IOWA DNR 2020 surveillance wild deer herd CWD 21 new positive deer and added two new counties
IOWA DNR 2020 surveillance wild deer herd CWD 21 new positive deer and added two new counties
21 deer test positive for chronic wasting disease
The Iowa Department of Natural Resources’ 2020 surveillance of Iowa’s wild deer herd for the presence of chronic wasting disease has yielded 21 new positive deer, and has added two new counties to the list where positive deer have been found.
The new positive deer were all from either an existing chronic wasting disease zone or adjacent to an existing zone. Two new counties were added to list where deer have tested positive. Jackson County had a positive deer that was taken just south of the existing Dubuque disease management zone, and Appanoose County had a positive deer taken just northeast of the existing Corydon disease management zone.
“Although we expect some spread just outside of our existing zones, it’s not what we like to see,” said Tyler Harms, deer program leader for the Iowa DNR. “We will reassess the boundaries of our existing zones to encompass these new positives.”
The Iowa DNR has a map online at https://www.iowadnr.gov/Hunting/Deer-Hunting/Deer-Disease-Information showing where the positive deer have been taken. To date, 111 wild Iowa deer have tested positive for the disease since 2013 when it was first discovered in the state.
“We rely heavily on our hunters to help us respond to this disease by increasing antlerless harvest in our disease management zones,” Harms said. “We know increased harvest is the best way to slow the spread and it helps increase sampling in these zones so we can monitor disease prevalence and spread. We continue to encourage hunters to harvest additional antlerless deer in these disease management zones.”
The 2020 sampling year ends March 31 and while most of the deer samples are collected during the hunting seasons, the DNR does collect samples from road killed deer and suspected sick deer near the deer disease management zones annually beginning April 1.
Media Contact: Tyler Harms, Biometrician, Wildlife Bureau, Iowa Department of Natural Resources, 515-777-5378.
Iowa Chronic Wasting Disease CWD TSE Prion Update 91 Positive as of December 3, 2020
DNR News Releases
Virtual meeting on fatal deer disease scheduled for Dec. 3
12/1/2020 1:24:00 PM View Count 972 Return
The Iowa Department of Natural Resources (DNR) will be hosting a virtual meeting on Dec. 3, 2020 at 12 p.m., to discuss the status of chronic wasting disease in Iowa. The meeting will be broadcast via Facebook Live at facebook.com/IowaDNR to provide Iowans the opportunity to ask questions. To attend via Zoom, go to https://us02web.zoom.us/j/87404715461?pwd=TjZhanI2NjlGQzM2em42T0xiRkQ0QT09 and enter the passcode: CWD2020!
The meeting will be recorded and available for viewing after the meeting on the Iowa DNR YouTube channel after the event is over and the video is outfitted with closed captioning.
Typically, the Iowa DNR would host in-person public meetings to provide citizens the opportunity to ask questions and voice concerns. However, a virtual meeting can get information out to a broader audience while adhering to COVID-19 guidelines.
Tyler Harms, deer program leader for the Iowa DNR, encourages hunters to either attend this meeting or watch the recorded presentation, especially if they plan to hit the field for the upcoming shotgun seasons.
“We feel it is important for hunters to be armed with information on this disease as we enter our most popular deer hunting seasons of the year,” he said.
Harms said that testing harvested deer is one of the best and easiest ways hunters can help the DNR monitor the spread of the disease.
“Our surveillance program relies heavily on voluntary samples from hunters, and we encourage anyone interested in helping with this effort to contact your local DNR wildlife unit if you are interested in getting your deer tested, especially those hunting in counties where chronic wasting disease has been found,” Harms said.
Since 2013, the fatal disease has been found in wild deer in eight Iowa counties, including Allamakee, Clayton, Winneshiek, Fayette, and Dubuque in the northeast, Wayne and Decatur in the south, and Woodbury in the west. The Iowa DNR has tested nearly 85,000 tissue samples from wild deer for chronic wasting disease since monitoring began in 2002. So far, there have been 91 positive tests.
Each year the DNR collects deer tissue samples from every county in Iowa, with efforts focused on portions of northeast and eastern Iowa near Wisconsin, Minnesota, Illinois, south-central Iowa near Missouri, and along the Missouri River near Nebraska where the disease has been detected. Additional testing has been conducted in Pottawattamie, Cerro Gordo, Van Buren, and Davis counties, following positive tests from captive facilities. All counties have at least 15 samples collected annually. The disease has been found in every state around Iowa.
“Deer hunting is an important tradition for many Iowans, and we want to make sure we’re doing everything we can to monitor and slow the spread of this disease to maintain a healthy deer herd for future generations,” Harms said.
The Iowa DNR has more information about chronic wasting disease and other infectious diseases online at www.iowadnr.gov/cwd.
TUESDAY, JANUARY 26, 2021
Iowa Chronic Wasting Disease CWD TSE Prion Update 91 Positive as of December 3, 2020
Nov. 22, 2019
Iowa Positive tests were confirmed on farms in Van Buren County DES MOINES, Iowa (Nov. 22, 2019
Two Cases of Chronic Wasting Disease Found at Deer Farms
Positive tests were confirmed on farms in Van Buren County DES MOINES, Iowa (Nov. 22, 2019) — The Iowa Department of Agriculture and Land Stewardship has confirmed that Chronic Wasting Disease (CWD) has been found in captive white-tail deer on two separate farms in Van Buren County, Iowa. Both sites are quarantined while the Department works to trace potential exposures and contain the disease.
There is no evidence that CWD can spread to humans, pets or domestic livestock. CWD is a neurological disease that only affects deer, elk and moose. It is caused by an abnormal protein called a prion and impacts the brain of the infected animal. The prions can attach to soil and spread the disease among deer. Symptoms of the disease include excessive salivation, thirst and urination, loss of appetite, progressive weight loss, listlessness as well as drooping ears and head.
The disease was detected as part of the Department’s voluntary CWD monitoring program. Participating producers test deceased farm-raised deer and elk over 12 months of age. Positive test results must be reported to the Iowa Department of Agriculture.
Chronic Wasting Disease was first identified in captive mule deer at a research facility in Colorado in 1967. The disease was then found in Wisconsin in 2002. Since 2002, Iowa has tested for CWD in 7,447 captive deer and elk as part of its surveillance program. The last confirmed case in Iowa was in Buchanan County in 2016.
To learn more about CWD, visit https://iowaagriculture.gov/animal-industry-bureau/chronic-wasting-disease
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Iowa’s Chronic Wasting Disease (CWD) Herd Certification Program (HCP)
CWD Program Standards
ADT/Traceability Fact sheet for interstate transport of Cervids
Regulatory Sample Collection
TUESDAY, FEBRUARY 25, 2020
Iowa Chronic Wasting Disease CWD TSE Prion Cases Climb To 89 positive To Date in Wild Cervid
Public meeting on fatal deer disease set for March 10 in Leon
Leon, Iowa - Deer hunters who hunt in Decatur County take note– chronic wasting disease has shown up in your area. A hunter harvested wild deer taken during the first shotgun season in Decatur County has tested positive for chronic wasting disease.
The Iowa Department of Natural Resources (DNR) has scheduled a meeting on March 10, at 7 p.m., in the Central Decatur CSD, 1201 NE Poplar, in Leon, to discuss the status of chronic wasting disease in Iowa and how deer hunters can help stop or slow the spread of this disease.
Tyler Harms, wildlife biologist for the Iowa DNR, will coordinate the meeting. He said there are several things hunters can do today to help monitor for the disease.
“The first and most important is to allow sampling of hunter harvested deer,” he said. “Second, is to remove any mineral blocks and feeders that unnaturally concentrates deer and increases the chance of spreading any disease and finally report any sick or emaciated deer to the DNR.
“We want people to come to this meeting, ask their questions, hear the concerns from other hunters,” Harms said. “Deer hunting is an important tradition and, for some, a large part of their identity. It is also important to us and we need to work together to combat this disease. Our goal is to provide quality deer hunting today, tomorrow, and for future generations.”
The Iowa DNR has tested nearly 74,000 deer tissue samples for chronic wasting disease since monitoring began in 2002. The disease first appeared in Iowa’s wild deer herd in 2013. So far, there have been 89 positive tests.
The Iowa DNR sets an annual goal of collecting 6,900 deer tissue samples. The effort has focused on portions of northeast and eastern Iowa near Wisconsin, Illinois, and south-central Iowa near Missouri, where the disease has been detected. Additional testing has been conducted in Pottawattamie, Cerro Gordo and Davis counties, following positive tests from captive facilities. All counties have at least 15 samples collected annually. The disease has been found in every state around Iowa.
Chronic wasting disease is a neurological disease belonging to the family of diseases known as transmissible spongiform encephalopathies, or prion diseases. It attacks the brain of infected deer and elk causing the animals to lose weight, display abnormal behavior, lose body functions and die. It is always fatal to the infected animal.
“Deer hunting is one of Iowa’s great traditions. We want to educate and work with our hunters so we continue to have the best deer herd in the country for generations to come,” he said.
The Iowa DNR has more information about chronic wasting disease and other infectious disease online at www.iowadnr.gov/cwd. ;
Media Contact: Andy Kellner, Wildlife Biologist, Iowa Department of Natural Resources, 515-975-8318.
MONDAY, FEBRUARY 10, 2020
Iowa CWD TSE Prion 2019/20 (confirmed or suspect) 43 cases to date Wild Cervid
Iowa CWD TSE Prion 2019/20 (confirmed or suspect) 43 cases to date Wild Cervid
Captive Population Positives (5)
Map Date February 4, 2020
SUNDAY, NOVEMBER 24, 2019
Iowa Two Cases of Chronic Wasting Disease Found at Deer Farms
THURSDAY, FEBRUARY 08, 2018
Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season
THURSDAY, MARCH 08, 2018
Wisconsin CWD-Positive Deer Found on Washington County Farm
FRIDAY, JULY 29, 2016
IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO DATE 304 CASES WILD AND CAPTIVE REPORT UPDATE JULY 2016
THURSDAY, FEBRUARY 08, 2018
Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season
TUESDAY, JANUARY 23, 2018
Iowa Preliminary CWD TSE Prion Minimal Low Testing Reports 2 Confirmed With 5 Suspects To Date for 2017 Season
TUESDAY, MARCH 14, 2017
Iowa 12 deer test positive for chronic wasting disease from 2016-17 hunting seasons
WEDNESDAY, FEBRUARY 01, 2017
Iowa Clayton County deer tests positive for chronic wasting disease
THURSDAY, JANUARY 26, 2017
IOWA DNR CONFIRMS 9 CASES CWD from hunter-harvested deer from near Harpers Ferry during the 2016 hunting seasons
FRIDAY, JULY 29, 2016
IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO DATE 304 CASES WILD AND CAPTIVE REPORT UPDATE JULY 2016
WEDNESDAY, FEBRUARY 01, 2017
Tuesday, December 20, 2016
IOWA CHRONIC WASTING DISEASE FOUND AT A DEER FARM IN BUCHANAN COUNTY
Friday, July 29, 2016
IOWA CHRONIC WASTING DISEASE CWD TSE PRION TOTAL TO DATE 304 CASES WILD AND CAPTIVE REPORT UPDATE JULY 2016
SUNDAY, JANUARY 24, 2016
IOWA CHRONIC WASTING TSE PRION DISEASE UPDATE
Iowa Supreme Court rules law allows quarantine of CWD deer, not land
This is very, very concerning imo.
IF this ruling is upheld as such ;
''The Iowa Supreme Court upheld the district court ruling — saying the law gives the DNR only the authority to quarantine the deer — not the land. The ruling says if the Iowa Legislature wants to expand the quarantine powers as suggested by the DNR, then it is free to do so.''
IF a 'precedent' is set as such, by the Legislature not intervening to expand quarantine powers to the DNR for CWD TSE Prion, and the precedent is set as such that the cervid industry and land there from, once contaminated with the CWD TSE Prion, are free to repopulate, sell the land, etc, imo, this will blow the lid off any containment efforts of this damn disease CWD TSE Prion. The Iowa Supreme Court did not just pass the cwd buck down the road, the Supreme Court of Iowa just threw the whole state of Iowa under the bus at 100 MPH. all those healthy deer, while the litigation was going on, well, they were incubating the cwd tse prion, loading up the land even more, and in the end, 79.8% of those healthy looking deer had CWD TSE Prion. what about the exposure to the other species that come across that land, and then off to some other land? this makes no sense to me, if this is set in stone and the Legislation does not stop it, and stop if fast, any containment of the cwd tse prion will be futile, imo...terry
FRIDAY, JUNE 16, 2017
Iowa Supreme Court rules law allows quarantine of CWD deer, not land
see old history of this CWD blunder in Iowa here
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease ***
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
For Immediate Release
Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov Share on facebook Share on twitter Share on email Share on print More Sharing Services 1
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
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INFORM: Cervid Health and States Indemnity FY 2015
USDA Animal and Plant Health Inspection Service sent this bulletin at 09/19/2014 05:22 PM EDT
Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS) received a total of $3 million in appropriated funding to support cervid health activities in fiscal year (FY) 2014, and made approximately $1.0 million of this funding available for indemnity of chronic wasting disease (CWD) positive, suspect, and exposed farmed cervids. All of the available FY2014 indemnity funding was used to depopulate three CWD-infected herds. However, several States have asked about the availability of Federal indemnity funds for CWD-exposed animals in the future.
VS plans to offer Federal indemnity for CWD-exposed cervids beginning in FY2015. Briefly, we will prioritize the highest risk CWD-exposed animals for indemnity based on the availability of funding. Any newly reported CWD-positive herds will be considered for indemnity as they are identified, based first on funding availability and secondly on the risk presented by the herd.
We will reassess our fiscal year funding on a quarterly basis so that providing indemnity for exposed animals does not exhaust available funding early in the fiscal year. By taking this fiscally cautious approach, we hope to provide indemnity for positive herds identified later in the fiscal year while removing high-risk animals from the landscape as soon as possible to minimize the risk for disease spread. Further, removal and testing of these exposed animals will provide a better understanding of the disease risk presented by these animals/herds.
VS plans to work with our State and industry stakeholders on the criteria to assess the risk and on the process through which States can request this indemnity. These will be finalized in a VS Guidance Document in the near future. We look forward to working with you to implement this process in the coming year.
***
how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms ???
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.
SUMMARY:
*** see history of this CWD blunder here ;
Wednesday, August 21, 2013
IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013
snip...
5. On July 16, 2012, DNR received a notice from the Texas Veterinary Medical Diagnostic Lab ("Texas Vet Lab”) that a sample from an adult male deer killed at Pine Ridge tested presumptively positive for CWD. (DNR has an agreement with the Texas Vet Lab to run these preliminary tests.) Because the Texas Vet Lab found this presumptive positive result, protocols required the sample to be sent to the National Veterinary Services Laboratory ("National Lab”) in Ames, Iowa for final confirmation. On July 18, 2012, the National Lab confirmed the positive CWD result in the deer.
6. On July 19, 2012, DNR notified the Brakkes of the positive test by phone. Mr. Brakke was out of state.
snip...
12. The Brakkes depopulated the Hunting Preserve, as specified in the Agreement, from September 10, 2012 to January 31, 2013. As part of this effort, the Brakkes, the staff and their customers killed 199 captive deer and nine captive elk. The DNR obtained 170 CWD samples. (Samples were not taken from fawns and one adult female who was killed in a manner that made sampling impossible.) Of these 199 deer, two additional adult male deer tested positive for CWD. Information provided by the Brakkes confirmed that these two additional deer originated from the Brakke Breeding Facility.
13. DNR installed, with the Brakke's permission, an interior electric fence on October 1 and 2, 2012.
14. The Brakkes cleaned and disinfected, under DNR supervision, the feeders and ground surrounding the feeders on April 5, 2013.
