Escaped buck from deer farm killed by bow hunter, chronic wasting disease test results pending
By Tony Kennedy and Dennis Anderson Star Tribune staff writers NOVEMBER 6, 2019 — 12:22AM
A 27-point trophy buck that escaped from an Olmsted County deer farm in April was killed by a bow hunter last week on public land near Elba, state officials confirmed Tuesday.
The thickly antlered, nontypical whitetail was still carrying an identification tag in its ear and the Board of Animal Health confirmed it was the same buck reported missing in April by a producer of trophy deer. The animal escaped through a storm-damaged fence, a Department of Natural Resources official said, adding that other escapees were recovered within 72 hours.
Captive deer herds have been linked by state wildlife officials to three of Minnesota’s four outbreaks of chronic wasting disease (CWD) in wild deer. The 27-pointer was kept by the hunter who shot it, but the Board of Animal Health was able to obtain tissue samples from the animal to determine if it was infected with the always fatal, highly contagious wasting disease. Test results are pending. The deer’s owner was fined $250 for allowing it to be at large in the wild.
Hunting spot hints
snip...see full story here;
Tony Kennedy is an outdoors writer covering Minnesota news about fishing, hunting, wildlife, conservation, camping, natural resource management, public land, forests and water.
tony.kennedy@startribune.com
i hope and pray that the testing comes back negative...terry
''Captive deer herds have been linked by state wildlife officials to three of Minnesota’s four outbreaks of chronic wasting disease (CWD) in wild deer.''
Wednesday, February 10, 2016
***> Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***
FRIDAY, OCTOBER 11, 2019
Minnesota Officials Burn, Bury, Worry As Chronic Wasting Spreads
MONDAY, NOVEMBER 04, 2019
Minnesota 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?
FRIDAY, FEBRUARY 15, 2019
Minnesota New CWD-positive deer in Crow Wing County and southeastern Minnesota require additional disease monitoring and management
THURSDAY, DECEMBER 06, 2018
Minnesota Wild deer identified as presumptive positive for CWD outside of disease management zone first in Houston County
FRIDAY, NOVEMBER 09, 2018
Minnesota CWD TSE Prion detected four harvested samples from farmed deer quarantined farm Crow Wing County
SATURDAY, APRIL 21, 2018
MINNESOTA STATE AUDITORS Board of Animal Health has failed to enforce some laws relating to deer and elk farms A CWD TSE PRION GLOBAL UPDATE
THURSDAY, APRIL 12, 2018
Minnesota DNR's 10-year CWD TSE Prion deer plan?
SATURDAY, MARCH 03, 2018
Minnesota CWD All seven of the remaining white-tailed deer on farm Positive
MONDAY, AUGUST 28, 2017
Minnesota CWD tests mandatory for deer harvested in central, north-central and southeast
SUNDAY, AUGUST 20, 2017
Minnesota Fearing spread of CWD, agency pushing animal health board to suspend farmer's license
FRIDAY, JANUARY 20, 2017
Minnesota Chronic Wasting Disease investigation traces exposure to Meeker County farm
FRIDAY, DECEMBER 08, 2017
Minnesota Chronic wasting disease update: second deer tests positive on Winona County farm
FRIDAY, NOVEMBER 24, 2017
Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting CWD TSE PRION DISEASE risk factors
WEDNESDAY, NOVEMBER 22, 2017
Minnesota Chronic Wasting Disease discovered in Winona County farm
WEDNESDAY, NOVEMBER 15, 2017
Minnesota DNR 7 deer test presumptive positive in southeast’s CWD management zone
THURSDAY, NOVEMBER 09, 2017
Minnesota CWD TSE Prion Disease not detected in latest round of CWD tests on farmed deer herd in Crow Wing County?
Friday, August 05, 2016
MINNESOTA CHRONIC WASTING DISEASE SURVEILLANCE AND TESTING CWD TSE PRION UPDATE
TUESDAY, NOVEMBER 22, 2016
Minnesota Tests confirm 2 CWD-positive deer near Lanesboro
TESTS CONFIRM 2 CWD-POSITIVE DEER NEAR LANESBORO
November 22, 2016
DNR initiates disease response plan; offers hunters information on field dressing
Test results show two deer harvested by hunters in southeastern Minnesota were infected with Chronic Wasting Disease, according to the Department of Natural Resources.
One deer has been confirmed as CWD-positive. Confirmation of the second is expected later this week. The deer, both male, were killed near Lanesboro in Fillmore County during the first firearms deer season.
The two deer were harvested approximately 1 mile apart. These are the only deer to test positive from 2,493 samples collected Nov. 5-13. Results are still pending from 373 additional test samples collected during the opening three days of the second firearms season, Nov. 19-21.
CWD is a fatal brain disease to deer, elk and moose but is not known to affect human health. While it is found in deer in states bordering southeastern Minnesota, it was only found in a single other wild deer in Minnesota in 2010.
