Friday, June 23, 2017

Chronic Wasting Disease possibly unleashed in Mississippi

Chronic wasting disease possibly unleashed in Mississippi 

Brian Broom , The Clarion-LedgerPublished 7:53 a.m. CT June 23, 2017 | Updated 5 hours ago 

A tornado that ripped through Lamar County and an illegal deer enclosure have heightened concerns over the introduction of chronic wasting disease into Mississippi's deer herd. That concern has led to a federal judge calling for CWD testing.

The story began in 2009. According to a US Attorney at the time, Gregory K. Davis, two Mississippi men and a Texas man conspired to illegally import white-tailed deer into Mississippi from Texas. The three continued to import deer from Texas and place them in a high-fence enclosure on Coleman Virgil Slade's property in Lamar County until 2012.

A federal and state investigation followed and the three were convicted in federal court.

Coleman Virgil Slade, 70, of Purvis, Mississippi, Don Durrett, 72, of Aspermont, Texas, and Dewayne Slade, 44, of Purvis, Mississippi, pled guilty on Aug. 31, 2016 to violating the Lacey Act.

Durrett and Dewayne Slade pled guilty to a misdemeanor conspiracy count and were each sentenced to a $10,000 fine, given three years of probation and lost their hunting rights for one year.

Coleman Virgil Slade pled guilty to a felony conspiracy count and was scheduled for sentencing on November 21, 2016, but his sentencing was postponed until Jan. 17, 2017. He was required to pay a $10,000 fine, assessments, and forfeited a pickup and trailer. 

Coleman Virgil Slade was also required to pay restitution for depopulation and testing of the remaining deer within the enclosure, but before Starrett could determine the amount, disaster struck.

"Four days after the sentencing (January 21, 2017) an EF3 tornado bisected the property in question and destroyed thousands of linear feet of fencing that enclosed the 420 acre parcel owned by defendant or his family," Starrett wrote in his restitution order earlier this month. "Because of the terrain and other special circumstances, the fencing was on the ground and destroyed for a number of months.

"The result is that native deer are free to move on and off of the subject property and the formerly enclosed deer and exposed native deer are free to move on and off of the property."

The restitution order states than none of the deer tested before the fence was damaged were found to carry CWD. However, the remaining deer that came from Texas, which is a CWD-positive state, are on the loose.

Deer in Mississippi are often exposed to diseases, but not any like CWD. ...


for full article, see;

Chronic wasting disease moves closer to Mississippi 

Brian Broom , The Clarion-Ledger Published 4:31 a.m. CT March 3, 2016 | Updated 3:59 p.m. CT March 5, 2016


CWD in Mississippi?

CWD has kept its distance from Mississippi, but now with a case documented about 200 miles from the western border, concern about a possible outbreak has increased.

"Any time there's a CWD case it concerns me because it shows it's an ever-spreading disease," said Chad Dacus, director of the Mississippi Department of Wildlife, Fisheries and Parks' Wildlife Bureau.

Due to concerns over the disease, Mississippi does not allow the importation of white-tailed deer and conducts tests for the disease annually.

"Since 2002, we've sampled over 12,000 deer in Mississippi, and we've never found CWD in any of those animals," Dacus said.

Dacus said most of the deer sampled were tested during spring health checks, but a limited number of tests were performed on deer that exhibited symptoms of illness. According to CWDA, indicators of the disease in white-tailed deer include weight loss, listlessness, lowering of the head, a blank expression and walking in a set pattern.

If a deer is observed exhibiting symptoms of the disease, Dacus said to let someone at MDWFP know about it.

"Contact one of our officers or biologists," Dacus said. "We'll try to get it sampled and tested."

so, from 2002 to March 3, 2016, the state of Mississippi has tested for CWD 12,000 deer, that would be about 14 years. about 857 test for CWD annually over 14 years. there are around 1.75 MILLION deer in Mississippi. Folks, that's not enough testing for CWD...imo...terry

Department of Justice U.S. Attorney’s Office Southern District of Mississippi FOR IMMEDIATE RELEASE Tuesday, September 6, 2016 Three Plead Guilty to Importing White-Tailed Deer in Mississippi

Hattiesburg, Miss. – Coleman Virgil Slade, 70, of Purvis, Mississippi, Don Durrett, 72, of Aspermont, Texas, and Dewayne Slade, 44, of Purvis, Mississippi, pled guilty on Wednesday, August 31, 2016, to conspiracy to violate the Lacey Act by importing live white-tailed deer into Mississippi, announced U.S. Attorney Gregory K. Davis, Special Agent in Charge Luis Santiago with the U.S. Fish and Wildlife Service, and Special Agent in Charge Dax Roberson with the U.S. Department of Agriculture – Office of Inspector General (USDA OIG).

