Chronic Wasting Disease: Oklahoma Chronic Wasting Disease CWD of Deer and Elk Surveillance, Testing, and Preparedness

Hunting: Oklahoma Department of Wildlife Conservation 2015-2016 Harvest Report is updated weekly. Sportsmen have the option to exclude their name; however, your deer harvest information will still appear on the ... www.wildlifedepartment.com www.wildlifedepartment.com/hunting/deer.htm

Oklahoma Chronic Wasting Disease (CWD) of Deer and Elk Surveillance, Testing, and Preparedness

Chronic Wasting Disease CWD of Deer and Elk

Key Points

1. At this point there is no known cases of CWD in wild deer and elk in Oklahoma.

2. There has been no known transmission of CWD from deer or elk to any other animals or people even in states where CWD is found.

3. It is always wise to use common sense when handling any meat or when dealing with sick or injured animals.

For more information about CWD log on to www.cwd-info.org

"In 2006 more than 1,626 hunter harvested deer and elk were sampled in Oklahoma and all tested negative for chronic wasting disease. To date, some 7,088 animals have been tested statewide as part of The Wildlife Department's monitoring program and all have tested negative for CWD. The Department will continue to monitor the state's deer and elk herds through additional testing."

What is Chronic Wasting Disease (CWD)?

It was 35 years ago and the biologists were baffled. Blood work showed nothing unusual, liver and kidney tests turned up negative for all known diseases, but the mule deer were still wasting away to skin and bones. It could have been straight out of an episode of “The X Files.”

A few of the captive deer at the Colorado Division of Wildlife’s research facilities in Fort Collins had begun to lose weight on a diet that sustained other deer. They drank incessantly and spent much of their time standing listlessly in their corrals. The biologists knew they had a unique syndrome on their hands, but it was like nothing they had ever seen before.

Captive deer at Wyoming Game and Fish Department's Sybille Research Unit were soon showing signs of the mystery disease. Because the Colorado and Wyoming facilities regularly traded deer and elk, the appearance of the disease in Wyoming came as no great surprise.

Over the next 10 years, researchers worked to understand the origin and causes of the affliction, but their studies led to more questions than answers.

One thing was certain, the disease was deadly. Between 1974 and 1979, 66 mule deer and one black-tailed deer were held captive in Colorado and Wyoming research corrals. Of those, 57 contracted the strange disease and not one survived.

The search went on for the cause of the disease. Viruses, bacteria and nutritional deficiencies were all ruled out. Biologists named it "chronic wasting disease” (CWD), identifying the disease’s most devastating outward symptom, irreversible weight loss.

The first break in the case came in 1978, when wildlife veterinarian Beth Williams began analyzing tissues of affected animals. She found microscopic holes in brain and nerve tissues of the deer. The disease was turning the brains of these deer into Swiss cheese.

This finding put Chronic Wasting Disease into a small category of diseases labeled transmissible spongiform encephalopathies (TSE). As pathologists looked into CWD further, they began to see similarities between it and scrapie, a TSE that affects sheep.

Sheep and goats have been affected by scrapie in Europe for centuries. In all those years, no other type of animal has ever come down with the disease, including generations of shepherds who work with their flocks daily and consumers who eat their meat and drink their milk.

Although they now knew CWD was related to scrapie and other TSEs, this helped little because at the time pathologists knew little about the cause of this disease either. The scientific camps began to stake their claim on the origins of these enigma diseases. Some thought it was a genetic illness, others assumed it was a virus too small to be detected by existing techniques. Several different scientists were pursuing proof of their favorite theories.

In the meantime, unsettling news was reported from the field. In March 1981, biologists in north Colorado brought in a sick elk that turned out to be suffering from chronic wasting disease. The disease had somehow spread from captive animals into free-ranging herds.

Cervids (animals such as white-tailed deer and elk ) seemed to be the target of CWD, no other animals including cattle, horses or humans have been affected by CWD. The disease spread incrementally through northcentral Colorado affecting mule deer, white-tailed deer and elk. In 1986, CWD claimed an elk in southeastern Wyoming, the first confirmed case of the disease in a wild animal outside of Colorado.

Although this was not exactly a raging disease outbreak, the spread of the disease had started and wildlife vets and biologists were concerned. They knew little about it, and knew nothing about how to stop it.

Today, 34 years since the disease was discovered, pathologists have learned more about the disease, but still have much to learn before they fully understand it. However slowly, CWD has continued to creep across the United States and Canada, currently impacting either captive or free-ranging deer in nine states and a pair of Canadian provinces. This includes a closely monitored captive elk herd in central Oklahoma.

It is now generally accepted that prions, naked proteins with the ability to duplicate and multiply, are the culprits to blame for CWD and other TSE’s. There remains no known cure or even a reliable method of disinfecting contaminated areas. Biologists in Fort Collins, Colorado, where the disease was first discovered, found out how resilient these prions can be. They set out in an intensive effort to rid the research facilities of CWD. All captive deer and elk were killed and buried. Personnel then plowed up the soil in the pens in an effort to bury possible disease organisms and structures and pastures were repeatedly treated with a powerful disinfectant. A year later, 12 elk calves from the wild were released in the sanitized holding areas. In the next five years, two of these elk died from chronic wasting disease.

Fortunately, Oklahoma’s free-ranging deer herd is not known to carry the disease. Over the past three years biologists and veterinarians have examined almost 400 deer and elk taken during Oklahoma's hunting seasons as part of the Department’s CWD monitoring program. All samples obtained from animals taken from the wild have tested negative and biologists will continue to closely monitor the deer and elk herd for signs of the disease.

Currently, detecting the disease is far from simple. The only acceptable test is a microscopic examination of an animal’s brain stem. There are no live animal tests and only a handful of laboratories and pathologists are qualified to administer the brain test.