The DNR discovered the disease when sampling hunter-killed deer this fall in southeastern Minnesota as part of its CWD surveillance program. Dr. Lou Cornicelli, DNR wildlife research manager, said hunter and landowner cooperation on disease surveillance is the key to keeping the state’s deer herd healthy.
“We were proactively looking for the disease, a proven strategy that allows us to manage CWD by finding it early, reacting quickly and aggressively to control it and hopefully eliminating its spread,” he said.
It is unknown how the two CWD-positive deer, which were harvested 4 miles west of Lanesboro in deer permit area 348, contracted the disease, Cornicelli said.
“We want to thank hunters who have brought their deer to our check stations for sampling,” he said. “While finding CWD-positive deer is disappointing, we plan to work with hunters, landowners and other organizations to protect the state’s deer herd and provide hunters the opportunity to pass on their deer hunting traditions.”
These are the first wild deer found to have CWD since a deer harvested in fall 2010 near Pine Island tested positive. It was found during a successful disease control effort prompted by the detection in 2009 of CWD on a domestic elk farm. The DNR, landowners and hunters worked together to sample more than 4,000 deer in the Pine Island area from 2011 to 2013, and no additional infected deer were found.
The National Centers for Disease Control and Prevention as well as the World Health Organization have found no scientific evidence that the disease presents a health risk to humans who come in contact with infected animals or eat infected meat. Still, the CDC advises against eating meat from animals known to have CWD...
snip...see more here;
TUESDAY, NOVEMBER 22, 2016
Minnesota Tests confirm 2 CWD-positive deer near Lanesboro
Thursday, September 19, 2013
Chronic Wasting Disease CWD surveillance, deer feeding ban continues in southeastern Minnesota
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Friday, May 25, 2012
Chronic Wasting Disease CWD found in a farmed red deer from Ramsey County Minnesota
SATURDAY, MARCH 17, 2012
Minnesota CWD DNR, Can chronic wasting disease jump from deer to humans? yes, maybe some day YOUTUBE
Tuesday, January 25, 2011
Minnesota, National Veterinary Services Laboratory in Ames, Iowa, has confirmed CWD case near Pine Island
Friday, January 21, 2011
MINNESOTA HIGHLY SUSPECT CWD POSITIVE WILD DEER FOUND NEAR PINE ISLAND
Saturday, October 31, 2009
Elk from Olmsted County herd depopulated to control CWD Three additional elk from the 558-head herd tested positive
Tuesday, January 27, 2009
Chronic Wasting Disease found in a farmed elk from Olmsted County ST. PAUL, Minn.
CHRONIC WASTING DISEASE UPDATE September 6, 2002
Minnesota has announced the finding of CWD in a captive elk in Aitkin County. The animal was a five-year-old male. It had been purchased from a captive facility in Stearns County in August of 2000. The herd where the elk was found has been placed under quarantine as has two additional facilities where the infected elk had resided prior to it coming to the farm in Aitkin County. Minnesota DNR officials will test wild deer in the area to determine if there is any sign of CWD in the free-ranging population. This is the first case of CWD in either captive or freeranging cervids in Minnesota. Several more states have passed bans on the importation of deer and elk carcasses from states where CWD has been found in wild animals. Previously the states of Colorado, Illinois and Iowa and the province of Manitoba had passed such bans. The states of Vermont, Oregon and Missouri have enacted similar bans. Numerous states have issue voluntary advisories to their out-of-state hunters encouraging them not to bring the carcass or carcass parts of deer and elk into their state. The bans do permit the importation of boned out meat, hides or cape with no meat attached, clean skull cap with antler attached, finished taxidermy heads or the ivories of elk. The state of Georgia has recently banned the importation of live cervids into that state also. Some citizens of Colorado have formed a new political action group called Colorado Wildlife Defense (just happens that the acronym is CWD). The stated goal of this group are; Elimination of big game diseases, especially CWD; promotion of healthy wildlife habitat; promotion of scientifically sound wildlife research; promotion of a discussion of the ethics of hunting and wildlife management; education of the hunting and non hunting public. Their action plan calls for; requiring double fencing of all game farms at owners expense; all game farmers provide annual proof of bonding; prohibit new licenses for deer and elk farms; prohibit expansion in acreage of existing game farms; prohibit the transfer of game farm licenses; prohibit charging for hunting behind high wire; prohibit blocking of traditional migratory paths by high fences; requiring game farms to maintain environmental controls and prohibit the escape of contaminated water or soil; requiring immediate reporting of missing deer or elk from game farms; and requiring all game farm deer and elk to be tested for brucellosis and TB. Wisconsin has announced that 7 more free-ranging deer have tested positive for CWD. They have expanded their eradication zone by an additional 15 square miles to cover these findings. The total number of free-ranging CWD positive in Wisconsin is now 31 white-tail deer.