15. On April 26, 2013, the Brakkes hand-delivered a notice to the DNR’s Chief of Law Enforcement Bureau, notifying the DNR that they would no longer operate a hunting preserve on the Quarantined Premises. The Brakkes did not reveal any plans to remove the fence around the Quarantined Premises or to remove the gates to and from the Quarantined Premises in this April 26, 2013 letter.
16. On June 3, 2013, DNR became aware that sections of the exterior fence surrounding the Quarantined Premises had been removed and that some, if not all, of the exterior gates to and from the Quarantined Premises were open.
17. On June 4, 2013, DNR received reports from the public in the area that four wild deer were observed inside the Quarantined Premises.
18. On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened; and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.
IV. CONCLUSIONS OF LAW
snip...
On June 5, 2013,
DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.
***79.8 percent of the deer tested positive for the disease ***
***test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). ***
For Immediate Release
Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov Share on facebook Share on twitter Share on email Share on print More Sharing Services 1
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
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IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013
IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY CONSENT ORDER
IN THE MATTER OF:
TOM & RHONDA BRAKKE D/B/A PINE RIDGE HUNTING LODGE Davis County, Iowa
EMERGENCY CONSENT ORDER NO. 2013-HP-
TO: Tom and Rhonda Brakke, Owners of Pine Ridge Hunting Lodge 22529 Balsam Ave. Clear Lake, IA 50428
1. SUMMARY
This Emergency Consent Order is entered into between the Director of the lowe Department of Naturel Resources (“DNR”) and Tom and Rhonda Brakke D/B/A Pine Ridge Hunting Lodge (“the Brakkes”) related to violations alleged by the DNR to have occurred at the premises they previously managed as a hunting preserve, Pine Ridge Hunting Lodge (“Pine Ridge”). This Emergency Consent Order is entered into between the parties for the purpose of settling the issues which were the subject of a hearing for a stay of the Emergency Order issued by the DNR on June 5, 2013 ("Emergency Order”).
This Emergency Consent Order supersedes the Emergency Order issued on June 6, 2013 with respect to sections V.5 and V.6 only and only to the extent the terms here in are inconsistent with the terms of sections V.5 and V.6 of such Emergency Order. Nothing herein shall be construed in any way as an admission of any issues or liability by any of the parties to this Emergency Consent Order.
Questions regarding this Emergency Consent Order should be directed to:
Relating to technical requirements (DNR): Dr. Dale Garner, Wildlife Bureau Chief Iowa Department of Natural Resources 502 East Ninth Street Des Moines, Iowa 50319 Phone: 515-281-6156
Relating to legal requirements (DNR): Kelley Myers, Attorney for the DNR Iowa Department of Natural Resources 502 East Ninth Street Des Moines, iowa 50319 Phone: 515-281-5534
Angie Bruce, Wildlife Bureau Executive Officer Iowa Department of Natural Resources 502 East Ninth Street Des Moines, Iowa 50319 Phone: 515-281-8070
Relating to technical requirements (Brakkes): Relating to legal requirements (Brakkes):
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lOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY CONSENT ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PlNE RIDGE HUNTlNG PRESERVE
Tom Brakke 22529 Balsam Avenue Clear Lake, IA 50428 Phone: (641)425-2095
Rebecca A. Bromrnel BrownWinick 666 Grand Avenue, Suite 2000 Des Moines, IA 50309 Phone: (515)242-2452
ll. PROCEDURAL BACKGROUND
1. DNR issued an Emergency Order on June 6, 2013, which required the Brakkes to comply with six separate provisions.
2. - Upon issuance of the Emergency Order, DNR requested the Iowa Department of Inspections and Appeals to set the case for a contested case hearing consistent with Iowa Code chapter 17A and 561 lAC chapter 7.
3. The Brakkes, through their counsel, appealed the Emergency Order on June 25, 2013. The Brakkes, through their counsel, flied a Motion for Stay on June 27, 2013, requesting the administrative law judge stay the Emergency Order.
4. The presiding administrative law judge, Judge Heather Palmer, issued the Notice for Hearing on June 18, 2013.
5. The parties, in prehearing conference with the judge, agreed that the hearing would be treated as a hearing on a motion for a stay, consistent with 561 lAC section 7.18(5).
6. The parties agreed to settle prior to the judge deciding whether to issue a stay ofthe Emergency Order. This Emergency Consent Order includes the terms of that settlement.
III. ORDER
THEREFORE, DNR orders and the Brakkes agree, without admitting any fault or any liability, to do the following:
1. The parties agree that an electrified fence just inside the existing high perimeter fence shall be restored or reconstructed on the following terms:
a. Electric Fence. The Brakkes shall maintain such electrified fence until such time as described in paragraph b below. The following terms shall apply to the electric fence:
i. Initiation of the construction and reconstruction efforts must commence by July 10, 2013, and be completed by July 22, 2013 unless unforeseen conditions are encountered or extenuating circumstances arise.
ii. The Brakkes and DNR shall split the cost of the materials for and/or installation of the fence 50-50. DNR intends to provide its staff for labor
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IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY CONSENT ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
and such labor costs shall be the responsibility of DNR and not included in the costs to be divided with the Brakkes.
iii. The fence shall be installed in such a manner as to ensure its effectiveness but also ease its maintenance. This may require, among other features, attachment to existing perimeter fencing so that the electrified portions come up from the ground at an approximate 45 degree angle. Regardless of the design, the fence must include an electrified wire every linear foot for at least three feet. The final design, which should be consistent with this section, shall be subject to the approval of at least one of the DNR’s biologists identified in paragraph c below and the Brakkes. The fence should be designed and installed in a manner that the 50 percent amount to be paid by the Brakkes for such fence does not exceed the amount the Brakkes paid pursuant to the September 7, 2012 Agreement for Chronic Wasting Disease Recovery Plan at Pine Ridge Hunting Lodge, unless otherwise agreed to by the parties.
iv. After construction is complete, the Brakkes shall be solely responsible for all fence repairs, maintenance and associated costs, except as stated in paragraph 3(a)(vii) below.
v. One of the DNR Wildlife biologists identified in paragraph c shall conduct a weekly internal perimeter fence inspection and shall note all reasonable repairs that must be made to make and keep the fence functional. All necessary repairs identified by the biologist shall be submitted to the Brakkes in writing and completed within 24 hours from the date of the submission, unless such repairs cannot be reasonably completed within such time but provided such repairs are completed within a reasonable time thereafter.
vi. One of the DNR Wildlife biologists identified in paragraph c shall conduct an internal perimeter fence inspection at the washout locations along the perimeter of Pine Ridge within one day of a significant rain event and shall note all reasonable repairs that must be made to make and keep the fence functional. All necessary repairs identified by the biologist shall be submitted to the Brakkes in writing and completed within 24 hours of the date of the submission, unless such repairs cannot be reasonably completed within such time but provided such repairs are completed within are reasonable time thereafter.
vii. If during their inspection, one of the biologist observes a breach or other damage to either the perimeter or electric fence that requires immediate action to prevent animal release or harm, DNR shall repair such damage on the spot and at its own expense. The biologist shall notify the Brakkes of such repairs and direct them to make additional repairs if needed.
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IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY CONSENT ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
viii. At no time during the time in which the electric fence is required shall the DNR wildlife biologists identified in paragraph c enter Pine Ridge without first providing notice to the Brakkes.
ix. The electric fence requirements set forth herein shall terminate once depopulation, as set forth below, is completed and such depopulation is confirmed by DNR.
b. Depopulation. The Brakkes shall depopulate the wild deer on Pine Ridge or shall authorize one of the DNR Wildlife biologists identified in paragraph c, to conduct such activities, as soon as is practicable or feasible given weather and terrain conditions. The following conditions shall apply:
i. The Brakkes may destroy the deer through any lawful means or may rely on the DNR Wildlife Biologists identified in paragraph c below to conduct such depopulation.
ii. Depopulation activities shall occur until the DNR Wildlife biologists conclude that all wild deer on Pine Ridge are destroyed or are likely destroyed. Such judgment shall be based on the observation and professional judgment of the biologist. To that end, the biologist must be provided with reasonable access to Pine Ridge to make such judgment.
iii. Depopulation activities must occur prior to the end of the 2013-2014 hunting season.
iv. Any deer destroyed pursuant to this Emergency Consent Order shall be immediately provided to or made available to DNR staff identified in paragraph c in order to ensure that testing and disposal can occur. DNR shall collect requisite samples and submit them for CWD testing. DNR shall share all results related to deer killed-on Pine Ridge with the Brakkes upon receipt of the same. DNR shall be responsible for all testing and disposal costs related to these efforts.
c. DNR Wildlife Staff. The Brakkes shall refer all communications related to fencing orde population to the following DNR Wildlife Staff: Dr. Dale Garner, Wildlife Bureau Chief, Angi Bruce, Executive Officer 3; Bill Ohde, Wiidlife District Supervisor; Keith Wilcox, Natural Resources Technician 2; Lincoln Utt, Natural Resources Technician 1; and Darwin Emmons, Natural Resources Technician 1. The Brakkes may suggest additions to this list during the term of this Emergency Consent Order with such request being made, in writing or email, to Dr. Dale Garner.
2. The Brakkes shall not be required to submit an operational plan, as described in section V.6 of the Emergency Order, pending a hearing on the merits or resolution of this case.
IV. DISPOSITION OF MOTION FOR STAY
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IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY CONSENT ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
This Emergency Consent Order resolves the Motion for Stay filed by the Brakkes on June 27, 2013. DNR acknowledges the Brakkes have appealed the Emergency Order and such portions that are subject to their appeal may be heard in the hearing on the merits that is tentatively set for November of 2013 regardless of this Emergency Consent Order.
V. NONCOMPLIANCE
Failure to knowingly comply with this Emergency Consent Order may result in referral of this matter to the Attorney General or any other appropriate legal authority for relief as allowed by law.
CHUCK GIPP, DIRECTOR Iowa Department of Natural Resources
Dated this 3rd day of July, 2013
TOM BRAKKE, CO-OWNER Pine Ridge Hunting Lodge
Dated this 3 day of July, 2013
CC: Kelley Myers, Rebecca Brommel
IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY ORDER
IN THE MATTER OF:
TOM & RHONDA BRAKKE D/B/A PINE RIDGE HUNTING LODGE Davis County, Iowa
EMERGENCY ORDER
NO. 2013-HP-
TO: Tom and Rhonda Brakke, Owners of Pine Ridge Hunting Lodge 22529 Balsam Ave. Clear Lake, IA 50428
I. SUMMARY
This Emergency Order is issued by the Director of the Iowa Department of Natural Resources ("DNR") to Tom and Rhonda Brakke D/B/A Pine Ridge Hunting Lodge ("the Brakkes”) for the purpose of resolving violations which occurred when the Brakkes removed portions of the fence surrounding the premises they manage or have managed as a hunting preserve, Pine Ridge Hunting Lodge, an area under quarantine for chronic wasting disease ("CWD"). This Emergency Order requires the Brakkes to stop immediately the deconstruction of the fence surrounding the Pine Ridge Hunting Lodge hunting preserve ("Quarantined Premises"); to restore immediately the portions of the fence so removed or degraded; to maintain the fence as an adequate quarantine around the Quarantined Premises for a period of five years; to close immediately and keep closed all gates to return the Quarantined Premises to a closed state; to authorize DNR to access the Quarantined Premises for a limited duration for the purposes of depopulating any deer that may be present; and to submit and agree to execute a plan designed to prevent the spread of CWD from the Quarantined Premises.
Questions regarding this Emergency Order should be directed to:
Relating to technical requirements:
Relating to legal requirements:
Dr. Dale Garner, Wildlife Bureau Chief Iowa Department of Natural Resources 502 East Ninth Street Des Moines, Iowa 50319 Phone: 515-281-6156
Kelley Myers, Attorney for the DNR Iowa Department of Natural Resources 502 East Ninth Street Des Moines, Iowa 50319 Phone: 515-281-5634
Angie Bruce, Wildlife Bureau Executive Officer Iowa Department of Natural Resources 502 East Ninth Street Des Moines, Iowa 50319 Phone: 515-281-8070
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IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
II. JURISDICTION
Pursuant to Iowa Code section 484C.4, which requires the Director to enforce the hunting preserve program and requirements; Iowa Code section 456A.23, which requires the DNR to protect wild animals and enforce by proper actions and proceedings the laws, rules and regulations relating to them; Iowa Code section 456A.25, which authorizes the Director to issue an order after investigation has occurred to secure compliance with the laws and rules DNR is entrusted to enforce; 571 Iowa Administrative Code ("IAC") section 115.10, requiring the Brakkes to maintain the quarantine for a period of at least five years; and 561 IAC section 7.18, which is incorporated by reference in 571 IAC chapter 7, which authorizes the Director to issue an emergency order requiring cessation of an activity and requiring an affirmative action when necessary to prevent or avoid immediate danger to the welfare of the state, DNR has jurisdiction to issue this Emergency Order.
III. STATEMENT OF FACTS
1. The wild deer hunting industry generates approximately $200 million annually for Iowa’s economy and is responsible for the creation of over 2000 jobs, annually. In addition, the tax revenue for the state and federal governments attributed to this wild deer hunting industry in Iowa is approximately $30 million combined, annually. In addition, wild deer are native to the State of Iowa and constitute a public resource held in trust by the state of Iowa.
2. Iowa Code authorizes the establishment and management of hunting preserves. These facilities are fenced facilities wherein customers traditionally pay the operator to participate in a hunt on the fenced property. The deer within the hunting preserve are whitetail and considered preserve deer. Wild animals may not be caught to populate the hunting preserve (except for some remaining deer upon the initial erection of the fences and after diligent efforts to remove those wild deer); instead, the hunting preserves are populated by natural breeding on the preserve grounds and by introduction of farm deer provided by breeding facilities.
3. Consistent with its statutory and administrative authorities, DNR manages diseases in deer, in particular CWD, because wild deer roam many hundreds of miles and can transmit CWD through saliva, nasal fluid, urine and excrement. The spread of CWD is made more virulent by virtue of the fact that CWD is not a virus or bacteria; it is a disease caused by transmissible spongiform encephalopathies (TSEs) or prions. These prions are infectious and self-propagating, meaning they can live without an animal host in the ground, and no known cure exists. The spread of this disease appears more likely where deer are crowded or congregated, which is why CWD testing is done at hunting preserves in Iowa. Other states that have experienced CWD outbreaks in the wild herd have not been able to stop them. The costs of CWD outbreaks are both financial, in lost hunting revenues for local businesses and farmers and lost tax revenues related to the hunting and traveling associated with hunting, as well as social, with the stigmatizing of one of Iowa’s cherished local traditions.
4. The Brakkes operated the Pine Ridge Hunting Lodge ("Pine Ridge") as a hunting preserve, authorized by Iowa Code chapter 484C and regulated by 571 IAC chapter 115. DNR issued the most recent license to the Brakkes to operate the hunting preserve at Pine Ridge from July 1, 2012 to June 30, 2013.
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IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
5. On July 16, 2012, DNR received a notice from the Texas Veterinary Medical Diagnostic Lab ("Texas Vet Lab”) that a sample from an adult male deer killed at Pine Ridge tested presumptively positive for CWD. (DNR has an agreement with the Texas Vet Lab to run these preliminary tests.) Because the Texas Vet Lab found this presumptive positive result, protocols required the sample to be sent to the National Veterinary Services Laboratory ("National Lab”) in Ames, Iowa for final confirmation. On July 18, 2012, the National Lab confirmed the positive CWD result in the deer.
