New Mexico Chronic Wasting Disease CWD TSE PrP Confirmed February 2022
NM528 28 x552857 Detected
NM530 28 1541x22, 3927798 Detected
2002 to 2016 Chronic Wasting Disease CWD TSE PrP Confirmed in 58 Cases in New Mexico...
Some Facts about CWD in New Mexico CWD is the acronym for Chronic Wasting Disease
New Mexico Department of Game and Fish began testing suspect deer for CWD in the 1990’s
The first case of CWD in New Mexico was confirmed in 2002. This was a deer from Main Post on White Sands Missile Range
Since 2002, CWD has been detected in both free-ranging deer and elk
Found in Units 19, 28, and 34
In New Mexico, CWD has not been found in any Class A Game Park
Cumulative positive animals found with CWD in New Mexico since 2002 is 59 as of 1 January 2018 and includes:
Harvested animals submitted by hunters
Animals collected because they were found ill or otherwise abnormal
Animals captured specifically for surveillance testing from high-risk sites
In addition to deer and elk, the Department has tested a limited number of oryx, bighorn sheep, antelope, and mountain lions
CWD was not detected in any species except deer and elk
Species that are not in the deer family are considered low-risk, and the Department does not routinely test low-risk species History Discussion of Chronic Wasting Disease (CWD) began among Department personnel in the early 1990’s. At the time, deer at Brazos were numerous and concentrated, and reports of deer in very poor condition were common. After a deer began sleeping on the doormat at the front door of a home, the Department collected the deer and submitted the first suspected CWD case. The test came back negative from Veterinary Diagnostic Services in Albuquerque.
CWD was found only in Colorado and Wyoming and seemed to be a remote risk even after the disease was detected in Nebraska. When CWD was detected in Wisconsin in early 2002, the risk of spread became real and proximate. New Mexico followed Wisconsin with CWD detected in a White Sands deer during March of 2002. A CWD advisory board was convened from several agencies. Surveillance was planned for the area of the index case. Department personnel, with strong public support, opposed any attempts to depopulate the mule deer in the area of the index case to eliminate or reduce prevalence of CWD.
The first CWD symposium was convened in Denver, CO during in August of 2002. At that meeting, a group met to assist New Mexico with surveillance. In December, persons from National Park Service and Colorado Veterinary Diagnostic Laboratory came to New Mexico to capture deer at the White Sands cantonment area. High winds hampered capture with clover traps, and chemical immobilization was difficult. Of 5 deer killed or captured, 3 were positive with CWD. This operation was the first application of ante-mortem testing with tonsillar tissue for management purposes.
The Department instituted mandatory check-in and check-out of hunters in Game Management Unit (GMU) 19 for the following hunting season in January 2003. It was also mandatory during that hunt for hunters to present all harvested deer for tissue collection and CWD testing. Two hunter-killed deer from Dripping Springs and the adjacent Organ Mountains yielded positive tests. Since then, check-in and check-out of hunters in GMU 19 and presentation of harvested deer for CWD testing have remained mandatory. No more hunter-harvested deer from GMU 19 have tested positive for CWD since that time. Additional positive deer have been collected from GMU 19, but they have been reported suspect animals or deer captured through surveillance. To date, the cumulative total of CWD detections in GMU 19 is 19.
Early in 2005, a sick, lethargic, emaciated deer was reported in Timberon, NM, GMU 34. That deer was collected and CWD was confirmed. This was the first case of CWD in GMU 34. During the hunting season of 2005, the first elk with CWD were tested. One was a reported CWD suspect, and the other was a sport-harvested elk; both were free-ranging animals. To date, the cumulative total of positive CWD tests from GMU 34 is 13, 8 deer and 5 elk.
During the 2007 hunt, a youth hunter harvested a buck deer appearing normal from GMU 28. The positive CWD test was the first case confirmed in GMU 28. It is now mandatory for GMU 28 hunters to present their harvested deer and elk so tissues can be collected for testing. Personnel from Fort Bliss collect tissue from harvested deer during the hunt, and now CWD positive deer are harvested each year. Prevalence seems higher in GMU28 than any other area, and the Department has done more ante-mortem surveillance in GMU 28 than any other unit. To date, the cumulative number of positive CWD tests is 26, and of those, 4 were harvested elk.
CWD has not been detected in species other than deer and elk in New Mexico. Tissues from bighorn, antelope, oryx, and cougar have been tested. Other states have also done surveillance in other species, but in the United States, CWD has not been detected in any species outside the family, Cervidae.
Surveillance Methodology From the beginning, the Department has encouraged successful hunters to present heads of harvested deer and elk for CWD testing. The Department submits tissues for CWD testing at no cost to hunters. Hunters who participate are entered into a random draw for hunting license authorizations. This has served as an incentive for hunters to present their harvested deer or elk heads for testing to increase the extent of surveillance.
In 2003, over 800 tissues were tested. Currently, the Department receives 200-300 tissues annually for testing. Most of these tissues are collected at established collection sites. Each year, collection sites are established in GMU 34 and GMU 28. GMU 19 hunters contact the Department by phone for tissue collection. Fewer than 100 hunters present their harvested deer or elk heads at a Department office, though each office is prepared to collect tissues from hunters.
The Department conducts targeted surveillance through capture and ante-mortem testing at herds deemed to be at high risk. The Department has also done advance ante-mortem testing in populations from which deer were subsequently translocated.
All deer or elk found or reported to be sick or abnormal are collected and tested irrespective of clinical symptoms. Surveillance among abnormal animals is among the most effective methods to detect presence of CWD.
Game Parks Game parks in New Mexico increase risk for CWD because translocation of animals is central to the business. Most game parks in New Mexico are dedicated to hunting. These are high-fenced areas, and management of the animals inside is negligible. A very few game parks support managed breeding for production and sale of live animals. Animals in production facilities are closely confined at high densities and fed rationed feed. If infected, CWD spreads rapidly under such conditions. Class A Park rules do not mandate surveillance testing in the absence of confirmed CWD. None of the game parks elects to test any of their cervids.
Rules to import cervids into New Mexico game parks are thorough, and, if followed, reduce risk of bringing CWD into game parks. The Department is certified by USDA to administer the federal Herd Certification Program. Because game parks are isolated and not closely monitored, compliance with importation rules is unknown. No restrictions exist to hinder or regulate intrastate movement and trade among game parks within New Mexico. Natural reproduction occurs within hunting game parks, but is unmanaged.
The Department has conducted depopulation of 4 game parks since 2002. Tissues were collected during depopulations, and no positive tests resulted.
The Department has quarantine authority and has exercised it once for a case in which a New Mexico game park became a trace forward facility in an epidemiological investigation from Colorado. This quarantine lasted until 5 years from the time of the importation at issue. The Director of the Department has authority to declare an animal health emergency and suspend existing rules or implement special measures. A moratorium on importation was declared in the early 2000’s, as CWD was being detected in many new states. Currently, CWD appears to be spreading largely through human-mediated movements of cervids, and in January 2018, the Director of the Department declared a moratorium on importation for an indefinite duration. That moratorium remains in effect at the time of this writing.
Management Actions The Department established rules to prevent spread of CWD through carcass transport shortly after the first confirmed case. In CWD positive areas, hunters must leave high-risk material in the game management unit of harvest. Hunters may remove only boned meat, hide, antlers, cleaned skull caps, and teeth. The remainder of the carcass must be left in in the field.
All deer and elk reported to be abnormal are now investigated. Those animals found by Department personnel to be significantly abnormal or compromised are collected. All such animals are defined as CWD suspects, and personnel collect the proper tissues for CWD testing. When possible and appropriate, full necropsies are performed in addition to CWD testing. This protocol allows the Department to understand some causes of unexplained mortality. This policy has resulted in a number of detections of CWD positive animals.
The Department encourages hunters to present the heads of recent legally harvested deer and elk for CWD testing. Incentives for hunters are offered by the Department to increase surveillance through hunter harvest. This has been the best way for the Department to conduct tests from animals in all parts of the state.
Some evidence exists that among deer, males might be more likely to get CWD. Buck-only hunting in New Mexico might be a factor helping keep the prevalence of CWD as low as possible. Special rules that facilitate maximum harvest in areas of high deer density also might help reduce CWD prevalence by reducing deer density. Such rules have been implemented in parts of New Mexico.
Regulations to reduce risk of transporting CWD into New Mexico have been implemented and modified. Two complete importation moratoriums have been imposed by the Department. During times importation is allowed, source herds must document and verify their testing and inventory tracking. Since the U.S. Department of Agriculture implemented its Herd Certification Program, the Department has relied on herd certification to approve importations and minimize risk of importing more CWD.
The Department has conducted 4 depopulations of game parks. The first was a game park stocked from a Colorado game park in which CWD was confirmed after elk from that game park were translocated to New Mexico. Two depopulations resulted when game parks wanted to cease operating the facility. To minimize risk to free-ranging cervids outside the high fence, the Department removed all cervids within one of the closing game parks. The game park was located in an area where CWD was not found and this park had not translocated elk for many years. Most, and maybe all, cervids were removed from this park before the fences were struck. If any deer or elk remained, they were considered to pose very low risk. The most recent depopulation was removal of cervids from a high-fenced paddock not licensed as a game park. Cervids were of unknown origin, and all were destroyed.
A crematory was installed at Department headquarters. The crematory is sized for up to 1200 pound batches in cases of disease outbreak. Temperatures within the burn chamber are adequate to inactivate the CWD infective agent, according to published studies. This crematory is deployed to dispose all CWD high-risk cervid or other suspect material.
Future The Department has conducted surveillance since CWD was detected in 2002. The distribution of CWD is determined from these data, and the long duration of surveillance gives high confidence to Department estimates of distribution. At present, CWD exists among deer and elk in the Organ Mountains, the Sacramento Mountains, and the Hueco Mountains.
With continued spread of CWD across North America, New Mexico will increase surveillance efforts across the state in years to come. Tissue collection will be increased at border areas through hunter participation and through active surveillance. In particular, tissue collection efforts will be increased at the eastern border with Texas through collection stations with notice to hunters. Surveillance will be conducted at the northern border through increased contact with hunters and through active surveillance in herds at increased risk from southward movement of CWD from Colorado. Although CWD is not known to occur in Arizona, the Department will increase tissues collected from the western part of the state. This will be done through increased hunter contact and through active collection during Department capture operations. All personnel collecting tissues will be trained and meet competencies for collection. The Department cannot risk or pay for tests that are inconclusive because of technician error.
Today, it is mandatory for hunters in GMU 19 and 28 to submit harvested animals for testing. This rule is casually enforced. In the future, enforcement in these two areas will be more active, and that can occur with very little additional effort. These hunts are limited in number, and access points are few making it straightforward to track licenses and hunters.
If prevalence of CWD appears to be increasing more quickly, the Department could respond with more aggressive hunting in areas of high CWD prevalence or in areas of high deer or elk density. Harvest of males could be increased with some rule changes. Such management might make more sense under future conditions.
No testing from mortality or hunter harvest is currently required in game parks. The Department could consider imposing mandatory testing in game parks to have some knowledge of CWD status within privately held cervids. Such regulations could be implemented within the framework of the federal Herd Certification Program. Additionally, some regulation and restriction could be imposed on intrastate translocation of privately owned cervids. Currently, only a notice of intent is required for game park owners to move cervids within the state.
Conclusion At the time of the first case of CWD, it was decided not to attempt to eliminate the infected herd of deer in GMU 19. CWD eradication through herd elimination is probably not possible now. Currently, no known vaccine or treatment is known to prevent infection, contagion, or spread of CWD. No treatment exists to cure or prolong survival of animals infected with CWD. CWD has spread from deer to elk to moose in North America. Despite clinical trials in primates and transgenic mice, most scientists still think it unlikely that CWD will readily transmit to humans. Evidence exists that the substrate can become infective in areas of high CWD prevalence. The hunting public in New Mexico continues to be largely unconcerned. However, if CWD becomes perceived to be a human health risk, that complacent sentiment could change. Hunter concern and fear could conceivably reduce participation in hunting and significantly impact New Mexico Game and Fish and other agencies in the United States that regulate and depend on hunting and license sales for revenue...snip...see full text;
SUNDAY, AUGUST 15, 2021
New Mexico CWD TEST RESULTS: 1/19/2021 update
NM18-290 28 3418801 Detected
NM18-293 28 3446090 Detected
NM475 29 3460171 Detected
NM518 28 3464748 Detected
NM515 28 3500214 Detected
NM778 34 3510401 Detected
https://www.wildlife.state.nm.us/download/conservation/invasives-diseases/CWD-Results-01_19_2021.pdf
https://chronic-wasting-disease.blogspot.com/2021/08/new-mexico-cwd-test-results-1192021.html
NEW Mexico CWD TSE Prion confirmed cases 58 detected through December 2016.
since December 2016, is anyone's guess, who's looking ???
cwd must be bad in New Mexico considering the lack of CWD TSE Prion updates and lack of testing, imo.
i thought NM was going to step up to the plate, but instead, there just feeding from the same plate as TAHC et al, out of sight, out of mind, imo...terry
http://www.wildlife.state.nm.us/conservation/invasive-species-and-diseases/chronic-wasting-disease/
NEW Mexico 2019-2020 Hunting Report CWD, mums the word, not much said;
FRIDAY, FEBRUARY 08, 2019
New Mexico Chronic Wasting Disease CWD TSE Prion Update 2018-2019?
https://chronic-wasting-disease.blogspot.com/2019/02/new-mexico-chronic-wasting-disease-cwd.html
WEDNESDAY, FEBRUARY 07, 2018
New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.
http://chronic-wasting-disease.blogspot.com/2018/02/new-mexico-bans-all-live-cervid.html
THURSDAY, NOVEMBER 02, 2017
New Mexico Chronic Wasting Disease CWD Figures 2016 - 2017 Update ???
http://chronic-wasting-disease.blogspot.com/2017/11/new-mexico-chronic-wasting-disease-cwd.html
THURSDAY, SEPTEMBER 22, 2016
New Mexico CWD confirmed in 5 McGregor Range deer during the 2015-16 hunting season
http://chronic-wasting-disease.blogspot.com/2016/09/new-mexico-cwd-confirmed-in-5-mcgregor.html
Wednesday, March 25, 2015
Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015
http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-cases.html
i got this in an email years back...