In 2000, a elk farmer in Wisconsin received elk from a CWD exposed herd in Colorado. At that time, the farmer advised the Wisconsin Department of Agriculture that both animals from the exposed herd in Colorado were dead. He has now advised Wisconsin Ag. that he was mistaken and that one of the animals is still alive in his herd. The second draft of the implementation documents for the National CWD Plan was distributed to committee members and others on Friday, August 30. The final documents are due to APHIS and USFWS on Friday, September 13. The herd of captive elk in Oklahoma that had been exposed to CWD will be destroyed this week. This herd had an elk test positive for CWD in 1997 but the depopulation of the herd was not agreed to by the owners and federal representatives until this week. Since the discovery of CWD in the herd, the remaining animals have been under quarantine, however, in the meantime the herd has dropped from 150 animals to 74. Due to a lack of communication, not all of the 76 animals that died in the interim were tested for CWD. All remaining animals will be tested but the true degree of infection rate of the herd will never be known.
The owners of the facility will not be permitted to restock the area with cervids for a period of five years. A New York based organization, BioTech Research Fund I LLC has committed a $1 million line of credit to fund commercialization of tests for brain-wasting disorders and production of various vaccines to Gene-Thera of Wheat Ridge, Colorado. Gene-Thera has spent three years developing new ways not only to diagnose CWD, but create vaccines for mad cow disease, E. coli contaminants and foot-and-mouth disease. Its tests for CWD have been successful in more than 100 samples from Colorado and Wisconsin according to company officials. Gene-Thera plans to license and market some o fits disease test kits by the end of the year, then begin volume distribution by mid-2003. The abstracts of the presentations from the CWD Conference in Denver August 6 and 7 have been posted on the Colorado Division of Wildlife web site. You will need adobe acrobat reader to read them.
The Division web site is: http://wildlife.state.co.us/CWD/Symposium_booklet.pdf
Minnesota: Second case in a game farmed elk discovered in Stearns Co.
This is a trace forward from the previously affected game farm in Aitkins Co. An additional game farm in Benton Co is under quarantine.
snip...
Supporting Documents: Colorado: CWD-Exposed Elk Used in 1990 Study- Wildlife officials call W. Slope move a mistake
Date: January 17, 2003 Source: Denver Post Contacts: Theo Stein Environment Writer
The Colorado Division of Wildlife knowingly used a herd of captive elk exposed to chronic wasting disease in a grazing study on the Western Slope in January 1990, possibly introducing the disease to the elk-rich area. "It was a bad call," said Jeff Ver Steeg, the division's top game manager. "I can't deny it." About 150 wild elk were allowed to graze in the same pens near Maybell after the research herd was removed and may have picked up the abnormal protein that causes the disease from the feces and urine left by the captive elk. While the Division of Wildlife has expressed concern before that its animals might have helped spread CWD, this is the first time the agency has acknowledged it knowingly moved elk exposed to CWD deep into an area where the disease was not known to already exist. Studies that could help determine the source of CWD on the Western Slope are incomplete, and officials say what data that do exist are so new and so spotty they may not provide all the answers. So far, it appears that less than 1 percent of deer and elk in the area are infected, compared with as much as 15 to 20 percent in hotspots in northeastern Colorado. But as wildlife officials grapple with CWD's appearance in northwestern Colorado, officials now admit the decision to continue the grazing study over the objections of some biologists was an error. At the time, biologists wanted to see whether elk grazing on winter range depleted forage that ranchers wanted for fattening cattle in spring. "I think in hindsight a lot of good people probably did some dumb things, myself included," said Bruce Gill, a retired wildlife manager who oversaw research efforts and remembers the debate over the project. "Had we known CWD would explode into such a potentially volatile ecologic and economic issue, we wouldn't have done it." Elk ranchers, who have been blamed for exporting the disease from its stronghold on the Colorado and Wyoming plains to seven states and two Canadian provinces, say the agency's belated disclosure smacks of a coverup. "It's pure negligence," said Jerry Perkins, a Delta banker and rancher who is now demanding a legislative inquiry. "If I'd have moved animals I knew to be infected around like that, I'd be in jail." Grand Junction veterinarian and sportsman Dick Steele said he faults the agency for not disclosing information about CWD-exposed research animals before October, when information was posted on the Division of Wildlife website. "This went way beyond poor judgment," he said. "My main concern is that this has been hidden for the last 12 years. It would have been real important to our decision-making process on how to deal with CWD." While the Maybell information is new, Perkins and other ranchers have long suspected Division of Wildlife research facilities near Meeker and Kremmling, which temporarily housed mule deer kept in heavily infected pens at the Fort Collins facility, have leaked CWD to the wild. Fear of an outbreak led the agency to sample 450 deer around the Meeker and Kremmling facilities. None tested positive, but the sample size was only large enough to detect cases if the infection rate was greater than 1 percent. This fall, tests on 23,000 deer and elk submitted by hunters statewide have revealed 48 CWD cases north of Interstate 70 and west of the Continental Divide. Biologists believe the infection rate in that area, which includes the Maybell, Meeker and Kremmling sites, is still well below 1 percent. But CWD has never been contained in a wild population, so experts fear the problem will grow worse.