6. On July 19, 2012, DNR notified the Brakkes of the positive test by phone. Mr. Brakke was out of state.
7. On July 23, 2012, DNR met with the Brakkes to initiate an epidemiological investigation. This investigation would help determine where the infected deer came from and make preliminary assessments about the extent of the exposure. The Brakkes provided information including their herd inventory and photographic evidence of the animals killed on the date the infected deer was killed. Also present at this meeting were representatives from the Iowa Department of Agriculture and Land Stewardship ("IDALS"), the United States Department of Agriculture ("USDA") and the Iowa Whitetail Deer Association, an Iowa non-profit organization. IDALS regulates breeding programs that sometimes populate hunting preserves. USDA regulates interstate transport of captive deer; its veterinarian designated as the Area Veterinarian in Charge would have been involved to determine if the diseased captive deer are or may have been moved through interstate commerce and/or transport.
8. Based on information provided by the Brakkes, DNR concluded that captive deer killed on the Hunting Preserve on the same day as the infected deer were located in Florida, New Hampshire, Tennessee and Iowa. Between July 27, 2012 and August 6, 2012, DNR worked with law enforcement officials from those other states to collect samples from the antlers of those deer for DNA testing. These tests would help to identify the origin of the infected deer and verify Brakke's prior documents that the infected deer came from the breeding facility run by the Tom and Rhonda Brakke in Cerro Gordo County, Iowa ("Brakke’s Breeding Facility"). These samples were obtained in a manner to preserve the chain of custody.
9. On August 10, 2012, the Wyoming Game and Fish Wildlife Forensic and Fish Health Laboratory ("Wyoming Lab") provided DNR results for the seven specimens provided to it. (DNR has an agreement with the Wyoming Lab to conduct DNA testing.) The results confirmed that the infected deer originated from the Brakke's Breeding Facility.
10. On August 13, 2012, DNR notified the Brakkes of the DNA results by telephone. DNR advised the Brakkes that they would need to meet with DNR to develop a plan to address the CWD infection at the Hunting Preserve. DNR would have also been communicating with IDALS consistent with the Plan.
11. On September 7, 2012, DNR and the Brakkes executed an agreement ("Agreement") to depopulate the Hunting Preserve by January 31, 2013, and to clean and disinfect the Hunting Preserve. It also contained a general Compliance with Laws provision, which required the Brakkes to comply with all applicable federal, state and local laws and regulations, including without limitation the rules described in 571 Iowa Administrative Code section 115.10 related to the maintenance of a
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IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
quarantine on the Quarantined Premises and the prohibition of deer movement in or out of the Quarantined Premises.
12. The Brakkes depopulated the Hunting Preserve, as specified in the Agreement, from September 10, 2012 to January 31, 2013. As part of this effort, the Brakkes, the staff and their customers killed 199 captive deer and nine captive elk. The DNR obtained 170 CWD samples. (Samples were not taken from fawns and one adult female who was killed in a manner that made sampling impossible.) Of these 199 deer, two additional adult male deer tested positive for CWD. Information provided by the Brakkes confirmed that these two additional deer originated from the Brakke Breeding Facility.
13. DNR installed, with the Brakke's permission, an interior electric fence on October 1 and 2, 2012.
14. The Brakkes cleaned and disinfected, under DNR supervision, the feeders and ground surrounding the feeders on April 5, 2013.
15. On April 26, 2013, the Brakkes hand-delivered a notice to the DNR’s Chief of Law Enforcement Bureau, notifying the DNR that they would no longer operate a hunting preserve on the Quarantined Premises. The Brakkes did not reveal any plans to remove the fence around the Quarantined Premises or to remove the gates to and from the Quarantined Premises in this April 26, 2013 letter.
16. On June 3, 2013, DNR became aware that sections of the exterior fence surrounding the Quarantined Premises had been removed and that some, if not all, of the exterior gates to and from the Quarantined Premises were open.
17. On June 4, 2013, DNR received reports from the public in the area that four wild deer were observed inside the Quarantined Premises.
18. On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened; and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.
IV. CONCLUSIONS OF LAW
1. Iowa Code section 484C.3 authorizes the DNR to adopt rules to administer the Preserve Whitetail program authorized by Iowa Code chapter 484C. DNR, through the Natural Resource Commission, has adopted rules in 571 IAC chapter 104 and 115 to limit movement of captive deer, monitor diseases among captive deer and establish requirements for hunting preserves authorized by the Preserve Whitetail program.
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IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
2. Iowa Code section 484C.4 authorizes the DNR to develop, administer and enforce hunting preserve programs consistent with the requirements both in Iowa Code chapter 484C and rules promulgated pursuant thereto.
3. Iowa Code section 484C.6(1) requires fences installed in and around hunting preserves to comply with rules adopted by the DNR; this requirement would include the fencing requirements found in 571 IAC section 115.10 and discussed in paragraph 6 of this section below. The Agreement, through the Compliance with Laws provision, requires the maintenance of a quarantine on the Quarantined Premises and the prohibition of deer movement in or out of the Quarantined Premises; such requirement would survive termination of the Agreement by virtue of being law.
4. Iowa Code section 484C.12(1) requires that any whitetail deer confined in hunting preserves are free of diseases and authorizes DNR to establish a quarantine for the infected whitetail population. The facts stated above demonstrate that CWD was found within the Brakkes whitetail population at the Quarantined Premises and that Brakkes were knowledgeable of such determination.
5. Iowa Code section 484C.12(2) requires the landowner and an epidemiologist appointed by the DNR, to develop a plan in the event a reportable disease, such as CWD, is found. The plan must include the eradication of the reportable disease among the preserve whitetail population as well as a plan both to reduce and eliminate the reportable disease and to prevent the spread of disease to other animals. The plan must comply with the DNR's rules, must be approved by the DNR and must be incorporated into an agreement between the landowner, or the Iandowner’s veterinarian, and epidemiologist appointed by the DNR. The facts stated above demonstrate that the Brakkes worked with the DNR to depopulate the Quarantined Area but that the Brakkes did not develop a future operational plan to address how they would continue to prevent the spread of disease to other animals.
6. 571 IAC section 115.10 requires a five-year quarantine be placed on a preserve and any remaining animals on the preserve when CWD is found in any animals on a preserve. (Currently CWD is only found in the animal family cervidae, which include deer and elk.) The rules prohibit animal movement in or out of the preserve during the quarantine period. The facts stated above demonstrate that the Brakkes have violated this rule requirement in their removal of the fence and opening ofthe gates.
7. Iowa Code section 17A.18A authorizes the Director of the DNR to take action necessary to prevent or avoid immediate danger to the public welfare. The Brakke’s failure to maintain the quarantine of the Quarantined Premises will allow for the spread of CWD beyond a captive herd. Once wild deer are exposed to CWD that exists on the Quarantined Area, DNR will not have a mechanism to limit the exposure to the remainder of the wild deer population. Iowa's wild deer herd serves a multi-million dollar industry in the state of Iowa and provides over $15 million in tax revenue to the state. The spread of CWD into the wild population would cripple the whitetail hunting industry in Iowa.
8. 561 IAC section 7.18 (which is incorporated by reference in 571 IAC chapter 7) authorizes the Director of the DNR to issue this Emergency Order to the extent necessary to prevent
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IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
or avoid immediate danger to the welfare of the citizens of Iowa. This authority authorizes the Director of the DNR to require a person or persons to immediately cease an offending activity or take an affirmative action to avoid or mitigate the offending action. This emergency action is necessary for the reasons stated in paragraph 7 of this section.
V. ORDER
THEREFORE, DNR orders the Brakkes to do the following immediately:
1. The Brakkes shall immediately discontinue the deconstruction of the fence surrounding the Quarantined Premises.
2. The Brakkes shall completely restore the portions of the fence surrounding the Quarantined Premises that have been removed or degraded by no later than June 7, 2013.
3. The Brakkes shall maintain the fence surrounding the Quarantined Premises, as an adequate quarantine until December 28, 2017, which is a period of five years from date of the last positive CWD diagnosis on the Quarantined Premises, which was December 28, 2012.
4. The Brakkes shall close by June 7, 2013, and keep closed, all gates to and from the Quarantined Premises to return the Quarantined Premises to a closed state.
5. The Brakkes shall authorize DNR officials to access the Quarantined Premises for a period of four weeks from date the Brakkes satisfy paragraphs 1 and 2 of this section for the purposes of depopulating any deer that may be on the Quarantined Premises. DNR shall recover and test those deer, if any, for CWD and report the findings to the Brakkes.
6. The Brakkes shall submit an operational plan, consistent with Iowa Code section 484C.12(2) that demonstrates how they shall comply with the quarantine requirements imposed by 571 IAC section 115.10. It shall be designed to prevent the spread of CWD to other animals. Such plan shall be reviewed by the DNR and shall be memorialized in an agreement among the Brakkes or the Brakkes’ veterinarian, the DNR and the State of Iowa's epidemiologist.
VI. HEARING
Pursuant to Iowa Code section 17A.18A(5), this Emergency Order is being transmitted to the Department of Inspections and Appeals so that the order may be set for immediate hearing before an Administrative Law Judge. You will be promptly notified of the hearing time and place. Consistent with 561 IAC section 7.18(5) (incorporated by reference into 571 IAC chapter 7), you may seek a stay of this Emergency Order consistent with the procedures identified therein.
VII. NONCOMPLIANCE
Failure to comply with this Emergency Order may result in referral of this matter to the Attorney General to obtain injunctive relief, any civil penalties authorized by Iowa Code section 484C.13 and any civil damages attributed to the spread of CWD from the Quarantined Premises to
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IOWA DEPARTMENT OF NATURAL RESOURCES EMERGENCY ORDER ISSUED TO: TOM AND RHONDA BRAKKE D/B/A PINE RIDGE HUNTING PRESERVE
the wild and other captive herds in the state or to the Davis County Attorney's Office for criminal prosecution consistent with Iowa Code section 484C.13.
CHUCK GIPP, DIRECTOR Iowa Department of Natural Resources
Dated this 6th day of June, 2013
CC: Kelley Myers
Iowa Judge Rules against IDALS Motion to Consolidate Brakke Cases
July 23, 2013
Iowa Judge Rules against IDALS Motion to Consolidate Brakke Cases
Iowa Assistant Attorney General to Inquire Constitutionality of CWD Standards Rationale Today, July 23, 2013, the Iowa Administrative Legal Judge ruled against a motion request by the Iowa Department of Land Stewardship (IDALS) to merge the two contested cases (Ag and IDNR) filed by the Brakke family into one. The motion would also delay hearing the merits for both cases until November. Tom and Rhonda Brakke filed suit against IDALS last fall to seek indemnity for their animals on their breeder farm. The Brakke’s filed a second suit against the Iowa Department of Natural Resources (IDNR) in July 2013, after the IDNR issued an emergency order quarantining their 330 acres until December 28, 2017. The Brakke’s believe the two lawsuits are separate jurisdictions and constitutional takings even though they are both related to the exposure of Chronic Wasting Disease. In a statement issued by the Iowa Assistant Attorney General, "Both cases will involve a constitutional takings analysis, and that analysis will involve some level of discussion of the cience and rationale behind IDALS' and DNR's Chronic Wasting Disease (CWD) quarantines policies and the USDA's Program Standards for CWD exposed herds or property." The American Cervid Alliance will distribute updates regarding the Iowa cases as they become available.
Iowa Scrapie TSE Prion Surveillance Sheep and Goats ???
Iowa Progress: Since 1993, the state of Iowa has had 86 herds that have been infected with Scrapie and has made steady progress in eradicating Scrapie. The chart below shows the number of Scrapie Infected Flocks detected in Iowa since the calendar year 2002. The last case of Scrapie in an Iowa producer’s herd was in a goat herd in January 2014. This producer also had sheep that had been diagnosed with Scrapie in 2013.
Scrapie surveillance:
The USDA sets minimum goals for Scrapie sampling for each state. This sampling can be done at Slaughter or On-Farm.
Iowa has never had a problem reaching our goal for sheep but since the Scrapie goat herd in NW IA was discovered in January 2014, the USDA has increased our goat surveillance goal.
We have never been able to reach our increased surveillance goals for goats due to the fact that Iowa has no slaughter plants for adult goats and not all goats are required to have Scrapie ID.
For Immediate Release Monday, July 23, 2012
Dustin Vande Hoef Communications Director 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov
Contact: Kevin Baskins, DNR 515-281-8395
CHRONIC WASTING DISEASE FOUND IN IOWA
DES MOINES – A white-tail deer at a hunting preserve in Davis County has become the first positive detection of chronic wasting disease (CWD) in Iowa. The positive sample was verified this week, and DNR is working closely with the State Veterinarian on this isolated incident.
There is no evidence that CWD can spread to humans, pets or domestic livestock such as pork, beef, dairy, poultry, sheep or goats.
The Davis County facility where the animal was held has been inspected by the Iowa Department of Natural Resources (DNR) and Iowa Department of Agriculture and Land Stewardship (IDALS) to ensure that any remaining deer remain contained. The facility is surrounded by an eight-foot fence. A quarantine has also been issued for the facility.
“Given all of Iowa’s surrounding states have confirmed cases of CWD, Iowa DNR was prepared to address this isolated incident,” said DNR Deputy Director Bruce Trautman.
The DNR and IDALS have a CWD response plan in place to address the disease.
“We have a CWD surveillance program in place to test deer, elk and moose at the facilities that raise farm deer and we have worked closely with DNR to plan for a possible finding of the disease,” said Iowa State Veterinarian Dr. David Schmitt.
Iowa has tested 42,557 wild deer and over 4,000 captive deer and elk as part of the surveillance program since 2002 when CWD was found in Wisconsin.
The DNR will increase testing of wild deer in the area by working with hunters and landowners to collect samples from hunter harvested deer beginning this fall.
CWD is a neurological disease that only affects deer, elk and moose. It is caused by an abnormal protein, called a prion, which affects the brains of infected animals, causing them to lose weight, display abnormal behavior and lose bodily functions. Signs include excessive salivation, thirst and urination, loss of appetite, progressive weight loss, listlessness and drooping ears and head.
The prions can attach to soil and spread the disease among deer. Chronic wasting disease was first identified in captive mule deer at a research facility in Colorado in 1967. Prior to the positive detection in Iowa, CWD had been detected in every bordering state.
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A Newsletter for the Iowa Sheep Industry ❖ December 2013
Scrapie Eradication Progress
by Gregory S. Schmitt, DVM
The National Scrapie Eradication Program (NSEP) started in 2001.
The goal for the NSEP is to have Scrapie eradicated by 2017.
U.S. Progress: This past Fiscal Year (FY13 = October 1, 2012 to September 30, 2013) there were 11 newly identified Infected and Source flocks in the nation.
Two of these were goat herds.
In Fiscal Year 2011 there were 15 newly identified Infected and Source flocks and in FY 2012 there were 8.
This is down from a high of 181 in FY 2005.
Iowa progress:
Until this year, Iowa’s last case of Scrapie was found in July 2010.
This fall Iowa identified 1 new Source and 4 new infected flocks in NW Iowa.
The 4 Infected flocks occurred as a result of sales of breeding sheep out of the Source flock to other sheep producers.
Flock cleanup is ongoing in these flocks.
There have been a total of 82 sheep flocks in Iowa that have been found to be infected with Scrapie since the accelerated National Scrapie Eradication Program (NSEP) started in November 2001.
In Fiscal Year 2005, Iowa had a high of 15 newly found Source or Infected flocks.
Iowa Animal Health News Volume 9, Issue 1 March, 2008
Iowa Progress: Since the program began in 11/01, 60 scrapie-infected flocks have been found in Iowa, with 7 of those found in 2007. Each year the number of flocks found to be infected with scrapie decreases in Iowa, so we are hopeful that we are making real progress. Most infected flocks are found through scrapie slaughter surveillance of adult breeding sheep. Although not all adult ewes are tested at slaughter, records show that among our Iowa sheep flocks with more than 50 head, that 70% of them have had at least one ewe sampled for scrapie at slaughter.
