deer that escaped farm had chronic wasting disease CWD
THURSDAY, JANUARY 23, 2020
Wisconsin Confirms CWD Detected In Marquette and Marathon County
WEDNESDAY, JANUARY 08, 2020
Wisconsin Chronic Wasting Disease CWD TSE Prion Positives in Farm-raised Deer in 2019
The majority of the positives have come after 2013 when DATCP began letting some deer farms and hunting ranches continue operating after CWD was detected on their property.
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
TUESDAY, JUNE 09, 2020
Wisconsin Trempealeau County Deer Farm Tests Positive for CWD Release Date: June 9, 2020
***Wyoming CWD TSE Prion
Wyoming, to date, has, as of February 2020, CWD had been identified in 31 of 37 (84%) of the state’s mule deer herds, in nine of 36 (25%) of the state’s elk herds, and generally wherever white-tailed deer occur in Wyoming (white-tailed deer herd units are loosely defined in Wyoming outside of the Black Hills). In contrast, CWD remains very rare in moose, and has only been detected in one targeted moose in 2008, with 1,198 moose tested to date....tss
Wyoming Chronic Wasting Disease Management Plan
Wyoming Game and Fish Department Cheyenne, Wyoming July 2020
As of February 2020, CWD had been identified in 31 of 37 (84%) of the state’s mule deer herds, in nine of 36 (25%) of the state’s elk herds, and generally wherever white-tailed deer occur in Wyoming (white-tailed deer herd units are loosely defined in Wyoming outside of the Black Hills). In contrast, CWD remains very rare in moose, and has only been detected in one targeted moose in 2008, with 1,198 moose tested to date. Prevalence estimates vary between herds, although deer herds generally exhibit significantly higher prevalence than sympatric elk herds (Table 1). In the majority of mule deer herd units where statistically significant sample sizes have been obtained, prevalence has steadily increased since its initial discovery within that herd. However, in some southeastern Wyoming mule 12 deer herds where the disease has long been established, CWD prevalence has either somewhat declined from peak levels and/or has remained relatively static, albeit at levels high enough to likely impact population performance. Overall, prevalence tends to be higher in southeastern Wyoming, where the disease has long been established, but is quickly becoming more common and widespread in much of the state.
Figure 2. Known CWD distribution in Wyoming deer and elk hunt areas (2019).
Table 1. CWD prevalence in sympatric Wyoming mule deer and elk herd units based on adult mule deer bucks and adult male and female elk (2016-2018).
Wyoming Game and Fish Department
2018/2019 Chronic Wasting Disease Surveillance Report
May 2020
2019 Results and Discussion:
A total of 5,067 deer, elk, and moose samples were analyzed by the WH Lin 2019. From the total samples received, 3,018 were from hunter-killed adult male mule deer, adult male white-tailed deer, adult elk, and adult moose. Of these, 354 tested positive for CWD representing 213 mule deer, 124 white-tailed deer, and 17 elk (Table 4).
Table 4. Distribution of hunter-killed samples and proportion of positives according to species.
2018 Results and Discussion:
A total of 5,694 deer, elk, and moose samples were analyzed by the WH L. From the total samples received, 3,688 were from hunter-killed adult male mule deer, adult male white-tailed deer, adult elk, and adult moose. Of these, 370 tested positive for CWD representing 263 mule deer, 67 whitetailed deer, and 40 elk (Table 1). All moose tested for CWD were negative.
Non-Target Deer Herd Units 2019.
Chronic wasting disease was documented for the first time in the Sublette herd unit, which resulted in an initial CWD prevalence of 2.8%. In areas with a sample size of ≥ 40 (80% CI), prevalence in the Laramie Mountains herd increased from 23.5% (avg. 2015-2018) to 28.6% in 2019, prevalence in the Upper Shoshone remained constant, Pumpkin Buttes prevalence dropped from 8.8% to 4.8%.
CWD in Western Wyoming. The identification of two, hunter harvested, CWD positive mule deer bucks in deer HA 152 this year extended CWD’s distribution in western Wyoming. Other positives in the general geographic area include GTNP, where a positive road-kill mule deer was discovered in 2018, deer HA 145 which had a positive CWD targeted mule deer in 2016, and deerHA 139 near Pinedale, which had one positive CWD targeted mule deer in 2017, and another in 2019.