Subject: New Mexico Chronic Wasting Disease CWD Statistics To Date
Sample_Number GMU Sampling_Date DOK Zone Easting Northing Kill_Location CWD_Test SignsORComments Kill_Info Tissue Species_Type
NM02-09 19 6/1/2002 6/1/2002 13 359899 3583583 WSMR main post (first CWD Positive in NM) Positive First CWD positive deer in New Mexico CWD Area Obex Deer
NM03-50-12 19 11/4/2002 11/4/2002 13 361000 3582000 WSMR Post Positive Deer
NM03-50-16 19 11/12/2002 11/12/2002 13 361000 3582000 WSMR Post Positive Deer
NM03-232-42 19 12/17/2002 12/17/2002 13 361000 3581000 WSMR Positive took tonsil sample, eartag 476 purple Tonsil Biopsy Tonsil & Lymph node Deer
NM03-232-41 19 1/1/2003 1/1/2003 13 351000 3581000 Organ Mtns. Positive no signs Hunter Harvest Lymph node & Obex Deer
NM03-227-17 19 1/4/2003 1/4/2003 13 348000 3577900 Dripping Springs Positive looked healthy Hunter Harvest Lymph node Deer
NM04-BURKETT-1114-004 19 11/14/2003 11/14/2003 13 359919 3583574 WSMR MAIN POST, BLDG. 100 Positive DOE SEVERELY EMACIATED, CAUSE OF DEATH UNKN. CWD Area Lymph node Deer
NM05-232-07 34 1/13/2004 1/13/2005 13 463977 3608839 15 miles NE of Pinon Positive Hunter reported convulsions, vomit, death CWD Suspect Obex Deer
NM05-50-38 19 12/14/2004 12/14/2004 13 346464 3566415 West Organs, W of Massey Tank Positive Tonsil Biopsy, eartag 478 Orange Tonsil Biopsy Tonsil Deer
NM05-50-36 19 12/14/2004 12/14/2004 13 349493 3578747 West Organs, W of Dripping Spring Visitor Center Positive Tonsil Biopsy, eartag # 249 Orange, 1st recapture (doe found & put down on 5/5/2005) Tonsil Biopsy Tonsil Deer
NM06-48-16 19 4/5/2005 4/5/2005 13 347623 3579382 WSMR - Tag # 482 Positive Tonsil Biopsy Tonsil Deer
NM05-50-85 19 4/11/2005 13 358175 3588385 WSMR, SW of Antelope Hill Positive eartag: 484 Purple CWD Area Tonsil Deer
NM05-50-59 19 4/15/2005 4/15/2005 13 346855 3577310 SW of Dripping springs Positive eartag: 490 Purple CWD Area Tonsil Deer
NM05-12-02 34 6/6/2005 6/5/2005 13 435000 3611500 Timberon Positive Very Poor BC, old doe CWD Suspect Lymph node Deer
NM06-10-01 34 10/1/2005 10/1/2005 13 445449 3623454 Hughes Canyon Positive Poor condition, could not stand CWD Suspect Obex Elk
NM06-206-03 34 10/3/2005 10/3/2005 13 440452 3625273 Wayland Canyon Positive Healthy, herding cows Hunter Harvest Obex Elk
NM06-48-05 19 12/10/2005 13 360273 3587275 Antelope Hill Positive 708 Tonsil Biopsy Tonsil Deer
NM06-127-15 34 3/24/2006 3/24/2006 13 433877 3612203 123 Waialae Dr. Timberon Positive Drooling, wobbly, and losing weight CWD Suspect Lymph node Deer
NM06-50-09 19 4/21/2006 4/21/2006 13 346665 3563768 N of sewage plant (Bishops Cap) Positive Capture #224, Game and fish tag 575 purple, 207 orange CWD Area Tonsil Deer
NM06-WSMR-08 19 6/2/2006 6/2/2006 13 343263 3743696 WSMR SW of Red Butte-Stallion range Positive Lion depredation study animal #19, Game and fish tag #246, orange lymph nodes collected Found Dead Lymph node Deer
NM06-147-02 34 8/12/2006 8/12/2006 13 432633 3612182 Abbyville St. Timberon, NM Positive Stumbling, foaming at mouth, disoriented CWD Area Deer
NM07-WMD-70 34 10/27/2006 10/27/2006 13 445000 3608000 West of Pinon Positive NA Hunter Harvest Lymph node Deer 07-16149 19 7/13/2007 7/13/2007 13 349000 3564000 South of Bishop's Cap Positive Sick, emaciated, salivating, urinating. Collectey by Richard McDonald. CWD Suspect Deer
NM08-0145 28 10/14/2007 10/14/2007 13 427000 3598000 Mc Gregor Positive none Hunter Harvest Deer
NM08-0528 34 10/30/2007 10/28/2007 13 451000 3578000 Southern Cross Ranch Positive Hunter Harvest Deer
NM07-WSMR-81 19 12/13/2007 12/13/2007 13 361084 3588638 MAIN POST Positive RECAPTURE DOE SEQ #80 CWD Area Deer
NM08-0630 28 10/12/2008 10/12/2008 13 441500 3599300 McGregor Range Positive Hunter Harvest Deer
NM08-0635 28 10/13/2008 10/12/2008 13 442600 3600300 McGregor Positive Hunter Harvest Deer
NM09-321 34 10/29/2008 10/25/2008 13 443000 3603000 Chuck Brown's Ranch Positive Small, emaciated, tick infested Hunter Harvest Deer
NM09-241 34 3/2/2009 3/1/2009 13 439367 3634869 Rio Penasco Positive Sick, reported by landowner, collected by Ben Byrd CWD Suspect Elk
NM10-302 34 12/6/2009 12/6/2009 13 439522 3632464 Wills Canyon Positive Sunken hips, Drewling, Not moving well (possible wounded) CWD Suspect Elk
NM09-339 28 5/9/2010 13 435976 3598058 Positive R 44 Ylw Lft 149.244 CWD Area Deer
NM09-182 28 10/10/2010 10/10/2010 13 434000 3602000 TA 13, GU4 Positive Hunter Harvest Deer
NM11-201 28 11/17/2010 11/17/2010 13 432402 3595093 McGregor Positive R ear 12 purple l ear 149.484 CWD Area Deer
NM08-0253 34 11/27/2010 11/27/2010 13 431000 3621000 Sac. Lookout Positive Hunter Harvest Elk
NM11-364 28 3/12/2011 3/12/2011 13 435747 3599058 McGregor Positive Rt ear: 10 pur Lft ear: 149.323 CWD Area Deer
NM11-367 28 3/13/2011 3/13/2011 13 430236 3596459 McGregor Positive Rt ear: 9 pur Lft ear: 149.426 CWD Area Deer
NM11-368 28 3/13/2011 3/13/2011 13 436668 3594474 McGregor Positive Rt ear: 25 Blue Lft ear: 149.184 CWD Area Deer
NM08-062 28 10/9/2011 10/9/2011 13 406700 3544700 McGregor Range South End Positive Hunter Harvest Deer
NM08-061 28 10/9/2011 10/9/2011 13 463900 3598800 McGregor Range Positive Hunter Harvest Deer
NM08-066 28 10/10/2011 10/9/2011 13 405238 3542644 McGregor Range Positive Hunter Harvest Deer
NM11-388 28 2/17/2012 2/17/2012 13 403607 3546117 Ft Bliss- McGregor Positive Left ear 60 yellow, Pregnant Collar 150.662 Rectal Biopsy Deer
NM11-391 28 2/18/2012 2/18/2012 13 416507 3576920 McGregor Positive Rt ear 56 yellow Collar 151.761 4 dars 1 stick 1 break 1 miss Rectal Biopsy Deer
NM14-4 28 12/11/2013 12/9/2013 13 432000 3606000 McGregor Positive Hunter Harvest Elk
NM14-6 28 12/11/2013 12/11/2013 13 431000 3604000 McGregor Positive Hunter Harvest Elk
NM14-5 28 12/11/2013 12/11/2013 13 431000 3604000 McGregor Positive Hunter Harvest Elk
NM14-62 19 2/12/2014 2/12/2014 13 348333 3598384 NASA Positive CWD Suspect Deer
NM14-343 19 4/6/2014 4/5/2014 13 343000 3575000 Mathis home Positive Suspect- near water, sick. Study deer. Collected by Pat Mathis. CWD Suspect Deer
http://chronic-wasting-disease.blogspot.com/2017/11/new-mexico-chronic-wasting-disease-cwd.html
SUNDAY, AUGUST 15, 2021
New Mexico CWD TEST RESULTS: 1/19/2021 update
NM18-290 28 3418801 Detected
NM18-293 28 3446090 Detected
NM475 29 3460171 Detected
NM518 28 3464748 Detected
NM515 28 3500214 Detected
NM778 34 3510401 Detected
https://www.wildlife.state.nm.us/download/conservation/invasives-diseases/CWD-Results-01_19_2021.pdf
https://chronic-wasting-disease.blogspot.com/2021/08/new-mexico-cwd-test-results-1192021.html
Wednesday, March 18, 2015
Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015
http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-confirmed.html
Friday, April 04, 2014
No New Positives Found in 2013-14 Trans Pecos CWD Surveillance
http://chronic-wasting-disease.blogspot.com/2014/04/no-new-positives-found-in-2013-14-trans.html
Monday, February 11, 2013
TEXAS CHRONIC WASTING DISEASE CWD Four New Positives Found in Trans Pecos
http://chronic-wasting-disease.blogspot.com/2013/02/texas-chronic-wasting-disease-cwd-four.html
Tuesday, July 10, 2012
Chronic Wasting Disease Detected in Far West Texas
http://chronic-wasting-disease.blogspot.com/2012/07/chronic-wasting-disease-detected-in-far.html
Monday, March 26, 2012
Texas Prepares for Chronic Wasting Disease CWD Possibility in Far West Texas
http://chronic-wasting-disease.blogspot.com/2012/03/texas-prepares-for-chronic-wasting.html
***for anyone interested, here is some history of CWD along the Texas, New Mexico border, and my attempt to keep up with it...terry
snip...
see history CWD Texas, New Mexico Border ;
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILES FROM TEXAS BORDER
http://chronic-wasting-disease.blogspot.com/2012/03/3-cases-of-cwd-found-new-mexico-mule.html
***> TEXAS HISTORY OF CWD <***
Singeltary telling TAHC, that CWD was waltzing into Texas from WSMR around Trans Pecos region, starting around 2001, 2002, and every year, there after, until New Mexico finally shamed TAHC et al to test where i had been telling them to test for a decade. 2012 cwd was detected first right there where i had been trying to tell TAHC for 10 years.
***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History <***
http://chronic-wasting-disease.blogspot.com/2017/08/texas-chronic-wasting-disease-cwd-tse.html
Sunday, October 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009
2009 Summary of Chronic Wasting Disease in New Mexico New Mexico Department of Game and Fish
http://chronic-wasting-disease.blogspot.com/2009/10/cwd-new-mexico-spreading-south-to-texas.html
Acta Zool. Mex vol.35 Xalapa 2019 Epub 29-Nov-2019 https://doi.org/10.21829/azm.2019.3502203 ARTÍCULOS CIENTÍFICOS
Impacts of chronic wasting disease on a low density mule deer (Odocoileus hemionus) population in the San Andres Mountains, Chihuahuan Desert, New Mexico
Louis C. Bender1
Cristina L. Rodden2
Pat Mathis2
Mara E. Weisenberger3
Octavio C. Rosas Rosas4 *
Patrick C. Morrow2
Brock D. Hoenes5
1Extension Animal Sciences and Natural Resources, New Mexico State University, Las Cruces, NM 88003, USA. <lbender@nmsu.edu>
2Environmental Stewardship Division, U.S. Department of the Army, White Sands Missile Range, WSMR, NM 88002, USA. <cristina.l.rodden.civ@mail.mil>; <patrick.l.mathis2.ctr@mail.mil>; <patrick.c.morrow.civ@mail.mil>
3San Andres National Wildlife Refuge, Las Cruces, NM 88012, USA. <mweisenberger@blm.gov>
4Colegio de Postgraduados, Campus San Luis Potosí, Iturbide No. 73, Salinas, San Luis Potosí, México. <octaviocrr@colpos.mx>
5Washington Dept. of Fish and Wildlife, 600 Capitol Way N., Olympia, WA 98501, USA. Brock.Hoenes@dfw.wa.gov
ABSTRACT:
Chronic wasting disease (CWD), a contagious neurodegenerative disease of cervids, is becoming increasingly prevalent in the arid Southwest including the Chihuahuan Desert ecoregion. Population effects of CWD are uncertain, particularly in arid environments, as previous work has been on relatively high density deer populations in semi-arid or temperate environments. In 2002, CWD was detected in a low density mule deer (Odocoileus hemionus) population in the arid San Andres Mountains, a Chihuahuan Desert range in southern New Mexico. We determined prevalence and distribution of CWD, and mortality and movements of deer, to assess the potential impact on low density deer populations in arid environments. Repeated seasonal primarily ante-mortem sampling found stable prevalence of 0.000-0.091, 2003-2008. Annual CWD mortality rate was <0.02, including deer that were culled. Monitoring of adult radio-collared deer showed no dispersal movements away from home ranges, with maximum movements of ≤20 km; similarly, no juveniles dispersed from maternal ranges. Distribution of infected deer was strongly related to presence of other infected deer. Annual survival rates of mule deer and population rate-of-increase suggested little effect of CWD on population-level mortality given observed prevalence. Transmission and reservoirs of CWD in the SAM were likely limited by low deer densities, patchy distribution, and environmental characteristics (i.e., low clay content of soils) unfavorable to prion persistence, characteristics that are typical of most mule deer populations in the Chihuahuan Desert ecoregion.