National Progress: As a result of a good collaborative effort between the sheep industry and the government, there has been a 34% decrease, between 2006 and 2007 in the percent of scrapie-positive sheep tested at slaughter, and the number of infected flocks also dropped by 38%. These drops were observed even though the number of sheep sampled at slaughter every year has increased. These numbers indicate that we are truly making progress in eradicating scrapie from the U.S. A total of 329 scrapie-infected sheep were found nationally testing during fiscal year 2007 through a combination of slaughter and on-the-farm testing. Twenty-four of those sheep were found in Iowa, with ten of those found at slaughter and the rest through on-the-farm testing that results from animals traced from infected flocks and animals found in infected flocks.
Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.
TUESDAY, JANUARY 12, 2021
Annual Scrapie Report Available for Fiscal Year 2020 USA October 1, 2019 to September 30, 2020
Research Paper
Management of chronic wasting disease in ranched elk: conclusions from a longitudinal three-year study
N.J. Haley,D.M. Henderson,R. Donner,S. Wyckoff,K. Merrett,J Tennant,
Pages 76-87 | Received 09 Oct 2019, Accepted 28 Jan 2020, Published online: 07 Feb 2020
Download citation https://doi.org/10.1080/19336896.2020.1724754
ABSTRACT
Chronic wasting disease is a fatal, horizontally transmissible prion disease of cervid species that has been reported in free-ranging and farmed animals in North America, Scandinavia, and Korea. Like other prion diseases, CWD susceptibility is partly dependent on the sequence of the prion protein encoded by the host’s PRNP gene; it is unknown if variations in PRNP have any meaningful effects on other aspects of health. Conventional diagnosis of CWD relies on ELISA or IHC testing of samples collected post-mortem, with recent efforts focused on antemortem testing approaches. We report on the conclusions of a study evaluating the role of antemortem testing of rectal biopsies collected from over 570 elk in a privately managed herd, and the results of both an amplification assay (RT-QuIC) and conventional IHC among animals with a several PRNP genotypes. Links between PRNP genotype and potential markers of evolutionary fitness, including pregnancy rates, body condition, and annual return rates were also examined. We found that the RT-QuIC assay identified significantly more CWD positive animals than conventional IHC across the course of the study, and was less affected by factors known to influence IHC sensitivity – including follicle count and PRNP genotype. We also found that several evolutionary markers of fitness were not adversely correlated with specific PRNP genotypes. While the financial burden of the disease in this herd was ultimately unsustainable for the herd owners, our scientific findings and the hurdles encountered will assist future CWD management strategies in both wild and farmed elk and deer.
KEYWORDS: Prion, elk, RAMALT, RT-QuIC, antemortem
snip...
This manuscript describes one such property, a herd of over 570 elk maintained on 3500 acres of fenced habitat in northwestern Colorado.
snip...
Return rate of CWD positive animals In the 2017 sampling period, 315 animals were tested for CWD antemortem. Of those, 71 tested positive by IHC, RT-QuIC, or both. Thirty-four infected animals (thirty-three cows and one bull) were euthanized and confirmed CWD positive post-mortem, with the remaining thirty-seven animals (Twenty-six bulls and eleven cows) released back onto the property. Of those animals which were released, four were harvested in the fall of 2017 and were found to be CWD positive post-mortem. Three of the remaining thirty (10%) returned for the 2018 sampling period, the remainder were lost in the field and went untested. All three were 132ML heterozygous animals, each positive again on antemortem testing in year three. In contrast, 120 of the 329 animals negative by antemortem testing were harvested in the fall of 2017, with 26 found to be CWD positive (21.7%). Of the remaining 209 animals, 141 returned for the 2018 sampling period (67.5%), with the remaining animals presumed lost in the field, untested. (Table 1 and Figure 1)
Over the course of the entire study, four of forty-nine CWD positive 132MM animals released back onto the property (8.2%) returned for a second year of sampling. Nine of thirty-three 132ML animals positive for CWD returned for a second year of sampling (27%), a return rate that was significantly greater than that of CWD positive 132MM animals (risk ratio: 3.34, p = 0.03). The lone 132LL cow identified during the course of antemortem testing in year two did not return for sampling in year three. Cumulatively, just 13 of 82 animals identified as CWD positive and released onto the property returned the following year (15.9%). These low rates of yearly return are in stark contrast to the cumulative return rate for CWD negative animals. For animals homozygous for the 132M allele, 107/144 returned in year two, and 28/69 returned in year three (63% overall). For 132ML heterozygous animals, 170/221 returned in year two, with 62/181 returning in year three (58% overall). Twenty-five of thirty-five animals homozygous for the 132L allele returned in year two, with fifteen of thirty-five returning in year three (57% overall). Cumulatively, 60% of animals negative for CWD returned the following year – a yearly return rate nearly over 3.5 times that of CWD positive animals (risk ratio: 3.62, p < 0.001; 95% confidence interval 1.96–6.69).
snip...
Discussion
While reports on the management of chronic wasting disease in wild deer and elk are many and varied [33–43], rare is the case presented for managing the disease in farmed cervids. Almost without exception, farmed cervids are immediately placed under quarantine and eventually depopulated when CWD is discovered on site [12]. This manuscript reports our efforts to manage CWD in a large elk herd, in a controlled setting with endemic CWD, through the use of annual live animal testing and targeted culling of CWD positive cows. Although the herd owners were presented with additional management directives, including culling of CWD positive bulls and those animals positive by an amplification assay (RT-QuIC), they were not implemented due to concern regarding its potential impact on hunting revenue. Ultimately, we could not completely evaluate our management practices, as the herd was slowly depopulated after the final sampling period due to the financial burden brought by the disease.
snip...see full text;
1999
Oklahoma:
-- In June,1998 CW) was diagnosed in a captive elk in Oklahoma.
-- The Oklahoma herd received more than 80 elk from commercial sources in Montana and Idaho.
-- Animals from the same origins as the Oklahoma herd went to 13 other ranches in Colorado, Idaho, Iowa, Montana, Nebraska, Alberta, and Saskatchewan in the past 11 years, plus many secondary movements. [8]
-- no control or surveillance program.
Utah:
-- one trace-back zoo in Salt Lake City from elk possibly associated to Oklahoma game farm.
-- One 30 year old hunter dying of CJD of unknown origin (not familial or iatrogenic).
-- 135 deer sampled in 1998, 90 tested, all negative so far, pathology done in-state. Unpublished UF&G.
Montana:
-- Single trace-back elk game farm under quarantine from Oklahoma case, though importer destroyed ear tag.
-- Single trace-forward elk game farm that had bought elk from trace-back game farm connected to Oklahoma
Montana to Survey for Chronic Wasting Disease
Montana FWP web site
During the upcoming fall big game hunting season, Fish, Wildlife & Parks' Wildlife Laboratory will be conducting surveys for Chronic Wasting Disease (CWD) in FWP administrative regions 2, 3, 4, 5 and 7. The surveys will include collection of heads from mule deer, white-tailed deer and elk. Sampled animals will be tagged at check stations to indicate that the head was removed for the CWD survey to prevent enforcement problems with evidence of sex. Specific brain tissues and tonsils will be extracted from the heads. Laboratory technicians will be assisting at several check stations to collect the tissues and these will be forwarded to a laboratory where histologic sections will be examined by a pathologist to look for lesions typical of CWD.
CWD has been identified in wild deer and elk in Colorado and Wyoming and in seven game farms in South Dakota, Nebraska, Oklahoma and Saskatchewan. For the past several years, Montana FWP monitored a limited number of big game animals for CWD and has found no evidence of the disease in free ranging wildlife. CWD was not believed to be present in Montana game farms until late June of this year, when the Department of Livestock notified FWP that a game farm elk reportedly shipped from Montana to Oklahoma was confirmed with CWD.
FWP has proposed increasing the surveillance for this disease in wild elk and deer. The surveillance will provide monitoring the southern perimeters of the state where the disease is most likely to naturally spread from Wyoming and Colorado. Emphasis will be placed on animals that are 1.5 years old and older of both sexes.
Tom Palmer of Montana FWP writes us about concerning a leaked "secret memo" circulating on the Internet:
"We don't have "internal" memos and this notion of something being "leaked" is odd. All of FWP's communications are open, public, and straight forward. The .memo released to the press by FWP and Gov. Marc Racicot. FWP is taking the CWD threat to wildlife very seriously.
Karen Zachheim, our Game Farm Coordinator, will send you any material requested .Should you want to talk to Karen about the CWD issue, call 406-444-4039, or Paul Sihler in the Director's office at 406-444-5620. If the material doesn't arrive early next week, please call me (406-444-3051)."
Montana has 93 game farms with 4,000 animals; 12 further facilities approved. Elk hunters pend an estimate $75 million per year for 22,000 elk, deer hunters $68 million to kill 75,000 mule deer and 60,000 white-tailed deer.
snip...
Montana to Survey for Chronic Wasting Disease
For Montanans, ultimately, the choice looms between the competing visions offered by Bob Spoklie and our Western neighbors. Montana lawmakers should follow Wyoming's lead and remove our wildlife heritage from the private marketplace.
***> For the sake of both the hunter and the hunted, private elk farms should be banned."
Trace-back: A game farm, zoo, or research facility that sold an elk or deer to a second facility where CWD was later positively diagnosed for the first time. The trace-back farm is presumed to be contaminated even if it has never reported CWD. Examples: Colorado has numerous trace-back game farms among the 11 in the Ft. Collins disease epicenter; improbably, none of these have ever reported CWD. Ear tags had been discarded in the Oklahoma CWD elk case, causing uncertainty in trace-back (limited to Montana, Idaho, or Utah).
-- The Oklahoma herd received more than 80 elk from commercial sources in Montana and Idaho.
-- Animals from the same origins as the Oklahoma herd went to 13 other ranches in Colorado, Idaho, Iowa, Montana, Nebraska, Alberta, and Saskatchewan in the past 11 years, plus many secondary movements. [8]
Montana:
-- Single trace-back elk game farm under quarantine from Oklahoma case, though importer destroyed ear tag.
-- Single trace-forward elk game farm that had bought elk from trace-back game farm connected to Oklahoma
Montana to Survey for Chronic Wasting Disease Montana FWP web site During the upcoming fall big game hunting season, Fish, Wildlife & Parks' Wildlife Laboratory will be conducting surveys for Chronic Wasting Disease (CWD) in FWP administrative regions 2, 3, 4, 5 and 7. The surveys will include collection of heads from mule deer, white-tailed deer and elk. Sampled animals will be tagged at check stations to indicate that the head was removed for the CWD survey to prevent enforcement problems with evidence of sex. Specific brain tissues and tonsils will be extracted from the heads. Laboratory technicians will be assisting at several check stations to collect the tissues and these will be forwarded to a laboratory where histologic sections will be examined by a pathologist to look for lesions typical of CWD. CWD has been identified in wild deer and elk in Colorado and Wyoming and in seven game farms in South Dakota, Nebraska, Oklahoma and Saskatchewan. For the past several years, Montana FWP monitored a limited number of big game animals for CWD and has found no evidence of the disease in free ranging wildlife. CWD was not believed to be present in Montana game farms until late June of this year, when the Department of Livestock notified FWP that a game farm elk reportedly shipped from Montana to Oklahoma was confirmed with CWD.
FWP has proposed increasing the surveillance for this disease in wild elk and deer. The surveillance will provide monitoring the southern perimeters of the state where the disease is most likely to naturally spread from Wyoming and Colorado. Emphasis will be placed on animals that are 1.5 years old and older of both sexes.
Tom Palmer of Montana FWP writes us about concerning a leaked "secret memo" circulating on the Internet:
"We don't have "internal" memos and this notion of something being "leaked" is odd. All of FWP's communications are open, public, and straight forward. The .memo released to the press by FWP and Gov. Marc Racicot. FWP is taking the CWD threat to wildlife very seriously.
Karen Zachheim, our Game Farm Coordinator, will send you any material requested .Should you want to talk to Karen about the CWD issue, call 406-444-4039, or Paul Sihler in the Director's office at 406-444-5620. If the material doesn't arrive early next week, please call me (406-444-3051)."
Montana has 93 game farms with 4,000 animals; 12 further facilities approved. Elk hunters pend an estimate $75 million per year for 22,000 elk, deer hunters $68 million to kill 75,000 mule deer and 60,000 white-tailed deer.
MONTANA
Karen Zachiem with Montana Parks and Wildlife reported that Montana allows game farming. Initial regulations were inadequate to protect the state's wildlife resources. The state has tried to tighten up regulations related to game farming, resulting in a series of lawsuits against the state from elk ranchers. Zachiem reported that the tightening of regulations was in response to the discovery of TB in wildlife (elk, deer, and coyotes) surrounding a TB infected game farm. TB has been found on several game farms in Montana. Also, they have had problems with wildlife entering game farms as well as game farm animals escaping the farms. Finally, there has been a growth in shooting ranches in Montana. Game farmers allow hunters to come into enclosures to kill trophy game farm animals, raising the issues of fair chase and hunting ethics.
Keep 'em wild: Montana should ban canned hunts. Whitefish elk farm draws fire from hunters, biologists By STEVE THOMPSON Missoula Independent, also the Whitefish Pilot 13 Sep 1998 Ph: 406/862-3795 Fax: 406/862-5344 "Although not everyone sees it the same way, Kalispell legislator Bob Spoklie says his controversial plan to develop an elk shooting gallery on 160 acres near Whitefish is rooted in the richest of Montana traditions-private property, pleasure and profit. Flaring like a bull elk in rut, Spoklie rages against those who disagree with his intentions. "These are not public wildlife," Spoklie told me angrily. "These are our animals and not anyone else's. We'll do as we please." If his political opponents succeed in banning canned elk hunts, Spoklie warns, the next step will be to eliminate all public hunting. "That's the real agenda here," he said.
By contrast, next door in Wyoming, the suggestion that Rocky Mountain elk can be penned, hand-fed and then shot is more than a disgusting notion. It's illegal. In fact, the Cowboy State has gone so far as to prohibit all private game farms. Utah also prohibits canned elk hunts. Listening to Spoklie, one might be convinced that Utah and Wyoming are governed by a bunch of socialist, animal-rights activists. But the truth is those states are hardly run by left-wing zealots. Rather, lawmakers there have chosen to honor a Western tradition as deeply rooted as Spoklie's rather crass libertarianism.
This conservation heritage was pioneered by Theodore Roosevelt and others who established wildlife as a public commons. Wildlife laws in those states seek to protect hunters' fair-chase pursuit of healthy, free-ranging game. According to Dick Sadler, a long-time Democratic legislator in Wyoming now retired, elk hunting farms violate the very spirit of the West. In the 1970s, he joined forces with Republican John Turner to pass landmark legislation which banned game farms. Sadler and Turner had researched game farms in other states, and they came away with a bitter taste.
Spoklie, however, says elk and other big game have been converted to private livestock around the world. "Montana is so far behind that we think we're leading," he says. As the founder of the Montana Alternative Livestock Association, Spoklie is clearly frustrated about the clamor surrounding his attempts to domesticate elk in Whitefish. But then he has been one of the chief lobbyists for the game farm industry. Due in large part to his influence, Montana legislators have resisted attempts to copy Wyoming's game farm ban, including former Florence Senator Terry Klampe's proposed moratorium in 1995.
But Sadler, a lifelong hunter, offers the following evidence for what's wrong with canned hunting: "I saw a film of one of those canned hunts in Michigan, where the guys get up and have a big breakfast, put on their hunting clothes, walk outside, shoot the animals in an enclosure and then congratulate themselves. "That was one of the most disgusting things I've ever seen."
As the proposal to ban game farms wound through the Wyoming legislature, though, Sadler focused on more pragmatic arguments. Today, he still complains about the threat of disease transmission to wild animals, genetic pollution and loss of habitat to enclosures.
