Confirmed Cases of Chronic Wasting Disease in New Mexico
GMU Collection Date Kill Date Location Tissue Species
19 June 1, 2002 June 1, 2002 WSMR main post (first CWD Positive in NM) CWD Area Deer
19 November 4, 2002 November 4, 2002 WSMR Main Post CWD Area Deer
19 November 12, 2002 November 12, 2002 WSMR Main Post CWD Area Deer
19 December 17, 2002 December 17, 2002 WSMR Main Post Tonsil Biopsy Deer
19 January 1, 2003 January 1, 2003 Organ Mtns. Hunter Harvest Deer
19 January 4, 2003 January 4, 2003 Dripping Springs Hunter Harvest Deer
19 November 14, 2003 November 14, 2003 WSMR MAIN POST CWD Area Deer
34 January 13, 2004 January 13, 2005 15 miles NE of Pinon CWD Suspect Deer
19 December 14, 2004 December 14, 2004 West Organs, W of Massey Tank Tonsil Biopsy Deer
19 December 14, 2004 December 14, 2004 West Organs, W of Dripping Spring Visitor Center Tonsil Biopsy Deer
19 April 5, 2005 April 5, 2005 WSMR - Tag # 482 Tonsil Biopsy Deer
19 April 11, 2005 WSMR, SW of Antelope Hill CWD Area Deer
19 April 15, 2005 April 15, 2005 SW of Dripping springs CWD Area Deer
34 June 6, 2005 June 5, 2005 Timberon CWD Suspect Deer
34 October 1, 2005 October 1, 2005 Hughes Canyon CWD Suspect Elk
34 October 3, 2005 October 3, 2005 Wayland Canyon Hunter Harvest Elk
19 December 10, 2005 Antelope Hill Tonsil Biopsy Deer
34 March 24, 2006 March 24, 2006 Timberon CWD Suspect Deer
19 April 21, 2006 April 21, 2006 N of sewage plant (Bishops Cap) CWD Area Deer
19 June 2, 2006 June 2, 2006 WSMR SW of Red Butte, Stallion range Found Dead Deer
34 August 12, 2006 August 12, 2006 Timberon CWD Area Deer
34 October 27, 2006 October 27, 2006 West of Pinon Hunter Harvest Deer
19 July 13, 2007 July 13, 2007 South of Bishop's Cap CWD Suspect Deer
28 October 14, 2007 October 14, 2007 Mc Gregor Hunter Harvest Deer
34 October 30, 2007 October 28, 2007 Unit 34 private land Hunter Harvest Deer
19 December 13, 2007 December 13, 2007 WSMR Main Post CWD Area Deer
28 October 12, 2008 October 12, 2008 McGregor Range Hunter Harvest Deer
28 October 13, 2008 October 12, 2008 McGregor Hunter Harvest Deer
34 October 29, 2008 October 25, 2008 Private land Hunter Harvest Deer
34 March 2, 2009 March 1, 2009 Rio Penasco CWD Suspect Elk
34 December 6, 2009 December 6, 2009 Wills Canyon CWD Suspect Elk
28 May 9, 2010 CWD Area Deer
28 October 10, 2010 October 10, 2010 McGregor Range Hunter Harvest Deer
28 November 17, 2010 November 17, 2010 McGregor CWD Area Deer
34 November 27, 2010 November 27, 2010 Lookout Station Hunter Harvest Elk
28 March 12, 2011 March 12, 2011 McGregor CWD Area Deer
28 March 13, 2011 March 13, 2011 McGregor CWD Area Deer
28 March 13, 2011 March 13, 2011 McGregor CWD Area Deer
28 October 9, 2011 October 9, 2011 McGregor Range Hunter Harvest Deer
28 October 9, 2011 October 9, 2011 McGregor Range South Hunter Harvest Deer
28 October 10, 2011 October 9, 2011 McGregor Range Hunter Harvest Deer
28 February 17, 2012 February 17, 2012 McGregor Rectal Biopsy Deer
28 February 18, 2012 February 18, 2012 McGregor Rectal Biopsy Deer
34 October 27, 2012 October 27, 2012 Timberon Hunter Harvest Deer
28 October 5, 2013 October 5, 2013 McGregor Hunter Harvest Deer
28 December 11, 2013 December 9, 2013 McGregor Hunter Harvest Elk
28 December 11, 2013 December 11, 2013 McGregor Hunter Harvest Elk
28 December 11, 2013 December 11, 2013 McGregor Hunter Harvest Elk
19 February 12, 2014 February 12, 2014 NASA CWD Suspect Deer
19 April 6, 2014 April 5, 2014 East of Las Cruces CWD Suspect Deer
28 November 21, 2015 November 21, 2015 McGregor Range Deer
28 November 21, 2015 November 21, 2015 McGregor Range Hunter Harvest Deer
28 November 21, 2015 December 21, 2015 McGregor Range Hunter Harvest Deer
28 November 22, 2015 November 21, 2015 McGregor Range Hunter Harvest Deer
28 November 22, 2015 November 22, 2015 McGregor Range Hunter Harvest Deer
28 November 27, 2016 November 26, 2016 McGregor Range Hunter Harvest Deer
28 November 27, 2016 November 27, 2016 McGregor Range Hunter Harvest Deer
28 December 12, 2016 December 12, 2016 McGregor Range Hunter Harvest Elk
Showing 1 to 58 of 58 entries
2019–2020 Chronic Wasting Disease
Chronic Wasting Disease Rules Apply to Units 19, 28 and 34
It is unlawful to transport outside the GMU any deer or elk or their parts taken from any chronic wasting disease (CWD) control area designated by the director of the New Mexico Department of Game and Fish. The exceptions are:
• Meat that is cut and wrapped either privately or commercially.
• Quarters or other portions of meat with no part of the head or spinal column attached.
• Meat that has been boned out.
• Hides with no heads attached.
• Clean skull plates with antlers attached; Skull plate must be immersed in a bath of at least one part chlorine bleach and two parts water with all meat and tissue removed.
• Antlers with no meat or tissue attached.
• Upper canine teeth, also known as ivories.
• Finished heads mounted by a taxidermist.
• By prior arrangement, a harvested deer or elk or their parts may be moved to an NMDGF office.
You may not remove the whole head and spinal column. You must keep proof of sex with all game species until you get the game to the place where it will be consumed or placed in cold storage.
Win an Elk or Oryx Incentive Authorization by Helping
Test for Chronic Wasting Disease!
To participate, bring your freshly harvested deer or elk head to any NMDGF office or field collection station, where tissues can be collected for CWD testing. In Units 19, 28 and 34 hunters must present the head for testing within the unit where the animal was harvested. Hunters must deliver the unfrozen head within 48 hours of killing the animal to be eligible. Participating hunters may be selected by drawing to receive an elk or oryx incentive authorization. Incentive Authorizations can be used by the recipient or by any individual of the recipient’s choice through sale, barter or gift.
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.
***>In 2003, over 800 tissues were tested.
***> Currently, the Department receives 200-300 tissues annually for testing.
***> 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.
are you kidding me?
***>In 2003, over 800 tissues were tested.
***> Currently, the Department receives 200-300 tissues annually for testing.
i am extremely, very very concerned about the very low numbers for chronic wasting disease cwd tse prion tissue samples collected and tested in New Mexico over the years, and what New Mexico conclusion of said cwd tse prion surveillance, considering these low figures...terry
THURSDAY, NOVEMBER 02, 2017
New Mexico Chronic Wasting Disease CWD Figures 2016 - 2017 Update ???
THURSDAY, SEPTEMBER 22, 2016
New Mexico CWD confirmed in 5 McGregor Range deer during the 2015-16 hunting season
TEXAS Animal Health Commission Accepting Comments on Chronic Wasting Disease Rule Proposal
Considering the seemingly high CWD prevalence rate in the Sacramento and Hueco Mountains of New Mexico, CWD may be well established in the population and in the environment in Texas at this time.
Monday, March 26, 2012
3 CASES OF CWD FOUND NEW MEXICO MULE DEER SEVERAL MILS FROM TEXAS BORDER
CWD in New Mexico ;
What is the Department doing to prevent the spread of CWD?
Chronic wasting disease (CWD) was recently detected in a mule deer from Unit 34. Until 2005, CWD had only been found in Unit 19. With this discovery, the Department will increase its surveillance of deer and elk harvested in Units 29, 30 and 34.
Lymph nodes and/or brain stems from every harvested deer and brain stems from all elk taken in Unit 34 will be sampled.
snip...
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwd_flyer.pdf
http://www.wildlife.state.nm.us/documents/cwdcontrolmap.pdf
http://list.uvm.edu/cgi-bin/wa?A2=ind0512b&L=safety&P=11092
http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html
http://www.wildlife.state.nm.us/documents/CWD_QandA.pdf
CWD SURVEILLANCE TEXAS
http://www.tpwd.state.tx.us//huntwild/wild/diseases/cwd/management_plan/status/
2011 – 2012
Friday, October 28, 2011
CWD Herd Monitoring Program to be Enforced Jan. 2012 TEXAS
Greetings TAHC et al,
A kind greetings from Bacliff, Texas.
In reply to ;
Texas Animal Health Commission (TAHC) Announcement October 27, 2011 I kindly submit the following ;
SUNDAY, OCTOBER 04, 2009
CWD NEW MEXICO SPREADING SOUTH TO TEXAS 2009
here is some old history of cwd tse prion New Mexico and Texas
New Mexico Department of Game and Fish
Media contact: Dan Williams, (505) 476-8004
Public contact: (505) 476-8000
dan.williams@state.nm.us
FOR IMMEDIATE RELEASE, JULY 7, 2006:
3 SOUTHERN NEW MEXICO DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
SANTA FE – Three deer in southern New Mexico have tested positive for chronic wasting disease, bringing the total number of confirmed CWD-infected deer in the state to 15 since the first infected deer was discovered in 2002.
The Department received test results Wednesday from the state Veterinary Diagnostic Services laboratory in Albuquerque that two wild deer captured near the White Sands Missile Range headquarters east of Las Cruces had tested positive for chronic wasting disease. A third wild deer captured in the small community of Timberon in the southern Sacramento Mountains also tested positive for the disease.