Key words: Chihuahuan Desert; chronic wasting disease; mule deer; New Mexico; Odocoileus hemionus; San Andres Mountains
RESUMEN:
La enfermedad crónica degenerativa (por sus siglas en inglés: CWD), una enfermedad neurodegenerativa contagiosa de los cérvidos, se está haciendo cada vez más frecuente en el suroeste árido americano incluyendo la ecoregión del desierto de Chihuahua. Los efectos de la CWD sobre poblaciones de cérvidos silvestres son inciertos, particularmente en ambientes áridos, ya que el trabajo previo ha estado en poblaciones de ciervos de densidad relativamente alta en ambientes semi-áridos o templados. En 2002, la CWD fue detectada en una población de venado bura (Odocoileus hemionus) de baja densidad en las áridas montañas de San Andrés, una región del Desierto Chihuahuense en el sur de Nuevo México. Se determinó la prevalencia y distribución de CWD, y la mortalidad y los movimientos de los venados, para evaluar su impacto potencial en poblaciones de baja densidad en ambientes áridos. En el muestreo ante-mortem previo repetido estacionalmente se encontró prevalencia estable de 0,000-0,091, 2003-2008. La tasa anual de mortalidad por CWD fue <0,02, incluyendo venados que fueron sacrificados. El monitoreo de venados con radio-collares adultos no mostró movimientos de dispersión fuera de los rangos de origen, con movimientos máximos de ≤20 km; de manera similar, no hay juveniles dispersos de los rangos maternos. La distribución de los venados infectados estaba fuertemente relacionada con la presencia de otros venados infectados. Las tasas anuales de supervivencia del venado mula y la tasa de aumento de la población sugirieron un efecto pequeño de la CWD en la mortalidad a nivel de la población dada la prevalencia observada. La transmisión y los depósitos de CWD en el SAM (Montañas San Andrés) fueron probablemente limitados por la baja densidad de los venados, su distribución irregular y las características ambientales (es decir, bajo contenido de arcilla de los suelos) desfavorables a la persistencia de priones, características típicas de la mayoría de las poblaciones de venados bura en la ecorregión del Desierto Chihuahuense.
Palabras clave: Desierto Chihuahuense; enfermedad crónico-degenerativa; venado bura; Nuevo México; Odocoileus hemionus; Montañas San Andrés
INTRODUCTION
Chronic wasting disease (CWD) is becoming increasingly widespread in the arid Southwest, including the Chihuahuan Desert ecoregion (https://www.cwd-info.org). Chronic wasting disease (CWD) is a contagious neurodegenerative disease of cervids. Although CWD results in the eventual death of infected individuals (Williams et al., 2001, 2002), the effect of CWD on populations is less certain (Miller et al., 2006, 2008; Wasserberg et al., 2009; Almberg et al., 2011; Saunders et al., 2012), and impacts and control options depend upon prevalence and mode of transmission (Miller et al., 2006; Wasserberg et al., 2009; Almberg et al., 2011; Saunders et al., 2012). Generally, management actions aimed at broad-scale population reductions or targeted animal removals in areas where CWD is established have failed to eliminate or prevent the spread of CWD (Saunders et al., 2012). Culling as a control strategy assumes that transmission is primarily direct and density dependent (Miller et al., 2006; Conner et al., 2007; Wasserberg et al., 2009), whereas much evidence supports indirect frequency dependent transmission of CWD (Miller et al., 2006; Wasserberg et al., 2009; Almberg et al., 2011; Potapov et al., 2013). Indirect transmission and long persistence of infectious prions in the environment (Miller et al., 2004) make it difficult or impossible to eliminate CWD from populations (Miller et al., 2006; Wasserberg et al., 2009; Almberg et al., 2011; Saunders et al., 2012). Management of CWD thus may depend upon disrupting transmission pathways (Miller et al., 2006), which requires understanding of ecological factors associated with presence of CWD because local environmental conditions may strongly affect probability of CWD transmission among hosts (Almberg et al., 2011; Walter et al., 2011; Saunders et al., 2012).
In the desert Southwestern USA, CWD was first detected in 2002 in a low density (ca. <1/km2; Bender et al., 2012) mule deer (Odocoileus hemionus) population in the San Andres Mountains (SAM), a Chihuahuan Desert range in south-central New Mexico. Virtually all field studies on population effects or environmental correlates of CWD have occurred in relative high density mule or white-tailed deer (O. virginianus) populations in the semi-arid or temperate Rocky Mountains, Canada, and the Midwestern USA (Saunders et al., 2012). These ecological conditions are dissimilar to the Chihuahuan Desert habitats of the Southwestern USA and Mexico, which are more arid and characterized by patchy, low density mule deer populations (Galindo-Leal, 1993; Sánchez-Rojas & Gallina, 2000; Esparza-Carlos et al., 2011; Bender et al., 2012), complicating management based on previous work and creating uncertainty regarding the potential impact and means of control of CWD in arid environments.
In the Southwestern USA and Mexico, mule deer are a resource of significant ecological and economic importance (Galindo-Leal, 1993; Heffelfinger, 2006; Little & Berrens, 2008; Bender et al., 2012). Because increasing mule deer populations is a priority for management agencies and private landowners in the Chihuahuan Desert ecoregion, information is needed on CWD in low density deer populations in arid Southwestern environments to develop informed management options. Our goal was to determine the population significance and identify behavioral and environmental factors associated with the presence of CWD in mule deer in the SAM. Our specific objectives included: (1) determine prevalence of CWD; (2) assess the role of CWD in mule deer mortality; and (3) assess the likelihood of spread of CWD due to mule deer movements or dispersal from CWD-positive areas.
MATERIAL AND METODS
Study area. The greater San Andres Mountains area encompasses ca. 11,000 km2 in south-central New Mexico (Fig. 1) in the Chihuahuan Desert ecoregion, including areas of San Andres National Wildlife Refuge (SANWR), White Sands Missile Range (WSMR), NASA’s White Sands Test Facility, and the Jornada Experimental Range. The SAM and surrounding terrain include playas, rugged mountain peaks and canyons, rolling grasslands, sand dunes, lava flows, and scattered springs and ponds (Muldavin et al., 2000). Precipitation averages 150-300 mm annually depending upon elevation, with the bulk of moisture occurring as short, intense rainstorms from July through September. Snowfall averages <100 mm, is short-lived, and occurs only at high elevations. Temperatures of the area range from -23 to 41oC. Major vegetation communities included desert and semidesert grassland, Chihuahuan desert scrub, and Great Basin conifer woodland (Muldavin et al., 2000). Other large herbivores present included oryx (Oryx gazella gazella), desert bighorn (Ovis canadensis mexicanus), javelina (Pecari tajacu), and a limited number of elk (Cervus elaphus). Livestock were present only on the periphery of our study area, and hunting of mule deer similarly occurred only on the periphery of the study area.
Figure 1 Composite minimum convex polygons of all locations of juvenile mule deer (solid polygon) superimposed on annual 100% minimum convex polygons of all adult female home ranges in the Stallion Range Center, Main Post, and Dripping Springs chronic wasting disease areas, San Andres Mountains. Solid outline is White Sands Missile Range boundary; dashed outline is 100% minimum convex polygon of all mule deer locations.
Mortality. We monitored survival, causes of mortality, nutritional condition, and movements of 169 (n = 21-26 adult males and 37-62 adult females annually) radio-collared deer in the SAM, December 2003-2009, as a component of a larger mule deer population project (see Bender et al., 2012 for detailed methods). We monitored radio-collared deer biweekly, located all mortalities, and performed a field necropsy or removed the carcass for a lab necropsy to determine cause of death (Bender et al., 2012). We also collected biological samples including obex and pharyngeal lymph nodes to help differentiate CWD from other causes-of-mortality. Last, we calculated annual mortality rates due to CWD (Heisey & Fuller, 1985; Bender et al., 2012).
Additionally, we captured neonate and other juvenile (<1-year-old) mule deer by hand, June-September 2005-2008, and by aerial net gunning in December and March-April 2005-2008 and 2010. Juveniles were equipped with ear tag radio-transmitters (Advanced Telemetry Systems, Asanti, Minnesota, USA) and monitored for survival and movements in association with adult deer (Hoenes, 2008).
CWD sampling. We used tonsillar biopsies to detect CWD (Wolfe et al., 2002) during annual December and April captures, 2003-2008 (Bender et al., 2012). We obtained lymphoid follicle samples from immobilized deer starting at the rostral rim of the tonsillar sinus and taking 2-4 samples beginning at the rim and including the sinus using biopsy forceps with a 6-mm cup. We preserved extracted tonsillar tissue in 10% neutral buffered formalin and submitted samples for histopathology and immunohistochemistry (IHC) following Miller and Williams (2002).
We also tested radio-collared and other deer from the SAM that died between capture periods for CWD using obex or pharyngeal lymph nodes and either the IHC or ELISA tests (Williams et al., 2001) (n = 28, December 2003-December 2009, respectively). We calculated prevalence (i.e., the proportion of a population that is affected with a particular disease at a given time [Merriam-Webster Medical Dictionary; https://www.merriam-webster.com/medical/prevalence]) for each capture period, where prevalence = number of samples testing positive for CWD/total numbers of samples. We compared prevalence among captures and sexes using Fisher’s exact tests (Zar, 1996) and trend in prevalence using Spearman rank correlation (Zar, 1996). We calculated SE for prevalence for each capture period using the binomial approximation assuming a population size of 2000 (Zar, 1996).
Deer movements. We located radio-collared deer approximately biweekly, recorded locations with a hand-held GPS, and plotted locations on GIS basemaps using ArcGIS 10.0 (ESRI, Redlands, California, USA). We constructed 100% minimum convex polygon home ranges for each deer to determine geographic extent of annual use areas (Hoenes, 2008). We defined dispersal as leaving the study area (defined as an inclusive 100% MCP of all adult deer locations) and establishing a home range outside of the study area. We also determined maximum distances between any 2 locations for each deer.
We used multi-response permutation procedures (MRPP; Slauson et al., 1991) to compare geographic distributions of locations of juveniles and adult deer from their maternal home range area. We used 100% MCP annual home ranges for all deer captured in the 3 centers of CWD (Stallion Range Center, Dripping Springs, and Main Post; Fig. 1) to determine the maximum extent of ranges of individual deer located in areas where CWD was detected. We then constructed a pooled 100% MCP of all locations of juveniles (from capture through age 1.5) to determine extent of juvenile movements relative to maternal home ranges in areas of CWD presence. We also used MRPP to compare the spatial distributions of each CWD-positive deer with (1) spatial distributions of all other CWD-positive mule deer and (2) spatial distributions of all mule deer not testing positive for CWD in the SAM.
RESULTS
Mortality. A total of eight captured deer (seven females, one male) tested positive for CWD at capture or post-mortem (see CWD Prevalence, below). Of these, two mortalities were ultimately attributed to CWD (Bender et al., 2012). These included one radio-collared female that was proximately killed by a puma (Puma concolor), and one radio-collared female that died from unknown causes approximately six months after testing positive for CWD for a 2nd time (she had previously tested positive two years prior to the second positive test). Of the remaining six deer that tested positive for CWD, two females (one radio-collared, one uncollared) were subsequently culled; one female’s radio-collar malfunctioned and had unknown fate; and three uncollared individuals (one male, two female) had unknown fates. These individuals were censored from survival analyses in Bender et al. (2012). Thus, deaths ultimately attributable to CWD accounted for two of 72 total deer deaths (50 adult females, 22 adult males) documented during our study (Bender et al., 2012).
Of 28 total mortalities of radio-collared deer from which obex or pharyngeal lymph samples were obtained, 1 individual was positive for CWD. This adult female was the puma kill noted above. She was previously tested at capture approximately 1.5 y prior to death and was CWD-negative at that time.
During our study (2004-2009), annual survival rates ranged from 0.74 (SE = 0.10) to 0.92 (SE = 0.15) for adult males, and from 0.74 (SE = 0.06) to 0.86 (SE = 0.05) for adult females (Bender et al., 2012). In our general survival analysis (Bender et al., 2012), we did not discriminate between disease-related mortality factors when estimating cause-specific mortality rates. Separating the disease-related causes-of-mortality in Bender et al. (2012), CWD-specific annual mortality rate averaged 0.01 (range = 0.00-0.02; n = six years) for females and 0.00 for males. If deer that tested positive for CWD but were censored from our general survival analysis (Bender et al., 2012) were included and treated as mortalities the month following capture or when culled, mean CWD-specific annual mortality rate increased to 0.02 (range = 0.00-0.07) for females and 0.01 (range = 0.00-0.04) for males.
CWD prevalence. We captured a total of 445 adult mule deer, including 226 different individuals and 219 recaptures. We performed a total of 364 biopsies, of which >251 resulted in extraction of tonsillar tissue with successful extraction ranging from 65-96% per capture. Seven mule deer (including the adult female which tested positive in both December 2005 and December 2007) were CWD-positive, for a prevalence of 0.000-0.091 among captures (Table 1). Mean prevalence of CWD was 0.025 (SE = 0.010) among all captures (Table 1). Prevalence among capture periods did not differ (Fischer’s exact P = 0.492), nor did prevalence between males and females (0.011 v. 0.031; Fischer’s exact P = 0.314) based on capture samples only, all project deer (0.010 v. 0.034; Fischer’s exact P = 0.224), or all deer sampled in the SAM (0.033 v. 0.049; Fischer’s exact P = 0.481; this included targeted removals of deer that appeared to be “sick”). There was no trend in prevalence over captures (r s = -0.200; P = 0.548).
Table 1 Numbers of deer sampled (No. Sampled), numbers of successful extraction of tonsillar tissue (No. Extracted), number of deer testing positive (No. Positive), and prevalence (No. Positive / No. Extracted) (SE) of chronic wasting disease in mule deer inhabiting the San Andres Mountains. Also shown is prevalence (SE) including all deer sampled (this includes mortalities, hunter harvest, culled deer, deer-vehicle collisions, etc., in addition to samples collected during captures).
Post-mortem tests of 28 project deer that died between capture periods resulted in one additional CWD-positive deer identified in June 2006. Including these deer, observed prevalence of CWD ranged from 0.000-0.079% (Table 1), with a mean among collection periods of 0.025 (SE = 0.010).
Deer movements. No radio-collared deer emigrated from the SAM. Maximum spread of movements (i.e., maximum distance between any two location points) was <20 km for bucks and <15 km for does.
We captured and radio-tagged 18, 37, 26, and 18 neonates, 2005-2008, respectively. We also captured additional six to nine-month-old juveniles in December 2007 (n = 6), April 2008 (n = 5), and March-April 2010 (n = 7). A total of ten, ten, seven, eight, and seven juveniles survived through age 1.5, 2005-2009, and none of these 42 juveniles dispersed from the immediate area of their maternal home range (Fig. 1) nor did the geographic distribution of their locations differ from adult deer in their maternal home range area (P >0.896).
We identified 13 positive test locations of CWD (includes project deer and all other deer tested from the SAM, including hunter harvests and targeted culls) associated with three geographic areas, the Main Post/Headquarters and Stallion Range Center on WSMR, and Dripping Springs Recreational Area on Bureau of Land Management ownership, immediately across the Organ Range from Main Post (Fig. 1). Distributions of all CWD-positive deer were significantly related (P <0.0004) to distributions of other CWD-positive deer, but not non-CWD deer (P >0.778). The lone exception was the single CWD-positive deer from Stallion Range Center, whose distribution was not related to other CWD-positive deer or all other mule deer in general (P >0.667).