It was the Republican Turner, who later became George Bush's Fish and Wildlife Service director, who invoked the West's sporting heritage. "Turner's argument to the legislature was that you can't take a magnificent animal like an elk and allow some slob to shoot it inside a fence," Sadler says. Ultimately, most Wyoming legislators agreed that it just wasn't proper to domesticate and commercialize a wild animal like elk.
To Spoklie's dismay, the debate locally is getting louder, and his loudest opponents are sportsmen. Making the biggest waves are the Montana Wildlife Federation, the Rocky Mountain Elk Foundation, Orion: The Hunter's Institute, and a coalition of neighbors and hunters in the Whitefish area.
Orion's founder Jim Posewitz, a retired wildlife biologist, says canned hunts jeopardize public acceptance of the real thing. A leading advocate of "fair chase" hunting, which emphasizes the almost sacred relationship between hunter and prey, Posewitz argues that the majority of non-hunting Americans will tolerate hunting only if it is conducted with the highest ethics. "Game farms are an abomination," he says.
Spoklie, an appointed lawmaker who recently lost the Republican primary election, dismisses such statements as "differences of philosophy" that don't stack up against private property rights. If someone's willing to pay thousands of dollars to shoot a penned elk, then that's good both for him and Montana's economy, he says.
Karen Zackheim, game farm coordinator for the state Department of Fish, Wildlife and Parks, says the issue goes beyond philosophy. The most pressing statewide concern, she says, is chronic wasting, an elk version of mad cow disease. The little known disease, for which there is neither a test nor a cure, recently killed captive elk in several Western states and has spread to wild game in some places. Zackheim also has identified other potential problems with the Spoklie elk farm.
Spoklie makes it clear that Zackheim and others should butt out. And some Montana lawmakers seem willing to listen to him, having recently stripped state wildlife officials of some oversight responsibilities. Now, Spoklie would prefer even less state oversight, including his permit application currently under review.
For Montanans, ultimately, the choice looms between the competing visions offered by Bob Spoklie and our Western neighbors. Montana lawmakers should follow Wyoming's lead and remove our wildlife heritage from the private marketplace. For the sake of both the hunter and the hunted, private elk farms should be banned."
Governments say Mr. McEwen, 30, has the classical strain, but some scientists question that diagnosis. They say it's possible the Utah man, who was an occasional hunter, is the first known victim of a newer strain contracted by eating deer and elk -- much the same way some in Britain contracted "mad cow disease" from eating infected beef in the 1980s.
Sent: Mon, Feb 3, 2020 11:43 am
Subject: Montana Chronic Wasting Disease CWD TSE Prion in Eastern Part of State Game Farm Elk
Montana Chronic Wasting Disease CWD TSE Prion in Eastern Part of State Game Farm Elk
Shultz, Thomas / Monday, February 3, 2020 / Categories: Department of Livestock
Chronic Wasting Disease (CWD) in Eastern Montana Game Farm Elk
FOR IMMEDIATE RELEASE:
January 31, 2020
CONTACT:
Dr. Tahnee Szymanski, MT Dept. of Livestock, (406) 444–5214, tszymanski@mt.gov
Dr. Marty Zaluski, MT Dept. of Livestock, (406) 444 –2043, mzaluski@mt.gov
The Department of Livestock Reports Finding of Chronic Wasting Disease (CWD) in Eastern Montana Game Farm Elk
Helena, Mont.- On January 31, 2020, the Montana Department of Livestock reported that a single game farm elk in eastern Montana has been confirmed positive for Chronic Wasting Disease (CWD). The disease has not been identified in domestic cervids in Montana since 1999.
The CWD positive animal was found as a result of surveillance required by the United States Department of Agriculture CWD Herd Certification Program (HCP) which requires all deaths in captive animals greater than 12 months of age be tested. The affected animal appeared healthy and was slaughtered for meat. The infection was confirmed by the National Veterinary Services Laboratories in Ames, Iowa through the identification of the prion in tissue samples collected from the animal.
The Department placed the herd under quarantine and is conducting an epidemiological investigation. Montana law requires CWD positive game farm herds undergo complete depopulation and post-mortem herd testing, or quarantine of the entire herd for a period of five years from the last CWD positive case.
“An epidemiologic investigation will be conducted, but at this time, the source of the disease is unknown,” stated State Veterinarian Dr. Marty Zaluski. “We will look at historical elk movements associated with this captive herd and proximity to infected wildlife to try to determine the source of exposure.”
Montana Fish Wildlife and Parks (FWP) has documented CWD in wild cervids across much of Montana through surveillance that began in 2017. In 2019, approximately 7,000 wild deer, elk, and moose were sampled statewide, with 140 testing positive for CWD.
CWD is a progressive, fatal disease that affects the nervous system of white-tailed deer, mule deer, elk, and moose. Transmission can occur through direct contact between animals, urine, feces, saliva, blood and antler velvet. Infected carcasses may serve as a source of environmental contamination and can infect other animals. Infected animals may carry the disease for years without showing signs of illness, but in later stages, signs may include progressive weight loss, lack of coordination and physical debilitation.
There is no known transmission of CWD to humans. However, the Centers for Disease Control and Prevention (CDC) recommends hunters harvesting an animal in areas with a known CWD presence have their animal tested. If the animal tests positive, the CDC advises against eating the meat.
The mission of the Montana Department of Livestock is to control and eradicate animal diseases, prevent the transmission of animal diseases to humans, and to protect the livestock industry from theft and predatory animals. For more information on the Montana Department of Livestock, visit http://liv.mt.gov/.
***Oklahoma CWD TSE Prion
Oklahoma, to date, CWD has been detected in 6 cases of CWD TSE Prion documented to date in Captive Cervid...tss
1st cwd positive captive 1998, 2nd cwd positive captive 2019, 3 cwd positives from that herd depopulation, with 1 additional Trace Out CWD Trace Out Positive, equal to date 6 captive CWD positives in Oklahoma to date, and since my confirming these figures the last time via phone, i am told now i will have to fill out a FOIA request for any further reports of CWD TSE Prion in captive herds in Oklahoma.
THURSDAY, NOVEMBER 19, 2020
Oklahoma Proper Carcass Disposal Cervid Importation with 6 cases of CWD TSE Prion documented to date in Captive Cervid
TUESDAY, JANUARY 07, 2020
Oklahoma Farmed Elk Lincoln County CWD Depopulation 3 Positive Elk with 1 Additional Dead Trace Out Confirmed Positive
FRIDAY, FEBRUARY 07, 2020
Montana 142 animals tested positive for CWD thus far during 2019/20 sampling
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...
(the map on page 71, cwd marked in red, is shocking...tss)
CWD Advisory Group
Testing Waiver
A Colorado alternative livestock producer who has had no CWD positive tests in the previous 60 months and who has had at least 60 months of CWD surveillance status may apply for a waiver from the mandatory surveillance requirements. Application to Waive CWD Sample Submission for Imported Elk
ORIGIN OF CHRONIC WASTING DISEASE TSE PRION?
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;
''it pains me to no end to even contemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA viewed it as a wildlife problem and consequently not their province!” page 26.
SATURDAY, FEBRUARY 01, 2020
Colorado confirmed CWD TSE Prion in 24 game management units in the state where it previously hadn’t been found
THURSDAY, MAY 14, 2020
COLORADO As of February 2020, CWD has been detected in 33 of 54 deer herds, 14 of 43 elk herds, and 2 of 9 moose herds
SUMMARY MINUTES OF THE 407th COMMISSION MEETING Texas Animal Health Commission
September 22, 2020
Chronic Wasting Disease (CWD):
A new CWD positive breeding herd was disclosed in February 2020 in Kimble County. This herd depopulation was completed in July 2020. Including the two index positive deer, an additional eight more positive deer were disclosed (approximate herd prevalence 12%). Since July 2015 and prior to this discovery, five positive captive breeder herds have been disclosed and four of those are in Medina County. One herd in Lavaca and three herds in Medina County were depopulated leaving one large herd in Medina County that is managed on a herd plan. A new zone was established in Val Verde County in December 2019 as a result of a positive free-ranging White-tailed Deer (WTD). A second positive WTD was also disclosed in February 2020 in the same area.
Item 17 – Consideration of and Possible Action on Regulation ADOPTION Regarding Ms. Mary Luedeker provided the background and overview of the regulation proposal.
(a) Chapter 40, Chronic Wasting Disease
On December 18, 2019, the commission received confirmation that a free ranging 5.5-year-old female white-tailed deer killed in Val Verde County tested positive for CWD. The Executive Director issued an order declaring a high-risk containment zone for portions of Val Verde County on December 20, 2019. This proposed rulemaking would replace the Executive Order and establish a Containment Zone (CZ) 4 in §40.6(b)(1)(D) and Surveillance Zone (SZ) 4 in §40.6(b)(2)(D) for Val Verde County.
40.6(b)(1)(D) Containment Zone 4. That portion of the state lying within the boundaries of a line beginning in Val Verde County at the International Bridge and proceeding northeast along Spur 239 to U.S. 90; thence north along U.S. 90 to the intersection of U.S. 277/377, thence north along U.S. 277/377 to the U.S. 277/377 bridge at Lake Amistad (29.496183°, -100.913355°), thence west along the southern shoreline of Lake Amistad to International Boundary at Lake Amistad dam, thence south along the Rio Grande River to the International Bridge on Spur 239. 40.6(b)(2)(D) Surveillance Zone 4. That portion of the state lying within a line beginning in Val Verde County at the confluence of Sycamore Creek and the Rio Grande River (29.242341°, - 100.793906°); thence northeast along Sycamore Creek to U.S. 277; thence northwest on U.S. 277 to Loop 79; thence north along Loop 79 to the Union Pacific Railroad; thence east along the Union Pacific Railroad to Liberty Drive (north entrance to Laughlin Air Force Base); thence north along Liberty Drive to U.S. 90; thence west along U.S. 90 to Loop 79; thence north along Loop 79 to the American Electric Power (AEP) Ft. Lancaster-to-Hamilton Road 138kV transmission line (29.415542°, -100.847993°); thence north along the AEP Ft. Lancaster-to-Hamilton Road 138kV transmission line to a point where the AEP Ft. Lancaster-to-Hamilton Road 138kV transmission line turns northwest (29.528552°, -100.871618°); thence northwest along the AEP Ft. Lancasterto-Hamilton Road 138kV transmission line to the AEP Ft. Lancaster-to-Hamilton Road maintenance road (29.569259°, -100.984758°); thence along the AEP Ft. Lancaster-to-Hamilton Road maintenance road to Spur 406; thence northwest along Spur 406 to U.S. 90; thence south along U.S. 90 to Box Canyon Drive; thence west along Box Canyon Drive to Bluebonnet Drive; thence southwest along Bluebonnet Drive to Lake Drive; thence south along Lake Drive to Lake Amistad (29.513298°, -101.172454°), thence southeast along the International Boundary to the International Boundary at the Lake Amistad dam; thence southeast along the Rio Grande River to the confluence of Sycamore Creek (29.242341°, -100.793906°).
On January 28, 2020, the commission received confirmation that a 4.5-year-old male white-tailed deer and a 3.5-year-old female white-tailed deer killed in Medina County tested positive for CWD. The proposed amendment takes the location of these mortalities into consideration and establishes Containment Zone 3 boundaries in §40.6(b)(1)(C) for Medina and Uvalde counties. The proposed
13
SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020
change to §40.6(b)(2)(C) extends the surveillance zone boundaries from F.M. 187 to the Sabinal River in Uvalde County.
40.6(b)(1)(C) Containment Zone 3. That portion of the state lying within Bandera, Medina and Uvalde counties and depicted in the following figure and more specifically described by the following latitude-longitude coordinate pairs:
Boundaries consist of properties under the same ownership or management for facilities operating under a herd plan due to a positive result in a CWD susceptible species in Medina and Uvalde counties.
40.6(b)(2)(C) Surveillance Zone 3. That portion of the state within the boundaries of a line beginning at U.S. 90 in Hondo in Medina County; thence west along U.S. 90 to the Sabinal River F.M. 187 in Uvalde County; thence north along F.M. 187 to F.M. 470 in Bandera County; thence east along F.M. 470 to Tarpley in Bandera County; thence south along F.M. 462 to U.S. 90 in Hondo.
On February 26, 2020, the commission received confirmation that a 5.5-year-old female white-tailed deer held in a deer breeding facility in Kimble County tested positive for CWD. The proposed amendment would establish Surveillance Zone 5 in Kimble County in §40.6(b)(2)(E). This proposal does not create a CZ in Kimble County because the detection was in a breeder deer facility, which is required by law to be designed and built to both prevent the free movement of deer and contact with freeranging deer. Second, the facility where CWD was discovered is operating under a commission herd plan, which restricts deer movement and requires CWD testing at an equal or higher level to what is required in a CZ.
40.6(b)(2)(E) Surveillance Zone 5. That portion of the state lying within the boundaries of a line beginning on U.S. 83 at the Kerr/Kimble County line; thence north along U.S. 83 to I.H. 10; thence northwest along on I.H. 10 to F.M. 2169; thence east along F.M. 2169 to County Road (C.R.) 410; thence east along C.R. 410 to C.R. 412; thence south along C.R. 412 to C.R. 470; thence east along C.R. 470 to C.R. 420; thence south along C.R. 420 to F.M. 479; thence east along F.M. 479 to C.R. 433; thence south along C.R. 433 to U.S. 290; thence west along U.S. 290 to I.H. 10; thence southeast along I.H. 10 to the Kerr/Kimble County line; thence west along the Kerr/Kimble County line to U.S. 83.
An opportunity for public comment was offered and instructions for unmuting lines and for the speaker to identify themselves was detailed. There was no public comment concerning the Rule Adoption. The motion to ADOPT the amendments to Chapter 40, Chronic Wasting Disease passed.
SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020
Scrapie: The flock identified in April 2016 remains under quarantine in Hartley County.
WEDNESDAY, SEPTEMBER 09, 2020
TEXAS TAHC CWD TSE Prion SUMMARY MINUTES OF THE 406th COMMISSION MEETING
FRIDAY, OCTOBER 16, 2020
TAHC Rules and Resources for Harvesting Exotic CWD Susceptible Species this 2020-21 Hunting Season
Sent: Sun, Aug 30, 2020 10:37 am
Subject: Texas CWD TSE Prion 3 More Documented, 185 Cases To Date
Texas CWD TSE Prion 3 More Documented, 185 Cases To Date
Sent: Thu, Jul 9, 2020 10:00 am
Subject: Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date
CWD Positives in Texas
CWD Positive
Confirmation Date Free Range/Captive County Source Species Sex Age
2020-07-30 Breeder Deer Kimble Facility #6 White-tailed Deer M 3
2020-07-29 Free Range El Paso N/A Mule Deer M 2.5
2020-06-25 Free Range El Paso N/A Mule Deer F 5.5
SUNDAY, AUGUST 30, 2020
Texas CWD TSE Prion 3 More Documented, 185 Cases To Date
Subject: Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date
Texas CWD TSE Prion Jumps To 182 Confirmed Cases
2020-06-25 Free Range El Paso N/A Mule Deer F 5.5
2020-06-16 Free Range El Paso N/A Mule Deer M 5.5
2020-06-10 Breeder Release Site Medina Facility #3 White-tailed Deer F 5.5
2020-06-10 Breeder Release Site Medina Facility #3 White-tailed Deer M 3.5
2020-06-10 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 5.5
2020-06-09 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 2.5
2020-06-09 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 4.5
2020-05-22 Free Range Hartley N/A Mule Deer M 4.5
2020-05-22 Free Range Hartley N/A Mule Deer F 5.5
2020-05-22 Free Range Hartley N/A Mule Deer M 4.5
2020-05-22 Free Range Dallam N/A Mule Deer M 2.5
2020-05-22 Free Range Hartley N/A Mule Deer M 5.5
2020-05-22 Free Range Hartley N/A Mule Deer M 5.5
SUNDAY, MARCH 08, 2020
Texas CWD TSE Prion Confirms 169 Positive To Date
THURSDAY, JULY 09, 2020
Texas CWD TSE Prion Jumps BY 13 To 182 Confirmed Cases To Date
SATURDAY, JULY 04, 2020
TAHC CHAPTER 40 CHRONIC WASTING DISEASE 406th COMMISSION MEETING AGENDA June 23, 2020 8:30 A.M.