Target Elk Herd Units for 2019.
Three elk herd units were targeted for the 2019 season; only the Snowy Range herd unit reached the 200 sample goal in the first year (Table 7). CWD prevalence in the Snowy Range showed a slight decrease from the previous four-year average of 2.8%.
https://wgfd.wyo.gov/WGFD/media/content/PDF/Vet%20Services/2018-2019-CWD-Surveillance-Report-wo-points.pdf
Wyoming CWD Dr. Mary Wood
''first step is admitting you have a problem''
''Wyoming was behind the curve''
wyoming has a problem...
THURSDAY, NOVEMBER 12, 2020
Wyoming Game and Fish Department has confirmed a new hunt area where an elk has tested positive for chronic wasting disease (CWD)
FRIDAY, SEPTEMBER 18, 2020
CWD found in new deer and elk hunt areas in northeast Wyoming
THURSDAY, OCTOBER 08, 2020
Wyoming Chronic wasting disease 2020 surveillance and monitoring
Fri, Jan 24, 2020 2:29 pm
Wyoming Game & Fish Discovers CWD-Positive Mule Deer in Pinedale, Discourages Feeding of Wildlife
''As of September 2019, CWD has been identified in 31 of 37 (84%) Wyoming mule deer herds, nine of 36 (25%) elk herds, and generally wherever white-tailed deer occur. Increasing prevalence and distribution of CWD has the potential to cause widespread and long-term negative impacts to Wyoming’s cervid populations. Prevalence of this disease in chronically infected Wyoming deer herds has exceeded 40%, with one elk herd exhibiting nearly 15% prevalence.''
''for the first time, there is clear evidence that CWD is adversely affecting the overall health and viability of some herds.''
SATURDAY, DECEMBER 08, 2018
Wind Cave elk capture project to limit spread of disease or Planned elk drive from Wind Cave National Park raises question about spread of disease?
WEDNESDAY, NOVEMBER 12, 2014
Shenandoah National Park, Chronic Wasting Disease Management Plan/Environmental Assessment
Wednesday, October 29, 2014
Chronic wasting disease now rings Greater Yellowstone in Wyoming
Tuesday, March 05, 2013
Chronic Wasting Disease Management Plan/Environmental Impact Statement, Shenandoah National Park Virginia
Tuesday, February 26, 2013
Planned elk drive from Wind Cave National Park raises question about spread of disease
snip...
just when you think it can’t get worse, dumb and dumber step up to the plate. this is about as dumb, if not dumber, than the blunder at Colorado Division of Wildlife Foothills Wildlife Research Facility in Fort Collins, where cwd was first documented. sometimes, you just can’t fix stupid. ...tss this should never happen!
Friday, November 16, 2012
Yellowstone elk herds feeding grounds, or future killing grounds from CWD
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.
FRIDAY, DECEMBER 06, 2019
Estimating relative CWD susceptibility and disease progression in farmed white-tailed deer with rare PRNP alleles
MONDAY, NOVEMBER 16, 2020
North America coyotes or pumas can serve as a vehicle for prions contributing to the spread of the infectious agent in the environment
Canada CWD TSE Prion Confirmed in Five Herds
Canada Federally Reportable Terrestrial Diseases
The number of confirmed cases of federally reportable diseases affecting terrestrial animals has been updated to include the month of October 2020.
In October, chronic wasting disease was confirmed in five herds.