DISCUSSION
Chronic wasting disease was at most a minor direct mortality factor in the SAM, with annual mortality rates <0.01 (or <0.02 if censored individuals were classed as mortalities immediately following capture or at culling). Prevalence data suggested a similar impact. Maximum potential annual mortality from CWD based on the highest annual prevalence we observed (9%) and a disease duration of two or three would be 0.05 and 0.03, respectively. All of these rates would be less than the mortality rates of mule deer due to senescence alone (approximately 0.08-0.10 based on a 12 or 10 year lifespan). Moreover, average annual mortality of radio-collared mule deer in the SAM was 0.19 for adult females and 0.16 for adult males (Bender et al., 2012). Thus, CWD-specific mortality rate (including censored deer) accounted for only 6% (males) to 11% (females) of observed mean annual mortality. Using prevalence data and assuming a typical 2-3 y disease duration, maximum potential mortality in the SAM (0.03-0.05) was ≤16-26% (females) or ≤19-31% (males) of the total observed mortality of mule deer. Level of adult mortality was not limiting population growth of mule deer in the SAM (Hoenes, 2008; Bender et al., 2012), and adult survival was higher than seen in other populations in arid New Mexico (Bender et al., 2011, 2012). Thus, effects of CWD on population-level mortality of deer were not resulting in any significant impacts on population rate of increase given observed prevalence. This was seen despite an older population age structure due to minimal harvesting and relatively low productivity (Hoenes, 2008; Bender et al., 2012).
Previously, CWD was shown to predispose mule deer to other mortality factors, including deer-vehicle collisions (Krumm et al., 2005) and puma predation (Krumm et al., 2010). Predisposition likely results from poor nutritional condition or lack of environmental awareness as the disease progresses (Williams et al., 2001). In the SAM, one CWD-positive female had her cause-of-death classified as unknown-not predation (Bender et al., 2012) approximately six months after testing positive at capture. She was not severely emaciated at death and was in better condition than the average lactating female at capture the previous autumn (percent ingesta-free body fat = 6.0% v. a mean of 5.1% [SE = 0.2] for lactating females; L. Bender, unpublished data). Similarly, of 28 post-mortem tests, one puma-killed female subsequently tested positive for CWD. This female was extremely emaciated (femur marrow fat <20%; Cook et al., 2001, L. Bender, unpublished data) at death, indicating a high degree of predisposition to mortality. Our results therefore at least partially support CWD predisposing deer to other mortality factors, and thus mortality from CWD is likely compensatory to some degree (Krumm et al., 2010).
Chronic wasting disease was rare in the SAM and deer densities were much lower than in other sites where CWD is present, characteristics which make sustaining a CWD epidemic less likely (Miller et al., 2006). Most (92%) CWD-positive deer were located in either the White Sands Main Post area, a residential development, or the Dripping Springs Recreation Area, both high human-use areas. Results from Colorado also found higher prevalence associated with developed habitats (Farnsworth et al., 2005). Deer associated with human developments tend to be tamer, have higher population densities, and are frequently present at water sites, feeders, and other concentration areas, which increases the likelihood of close contact and potentially disease transmission (Farnsworth et al., 2005; Miller et al., 2006, 2008). Because CWD prions can be transferred via saliva (Mathiason et al., 2006), excreta (Miller et al., 2006; Gultekin et al., 2009), and other tissues, deer in these areas may be more likely to be exposed because of higher frequency of contact with infectious prions, resulting in a positive association of CWD and human-developed areas. Similarly, because developed areas can act as refugia from hunting, deer often show older age structure in such areas, which further increases the opportunity for exposure to CWD (Farnsworth et al., 2005).
The spatial distribution of disease can be related to the distribution or movement patterns of hosts or vectors (Conner & Miller, 2004). For mule deer, potential movements hypothesized to spread CWD among populations include seasonal migrations, dispersal of juveniles, and dispersal or other long range movements of adults (such as movements of adult males during the rut) (Conner & Miller, 2004; Conner et al., 2007). No radio-collared deer emigrated from the SAM during our study, and maximum spread of movements was <20 km, indicating that deer movements were localized. Similarly, no radio-tagged juveniles that survived through age 1.5 emigrated from the SAM and all remained within or adjacent to their maternal home range (Fig. 1). Because dispersal of juveniles is the most common means of long-range movement among populations of deer (Kie & Czech, 2000), dispersal of juveniles would be a likely mechanism for spread of CWD from the SAM to adjacent habitats. However, work in Colorado suggested that migratory movements were more likely to spread CWD among populations than was dispersal (Conner & Miller, 2004). Further, prevalence of CWD is more common in older deer due to increased exposure time (Farnsworth et al., 2005), and thus juveniles show lower prevalence in part because they are exposed to infective deer or other infectious material for a short time prior to dispersal and the slow progression of the disease in individuals (Williams et al., 2001, 2002). Mule deer in the SAM are non-migratory, and lack of migratory movements in combination with the lack of dispersal indicates that the likelihood of spread of CWD to adjacent populations was low.
It is possible albeit unlikely that deer from other populations move to the SAM and return to their original ranges. Given the large proportion of radio-collared deer in areas associated with CWD in the SAM (at times approximately 50% of the local deer) and the timing of captures (December and April), if such movements occurred during the most likely biological period (i.e., the rut in December), it is highly probable that some of these deer would have been captured and these movements seen as a dispersal from the SAM. Conner and Miller (2004) hypothesized that epidemics of CWD may be more rapid in populations where deer are sedentary and have small home ranges, noting that prevalence of CWD rose to >50% in a captive population in <7 years. Mule deer in the SAM are sedentary, patchily distributed, and show small home ranges (females = 8-16 km2, males = 11-33 km2) (Hoenes, 2008; Bender et al., 2012), and thus fit this hypothesis. Further, distributions of CWD-positive deer in the SAM were strongly spatially correlated, similar to results from Wisconsin which showed that probability of infection was related to numbers of nearby infected deer (Grear et al., 2010). However, prevalence of CWD in the SAM did not increase over time (Table 1), indicating that free-ranging deer may not be predisposed to a significant population impact simply because of small, sedentary ranges. The low and stable prevalence of CWD in the SAM may be due to the low population density and patchy distribution of deer. Miller et al. (2006) suggested that CWD epidemics may not be sustained in areas where <200 deer comprised a wintering (i.e., close geographic proximity) group. Additionally, high clay content of soils may enhance the environmental persistence and infectivity of prions (Almberg et al., 2011; Walter et al., 2011). Clay content of soils in CWD areas of the SAM is low (primarily Nickel [<15% clay]-Upton [15-30% clay] associations or rock outcrops; Bulloch & Neher, 1980), which may limit environmental accumulation of prions. The combination of low deer densities, patchy deer distribution, and poor edaphic characteristics for prion accumulation likely contributed to observed trends in prevalence of CWD in the SAM. These characteristics are also typical of most mule deer populations in the arid Southwestern USA and Mexico (Galindo-Leal, 1993; Sánchez-Rojas & Gallina, 2000; Esparza-Carlos et al., 2011; Bender et al., 2011, 2012).
The single exception to a contagious distribution of CWD-positive deer in the SAM was the single CWD-positive female from the Stallion Range Center. The range of this individual was well separated from other CWD-positive deer (Fig. 1). This disjunct occurrence highlights the uncertainty over mode of transmission or infection with CWD as no other individuals in this small subpopulation (<50 deer) tested positive, despite 32 tonsillar biopsies performed at capture and several post-mortem samples.
CONCLUSIONS
Prevalence and mortality data show that CWD had little population-level effect on mule deer in the SAM, likely because of low deer density, patchy distribution, and soil characteristics that do not favor accumulation or infectivity of prions, characteristics that are typical of mule deer populations in the Chihuahuan Desert habitats (Galindo-Leal,1993; Sánchez-Rojas & Gallina, 2000; Esparza-Carlos et al., 2011; Bender et al., 2012). This was reflected in growth of the mule deer population, which more than doubled (an average increase of >13% annually) from 2007 to 2014 in areas surveyed originally in 2007 (Bender et al., 2012; L. Bender, unpublished data). Because transmission of CWD is at least partially indirect, culling has been ineffective in controlling CWD (Conner et al., 2007) and annual removals may need to exceed 45% of the deer population to control CWD (Miller et al., 2006). Such a level of removal would quickly eliminate mule deer from many arid Southwestern habitats, given the relatively low deer density and productivity seen in mule deer populations in arid environments (Galindo-Leal, 1993; Sánchez-Rojas & Gallina, 2000; Lomas & Bender, 2007; Bender et al., 2011, 2012). Culling would also only lower CWD prevalence, not eliminate CWD (Wasserberg et al., 2009). Consequently, culling mule deer to manage CWD would likely be ineffective unless the population was exterminated in the SAM or similar populations, and prions did not persist in the environment. Further, the low prevalence of CWD in the SAM (approximately 2.5% over time) suggests that CWD in other areas of the Southwest could well be present, because low prevalence makes detection difficult. This was corroborated by detection of CWD-positive deer and elk in the southern and central Sacramento Mountains, a distance of ≥65 km from the nearest location of a CWD-positive deer in the SAM.
ACKNOWLEDGEMENTS.
We thank the U.S. Department of Defense-White Sands Missile Range, U.S. Fish and Wildlife Service-San Andres National Wildlife Refuge, U.S. Bureau of Land Management-Las Cruces Field Office, New Mexico Department of Game and Fish, and U.S. Geological Survey for funding this project. The New Mexico State University, Agricultural Experiment Station and Cooperative Extension Service provided additional financial support. We thank J. Barnitz, A. Bennett, K. Cobble, and K. Mower for field and logistical assistance. We thank D. Childress, R. Bodwin, and E. Watters for flight support for capture and surveys. All activities were in compliance with NMSU IACUC # 2003-023 and 2009-205.
CHRONIC WASTING DISEASE CASES CWD STATUS OF CAPTIVE HERDS AS OF February 2022
CHRONIC WASTING DISEASE CASES CWD STATUS OF CAPTIVE HERDS
Date of Index Case Confirmation Index Case State County Species Herd Type HCP Enrolled HCP Certified Number of Animals Herd Status
2/23/2022 4.5 Y Male PA Lancaster WTD Shooter No No 93 Quarantine
1/12/2022 6.5 Y Female WV Hardy WTD Shooter Yes Yes 18 Quarantine
1/5/2022 4.5 Y Female PA Lycoming WTD Shooter No No 177 Quarantine
11/8/2021 3 Y Male WI Waukesha WTD/ Elk Breeder Yes Yes 22 Quarantine
11/4/2021 2, 3 Y Male MI Kent Elk Breeder Yes Yes 0 Depopulated
10/18/2021 9 Y Female WI Portage WTD Shooter No No 370 Quarantine
10/14/2021 11.5 Y Female PA Fulton WTD Hobby No No 1 Quarantine
10/14/2021 2.5 Y Male PA Bedford WTD Breeder No No 70 Quarantine
10/12/2021 4.5 Y Female PA Indiana Red Deer Shooter No No 14 Quarantine
10/5/2021 1.5 Y Male PA Bedford WTD Shooter No No 50 Quarantine 9/27/2021 Y Male WI Vilas WTD Shooter No No Quarantine
9/27/2021 4.5 Y Male PA Huntingdon WTD Breeder No No 137 Quarantine
9/21/2021 1 Y Male PA Blair WTD Breeder No No 26 Quarantine
9/9/2021 3.5 Y Male PA Bedford WTD Breeder No No 36 Quarantine
9/2/2021 11 Y Female WI Outagamie WTD Breeder Yes Yes 31 Quarantine
8/31/2021 1 Y Female WI Langlade WTD Breeder Yes Yes 58 Quarantine
8/31/2021 2 Y Male WV Hampshire WTD Breeder Yes Yes 23 Quarantine
8/26/2021 4 Y Male PA Bedford WTD Shooter No No >200 Quarantine
8/24/2021 3Y Female TX Duval WTD Breeder No No 188 Quarantine
8/11/2021 6 Y Female WI Taylor WTD Breeder Yes Yes 220 Quarantine
8/9/2021 9 Y Male WI Sauk WTD Hobby No No 1 Quarantine
7/15/2021 4 Y Female MI Montcalm WTD Breeder No No 109 Quarantine
6/15/2021 4 Y Female TX Uvalde WTD Breeder & Shooter No No 1000+ Quarantine
5/28/2021 9 Y Female PA Bedford WTD Breeder No No 29 Quarantine
5/12/2021 2.5 Y Male PA Warren WTD Shooter No No 19 Depopulated
5/10/2021 3 Y Female MN Beltrami WTD Breeder No No 61 Depopulated
4/20/2021 Six positives PA Bedford WTD Breeder Traceback No No 87 Depopulated
4/20/2021 1.5 Y Male TX Mason WTD Breeder Traceback Yes Yes 93 Depopulated
4/20/2021 1.5 Y Male TX Matagorda WTD Breeder Traceback Yes No 221 Depopulated
4/18/2021 2.5 Y Male MI WTD Shooter No No ukn Quarantine
3/30/2021 3.5 Y, 2.5 Y, 3.5Y TX Uvalde WTD Breeder Yes Yes 61 Quarantine
3/30/2021 2.5 Y & 1.5 Y TX Uvalde WTD Breeder Yes No 318 Quarantine
3/29/2021 3Y Female TX Hunt WTD Breeder Yes No 381 Quarantine
3/29/2021 4 Y Female PA Blair WTD Breeder No NA 11 Quarantine
3/19/2021 3.75 Y Male PA Bedford WTD Hobby No NA 8 Quarantine
3/3/2021 4 Y Male MI Montcalm WTD Shooter No NA 14 Quarantine
2/8/2021 3.5 Y Male PA Blair WTD Shooter No NA 19 Quarantine
12/30/2020 Ukn Y Female PA Bedford WTD Shooter No NA 51 Quarantine
12/15/2020 2.5 Y Female PA Fulton WTD Hobby No NA 19 Quarantine
11/18/2020 2.5 Y Female KS Rawlins MD Breeder Yes Yes 70 Quarantine
10/29/2020 2 Y Male PA Somerset WTD Shooter No No 0 Depopulated
10/14/2020 2 Y Male SD Custer Elk Breeder/Hobby No NA 6 Quarantine
10/14/2020 2.5 Y Female MN Houston WTD Breeder Yes yes 49 Quarantine
10/1/2020 MT WTD Breeder No NA 17 Depopulated
10/1/2020 4 Y Male WI Washburn WTD Breeder Yes No 21 Quarantine
9/23/2020 6 Y Female UT Duchesne Elk Breeder No NA 55 Partial Depopulation/ Quarantine
7/2/2020 3 Y Female KS Osage Elk Breeder Yes Yes 20+ Depopulated
Updated February 2022
snip...see full list ;
CWD Quarantines equal CWD time bomb waiting to go off...terry
***> Texas Chronic Wasting Disease CWD TSE Prion Confirmed Positive Jumps By 91 Total To Date 361 Cases
TEXAS CWD TRACKING
CWD Positive
Confirmation Date Free Range/Captive County Source Species Sex Age
Pending Breeder Deer Kimble Facility #6 White-tailed Deer Unknown 3.5
Pending Breeder Deer Hunt Facility #9 White-tailed Deer M 1.9
N/A Free Range Hartley N/A Mule Deer M 5.5
2022-01-25 Free Range Medina N/A White-tailed Deer F 5.5
2022-01-12 Breeder Deer Hunt Facility #9 White-tailed Deer M 1.5
2022-01-12 Breeder Deer Hunt Facility #9 White-tailed Deer F 3.5
2022-01-12 Breeder Release Site Medina Facility #3 Red Deer F 4.5
2022-01-12 Free Range Hartley N/A White-tailed Deer M 3.5
2022-01-12 Free Range Hartley N/A Mule Deer M 5.5
2022-01-12 Free Range Hartley N/A Mule Deer M 4.5
2022-01-12 Free Range Hartley N/A Mule Deer M 5.5
2022-01-12 Free Range Hartley N/A Mule Deer F 3.5
2022-01-12 Breeder Deer Kimble Facility #6 White-tailed Deer Unknown 5.5
2022-01-12 Free Range Hartley N/A Mule Deer M 3.5
2022-01-12 Free Range Hartley N/A Mule Deer M 7.5
2022-01-10 Free Range Medina N/A White-tailed Deer M 4.5
2022-01-10 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.3
2022-01-10 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 5.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer F 1.4
2022-01-07 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 5.4
2022-01-06 Free Range Medina N/A White-tailed Deer M 2.5
2021-12-28 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2021-12-28 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 3.4
2021-12-13 Free Range Medina N/A White-tailed Deer M 3.5
2021-12-13 Breeder Deer Duval Facility #13 White-tailed Deer F 4.4
2021-12-13 Free Range El Paso N/A Mule Deer F 4.5
2021-10-18 Breeder Deer Medina Facility #4 White-tailed Deer M 4
2021-10-12 Breeder Deer Hunt Facility #9 White-tailed Deer F 8.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 1.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.2
2021-10-12 Breeder Deer Uvalde Facilities #7 & 8 White-tailed Deer M 2.1
Showing 1 to 100 of 361 entries Previous Next
National CWD Tracking Map
“Regarding the current situation involving CWD in permitted deer breeding facilities, TPWD records indicate that within the last five years, the seven CWD-positive facilities transferred a total of 2,530 deer to 270 locations in 102 counties and eight locations in Mexico (the destinations included 139 deer breeding facilities, 118 release sites, five Deer Management Permit sites, and three nursing facilities).'' ...