If there is a bright side to chronic wasting disease it is that it reminds how valuable our deer are. It wasn’t that long ago that deer seemed headed down the same path as the buffalo and the passenger pigeon, over-exploited and pushed out by land-hungry settlers. Through the tireless work of biologists and sportsmen, deer have been restored to once unthinkable numbers in Oklahoma and across their native range.

A deer is a symbol of grace and it provides a succulent, nutritious meal. It is that and more, it is a wild animal that makes the woods a better place just for being there. It is as American as they come, inhabiting just about every ecotone on this continent.

To know that a disease as serious as CWD is spreading should pain everyone who has ever marveled at a deer slinking over a barbed wire fence. But it is no surprise that it was hunters who were the first to step up to the plate for the animals. In Oklahoma, a CWD monitoring program is in place thanks to funds provided through hunter’s licenses. In Wisconsin, it is hunters who have taken on the grim task of thinning out the deer herd to prevent the spread of CWD, and across the United States it is sportsmen who are carrying much of the financial burden to pay for biologists, veterinarians and pathologists to study the disease.

Is Venison Safe to Eat?

According to current research, there is no scientific evidence linking CWD to human diseases. It is recommended that hunters practice standard safety practices when handling any wild game, or any meat for that matter, as general precautionary measures.

These practices include washing your hands after handling raw meat and cooking the meat at an appropriate temperature.

"In my opinion, venison is just as safe as any other game meat," said Mike Shaw, head deer biologist for the Oklahoma Department of Wildlife Conservation.

Even in the parts of Wyoming and Colorado where chronic wasting disease is found, less than six percent of deer are infected.

A few precautions are recommended:

1) Don't shoot an animal that is acting abnormally or looks sick. 2) Wear rubber or latex gloves when you field-dress your animal. 3) Don't eat deer brains or spinal cord. 4) Bone out your deer meat and discard the brain, spinal cord, eyes, spleen, and lymph nodes.

Prions: New germs

In 1972 neurologist Stanley Prusiner lost a patient to Creutzfeldt-Jakob disease, a TSE that affect humans. Prusiner was serving his residency at the University of California’s School of Medicine and was astounded by the lack of information about the rare disease.

Two years later he set up his own laboratory at the University of California-San Francisco and set out to get to the root cause of scrapie, Creutzfeldt-Jakob and other TSE’s.

He took two known facts about the disease and came up with an astounding conclusion. He knew that scrapie infected tissue showed no signs of foreign DNA. He also knew that the only disinfectant techniques that affected the scrapie "germ" were those techniques that broke down not only DNA, but also proteins. From these two facts he assumed that the scrapie "germ" was a simple protein without DNA.

The notion seemed impossible in scientific circles. Since the 1950’s scientists had been working on the basis that proteins were duplicated using a blueprint provided by DNA. Prusiner was saying that these proteinaceous infectious particles, or prions for short, could recreate themselves without ever using DNA. His theory was accepted with just about the same enthusiasm that early mapmakers shared with Columbus when he told them the earth was round.

Prusiner spent the next two decades proving his theory and his efforts were rewarded in 1997 when he won the Nobel Prize for medicine. Although a few skeptics still remain, it is now generally accepted that prions play a causative role in CWD and other TSE’s.

The Worth of a Healthy Deer Herd

Wildlife agencies across the United States are scrambling to protect deer herds in their areas from the ravaging effects of CWD.

It is no wonder why. Not only are deer a beautiful natural resource and part of a rich hunting heritage, they also provide a significant economic impact. The annual pilgrimage of hunters into the woods each fall means big bucks, in more ways than one. In Oklahoma alone, 261,000 hunters, most of which are deer hunters, spent over $2.6 million on hunting expenditures according to a recent survey. While hunters are after deer, they spend money to gas their vehicles, eat meals and purchase equipment. These dollars go back into Oklahoma communities, particularly those in rural areas.

In an effort to keep Oklahoma’s deer safe from CWD, the Wildlife Conservation Commission has suspended the import of live deer and elk into the state from states that have CWD in their free-ranging deer herds. By suspending import of potentially infected animals, the Department hopes to avoid the consequences of the disease and the potential costs of controlling CWD. The detection of the disease has had immense economic impact on states such as Wisconsin where the disease was discovered last year. Within the first month after detection, the Wisconsin wildlife management agency spent approximately $250,000 in control and public information efforts and will spend upwards of $2.5 million this year as a result of CWD control efforts. The agency continues to try to control the spread of the disease and has publicly outlined plans to kill all 30,000 estimated animals in the focal area where infected animals have been found.

Wisconsin is not the only state fighting CWD. As an example, a supplemental appropriation of $300,143 has been made in Colorado to help combat the disease and more appropriations are being considered. Saskatchewan has spent approximately $30 million in attempts at eradicating the disease in infected commercially operated game farms.

http://www.wildlifedepartment.com/hunting/cwd.htm

http://www.wildlifedepartment.com/hunting/deer.htm

*** While elk were historically found in Oklahoma, the majority of the current private lands elk population found in the state is the result of animals that were either intentionally liberated or escaped from a captive facility.

http://www.wildlifedepartment.com/media/proposed_changes.htm

*** Chronic Wasting Disease (CWD) in deer and elk – *** has been recently confirmed in a captive elk herd in Oklahoma County

FEBRUARY 2001 NEWS RELEASES

A degenerative brain disease similar to mad cow disease - called Chronic Wasting Disease (CWD) in deer and elk – *** has been recently confirmed in a captive elk herd in Oklahoma County, but has never been documented in wild deer or elk in Oklahoma. Even if the disease did exist in wild herds, there has never been a confirmed case of a hunter contracting it through hunting or eating venison. http://www.wildlifedepartment.com/newsreleasearchive/2001/02-01nr.htm

Deer Management Assistance Program: Erik Bartholomew - (405) 385-1791 erik.bartholomew@odwc.ok.goverik.bartholomew@odwc.ok.gov; doug.schoeling@odwc.ok.govdoug.schoeling@odwc.ok.gov; nichole.carrillo@ag.ok.gov

Oklahoma Chronic Wasting Disease CWD TSE Prion Surveillance and Testing History ???