The Division of Wildlife says it will be months before a statistical analysis of the fall's sampling results can be completed, an exercise that may shed light on the disease's origin on the Western Slope. "We're just not going to speculate at this point," said Ver Steeg of the possible Maybell connection. "This is one possibility, but certainly not the only possibility." Some biologists think a defunct elk ranch near Pagoda, which had dozens of unexplained deaths in the mid-'90s, is another, a suggestion Perkins rejects. "It may be inconclusive to them," said Perkins. "It isn't inconclusive to us."
WEDNESDAY, APRIL 17, 2019
Minnesota Board of Animal Health CWD positive Crow Wing County deer farm depopulated
***> for those legislators that believe in all things stupid, like ted nugent, and say that cwd is not adversely affecting deer, look no further than Colorado, here's your sign...
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.
snip...
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 ( http://www.colorado.gov/pacific/cdphe/priondiseases ) for the most current recommendations on carcass testing and other preventive measures.
To minimize exposure to CWD and other diseases of potential concern, Colorado Parks and Wildlife (CPW) and state public health officials advise hunters not to shoot, handle or consume any deer, elk or moose that is acting abnormally or appears to be sick. When fielddressing game, wear rubber gloves and minimize the use of a bone saw to cut through the brain or spinal cord (backbone). Minimize contact with brain or spinal cord tissues, eyes, spleen or lymph nodes. Always wash hands and utensils thoroughly after dressing and processing game meat.
(the map on page 71, cwd marked in red, is shocking...tss)
TUESDAY, SEPTEMBER 17, 2019
Michigan House Bill 4687 State Legislators Turn To Draft Dodger Ted Nugent To Make Scientific Decisions over DNR on CWD TSE Prion
THURSDAY, OCTOBER 24, 2019
Michigan DNR reports CWD deer in Hamilton Township, Gratiot County 131 positive to date
TEXAS CWD TSE PRION STRAIN UNLIKE ANYTHING EVER SEEN
“Wow,” he said. “Unlike anything we've seen before.”
The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.
snip...
THURSDAY, SEPTEMBER 05, 2019
Unique Profile of The Texas CWD TSE Prion isolates, the TSE Prion CWD, Scrapie, BSE in Livestock, and CJD in Humans
FRIDAY, OCTOBER 18, 2019
TAHC Exotic CWD Susceptible Species Rules, Regulations, TSE PRION, WHEAT, GRAINS, HAY, STRAY, GLOBAL CONCERNS GROW, UPDATE, October 17, 2019
SATURDAY, SEPTEMBER 28, 2019
Texas CWD TSE Prion aka Mad Deer Disease Detected Free Range Mule Deer El Paso 145 Positive To Date
FRIDAY, JULY 19, 2019
Texas CWD 6,735 samples, 12 tested positive for CWD, additional 62 WTD from permitted breeder facilities tested positive also
TUESDAY, MARCH 05, 2019
TAHC CWD TSE PRION AT 144 POSITIVE MINUTES OF THE 401st COMMISSION MEETING Texas Animal Health Commission August 7, 2018
SUNDAY, JUNE 02, 2019
WISCONSIN THE KILLER AMONG US CWD TSE PRION JANUARY 31, 2008 revisited May 2019
Greetings TSE Prion world, Milwaukee Magazine, and Mary Van de Kamp Nohl.
i thought i would post again, after over a decade, an article that was printed in the Milwaukee Journal Magazine some 11 years ago about chronic wasting disease cwd tse prion in deer and elk. this was a brilliantly written article about aka mad deer disease. i wanted to post this again in full, and then update the article with the latest science up to 2019, and what kind of dire straights we are in right now with the cwd tse prion, and how, by letting corporate America regulated itself, will not work, and in some cases, it could kill you, and in other cases, release a plague on us all, which in this case, is exactly what happened. wake up America, here's your sign...
THE KILLER AMONG US
how is Wisconsin and Texas doing after the Texas Deer Czar, aka Dr. Dough, went up to Wisconsin to fix the cwd tse prion problem, hows that working out???
WEDNESDAY, MARCH 06, 2019
Wisconsin Continues to Ignore CWD TSE Prion, as the disease continues to mount, the Governor flounders, more wild deer positive
SATURDAY, JULY 13, 2019
Wisconsin CWD research planned at Buckhorn Flats property
FRIDAY, JANUARY 26, 2018
WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE
deer czar from Texas, Dr. Dough, goes to Wisconsin to solve the cwd problem...
CWD, Wisconsin, Texas, and Dr. James Kroll
OPINION BLOG
These are just two insights into the man who has been asked to provide analysis and recommended changes to Wisconsin’s deer management program.