It is apparent that prior to the recent emergency rules, the CWD detection rules were ineffective at detecting CWD earlier in the deer breeding facilities where it was eventually discovered and had been present for some time; this creates additional concern regarding adequate mitigation of the risk of transferring CWD-positive breeder deer to release sites where released breeder deer come into contact with free-ranging deer...
Commission Agenda Item No. 5 Exhibit B
DISEASE DETECTION AND RESPONSE RULES
PROPOSAL PREAMBLE
1. Introduction.
snip...
A third issue is the accuracy of mortality reporting. Department records indicate that for each of the last five years an average of 26 deer breeders have reported a shared total of 159 escapes. Department records for the same time period indicate an average of 31 breeding facilities reported a shared total of 825 missing deer (deer that department records indicate should be present in the facility, but cannot be located or verified).
Listen here;
Nov 3, 2021
Nov 4, 2021
Counties where CWD Exposed Deer were Released, September 2021
Number of CWD Exposed Deer Released by County, September 2021
Control of Chronic Wasting Disease OMB Control Number: 0579-0189 APHIS-2021-0004 Singeltary Submission
Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification
SATURDAY, FEBRUARY 26, 2022
Texas Chronic Wasting Disease CWD TSE Prion Confirmed Positive Jumps By 91 Total To Date 361 Cases
FRIDAY, APRIL 30, 2021
Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
WEDNESDAY, DECEMBER 04, 2013
Chronic Wasting Disease CWD and Land Value concerns?
TUESDAY, APRIL 13, 2021
Implications of farmed-cervid movements on the transmission of chronic wasting disease
TRUCKING TRANSPORTING CERVID CHRONIC WASTING DISEASE TSE PRION VIOLATING THE LACEY ACT
MONDAY, MARCH 05, 2018
TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES
SATURDAY, JULY 09, 2016
Texas Intrastate – within state movement of all Cervid or Trucking Chronic Wasting Disease CWD TSE Prion Moratorium
THURSDAY, AUGUST 20, 2015
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks and CWD
SUNDAY, MARCH 20, 2022
CHRONIC WASTING DISEASE CASES CWD STATUS OF CAPTIVE HERDS AS OF February 2022
Published: 06 September 2021
***> Chronic wasting disease: a cervid prion infection looming to spillover
Alicia Otero, Camilo Duque Velásquez, Judd Aiken & Debbie McKenzie
Veterinary Research volume 52, Article number: 115 (2021)
FRIDAY, FEBRUARY 11, 2022
Passage of the CWD agent through meadow voles results in increased attack rates and decreased incubation periods in raccoons
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
MONDAY, APRIL 19, 2021
Evaluation of the application for new alternative biodiesel production process for rendered fat including Category 1 animal by-products (BDI-RepCat® process, AT) ???
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
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
5 or 6 years quarantine is NOT LONG ENOUGH FOR CWD TSE PRION !!!
QUARANTINE NEEDS TO BE 21 YEARS FOR CWD TSE PRION !
FRIDAY, APRIL 30, 2021
Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land?
***> 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
and so it seems...
Scrapie Agent (Strain 263K) Can Transmit Disease via the Oral Route after Persistence in Soil over Years
Published: May 9, 2007
snip...
Our results showed that 263K scrapie agent can persist in soil at least over 29 months. Strikingly, not only the contaminated soil itself retained high levels of infectivity, as evidenced by oral administration to Syrian hamsters, but also feeding of aqueous soil extracts was able to induce disease in the reporter animals. We could also demonstrate that PrPSc in soil, extracted after 21 months, provides a catalytically active seed in the protein misfolding cyclic amplification (PMCA) reaction. PMCA opens therefore a perspective for considerably improving the detectability of prions in soil samples from the field.
snip...
***> This is very likely to have parallels with control efforts for CWD in cervids. <***
Paper
Rapid recontamination of a farm building occurs after attempted prion removal
Kevin Christopher Gough BSc (Hons), PhD Claire Alison Baker BSc (Hons) Steve Hawkins MIBiol Hugh Simmons BVSc, MRCVS, MBA, MA Timm Konold DrMedVet, PhD, MRCVS … See all authors
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
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...
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.
***>This is very likely to have parallels with control efforts for CWD in cervids.
***> 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
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
***> 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
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.
***> 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.
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
Pathogens. 2020 Apr; 9(4): 311.
Published online 2020 Apr 23. doi: 10.3390/pathogens9040311
PMCID: PMC7238116
PMID: 32340296
Long-Term Incubation PrPCWD with Soils Affects Prion Recovery but Not Infectivity
Alsu Kuznetsova,1 Debbie McKenzie,2 Catherine Cullingham,3 and Judd M. Aiken1,*
Abstract
Chronic wasting disease (CWD) is a contagious prion disease of cervids. The infectious agent is shed from animals at the preclinical and clinical stages of disease where it persists in the environment as a reservoir of CWD infectivity. In this study, we demonstrate that long-term incubation of CWD prions (generated from tg-mice infected with deer or elk prions) with illite, montmorillonite (Mte) and whole soils results in decreased recovery of PrPCWD, suggesting that binding becomes more avid and irreversible with time. This continual decline of immunoblot PrPCWD detection did not correlate with prion infectivity levels. Bioassay showed no significant differences in incubation periods between mice inoculated with 1% CWD brain homogenate (BH) and with the CWD-BH pre-incubated with quartz or Luvisolic Ae horizon for 1 or 30 weeks. After 55 weeks incubation with Chernozem and Luvisol, bound PrPCWD was not detectable by immunoblotting but remained infectious. This study shows that although recovery of PrPCWD bound to soil minerals and whole soils with time become more difficult, prion infectivity is not significantly altered. Detection of prions in soil is, therefore, not only affected by soil type but also by length of time of the prion–soil interaction.
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4. Conclusions
The binding of prions to soil minerals and other soil constituents impacts PrPCWD recovery. During extended incubation with soils, PrP signal on immunoblots continuously declined until it was no longer detectable after 25 weeks in soils with loamy-clay texture and Mte minerology. PrPCWD infectivity did not, however, decrease after 30 weeks incubation with quartz and the Luvisolic Ae soil horizon. At 55 weeks incubation in Chernozem and Luvisol, CWD-BH remained infectious. We studied a wide variety of soil types (from prairie, mountain and boreal regions) and showed decreased PrPCWD signal recovery (as measured by immunoblotting) with retention of infectivity. The decrease in PrPCWD recovery was particularly dramatic in soils from the prairie region. Regardless of soil minerology, texture and humus content, detection of PrPCWD in environmental soil samples is a challenge after long-term incubation. These findings provide important information on the behavior of prions in natural environments, but complicate analysis of environmental samples.
Keywords: prion protein, soil, CWD, prolonged incubation, CWD infectivity, prion detection
Prion. 2012 Jul 1; 6(3): 302–308. doi: 10.4161/pri.20025 PMCID: PMC3399538 PMID: 22561162
Temperature influences the interaction of ruminant PrPTSE with soil
Ben C. Maddison, 1 Jonathan P. Owen, 1 Maged A. Taema, 2 George Shaw, 3 and Kevin C. Gough 2 , *
Abstract
Ovine scrapie and cervid chronic wasting disease can be transmitted in the absence of animal-to-animal contact, and environmental reservoirs of infectivity have been implicated in their spread and persistence. Investigating environmental factors that influence the interaction of disease-associated PrP with soils is imperative to understanding what is likely to be the complex role of soil in disease transmission. Here, we describe the effects of soil temperature on the binding/desorption and persistence of both ovine scrapie- and bovine BSE-PrPTSE. Binding of PrPTSE to a sandy loam soil at temperatures of 4°C, 8–12°C and 25–30°C demonstrated that an increase in temperature resulted in (1) a decrease in the amount of PrPTSE recovered after 24 h of interaction with soil, (2) an increase in the amount of N-terminal cleavage of the prion protein over 11 d and (3) a decrease in the persistence of PrPTSE on soil over an 18 mo period.
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In the present study we investigated the effects of soil temperature in the range 4°C to 30°C on the interaction of BSE- and scrapie-PrPTSE with a complex soil matrix. Lower soil temperatures resulted in increased levels of PrPTSE recovery and persistence over an 18-mo incubation period. A low soil temperature also resulted in less cleavage of the N-terminal domain of PrPTSE after an 11-d interaction. These effects of temperature on PrPTSE-soil interaction were likely to be exerted through both microbial activity and abiotic cleavage mechanisms. Together, the data indicate that for the recoverable fraction of PrPTSE, soils at lower temperature may release increased levels of PrPTSE.
A recent study using transmissible mink encephalopathy reported a correlation between the level of desorption of PrPTSE from soil and the infectivity titer of the sample.25 If such a correlation is also true for ovine scrapie and bovine BSE, the data presented here indicate that the bioavailability of prions in soil for the environmental transmission of scrapie or BSE may be influenced by the temperature of the soil. However, it remains to be seen whether the reported influence of temperature on prion interaction with a sandy-loam soil is consistent with other soil types. Of course, it should also be considered that temperature would be just one of a range of factors influencing the bioavailability of prions from soil; other factors would likely include soil type, prion strain and the biological matrix of the prion source. Scrapie and CWD are known to be spread by environmental routes and therefore understanding the range of factors that influence the persistence of environmental prions is vital in developing eradication programmes.
Keywords: BSE, environment, prion, scrapie, soil, transmission
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.
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***>>> 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.
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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
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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.
Published: 07 October 2021
Review on PRNP genetics and susceptibility to chronic wasting disease of Cervidae
Katayoun Moazami-Goudarzi, Olivier Andréoletti, Jean-Luc Vilotte & Vincent Béringue
Veterinary Research volume 52, Article number: 128 (2021) Cite this article
Abstract
To date, chronic wasting disease (CWD) is the most infectious form of prion disease affecting several captive, free ranging and wild cervid species. Responsible for marked population declines in North America, its geographical spread is now becoming a major concern in Europe. Polymorphisms in the prion protein gene (PRNP) are an important factor influencing the susceptibility to prions and their rate of propagation. All reported cervid PRNP genotypes are affected by CWD. However, in each species, some polymorphisms are associated with lower attack rates and slower progression of the disease. This has potential consequences in terms of genetic selection, CWD diffusion and strain evolution. CWD also presents a zoonotic risk due to prions capacity to cross species barriers. This review summarizes our current understanding of CWD control, focusing on PRNP genetic, strain diversity and capacity to infect other animal species, including humans.
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CWD positive animals with extended time before they succumb to disease likely represent a source of chronic prion shedding within populations and may contribute to environmental contamination.
***> CWD positive animals with extended time before they succumb to disease likely represent a source of chronic prion shedding within populations and may contribute to environmental contamination. <***
Genes (Basel) . 2021 Sep 10;12(9):1396. doi: 10.3390/genes12091396.