Oklahoma

Chronic Wasting Disease Surveillance in Oklahoma: Chronic Wasting Disease (CWD) is a progressive, fatal, degenerative neurological disease that affects deer, elk, and moose. First recognized in 1967 in captive mule deer in Colorado, CWD now affects free-ranging cervids in at least 15 states and 2 Canadian provinces. Research suggests that transmission may occur via several routes, with environmental contamination likely playing a significant role. In 1998, a captive elk herd in central Oklahoma was diagnosed with CWD. Infected animals in this herd originated in Montana, and although the herd was depopulated in September 2002, there remains the concern for possible exposure of native wild deer populations. Since that time numerous captive cervid facilities have developed in Oklahoma. Additionally, CWD has been located in free-ranging animals in multiple states including Texas, Kansas, Colorado, New Mexico, and Missouri. From 1997 to 2012, the Oklahoma Department of Wildlife Conservation (ODWC) in cooperation with the U.S. Department of Agriculture (Animal and Plant Health Inspection Service) Veterinary Services, and the Oklahoma Department of Agriculture took a proactive approach to protect Oklahoma¿s deer and elk resource. This approach helped to reassure hunters, the general public, deer processors, taxidermists, rendering companies, and the state¿s trading partners that Oklahoma¿s wild deer population is free of CWD and to reduce the potential threat to human health concerns. The U.S. Fish and Wildlife Service (USFWS) funding supplied to ODWC is to conduct surveillance for CWD in Oklahoma and at the Wichita Mountains National Wildlife Refuge (WMNWR). Funding received during the first year of this project will focus on CWD surveillance in southwest Oklahoma, which includes the WMNWR. Surveillance will shift to other regions of Oklahoma in subsequent years if funding is available. Funding for this project was received through the USFWS National Wildlife Refuge System Wildlife Health Office. As such, eligible entities for this funding are USFWS divisions and programs or State wildlife management agencies that form partnerships with one or more USFWS National Wildlife Refuges. Hence, ODWC is one such entity and responsible for the management of white-tailed deer and elk populations in Oklahoma. WMNWR and ODWC formed such a partnership in order to jointly utilize this funding and conduct CWD surveillance in Oklahoma and on the WMNWR. Depending upon funding allocations, this project could be funded for up to 5 years. Federal Grant Title: Chronic Wasting Disease Surveillance in Oklahoma Federal Agency Name: Fish and Wildlife Service Grant Categories: Natural Resources Type of Opportunity: Discretionary Funding Opportunity Number: F14AS00385 Type of Funding: Grant CFDA Numbers: 15.650 CFDA Descriptions: Research Grants (Generic) Current Application Deadline: Aug 14, 2014 Notice of Intent to Award Single Source Original Application Deadline: Aug 14, 2014 Notice of Intent to Award Single Source Posted Date: Aug 8, 2014 Creation Date: Aug 8, 2014 Archive Date: Aug 7, 2015 Total Program Funding: $32250 Maximum Federal Grant Award: $32250 Minimum Federal Grant Award: $6450 Expected Number of Awards: 1 Cost Sharing or Matching: No

Applicants Eligible for this Grant State governments Grant Announcement Contact Michelle L. Willcox, Grants Specialist, 505-248-7486 michelle_willcox@fws.gov michelle_willcox@fws.gov

Fish and Wildlife Service 703-358-2459

http://www.federalgrants.com/Chronic-Wasting-Disease-Surveillance-in-Oklahoma-47559.html

Ear tags had been discarded in the Oklahoma CWD elk case, causing uncertainty in trace-back (limited to Montana, Idaho, or Utah). Oklahoma:

-- In June,1998 CW) was diagnosed in a captive elk in Oklahoma.

-- The Oklahoma herd received more than 80 elk from commercial sources in Montana and Idaho.

-- Animals from the same origins as the Oklahoma herd went to 13 other ranches in Colorado, Idaho, Iowa, Montana, Nebraska, Alberta, and Saskatchewan in the past 11 years, plus many secondary movements. [8]

-- no control or surveillance program.

Utah:

-- one trace-back zoo in Salt Lake City from elk possibly associated to Oklahoma game farm.

-- One 30 year old hunter dying of CJD of unknown origin (not familial or iatrogenic).

-- 135 deer sampled in 1998, 90 tested, all negative so far, pathology done in-state. Unpublished UF&G.

Montana:

-- Single trace-back elk game farm under quarantine from Oklahoma case, though importer destroyed ear tag.

-- Single trace-forward elk game farm that had bought elk from trace-back game farm connected to Oklahoma

Iowa, Illinois, Texas, and Wisconsin:

-- These states have trace-forward herds from an infected herd in Nebraska.

-- Missouri also sold elk from this herd at auction to buyers in unknown states.

-- Wisconsin has additional trace-forward game farms from affected South Dakota game farms [7]

-- Michigan allows deer to concentrate at bait stations, spread of tuberculosis attributed to this in NE Lower Peninsula [7].

Vermont:

-- ancedotal trace-forward herds from Colorado and Wyoming

Idaho:

-- no reported CWD, possible trace-back herd based on Oklahoma case, hold order on elk farm.