The discoveries of the infected deer were part of the Department's ongoing efforts to monitor the disease, which to date has been confined to the southern Sacramento Mountains southeast of Cloudcroft and areas surrounding the Organ Mountains near Las Cruces. Two wild elk from the southern Sacramento Mountains tested positive for the disease in December 2005.
Chronic wasting disease is a fatal neurological illness that afflicts deer, elk and moose. There is no evidence of CWD being transmitted to humans or livestock. The disease causes animals to become emaciated, display abnormal behavior and lose control of bodily functions. To date, it has been found in captive and wild deer, elk and moose in eight states and two Canadian provinces.
For more information about CWD in New Mexico and how hunters can assist in research and prevention, please visit the New Mexico Department of Game and Fish Web site, www.wildlife.state.nm.us . More information about CWD also can be found on the Chronic Wasting Disease Alliance site at www.cwd-info.org/ .
###
http://www.wildlife.state.nm.us/publications/press_releases/documents/2006/0707CWD.htm
SEE MAP NM
http://www.wildlife.state.nm.us/documents/cwdcontrolmap.pdf
SEE SAMPLING MAP TEXAS
CWD Sampling Maps
Three Year Summary of Hunter-Kill CWD Sampling (as of August 31, 2005)
http://www.tahc.state.tx.us/animal_health/diseases/cwd/CWD_Sampling_Aug2005.pdf
CWD Sampling Maps
Three Year Summary of Hunter-Kill CWD Sampling (as of August 31, 2005)
USDA CWD Maps
March 2006 — Current Distribution of CWD
TAHC CWD Monitoring Program Information
CWD Sample Submission and Costs
2006 Factsheet For Producers Enrolling in the Complete Herd Monitoring Program
USDA CWD Maps
March 2006 — Current Distribution of CWD
TAHC CWD Monitoring Program Information
CWD Sample Submission and Costs
2006 Factsheet For Producers Enrolling in the Complete Herd Monitoring Program
----- Original Message -----
From: "Terry S. Singeltary Sr."
To:
Sent: Monday, June 27, 2005 6:51 PM
Subject: CWD TWO NEW CASES NEAR WHITE SANDS MISSLE RANGE NEW MEXICO
##################### Bovine Spongiform Encephalopathy #####################
From: TSS
Subject: CWD TWO NEW CASES NEAR WHITE SANDS MISSLE RANGE NEW MEXICO
Date: June 27, 2005 at 4:43 pm PST
New Mexico Department of Game and Fish
Contact: Dan Williams, (505) 476-8004
dan.williams@state.nm.us
FOR IMMEDIATE RELEASE, JUNE 24, 2005:
TWO MULE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
ANGLER LANDS STATE RECORD BLUE CATFISH AT ELEPHANT BUTTE LAKE
TWO MULE DEER TEST POSITIVE FOR CHRONIC WASTING DISEASE
SANTA FE – Two mule deer captured in the Organ Mountains as part of an ongoing research project near White
Sands Missile Range have tested positive for chronic wasting disease (CWD), a fatal neurological disease that
attacks the brains of infected deer and elk, the Department of Game and Fish announced.
The number of confirmed CWD cases in New Mexico now stands at 11 since 2002, when the disease was first
confirmed in a deer found near the eastern foothills of the Organ Mountains. All 11 CWD-infected deer were found
in the same general area of southern New Mexico. The origin of the disease in New Mexico remains unknown.
The carcasses of the infected deer will be incinerated, said Kerry Mower, the Department’s lead wildlife disease
biologist.
Chronic wasting disease causes animals to become emaciated, display abnormal behavior, lose bodily functions
and die. The disease has been found in wild deer and elk, and in captive deer and elk, in eight states and two
Canadian provinces. There currently is no evidence of CWD being transmitted to humans or livestock.
Mower said the most recent CWD-positive deer showed no obvious physical signs of having the disease. They
were captured in April 2005 and tested as part of a 3-year-old research project studying deer population dynamics
in southern New Mexico. More than 140 deer have been captured alive and tested for the study, in which
researchers hope to find the cause of a 10-year decline in the area deer population. Study participants include the
Department of Game and Fish, the U.S. Army at White Sands Missile Range and Fort Bliss, Bureau of Land
Management, U.S. Geological Survey at New Mexico State University, and San Andres National Wildlife Refuge.
Hunters can assist the Department in its CWD research and prevention efforts by bringing their fresh, legally
harvested deer or elk head to an area office, where officers will remove the brain stem for testing. Participants will
be eligible for drawings for an oryx hunt on White Sands Missile Range and a trophy elk hunt on the Valle Vidal.
For more information about the drawing and chronic wasting disease, visit the Department web site at
www.wildlife.state.nm.us.
http://www.wildlife.state.nm.us/publications/press_releases/documents/0624CW Dandcatfish.pdf
SEE MAP ;
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdf
Greetings list members,
I am deeply concerned with these CWD mad deer so close to the Texas border.
WHAT keeps them from crossing the border to Texas ???
IF these illegal aliens can so easily cross our borders, why not these infected deer?
maybe we should get these minute men to start watching for mad deer coming in to Texas from New Mexico.
I mentioned my concerns several other times before;
-------- Original Message --------
Subject: Current status of CWD testing in Texas
Date: Tue, 10 May 2005 09:09:47 -0500
From: "kschwaus"
To:
Mr. Singeltary,
I was asked to provide you with the following information. If you have any other questions regarding CWD sampling in Texas, please do not hesitate to give me a call. My office number is below.
Below I have included a chart showing CWD samples that have been tested since the fall of 2002 through the present at the eco-region level. The second chart shows the totals on a given year. The unknown location samples come from private individuals sending in samples directly to the Texas Veterinary Medical Diagnostic Lab (TVMDL). Due to the confidentiality laws that the TVMDL operates under, they are unable to provide TPWD with the location of those samples.
Region Population Estimate
Sampling from Fall 2002 to Present
Pineywoods
502,521
975
Gulf Prairie
90,664
441
Post Oak Savannah
291,119
1146
Black Land Prairies
54,505
153
Cross Timbers
441,031
1015
Edwards Plateau
1,608,390
1618
South Texas Plains
500,183
1253
Rolling Plains
231,358
352
High Plains
49,981
81
Trans Pecos
148,174
173
Unknown Location
1,896
Total
3,917,926
9,103
Samples Collected By
2002-03
2003-04
2004-Present
TPWD
1,722
2,955
2,540
Private (unknown location)
326
608
952
Total
2,048
3,563
3,492
Thank you,
Kevin Schwausch
Big Game Program Specialist
Texas Parks & Wildlife Department
PO Box 1394
Burnet, TX 78611
512-756-4476
===============================
I would like to thank Kevin and TPWD for there prompt reply with updated data.
I am still concerned about the Texas, New Mexico border and New Mexico's apparent lack of CWD testing updates. Makes one wonder about there CWD testing program. NO report/reply back from New Mexico about there CWD testing update yet. ...
TSS
===================
-------- Original Message --------
Subject: CWD SURVEILLANCE TEXAS UPDATE (kinda)
Date: Mon, 9 May 2005 14:52:48 -0500
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@aegee.org
##################### Bovine Spongiform Encephalopathy #####################
IMPLEMENTATION OF A GEOGRAPHICALLY FOCUSED CWD SURVEILLANCE PROGRAM FOR FREE-RANGING CERVIDS
A geographically-focused free-ranging cervid Monitoring Program was implemented during the fall 2002 deer-hunting season. Brain stem samples from hunter-killed deer will be obtained from TPWD Wildlife Management Areas (WMA), State Parks, and where otherwise available with hunter and/or landowner permission, from deer taken on private land. Volume 1, Sixth Edition of United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services, Regulatory Statistics (Appendix D1) indicates that 148 samples is sufficient to detect disease at two per-cent prevalence, regardless of the population size. Therefore the goal is to acquire 148 samples from each of the State's ten ecoregions provided adequate sampling distribution is achieved across each ecoregion. The five year 2002 -2006, goal is to cumulatively collect 459 samples from each of the ten ecoregions. The cumulative sample would be used statistically to detect CWD at one per-cent prevalence level with 99 per-cent confidence. However, funding from APHIS/USDA could provide the necessary funds for sampling at the one per-cent prevalence level each year. TAHC conducted a risk assessment of counties where deer and elk have been imported and where high densities of free-ranging deer occur. The assessment was conducted for USDA funding consideration. The risk assessment was based on limited number of criteria. Since CWD could potentially occur anywhere in Texas, monitoring efforts would be focused to achieve a stratified sampling scheme across each ecoregion of the State.
Confidentiality laws restrict the type of data TPWD personnel can collect as it relates to a specific parcel of land. Therefore, personnel will ensure that no property specific information is collected (i.e. ranch name or exact location) without the landowner's written permission. The following are guidelines for data and sample collection distributed to TPWD personnel prior to sample collection:
1. A Texas Veterinary Medical Diagnostic Laboratory (TVMDL) Accession Form must be submitted with brain stem samples.
2. The most important items to be filled out are the TPWD employee name, address and phone number, and "Patient/Deer ID". County of Kill can be recorded on the bottom of the form, but DO NOT report any information that identifies the specific parcel of land.
3. The "Patient/Deer ID" number MUST BE specific to the field data sheet the employee is using to record data.
4. Specific CWD field data sheets will not be provided, as current field data sheets (i.e. Age/Weight Antler Data Sheets, Hunter Check Station Data Sheets, etc.) will be appropriate in most cases. Field staff may produce their own CWD data sheet if necessary.
5. The field data sheet must contain:
1. Employee Name
2. Sample Number (same as Patient/Deer ID on TVMDL Accession Form
3. Sample Date
4. Deer Age
5. Deer Sex
6. County of Kill
7. Hunter Name
8. Hunting License Number
9. Ranch name or tract name/location ONLY with landowner permission.
6. Should a CWD positive be detected, TAHC will use hunter contact information to conduct CWD investigation under their regulatory authority.