Selective Breeding for Disease-Resistant PRNP Variants to Manage Chronic Wasting Disease in Farmed Whitetail Deer
Nicholas Haley 1, Rozalyn Donner 1, Kahla Merrett 1, Matthew Miller 1, Kristen Senior 1
Affiliations expand
PMID: 34573378 DOI: 10.3390/genes12091396
Abstract
Chronic wasting disease (CWD) is a fatal transmissible spongiform encephalopathy (TSE) of cervids caused by a misfolded variant of the normal cellular prion protein, and it is closely related to sheep scrapie. Variations in a host's prion gene, PRNP, and its primary protein structure dramatically affect susceptibility to specific prion disorders, and breeding for PRNP variants that prevent scrapie infection has led to steep declines in the disease in North American and European sheep. While resistant alleles have been identified in cervids, a PRNP variant that completely prevents CWD has not yet been identified. Thus, control of the disease in farmed herds traditionally relies on quarantine and depopulation. In CWD-endemic areas, depopulation of private herds becomes challenging to justify, leading to opportunities to manage the disease in situ. We developed a selective breeding program for farmed white-tailed deer in a high-prevalence CWD-endemic area which focused on reducing frequencies of highly susceptible PRNP variants and introducing animals with less susceptible variants. With the use of newly developed primers, we found that breeding followed predictable Mendelian inheritance, and early data support our project's utility in reducing CWD prevalence. This project represents a novel approach to CWD management, with future efforts building on these findings.
Keywords: CWD; PRNP; deer; prion; resistance; selective breeding; susceptibility.
***> While resistant alleles have been identified in cervids, a PRNP variant that completely prevents CWD has not yet been identified.
In Moore et al., reindeer carrying allele E had longer survival-times following intracranial exposure [24]. In the same experiment, a reindeer with a genotype carrier of E, found dead without showing clinical signs ~13 months post-intracranial inoculation, had no histopathological lesions or PrPSc deposition at post-mortem examination.
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Our data support the notion that PRNP genetic variation modulates CWD susceptibility rather than conferring complete resistance. This is in agreement with experimental observations of reindeer-developing CWD after intracranial inoculation regardless of PRNP genotype [24].
***> Our data support the notion that PRNP genetic variation modulates CWD susceptibility rather than conferring complete resistance.
Published: 27 May 2021
White-tailed deer S96 prion protein does not support stable in vitro propagation of most common CWD strains
Alicia Otero, Camilo Duque Velásquez, Judd Aiken & Debbie McKenzie
Scientific Reports volume 11, Article number: 11193 (2021) Cite this article
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Abstract
PrPC variation at residue 96 (G/S) plays an important role in the epidemiology of chronic wasting disease (CWD) in exposed white-tailed deer populations. In vivo studies have demonstrated the protective effect of serine at codon 96, which hinders the propagation of common CWD strains when expressed in homozygosis and increases the survival period of S96/wt heterozygous deer after challenge with CWD. Previous in vitro studies of the transmission barrier suggested that following a single amplification step, wt and S96 PrPC were equally susceptible to misfolding when seeded with various CWD prions. When we performed serial prion amplification in vitro using S96-PrPC, we observed a reduction in the efficiency of propagation with the Wisc-1 or CWD2 strains, suggesting these strains cannot stably template their conformations on this PrPC once the primary sequence has changed after the first round of replication. Our data shows the S96-PrPC polymorphism is detrimental to prion conversion of some CWD strains. These data suggests that deer homozygous for S96-PrPC may not sustain prion transmission as compared to a deer expressing G96-PrPC.
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The protective effect of S96 and H95 alleles was further demonstrated by experimental oral infection in white-tailed deer expressing these amino acid substitutions19. Among the alleles of the PRNP gene associated with a lower CWD incidence and extended preclinical phase, S96 has the highest allelic frequency (~ 25%) after the wt allele in several white-tailed deer populations from the United States and Canada26,27,31. Subsequent independent transmission and epidemiological studies have demonstrated that deer homozygous and heterozygous for S96-PrPC are, compared to wt/wt deer, less susceptible to CWD infection, present prolonged survival times, show delayed prion accumulation and are generally at a significantly earlier stage of disease when deer herds are depopulated23,31,32,33.
***> Subsequent independent transmission and epidemiological studies have demonstrated that deer homozygous and heterozygous for S96-PrPC are, compared to wt/wt deer, less susceptible to CWD infection, present prolonged survival times,
Prion protein polymorphisms associated with reduced CWD susceptibility limit peripheral PrPCWD deposition in orally infected white-tailed deer
Alicia Otero1 , Camilo Duque Velásquez4,5, Chad Johnson3 , Allen Herbst2,5, Rosa Bolea1 , Juan José Badiola1 , Judd Aiken2,5 and Debbie McKenzie4,5*
Abstract
Background: Chronic wasting disease (CWD) is a prion disease affecting members of the Cervidae family. PrPC primary structures play a key role in CWD susceptibility resulting in extended incubation periods and regulating the propagation of CWD strains. We analyzed the distribution of abnormal prion protein (PrPCWD) aggregates in brain and peripheral organs from orally inoculated white-tailed deer expressing four different PRNP genotypes: Q95G96/ Q95G96 (wt/wt), S96/wt, H95/wt and H95/S96 to determine if there are substantial differences in the deposition pattern of PrPCWD between different PRNP genotypes.
Results: Although we detected differences in certain brain areas, globally, the different genotypes showed similar PrPCWD deposition patterns in the brain. However, we found that clinically affected deer expressing H95 PrPC , despite having the longest survival periods, presented less PrPCWD immunoreactivity in particular peripheral organs. In addition, no PrPCWD was detected in skeletal muscle of any of the deer.
Conclusions: Our data suggest that expression of H95-PrPC limits peripheral accumulation of PrPCWD as detected by immunohistochemistry. Conversely, infected S96/wt and wt/wt deer presented with similar PrPCWD peripheral distribution at terminal stage of disease, suggesting that the S96-PrPC allele, although delaying CWD progression, does not completely limit the peripheral accumulation of the infectious agent.
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The significantly longer incubation periods observed in deer with H95-PRNP alleles may not impact secretion of CWD (i.e., less CWD secreted over longer time periods). The emergence of new CWD strains could implicate a zoonotic potential [20].
Keywords: Prions, Prion diseases, Chronic wasting disease, CWD, PrPCWD, Peripheral tissues, Polymorphisms, Deer
***> Selective Breeding
***> less susceptible to CWD infection, present prolonged survival times...
this is very disturbing. with all the hype about selective breeding with different alleles, and presenting longer survival times with cwd, this would only allow the spreading of the cwd tse prion to last longer in the given environment imo., and as such has been stated in scientific literature...terry
With cervids, however, resistance based on the PRNP allele alone is not absolute, and is better characterized as a delayed progression [18,25]
Volume 23, Number 9—September 2017 Research Letter
Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion
Allen Herbst1, Camilo Duque Velásquez1, Elizabeth Triscott, Judd M. Aiken, and Debbie McKenzieComments to Author Author affiliations: University of Alberta, Edmonton, Alberta, Canada
Abstract
Human and mouse prion proteins share a structural motif that regulates resistance to common chronic wasting disease (CWD) prion strains. Successful transmission of an emergent strain of CWD prion, H95+, into mice resulted in infection. Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.
P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD
In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible.
***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
PRION 2016 CONFERENCE TOKYO
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.'' c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§
Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g
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Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.
THURSDAY, DECEMBER 16, 2021
Detection of CWD prions in naturally infected white‑tailed deer fetuses and gestational tissues by PMCA
THURSDAY, DECEMBER 16, 2021
RT‑QuIC detection of CWD prion seeding activity in white‑tailed deer muscle tissues
ARS RESEARCH Generation of human chronic wasting disease in transgenic mice
Publication Acceptance Date: 9/8/2021
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
Title: Generation of human chronic wasting disease in transgenic mice
Author item WANG, ZERUI - Case Western Reserve University (CWRU) item QIN, KEFENG - University Of Chicago item CAMACHO, MANUEL - Case Western Reserve University (CWRU) item SHEN, PINGPING - Case Western Reserve University (CWRU) item YUAN, JUE - Case Western Reserve University (CWRU) item Greenlee, Justin item CUI, LI - Jilin University item KONG, QINGZHONG - Case Western Reserve University (CWRU) item MASTRIANNI, JAMES - University Of Chicago item ZOU, WEN-QUAN - Case Western Reserve University (CWRU)
Submitted to: Acta Neuropathologica Publication Type: Peer Reviewed Journal Publication Acceptance Date: 9/8/2021 Publication Date: N/A Citation: N/A
Interpretive Summary: Prion diseases are invariably fatal neurologic diseases for which there is no known prevention or cure. Chronic wasting disease (CWD) is the prion disease of deer and elk and is present in farmed and free ranging herds throughout North America. To date there is no clear evidence that the CWD agent could be transmitted to humans. This manuscript describes the use of an in vitro technique, cell-free serial protein misfolding cyclic amplification (sPMCA), to generate a CWD prion that is infectious to transgenic mice expressing the human prion protein. This study provides the first evidence that CWD prions may be able to cause misfolding in the human prion protein. This information will impact medical experts and those involved in making policy for farmed cervids and wildlife.
Technical Abstract: Chronic wasting disease (CWD) is a cervid spongiform encephalopathy or prion disease caused by the infectious prion or PrPSc, a misfolded conformer of cellular prion protein (PrPC). It has rapidly spread in North America and also has been found in Asia and Europe. In contrast to the zoonotic mad cow disease that is the first animal prion disease found transmissible to humans, the transmissibility of CWD to humans remains uncertain although most previous studies have suggested that humans may not be susceptible to CWD. Here we report the generation of an infectious human PrPSc by seeding CWD PrPSc in normal human brain PrPC through the in vitro cell-free serial protein misfolding cyclic amplification (sPMCA). Western blotting confirms that the sPMCA-induced proteinase K-resistant PrPSc is a human form, evidenced by a PrP-specific antibody that recognizes human but not cervid PrP. Remarkably, two lines of humanized transgenic (Tg) mice expressing human PrP-129Val/Val (VV) or -129Met/Met (MM) polymorphism develop prion disease at 233 ± 6 (mean ± SE) days post-inoculation (dpi) and 552 ± 27 dpi, respectively, upon intracerebral inoculation with the sPMCA-generated PrPSc. The brain of diseased Tg mice reveals the electrophoretic profile of PrPSc similar to sporadic Creutzfeldt-Jakob disease (sCJD) MM1 or VV2 subtype but different neuropathological patterns. We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.
''The brain of diseased Tg mice reveals the electrophoretic profile of PrPSc similar to sporadic Creutzfeldt-Jakob disease (sCJD) MM1 or VV2 subtype but different neuropathological patterns.''
''We believe that our study provides the first evidence that CWD PrPSc is able to convert human PrPC into PrPSc in vitro and the CWD-derived human PrPSc mimics atypical sCJD subtypes in humanized Tg mice.''
Published: 26 September 2021
Generation of human chronic wasting disease in transgenic mice
Zerui Wang, Kefeng Qin, Manuel V. Camacho, Ignazio Cali, Jue Yuan, Pingping Shen, Justin Greenlee, Qingzhong Kong, James A. Mastrianni & Wen-Quan Zou
Acta Neuropathologica Communications volume 9, Article number: 158 (2021)
Abstract
Chronic wasting disease (CWD) is a cervid prion disease caused by the accumulation of an infectious misfolded conformer (PrPSc) of cellular prion protein (PrPC). It has been spreading rapidly in North America and also found in Asia and Europe. Although bovine spongiform encephalopathy (i.e. mad cow disease) is the only animal prion disease known to be zoonotic, the transmissibility of CWD to humans remains uncertain. Here we report the generation of the first CWD-derived infectious human PrPSc by elk CWD PrPSc-seeded conversion of PrPC in normal human brain homogenates using in vitro protein misfolding cyclic amplification (PMCA). Western blotting with human PrP selective antibody confirmed that the PMCA-generated protease-resistant PrPSc was derived from the human PrPC substrate. Two lines of humanized transgenic mice expressing human PrP with either Val or Met at the polymorphic codon 129 developed clinical prion disease following intracerebral inoculation with the PMCA-generated CWD-derived human PrPSc. Diseased mice exhibited distinct PrPSc patterns and neuropathological changes in the brain. Our study, using PMCA and animal bioassays, provides the first evidence that CWD PrPSc can cross the species barrier to convert human PrPC into infectious PrPSc that can produce bona fide prion disease when inoculated into humanized transgenic mice.
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It is worth noting that the annual number of sporadic CJD (sCJD) cases in the USA has increased, with the total number of suspected and confirmed sCJD cases rising from 284 in 2003 to 511 in 2017 (https://www.cdc.gov/prions/cjd/occurrence-transmission.html). The greatly enhanced CJD surveillance and an aging population in the USA certainly contributed to the observed increase in annual sCJD case numbers in recent years, but the possibility cannot be excluded that some of the increased sCJD prevalence is linked to CWD exposure.
In the present study, using serial protein misfolding cyclic amplification (sPMCA) assay we generate PrPSc by seeding CWD prions in normal human brain homogenates. Importantly, we reveal that two lines of humanized Tg mice expressing human PrP-129VV and 129MM develop prion diseases upon intracerebral inoculation of the abnormal PrP generated by sPMCA. We believe that our study provides the first opportunity to dissect the clinical, pathological and biochemical features of the CWD-derived human prion disease in two lines of humanized Tg mice expressing two major human PrP genotypes, respectively.
i thought i might share some news about cwd zoonosis that i got, that i cannot share or post to the public yet, i promised for various reasons, one that it will cause a shit storm for sure, but it was something i really already knew from previous studies, but, i was told that ;
==================
https://www.nature.com/articles/srep11573
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
''As you can imagine, 2 and 5 (especially 5) may raise alarms. The evidence we have for 4 are not as strong or tight as I would like to have. At this point, please do not post any of the points publicly yet, but you can refer to points 1-3 in private discussions and all 5 points when discussing with relevant public officials to highlight the long-term risks of CWD zoonosis.''
====================
so, i figure your as about as official as it gets, and i think this science is extremely important for you to know and to converse about with your officials. it's about to burn a whole in my pocket. this is about as close as it will ever get for cwd zoonosis to be proven in my time, this and what Canada Czub et al found with the Macaques, plus an old study from cjd surveillance unit back that showed cjd and a 9% increase in risk from folks that eat venison, i will post all this below for your files Sir. i remember back in the BSE nvCJD days, from when the first BSE case in bovine was confirmed around 1984 maybe 83, i forget the good vets named that screwed it up first, Carol something, but from 83ish to 95 96 when nvCJD was linked to humans from BSE in cattle, so that took 10 to 15 years. hell, at that rate, especially with Texas and cwd zoonsis, hell, i'll be dead before it's official, if ever, so here ya go Sir. there was a grant study on cwd zoonosis that had been going on for some time, i followed it over the years, then the grant date for said study had expired, so, i thought i would write the good Professor about said study i.e. Professor Kong, CWRU et al. i will post the grant study abstract first, and then after that, what reply i got back, about said study that i was told not to post/publish...