-- elk ranchers forced regulatory change to ag department to avoid regs.

http://www.mad-cow.org/99feb_cwd_special.html

PROGRAM GUIDELINES FOR OKLAHOMA CHRONIC WASTING DISEASE (CWD) CERVID SURVEILLANCE AND CERTIFICATION STATUS PROGRAM

http://www.oda.state.ok.us/ais/aiscervidaemonitor.pdf

Dec. 19, 2013

A service of the Oklahoma Department of Wildlife Conservation

Wildlife Department offering online public comment period for proposed regulation changes

Sportsmen have the opportunity to log on to wildlifedepartment.com to voice their thoughts on a list of Oklahoma hunting and fishing related rule change proposals.

Most notable is a proposal to expand private lands elk hunting opportunity to statewide. For several years elk have been hunted on private lands in Caddo, Comanche, and Kiowa counties in southwest Oklahoma. More recently, Adair, Cherokee, Delaware, Mayes, Muskogee and Sequoyah counties in the northeast part of the state were added to the list of locations where these animals could be pursued by hunters.

While elk were historically found in Oklahoma, the majority of the current private lands elk population found in the state is the result of animals that were either intentionally liberated or ***escaped from a captive facility. A recent survey showed that at least 30 of the state's 77 counties are home to elk. The proposal will allow elk hunting opportunity in every county of the state. The popular controlled hunts program will not be affected by this proposal and will continue to offer hunters lucky enough to draw a permit the chance to pursue elk on certain state and federal managed areas.

http://www.wildlifedepartment.com/newsreleasearchive/2013/1213.htm

===================let’s review a few things shall we==================

Chronic Wasting Disease (CWD) of Deer and Elk

Key Points

1. At this point there is no known cases of CWD in wild deer and elk in Oklahoma.

2. There has been no known transmission of CWD from deer or elk to any other animals or people even in states where CWD is found.

3. It is always wise to use common sense when handling any meat or when dealing with sick or injured animals.

For more information about CWD log on to www.cwd-info.org

What is Chronic Wasting Disease (CWD)?

snip...

Is Venison Safe to Eat?

These practices include washing your hands after handling raw meat and cooking the meat at an appropriate temperature.

"In my opinion, venison is just as safe as any other game meat," said Mike Shaw, head deer biologist for the Oklahoma Department of Wildlife Conservation.

snip...

http://www.wildlifedepartment.com/hunting/cwd.htm

http://www.wildlifedepartment.com/hunting/deer.htm

Monthly Activity Report Wildlife Division: February Alan Peoples, Chief Bill Dinkines, Assistant Chief Wildlife & Lands Management

CWD-95-12- Attended SE Deer Study Group meeting in Destin, FL. Reviewed literature from other states regarding new CWD cases in Virginia, Missouri, and West Virginia. Discussed CWD response plan with USDA HVIC. Provided CWD status update for Oklahoma at SEDSG meeting in Florida.

http://www.wildlifedepartment.com/employee/2012/april/wildlife.pdf

Monthly Activity Report Wildlife Division: March Alan Peoples, Chief Bill Dinkines, Assistant Chief Wildlife & Lands Management

CWD9512- Assisted with 2 roadkill deer in NW OKC for CWD samples. Removed obex from roadkilled deer. Disposed of heads. Traveled to reported roadkill location, evaluated deer for suitability. Removed unsuitable roadkill from roadway. Researched IR camera purchase. Researched and purchased digital camera.

http://www.wildlifedepartment.com/employee/2012/may/wildlife.pdf

Monthly Activity Report Wildlife Division: January, 2013 Alan Peoples, Chief Bill Dinkines, Assistant Chief Wildlife & Lands Management

095-CWD-13- Pulled CWD sample on road-killed deer. Prepared quarterly report, determined rollover/add-on for next budget cycle. Submitted paperwork to APHIS. Checked on and purchased equipment for CWD grant.

http://www.wildlifedepartment.com/employee/2013/March/Wildlife%20Feb.pdf

Monthly Activity Report Wildlife Division: April, 2013 Alan Peoples, Chief Bill Dinkines, Assistant Chief Wildlife & Lands Management

095-CWD-13- Held a meeting with ODAFF regarding captive cervid program and shared concerns regarding transmission of CWD from captive herds to native animals. Met with ODWC Wildlife Div. staff prior to ODAFF meeting to solidify Dept. position.

http://wildlifedepartment.com/employee/2013/July/Wildlife.pdf

Monthly Activity Report Wildlife Division: April, 2014 Alan Peoples, Chief Bill Dinkines, Assistant Chief Wildlife & Lands Management

F12AF00615- Big Game: Entered deer data from DMAP, DCAP and check station books onto spreadsheets. Entered student data for deer ages into spreadsheet. Completed DMAP summaries for each cooperator. Made copy of age sheets for each DMAP cooperator. Mailed DMAP summary packets. Sent DMAP summaries to each biologist for their properties. Bundled 10,000 carcass tags for 2014 season. Updated 2013 DMAP compliance spreadsheet. Made new 2014 spreadsheets for DMAP by biologists and by county. Aged deer jaws. Entered data, prepped data, edited data, and began SAS runs of data, started building tables for BGR. Research trailer and gun for SCI grant, prepped, and submitted grants request. Prep for field day in Okmulgee. Discuss CWD funding opportunity, responded to RMEF grant department on Dewey County survey, Send IE 2014-15 deer season dates. Submitted samples to SCWDS for testing. Discussions with supervisors about long range deer plan.

http://www.wildlifedepartment.com/employee/2014/may/wildlife.pdf

FEBRUARY 2001 NEWS RELEASES

> A degenerative brain disease similar to mad cow disease - called Chronic Wasting Disease (CWD) in deer and elk - has been recently confirmed in a captive elk herd in Oklahoma County Oklahoma Venison and Elk Safe To Eat

Recent media reports linking eating wild deer meat to a form of “mad cow disease” have been sensationalized, and hunters should not been worried about their venison, according to officials with the Oklahoma Department of Wildlife Conservation.