2020 October 2 Alberta Elk
2020 October 14 Alberta Elk
2020 October 21 Saskatchewan Elk
2020 October 21 Alberta Elk
2020 October 28 Alberta Elk
SUNDAY, NOVEMBER 22, 2020
Canada October 2020 CWD TSE Prion Confirmed in Five Herds
THURSDAY, SEPTEMBER 10, 2020
Saskatchewan, Canada, Chronic Wasting Disease CWD TSE Prion
THURSDAY, JANUARY 23, 2020
Canadian Food Inspection Agency (CFIA) has updated the following chapter of the Accredited Veterinarian's Manual: Chapter 13 Chronic Wasting Disease Herd Certification Programs
TUESDAY, NOVEMBER 17, 2020
Finland Transmissible Spongiform Encephalopathy TSE was found in a killed moose in Laukas
SATURDAY, MARCH 10, 2018
FINLAND REPORTS FIRST CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN A moose or European elk (Alces alces)
http://chronic-wasting-disease.blogspot.com/2018/03/finland-reports-first-case-of-chronic.html
THURSDAY, SEPTEMBER 26, 2019
Sweden The third case of CWD in moose in Arjeplog is now established
https://chronic-wasting-disease.blogspot.com/2019/09/sweden-third-case-of-cwd-in-moose-in.html
SATURDAY, JUNE 01, 2019
Sweden Documents Another Case of Chronic Wasting Disease CWD TSE Prion Norrbotten
FRIDAY, APRIL 12, 2019
Sweden Wasting Disease (CWD) discovered on moose in Norrbotten County
FRIDAY, OCTOBER 09, 2020
Norway Regulatory process VKM order for CWD TSE Prion after discovery on the Hardangervidda in 2020
MONDAY, SEPTEMBER 14, 2020
Norway Chronic Wasting Disease (CWD) identified in a wild reindeer at Hardanger Plateau
FRIDAY, SEPTEMBER 11, 2020
Norway Skrantesjuke CWD TSE Prion detected on reindeer buck from Hardangervidda
WEDNESDAY, APRIL 01, 2020
Norway Chronic Wasting Disease CWD TSE Prion Skrantesjuke 2 Positive Moose for 2019
MONDAY, NOVEMBER 18, 2019
Norway Chronic Wasting Disease CWD TSE Prion Detected in Sixth Moose
WEDNESDAY, MARCH 06, 2019
Norway The Madness Continues in Nordfjella Chronic Wasting Disease CWD TSE Prion
THURSDAY, FEBRUARY 14, 2019
Norway Eradication of Chronic Wasting Disease is not completed
SUNDAY, JULY 14, 2019
Korea Chronic Wasting Disease CWD TSE Prion additional cases were observed in red deer, sika deer, and their crossbred deer in 2010 and 2016, beyond that, anyone's guess
WEDNESDAY, MAY 29, 2019
Incomplete inactivation of atypical scrapie following recommended autoclave decontamination procedures USDA HERE'S YOUR SIGN!
THURSDAY, DECEMBER 19, 2019
The emergence of classical BSE from atypical/Nor98 scrapie
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
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
Fri, Nov 13, 2020 10:50 am
Subject: CWD TSE PRION, SCRAPIE, BSE, AND PORCINE, PIGS, WILD BOAR, ZOONOTIC ZOONOSIS RISK FACTORS AND POTENTIALS
CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020
zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum
4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein.
***> PIGS, WILD BOAR, CWD <***
***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE
HYPOTHOSIS AND SPECIFIC AIMS
HYPOTHOSIS
BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS
Final Report – CJD Foundation Grant Program A.
Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.
Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018
Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item MOORE, SARAH - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 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.
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP
Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.
Interpretive Summary:
Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.
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.
Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation
S. Jo Moore1,2, M. Heather West Greenlee3, Naveen Kondru3, Sireesha Manne3, Jodi D. Smith1, Robert A. Kunkle1, Anumantha Kanthasamy3 and Justin J. Greenlee1* + Author Affiliations
1Virus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, Iowa, United States of America 2Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee, United States of America 3Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, Iowa, United States of America
ABSTRACT
Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (‘market weight’ groups). The remaining pigs (‘aged’ groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.
IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months post-inoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results in orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.
FOOTNOTES
↵*Corresponding author: Email: justin.greenlee@ars.usda.gov This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.