Kroll’s insights are from an article entitled “Which Side of the Fence Are You On?”
by Joe Nick Patoski for a past edition of Texas Monthly.
If nothing more, the article gives an unabashed look into the mind-set that will be providing the Wisconsin DNR with recommendations on how to change their deer management practices.
James Kroll (also known as “Deer Dr.”) was appointed to the Wisconsin “deer czar” position last fall.
He was hired by the Department of Administration and instructed to complete a review of the state’s deer management program.
Here’s a sample of the article:
“Game Management,” says James Kroll, driving to his high-fenced, two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.”
Kroll, also known as Dr. Deer, is the director of the Forestry Resources Institute of Texas at Stephen F. Austin State University, and the “management” he is referring to is the sort practiced by the State of Texas.
The 55-year-old Kroll is the leading light in the field of private deer management as a means to add value to the land.
His belief is so absolute that some detractors refer to him as Dr. Dough, implying that his eye is on the bottom line more than on the natural world.
Kroll, who has been the foremost proponent of deer ranching in Texas for more than thirty years, doesn’t mind the controversy and certainly doesn’t fade in the heat.
People who call for more public lands are “cocktail conservationists,” he says, who are really pining for socialism.
He calls national parks “wildlife ghettos” and flatly accuses the government of gross mismanagement.
He argues that his relatively tiny acreage, marked by eight-foot fences and posted signs warning off would-be poachers, is a better model for keeping what’s natural natural while making money off the land.
snip...
It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin.
In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.
FRIDAY, JUNE 01, 2012
TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS
THURSDAY, MARCH 29, 2012
TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT CALLING KETTLE BLACK
WEDNESDAY, OCTOBER 03, 2018
WISCONSIN CAVES TO GAME FARM INDUSTRY AGAIN WHILE STATE FALLS FURTHER INTO THE ABYSS OF MAD DEER DISEASE CWD TSE PRION
TUESDAY, NOVEMBER 20, 2018
WISCONSIN Captive CWD TSE Prion Lotto Entitlement Program Pays Out Again Indemnity From Taxpayers $330,000 To Farmers So Far This Year
TUESDAY, SEPTEMBER 25, 2018
Wisconsin CWD TSE PRION PLAN preferred option disposal in a landfill OR public land is acceptable to leave the carcass in the spot of the kill
stupid is, as stupid does, sometimes you can't fix stupid...tss
WEDNESDAY, JUNE 13, 2018
Wisconsin DATCP NVSL confirmed 21 WTD from a deer farm Iowa County tested positive for chronic wasting disease (CWD)
FRIDAY, FEBRUARY 16, 2018
Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion
FRIDAY, FEBRUARY 16, 2018
Wisconsin Stop private deer industry from trucking CWD across state Durkin: Stop private deer industry from trucking CWD across state
MONDAY, MARCH 05, 2018
TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES
MONDAY, MARCH 20, 2017
Wisconsin CWD TSE Prion Annual Roundup 441 positive
Sunday, May 08, 2016
*** WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE ABYSS UPDATE ***
Wisconsin Chronic Wasting Disease CWD TSE Prion
Wednesday, February 10, 2016
***> Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***
Sunday, January 17, 2016
*** Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of $298,770 for 228 white-tailed deer killed on farm ***
MONDAY, NOVEMBER 26, 2018
Wisconsin CWD spreads on deer and elk farms as control efforts stumble
MONDAY, DECEMBER 10, 2018
Wisconsin DATCP Confirms 11 additional animals from a deer farm in Washington County tested positive for CWD TSE Prion
FRIDAY, FEBRUARY 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al
Monday, January 16, 2012
9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised
Wednesday, November 16, 2011
***> Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Thursday, April 28, 2011
Chronic Wasting Disease Testing and Prevalence Wisconsin April 2011
Thursday, March 18, 2010
175 DEER TEST POSITIVE FOR CWD IN WISCONSIN
MONDAY, FEBRUARY 11, 2019
Wisconsin DATCP Confirms CWD-Positive Deer in Forest County Breeder to Hunting Farm
WEDNESDAY, FEBRUARY 20, 2019
Wisconsin Additional CWD detections in more wild deer in Eau Claire County
THURSDAY, OCTOBER 03, 2019
Tennessee Madison County deer sampled within 10 miles of Crockett and Gibson counties has tested positive for CWD, Declared High Risk
MONDAY, SEPTEMBER 23,
2019 Tennessee More deer test positive for Chronic Wasting Disease in Tennessee, sharp rise expected
WEDNESDAY, NOVEMBER 06, 2019
Montana Carbon County deer tests positive for CWD TSE Prion
THURSDAY, OCTOBER 24, 2019