7. Make sure the container containing the brain stem sample is legibly identified with the sample number, deer age and sex, county of kill and date. Although the sample number is all that is needed, additional information will help resolve any problems should batches of samples be combined.
8. Should a landowner retain deer heads for our sampling purposes, remind the landowner to issue the hunters a proof of sex document as provided for in TAHC 65.10 (c). In addition, a Wildlife resource document (PWD 905) must accompany the head until the carcass reaches a final destination and finally processed.
9. Samples MAY NOT be taken from legally harvested deer without the hunter's consent.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/imp lementation/
ACTIONS SHOULD A CWD POSITIVE BE DETECTED
Should sampling detect a CWD positive animal, TAHC and TPWD would activate the Media Response Plan (Appendix F).
TAHC and TPWD would immediately begin review of the information at hand and determine the action to be taken within the Response Plan (Appendix C.)
The first action should be to inform landowners adjacent to the property containing the CWD positive and hold a meeting with advisory committees and affected landowner to discuss plans for secondary sampling. Planning for secondary sampling, investigating movements of deer into and away from property for further actions would then be the next step. The secondary sampling is critical for determining distribution and prevalence of the disease.
As distribution and prevalence is being determined, information review and discussions with TPWD advisory committees (e.g., Private Lands Advisory Board, Hunting Advisory Committee, White-tailed Deer Advisory Committee etc.) and landowners would take place in order to determine the appropriate management action to be taken.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/det ection/
APPENDIX A: Results of CWD Sampling
Sampling and testing results for CWD from June, 2002 to April 1, 2003 are presented below:
Sampling and testing results for CWD from June, 2002 to April 1, 2003
TPWD TAHC Private Sector
1349 CWD Negative Deer 335 CWD Negative Deer 336 CWD Negative Deer
23 CWD Negative Exotics No Exotics No Exotics
1372 Total 335 Total 336 Total
The Grand Total of all samples collected and known 4/1/03 is 2043 of which 2020 deer and 23 exotics were found CWD negative. Samples were collected from 143 of 254 counties in Texas, and seven counties had 50 or more samples collected. Five ecoregions had 160 or more samples collected (150 samples from each ecoregion was the goal). The geographic distribution of sampling is currently not considered adequate for determining whether or not CWD exists in Texas (see map pg. 15). The goal is to improve upon distribution of samples collected within ecoregions and within counties. The goal of 2003-2004 and the next three to five years, is to collect 5000 samples (500 from each ecoregion) each sample year. The increased sampling is to have a 99 per-cent confidence level in detecting CWD if only one per-cent of the population is infected. Long-term surveillance sampling for CWD is required, as little is known about the incubation and infectious periods of the disease.
fig1AppendixA (18K)
SEE MAP OF TEXAS CWD TESTING
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/ima ges/fig1AppendixA.png
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/app endix_a/
APPENDIX B: Chronic Wasting Disease - Status of Current Knowledge
Occurrence and Distribution
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy, which is a disease that alters the structure of the brain, in a way that resembles a sponge-like appearance and texture. Much is not known about CWD, including its origin, exact mode of transmission, and the causative or etiological agent. The source of CWD may be related in some way to scrapie in domestic sheep; it may "represent a spontaneous, naturally occurring" form of this disease in cervids thought to be caused by a "low virus infection." A more plausible theory is that CWD is caused by a point mutation of a membrane-bound protein resulting in accumulations of proteinase-resistant proteins called "prions" in the brain (medulla oblongata), tonsils (in deer only), and lymphoid tissue.
The only known long-term distribution of CWD in free-ranging susceptible cervids includes two contiguous local areas in northeastern Colorado and southeastern Wyoming. Up to 15% and less than 1% prevalence were reported for mule deer and elk, respectively, in certain management units. Two cases of CWD occurred in mule deer in the southwestern corner of the panhandle of Nebraska, which is close to the endemic area of Colorado and Wyoming. Both of these latter animals were close enough to have originated from the endemic area. More recently, CWD was diagnosed in deer in Nebraska within and outside a fenced pasture of a captive operation where elk were diagnosed with the disease. Infections in captive elk also have been documented in Colorado, Wyoming, Montana, Oklahoma, South Dakota, and Kansas. In early 2002, CWD was detected in free-ranging white-tailed deer in South Dakota and Wisconsin, later the disease was found in breeder pens in northern Wisconsin. Cases of CWD have been documented in captive elk and free ranging mule deer in Saskatchewan and Ontario as well. New Mexico discovered CWD in a free-ranging mule deer on the White Sands Missile Range, Minnesota found CWD in a captive elk herd, Illinois detected CWD in a free-ranging white-tailed deer and an infected white-tailed deer was found in a breeding facility in Alberta.
Incubation, Transmission, and Clinical Course of CWD
Incubation time, that time from infection to appearance of clinical signs, typically is less than 2 years (18-24 months). However, incubation time can be variable and ranges up to 36 months. The exact mode of transmission of CWD is unknown; however, circumstantial and experimental data indicate horizontal (or lateral) transmission in captive susceptible cervids, either by direct animal-to-animal contact or by environmental contamination. For susceptible cervids, the routes of transmission are presumed to be by exposure to saliva, urine, feces, or placental tissue, with infection occurring through the alimentary canal (mouth/nose - esophagus - stomach - intestines). If this transmission mode is confirmed for free-ranging deer or elk, it could potentially exacerbate the risk of infection. In contrast to outbreaks of mad cow disease, where exposure to animal protein-contaminated feed was documented, this has not been the case for captive or wild cervids infected with CWD. Presently, feed contamination is not considered a likely underlying transmission mechanism. Whereas, the importance of maternal transmission (mother to fetus or nursing young) as a mode of scrapie transmission in domestic sheep has at least been debated, its importance relative to CWD persistence in captive and wild cervid herds has been contraindicated thus far by current reports. Although the route of agent shedding from infected individuals is presently unknown, it is believed that the rate of agent shedding may very well increase as the disease progresses. Thus far, evidence also indicates that there is no difference between males and females or across age classes in susceptibility to CWD.
Importantly, natural transmission of TSEs (i.e., BSE, CWD) between domesticated bovines (i.e., cattle, bison), sheep and cervids has not been documented. Deer, domestic cattle and sheep have been experimentally inoculated with brain tissue containing (PrP(res)) from CWD - infected mule deer, and 2 years later, only the deer have become infected with CWD. However, healthy deer have been inoculated with brain tissue from scrapie-infected sheep, and the deer developed spongiform encephalopathy.
The clinical course of CWD is about 12 months. That is, once clinical signs are apparent, cervids rarely survive more than 12 months. Chronic wasting disease is a progressive, fatal disease, with no vaccine to prevent the disease or treatment for reversing the disease (recovery), and there is no evidence of immunity. There has been no effective, practical ante mortem (live-animal) test for diagnosis until recently; a live-test for deer (not elk) involving tonsil biopsy and immunohistochemical analysis for (PrR (res)) accumulation has demonstrated promise, and may be more sensitive than the post-mortem analysis of the obex of the medulla oblongata in the brain. The practicality of this test remains to be decided.
Clinical Signs of CWD
All signs or symptoms of CWD do not occur in all cases, and many of these signs are symptoms of other diseases and conditions as well. Further, the occurrence and severity of symptoms will depend in part on the stage (early versus advanced) of the disease. Below is a comprehensive list of the clinical signs of CWD: (1) loss of fear of humans; (2) nervousness or hyper-excitability; (3) teeth-grinding; (4) ataxia or loss of coordination; (5) notable weakness; (6) intractability; (7) inability to stand; (8) rough dull hair coat; (9) excessive salivation; (10) flaccid, hypotonia of the facial muscles; (11) drooping of the head and ears; (12) excessive thirst (polydipsia); (13) excessive urination (polyuria); (14) esophageal hypotonia and dilation, difficulty swallowing, and regurgitating ruminal fluid and ingesta; and (15) severe emaciation and dehydration.
It is important to note that while some primary symptoms may be directly related to CWD, others may be secondary, more of a consequence of the deteriorating body condition (emaciation) and related physiology (e.g., pneumonia, abscesses, enteritis, or internal parasitism that may often cause emaciation).
Pathological Signs of CWD
Pathological signs of the disease include:
(1) emaciation associated with absence or serous atrophy of subcutaneous and visceral adipose tissue or fat, and yellow gelatinous bone marrow;
(2) sub acute to chronic bronchopneumonia;
(3) digestive tract (abomasal or omasal) ulcers;
(4) enlarged adrenal glands;
(5) watery or frothy rumen contents; and
(6) histological lesions.
These lesions have primarily and most consistently been observed in the brain and spinal cord. (7) Immunohistochemistry (IHC) is very sensitive and specific to CWD and is typically used to confirm diagnoses by measuring accumulations of proteinase-resistant prion protein (PrP(res)) in brain tissues (specifically in the obex of the medulla oblongata) of infected deer and elk. This prion protein is indistinguishable from the scrapie-associated prion protein (PrP(Sc)) found in brain tissues of domestic sheep infected with scrapie, but other differences have been noted. (PrP(res)) has not been detected in uninfected cervids. This test can detect CWD infection before lesions are observable; however, IHC (+) results are not detected until at least three months after infection. Lesions do not always accompany (PrP(res)) accumulation and IHC (+) results. (8) Scrapie associated fibrils (SAFs) have been observed by electron microscopy in the brain tissue of infected cervids, but not in uninfected cervids. (9) Generally, blood (whole blood and serum) and urine profiles have remained within the normal range, with the exception that certain characteristics have reflected the emaciated condition of the infected animals. Low specific gravity of the urine, is the one urine characteristic that may be directly related to CWD, specifically to degenerative encephalopathic changes in the hypothalamus. The hypothalamus is important in regulating anti diuretic hormone, which influences concentrations of urinary electrolytes (e.g., Na) and osmolality.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/app endix_b/
APPENDIX C: Importation of Susceptible Cervids
On March 20, 2002, the Texas Animal Health Commission, and Texas Parks and Wildlife Commission issued separate orders to prohibit the entry of all elk, white-tailed deer, black-tailed deer, and mule deer into Texas.