TUESDAY, JANUARY 28, 2020
Mississippi MDWFP North MS CWD Management Zone Since October 2019, 25 CWD-positive deer have been detected from this zone
CWD WEBINAR CWD YESTERDAY! December 11, 2019
Dr. Mckenzie and CIDRAP on CWD TSE Prion
122: Prions and Chronic Wasting Disease with Jason Bartz
Texas CWD Symposium: Transmission by Saliva, Feces, Urine & Blood
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
''On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis. ''
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO
cwd update on Wisconsin from Tammy Ryan...
Wyoming CWD Dr. Mary Wood
''first step is admitting you have a problem''
''Wyoming was behind the curve''
wyoming has a problem...
TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?
OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?
apparently, no ID though. tell me it ain't so please...
23:00 minute mark
''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''
Wyoming CWD Dr. Mary Wood
''first step is admitting you have a problem''
''Wyoming was behind the curve''
wyoming has a problem...
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
SATURDAY, JANUARY 19, 2019
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
FRIDAY, DECEMBER 20, 2019
TEXAS ANIMAL HEALTH COMMISSION EXECUTIVE DIRECTOR ORDER DECLARING A CHRONIC WASTING DISEASE HIGH RISK AREA CONTAINMENT ZONE FOR PORTIONS OF VAL VERDE COUNTY
TUESDAY, DECEMBER 31, 2019
In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus
SUNDAY, AUGUST 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
SUNDAY, FEBRUARY 16, 2020
***> Jerking for Dollars, Are Texas Politicians and Legislators Masturbating Deer For Money, and likely spreading CWD TSE Prion?
TUESDAY, FEBRUARY 04, 2020
TEXAS REPORTS 20 NEW CWD TSE PRION CASES 3 WILD 17 BREEDER 166 POSITIVE TO DATE
FRIDAY, MAY 22, 2020
TPW Commission has adopted rules establishing Chronic Wasting Disease (CWD) management zones to further detection and response efforts among WTD
SUNDAY, MARCH 01, 2020
Texas As one CWD investigation continues, another launches...THE FULL MONTY!
SATURDAY, DECEMBER 02, 2017
TEXAS TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play
SUNDAY, JANUARY 22, 2017
Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry
*** TEXAS TAHC OLD STATISTICS BELOW FOR PAST CWD TESTING ***
CWD TEXAS TAHC OLD FILE HISTORY
updated from some of my old files, some of the links will not work.
*** Subject: CWD testing in Texas ***
Date: Sun, 25 Aug 2002 19:45:14 –0500
From: Kenneth Waldrup
To: flounder@wt.net
snip...see ;
MONDAY, AUGUST 14, 2017
*** Texas Chronic Wasting Disease CWD TSE Prion History ***
2021 Transmissible Spongiform Encephalopathy TSE Prion End of Year Report 2020
CJD FOUNDATION VIRTUAL CONFERENCE CJD Foundation Research Grant Recipient Reports Panel 2 Nov 3, 2020
zoonotic potential of PMCA-adapted CWD PrP 96SS inoculum
4 different CWD strains, and these 4 strains have different potential to induce any folding of the human prion protein.
***> PIGS, WILD BOAR, CWD <***
***> POPULATIONS OF WILD BOARS IN THE UNITED STATES INCREASING SUPSTANTUALLY AND IN MANY AREAS WE CAN SEE A HIGH DENSITY OF WILD BOARS AND HIGH INCIDENT OF CHRONIC WASTING DISEASE
HYPOTHOSIS AND SPECIFIC AIMS
HYPOTHOSIS
BSE, SCRAPIE, AND CWD, EXPOSED DOMESTIC PIGS ACCUMULATE DIFFERENT QUANTITIES AND STRAINS OF PRIONS IN PERIPHERAL TISSUES, EACH ONE OF THEM WITH PARTICULAR ZOONOTIC POTENTIALS
Final Report – CJD Foundation Grant Program A.
Project Title: Systematic evaluation of the zoonotic potential of different CWD isolates. Principal Investigator: Rodrigo Morales, PhD.
Systematic evaluation of the zoonotic potential of different CWD isolates. Rodrigo Morales, PhD Assistant Professor Protein Misfolding Disorders lab Mitchell Center for Alzheimer’s disease and Related Brain Disorders Department of Neurology University of Texas Health Science Center at Houston Washington DC. July 14th, 2018
Conclusions and Future Directions • We have developed a highly sensitive and specific CWD-PMCA platform to be used as a diagnostic tool. • Current PMCA set up allow us to mimic relevant prion inter-species transmission events. • Polymorphic changes at position 96 of the prion protein apparently alter strain properties and, consequently, the zoonotic potential of CWD isolates. • Inter-species and inter-polymorphic PrPC → PrPSc conversions further increase the spectrum of CWD isolates possibly present in nature. • CWD prions generated in 96SS PrPC substrate apparently have greater inter-species transmission potentials. • Future experiments will explore the zoonotic potential of CWD prions along different adaptation scenarios, including inter-species and inter-polymorphic.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item MOORE, SARAH - Orise Fellow item Kunkle, Robert item KONDRU, NAVEEN - Iowa State University item MANNE, SIREESHA - Iowa State University item SMITH, JODI - Iowa State University item KANTHASAMY, ANUMANTHA - Iowa State University item WEST GREENLEE, M - Iowa State University item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 month challenge groups). The remaining pigs (>6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP
Author item MOORE, S - Orise Fellow item Kokemuller, Robyn item WEST-GREENLEE, M - Iowa State University item BALKEMA-BUSCHMANN, ANNE - Friedrich-Loeffler-institut item GROSCHUP, MARTIN - Friedrich-Loeffler-institut item Greenlee, Justin Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 5/10/2018 Publication Date: 5/22/2018 Citation: Moore, S.J., Kokemuller, R.D., West-Greenlee, M.H., Balkema-Buschmann, A., Groschup, M.H., Greenlee, J.J. 2018. The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP. Prion 2018, Santiago de Compostela, Spain, May 22-25, 2018. Paper No. WA15, page 44.
Interpretive Summary:
Technical Abstract: We have previously shown that the chronic wasting disease (CWD) agent from white-tailed deer can be transmitted to domestic pigs via intracranial or oral inoculation although with low attack rates and restricted PrPSc accumulation. The objective of this study was to assess the potential for cross-species transmission of pig-passaged CWD using bioassay in transgenic mice. Transgenic mice expressing human (Tg40), bovine (TgBovXV) or porcine (Tg002) PRNP were inoculated intracranially with 1% brain homogenate from a pig that had been intracranially inoculated with a pool of CWD from white-tailed deer. This pig developed neurological clinical signs, was euthanized at 64 months post-inoculation, and PrPSc was detected in the brain. Mice were monitored daily for clinical signs of disease until the end of the study. Mice were considered positive if PrPSc was detected in the brain using an enzyme immunoassay (EIA). In transgenic mice expressing porcine prion protein the average incubation period was 167 days post-inoculation (dpi) and 3/27 mice were EIA positive (attack rate = 11%). All 3 mice were found dead and clinical signs were not noted prior to death. One transgenic mouse expressing bovine prion protein was euthanized due to excessive scratching at 617 dpi and 2 mice culled at the end of the study at 700 dpi were EIA positive resulting in an overall attack rate of 3/16 (19%). None of the transgenic mice expressing human prion protein that died or were euthanized up to 769 dpi were EIA positive and at study end point at 800 dpi 2 mice had positive EIA results (overall attack rate = 2/20 = 10%). The EIA optical density (OD) readings for all positive mice were at the lower end of the reference range (positive mice range, OD = 0.266-0.438; test positive reference range, OD = 0.250-4.000). To the authors’ knowledge, cervid-derived CWD isolates have not been successfully transmitted to transgenic mice expressing human prion protein. The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
MONDAY, JANUARY 04, 2021
NC1209: North American interdisciplinary chronic wasting disease research consortium Singeltary Submission January 2021
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, AUGUST 1997 MAD COW FEED BAN WAS A SHAM, AS I HAVE STATED SINCE 1997! 3 FAILSAFES THE FDA ET AL PREACHED AS IF IT WERE THE GOSPEL, IN TERMS OF MAD COW BSE DISEASE IN USA, AND WHY IT IS/WAS/NOT A PROBLEM FOR THE USA, and those are;
BSE TESTING (failed terribly and proven to be a sham)
BSE SURVEILLANCE (failed terribly and proven to be a sham)
BSE 589.2001 FEED REGULATIONS (another colossal failure, and proven to be a sham)
these are facts folks. trump et al just admitted it with the feed ban.
see;
FDA Reports on VFD Compliance
John Maday
August 30, 2019 09:46 AM VFD-Form 007 (640x427)
Before and after the current Veterinary Feed Directive rules took full effect in January, 2017, the FDA focused primarily on education and outreach. ( John Maday ) Before and after the current Veterinary Feed Directive (VFD) rules took full effect in January, 2017, the FDA focused primarily on education and outreach to help feed mills, veterinarians and producers understand and comply with the requirements. Since then, FDA has gradually increased the number of VFD inspections and initiated enforcement actions when necessary. On August 29, FDA released its first report on inspection and compliance activities. The report, titled “Summary Assessment of Veterinary Feed Directive Compliance Activities Conducted in Fiscal Years 2016 – 2018,” is available online.
SUNDAY, SEPTEMBER 1, 2019
***> FDA Reports on VFD Compliance
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
THURSDAY, SEPTEMBER 26, 2019
Veterinary Biologics Guideline 3.32E: Guideline for minimising the risk of introducing transmissible spongiform encephalopathy prions and other infectious agents through veterinary biologics
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
snip...
[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
snip...see full archive and more of this;
MONDAY, NOVEMBER 23, 2020
***> Chronic Wasting Disease CWD TSE Prion Cervid State by State and Global Update November 2020
MONDAY, NOVEMBER 30, 2020
***> REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRION
see updated concerns with atypical BSE from feed and zoonosis...terry
THE tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
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]
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
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
PRION CONFERENCE 2010 ABSTRACT REFERENCE
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
The effectiveness of on-farm decontamination methods for scrapie - SE1865
Description
Scrapie infectivity persists on farms where infected animals have been removed1. Recently we have demonstrated that it is possible to detect environmental scrapie contamination biochemically using serial Protein Misfolding Cyclic Amplification (sPMCA)2, allowing the monitoring of scrapie infectivity on farm premises. Ongoing Defra study SE1863 has compared pen decontamination regimes on a scrapie-infected farm by both sheep bioassay and sPMCA. For bioassay, scrapie-free genetically susceptible lambs were introduced into pens decontaminated using distinct methodologies, all pens contained scrapie-positive lambs within 1 year. Remarkably this included lambs housed within a pen which had been jet washed/chloros treated, followed by regalvanisation/ replacement of all metalwork and painting of all other surfaces.
We have recently demonstrated using sPMCA, that material collected on swabs from vertical surfaces at heights inaccessible to sheep within a barn on the same scrapie affected farm contained scrapie prions (unpublished observations). We hypothesise that scrapie prions are most likely to have been deposited in these areas by bioaerosol movement. We propose that this bioaerosol movement contributes to scrapie transmission within the barn, and could account for the sheep that became positive within the pen containing re-galvanised/new metalwork and repainted surfaces (project SE1863). It is proposed that a thorough decontamination that would minimise prion-contaminated dust, both within the building and its immediate vicinity, is likely to increase the effectiveness of current methods for decontaminating farm buildings following outbreaks of scrapie. The proposed study builds on our previous data and will thoroughly investigate the potential for farm building scrapie-contamination via the bioaerosol route, a previously unrecognised route for dissemination of scrapie infectivity. This route could lead to the direct infection of healthy animals and/or indirect transmission of disease via contamination of surfaces within animal pens. The proposed study would analyse material collected using air samplers set up within “scrapie-infected” barns and their immediate vicinity, to confirm that prion containing material can be airborne within a scrapie infected farm environment. The study would incorporate a biochemical assessment of different surface decontamination methods, in order to demonstrate the best methodology and then the analysis of air and surface samples after a complete building decontamination to remove sources of dust and surface bound prions from both the building and its immediate vicinity. Analysis of such surface and air samples collected before and after treatment would measure the reduction in levels of infectivity. It is envisaged that the biochemical demonstration of airborne prions and the effective reduction in such prion dissemination would lead to a sheep bioassay experiment that would be conducted after a full farm decontamination. This would fully assess the effectiveness of an optimised scrapie decontamination strategy.
This study will contribute directly to Defra policy on best practice for on-farm decontamination after outbreaks of scrapie; a situation particularly relevant to decontamination after scrapie cases on goat farms where no genetic resistance to scrapie has currently been identified, and where complete decontamination is essential in order to stop recurrence of scrapie after restocking.
Objective
Phase 1
• Determine the presence and relative levels of airborne prions on a scrapie infected farm.
• Evaluate different pen surface decontamination procedures.
Phase 2
• Determine the presence of any airborne prions in a barn after a full decontamination.
Phase 3
• Further assess the efficacy of the decontamination procedure investigated in phase 2 by sheep bioassay.
Time-Scale and Cost
From: 2012
To: 2016
Cost: £326,784
Contractor / Funded Organisations
A D A S UK Ltd (ADAS)
Keywords Animals Fields of Study Animal Health
The Effectiveness of on-Farm Decontamination Methods for Scrapie
Institutions ADAS
Start date 2012
End date 2016
Objective Phase 1
Determine the presence and relative levels of airborne prions on a scrapie infected farm. Evaluate different pen surface decontamination procedures.
Phase 2
Determine the presence of any airborne prions in a barn after a full decontamination.
Phase 3
Further assess the efficacy of the decontamination procedure investigated in phase 2 by sheep bioassay.
More information
Scrapie infectivity persists on farms where infected animals have been removed1. Recently we have demonstrated that it is possible to detect environmental scrapie contamination biochemically using serial Protein Misfolding Cyclic Amplification (sPMCA)2, allowing the monitoring of scrapie infectivity on farm premises. Ongoing Defra study SE1863 has compared pen decontamination regimes on a scrapie-infected farm by both sheep bioassay and sPMCA. For bioassay, scrapie-free genetically susceptible lambs were introduced into pens decontaminated using distinct methodologies, all pens contained scrapie-positive lambs within 1 year. Remarkably this included lambs housed within a pen which had been jet washed/chloros treated, followed by regalvanisation/replacement of all metalwork and painting of all other surfaces.