Pennsylvania NEWLY DETECTED CWD-POSITIVE DEER CAPTIVE-RAISED WILL EXPAND DMA 4 IN 2020
FRIDAY, NOVEMBER 01, 2019
South Dakota Chronic Wasting Disease CWD TSE Prion confirmed in Bennett County
MONDAY, OCTOBER 21, 2019
North Dakota Two mule deer taken in September have tested positive for Chronic Wasting Disease CWD TSE Prion Detected in McKenzie County
FRIDAY, OCTOBER 25, 2019
Wyoming CWD TSE Prion found in a new deer hunt area in Bighorn Mountains
THURSDAY, OCTOBER 03, 2019
Wyoming CWD TSE Prion found in deer west of Continental Divide
WEDNESDAY, OCTOBER 16, 2019
Arkansas Chronic Wasting Disease CWD TSE Prion 619 Positive Cases As Of September 15, 2019
THURSDAY, JUNE 06, 2019
Arkansas AGFC identified 241 new positive cases of CWD TSE Prion in white-tailed deer and five elk during the 2018-19 deer hunting season WD Management Zone expands to include Baxter, Scott and Stone counties
THURSDAY, FEBRUARY 21, 2019
Arkansas CWD TSE Prion Jumps To 605 Cases To Date As Of Jan. 10, 2019
TUESDAY, DECEMBER 18, 2018
Arkansas Two elk and As of Nov. 30, 2018, 155 new cases of CWD have been detected for CWD TSE Prion
FRIDAY, OCTOBER 11, 2019
Minnesota Officials Burn, Bury, Worry As Chronic Wasting Spreads
WEDNESDAY, OCTOBER 16, 2019
Kansas Chronic Wasting Disease CWD TSE Prion Update With 216 cervids Positive To Date
FRIDAY, OCTOBER 04, 2019
Indiana CWD TSE Prion Surveillance 2019 and before?
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
let's review some recent science on the environmental effects of the exposure of the cwd tse prion, it's not pretty...
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]
P-147 Infection and detection of PrPCWD in soil from CWD infected farm in Korea
Hyun Joo Sohn, Kyung Je Park, In Soon Roh, Hyo Jin Kim, Hoo Chang Park, Byounghan Kim
Animal and Plant Quarantine Agency (QIA), Korea
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 2010 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and feces of TSE-infected animals. Using serial protein misfolding cyclic amplification (sPMCA), we developed a detection method for CWD PrPSc in soil from CWD affected farm in 2010. We found to detect PrPSc in soil from CWD infected farm, but not detect PrPSc in soil of wild cervid habitats and normal cervid farm in Korea. We also tried the bioassay on transgenic mice overexpressing elk prion protein (TgElk mice) to confirm infectivity of CWD-infected farm soil and washing solution of it. As the results, there was the presence of infectious prions in them. The attack rates were each 12.5% (1/8, soil) and 100% (6/6, soil washing solution). Our method appears to be a very useful technique for monitoring PrPSc levels in environmental conditions.
Prion 2016 Conference Poster Abstracts
Prion 2016 Oral Abstracts
Prion 2016 Prion Diseases in Animals
Prion 2016 Prion Diseases in Humans
see full text;
PRION CONFERENCE 2019
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.
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
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 ***
TUESDAY, OCTOBER 01, 2019
Genetic susceptibility to chronic wasting disease cwd tse prion?
i am concerned with the fact, the longer you can delay death with cwd, you risk having a cwd tse prion infected deer live longer in the wild or captive, thus giving more time to spread disease. you also risk developing a super cwd tse strain imo. we already have multiple strains, with what seems to be a super strain of cwd in Texas. also, with scrapie, they thought arr was resistant in sheep, until it was not...
2019
Chronic Wasting Disease In Cervids: Zoonosis there from, has it already happened, and is it being misdiagnosed as sporadic cjd?
> However, to date, no CWD infections have been reported in people.
key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Prion 2017 Conference
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
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see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry
PRION 2019 ABSTRACTS
1. Interspecies transmission of the chronic wasting disease agent
Justin Greenlee
Virus and Prion Research Unit, National Animal Disease Center, USDA Agriculture Research Service
ABSTRACT
The presentation will summarize the results of various studies conducted at our research center that assess the transmissibility of the chronic wasting disease (CWD) agent to cattle, pigs, raccoons, goats, and sheep. This will include specifics of the relative attack rates, clinical signs, and microscopic lesions with emphasis on how to differentiate cross-species transmission of the CWD agent from the prion diseases that naturally occur in hosts such as cattle or sheep. Briefly, the relative difficulty of transmitting the CWD agent to sheep and goats will be contrasted with the relative ease of transmitting the scrapie agent to white-tailed deer.