On August 25, 2002, Texas Animal Health Commission adopted entry requirements for black-tailed deer, elk, or other cervid species determined to be susceptible to CWD. All mule deer and white-tailed deer held under authority of Scientific Breeder Permits are also required to obtain a purchase permit and, in some cases, a transport permit from Texas Parks and Wildlife Department in order to enter the state. All requests for entry must be made in writing and accompanied with the information necessary to support import qualification of the animal(s). Requests for entry and supporting documentation should be received by the TAHC at least 10 working days prior to the proposed entry date. The processing of the application can be expedited by assuring that all of the necessary documentation has been provided and that the necessary staff is available for review. The application must be accompanied by an owner's statement stating that to his/her knowledge the animals (or donor animals) to be imported have never come in contact with equipment or resided on a premise where CWD was ever diagnosed.
Entry Requirements: The applicant must identify the herd of origin and the herd of destination on both the permit application and the certificate of veterinary inspection. The susceptible cervid(s) to be imported into this state, shall be identified to their herd of origin by a minimum of two official/approved unique identifiers to include, but not limited to, legible tattoo, USDA approved ear tag, breed registration or other state approved permanent identification methods. If a microchip is used for identification, the owner shall provide the necessary reader. A certificate of veterinary inspection completed by an accredited veterinarian shall accompany the shipment. Additionally, the herd of origin must meet the following criteria:
1. In states where there is a state approved CWD monitoring program which meets the requirements provided in Section D of Appendix C (below) and where CWD has not been identified in a susceptible species, then all elk, white-tailed deer, mule deer, and black-tailed deer to be imported must originate from a herd that has been in a state-approved complete herd certification program for a minimum of three years (or current federal standards).
2. From states which do not have a CWD monitoring program which meets the standards provided in Section D of Appendix C (below) and where CWD has not been identified in a susceptible species, then all elk, white-tailed deer, mule deer, and black-tailed deer shall originate from herds that have complete herd records, including, but not limited to, complete and detailed herd inventories, records of deaths, laboratory results, and sales and purchase receipts, for a minimum of five years. Complete documents which support this type of status shall be submitted with the permit application.
3. In states where CWD has been identified in a susceptible species, then elk, white-tailed deer, mule deer, and black-tailed deer (or other susceptible species) to be imported must originate from a herd that has been in a state-approved complete herd monitoring program, as provided in Section D of Appendix C (below) for a minimum of five years.
4. A state-approved chronic wasting disease monitoring program must be certified by the Texas State Veterinarian as meeting the following minimum standards:
1. In states where CWD has been found in free-ranging wildlife, the state program shall have perimeter fencing requirements adequate to prevent ingress, egress or contact with susceptible cervids.
2. Surveillance based on testing of susceptible cervid deaths over 16 months of age is required of all herds within a complete herd monitoring program. Surveillance sampling at commercial slaughter and at shooter operations should be at least 10 percent of the number slaughtered annually.
3. A good quality sampling program where state and federal officials have the authority to adjust herd status if poor quality samples, particularly samples that are from the wrong portion of the brain, are routinely submitted from a premise. Laboratory analysis of the brain stem by United States Department of Agriculture (USDA) approved lab is recognized as the current standard for CWD diagnosis. Other laboratory analyses may be accepted as validated or accepted by USDA/Animal and Plant Health Inspection Service (APHIS).
4. Physical herd inventory with annual verification reconciling animals and identification with records by an accredited veterinarian or state or federal personnel is required. Inventory is to include a cross check of all animal identifications with the herd inventory and specific information on the disposition of all animals not present.
5. Premise locations must be specifically identified by GIS or detailed description during the initial herd inventory.
6. Herd additions are allowed from herds with equal or greater time in an approved state CWD monitoring program with no negative impact on the certification status of the receiving herd. If herd additions are acquired from a herd with a later date of enrollment, the receiving herd reverts to the enrollment date of the sending herd. If a herd participating in the monitoring program acquires animals from a non-participating herd, the receiving herd must start over with new enrollment date based upon the date of acquisition of the animal(s). If a new herd begins with animals of a given status, that status will be retained by the new herd, based upon the lowest status of the animals received. Animals of different status which are commingled during marketing or transport will revert to the lowest status.
7. Elk, white-tailed deer, mule deer and black-tailed deer will only be allowed to enter the state of Texas if the state of origin lists CWD as a reportable disease and imposes an immediate quarantine on a herd and/or premise when a CWD positive animal is disclosed.
8. Animal health officials in the state of origin must have access to herd records for the appropriate number of years (three to five), including records of deaths and causes of death.
9. Section D also addresses entry requirements as they pertain to tuberculosis testing. However, these requirements are not included as a part of the Texas Chronic Wasting Disease Management Plan.
At the November 2002 meeting the TPWD Commission adopted regulations, to suspend the ban on importation of mule deer and white-tailed deer and provide for importation under TAHC requirements. Additionally, the TPW Commission adopted changes to Trap, Transportation, and Transplant rules, which will require a sample of deer to be tested for CWD on any property serving as a trap site for relocated deer. The rule sets forth the minimum sample size, requires the sample to be tested 100% negative by the Texas Veterinary Medical Diagnostic Laboratory and stipulates that all deer transported be uniquely marked with an ear tattoo prior to release.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/app endix_c/
APPENDIX D: Response Plan for CWD If Detected
1. If the Texas Veterinary Medical Diagnostic Laboratory reports a CWD positive test, the suspect sample will be immediately shipped to USDA Laboratory at Ames, Iowa for conformation of positive finding. The time between initial suspect finding and Ames Lab confirmation will be used to mobilize staff and groups for response plan initiation.
2. The confirmation notice of a positive would come through the USDA Veterinary Services Office in Austin, and USDA/VS personnel would be part of the response effort.
3. Governor's Office will be notified of the finding, as well as Commission members of both TAHC and TPWD.
4. CWD Media Response Plan will be activated (Appendix F).
5. Source location of CWD positive concerns:
1. The source location of the CWD positive animal and information about the area, landowners (to contact for cooperative discussions on further sampling, review of management plans), and the deer density within a 4-8 mile radius will be determined.
2. Should the source location of the CWD positive be in a Scientific Breeder facility or pen, TAHC will inform and work cooperatively with the landowner. TAHC may elect to monitor the herd with special conditions (i.e. double-fencing) or negotiate indemnification (cap established at $3000.00 for prime breeding animals) for eradication of the herd.
6. GIS locations and mapping for sampling will be utilized.
7. TAHC and TPWD will inform and work cooperatively with landowners and with landowner permission in the sample area that may be affected.
8. TAHC would determine sampling requirements. Sample numbers and the size of the area to be sampled will be determined based upon population numbers and the statistically-based numbers required for detecting CWD at a 2% prevalence level from "Regulatory Statistics Volume 1, Sixth Edition" (See Appendix D1). The numbers of animals to be sampled (projected at 150) would be collected throughout an area from 64-1056 square miles and not from a single property unless it is as large as the sample area around a positive. A square mile is 640 acres, in areas where the herd density is 1 deer per 5 acres an area of 64 square miles should contain 8192 deer (128 deer per section) and less than 3 deer per section will be sampled. In areas where the herd density is 1 deer per 200 acres an area of 1056 square miles should contain 3379 deer (3.2 deer section) a deer per 7 sections would be sampled. This sampling is not designed to reduce the population below viability.
9. Sampling will be conducted at no cost to the landowner in a cooperative manner to detect additional CWD positives, and sampling around any additional positive finds, to determine direction of spread, prevalence of the disease and to determine distribution. Additional samples would be taken surrounding any new positive to determine direction, but re-sampling again in an area previously sampled would not be necessary.
10. Simultaneously with the sampling, a joint investigation into movement of deer into or out of area will be conducted.
11. Identify geologic features or barriers, which may be used to limit population distribution, will be determined.
12. After distribution is determined, reasonable, responsible, and rational management strategies will be determined in association with landowners and applied as situations dictate following sampling activities, to include monitoring at appropriate intervals, herd reduction as a possible strategy, and eradication of local populations in limited appropriate circumstances. Strategies for possible treatments will also be discussed and reviewed with the TTT/MLDP Task Force/ White-tailed Deer Advisory Committee and the Private Lands Advisory Board.
13. TPWD will collect and take samples from cervids and transport sample to Texas Veterinary Medical Diagnostic Laboratory for analysis.
14. Options for CWD testing (i.e. ELISA test) within localities should a CWD-positive be detected will be considered and evaluated. The purpose would be to ensure reliable test results in a timely manner within the local area providing little interruption to hunting and recreation in the area.
15. TPWD must be prepared to make budget and personnel adjustments for the sampling.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/app endix_d/
APPENDIX D1
United States Department of Agriculture Animal and Plant Health Inspection Service Veterinary Services
REGULATORY STATISTICS
Volume 1
Sixth Edition
June 1983
By Victor C. Beal, Jr.
Table 2 - NUMBER NEEDED TO TEST TO BE 95% CONFIDENT THAT THE DISEASE WILL BE DETECTED IF PRESENT AT OR ABOVE FIVE LEVELS OF INCIDENCE OR CONTAMINATION
SEE FUZZY MATH BELOW ;
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/app endix_d1/
APPENDIX E: TAHC Rules for Monitoring CWD
Participating herds must have adequate perimeter fencing to prevent ingress and egress of cervids. Collection and submission of appropriate samples from all cases of mortality in animals over 16 months of age will accomplish surveillance in participating herds. Exemptions are provided for animals consigned to commercial slaughter operations with state or federal meat inspection. An annual inventory in participating herds shall be verified by a TAHC, USDA or accredited veterinarian. All animals over one year of age shall be identified with an official ear tag or other approved identification device. All animals less than one year of age shall be officially identified on a change of ownership.
Herd status designation shall be assigned on the basis of the number of years of participation provided that CWD is not confirmed in the herd:
1. Level A - One full year of participation.
2. Level B - Two to three years of participation.
3. Level C - Four to five years of participation.
4. Level D - Six years or more of participation.
Additions to Complete Monitored Herd:
1. Additions may originate from herds of equal or higher status with no change in the status of the receiving herd.
2. Additions may originate from herds of lower status with the receiving herd acquiring the lower status of the herd(s) involved.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/app endix_e/
APPENDIX F: Media Response Plan
A deer tissue sample tests positive for CWD in Texas, then the TPWD and TAHC officials have only a few hours to manage communication before news reaches the public section.