----Original Message-----
From: Terry Singeltary
To: Tracy.A.Nichols
Sent: Fri, Mar 30, 2018 12:51 pm
Subject: Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Greetings APHIS, USDA, Dr. Tracy Nichols, et al,
I wish to kindly submit my comments on the Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards please. i have submitted online and sent a hard copy to Dr. Nichols via email. i know that my concern may not be the same concern as others, but ramifications from cwd tse prion can be long lasting, and science is still emerging. however, the science today warrants immediate and further actions be taken. my comments, with reference materials, are as follows, and will be formatted in such a way, i will address issues by numbers 1-10, and under each one of my comments by each number, i will reference my comments with science to back up what i am stating/asking...thank you kindly, terry
snip...see full text;
WEDNESDAY, NOVEMBER 4, 2020
CWD TSE PRION, SCRAPIE, BSE, AND PORCINE, PIGS, WILD BOAR, ZOONOTIC ZOONOSIS RISK FACTORS AND POTENTIALS
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
SUNDAY, OCTOBER 11, 2020
Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ
THURSDAY, SEPTEMBER 24, 2020
The emergence of classical BSE from atypical/ Nor98 scrapie
WEDNESDAY, OCTOBER 28, 2020
EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission
----Original Message-----
From: Terry Singeltary
To: Tracy.A.Nichols
Sent: Fri, Mar 30, 2018 12:51 pm
Subject: Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018
Greetings APHIS, USDA, Dr. Tracy Nichols, et al,
I wish to kindly submit my comments on the Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards please. i have submitted online and sent a hard copy to Dr. Nichols via email. i know that my concern may not be the same concern as others, but ramifications from cwd tse prion can be long lasting, and science is still emerging. however, the science today warrants immediate and further actions be taken. my comments, with reference materials, are as follows, and will be formatted in such a way, i will address issues by numbers 1-10, and under each one of my comments by each number, i will reference my comments with science to back up what i am stating/asking...thank you kindly, terry
snip...see full text;
WEDNESDAY, NOVEMBER 4, 2020
CWD TSE PRION, SCRAPIE, BSE, AND PORCINE, PIGS, WILD BOAR, ZOONOTIC ZOONOSIS RISK FACTORS AND POTENTIALS
SUNDAY, NOVEMBER 08, 2020
OHIO CHRONIC WASTING DISEASE TSE PRION UPDATE TO DATE 24 CWD POSITIVES IN CAPTIVE CERVID ZERO IN WILD
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
SUNDAY, OCTOBER 11, 2020
Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ
THURSDAY, SEPTEMBER 24, 2020
The emergence of classical BSE from atypical/ Nor98 scrapie
WEDNESDAY, OCTOBER 28, 2020
EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission
WEDNESDAY, OCTOBER 28, 2020
EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission
WEDNESDAY, OCTOBER 28, 2020
EFSA Scientific Opinion Potential BSE risk posed by the use of ruminant collagen and gelatine in feed for non‐ruminant farmed animals
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
FRIDAY, OCTOBER 23, 2020
Scrapie TSE Prion Zoonosis Zoonotic, what if?
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.
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
FRIDAY, NOVEMBER 08, 2019
EFSA Panel on Biological Hazards (BIOHAZ) Update on chronic wasting disease (CWD) III
MONDAY, NOVEMBER 02, 2020
Successful transmission of the chronic wasting disease (CWD) agent to white-tailed deer by intravenous blood transfusion
WEDNESDAY, NOVEMBER 4, 2020
CWD TSE PRION, SCRAPIE, BSE, AND PORCINE, PIGS, WILD BOAR, ZOONOTIC ZOONOSIS RISK FACTORS AND POTENTIALS
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that: (1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; (2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; (3) Reliable essays can be established to detect CWD infection in humans; and (4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance
There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
Funding Agency
Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 5R01NS088604-04
Application # 9517118
Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2018-08-01
Budget End 2019-07-31 Support Year 4
Fiscal Year 2018
Total Cost Indirect Cost Institution Name Case Western Reserve University Department Pathology Type Schools of Medicine DUNS # 077758407 City Cleveland State OH Country United States Zip Code 44106
Related projects
NIH 2018
R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University
NIH 2017
R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University
NIH 2016
R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University
NIH 2015 R01 NS Cervid to human prion transmission
Kong, Qingzhong / Case Western Reserve University $337,507
Publications
Ashok, Ajay; Karmakar, Shilpita; Chandel, Rajeev et al. (2018) Prion protein modulates iron transport in the anterior segment: Implications for ocular iron homeostasis and prion transmission. Exp Eye Res 175:1-13
Kim, Chae; Xiao, Xiangzhu; Chen, Shugui et al. (2018) Artificial strain of human prions created in vitro. Nat Commun 9:2166 Asthana, Abhishek; Baksi, Shounak; Ashok, Ajay et al. (2017) Prion protein facilitates retinal iron uptake and is cleaved at the ?-site: Implications for retinal iron homeostasis in prion disorders. Sci Rep 7:9600
Orrú, Christina D; Yuan, Jue; Appleby, Brian S et al. (2017) Prion seeding activity and infectivity in skin samples from patients with sporadic Creutzfeldt-Jakob disease. Sci Transl Med 9:
Elezgarai, Saioa R; Fernández-Borges, Natalia; Eraña, Hasier et al. (2017) Generation of a new infectious recombinant prion: a model to understand Gerstmann-Sträussler-Scheinker syndrome. Sci Rep 7:9584
Choi, Jin-Kyu; Cali, Ignazio; Surewicz, Krystyna et al. (2016) Amyloid fibrils from the N-terminal prion protein fragment are infectious. Proc Natl Acad Sci U S A 113:13851-13856
Zhan, Yi-An; Abskharon, Romany; Li, Yu et al. (2016) Quiescin-sulfhydryl oxidase inhibits prion formation in vitro. Aging (Albany NY) 8:3419-3429 Nichols, Tracy A; Spraker, Terry R; Gidlewski, Thomas et al. (2016) Dietary magnesium and copper affect survival time and neuroinflammation in chronic wasting disease. Prion 10:228-50
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
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) <***
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" wt.net="">
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
===============
Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
snip...see full text;
MONDAY, FEBRUARY 25, 2019
***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
WEDNESDAY, AUGUST 5, 2020
1996-12-04: BBC - Horizon BSE1 - BSE2 The Invisible Enemy, The British Disease, CWD, sporadic CJD
MONDAY, OCTOBER 05, 2020
USA, UK, JAPAN, CJD TSE PRION STATISTICS UPDATE OCTOBER 2020
MONDAY, JANUARY 20, 2020
sporadic CJD one in a million, FAKE NEWS PEOPLE!
this myth has been incorrect for decades, and had been stated as such by a few, but again, the media is too lazy to do it's job and print the facts.
human tse prion, including 85%+ of all human tse i.e. sporadic cjd, is now one in 5,000!
ZOONOSIS OF SCRAPIE TSE PRION
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
***> why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man.
***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough.
***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
R. BRADLEY
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
***> 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. <***
Transmission of scrapie prions to primate after an extended silent incubation period
Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.
SNIP...
Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. 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.
The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.
We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.
Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.
The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.
Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.
Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.
Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.
Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.
In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... 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.
Like lambs to the slaughter
* 31 March 2001 *
Debora MacKenzie *
Magazine issue 2284
Suspect symptoms
What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?
Exclusive from New Scientist magazine
Four years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious.
The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.
Photo: Murdo McLeod
Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise.
He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals.
Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.
Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears.
To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.
"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris.
Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.
Brain damage Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health.
But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.
Deslys and colleagues were originally studying vCJD, not sCJD.
They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three.
Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.
As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain.
As expected, they all affected the brain in a different way from BSE and vCJD.
But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology. Multiple strains "The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys.
"You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie," she says.
In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar. But there are more than 20 strains of scrapie, and six of sCJD.
"You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys.
Bruce is cautious about the mouse results, but agrees they require further investigation.
Other trials of scrapie and sCJD in mice, she says, are in progress.
Deformed proteins People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways.
Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD. But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD.
"If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."
There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere.
Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain.
Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.
Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE.
And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.
More at: Proceedings of the National Academy of Sciences (vol 98, p 4142)
Correspondence about this story should be directed to letters@newscientist.com 1900 GMT, 28 March 2001
* New Scientist
http://www.newscientist.com/dailynews/news.jsp?id=ns9999560
http://www.newscientist.com/article.ns?id=mg16922840.300
http://www.newscientist.com/article.ns?id=mg16922840.300
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
FRIDAY, OCTOBER 23, 2020
Scrapie TSE Prion Zoonosis Zoonotic, what if?