CWD ZOONOSIS GRANT FIRST;
===============
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that: (1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; (2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; (3) Reliable essays can be established to detect CWD infection in humans; and (4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
Funding Agency Agency National Institute of Health (NIH) Institute National Institute of Neurological Disorders and Stroke (NINDS) Type Research Project (R01) Project # 1R01NS088604-01A1 Application # 9037884 Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND) Program Officer Wong, May Project Start 2015-09-30 Project End 2019-07-31 Budget Start 2015-09-30 Budget End 2016-07-31 Support Year 1 Fiscal Year 2015 Total Cost $337,507 Indirect Cost $118,756
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Professor Kongs reply to me just this month about above grant study that has NOT been published in peer reveiw yet...
=================================
Here is a brief summary of our findings:
snip...can't post, made a promise...tss
On Sat, Apr 3, 2021 at 12:19 PM Terry Singeltary <flounder9@verizon.net> wrote:
snip...
end...tss
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CWD ZOONOSIS THE FULL MONTY TO DATE
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.
SUNDAY, JULY 25, 2021
North American and Norwegian Chronic Wasting Disease prions exhibit different potential for interspecies transmission and zoonotic risk
''Our data suggest that reindeer and red deer from Norway could be the most transmissible CWD prions to other mammals, whereas North American CWD prions were more prone to generate human prions in vitro.''
MONDAY, JULY 19, 2021
***> U Calgary researchers at work on a vaccine against a fatal infectious disease affecting deer and potentially people
Prion Conference 2018 Abstracts
BSE aka MAD COW DISEASE, was first discovered in 1984, and it took until 1995 to finally admit that BSE was causing nvCJD, the rest there is history, but that science is still evolving i.e. science now shows that indeed atypical L-type BSE, atypical Nor-98 Scrapie, and typical Scrapie are all zoonosis, zoonotic for humans, there from.
HOW long are we going to wait for Chronic Wasting Disease, CWD TSE Prion of Cervid, and zoonosis, zoonotic tranmission to humans there from?
Studies have shown since 1994 that humans are susceptible to CWD TSE Prion, so, what's the hold up with making CWD a zoonotic zoonosis disease, the iatrogenic transmissions there from is not waiting for someone to make a decision.
Prion Conference 2018 Abstracts
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.
Background
Chronic wasting disease (CWD) is a prion disease of deer and elk that has been identified in freeranging cervids in 23 US states. While there is currently no epidemiological evidence for zoonotic transmission through the consumption of contaminated venison, studies suggest the CWD agent can cross the species barrier in experimental models designed to closely mimic humans. We compared rates of human prion disease in states with and without CWD to examine the possibility of undetermined zoonotic transmission.
Methods
Death records from the National Center for Health Statistics, case records from the National Prion Disease Pathology Surveillance Center, and additional state case reports were combined to create a database of human prion disease cases from 2003-2015. Identification of CWD in each state was determined through reports of positive CWD tests by state wildlife agencies. Age- and race-adjusted mortality rates for human prion disease, excluding cases with known etiology, were determined for four categories of states based on CWD occurrence: highly endemic (>16 counties with CWD identified in free-ranging cervids); moderately endemic (3-10 counties with CWD); low endemic (1-2 counties with CWD); and no CWD states. States were counted as having no CWD until the year CWD was first identified. Analyses stratified by age, sex, and time period were also conducted to focus on subgroups for which zoonotic transmission would be more likely to be detected: cases <55 years old, male sex, and the latter half of the study (2010-2015).
Results
Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states (rate ratio [RR]: 1.12, 95% confidence interval [CI] = 1.01 - 1.23), as did low endemic states (RR: 1.15, 95% CI = 1.04 - 1.27). Moderately endemic states did not have an elevated mortality rate (RR: 1.05, 95% CI = 0.93 - 1.17). In age-stratified analyses, prion disease mortality rates among the <55 year old population were elevated for moderately endemic states (RR: 1.57, 95% CI = 1.10 – 2.24) while mortality rates were elevated among those ≥55 for highly endemic states (RR: 1.13, 95% CI = 1.02 - 1.26) and low endemic states (RR: 1.16, 95% CI = 1.04 - 1.29). In other stratified analyses, prion disease mortality rates for males were only elevated for low endemic states (RR: 1.27, 95% CI = 1.10 - 1.48), and none of the categories of CWD-endemic states had elevated mortality rates for the latter time period (2010-2015).
Conclusions
While higher prion disease mortality rates in certain categories of states with CWD in free-ranging cervids were noted, additional stratified analyses did not reveal markedly elevated rates for potentially sensitive subgroups that would be suggestive of zoonotic transmission. Unknown confounding factors or other biases may explain state-by-state differences in prion disease mortality.
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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.
Prion disease is a fatal progressive neurodegenerative disease due to deposition of an abnormal protease-resistant isoform of prion protein. Typical symptoms include rapidly progressive dementia, myoclonus, visual disturbance and hallucinations. Interestingly, in patients with prion disease, the abnormal protein canould also be found in the peripheral nervous system. Case reports of prion deposition in peripheral nerves have been reported. Peripheral nerve involvement is thought to be uncommon; however, little is known about the exact prevalence and features of peripheral neuropathy in patients with prion disease.
We reviewed autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017. We collected information regarding prion protein diagnosis, demographics, comorbidities, clinical symptoms, physical exam, neuropathology, molecular subtype, genetics lab, brain MRI, image and EMG reports. Our study included 104 patients. Thirteen (12.5%) patients had either subjective symptoms or objective signs of peripheral neuropathy. Among these 13 patients, 3 had other known potential etiologies of peripheral neuropathy such as vitamin B12 deficiency or prior chemotherapy. Among 10 patients that had no other clear etiology, 3 (30%) had familial CJD. The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%). The Majority of cases wasere male (60%). Half of them had exposure to wild game. The most common subjective symptoms were tingling and/or numbness of distal extremities. The most common objective finding was diminished vibratory sensation in the feet. Half of them had an EMG with the findings ranging from fasciculations to axonal polyneuropathy or demyelinating polyneuropathy.
Our study provides an overview of the pattern of peripheral neuropathy in patients with prion disease. Among patients with peripheral neuropathy symptoms or signs, majority has polyneuropathy. It is important to document the baseline frequency of peripheral neuropathy in prion diseases as these symptoms may become important when conducting surveillance for potential novel zoonotic prion diseases.
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P177 PrP plaques in methionine homozygous Creutzfeldt-Jakob disease patients as a potential marker of iatrogenic transmission
Abrams JY (1), Schonberger LB (1), Cali I (2), Cohen Y (2), Blevins JE (2), Maddox RA (1), Belay ED (1), Appleby BS (2), Cohen ML (2)
(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.
Background
Sporadic Creutzfeldt-Jakob disease (CJD) is widely believed to originate from de novo spontaneous conversion of normal prion protein (PrP) to its pathogenic form, but concern remains that some reported sporadic CJD cases may actually be caused by disease transmission via iatrogenic processes. For cases with methionine homozygosity (CJD-MM) at codon 129 of the PRNP gene, recent research has pointed to plaque-like PrP deposition as a potential marker of iatrogenic transmission for a subset of cases. This phenotype is theorized to originate from specific iatrogenic source CJD types that comprise roughly a quarter of known CJD cases.
Methods
We reviewed scientific literature for studies which described PrP plaques among CJD patients with known epidemiological links to iatrogenic transmission (receipt of cadaveric human grown hormone or dura mater), as well as in cases of reported sporadic CJD. The presence and description of plaques, along with CJD classification type and other contextual factors, were used to summarize the current evidence regarding plaques as a potential marker of iatrogenic transmission. In addition, 523 cases of reported sporadic CJD cases in the US from January 2013 through September 2017 were assessed for presence of PrP plaques.
Results
We identified four studies describing 52 total cases of CJD-MM among either dura mater recipients or growth hormone recipients, of which 30 were identified as having PrP plaques. While sporadic cases were not generally described as having plaques, we did identify case reports which described plaques among sporadic MM2 cases as well as case reports of plaques exclusively in white matter among sporadic MM1 cases. Among the 523 reported sporadic CJD cases, 0 of 366 MM1 cases had plaques, 2 of 48 MM2 cases had kuru plaques, and 4 of 109 MM1+2 cases had either kuru plaques or both kuru and florid plaques. Medical chart review of the six reported sporadic CJD cases with plaques did not reveal clinical histories suggestive of potential iatrogenic transmission.
Conclusions
PrP plaques occur much more frequently for iatrogenic CJD-MM cases compared to sporadic CJDMM cases. Plaques may indicate iatrogenic transmission for CJD-MM cases without a type 2 Western blot fragment. The study results suggest the absence of significant misclassifications of iatrogenic CJD as sporadic. To our knowledge, this study is the first to describe grey matter kuru plaques in apparently sporadic CJD-MM patients with a type 2 Western blot fragment.
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P180 Clinico-pathological analysis of human prion diseases in a brain bank series
Ximelis T (1), Aldecoa I (1,2), Molina-Porcel L (1,3), Grau-Rivera O (4), Ferrer I (5), Nos C (6), Gelpi E (1,7), Sánchez-Valle R (1,4)
(1) Neurological Tissue Bank of the Biobanc-Hospital ClÃnic-IDIBAPS, Barcelona, Spain (2) Pathological Service of Hospital ClÃnic de Barcelona, Barcelona, Spain (3) EAIA Trastorns Cognitius, Centre Emili Mira, Parc de Salut Mar, Barcelona, Spain (4) Department of Neurology of Hospital ClÃnic de Barcelona, Barcelona, Spain (5) Institute of Neuropathology, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Barcelona (6) General subdirectorate of Surveillance and Response to Emergencies in Public Health, Department of Public Health in Catalonia, Barcelona, Spain (7) Institute of Neurology, Medical University of Vienna, Vienna, Austria.
Background and objective:
The Neurological Tissue Bank (NTB) of the Hospital Clínic-Institut d‘Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain is the reference center in Catalonia for the neuropathological study of prion diseases in the region since 2001. The aim of this study is to analyse the characteristics of the confirmed prion diseases registered at the NTB during the last 15 years.
Methods:
We reviewed retrospectively all neuropathologically confirmed cases registered during the period January 2001 to December 2016.
Results:
176 cases (54,3% female, mean age: 67,5 years and age range: 25-86 years) of neuropathological confirmed prion diseases have been studied at the NTB. 152 cases corresponded to sporadic Creutzfeldt-Jakob disease (sCJD), 10 to genetic CJD, 10 to Fatal Familial Insomnia, 2 to GerstmannSträussler-Scheinker disease, and 2 cases to variably protease-sensitive prionopathy (VPSPr). Within sCJD subtypes the MM1 subtype was the most frequent, followed by the VV2 histotype.
Clinical and neuropathological diagnoses agreed in 166 cases (94%). The clinical diagnosis was not accurate in 10 patients with definite prion disease: 1 had a clinical diagnosis of Fronto-temporal dementia (FTD), 1 Niemann-Pick‘s disease, 1 Lewy Body‘s Disease, 2 Alzheimer‘s disease, 1 Cortico-basal syndrome and 2 undetermined dementia. Among patients with VPSPr, 1 had a clinical diagnosis of Amyotrophic lateral sclerosis (ALS) and the other one with FTD.
Concomitant pathologies are frequent in older age groups, mainly AD neuropathological changes were observed in these subjects.
Discussion:
A wide spectrum of human prion diseases have been identified in the NTB being the relative frequencies and main characteristics like other published series. There is a high rate of agreement between clinical and neuropathological diagnoses with prion diseases. These findings show the importance that public health has given to prion diseases during the past 15 years. Continuous surveillance of human prion disease allows identification of new emerging phenotypes. Brain tissue samples from these donors are available to the scientific community. For more information please visit:
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P192 Prion amplification techniques for the rapid evaluation of surface decontamination procedures
Bruyere-Ostells L (1), Mayran C (1), Belondrade M (1), Boublik Y (2), Haïk S (3), Fournier-Wirth C (1), Nicot S (1), Bougard D (1)
(1) Pathogenesis and control of chronic infections, Etablissement Français du Sang, Inserm, Université de Montpellier, Montpellier, France. (2) Centre de Recherche en Biologie cellulaire de Montpellier, CNRS, Université de Montpellier, Montpellier, France. (3) Inserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Université Paris 06 UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, Paris, France.
Aims:
Transmissible Spongiform Encephalopathies (TSE) or prion diseases are a group of incurable and always fatal neurodegenerative disorders including Creutzfeldt-Jakob diseases (CJD) in humans. These pathologies include sporadic (sCJD), genetic and acquired (variant CJD) forms. By the past, sCJD and vCJD were transmitted by different prion contaminated biological materials to patients resulting in more than 400 iatrogenic cases (iCJD). The atypical nature and the biochemical properties of the infectious agent, formed by abnormal prion protein or PrPTSE, make it particularly resistant to conventional decontamination procedures. In addition, PrPTSE is widely distributed throughout the organism before clinical onset in vCJD and can also be detected in some peripheral tissues in sporadic CJD. Risk of iatrogenic transmission of CJD by contaminated medical device remains thus a concern for healthcare facilities. Bioassay is the gold standard method to evaluate the efficacy of prion decontamination procedures but is time-consuming and expensive. Here, we propose to compare in vitro prion amplification techniques: Protein Misfolding Cyclic Amplification (PMCA) and Real-Time Quaking Induced Conversion (RT-QuIC) for the detection of residual prions on surface after decontamination.
Methods:
Stainless steel wires, by mimicking the surface of surgical instruments, were proposed as a carrier model of prions for inactivation studies. To determine the sensitivity of the two amplification techniques on wires (Surf-PMCA and Surf-QuIC), steel wires were therefore contaminated with serial dilutions of brain homogenates (BH) from a 263k infected hamster and from a patient with sCJD (MM1 subtype). We then compared the different standard decontamination procedures including partially and fully efficient treatments by detecting the residual seeding activity on 263K and sCJD contaminated wires. We completed our study by the evaluation of marketed reagents endorsed for prion decontamination.