We have recently demonstrated using sPMCA, that material collected on swabs from vertical surfaces at heights inaccessible to sheep within a barn on the same scrapie affected farm contained scrapie prions (unpublished observations). We hypothesise that scrapie prions are most likely to have been deposited in these areas by bioaerosol movement. We propose that this bioaerosol movement contributes to scrapie transmission within the barn, and could account for the sheep that became positive within the pen containing re-galvanised/new metalwork and repainted surfaces (project SE1863). It is proposed that a thorough decontamination that would minimise prion-contaminated dust, both within the building and its immediate vicinity, is likely to increase the effectiveness of current methods for decontaminating farm buildings following outbreaks of scrapie. The proposed study builds on our previous data and will thoroughly investigate the potential for farm building scrapie contamination via the bioaerosol route, a previously unrecognised route for dissemination of scrapie infectivity. This route could lead to the direct infection of healthy animals and/or indirect transmission of disease via contamination of surfaces within animal pens. The proposed study would analyse material collected using air samplers set up within “scrapie-infected” barns and their immediate vicinity, to confirm that prion containing material can be airborne within a scrapie infected farm environment. The study would incorporate a biochemical assessment of different surface decontamination methods, in order to demonstrate the best methodology and then the analysis of air and surface samples after a complete building decontamination to remove sources of dust and surface bound prions from both the building and its immediate vicinity. Analysis of such surface and air samples collected before and after treatment would measure the reduction in levels of infectivity. It is envisaged that the biochemical demonstration of airborne prions and the effective reduction in such prion dissemination would lead to a sheep bioassay experiment that would be conducted after a full farm decontamination. This would fully assess the effectiveness of an optimised scrapie decontamination strategy.
This study will contribute directly to Defra policy on best practice for on-farm decontamination after outbreaks of scrapie; a situation particularly relevant to decontamination after scrapie cases on goat farms where no genetic resistance to scrapie has currently been identified, and where complete decontamination is essential in order to stop recurrence of scrapie after restocking.
Funding Source
Department for Environment, Food and Rural Affairs
Project source
View this project
Project number
SE1865
Categories
Foodborne Disease
Policy and Planning
Circulation of prions within dust on a scrapie affected farm
Kevin C Gough1 , Claire A Baker2 , Hugh A Simmons3 , Steve A Hawkins3 and Ben C Maddison2*
Abstract
Prion diseases are fatal neurological disorders that affect humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk are contagious prion diseases where environmental reservoirs have a direct link to the transmission of disease. Using protein misfolding cyclic amplification we demonstrate that scrapie PrPSc can be detected within circulating dusts that are present on a farm that is naturally contaminated with sheep scrapie. The presence of infectious scrapie within airborne dusts may represent a possible route of infection and illustrates the difficulties that may be associated with the effective decontamination of such scrapie affected premises.
snip...
Discussion We present biochemical data illustrating the airborne movement of scrapie containing material within a contaminated farm environment. We were able to detect scrapie PrPSc within extracts from dusts collected over a 70 day period, in the absence of any sheep activity. We were also able to detect scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m distance away from the scrapie contaminated buildings, suggesting that the chance of contamination of pasture by scrapie contaminated dusts decreases with distance from contaminated farm buildings. PrPSc amplification by sPMCA has been shown to correlate with infectivity and amplified products have been shown to be infectious [14,15]. These experiments illustrate the potential for low dose scrapie infectivity to be present within such samples. We estimate low ng levels of scrapie positive brain equivalent were deposited per m2 over 70 days, in a barn previously occupied by sheep affected with scrapie. This movement of dusts and the accumulation of low levels of scrapie infectivity within this environment may in part explain previous observations where despite stringent pen decontamination regimens healthy lambs still became scrapie infected after apparent exposure from their environment alone [16]. The presence of sPMCA seeding activity and by inference, infectious prions within dusts, and their potential for airborne dissemination is highly novel and may have implications for the spread of scrapie within infected premises. The low level circulation and accumulation of scrapie prion containing dust material within the farm environment will likely impede the efficient decontamination of such scrapie contaminated buildings unless all possible reservoirs of dust are removed. Scrapie containing dusts could possibly infect animals during feeding and drinking, and respiratory and conjunctival routes may also be involved. It has been demonstrated that scrapie can be efficiently transmitted via the nasal route in sheep [17], as is also the case for CWD in both murine models and in white tailed deer [18-20].
The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease
Author
item Greenlee, Justin item Moore, S - Orise Fellow item Smith, Jodi - Iowa State University item Kunkle, Robert item West Greenlee, M - Iowa State University Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: 8/12/2015 Publication Date: N/A Citation: N/A
Interpretive Summary:
Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.
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.
SOURCE REFERENCE 2018 PRION CONFERENCE ABSTRACT
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research
Title: Horizontal transmission of chronic wasting disease in reindeer
Author
item MOORE, SARAH - ORISE FELLOW item KUNKLE, ROBERT item WEST GREENLEE, MARY - IOWA STATE UNIVERSITY item Nicholson, Eric item RICHT, JUERGEN item HAMIR, AMIRALI item WATERS, WADE item Greenlee, Justin
Submitted to: Emerging Infectious Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/29/2016
Publication Date: 12/1/2016
Citation: Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.
Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD.
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal prion disease of cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, and CWD was recently reported in a free-ranging reindeer of Norway. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer, non-inoculated negative control reindeer were introduced into the same pen as the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to the CWDmd inoculated reindeer (indirect contact; n=2). Experimentally inoculated reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrPcwd). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (months PI). PrPcwd was detected in 5 out of 6 sentinel reindeer although only 2 out of 6 developed clinical disease during the study period (< 57 months PI). We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naïve reindeer both directly and indirectly.
***> 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.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
Gudmundur Georgsson1, Sigurdur Sigurdarson2, Paul Brown3
First Published: 01 December 2006 https://doi.org/10.1099/vir.0.82011-0 ABSTRACT 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 sheep-house 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.
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.
source reference Prion Conference 2015 abstract book
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
Sandra Pritzkow,1 Rodrigo Morales,1 Fabio Moda,1,3 Uffaf Khan,1 Glenn C. Telling,2 Edward Hoover,2 and Claudio Soto1, * 1Mitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, 6431 Fannin Street, Houston, TX 77030, USA
2Prion Research Center, Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA
3Present address: IRCCS Foundation Carlo Besta Neurological Institute, 20133 Milan, Italy *Correspondence: claudio.soto@uth.tmc.edu http://dx.doi.org/10.1016/j.celrep.2015.04.036
SUMMARY
Prions are the protein-based infectious agents responsible for prion diseases. Environmental prion contamination has been implicated in disease transmission. Here, we analyzed the binding and retention of infectious prion protein (PrPSc) to plants. Small quantities of PrPSc contained in diluted brain homogenate or in excretory materials (urine and feces) can bind to wheat grass roots and leaves. Wild-type hamsters were efficiently infected by ingestion of prion-contaminated plants. The prion-plant interaction occurs with prions from diverse origins, including chronic wasting disease. Furthermore, leaves contaminated by spraying with a prion-containing preparation retained PrPSc for several weeks in the living plant. Finally, plants can uptake prions from contaminated soil and transport them to aerial parts of the plant (stem and leaves). These findings demonstrate that plants can efficiently bind infectious prions and act as carriers of infectivity, suggesting a possible role of environmental prion contamination in the horizontal transmission of the disease.
INTRODUCTION
snip...
DISCUSSION
This study shows that plants can efficiently bind prions contained in brain extracts from diverse prion infected animals, including CWD-affected cervids. PrPSc attached to leaves and roots from wheat grass plants remains capable of seeding prion replication in vitro. Surprisingly, the small quantity of PrPSc naturally excreted in urine and feces from sick hamster or cervids was enough to efficiently contaminate plant tissue. Indeed, our results suggest that the majority of excreted PrPSc is efficiently captured by plants’ leaves and roots. Moreover, leaves can be contaminated by spraying them with a prion-containing extract, and PrPSc remains detectable in living plants for as long as the study was performed (several weeks). Remarkably, prion contaminated plants transmit prion disease to animals upon ingestion, producing a 100% attack rate and incubation periods not substantially longer than direct oral administration of sick brain homogenates.
Finally, an unexpected but exciting result was that plants were able to uptake prions from contaminated soil and transport them to aerial parts of the plant tissue. Although it may seem farfetched that plants can uptake proteins from the soil and transport it to the parts above the ground, there are already published reports of this phenomenon (McLaren et al., 1960; Jensen and McLaren, 1960;Paungfoo-Lonhienne et al., 2008). The high resistance of prions to degradation and their ability to efficiently cross biological barriers may play a role in this process. The mechanism by which plants bind, retain, uptake, and transport prions is unknown. We are currently studying the way in which prions interact with plants using purified, radioactively labeled PrPSc to determine specificity of the interaction, association constant, reversibility, saturation, movement, etc.
Epidemiological studies have shown numerous instances of scrapie or CWD recurrence upon reintroduction of animals on pastures previously exposed to prion-infected animals. Indeed, reappearance of scrapie has been documented following fallow periods of up to 16 years (Georgsson et al., 2006), and pastures were shown to retain infectious CWD prions for at least 2 years after exposure (Miller et al., 2004). It is likely that the environmentally mediated transmission of prion diseases depends upon the interaction of prions with diverse elements, including soil, water, environmental surfaces, various invertebrate animals, and plants.
However, since plants are such an important component of the environment and also a major source of food for many animal species, including humans, our results may have far-reaching implications for animal and human health. Currently, the perception of the riskfor animal-to-human prion transmission has beenmostly limited to consumption or exposure to contaminated meat; our results indicate that plants might also be an important vector of transmission that needs to be considered in risk assessment.
RIGINAL RESEARCH ARTICLE
Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
imageTimm Konold1*, imageStephen A. C. Hawkins2, imageLisa C. Thurston3, imageBen C. Maddison4, imageKevin C. Gough5, imageAnthony Duarte1 and imageHugh A. Simmons1
1Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK
2Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK
3Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK
4ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
5School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie-affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20).
Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22).
Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing.
Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building.
Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9).
The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep.
Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease.
It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled.
Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases.
Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA.
Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice.
In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals.
In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions).
As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28).
This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm.
This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc.
In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc.
Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing.
The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material.
In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12).
A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30).
This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model.
Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
WEDNESDAY, MARCH 13, 2019
CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood
Subject: Prion 2019 Conference
See full Prion 2019 Conference Abstracts
Transmissible Spongiform Encephalopathies in exotic species
In exotic species, the last one was in 2007.
SPECIES No. DATES AFFECTED
Ankole cow 2 1991, 95
Bison 1 1996
Cheetah 5 1992 – 98
Eland 6 1989 – 95
Gemsbok 1 1987
Kudu 6 1989 – 92
Asian Leopard Cat1 1 2005
Lion 5 1998 - 2007
Nyala 1 1986
Ocelot 3 1994 – 99
Oryx 2 1989, 92
Puma 3 1992 – 95
Tiger 3 1995 – 99
Data valid to 30 September 2019
1Felis (Prionailurus) bengalensis.
ZOO ANIMALS AND TSE PRION DISEASE
The 82 zoo animals with BSE:
Id TSE Genus Species Subsp Birth Origin Death Place of Death
654 x Microcebus murinus - 1997 U.Montpellier 1998 U.Montpellier
656 x Microcebus murinus - 1997 U.Montpellier 1998 U.Montpellier
481 + Eulemur fulvus mayottensis 1974 Madagascar 1992 Montpellier zoo
474 + Eulemur fulvus mayottensis 1974 Madagascar 1990 Montpellier zoo
584 - Eulemur fulvus mayottensis 1984 Montpellier 1991 Montpellier zoo
455 + Eulemur fulvus mayottensis 1983 Montpellier 1989 Montpellier zoo
- + Eulemur fulvus mayottensis 1988 Montpellier 1992 Montpellier zoo
- + Eulemur fulvus mayottensis 1995 Montpellier 1996 Montpellier zoo
- + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo
- + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo
- + Eulemur fulvus albifrons 1988 Paris 1992 Montpellier zoo
456 + Eulemur fulvus albifrons 1988 Paris 1990 Montpellier zoo
586 + Eulemur mongoz - 1979 Madagascar 1998 Montpellier zoo
- p Eulemur mongoz - 1989 Mulhouse 1991 Montpellier zoo
- p Eulemur mongoz - 1989 Mulhouse 1990 Montpellier zoo
- p Eulemur macaco - 1986 Montpellier 1996 Montpellier zoo
- p Lemur catta - 1976 Montpellier 1994 Montpellier zoo
- p Varecia variegata variegata 1985 Mulhouse 1990 Montpellier zoo
- p Varecia variegata variegata 1993 xxx 1994 Montpellier zoo
455 + Macaca mulatta - 1986 Ravensden UK 1992 Montpellier zoo
- p Macaca mulatta - 1986 Ravensden UK 1993 Montpellier zoo
- p Macaca mulatta - 1988 Ravensden UK 1991 Montpellier zoo
- p Saimiri sciureus - 1987 Frejus France 1990 Frejus zoo
700 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
701 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
702 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
703 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
704 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
705 pc eulemur hybrid - - Besancon zoo 1998 Besancon zoo
706 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
707 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
708 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
709 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
710 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
711 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
712 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
713 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
714 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
715 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
716 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
717 pc eulemur hybrid - - Strasbourg zoo 1998 Strasbourg zoo
x p genus species - - Lille zoo 1996 Lille zoo
y p genus species - - Lille zoo 1996 Lille zoo
z p genus species - - Lille zoo 1996 Lille zoo
1 + Actinonyx jubatus cheetah 1986 Marwell zoo 1991 Pearle Coast AU
Duke + Actinonyx jubatus cheetah 1984 Marwell zoo 1992 Colchester zoo? UK
Saki + Actinonyx jubatus cheetah 1986 Marwell zoo 1993 unknown UK
Mich + Actinonyx jubatus cheetah 1986 Whipsnade 1993 Whipsnade UK
Fr1 + Actinonyx jubatus cheetah 1987 Whipsnade 1997 Safari de Peaugres FR
Fr2 + Actinonyx jubatus cheetah 1991 Marwell zoo 1997 Safari de Peaugres Fr
xx + Actinonyx jubatus cheetah 19xx xxx zoo 199x Fota zoo IR
yy + Actinonyx jubatus cheetah 19xx yyy zoo 1996+ yyyy zoo UK
zz + Actinonyx jubatus cheetah 19xx zzz zoo 1996+ yyyy zoo UK
aaa + Felis concolor puma 1986 Chester zoo 1991 Chester zoo UK
yy + Felis concolor puma 1980 yyy zoo 1995 yyyy zoo UK
zz + Felis concolor puma 1978 zzz zoo 1995 zzzz zoo UK
xxx + Felis pardalis ocelot 1987 xxx 1994 Chester zoo UK
zzz + Felis pardalis ocelot 1980 zzz 1995 zzzz zoo UK
85 + Felis catus cat 1990+ various 1999+ various UK LI NO
19 + Canis familia. dog 1992+ various 1999+ various UK
Fota + Panthera tigris tiger 1981 xxx zoo 1995 xxxx zoo UK
yy + Panthera tigris tiger 1983 yyy zoo 1998 yyyy zoo UK
Lump + Panthera leo lion 1986 Woburn SP 1998 Edinburgh zoo UK [since 1994]
1 + Taurotragus oryx eland 1987 Port Lympne 1989 Port Lympne zoo UK
Moll + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK
Nedd + Taurotragus oryx eland 1989 xx UK 1991 not Port Lympne UK
Elec + Taurotragus oryx eland 1990 xx UK 1992 not Port Lympne Uk
Daph p Taurotragus oryx eland 1988 xx UK 1990 not Port Lympne UK
zzz + Taurotragus oryx eland 1991 zz UK 1994 zzz UK
yyy + Taurotragus oryx eland 1993 yy UK 1995 yyy UK
Fran p Tragelaphus strepsi. kudu 1985 London zoo 1987 London zoo UK
Lind + Tragelaphus strepsi. kudu 1987 London zoo 1989 London zoo UK
Karl + Tragelaphus strepsi. kudu 1988 London zoo 1990 London zoo UK
Kaz + Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK
Bamb pc Tragelaphus strepsi. kudu 1988 London zoo 1991 London zoo UK
Step - Tragelaphus strepsi. kudu 1984 London zoo 1991 London zoo UK
346 pc Tragelaphus strepsi. kudu 1990 London zoo 1992 London zoo UK
324 + Tragelaphus strepsi. kudu 1989 Marwell zoo 1992 London zoo UK
xxx + Tragelaphus angasi nyala 1983 Marwell zoo 1986 Marwell zoo UK
yy + Oryx gazella gemsbok 1983 Marwell zoo 1986 Marwell zoo UK
zz + Oryx gazella gemsbok 1994+ zzz zoo 1996+ zzzz zoo UK
xx + Oryx dammah scim oryx 1990 xxxx zoo 1993 Chester zoo UK
yy + Oryx leucoryx arab oryx 1986 Zurich zoo 1991 London zoo UK
yy + Bos taurus ankole cow 1987 yyy zoo 1995 yyyy zoo UK
zz + Bos taurus ankole cow 1986 zzz zoo 1991 zzzz zoo UK
xx + Bison bison Eu bison 1989 xxx zoo 1996 xxxx zoo UK
THURSDAY, DECEMBER 19, 2019
TSE surveillance statistics exotic species and domestic cats Update December 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.