Coleman Virgil Slade pled guilty to a felony conspiracy count. He will be sentenced on November 21, 2016, by U.S. District Judge Keith Starrett and faces a maximum penalty of five years in prison and a $250,000 fine.

Don Durrett and Dewayne Slade pled guilty to a misdemeanor conspiracy count and were each sentenced to a $10,000 fine, placed on three years of probation, and prohibited from hunting for one year.

According to the guilty pleas, from January of 2009 through December of 2012, the Slades and Durrett spent over $100,000 to purchase live white-tailed deer for delivery from Texas to Mississippi. It is illegal to import live white-tailed deer into Mississippi. However, the deer were transported to Lamar County, Mississippi, and placed in a high fence enclosure. The purchases and transportation to Mississippi of the live white-tailed deer were accomplished through false purchase and transportation records.

“The Department of Justice is committed to enforcing the Lacey Act and other federal laws to protect our wildlife resources,” said U.S. Attorney Gregory K. Davis. “We will continue to work closely with USDA OIG, U.S. Fish and Wildlife Service and the Mississippi Department of Wildlife, Fisheries and Parks to enforce the Lacey Act.”

U.S. Fish and Wildlife Service Special Agent in Charge Luis Santiago stated “We take our mission working with the Mississippi Department of Wildlife, Fisheries, and Parks and the citizens of Mississippi in conserving, protecting, and enhancing fish, wildlife, plants and their habitats very seriously. We will continue working vigorously investigating those who choose to violate state and federal laws.”

“I want to thank the US Attorney’s office, OIG special agents, and our law enforcement partners for their hard work on this investigation,” said USDA OIG Special Agent in Charge Dax Roberson, “USDA OIG is committed to pursuing individuals who commit criminal violations of the Lacey Act, which is intended to protect the health and well-being of America’s wildlife.”

This case was investigated by the U.S. Fish and Wildlife Service - Office of Law Enforcement, the U.S. Department of Agriculture – Office of Inspector General, and the Mississippi Department of Wildlife, Fisheries, and Parks. It was prosecuted by Deputy Criminal Division Chief Darren LaMarca.


Three charged with various violations of the federal Lacey Act for white-tailed deer importation from Texas to Mississippi



Title 40: Wildlife, Fisheries, and Parks

Part 2: Wildlife

Part 2, Chapter 2: White-tailed Deer


A. It is unlawful to import, transport, or possess any portion of a cervid carcass originating from any state, territory, or foreign country where the occurrence of Chronic Wasting Disease (CWD) has been confirmed by either the state wildlife agency, state agriculture agency, state veterinarian, United States Department of Agriculture (USDA) Animal Plant Health Inspection Service (APHIS), or the Canadian Food Inspection Agency (CFIA).

B. This rule shall not apply to the importation of:

1. Meat from cervids that has been completely deboned.

2. Antlers, antlers attached to cleaned skull plates or cleaned skulls where no tissue is attached to the skull.

3. Cleaned teeth.

4. Finished taxidermy and antler products.

5. Hides and tanned products.

6. Any portions of white-tailed deer originating from the land between the Mississippi River levees in Arkansas.

C. For the purpose of this rule, cervids include any member of the Cervidae family, including white-tailed deer, elk, moose, red deer, sika deer, fallow deer, mule deer and caribou.

History: Promulgated May 2016.

Source: MISS. CODE ANN. §§49-1-29, 49-4-4, 49-7-58, and 49-7-58.2.


Chronic Wasting Disease

Chronic wasting disease (CWD) is a progressively degenerative fatal disease that attacks the central nervous system of members of the deer family. To date, it has been diagnosed in elk, mule deer, black-tailed deer, white-tailed deer, and moose. CWD is one of a group of diseases known as transmissible spongiform encephalopathies (TSEs). These diseases are characterized as transmissible because they can be transmitted from one infected animal to another. They are further classified as spongiform due to the "spongy-like" areas which form in the brain of the infected animal, hence the encephalopathy portion of the name. 

 The scientific community generally accepts that the infectious agents of CWD are prions. Prions are abnormal proteins that seem to have the ability to alter the structure of normal proteins found in the body of the animal they enter. Logical natural methods of prion transmission include, but may not be limited to, secretions and excretions from infected animals. A study conducted at Colorado State University found that CWD can be transmitted experimentally from saliva and blood. Also, human activity contributes to environmental prion contamination. Prions are hideously durable and impervious to most disinfectants and natural conditions, remaining in the environment for years. 