Prior to Trigger Event, these items are complete and ready to go:
* Step-by-Step Media Response Plan
* Shell of news release announcing CWD find-Draft pending response plan protocols being developed between TPWD and TAHC.
* Identify news media spokespersons with TPWD and TAHC in Austin
o TAHC: (512) 719-0700. Media Contact: Carla Everett.
Spokespersons: Dr. Ken Waldrup, Dr. Max Coates, Dr. Linda Logan, Dr. Dan Baca, and Dr. Terry Conger.
o TPWD: (512) 389-8900. Media Contact: Steve Lightfoot. Spokespersons: Robert L. Cook, Ron George, Clayton Wolf, and Doug Humphreys
* Web site for news media and general public on CWD. Listings on site include:
* FAQ/Q&A sheet with basic facts on CWD
o http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/
* Names/contact info for local/regional experts who can speak about CWD in various regions of Texas.
* Streaming video of CWD educational video on Web for general public.
* Downloadable radio PSAs.
* High-resolution photos and video of animals with CWD.
Actions Needed:
* Gain a clear understanding of Texas operational plan for handling CWD outbreak, including likely sequence of events from initial find to confirmation, and approve policies concerning quarantines, stoppage of intrastate animal movement, and designation of infection zone for monitoring, sampling protocols and possible depopulation plan.
* Effective communication planning hinges on our through understanding of state's plan for dealing with a CWD outbreak.
* Obtain concurrence with media response plan from TAHC and TPWD.
* Make final these above-listed information instruments.
Trigger Event
Notification that a suspected case of CWD exists in Texas.
Notify media contacts at TAHC and TPWD.
* TAHC - Carla Everett, (512) 719-0700 or (800) 550-8242. ceverett@tahc.state.tx.us
* TPWD - Steve Lightfoot, (512) 389-4701 or (512) 565-3680. steve.lightfoot@tpwd.state.tx.us
Actions Needed:
* TAHC and TPWD confirm contacts and alternates, e-mail addresses, cell phone numbers and office and home phone numbers provided to Carla Everett and/or Steve Lightfoot for compilation, coordination and distribution to agency leadership and involved personnel from other entities.
* News release distributed to media, agency(s) personnel and commissioners, affected stakeholder groups and constituents.
* News conference called, depending on level of media response.
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TEXAS OLD STATISTICS BELOW FOR PAST CWD TESTING;
Subject: CWD testing in Texas
Date: Sun, 25 Aug 2002 19:45:14 -0500
From: Kenneth Waldrup
To: flounder@wt.net
CC: mcoats@tahc.state.tx.us
Dear Dr. Singletary,
In Fiscal Year 2001, seven deer from Texas were tested by the National Veterinary Services Laboratory (NVSL) for CWD (5 fallow deer and 2 white-tailed deer). In Fiscal Year 2002, seven elk from Texas were tested at NVSL (no deer). During these two years, an additional six elk and one white-tailed deer were tested at the Texas Veterinary Medical Diagnostic Laboratory (TVMDL). In Fiscal Year 2002, four white-tailed deer (free-ranging clinical suspects) and at least eight other white-tailed deer have been tested at TVMDL. One elk has been tested at NVSL. All of these animals have been found negative for CWD. Dr. Jerry Cooke of the Texas Parks and Wildlife Department also has records of 601 clinically ill white-tailed deer which were necropsied at Texas A&M during the late 1960's and early 1970's, and no spongiform encepalopathies were noted.
Thank you for your consideration.
Ken Waldrup, DVM, PhD Texas Animal Health Commission
========================
TEXAS CWD STATUS
Captive Cervids
There have been no reported CWD infections of captive elk or deer in Texas. There is currently no mandatory surveillance program for susceptible cervids kept on game farms, although, there has been voluntary surveillance since 1999, which requires owners of participating herds to maintain an annual herd inventory and submit samples for all mortalities of animals over 16 months of age.
Free-Ranging (Wild) Cervids
There have been no reported CWD infections of free-ranging susceptible cervids in Texas. Currently targeted surveillance of free-ranging cervids having clinical symptoms is ongoing in Texas with no positives identified. Additionally, sampling of hunter-killed animals was initiated statewide during the 2002-2003 deer hunting season and sampling will be continued for the next three to five years.
Historic Status
Some have speculated that CWD is "spontaneous" and may exist naturally at low levels, even in Texas. The Texas Wildlife Disease Project, a cooperative research project between TPWD and Texas A&M University (circa 1965-1975), was created to address two disease issues; a) low reproduction in Texas pronghorn and b) "circling disease" in white-tailed deer. One of the leading veterinary pathologists on this project was already suspicious that the etiology of "circling disease" was scrapie being transmitted from sheep to deer. During the project's existence, a total of 780 clinically affected animals (601 white-tailed deer, 7 mule deer, 2 elk, and 170 exotic deer and antelope) were collected. Tissues, including brain and lymph nodes, from the collected animals were examined for spongiform histological lesions, and all were found to be negative. Had CWD (a form of TSE, like scrapie) existed in Texas during this time frame, it is probable that these investigations would have detected these classic histological lesions, especially in clinically affected animals. It must be noted, however, that the current laboratory tests used to diagnose CWD were not available during the time the Wildlife Disease Project so it can not be stated with absolute certainty that CWD was not present.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/sta tus/
PLAN FOR MANAGEMENT OF THE DISEASE IN TEXAS
Diseases such as CWD tend to be managed more effectively when efforts are applied before or as the disease emerges, rather than after it becomes established. CWD is an emerging disease. The current number of known infections within private elk and deer breeding facilities varies markedly among states (and Canada) and is increasing steadily with continued and expanding surveillance and investigations. The geographic spread of CWD in free-ranging mule deer, white-tailed deer and elk is a concern. The recent discovery of CWD in free-ranging white-tailed deer in Wisconsin and Illinois, approximately 700 miles east of any previously known infection, and the discovery of several CWD positive mule deer in New Mexico, approximately 35 miles north of the Texas border were well out of the known boundaries of the disease.
The disease prevalence appears to be increasing in localized areas, although it is not clear whether this is due to increased incidence, or increased surveillance, reporting, and testing. Information from states with direct experience in managing CWD is being used for developing Texas plans as we learn from their experiences.
TPWD and TAHC are developing stepped up targeted and geographically-focused surveillance plans to monitor free-ranging deer for the presence of the disease and a rapid response plan to guide both TPWD and TAHC should CWD be detected in the State. TPWD and TAHC are also evaluating cervid management laws, rules, and policies for free ranging and scientific breeder permitted cervids under their authority to identify issues and potential weaknesses related to disease management. In these efforts, TPWD and TAHC will work with other agencies and organizations responsible for or are concerned about cervid disease management in an attempt to ensure comprehensive approaches to effective management of CWD risks (see Appendix C: Importation of Susceptible Cervids).
TAHC and TPWD have split jurisdictions and regulatory responsibilities, which creates challenges for both agencies (i.e., TAHC responsible for elk, TPWD responsible for white-tailed deer and mule deer). Both agencies will cooperate to resolve issues as they arise.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/pla n/
COMPONENTS OF THE PLAN
1. Education and information sharing with public, constituents, and other government agency personnel concerning CWD.
2. Ongoing targeted surveillance of clinical deer statewide (i.e., collecting and CWD- testing deer/elk exhibiting symptoms that may be consistent with CWD).
3. Development and implementation of a geographically-focused Monitoring Plan involving the sampling and CWD-testing of hunter-harvested deer.
4. TAHC Rules for Importation of Susceptible Cervids (Appendix C).
5. Response Plan for CWD should it occur in Texas(Appendix D).
6. TAHC rules for monitoring for CWD in breeding facilities (Appendix E).
7. Media Response plan development in the possible event of a positive CWD occurrence (Appendix F).
8. Advance education of relevant professionals such as resource agency personnel, private wildlife consultants, veterinarians, landowners, wildlife co-ops, taxidermists, and others
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/com ponents/
EDUCATION AND INFORMATION SHARING
TPWD/TAHC will help educate and share current information with the general public, constituent groups, and other government agency personnel. These efforts will include website updates, distribution of brochures, periodic news releases, public meetings, informational workshops, agency communications and reports. This information will include:
1) basic history and understanding of CWD;
2) its nationwide distribution, and status of knowledge of the disease (e.g., epidemiology, transmission, clinical signs, population effects);
3) other CWD related issues and concerns (e.g., carcass handling and meat consumption, transmission potential to humans and livestock, deer feeding); and
4) management and research actions being taken by TPWD and TAHC. Information may also be designed to focus on specific issues of importance to landowners, hunters, meat processors, taxidermists, deer feeders, veterinarians, rehabilitators, feed companies, feeder manufacturers and operators of captive deer and elk facilities.
Publication of technical findings of research in peer-reviewed journals and agency reports will be strongly encouraged. The more informed all agencies and the public (including hunters) become, the more effectively CWD risks will be managed in the future.
Informing and educating the public, constituents, TPWD and other agency personnel about CWD is essential. Development of informational brochures and leaflets for public and intra-/interagency distribution containing information about CWD being directed toward general public (including hunter) interests and concerns are a necessity. This information will be distributed as follows:
* Available at all TPWD offices statewide.
* Carried by Wildlife Biologists, Game Wardens and Park Peace Officers.
* Distributed to potential contact agencies and individuals.