Results:
The two amplification techniques can detect minute quantities of PrPTSE adsorbed onto a single wire. 8/8 wires contaminated with a 10-6 dilution of 263k BH and 1/6 with the 10-8 dilution are positive with Surf-PMCA. Similar performances were obtained with Surf-QuIC on 263K: 10/16 wires contaminated with 10-6 dilution and 1/8 wires contaminated with 10-8 dilution are positive. Regarding the human sCJD-MM1 prion, Surf-QuIC allows us to detect 16/16 wires contaminated with 10-6 dilutions and 14/16 with 10-7 . Results obtained after decontamination treatments are very similar between 263K and sCJD prions. Efficiency of marketed treatments to remove prions is lower than expected.
Conclusions:
Surf-PMCA and Surf-QuIC are very sensitive methods for the detection of prions on wires and could be applied to prion decontamination studies for rapid evaluation of new treatments. Sodium hypochlorite is the only product to efficiently remove seeding activity of both 263K and sCJD prions.
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WA2 Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Schatzl HM (1, 2), Hannaoui S (1, 2), Cheng Y-C (1, 2), Gilch S (1, 2), Beekes M (3), SchulzSchaeffer W (4), Stahl-Hennig C (5) and Czub S (2, 6)
(1) University of Calgary, Calgary Prion Research Unit, Calgary, Canada (2) University of Calgary, Faculty of Veterinary Medicine, Calgary, Canada, (3) Robert Koch Institute, Berlin, Germany, (4) University of Homburg/Saar, Homburg, Germany, (5) German Primate Center, Goettingen, Germany, (6) Canadian Food Inspection Agency (CFIA), Lethbridge, Canada.
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 found in spinal cord and brain of 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 preclinical 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. 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.
See also poster P103
***> 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.
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WA16 Monitoring Potential CWD Transmission to Humans
Belay ED
Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA.
The spread of chronic wasting disease (CWD) in animals has raised concerns about increasing human exposure to the CWD agent via hunting and venison consumption, potentially facilitating CWD transmission to humans. Several studies have explored this possibility, including limited epidemiologic studies, in vitro experiments, and laboratory studies using various types of animal models. Most human exposures to the CWD agent in the United States would be expected to occur in association with deer and elk hunting in CWD-endemic areas. The Centers for Disease Control and Prevention (CDC) collaborated with state health departments in Colorado, Wisconsin, and Wyoming to identify persons at risk of CWD exposure and to monitor their vital status over time. Databases were established of persons who hunted in Colorado and Wyoming and those who reported consumption of venison from deer that later tested positive in Wisconsin. Information from the databases is periodically cross-checked with mortality data to determine the vital status and causes of death for deceased persons. Long-term follow-up of these hunters is needed to assess their risk of development of a prion disease linked to CWD exposure.
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P166 Characterization of CJD strain profiles in venison consumers and non-consumers from Alberta and Saskatchewan
Stephanie Booth (1,2), Lise Lamoureux (1), Debra Sorensen (1), Jennifer L. Myskiw (1,2), Megan Klassen (1,2), Michael Coulthart (3), Valerie Sim (4)
(1) Zoonotic Diseases and Special Pathogens, National Microbiology Laboratory, Public Health Agency of Canada, Winnipeg (2) Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg (3) Canadian CJD Surveillance System, Public Health Agency of Canada, Ottawa (4) Division of Neurology, Department of Medicine Centre for Prions and Protein Folding Diseases, University of Alberta, Edmonton.
Chronic wasting disease (CWD) is spreading rapidly through wild cervid populations in the Canadian provinces of Alberta and Saskatchewan. While this has implications for tourism and hunting, there is also concern over possible zoonotic transmission to humans who eat venison from infected deer. Whilst there is no evidence of any human cases of CWD to date, the Canadian CJD Surveillance System (CJDSS) in Canada is staying vigilant. When variant CJD occurred following exposure to BSE, the unique biochemical fingerprint of the pathologic PrP enabled a causal link to be confirmed. However, we cannot be sure what phenotype human CWD prions would present with, or indeed, whether this would be distinct from that see in sporadic CJD. Therefore we are undertaking a systematic analysis of the molecular diversity of CJD cases of individuals who resided in Alberta and Saskatchewan at their time of death comparing venison consumers and non-consumers, using a variety of clinical, imaging, pathological and biochemical markers. Our initial objective is to develop novel biochemical methodologies that will extend the baseline glycoform and genetic polymorphism typing that is already completed by the CJDSS. Firstly, we are reviewing MRI, EEG and pathology information from over 40 cases of CJD to select clinically affected areas for further investigation. Biochemical analysis will include assessment of the levels of protease sensitive and resistant prion protein, glycoform typing using 2D gel electrophoresis, testing seeding capabilities and kinetics of aggregation by quaking-induced conversion, and determining prion oligomer size distributions with asymmetric flow field fractionation with in-line light scattering. Progress and preliminary data will be presented. Ultimately, we intend to further define the relationship between PrP structure and disease phenotype and establish a baseline for the identification of future atypical CJD cases that may arise as a result of exposure to CWD.
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Source Prion Conference 2018 Abstracts
Volume 24, Number 8—August 2018 Research Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions
Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)
Abstract Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted.
snip...
Discussion Characterization of the transmission properties of CWD and evaluation of their zoonotic potential are important for public health purposes. Given that CWD affects several members of the family Cervidae, it seems reasonable to consider whether the zoonotic potential of CWD prions could be affected by factors such as CWD strain, cervid species, geographic location, and Prnp–PRNP polymorphic variation. We have previously used an in vitro conversion assay (PMCA) to investigate the susceptibility of the human PrP to conversion to its disease-associated form by several animal prion diseases, including CWD (15,16,22). The sensitivity of our molecular model for the detection of zoonotic conversion depends on the combination of 1) the action of proteinase K to degrade the abundant human PrPC that constitutes the substrate while only N terminally truncating any human PrPres produced and 2) the presence of the 3F4 epitope on human but not cervid PrP. In effect, this degree of sensitivity means that any human PrPres formed during the PMCA reaction can be detected down to the limit of Western blot sensitivity. In contrast, if other antibodies that detect both cervid and human PrP are used, such as 6H4, then newly formed human PrPres must be detected as a measurable increase in PrPres over the amount remaining in the reaction product from the cervid seed. Although best known for the efficient amplification of prions in research and diagnostic contexts, the variation of the PMCA method employed in our study is optimized for the definitive detection of zoonotic reaction products of inherently inefficient conversion reactions conducted across species barriers. By using this system, we previously made and reported the novel observation that elk CWD prions could convert human PrPC from human brain and could also convert recombinant human PrPC expressed in transgenic mice and eukaryotic cell cultures (15).
A previous publication suggested that mule deer PrPSc was unable to convert humanized transgenic substrate in PMCA assays (23) and required a further step of in vitro conditioning in deer substrate PMCA before it was able to cross the deer–human molecular barrier (24). However, prions from other species, such as elk (15) and reindeer affected by CWD, appear to be compatible with the human protein in a single round of amplification (as shown in our study). These observations suggest that different deer species affected by CWD could present differing degrees of the olecular compatibility with the normal form of human PrP.
The contribution of the polymorphism at codon 129 of the human PrP gene has been extensively studied and is recognized as a risk factor for Creutzfeldt-Jakob disease (4). In cervids, the equivalent codon corresponds to the position 132 encoding methionine or leucine. This polymorphism in the elk gene has been shown to play an important role in CWD susceptibility (25,26). We have investigated the effect of this cervid Prnp polymorphism on the conversion of the humanized transgenic substrate according to the variation in the equivalent PRNP codon 129 polymorphism. Interestingly, only the homologs methionine homozygous seed–substrate reactions could readily convert the human PrP, whereas the heterozygous elk PrPSc was unable to do so, even though comparable amounts of PrPres were used to seed the reaction. In addition, we observed only low levels of human PrPres formation in the reactions seeded with the homozygous methionine (132 MM) and the heterozygous (132 ML) seeds incubated with the other 2 human polymorphic substrates (129 MV and 129 VV). The presence of the amino acid leucine at position 132 of the elk Prnp gene has been attributed to a lower degree of prion conversion compared with methionine on the basis of experiments in mice made transgenic for these polymorphic variants (26). Considering the differences observed for the amplification of the homozygous human methionine substrate by the 2 polymorphic elk seeds (MM and ML), reappraisal of the susceptibility of human PrPC by the full range of cervid polymorphic variants affected by CWD would be warranted.
In light of the recent identification of the first cases of CWD in Europe in a free-ranging reindeer (R. tarandus) in Norway (2), we also decided to evaluate the in vitro conversion potential of CWD in 2 experimentally infected reindeer (18). Formation of human PrPres was readily detectable after a single round of PMCA, and in all 3 humanized polymorphic substrates (MM, MV, and VV). This finding suggests that CWD prions from reindeer could be more compatible with human PrPC generally and might therefore present a greater risk for zoonosis than, for example, CWD prions from white-tailed deer. A more comprehensive comparison of CWD in the affected species, coupled with the polymorphic variations in the human and deer PRNP–Prnp genes, in vivo and in vitro, will be required before firm conclusions can be drawn. Analysis of the Prnp sequence of the CWD reindeer in Norway was reported to be identical to the specimens used in our study (2). This finding raises the possibility of a direct comparison of zoonotic potential between CWD acquired in the wild and that produced in a controlled laboratory setting. (Table).
The prion hypothesis proposes that direct molecular interaction between PrPSc and PrPC is necessary for conversion and prion replication. Accordingly, polymorphic variants of the PrP of host and agent might play a role in determining compatibility and potential zoonotic risk. In this study, we have examined the capacity of the human PrPC to support in vitro conversion by elk, white-tailed deer, and reindeer CWD PrPSc. Our data confirm that elk CWD prions can convert the human PrPC, at least in vitro, and show that the homologous PRNP polymorphisms at codon 129 and 132 in humans and cervids affect conversion efficiency. Other species affected by CWD, particularly caribou or reindeer, also seem able to convert the human PrP. It will be important to determine whether other polymorphic variants found in other CWD-affected Cervidae or perhaps other factors (17) exert similar effects on the ability to convert human PrP and thus affect their zoonotic potential.
Dr. Barria is a research scientist working at the National CJD Research and Surveillance Unit, University of Edinburgh. His research has focused on understanding the molecular basis of a group of fatal neurologic disorders called prion diseases.
Acknowledgments We thank Aru Balachandran for originally providing cervid brain tissues, Abigail Diack and Jean Manson for providing mouse brain tissue, and James Ironside for his critical reading of the manuscript at an early stage.
This report is independent research commissioned and funded by the United Kingdom’s Department of Health Policy Research Programme and the Government of Scotland. The views expressed in this publication are those of the authors and not necessarily those of the Department of Health or the Government of Scotland.
Author contributions: The study was conceived and designed by M.A.B. and M.W.H. The experiments were conducted by M.A.B. and A.L. Chronic wasting disease brain specimens were provided by G.M. The manuscript was written by M.A.B. and M.W.H. All authors contributed to the editing and revision of the manuscript.
Prion 2017 Conference Abstracts
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 ABSTRACTS REFERENCE
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.
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, did 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 $$$ ***
> However, to date, no CWD infections have been reported in people.
key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** 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).***
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 ===============
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
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
***> ''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
***> 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) <***
***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.
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***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
GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results regarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
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 emphasized by the finding that some strains of scrapie produce lesions identical to the once which characterize 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 scrapie problem urgent if the sheep industry is not to suffer grievously.
snip...
76/10.12/4.6
IN CONFIDENCE
SCRAPIE TRANSMISSION TO CHIMPANZEES
IN CONFIDENCE
reference...
RB3.20
TRANSMISSION TO CHIMPANZEES
1. Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.
2. We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, ilp and i/v) :
3. I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. Proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.
4. In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.
5. A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
6. A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans' susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday' s meeting.
R. Bradley
23 September 1990
CVO (+Mr Wells' comments)
Dr T W A Little
Dr B J Shreeve
90/9.23/1.1.
http://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
IN CONFIDENCE CHIMPANZEES
CODE 18-77 Reference RB3.46
Some further information that may assist in decision making has been gained by discussion with Dr Rosalind Ridley.
She says that careful study of Gajdusek's work shows no increased susceptibility of chimpanzees over New World Monkeys such as Squirrel Monkeys. She does not think it would tell you anything about the susceptibility to man. Also Gajdusek did not, she believes, challenge chimpanzees with scrapie as severely as we did pigs and we know little of that source of scrapie. Comparisons would be difficult. She also would not expect the Home Office to sanction such experiments here unless there was a very clear and important objective that would be important for human health protection. She doubted such a case could be made. If this is the case she thought it would be unethical to do an experiment abroad because we could not do it in our own country.
Retrospectively she feels they should have put up more marmosets than they did. They all remain healthy. They would normally regard the transmission as negative if no disease resulted in five years.
We are not being asked for a decision but I think that before we made one we should gain as much knowledge as we can. If we decided to proceed we would have to bear any criticisms for many years if there was an adverse view by scientists or media. This should not be undertaken lightly. There is already some adverse comment here, I gather, on the pig experiment though that will subside.
The Gibbs' (as' distinct from Schellekers') study is somewhat different. We are merely supplying material for comparative studies in a laboratory with the greatest experience of human SEs in the world and it has been sanctioned by USDA (though we do not know for certain yet if chimpanzees specifically will be used). This would keep it at a lower profile than if we conducted such an experiment in the UK or Europe.
I consider we must have very powerful and defendable objectives to go beyond Gibbs' proposed experiments and should not initiate others just because an offer has been made.
Scientists have a responsibility to seek other methods of investigative research other than animal experimentation. At present no objective has convinced me we need to do research using Chimpanzees - a species in need of protection. Resisting such proposals would enable us to communicate that information to the scientist and the public should the need arise. A line would have been drawn.
CVO cc Dr T Dr B W A Little Dr B J Shreeve
R Bradley
26 September 1990
90/9.26/3.2
http://web.archive.org/web/20090506041605/http://www.bseinquiry.gov.uk/files/yb/1990/09/26003001.pdf
this is tse prion political theater here, i.e. what i call TSE PRION POKER...tss
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs.
snip...
PAGE 26
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.
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 its 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.
snip...see;
IN CONFIDENCE
PERCEPTIONS OF UNCONVENTIONAL SLOW VIRUS DISEASE OF ANIMALS IN THE USA
GAH WELLS
REPORT OF A VISIT TO THE USA
APRIL-MAY 1989
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man.
***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough.
***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
MONDAY, FEBRUARY 25, 2019
***> MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. ***These circumstances represent a potential threat to blood, blood products, and plasma supplies.
Terry S. Singeltary
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