===
186. Serial detection of hematogenous prions in CWD-infected deer
Amy V. Nalls, Erin E. McNulty, Nathaniel D. Denkers, Edward A. Hoover and Candace K. Mathiason
Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA
CONTACT Amy V. Nalls amy.nalls@colostate.edu
ABSTRACT
Blood contains the infectious agent associated with prion disease affecting several mammalian species, including humans, cervids, sheep, and cattle. It has been confirmed that sufficient prion agent is present in the blood of both symptomatic and asymptomatic carriers to initiate the amyloid templating and accumulation process that results in this fatal neurodegenerative disease. Yet, to date, the ability to detect blood-borne prions by in vitro methods remains difficult.
We have capitalized on blood samples collected from longitudinal chronic wasting disease (CWD) studies in the native white-tailed deer host to examine hematogenous prion load in blood collected minutes, days, weeks and months post exposure. Our work has focused on refinement of the amplification methods RT-QuIC and PMCA. We demonstrate enhanced in vitro detection of amyloid seeding activity (prions) in blood cell fractions harvested from deer orally-exposed to 300 ng CWD positive brain or saliva.
These findings permit assessment of the role hematogenous prions play in the pathogenesis of CWD and provide tools to assess the same for prion diseases of other mammalian species.
Considering the oral secretion of prions, saliva from CWD-infected deer was shown to transmit disease to other susceptible naïve deer when harvested from the animals in both the
and preclinical stages69
of infection, albeit within relatively large volumes of saliva (50 ml). In sheep with preclinical, natural scrapie infections, sPMCA facilitated the detection of PrPSc within buccal swabs throughout most of the incubation period of the disease with an apparent peak in prion secretion around the mid-term of disease progression.70
The amounts of prion present in saliva are likely to be low as indicated by CWD-infected saliva producing prolonged incubation periods and incomplete attack rates within the transgenic mouse bioassay.41
snip...
Indeed, it has also been shown that the scrapie and CWD prions are excreted in urine, feces and saliva and are likely to be excreted from skin. While levels of prion within these excreta/secreta are very low, they are produced throughout long periods of preclinical disease as well as clinical disease. Furthermore, the levels of prion in such materials are likely to be increased by concurrent inflammatory conditions affecting the relevant secretory organ or site. Such dissemination of prion into the environment is very likely to facilitate the repeat exposure of flockmates to low levels of the disease agent, possibly over years.
snip...
Given the results with scrapie-contaminated milk and CWD-contaminated saliva, it seems very likely that these low levels of prion in different secreta/excreta are capable of transmitting disease upon prolonged exposure, either through direct animal-to-animal contact or through environmental reservoirs of infectivity.
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
HUNTERS, CWD TSE PRION, THIS SHOULD A WAKE UP CALL TO ALL OF YOU GUTTING AND BONING OUT YOUR KILL IN THE FIELD, AND YOUR TOOLS YOU USE...
* 1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
PMID: 8006664 [PubMed - indexed for MEDLINE]
Wednesday, September 11, 2019
Is the re-use of sterilized implant abutments safe enough? (Implant abutment safety) iatrogenic TSE Prion
SATURDAY, MARCH 16, 2019
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary Submission
MONDAY, NOVEMBER 23, 2020
***> Chronic Wasting Disease CWD TSE Prion Cervid State by State and Global Update November 2020
MONDAY, NOVEMBER 30, 2020
***> REPORT OF THE MEETING OF THE OIE SCIENTIFIC COMMISSION FOR ANIMAL DISEASES Paris, 9–13 September 2019 BSE, TSE, PRION
see updated concerns with atypical BSE from feed and zoonosis...terry
Monday, November 30, 2020
Tunisia has become the second country after Algeria to detect a case of CPD within a year
TUESDAY, NOVEMBER 17, 2020
The European Union summary report on surveillance for the presence of transmissible spongiform encephalopathies (TSE) in 2019 First published 17 November 2020
WEDNESDAY, OCTOBER 28, 2020
EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission
WEDNESDAY, OCTOBER 28, 2020
EFSA Scientific Opinion Potential BSE risk posed by the use of ruminant collagen and gelatine in feed for non‐ruminant farmed animals
WEDNESDAY, DECEMBER 2, 2020
EFSA Evaluation of public and animal health risks in case of a delayed post-mortem inspection in ungulates EFSA Panel on Biological Hazards (BIOHAZ) ADOPTED: 21 October 2020
i wonder if a 7 month delay on a suspect BSE case in Texas is too long, on a 48 hour turnaround, asking for a friend???
> However, to date, no CWD infections have been reported in people.
key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Prion 2017 Conference
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip…
see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
International Conference on Emerging Diseases, Outbreaks & Case Studies & 16th Annual Meeting on Influenza March 28-29, 2018 | Orlando, USA
Qingzhong Kong
Case Western Reserve University School of Medicine, USA
Zoonotic potential of chronic wasting disease prions from cervids
Chronic wasting disease (CWD) is the prion disease in cervids (mule deer, white-tailed deer, American elk, moose, and reindeer). It has become an epidemic in North America, and it has been detected in the Europe (Norway) since 2016. The widespread CWD and popular hunting and consumption of cervid meat and other products raise serious public health concerns, but questions remain on human susceptibility to CWD prions, especially on the potential difference in zoonotic potential among the various CWD prion strains. We have been working to address this critical question for well over a decade. We used CWD samples from various cervid species to inoculate transgenic mice expressing human or elk prion protein (PrP). We found infectious prions in the spleen or brain in a small fraction of CWD-inoculated transgenic mice expressing human PrP, indicating that humans are not completely resistant to CWD prions; this finding has significant ramifications on the public health impact of CWD prions. The influence of cervid PrP polymorphisms, the prion strain dependence of CWD-to-human transmission barrier, and the characterization of experimental human CWD prions will be discussed.
Speaker Biography Qingzhong Kong has completed his PhD from the University of Massachusetts at Amherst and Post-doctoral studies at Yale University. He is currently an Associate Professor of Pathology, Neurology and Regenerative Medicine. He has published over 50 original research papers in reputable journals (including Science Translational Medicine, JCI, PNAS and Cell Reports) and has been serving as an Editorial Board Member on seven scientific journals. He has multiple research interests, including public health risks of animal prions (CWD of cervids and atypical BSE of cattle), animal modeling of human prion diseases, mechanisms of prion replication and pathogenesis, etiology of sporadic Creutzfeldt-Jacob disease (CJD) in humans, normal cellular PrP in the biology and pathology of multiple brain and peripheral diseases, proteins responsible for the α-cleavage of cellular PrP, as well as gene therapy and DNA vaccination.
SATURDAY, FEBRUARY 23, 2019
Chronic Wasting Disease CWD TSE Prion and THE FEAST 2003 CDC an updated review of the science 2019
TUESDAY, NOVEMBER 04, 2014
Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011
Authors, though, acknowledged the study was limited in geography and sample size and so it couldn't draw a conclusion about the risk to humans. They recommended more study. Dr. Ermias Belay was the report's principal author but he said New York and Oneida County officials are following the proper course by not launching a study. "There's really nothing to monitor presently. No one's sick," Belay said, noting the disease's incubation period in deer and elk is measured in years. "
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS
resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
snip....
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
> However, to date, no CWD infections have been reported in people.
sporadic, spontaneous CJD, 85%+ of all human TSE, just not just happen. never in scientific literature has this been proven.
if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;
sporadic = 54,983 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
spontaneous = 325,650 hits https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
*** IF CWD is not a risk factor for humans, then I guess the FDA et al recalled all this CWD tainted elk tenderloin (2009 Exotic Meats USA of San Antonio, TX) for the welfare and safety of the dead elk. ...tss
Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease
Contact: Exotic Meats USA 1-800-680-4375
FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah’s Ark Processors LLC.
Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease found in elk and deer. The disease is caused by an abnormally shaped protein called a prion, which can damage the brain and nerves of animals in the deer family. Currently, it is believed that the prion responsible for causing CWD in deer and elk is not capable of infecting humans who eat deer or elk contaminated with the prion, but the observation of animal-to-human transmission of other prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has raised a theoretical concern regarding the transmission of CWD from deer or elk to humans. At the present time, FDA believes the risk of becoming ill from eating CWD-positive elk or deer meat is remote. However, FDA strongly advises consumers to return the product to the place of purchase, rather than disposing of it themselves, due to environmental concerns.
Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was packaged in individual vacuum packs weighing approximately 3 pounds each. A total of six packs of the Elk Tenderloins were sold to the public at the Exotic Meats USA retail store. Consumers who still have the Elk Tenderloins should return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX 78209. Customers with concerns or questions about the Voluntary Elk Recall can call 1-800-680-4375. The safety of our customer has always been and always will be our number one priority.
Exotic Meats USA requests that for those customers who have products with the production dates in question, do not consume or sell them and return them to the point of purchase. Customers should return the product to the vendor. The vendor should return it to the distributor and the distributor should work with the state to decide upon how best to dispose. If the consumer is disposing of the product he/she should consult with the local state EPA office.
#
RSS Feed for FDA Recalls Information11 [what's this?12]
USGS Outstanding in the Field podcast, Episode 3: Chronic Wasting Disease - Oh, Deer (Credit: USGS)
TUESDAY, DECEMBER 29, 2020
Chronic Wasting Disease: Can Science Save Our Dear Deer?
FRIDAY, JULY 26, 2019
Chronic Wasting Disease in Cervids: Implications for Prion Transmission to Humans and Other Animal Species
TUESDAY, JANUARY 21, 2020
***> 2004 European Commission Chronic wasting disease AND TISSUES THAT MIGHT CARRY A RISK FOR HUMAN FOOD AND ANIMAL FEED CHAINS REPORT UPDATED 2020
CWD TSE PRION AND ZOONOTIC, ZOONOSIS, POTENTIAL
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" wt.net="">
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler ===============
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
snip...see full text;
MONDAY, FEBRUARY 25, 2019
***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
***> In conclusion, sensory symptoms and loss of reflexes in Gerstmann-Sträussler-Scheinker syndrome can be explained by neuropathological changes in the spinal cord. We conclude that the sensory symptoms and loss of lower limb reflexes in Gerstmann-Sträussler-Scheinker syndrome is due to pathology in the caudal spinal cord. <***
***> The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.<***
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
***> All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.<***
***> In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***
TUESDAY, NOVEMBER 17, 2020
The European Union summary report on surveillance for the presence of transmissible spongiform encephalopathies (TSE) in 2019 First published 17 November 2020
FRIDAY, OCTOBER 30, 2020
Efficient transmission of US scrapie agent by intralingual route to genetically susceptible sheep with a low dose inoculum
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strains
PLEASE NOTE;
2.3.2. New evidence on the zoonotic potential of atypical BSE and atypical scrapie prion strainsNo
Olivier Andreoletti, INRA Research Director, Institut National de la Recherche Agronomique (INRA) – École Nationale Vétérinaire de Toulouse (ENVT), invited speaker, presented the results of two recently published scientific articles of interest, of which he is co-author: ‘Radical Change in Zoonotic Abilities of Atypical BSE Prion Strains as Evidenced by Crossing of Sheep Species Barrier in Transgenic Mice’ (MarinMoreno et al., 2020) and ‘The emergence of classical BSE from atypical/Nor98 scrapie’ (Huor et al., 2019).
In the first experimental study, H-type and L-type BSE were inoculated into transgenic mice expressing all three genotypes of the human PRNP at codon 129 and into adapted into ARQ and VRQ transgenic sheep mice. The results showed the alterations of the capacities to cross the human barrier species (mouse model) and emergence of sporadic CJD agents in Hu PrP expressing mice: type 2 sCJD in homozygous TgVal129 VRQ-passaged L-BSE, and type 1 sCJD in homozygous TgVal 129 and TgMet129 VRQ-passaged H-BSE.
WEDNESDAY, OCTOBER 28, 2020
***> EFSA Annual report of the Scientific Network on BSE-TSE 2020 Singeltary Submission
SUNDAY, OCTOBER 11, 2020
Bovine adapted transmissible mink encephalopathy is similar to L-BSE after passage through sheep with the VRQ/VRQ genotype but not VRQ/ARQ
THURSDAY, SEPTEMBER 24, 2020
The emergence of classical BSE from atypical/ Nor98 scrapie
FRIDAY, OCTOBER 23, 2020
Scrapie TSE Prion Zoonosis Zoonotic, what if?
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
https://www.nature.com/articles/srep11573
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).
Wednesday, February 16, 2011
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
MONDAY, DECEMBER 16, 2019
Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update
***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***
What if?
DECEMBER 2020 TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE BSE, SCRAPIE, CWD, CPD, PPD, CJD END OF YEAR REPORTS
MONDAY, DECEMBER 14, 2020
Experimental oral transmission of chronic wasting disease to sika deer (Cervus nippon)
TUESDAY, DECEMBER 01, 2020
Sporadic Creutzfeldt Jakob Disease sCJD and Human TSE Prion Annual Report December 14, 2020
TUESDAY, JANUARY 12, 2021
Wisconsin CWD TSE Prion 8,101 Positive With Wild Deer Testing Positive for CWD in Germania in Southwestern Shawano County
FRIDAY, JANUARY 22, 2021
Wisconsin DNR CONFIRMS CWD IN WOOD COUNTY WILD DEER; RENEWS BAITING AND FEEDING BANS
WEDNESDAY, NOVEMBER 4, 2020
CWD TSE PRION, SCRAPIE, BSE, AND PORCINE, PIGS, WILD BOAR, ZOONOTIC ZOONOSIS RISK FACTORS AND POTENTIALS
Saturday, January 23, 2021
Improved surveillance of surgical instruments reprocessing following the variant Creutzfeldt-Jakob disease crisis in England: findings from a 3-year survey
FRIDAY, JANUARY 22, 2021
Creutzfeldt Jakob Disease TSE Prion and Nutritional Supplements, Porcine Products, what you need to know
***> FDA DOES NOT have mandatory established specifications for animal-derived ingredients to ensure they are BSE free in Nutritional Supplements
***>''Implementing recent national guidelines to address the prions concern proved an eye-opener. Microscopic levels of proteins remain on many reprocessed instruments. The impact most of these residues, potentially including prions, may have on subsequent patients after sterilization remains debatable.''<***
DEAD people can't debate this, and it's a damn shame that after 5 decades, or more, of discussing this, we now know what to do, but still refuse to do it i.e. disposable instruments, jiminy cricket what the hell does it take, how many body bags of iatrogenic cjd (now called sporadic cjd in most cases still) does it take, i guess it's just too easy to call it sporadic cjd and go on down the road.
all iatrogenic cjd is, is sporadic cjd, before the iatrogenic event is discovered, traced back, provern, documented, put into the academic domain, and then finally the public domain, this very seldom happens, thus problem solved, it's all sporadic cjd, PLUS, SPORADIC CJD HAS NOW BEEN LINKED TO ATYPICAL AND TYPICAL BSE, SCRAPIE, AND NOW CWD.
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
11:56 AM
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