53. Evaluation of the inter-species transmission potential of different CWD isolates
Rodrigo Moralesa, Carlos Kramma,b, Paulina Sotoa, Adam Lyona, Sandra Pritzkowa, Claudio Sotoa
aMitchell Center for Alzheimer’s disease and Related Brain Disorders, Dept. of Neurology, McGovern School of Medicine University of Texas Health Science Center at Houston, TX, USA; bFacultad de Medicina, Universidad de los Andes, Santiago, Chile
ABSTRACT
Chronic Wasting Disease (CWD) has reached epidemic proportions in North America and has been identified in South Korea and Northern Europe. CWD-susceptible cervid species are known to share habitats with humans and other animals entering the human food chain. At present, the potential of CWD to infect humans and other animal species is not completely clear. The exploration of this issue acquires further complexity considering the differences in the prion protein sequence due to species-specific variations and polymorphic changes within species. While several species of cervids are naturally affected by CWD, white-tailed deer (WTD) is perhaps the most relevant due to its extensive use in hunting and as a source of food. Evaluation of inter-species prion infections using animals or mouse models is costly and time consuming. We and others have shown that the Protein Misfolding Cyclic Amplification (PMCA) technology reproduces, in an accelerated and inexpensive manner, the inter-species transmission of prions while preserving the strain features of the input PrPSc. In this work, we tested the potential of different WTD-derived CWD isolates to transmit to humans and other animal species relevant for human consumption using PMCA. For these experiments, CWD isolates homozygous for the most common WTD-PrP polymorphic changes (G96S) were used (96SS variant obtained from a pre-symptomatic prion infected WTD). Briefly, 96GG and 96SS CWD prions were adapted in homologous or heterologous substrate by PMCA through several (15) rounds. End products, as well as intermediates across the process, were tested for their inter-species transmission potentials. A similar process was followed to assess seed-templated misfolding of ovine, porcine, and bovine PrPC. Our results show differences on the inter-species transmission potentials of the four adapted materials generated (PrPC/PrPSc polymorphic combinations), being the homologous combinations of seed/substrate the ones with the greater apparent zoonotic potential. Surprisingly, 96SS prions adapted in homologous substrate were the ones showing the easiest potential to template PrPC misfolding from other animal species. In summary, our results show that a plethora of different CWD isolates, each comprising different potentials for inter-species transmission, may exist in the environment. These experiments may help to clarify an uncertain and potentially worrisome public health issue. Additional research in this area may be useful to advise on the design of regulations intended to stop the spread of CWD and predict unwanted zoonotic events.
56. Understanding chronic wasting disease spread potential for at-risk species
Catherine I. Cullingham, Anh Dao, Debbie McKenzie and David W. Coltman
Department of Biological Sciences, University of Alberta, Edmonton AB, Canada
CONTACT Catherine I. Cullingham cathy.cullingham@ualberta.ca
ABSTRACT
Genetic variation can be linked to susceptibility or resistance to a disease, and this information can help to better understand spread-risk in a population. Wildlife disease incidence is increasing, and this is resulting in negative impacts on the economy, biodiversity, and in some instances, human health. If we can find genetic variation that helps to inform which individuals are susceptible, then we can use this information on at-risk populations to better manage negative consequences. Chronic wasting disease, a fatal, transmissible spongiform encephalopathy of cervids (both wild and captive), continues to spread geographically, which has resulted in an increasing host-range. The disease agent (PrPCWD) is a misfolded conformer of native cellular protein (PrPC). In Canada, the disease is endemic in Alberta and Saskatchewan, infecting primarily mule deer and white-tail deer, with a smaller impact on elk and moose populations. As the extent of the endemic area continues to expand, additional species will be exposed to this disease, including bison, bighorn sheep, mountain goat, and pronghorn antelope. To better understand the potential spread-risk among these species, we reviewed the current literature on species that have been orally exposed to CWD to identify susceptible and resistant species. We then compared the amino acid polymorphisms of PrPC among these species to determine whether any sites were linked to susceptibility or resistance to CWD infection. We sequenced the entire PrP coding region in 578 individuals across at-risk populations to evaluate their potential susceptibility. Three amino acid sites (97, 170, and 174; human numbering) were significantly associated with susceptibility, but these were not fully discriminating. All but one species among the resistant group shared the same haplotype, and the same for the susceptible species. For the at-risk species, bison had the resistant haplotype, while bighorn sheep and mountain goats were closely associated with the resistant type. Pronghorn antelope and a newly identified haplotype in moose differed from the susceptible haplotype, but were still closely associated with it. These data suggest pronghorn antelope will be susceptible to CWD while bison are likely to be resistant. Based on this data, recommendations can be made regarding species to be monitored for possible CWD infection.
KEYWORDS: Chronic wasting disease; Prnp; wildlife disease; population genetics; ungulates
Thursday, May 23, 2019
Prion 2019 Emerging Concepts CWD, BSE, SCRAPIE, CJD, SCIENTIFIC PROGRAM Schedule and Abstracts
see full Prion 2019 Conference Abstracts
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
snip…full text;
SATURDAY, FEBRUARY 09, 2019
Experts: Yes, chronic wasting disease in deer is a public health issue — for people
FRIDAY, JULY 26, 2019
Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species
MONDAY, FEBRUARY 25, 2019
MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
WEDNESDAY, JULY 31, 2019
The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L
***> cattle, pigs, sheep, cwd, tse, prion, oh my!
***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006).
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period.