* Potential contact agencies/individuals (in alphabetical order) include:
o Cooperative Extension Service
o Exotic Wildlife Association
o Federal Natural resource and land management agencies, NPS, USFWS and USFS
o Governors Office, EOC
o Military installations
o Sportsmen Conservationists of Texas
o Texas Ag. Council
o Texas Agricultural Extension Service
o Texas Animal Health Commission
o Texas Chapter of the Wildlife Society
o Texas Deer Association
o Texas Department of Agriculture
o Texas Game Warden Association
o Texas Grain and Feed Association
o Texas Farm Bureau
o Texas Taxidermists Association
o Texas Veterinary Medical Diagnostic Laboratory
o Texas Veterinary Medical Association
o Texas Wildlife Association
o TSCRA (Texas and Southwestern Cattle Raisers Association)
o TS&GRA
o USDA/APHIS
o Wildlife rehabilitators
Should CWD occur it could have a significant adverse economical impact upon landowners, local communities and landowners possessing deer held under authority of Scientific Breeder Permits and elk. Special emphasis would be directed toward informing all constituents that potentially could be affected by the discovery of CWD in the State. These efforts could be accomplished through the completion of a general news packet, video releases, TPWD/TAHC web sites, as well as television and radio news releases, as well as partner publications and information systems.
Informing and educating TPWD wildlife biologists and law enforcement personnel is also critical, as these individuals will generally be the first lines of information for the public and press. Internal distribution of relevant information in a timely manner will aid TPWD personnel in addressing any CWD concerns from the public or constituent groups. As information is gathered regarding testing or other pertinent data, TPWD should present this information as requested at interagency meetings and professional meetings/symposia. These data should additionally be published peer-reviewed journals or TPWD Technical Reports. In addition, advance education of relevant professionals such as other resource agency personnel, private wildlife consultants, veterinarians, landowners, wildlife co-ops, taxidermists, feed store personnel, and other similar professions who may be contacted by the public and press for comments should be invited to education workshops.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/edu cation/
ONGOING TARGETED SURVEILLANCE OF CLINICAL DEER STATEWIDE
Collecting CWD clinical-free-ranging cervids began in late summer 2002. The collection of clinical deer has been reported by researchers in other states to be particularly useful in detecting the presence/absence of CWD in local areas statewide. TPWD will continue testing clinical free-ranging deer for CWD as they are encountered. Federal funding through APHIS/USDA may be available and would provide for increased sampling during FY-04 sampling period and beyond.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/management_plan/sur veillance/
Chronic Wasting Disease Testing
Submitting a Specimen for Testing
Texas Veterinary Medical Diagnostic Laboratory (TVMDL) will provide Immunohistochemistry (IHC) based testing for Chronic Wasting Disease (CWD), and screening for tuberculosis (TB) in cervids. These tests are available at the College Station and Amarillo Laboratories. Specimens required for testing are the obex of the brain, both retropharyngeal lymph nodes, and both tonsils. If both CWD and TB testing are requested, it is recommended that the entire head be shipped to the lab so each of those specimens can be identified and processed. Antlers should be removed from the head and the head, including a liberal amount of the soft tissue posterior to the pharynx, should be packed in multiple plastic bags to prevent leakage. A completed Texas Veterinary Medical Diagnostic Laboratory (TVMDL) Accession Form
or a letter with the name, address and telephone number of the submitter should be enclosed in a separate plastic bag. Specimens must be chilled within 2 hours after kill and should remain chilled during transit. For optimum results, specimens should arrive at the lab within 24 hours after kill. Charges are as follows:
Charges for Chronic Wasting Disease Testing
Note: There will be a $100.00 additional charge for carcass disposal if an entire carcass is submitted.
Brain removal $10.00
IHC test for CWD $30.00
TB Screen $15.00
Head Disposal $15.00
Total $70.00
Payment by check or money order must be included with specimens for testing to be completed. Credit Cards are not accepted. Specimens submitted for both CWD and TB screening will require a pre-payment of $65.00 or $50.00 if CWD testing alone is requested. Submission of previously removed obexs must include a $30.00 payment for each test to be completed. Please call 979-845-3414 if you have questions on specimen submittal or charges.
Texas Veterinary Medical Diagnostic Laboratory (TVMDL) Accession Form
The Texas Veterinary Medical Diagnostic Laboratory (TVMDL) Accession Form media download (PDF 270.3 KB) should be printed and filled out prior to submitting a sample. See instructions above.
http://www.tpwd.state.tx.us/hunt/chronic_wasting_disease/testing/
SEE MAP OF CWD ON THE BORDER OF NEW MEXICO VERY CLOSE TO TEXAS ;
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdf
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwd_flyer.pdf
NO update on CWD testing in Texas, New Mexico that i could find. I have inquired about it though, no reply yet...
-------- Original Message --------
Subject: CWD testing to date TEXAS ?
Date: Mon, 09 May 2005 12:26:20 -0500
From: "Terry S. Singeltary Sr."
To: kristen.everett@tpwd.state.tx.us
Hello Mrs. Everett,
I am most curious about the current status on CWD testing in Texas. could you please tell me what the current and past testing figures are to date and what geographical locations these tests have been in. good bust on the illegal deer trapping case. keep up the good work there.........
thank you, with kindest regards,
Terry S. Singeltary Sr. snip...tss Bacliff, Texas USA 77518
CJD WATCH
http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm
CJD Watch message board
http://disc.server.com/Indices/167318.html
-------- Original Message --------
Subject: CWD testing in New Mexico
Date: Mon, 09 May 2005 14:39:18 -0500
From: "Terry S. Singeltary Sr."
To: ispa@state.nm.us
Greetings,
I am most curious of the current and past CWD testing in New Mexico, and there geographical locations...
thank you,
Terry S. Singeltary SR. CJD Watch
-------- Original Message --------
Subject: CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS ?
Date: Mon, 16 Aug 2004 15:09:58 -0500
From: "Terry S. Singeltary Sr."
To: Bovine Spongiform Encephalopathy
Greetings List members,
as i stated in my previous email;
http://www.tahc.state.tx.us/news/pr/2004/2004Aug10_Anthrax_Confirmed.pdf
CWD has not been detected in Texas, SADLY, they have not tested enough from the total population to know if CWD is in Texas or not. time will tell though. IF they get serious about finding and documenting CWD in sufficient numbers here in TEXAS, sadly, i am afraid they will find it. ITs already at NM, Texas border, TSEs knows no borders. HOWEVER, with the recent finding of a CNS cow with high potential for BSE/TSE in TEXAS, with one high official over ruling another official that wanted it tested, with the high official winning out and the damn thing going to render without being tested, head spinal cord and all. THIS weighs heavy on the credibility of any surveillance for any TSE in TEXAS, and speaks a great deal for the over all surveillance of TSE in the USA...TSS
SO, i thought i would just see where these Ecoregions were, and just how the CWD testing was distributed. YOU would think that with the cluster of CWD bordering TEXAS at the WPMR in NM, you would have thought this would be where the major CWD testing samples were to have been taken? wrong! let's have a look at the sample testing. here is map of CWD in NM WPMR bordering TEXAS;
NEW MEXICO 7 POSITIVE CWD WHITE SANDS MISSILE RANGE MAP
http://www.wildlife.state.nm.us/conservation/disease/cwd/documents/cwdmap.pdf
NEXT, let's have a look at the overall distribution of CWD in Free-Ranging Cervids and see where the CWD cluster in NM WSMR borders TEXAS;
Current Distribution of Chronic Wasting Disease in Free-Ranging Cervids
http://www.aphis.usda.gov/vs/nahps/cwd/cwd-distribution.html
NOW, the MAP of the Exoregion where the samples were taken to test for CWD;
CWD SURVEILLANCE SAMPLE SUBMISSIONS TEXAS
http://www.tahc.state.tx.us/animal_health/diseases/cwd/CWD2003.gif
Ecoregions of TEXAS
http://www.tpwd.state.tx.us/images/tx-eco95.gif
IF you look at the area around the NM WSMR where the CWD cluster was and where it borders TEXAS, that ecoregion is called Trans Pecos region. Seems if my Geography and my Ciphering is correct ;-) that region only tested 55% of it's goal. THE most important area on the MAP and they only test some 96 samples, this in an area that has found some 7 positive animals? NOW if we look at the only other border where these deer from NM could cross the border into TEXAS, this area is called the High Plains ecoregion, and again, we find that the sampling for CWD was pathetic. HERE we find that only 9% of it's goal of CWD sampling was met, only 16 samples were tested from some 175 that were suppose to be sampled.
AS i said before;
> SADLY, they have not tested enough from the total population to > know if CWD is in Texas or not.
BUT now, I will go one step further and state categorically that they are not trying to find it. just the opposite it seems, they are waiting for CWD to find them, as with BSE/TSE in cattle, and it will eventually...
TSS
=====
2019
cwd tse prion, while rome burns, prepare for the storm
the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO
cwd update on Wisconsin from Tammy Ryan...
Wyoming CWD Dr. Mary Wood
''first step is admitting you have a problem''
''Wyoming was behind the curve''
wyoming has a problem...
SATURDAY, JANUARY 19, 2019
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
TUESDAY, JANUARY 29, 2019
TEXAS REPORTS 2 MORE CWD TSE PRION ALL WILD CERVID TOTAL TO DATE 141
TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?
apparently, no ID though. tell me it ain't so please...