A degenerative brain disease similar to mad cow disease - called Chronic Wasting Disease (CWD) in deer and elk - has been recently confirmed in a captive elk herd in Oklahoma County, but has never been documented in wild deer or elk in Oklahoma. Even if the disease did exist in wild herds, there has never been a confirmed case of a hunter contracting it through hunting or eating venison.

“Chronic Wasting Disease has occurred in Colorado and Wyoming for 30 years, but nobody who has hunted there or eaten venison from those animals has come down with CWD,” said Mike Shaw, wildlife research supervisor for the Wildlife Department. “A hunter from Vinita contracted Creuztfelt-Jacob Disease (CJD), a related spongiform encephalopathy, in 1999, but the National Center for Disease Control never established a positive connection to his eating deer meat. We even investigated the possible link by sampling 16 deer from the area where the man hunted. None of the deer tested positive for Chronic Wasting Disease. In addition, we have tested more than 200 deer from other parts of the state, and those deer have all been negative for CWD.”

In fact, nationally there are over 11 million big game hunters, and only two confirmed reports of hunters contracting Creuztfelt-Jacob Disease, Shaw said. The Center for Disease Control investigated both cases and concluded that their contracting CJD was coincidental to hunting.

“There is always a risk involved with handling any type of animals, domestic or wild, but that risk is very small,” he said. “The odds are many times greater that someone would be struck by lightning or die from a bee sting.”

Shaw said there are two precautions that anyone concerned about chronic wasting disease can take. Wearing protective gloves when dressing and butchering animals and avoiding consumption of brain and spinal cord tissue are good precautionary measures.

Dr. Gene Eskew, a veterinarian with the Oklahoma Department of Agriculture, said the captive elk in Oklahoma County are under quarantine, and they do not believe any infected elk have been killed for human consumption. Only four of the 140 elk have contracted the disease thus far. Agriculture Department officials will be watching for additional elk deaths, and will test the animals immediately through the National Veterinary Services Laboratory in Ames, Iowa.

“As a biological scientist who has studied deer most of my life, I can honestly say that I don’t see any danger in eating deer meat because there just isn’t any scientific evidence proving that Chronic Wasting Disease can cause Creuztfelt-Jacob Disease,” Shaw said. “There are far too many other things to worry about; real dangers like driving to work, having a heart attack because you don’t exercise enough or getting stung by a bee.

http://www.wildlifedepartment.com/newsreleasearchive/2001/02-01nr.htm

FEBRUARY 2001 NEWS RELEASES

http://www.wildlifedepartment.com/newsreleasearchive/2001/02-01nr.htm

http://soonersearch.ok.gov//agencies/wildlife/results.htm?cref=http%3A%2F%2Fwww.ok.gov%2Fsoonersearch%2Fxml%2Fcse_WilDep.xml&cof=FORID%3A9&q=chronic+wasting+disease+cwd&sa=Search&siteurl=www.wildlifedepartment.com%2Fsearch.htm&ref=www.wildlifedepartment.com%2Fchunt%2Fstep1.htm&ss=0j0j1

Farmed Cervidae

“Farmed Cervidae” are cervid species raised in captivity for the purpose of supplying the commercial hunting industry with livestock. In Oklahoma, the majority of this industry is whitetail deer with elk making up a smaller portion. These animals are intensively managed, fed, and selectively bred for antler mass, spread, and classification (typical vs. non-typical). Not all farmed cervidae are ultimately hunted, however. As global demand for venison rises, some animals are raised for slaughter, while other producers raise farmed cervidae for the sole purpose of hobby and enjoyment.

Current Topics

•License renewal applications for Farmed Cervidae Facilities will be mailed out in January and are due by April 1, 2016.

•Annual CWD Inventories and Triannual Tuberculosis/Brucellosis Testing is due between January 1, 2016 and April 1, 2016 for applicable herds.

•Cervid imports into Oklahoma from Missouri are once again permissible since Missouri is currently accepting cervid imports from Oklahoma.

Import Requirements

All cervidae imported into the state of Oklahoma must have the following: an approved permit application, valid certificate of veterinary inspection, proper identification, tuberculosis and brucellosis testing, and chronic wasting disease herd certification status. The permit application below explains these requirements in full. The veterinarian of the consignor in the exporting state completes and submits the permit application and certificate of veterinary inspection. The consignee of any import must hold a valid farmed cervidae facility license or commercial hunting area license. Cervidae imports are restricted from any county where Chronic Wasting Disease has been identified among free-ranging cervidae (map linked below).

•Cervidae Import Permit Application

•Import Requirements of Other States

• Map of CWD Positive Counties

Facility Licensing

Any farmed cervidae facility in Oklahoma maintaining whitetail deer, mule deer, red deer, or elk is required to be licensed by The Oklahoma Department of Agriculture. The purpose of facility licensing is multifold: to prevent the commingling of native cervidae with captive cervidae, to protect the farmed cervidae and hunting industries in Oklahoma from chronic wasting disease, and to protect the farmed cervidae and cattle industries of Oklahoma from the controlled diseases the two have in common. The Oklahoma Department of Wildlife Conservation licenses commercial hunting areas in Oklahoma where the majority of farmed cervidae are ultimately harvested.

•Farmed Cervidae License Application

•Oklahoma Farmed Cervidae Act & Rules

•Licensing Explained

• Carcass Disposal Regulations

Exotic Cervidae Species Registration

All species in the Cervidae Family (other than whitetail deer, mule deer, red deer, and elk) are currently considered “exotics” by Oklahoma regulations and are exempt from facility licensing. However, due to the concern of controlled diseases, owners of these species must register with the Oklahoma Department of Agriculture unless already licensed by the Oklahoma Department of Wildlife Conservation or USDA Animal Care. This registration will also help keep registrants informed of any emergency disease information.