This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.
snip.....
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip.....
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip.....
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip.....
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip.....
READ THIS VERY, VERY, CAREFULLY;
SUNDAY, SEPTEMBER 1, 2019
***> FDA Reports on VFD Compliance
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
THURSDAY, AUGUST 08, 2019
Raccoons accumulate PrPSc after intracranial inoculation with the agents of chronic wasting disease (CWD) or transmissible mink encephalopathy (TME) but not atypical scrapie
SUNDAY, SEPTEMBER 08, 2019
Wisconsin Laboratory Testing Options for Prion Diseases, Wisconsin Neurologists, Clinical Laboratory Directors, and Infection Preventionists, Please Distribute Widely
Preparing for the Storm
the British disease...NOT, the UKBSEnvCJD only theory was/is bogus $$$
*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video
*** sporadic CJD linked to mad cow disease
*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***
MONDAY, JUNE 24, 2019
APHIS, FSIS, USDA, FDA, Transmissible Spongiform Encephalopathy TSE, BSE, CWD, Scrapie, Camel TSE Prion Disease, CJD Humans
WEDNESDAY, JULY 31, 2019
The agent of transmissible mink encephalopathy passaged in sheep is similar to BSE-L
TUESDAY, JULY 30, 2019
Guidelines for reporting surveillance data on Transmissible Spongiform Encephalopathies (TSE) in the EU within the framework of Regulation (EC) No 999/2001 APPROVED: 9 July 2019
2002
CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002
CHRONIC WASTING DISEASE
JOINT OVERSIGHT HEARING BEFORE THE SUBCOMMITTEE ON FORESTS AND FOREST HEALTH JOINT WITH THE SUBCOMMITTEE ON FISHERIES CONSERVATION, WILDLIFE AND OCEANS OF THE COMMITTEE ON RESOURCES U.S. HOUSE OF REPRESENTATIVES ONE HUNDRED SEVENTH CONGRESS SECOND SESSION
May 16, 2002
Serial No. 107-117
snip...
Mr. MCINNIS. Today, this joint Subcommittee hearing will explore an issue of immeasurable importance to the growing number of communities in wide-ranging parts of this country, the growing incidence of Chronic Wasting Disease in North America’s wild and captive deer and elk populations. In a matter of just a few months, this once parochial concern has grown into something much larger and much more insidious than anyone could have imagined or predicted.
As each day passes, this problem grows in its size, scope, and consequence. One thing becomes clear. Chronic Wasting Disease is not a Colorado problem. It is a Wisconsin problem or a Nebraska or Wyoming problem. It is a national problem and anything short of a fully integrated, systematic national assault on this simply will not do, which is precisely why we brought our group together here today.
snip...
So this is a disease that is spreading throughout the continent and it is going to require a national response as well as the efforts that are currently taking place in States like Wisconsin, Colorado, Nebraska, Wyoming, the interest they now have down in Texas and some of the neighboring States that have large white-tailed deer population and also elk.
This is a huge issue for us, Mr. Chairman, in the State of Wisconsin. I want to commend Governor McCallum and your staff and the various agencies for the rapid response that you have shown, given the early detection of CWD after the last deer hunting season. The problem that we have, though, is just a lack of information, good science in regards to what is the best response, how dangerous is this disease. We cannot close the door, quite frankly, with the paucity of scientific research that is out there right now in regards to how the disease spreads, the exposure of other livestock herds—given the importance of our dairy industry in the State, that is a big issue—and also the human health effects.
MONDAY, OCTOBER 07, 2019
Chronic Wasting Disease (CWD) and Government Response Congressional Research Service May 17, 2019
WEDNESDAY, OCTOBER 02, 2019
Chronic Wasting Disease In Cervids: Prevalence, Impact And Management Strategies
WEDNESDAY, JUNE 26, 2019
Subcommittee Hearing: Chronic Wasting Disease: The Threats to Wildlife, Public Lands, Hunting, and Health
video
CWD, TSE, PRION, CATTLE, PIGS, HUMANS, PLANTS, WHEAT, GRAINS, HAY, STRAW, SOIL, OH MY!
WEDNESDAY, OCTOBER 16, 2019
Australia Assessment of bulk wheat from Canada Part B: Animal biosecurity risk advice, CWD TSE Prion concerns are mounting
THURSDAY, OCTOBER 17, 2019
Europe's uneven laws threaten scavengers and Spread Transmissible Spongiform Encephalopathy TSE Prion
do you know that in studies with scrapie (same as cwd tse prion, in fact, evidence shows this is where cwd came from), the tse prion agent can survive in soil and still be infectious for from 16 to 21 years, so, my next question is, when to property values start to sink, or have they already?
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
it's a damn shame no one took this seriously, because they knew, they (officials) have known, but it's corporate junk science that got us here, bottom line, and it's still happening $$$
Terry S. Singeltary Sr.
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