23:00 minute mark
''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''
SATURDAY, JANUARY 19, 2019
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
THURSDAY, MAY 17, 2018
Texas TAHC CWD TSE Prion Pay to Play Federal Indemnity Program, or what i call, ENTITLEMENT PROGRAM for Game Farm Industry
*** Hartley County Sheep with Scrapie, and CWD in Hartley county ???
*** Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play
Wednesday, May 04, 2016
TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission
TUESDAY, DECEMBER 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION
SUNDAY, DECEMBER 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry
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 <***
***> NORWAY CWD UPDATE December 2018
Report from the Norwegian Scientific Committee for Food and Environment (VKM) 2018: 16
Factors that can contribute to spread of CWD – an update on the situation in Nordfjella, Norway
Opinion of Panel on biological hazards of the Norwegian Scientific Committee for Food and Environment
13.12.2018
ISBN: 978-82-8259-316-8
ISSN: 2535-4019
Norwegian Scientific Committee for Food and Environment (VKM)
Po 222 Skøyen
0213 Oslo
Norway
FRIDAY, DECEMBER 14, 2018
Norway, Nordfjella VKM 2018 16 Factors that can contribute to spread of CWD TSE Prion UPDATE December 14, 2018
THURSDAY, OCTOBER 25, 2018
***> Norway New additional requirements for imports of hay and straw for animal feed from countries outside the EEA due to CWD TSE Prion
new link;
THURSDAY, FEBRUARY 07, 2019
CWD TSE Prion, and Processing your own meat
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
FRIDAY, FEBRUARY 08, 2019
Prion protein polymorphisms associated with reduced CWD susceptibility limit peripheral PrPCWD deposition in orally infected white-tailed deer
MONDAY, JANUARY 14, 2019
Evaluation of iatrogenic risk of CJD transmission associated with Chronic Wasting Disease TSE Prion in Texas TAHC TPWD
It is a dimension as vast as space and as timeless as infinity. It is the middle ground between light and shadow, between science and superstition, and it lies between the pit of man's fears and the summit of his knowledge. This is the dimension of imagination. It is NOT, an area which we call the Twilight Zone, but an area that believes junk science, and the very industries and lobbyist some Texas Hunters, the cervid industry, that insist on shoving the fake news down their throats, we call this ted nugent junk science, and in TEXAS, sometimes you just can't fix stupid, this is where the rubber meets the road, here's your sign!
chronic wasting disease cwd tse prion aka mad deer elk disease, if you consume a cwd tse prion positive cervid, then months, years, decades later, go on to have surgery, dental, ophthalmology, endoscopy, donate tissue, blood, organs, you then expose those medical theaters and tissue, blood, organs, that are incubating the infectious cwd tse prion disease, to everyone that comes in contact.
these are not memes, these are actual statements from hunters/industry in Texas about CWD tse prion.
God help them, and us...terry
''Got a call today from TPWD, I’ve got a mule deer that tested early positive for CWD. I’m soon to turn into a zombie because I have already been eating it. They advised not to consume any of the meat...too late! They want to come confiscate what meat is left once they get more results back from another lab.''
snip...
***> This is very likely to have parallels with control efforts for CWD in cervids.
Rapid recontamination of a farm building occurs after attempted prion removal
Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2
Abstract
The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity.
Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids.
Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent.
Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA).
A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay.
Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3.
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
snip...
As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.
Funding This study was funded by DEFRA within project SE1865.
Competing interests None declared.
Saturday, January 5, 2019
Rapid recontamination of a farm building occurs after attempted prion removal
***> NORWAY CWD UPDATE December 2018
Report from the Norwegian Scientific Committee for Food and Environment (VKM) 2018: 16
Factors that can contribute to spread of CWD – an update on the situation in Nordfjella, Norway
Opinion of Panel on biological hazards of the Norwegian Scientific Committee for Food and Environment
13.12.2018
ISBN: 978-82-8259-316-8
ISSN: 2535-4019
Norwegian Scientific Committee for Food and Environment (VKM)
Po 222 Skøyen
0213 Oslo
Norway
FRIDAY, DECEMBER 14, 2018
Norway, Nordfjella VKM 2018 16 Factors that can contribute to spread of CWD TSE Prion UPDATE December 14, 2018
THURSDAY, OCTOBER 25, 2018
***> Norway New additional requirements for imports of hay and straw for animal feed from countries outside the EEA due to CWD TSE Prion
new link;
SATURDAY, JANUARY 19, 2019
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS
MONDAY, JANUARY 14, 2019
Evaluation of iatrogenic risk of CJD transmission associated with Chronic Wasting Disease TSE Prion in Texas TAHC TPWD
It is a dimension as vast as space and as timeless as infinity. It is the middle ground between light and shadow, between science and superstition, and it lies between the pit of man's fears and the summit of his knowledge. This is the dimension of imagination. It is NOT, an area which we call the Twilight Zone, but an area that believes junk science, and the very industries and lobbyist some Texas Hunters, the cervid industry, that insist on shoving the fake news down their throats, we call this ted nugent junk science, and in TEXAS, sometimes you just can't fix stupid, this is where the rubber meets the road, here's your sign!
chronic wasting disease cwd tse prion aka mad deer elk disease, if you consume a cwd tse prion positive cervid, then months, years, decades later, go on to have surgery, dental, ophthalmology, endoscopy, donate tissue, blood, organs, you then expose those medical theaters and tissue, blood, organs, that are incubating the infectious cwd tse prion disease, to everyone that comes in contact.
these are not memes, these are actual statements from hunters/industry in Texas about CWD tse prion.
God help them, and us...terry
''Got a call today from TPWD, I’ve got a mule deer that tested early positive for CWD. I’m soon to turn into a zombie because I have already been eating it. They advised not to consume any of the meat...too late! They want to come confiscate what meat is left once they get more results back from another lab.''
snip...
SUNDAY, MAY 14, 2017
85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play
Wednesday, May 04, 2016
TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission
TUESDAY, DECEMBER 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION
SUNDAY, DECEMBER 14, 2014
TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry
***> TEXAS HISTORY OF CHRONIC WASTING DISEASE CWD TSE PRION
***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History
TUESDAY, JANUARY 29, 2019
TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?
NEWS RELEASE Texas Animal Health Commission “Serving Texas Animal Agriculture Since 1893” Andy Schwartz, DVM ● Interim Executive Director P.O. Box 12966 ● Austin, Texas 78711 ● (800) 550-8242 http://www.tahc.texas.gov For more information contact the Communications Dept. at 512-719-0750 or at callie.ward@tahc.texas.gov
________________________________________________________________________________________________________
April 22, 2016
Scrapie Confirmed in a Hartley County Sheep AUSTIN – Texas Animal Health Commission (TAHC) officials have confirmed scrapie in a Hartley County ewe. The ewe was tested by TAHC after the owner reported signs of weight loss and lack of coordination to their local veterinarian. The premises was quarantined and a flock plan for monitoring is being developed by the TAHC and USDA. “The TAHC is working closely with the flock owner, sharing all of the options for disease eradication,” said Dr. David Finch, TAHC Region 1 Director. “We are thankful the producer was proactive in identifying a problem and seeking veterinary help immediately.”
Texas leads the nation in sheep and goat production. Since 2008, there have been no confirmed cases of scrapie in Texas. The last big spike in Texas scrapie cases was in 2006 when nine infected herds were identified and the last herd was released from restrictions in 2013.
According to USDA regulations, Texas must conduct adequate scrapie surveillance by collecting a minimum of 598 sheep samples annually. Since USDA slaughter surveillance started in FY 2003, the percent of cull sheep found positive for scrapie at slaughter (once adjusted for face color) has decreased 90 percent.
Scrapie is the oldest known transmissible spongiform encephalopathies, and under natural conditions only sheep and goats are known to be affected by scrapie. It is a fatal disease that affects the central nervous system of sheep and goats. It is not completely understood how scrapie is passed from one animal to the next and apparently healthy sheep infected with scrapie can spread the disease. Sheep and goats are typically infected as young lambs or kids, though adult sheep and goats can become infected.
The most effective method of scrapie prevention is to maintain a closed flock. Raising replacement ewes, purchasing genetically resistant rams and ewes, or buying from a certified-free scrapie flock are other options to reduce the risk of scrapie. At this time the resistant genetic markers in goats have not been identified, therefore it is important to maintain your sheep and goat herds separately. The incubation period for Scrapie is typically two to five years. Producers should record individual identification numbers and the seller’s premise identification number on purchase and sales records. These records must be maintained for a minimum of five years. Producers should notify the Texas Animal Health Commission (800-550-8242) or the USDA-Austin Office (512-383-2400) if they have an adult sheep or goat with neurologic signs such as incoordination, behavioral changes, or intense itching with wool loss. Producers may order scrapie identification tags by calling 866-873-2824.
For more information, please visit our website at: http://www.tahc.texas.gov/animal_health/scrapie/scrapie.html.
###
PRION 2018 CONFERENCE
O3 Experimental studies on prion transmission barrier and TSE pathogenesis in large animals
Rosa Bolea(1), Acín C(1)Marín B(1), Hedman C(1), Raksa H(1), Barrio T(1), Otero A(1), LópezPérez O(1), Monleón E(1),Martín-Burriel(1), Monzón M(1), Garza MC(1), Filali H(1),Pitarch JL(1), Garcés M(1), Betancor M(1), GuijarroIM(1), GarcíaM(1), Moreno B(1),Vargas A(1), Vidal E(2), Pumarola M(2), Castilla J(3), Andréoletti O(4), Espinosa JC(5), Torres JM(5), Badiola JJ(1).
1Centro de Investigación en Encefalopatías y Enfermedades Transmisibles Emergentes, VeterinaryFaculty, Universidad de Zaragoza; Zaragoza,Spain.2 RTA, Centre de Recerca en Sanitat Animal (CReSA, IRTA-UAB) 3 4 INRA, ÉcoleVétérinaire, Toulouse, France.5CIC bioGUNE, Prion researchlab, Derio, Spain CISA- INIA, Valdeolmos, Madrid 28130, Spain.
Experimental transmission of Transmissible Spongiform Encephalopathies (TSE) has been understood and related with several factors that could modify the natural development of these diseases. In fact, the behaviour of the natural disease does not match exactly in each animal, being modified by parameters such as the age at infection, the genotype, the breed or the causative strain. Moreover, different TSE strains can target different animal species or tissues, what complicate the prediction of its transmissibility when is tested in a different species of the origin source. The aim of the experimental studies in large animals is to homogenize all those factors, trying to minimize as much as possible variations between individuals. These effects can be flattened by experimental transmission in mice, in which a specific strain can be selected after several passages. With this objective, several experimental studies in large animals have been developed by the presenter research team.
Classical scrapie agent has been inoculated in cow, with the aim of demonstrate the resistance or susceptibility of this species to the first well known TSE; Atypical scrapie has been inoculated in sheep (using several routes of infection), cow and pig, with the objective of evaluating the potential pathogenicity of this strain; Classical Bovine Spongiform Encephalopathy (BSE) has been inoculated in goats aiming to demonstrate if the genetic background of this species could protect against this strain; goat BSE and sheep BSE have been inoculated in goats and pigs respectively to evaluate the effect of species barrier; and finally atypical BSE has been inoculated in cattle to assess the transmissibility properties of this newly introduced strain.