Please submit the completed form below to nichole.carrillo@ag.ok.gov or Fax 405-522-0756.

Exotic Cervidae Owner Registration Form

Chronic Wasting Disease (CWD) Herd Certification Program (HCP)

The CWD HCP is a voluntary surveillance program designed to verify that a cervidae herd is low risk for CWD. Federal rule and program standards for interstate transport of cervidae and a national CWD HCP were passed in August 2012 and implemented by ODAFF. Herds that complete five years of the program with no evidence of CWD are designated as “certified” and are allowed to transport cervidae species interstate. Producers can purchase CWD certified cervidae and “inherit” the status of the original herd or can start with non-monitored animals at year one and work their way up through the program year-by-year. CWD herd certification not only allows herds to be moved interstate, it also adds value to a herd while helping producers protect the health of their animals. A CWD HCP application must be submitted to ODAFF and approved for participation in the program.

•CWD HCP Application and Inventory Form

•CWD Inventory and Inspections Explained Presentation

•Map of CWD Certified Veterinarians

•CWD HCP Federal Rule

• CWD HCP Program Standards

• USDA CWD HCP WebPage

http://www.oda.state.ok.us/ais/farmedcervidae.htm

*** Oklahoma Captive figures for CWD testing and surveillance will come at a later date, and this url will but updated...tss ***

*** •Cervid imports into Oklahoma from Missouri are once again permissible since Missouri is currently accepting cervid imports from Oklahoma.

Sunday, March 06, 2016

Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases mounting

http://chronic-wasting-disease.blogspot.com/2016/03/missouri-2015-2016-cwd-surveillance.html

2015-2016

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***

===============

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160

Tuesday, December 16, 2014

*** Evidence for zoonotic potential of ovine scrapie prions

Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics

Abstract

Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. ***The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. ***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

Subject terms: Biological sciences• Medical research At a glance

http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html

see more here ;

http://www.nature.com/ncomms/2014/141216/ncomms6821/extref/ncomms6821-s1.pdf

***The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans.***

***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

http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf

PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS

*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***

O18

Zoonotic Potential of CWD Prions

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

*** These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.

==================

***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

==================

P.105: RT-QuIC models trans-species prion transmission

Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD.

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.

================

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

================

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

*** 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.

http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm

http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html

*** 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).***

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249

*** 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.

http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf

now, let’s see what the authors said about this casual link, personal communications years ago. 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

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

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 ;

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html

CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.

Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.

https://www.organicconsumers.org/old_articles/madcow/killer123103.php

I urge everyone to watch this video closely...terry

*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***

http://zoomify.uzh.ch:8080/zoomify/videos/video-004/video-004.html

Envt.07:

Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease

***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.

http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975

Prions in Skeletal Muscles of Deer with Chronic Wasting Disease Rachel C. Angers1,*, Shawn R. Browning1,*,†, Tanya S. Seward2, Christina J. Sigurdson4,‡, Michael W. Miller5, Edward A. Hoover4, Glenn C. Telling1,2,3,§ snip...

Abstract The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. 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.

http://www.sciencemag.org/content/311/5764/1117.long

***********CJD REPORT 1994 increased risk for consumption of veal and venison and lamb***********

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994

Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss)

These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...

Table 9 presents the results of an analysis of these data.

There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).

Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.

There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).

The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).

The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).

snip...

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).

snip...

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

snip...

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf

CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249

”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

http://jgv.sgmjournals.org/content/87/12/3737.full

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

PL1

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.

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

see ;

http://www.tandfonline.com/doi/pdf/10.4161/pri.28467

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf

http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217

http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4

Wednesday, December 16, 2015

Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission

Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1

1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK

Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.

snip...

Discussion

Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).

Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.

This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.

PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.

Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification

http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full

Wednesday, December 16, 2015

*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***

http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html

Circulation of prions within dust on a scrapie affected farm

Kevin C Gough1, Claire A Baker2, Hugh A Simmons3, Steve A Hawkins3 and Ben C Maddison2*

Abstract

Prion diseases are fatal neurological disorders that affect humans and animals. Scrapie of sheep/goats and Chronic Wasting Disease (CWD) of deer/elk are contagious prion diseases where environmental reservoirs have a direct link to the transmission of disease. Using protein misfolding cyclic amplification we demonstrate that scrapie PrPSc can be detected within circulating dusts that are present on a farm that is naturally contaminated with sheep scrapie. The presence of infectious scrapie within airborne dusts may represent a possible route of infection and illustrates the difficulties that may be associated with the effective decontamination of such scrapie affected premises.

snip...

Discussion

We present biochemical data illustrating the airborne movement of scrapie containing material within a contaminated farm environment. We were able to detect scrapie PrPSc within extracts from dusts collected over a 70 day period, in the absence of any sheep activity. We were also able to detect scrapie PrPSc within dusts collected within pasture at 30 m but not at 60 m distance away from the scrapie contaminated buildings, suggesting that the chance of contamination of pasture by scrapie contaminated dusts decreases with distance from contaminated farm buildings. PrPSc amplification by sPMCA has been shown to correlate with infectivity and amplified products have been shown to be infectious [14,15]. These experiments illustrate the potential for low dose scrapie infectivity to be present within such samples. We estimate low ng levels of scrapie positive brain equivalent were deposited per m2 over 70 days, in a barn previously occupied by sheep affected with scrapie. This movement of dusts and the accumulation of low levels of scrapie infectivity within this environment may in part explain previous observations where despite stringent pen decontamination regimens healthy lambs still became scrapie infected after apparent exposure from their environment alone [16]. The presence of sPMCA seeding activity and by inference, infectious prions within dusts, and their potential for airborne dissemination is highly novel and may have implications for the spread of scrapie within infected premises. The low level circulation and accumulation of scrapie prion containing dust material within the farm environment will likely impede the efficient decontamination of such scrapie contaminated buildings unless all possible reservoirs of dust are removed. Scrapie containing dusts could possibly infect animals during feeding and drinking, and respiratory and conjunctival routes may also be involved. It has been demonstrated that scrapie can be efficiently transmitted via the nasal route in sheep [17], as is also the case for CWD in both murine models and in white tailed deer [18-20].