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE AND FRIENDLY FIRE, IATROGENIC SPREAD
WEDNESDAY, OCTOBER 31, 2018
***> PIG HEART VALVES and Potential Iatrogenic Transmissible Spongiform Encephalopathy TSE Prion Disease in Humans, what if?
MONDAY, OCTOBER 05, 2020
USA, UK, JAPAN, CJD TSE PRION STATISTICS UPDATE OCTOBER 2020
FRIDAY, OCTOBER 30, 2020
Analysis of Chinese patients with sporadic Creutzfeldt-Jakob disease
Sunday, November 1, 2020
Taiwan Incidence of and Mortality Due to Human TSE Prion Diseases Sees Significant Increase In Incidence After 2008
SATURDAY, SEPTEMBER 26, 2020
A nationwide trend analysis in the incidence and mortality of Creutzfeldt–Jakob disease in Japan between 2005 and 2014 with increasing trends of incidence and mortality
snip...
Overall, the AAPCs of age-adjusted CJD-associated mortality rates rose significantly over the study period (3.2%; 95% confidence interval [CI] 1.4–5.1%). The AAPC of the age-adjusted incidence rates also increased (overall 6.4%; 95% CI 4.7–8.1%). The CJD-associated increases in the mortality and incidence rates were especially prominent among adults over the age of 70 years. Given this trend in aging of population, the disease burden of CJD will continue to increase in severity. Our findings thus recommend that policymakers be aware of the importance of CJD and focus on preparing to address the increasing prevalence of dementia.
snip...
Volume 26, Number 8—August 2020
Sporadic Creutzfeldt-Jakob Disease among Physicians, Germany, 1993–2018 high proportion of physicians with sCJD were surgeons
THURSDAY, JULY 02, 2020
Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor:
In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally..
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
doi:10.1016/S1473-3099(03)00715-1 Copyright © 2003 Published by Elsevier Ltd. Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
Available online 29 July 2003.
Volume 3, Issue 8, August 2003, Page 463
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem..” ...
January 28, 2003; 60 (2) VIEWS & REVIEWS
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Ermias D. Belay, Ryan A. Maddox, Pierluigi Gambetti, Lawrence B. Schonberger
First published January 28, 2003, DOI: https://doi.org/10.1212/01.WNL.0000036913.87823.D6
Abstract
Transmissible spongiform encephalopathies (TSEs) attracted increased attention in the mid-1980s because of the emergence among UK cattle of bovine spongiform encephalopathy (BSE), which has been shown to be transmitted to humans, causing a variant form of Creutzfeldt-Jakob disease (vCJD). The BSE outbreak has been reported in 19 European countries, Israel, and Japan, and human cases have so far been identified in four European countries, and more recently in a Canadian resident and a US resident who each lived in Britain during the BSE outbreak. To monitor the occurrence of emerging forms of CJD, such as vCJD, in the United States, the Centers for Disease Control and Prevention has been conducting surveillance for human TSEs through several mechanisms, including the establishment of the National Prion Disease Pathology Surveillance Center. Physicians are encouraged to maintain a high index of suspicion for vCJD and use the free services of the pathology center to assess the neuropathology of clinically diagnosed and suspected cases of CJD or other TSEs.
Received May 7, 2002. Accepted August 28, 2002.
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
Terry S. Singeltary, retired (medically)
Published March 26, 2003
26 March 2003
Terry S. Singeltary, retired (medically) CJD WATCH
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?
Reply to Singletary Ryan A. Maddox, MPH Other Contributors: Published March 26, 2003
Mr. Singletary raises several issues related to current Creutzfeldt- Jakob disease (CJD) surveillance activities. Although CJD is not a notifiable disease in most states, its unique characteristics, particularly its invariably fatal outcome within usually a year of onset, make routine mortality surveillance a useful surrogate for ongoing CJD surveillance.[1] In addition, because CJD is least accurately diagnosed early in the course of illness, notifiable-disease surveillance could be less accurate than, if not duplicative of, current mortality surveillance.[1] However, in states where making CJD officially notifiable would meaningfully facilitate the collection of data to monitor for variant CJD (vCJD) or other emerging prion diseases, CDC encourages the designation of CJD as a notifiable disease.[1] Moreover, CDC encourages physicians to report any diagnosed or suspected CJD cases that may be of special public health importance (e.g...., vCJD, iatrogenic CJD, unusual CJD clusters).