Once the experiments have been carried out on large animal species, a collection of samples from animals studied were inoculated in different types of tg mice overexpressing PrPcin order to study the infectivity of the tissues, and also were studied using PMCA.
In summary, the parameters that have been controlled are the species, the strain, the route of inoculation, the time at infection, the genotype, the age, and the environmental conditions.
To date,
***> eleven of the atypical scrapie intracerebrally inoculated sheep have succumbed to atypical scrapie disease;
***> six pigs to sheep BSE;
***> one cow to classical scrapie;
***> nine goats to goat BSE and
***> five goats to classical BSE.
***> PrPSC has been demonstrated in all cases by immunohistochemistry and western blot.
=====> PRION CONFERENCE 2018
MONDAY, OCTOBER 1, 2018
Review: Update on Classical and Atypical Scrapie in Sheep and Goats
***> Our findings suggest that cattle exposure to atypical scrapie could be responsible of the occurrence of classical BSE in this species.
***> These results also raise some concerns about the current and future changes in the protection measures that were implemented to mitigate animal and human exposure to TSE agents.
Monday, November 30, 2009
***> USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period.
This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
2017 Annual Report
1a. Objectives (from AD-416):
Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.
1b. Approach (from AD-416):
The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.
3. Progress Report:
All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.
4. Accomplishments
1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.
Review Publications
Hwang, S., Greenlee, J.J., Nicholson, E.M. 2017. Use of bovine recombinant prion protein and real-time quaking-induced conversion to detect cattle transmissible mink encephalopathy prions and discriminate classical and atypical L- and H-type bovine spongiform encephalopathy. PLoS One. 12(2):e0172391.
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.
Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.
Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114. Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.
Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005.
FRIDAY, APRIL 20, 2018
*** Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies
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...
TUESDAY, MAY 31, 2011
Chronic Wasting Disease DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011
Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) A TOTAL FAILURE $$$
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.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.
snip.....
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip.....
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip.....
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip.....
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip.....
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
***> Wednesday, January 23, 2019
***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***
SUNDAY, DECEMBER 02, 2018
CWD TSE PRION, REGULATORY LEGISLATION, PAY TO PLAY, and The SPREAD of Chronic Wasting Disease
Prion Conference 2018
O5 Prion Disease in Dromedary Camels
Babelhadj B (1), Di Bari MA (2), Pirisinu L (2), Chiappini B (2), Gaouar SB (3), Riccardi G (2), Marcon S (2), Agrimi U (2), Nonno R (2), Vaccari G (2) (1) École Normale Supérieure Ouargla. Laboratoire de protection des écosystèmes en zones arides et semi arides University Kasdi Merbah Ouargla, Ouargla, Algeria; (2) Istituto Superiore di Sanità, Department of Food Safety, Nutrition and Veterinary Public Health, Rome, Italy (3) University Abou Bekr Bélkaid, Tlemcen, Algeria.
Prions are responsible for fatal and transmissible neurodegenerative diseases including CreutzfeldtJakob disease in humans, scrapie in small ruminants and bovine spongiform encephalopathy (BSE). Following the BSE epidemic and the demonstration of its zoonotic potential, general concerns have been raised on animal prions.
Here we report the identification of a prion disease in dromedary camels (Camelus dromedarius) in Algeria and designate it as Camel Prion Disease (CPD). In the last years, neurological symptoms have been observed in adult male and female dromedaries presented for slaughter at the Ouargla abattoir. The symptoms include weight loss, behavioral abnormalities and neurological symptoms such as tremors, aggressiveness, hyper-reactivity, typical down and upwards movements of the head, hesitant and uncertain gait, ataxia of the hind limbs, occasional falls and difficult getting up. During 2015 and 2016, symptoms suggestive of prion disease were observed in 3.1% of 2259 dromedaries presented at ante-mortem examination. Laboratory diagnosis was obtained in three symptomatic dromedaries, sampled in 2016 and 2017, by the detection of typical neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues.
Histopathological examination revealed spongiform change, gliosis and neuronal loss preferentially in grey matter of subcortical brain areas. Abundant PrPSc deposition was detected in the same brain areas by immunohistochemistry and PET-blot. Western blot analysis confirmed the presence of PK-resistant PrPSc, whose N-terminal cleaved PK-resistant core was characterized by a mono-glycosylated dominant form and by a distinctive N-terminal cleavage, different from that observed in BSE and scrapie.
PrPSc was also detected, by immunohistochemistry, in all sampled lymph nodes (cervical, prescapular and lumbar aortic) of the only animal from which they were collected.
The PRNP sequence of the two animals for which frozen material was available, showed 100% nucleotide identity with the PRNP sequence already reported for dromedary camel.
Overall, these data demonstrate the presence of a prion disease in dromedary camelswhose nature, origin and spread need further investigations. However, our preliminary observations on the rather high prevalence of symptomatic dromedaries and the involvement of lymphoid tissues, are consistent with CPD being an infectious disease. In conclusion, the emergence of a new prion disease in a livestock species of crucial importance for millions of people around the world, makes urgent to assess the risk for humans and to develop policies able to control the spread of the disease in animals and to minimize human exposure.
CDC
New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES
Mad Camel Disease
Volume 24, Number 6—June 2018 Research
Prion Disease in Dromedary Camels, Algeria
Abstract
Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.
SNIP...
The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.
Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (27) should be investigated to trace the possible origin of CPD from other countries.
Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (28). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (28).
On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (29). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (30).
Such genetic homogeneity also might be reflected in PRNP. Studies on PRNP variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep.
In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (13). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.
The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock.
***> IMPORTS AND EXPORTS <***
***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***
ZOONOSIS OF SCRAPIE TSE PRION
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
***> why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man.
***> I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough.
***> Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
R. BRADLEY
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***
Transmission of scrapie prions to primate after an extended silent incubation period
Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.
SNIP...
Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.
The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.
We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.
Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.
The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.
Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.
Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.
Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.
Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.
In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018
P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer
Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1)
(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada.
Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer.
Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection.
Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD.
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3
Correspondence
Gudmundur Georgsson ggeorgs@hi.is
1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland
2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland
3 Bethesda, Maryland, USA
Received 7 March 2006 Accepted 6 August 2006
In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.
TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION
*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION
SEE;
Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;
Some unofficial information from a source on the inside looking out -
Confidential!!!!
As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).
Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document
Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
=========================
***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20).
Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22).
Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing.
Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building.
Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9).
The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep.
Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease.
It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled.
Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases.
Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA.
Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice.
In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals.
In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions).
As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28).
This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm.
This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc.
In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc.
Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing.
The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material.
In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12).
A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30).
This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model.
Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
***> 2018 URGENT DATA <***
***2018***
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans.
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of humanized Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental human CWD samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental human CWD samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance
There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
Funding Agency
Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS088604-04
Application #
9517118
Study Section
Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30 Project End 2019-07-31 Budget Start 2018-08-01 Budget End 2019-07-31 Support Year 4 Fiscal Year 2018 Total Cost Indirect Cost Institution Name Case Western Reserve University Department Pathology Type Schools of Medicine DUNS # 077758407 City Cleveland State OH Country United States Zip Code 44106
Related projects
NIH 2018 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University
NIH 2017 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University
NIH 2016 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University
NIH 2015 R01 NS Cervid to human prion transmission Kong, Qingzhong / Case Western Reserve University $337,507
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
here is the latest;
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge). To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip...see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry
just out CDC...see;
Research Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions
Marcelo A. Barria
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) M. A. Barria et al.
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.
Molecular Barriers to Zoonotic Transmission of Prions
Marcelo A. Barria, Aru Balachandran, Masanori Morita, Tetsuyuki Kitamoto, Rona Barron, Jean Manson, Richard Knight, James W. Ironside, and Mark W. Headcorresponding author
snip...
The conversion of human PrPC by CWD brain homogenate in PMCA reactions was less efficient when the amino acid at position 129 was valine rather than methionine.
***Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.
snip...
However, we can say with confidence that under the conditions used here, none of the animal isolates tested were as efficient as C-type BSE in converting human PrPC, which is reassuring.
***Less reassuring is the finding that there is no absolute barrier to the conversion of human PrPC by CWD prions in a protocol using a single round of PMCA and an entirely human substrate prepared from the target organ of prion diseases, the brain.
Prion 2017 Conference Abstracts
CWD 2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009.
21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes.
Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product.
Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain).
Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments.
We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem.
Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes.
All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals.
Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing.
Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years.
Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017
DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE
DECIPHERING NEURODEGENERATIVE DISORDERS
VIDEO PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION
10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question...
''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)
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132 ;
also, see;
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.
snip...
The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.
zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm
***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE..116***
To date there is no direct evidence that CWD has been or can be transmitted from animals to humans.
However, initial findings from a laboratory research project funded by the Alberta Prion Research Institute (APRI) and Alberta Livestock Meat Agency (ALMA), and led by a Canadian Food Inspection Agency (CFIA) scientist indicate that CWD has been transmitted to cynomolgus macaques (the non-human primate species most closely related to humans that may be used in research), through both the intracranial and oral routes of exposure.
Both infected brain and muscle tissues were found to transmit disease.
Health Canada’s Health Products and Food Branch (HPFB) was asked to consider the impact of these findings on the Branch’s current position on CWD in health products and foods.
Summary and Recommendation:
snip...
Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle.
These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle.
*** WDA 2016 NEW YORK ***
We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions.
In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.
***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
Student Presentations Session 2
The species barriers and public health threat of CWD and BSE prions
Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University
Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein.
These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species.
The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time.
We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations.
We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.
***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
SATURDAY, JANUARY 27, 2018
CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE.
THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$
BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.
SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.
SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.
SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.
***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.***
CDC CWD TSE PRION UPDATE USA JANUARY 2018
As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk. CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast.. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand. Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd. As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids...
Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018
snip....
*** 2017-2018 CWD TSE Prion UPDATE
*** 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.
you can see more evidence here ;
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
WEDNESDAY, SEPTEMBER 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
PRION 2010
International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria
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 (216-119-163-189.ipset45.wt.net)
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.
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).***
Terry S. Singeltary Sr.
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