The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf

Wednesday, June 10, 2015

Zoonotic Potential of CWD Prions

LATE-BREAKING ABSTRACTS

http://chronic-wasting-disease.blogspot.com/2015/06/zoonotic-potential-of-cwd-prions.html

*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***

O18

Zoonotic Potential of CWD Prions

Chronic wasting disease (CWD) is a widespread and expanding prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern. Current literature generated with in vitro methods and in vivo animal models (transgenic mice, macaques and squirrel monkeys) reports conflicting results. The susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. In our earlier bioassay experiments using several humanized transgenic mouse lines, we detected protease-resistant PrPSc in the spleen of two out of 140 mice that were intracerebrally inoculated with natural CWD isolates, but PrPSc was not detected in the brain of the same mice. Secondary passages with such PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient prion transmission with clear clinical and pathological signs in both humanized and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD isolates in a new humanized transgenic mouse line led to clinical prion infection in 2 out of 20 mice. ***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.

==================

***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***

==================

P.105: RT-QuIC models trans-species prion transmission

Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious. Studies of the effects of primary or tertiary prion protein structures on trans-species prion transmission have relied primarily upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect. As an alternative strategy, we used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species prion conversion.

To assess trans-species conversion in the RT-QuIC system, we compared chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions, as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each prion was seeded into each host recombinant PrP (full-length rPrP of white-tailed deer, bovine or feline). We demonstrated that fCWD is a more efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests adaptation to the new host.

Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD. ***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.

================

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

================

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, Val erie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

*** 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 longe 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...TSS

===============

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

Friday, January 30, 2015

*** Scrapie: a particularly persistent pathogen ***

http://transmissiblespongiformencephalopathy.blogspot.com/2015/01/scrapie-particularly-persistent-pathogen.html

Tuesday, December 16, 2014

*** Evidence for zoonotic potential of ovine scrapie prions

Abstract

***Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE.

***The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans.

***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

Subject terms: Biological sciences• Medical research At a glance

http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html

see more here ;

http://www.nature.com/ncomms/2014/141216/ncomms6821/extref/ncomms6821-s1.pdf

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...

http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf

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

http://chronic-wasting-disease.blogspot.com/2012/12/defra-uk-what-is-risk-of-chronic.html

I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...

======

In the USA, under the Food and Drug Administrations 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.

======

31 Jan 2015 at 20:14 GMT

*** Ruminant feed ban for cervids in the United States? ***

31 Jan 2015 at 20:14 GMT

http://www.plosone.org/annotation/listThread.action?root=85351

Thursday, May 02, 2013

*** Chronic Wasting Disease (CWD) Texas Important Update on OBEX ONLY TEXTING

http://chronic-wasting-disease.blogspot.com/2013/05/chronic-wasting-disease-cwd-texas.html

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease

Authors

item Greenlee, Justin item Moore, S - item Smith, Jodi - item Kunkle, Robert item West Greenlee, M -

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A Technical Abstract: The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the two inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=317901

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=260467

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

Interspecies transmission studies afford the opportunity to better understand the potential host range and origins of prion diseases. Previous experiments demonstrated that white-tailed deer are susceptible to sheep-derived scrapie by intracranial inoculation. The purpose of this study was to determine susceptibility of white-tailed deer to scrapie after a natural route of exposure. Deer (n=5) were inoculated by concurrent oral (30 ml) and intranasal (1 ml) instillation of a 10% (wt/vol) brain homogenate derived from a sheep clinically affected with scrapie. Non-inoculated deer were maintained as negative controls. All deer were observed daily for clinical signs. Deer were euthanized and necropsied when neurologic disease was evident, and tissues were examined for abnormal prion protein (PrPSc) by immunohistochemistry (IHC) and western blot (WB). One animal was euthanized 15 months post-inoculation (MPI) due to an injury. At that time, examination of obex and lymphoid tissues by IHC was positive, but WB of obex and colliculus were negative. Remaining deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 MPI. Tissues from these deer were positive for scrapie by IHC and WB. Tissues with PrPSc immunoreactivity included brain, tonsil, retropharyngeal and mesenteric lymph nodes, hemal node, Peyer’s patches, and spleen. This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.

see full text ;

http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf

White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation

snip...

It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that

1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and

2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.

This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199251/?tool=pubmed

http://chronic-wasting-disease.blogspot.com/2011/10/white-tailed-deer-are-susceptible-to.html

2012

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

snip...

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.

*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf

2011

*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.

http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf

White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS

see full text ;

http://www.usaha.org/Portals/6/Reports/2010/report-cwal-2010.pdf

Monday, November 3, 2014

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

http://transmissiblespongiformencephalopathy.blogspot.com/2014/11/persistence-of-ovine-scrapie.html

PPo3-22:

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK

Key words: scrapie, evironmental persistence, sPMCA

Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.

http://www.prion2010.org/bilder/prion_2010_program_latest_w_posters_4_.pdf?139&PHPSESSID=a30a38202cfec579000b77af81be3099

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011

The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.