As noted in our article, strong evidence is lacking for a causal link between chronic wasting disease (CWD) of deer and elk and human disease,[2] but only limited data seeking such evidence exist. Overall, the previously published case-control studies that have evaluated environmental sources of infection for sporadic CJD have not consistently identified strong evidence for a common risk factor.[3] However, the power of a case-control study to detect a rare cause of CJD is limited, particularly given the relatively small number of subjects generally involved and its long incubation period, which may last for decades. Because only a very small proportion of the US population has been exposed to CWD, a targeted surveillance and investigation of unusual cases or case clusters of prion diseases among persons at increased risk of exposure to CWD is a more efficient approach to detecting the possible transmission of CWD to humans. In collaboration with appropriate local and state health departments and the National Prion Disease Pathology Surveillance Center, CDC is facilitating or conducting such surveillance and case- investigations, including related laboratory studies to characterize CJD and CWD prions.
Mr. Singletary also expresses concern over a recent publication by Asante and colleagues indicating the possibility that some sporadic CJD cases may be attributable to bovine spongiform encephalopathy (BSE).[4] The authors reported that transgenic mice expressing human prion protein homozygous for methionine at codon 129, when inoculated with BSE prions, developed a molecular phenotype consistent with a subtype of sporadic CJD. Although the authors implied that BSE might cause a sporadic CJD-like illness among persons homozygous for methionine, the results of their research with mice do not necessarily directly apply to the transmission of BSE to humans. If BSE causes a sporadic CJD-like illness in humans, an increase in sporadic CJD cases would be expected to first occur in the United Kingdom, where the vast majority of vCJD cases have been reported. In the United Kingdom during 1997 through 2002, however, the overall average annual mortality rate for sporadic CJD was not elevated; it was about 1 case per million population per year. In addition, during this most recent 6-year period following the first published description of vCJD in 1996, there was no increasing trend in the reported annual number of UK sporadic CJD deaths.[3, 5] Furthermore, surveillance in the UK has shown no increase in the proportion of sporadic CJD cases that are homozygous for methionine (Will RG, National CJD Surveillance Unit, United Kingdom, 2003; personal communication)..
References
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Diagnosis and reporting of Creutzfeldt-Jakob disease. JAMA 2001;285:733-734.
2. Belay ED, Maddox RA, Gambetti P, Schonberger LB. Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States. Neurology 2003;60:176-181.
3. Belay ED. Transmissible spongiform encephalopathies in humans. Annu Rev Microbiol 1999;53:283-314.
4. Asante EA, Linehan JM, Desbruslais M, et al. BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein. EMBO J 2002;21:6358-6366.
5. The UK Creutzfeldt-Jakob Disease Surveillance Unit. CJD statistics. Available at: http://www.cjd.ed.ac.uk/figures.htm. Accessed February 18, 2003.
Competing Interests: None declared.
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
2 January 2000 British Medical Journal U.S.
Scientist should be concerned with a CJD epidemic in the U.S., as well
15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S.
Volume 2: Science
4. The link between BSE and vCJD
Summary 4.29 The evidence discussed above that vCJD is caused by BSE seems overwhelming. Uncertainties exist about the cause of CJD in farmers, their wives and in several abattoir workers. It seems that farmers at least might be at higher risk than others in the general population. 1 Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrPSc found in vCJD.
***>It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people...end
BSE INQUIRY
SATURDAY, JUNE 23, 2018
CDC
***> Diagnosis of Methionine/Valine Variant Creutzfeldt-Jakob Disease by Protein Misfolding Cyclic Amplification
Volume 24, Number 7—July 2018 Dispatch
WEDNESDAY, OCTOBER 21, 2020
Human Prion Disease Surveillance in Washington State, 2006-2017
THURSDAY, NOVEMBER 19, 2020
NIH 2020 R01 NS Role of skin prions in disease transmission and diagnostic testing of human prion disease
Terry S. Singeltary Sr.
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