SUMMARY:

http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf

For Immediate Release Thursday, October 2, 2014

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).

http://www.iowaagriculture.gov/press/2014press/press10022014.asp

*** see history of this CWD blunder here ;

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/070313_consent_order.pdf

On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/060613_consent_order.pdf

The overall incidence of clinical CWD in white-tailed deer was 82%

Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)

https://cpw.state.co.us/Documents/Hunting/BigGame/CWD/PDF/ResearchArticles/JWDEpiCWD.pdf

Tuesday, February 23, 2016

ARKANSAS Detects First Chronic Wasting Disease CWD in a wild elk

http://chronic-wasting-disease.blogspot.com/2016/02/arkansas-detects-first-chronic-wasting.html

Friday, February 26, 2016

TEXAS Hartley County Mule Deer Tests Positive for Chronic Wasting Disease CWD TSE Prion

http://chronic-wasting-disease.blogspot.com/2016/02/texas-hartley-county-mule-deer-tests.html

Friday, February 05, 2016

TEXAS NEW CHRONIC WASTING DISEASE CWD CASE DISCOVERD AT CAPTIVE DEER RELEASE SITE

http://chronic-wasting-disease.blogspot.com/2016/02/texas-new-chronic-wasting-disease-cwd.html

Tuesday, February 23, 2016

*** Parks and Wildlife begins reducing deer population at Texas Mountain Ranch Chronic Wasting Disease CWD TSE Prion Update ***

*** I kindly would like to comment on a few statements from the TPWD et al ;

http://chronic-wasting-disease.blogspot.com/2016/02/parks-and-wildlife-begins-reducing-deer.html

Wednesday, March 18, 2015

Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-confirmed.html

Wednesday, March 25, 2015

Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-cases.html

Wednesday, February 10, 2016

*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***

http://chronic-wasting-disease.blogspot.com/2016/02/wisconsin-two-deer-that-escaped-farm.html

Tuesday, February 02, 2016

Illinois six out of 19 deer samples tested positive for CWD in the Oswego zone of Kendall County

http://chronic-wasting-disease.blogspot.com/2016/02/illinois-six-out-of-19-deer-samples.html

Friday, February 05, 2016

IOWA Two Wild Deer Test Positive for Chronic Wasting Disease in Allamakee County

http://chronic-wasting-disease.blogspot.com/2016/02/iowa-two-wild-deer-test-positive-for.html

Wednesday, March 02, 2016

Kansas Chronic Wasting Disease CWD TSE Prion 52 cases 2015 updated report 'ALARMING'

http://chronic-wasting-disease.blogspot.com/2016/03/kansas-chronic-wasting-disease-cwd-tse.html

Monday, March 07, 2016

Wyoming Game and Fish Department confirmed chronic wasting disease (CWD) in a buck mule deer that was found dead southeast of Lander

http://chronic-wasting-disease.blogspot.com/2016/03/wyoming-game-and-fish-department.html

Sunday, March 06, 2016

Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases mounting

http://chronic-wasting-disease.blogspot.com/2016/03/missouri-2015-2016-cwd-surveillance.html

Friday, January 29, 2016

NEBRASKA Three Positives for CWD Found in Recent Testing of Deer

http://chronic-wasting-disease.blogspot.com/2016/01/nebraska-three-positives-for-cwd-found.html

Friday, February 26, 2016

Pennsylvania Monitoring the Growing Threat of Chronic Wasting Disease CWD TSE Prion

http://chronic-wasting-disease.blogspot.com/2016/02/pennsylvania-monitoring-growing-threat.html

Thursday, January 21, 2016

INDIANA With end of long legal challenge last year, high-fence hunting operations currently unregulated

http://chronic-wasting-disease.blogspot.com/2016/01/indiana-with-end-of-long-legal.html

Wednesday, December 30, 2015

Michigan Deer suspected positive _confirmed_ for CWD found in Watertown Township; Jan. 12 public meeting set

http://chronic-wasting-disease.blogspot.com/2015/12/michigan-deer-suspected-positive-for.html

Tuesday, December 01, 2015

MICHIGAN 4TH WILD CHRONIC WASTING DISEASE CWD SUSPECT CONFIRMED

http://chronic-wasting-disease.blogspot.com/2015/12/michigan-4th-wild-chronic-wasting.html

Friday, November 20, 2015

ODNR Takes Action to Monitor Chronic Wasting Disease in Ohio's Deer Herd

http://chronic-wasting-disease.blogspot.com/2015/11/odnr-takes-action-to-monitor-chronic.html

Saturday, December 12, 2015

CHRONIC WASTING DISEASE CWD TSE PRION REPORT DECEMBER 14, 2015

http://chronic-wasting-disease.blogspot.com/2015/12/chronic-wasting-disease-cwd-tse-prion.html

Friday, August 14, 2015

*** Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation

http://chronic-wasting-disease.blogspot.com/2015/08/susceptibility-of-cattle-to-agent-of.html

Friday, August 14, 2015

Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015

http://transmissiblespongiformencephalopathy.blogspot.com/2015/08/carcass-management-during-mass-animal.html

Tuesday, September 22, 2015

*** Host Determinants of Prion Strain Diversity Independent of Prion Protein Genotype

http://transmissiblespongiformencephalopathy.blogspot.com/2015/09/host-determinants-of-prion-strain.html

Friday, August 28, 2015

*** Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection

http://chronic-wasting-disease.blogspot.com/2015/08/chronic-wasting-disease-cwd-tse-prion.html

Friday, February 05, 2016

*** Report of the Committee on Wildlife Diseases FY2015 CWD TSE PRION Detections in Farmed Cervids and Wild ***

http://chronic-wasting-disease.blogspot.com/2016/02/report-of-committee-on-wildlife.html

http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...

http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

AND THEY MEANT IT $$$

Saturday, February 6, 2016

*** Secretary's Advisory Committee on Animal Health; Meeting [Docket No. APHIS-2016-0007] Singeltary Submission ***

http://animalhealthreportpriontse.blogspot.com/2016/02/secretarys-advisory-committee-on-animal.html

Terry S. Singeltary Sr. flounder9@verizon.net