 Animals suffering from CWD typically behave abnormally by separating themselves from their usual social group. They often stand alone, with a drooped posture, and may not respond to human presence. As the disease progresses, they will appear very skinny on close examination and will salivate, drink, and urinate excessively. 

 As of October 2014, CWD has been diagnosed in 20 states and 2 Canadian Providences. CWD is currently present in wild cervid populations in Colorado, Wyoming, South Dakota, Nebraska, Wisconsin, New Mexico, Illinois, Utah, New York, West Virginia, Kansas, Virginia, Missouri, North Dakota, Pennsylvania, Saskatchewan, and Alberta. CWD is present in captive cervid populations in Minnesota, Oklahoma, Michigan, New York, Colorado, Kansas, Iowa, Nebraska, South Dakota, Wisconsin, Ohio, Pennsylvania, and Montana. Chronic Wasting Disease has not been found in Mississippi. 

 A total of 1,015 samples were taken from free-ranging white-tailed deer in Mississippi during the 2009 - 2010 sampling period. Samples were obtained from hunter-harvested animals, spring herd health evaluations, target animal surveillance, and road-killed animals. Samples were obtained from 71 counties. The samples were submitted to the Southeastern Cooperative Wildlife Disease Study at the University of Georgia following the 2009 - 2010 hunting season and were tested for evidence of the CWD agent using immunohistochemistry. Evidence of CWD was not detected in any of the tested samples. Samples are collected annually from sick and Heard Health Evaluation deer. 

 All public health officials maintain that venison is safe for human consumption. However, hunters who wish to take additional steps to avoid potential unnecessary contact with prions or environmental contamination can do the following: 

 Avoid shooting, handling, or consuming any animal that appears sick. Contact the MDWFP at (601) 432-2199 if you see or harvest an animal that appears sick.

Wear latex gloves when field dressing or processing deer.

Avoid eating or contact with brain, spinal cord, spleen, lymph nodes, or eyes.

Cut through the spinal cord only when removing the head. Use a knife designated solely for this purpose.

Bone out meat to avoid cutting into or through bones. Remove all fat and connective tissue to avoid lymph nodes.

Dispose of all carcass material, including the head, in a landfill or pit dug for carcass disposal purposes.

Either process your animal individually or request that it be processed without adding meat from other animals.

Disinfect knives and other processing equipment in a 50% bleach solution for a minimum of one hour.

Discontinue baiting and feeding which unnaturally concentrate deer.

Upper Mississippi River National Wildlife and Fish Refuge Chronic Wasting Disease Monitoring Metadata Updated: May 23, 2017 

The Refuge completed a Chronic Wasting Disease Surveillance and Management Plan (CWD Plan) in 2005. The goals of the Refuge’s CWD Plan are to: 1) minimize the impact of CWD on ungulate populations that reside or frequent refuge lands; 2) to ensure early, rapid, and accurate detection of CWD when it does occur on Refuge lands, and 3) to ensure coordination and communication with adjacent wildlife management agencies on CWD. Northwest Illinois and Northeast Iowa are separated by the Mississippi River and a large proportion of the land within the river valley is represented by properties managed by the Upper Mississippi River National Wildlife and Fish Refuge (Refuge). Interspersed with Refuge properties in the river valley are properties owned by the states of Illinois and Iowa, the US Army Corps of Engineers, and private entities. In addition to the bottomland forests, wetlands, grasslands and croplands within the river valley, the adjacent bluffs along both sides of the valley typically consist of mixed hardwood forests. The interspersion of habitat types in the river valley and adjacent bluffs provides optimal habitat for white-tailed deer and high deer populations support a substantial level of hunting opportunities each year. High deer populations in this region also results in a presumably high risk of disease transmission, including transmission of Chronic Wasting Disease (CWD).

Access & Use Information Public: This dataset is intended for public access and use. License: No license information was provided. If this work was prepared by an officer or employee of the United States government as part of that person's official duties it is considered a U.S. Government Work.

Beware of potential threat to state's deer 

STARKVILLE, Miss. -- Diseases are a big concern for deer biologists and managers.

Since the reestablishment of white-tailed deer across the Southeast, hemorrhagic disease has had a negative impact on their populations. Hemorrhagic disease in deer can be caused by epizootic hemorrhagic disease viruses, or bluetongue viruses, and is spread by black gnats.

These viruses occur each year. Much like the flu in humans, this disease is worse in incidence and severity in some years. However, biologists and hunters throughout the Southeast could soon be longing for the good ole days when hemorrhagic disease was the only big threat to deer populations.

Bill Hamrick Bill Hamrick Chad Dacus Chad M. Dacus In recent years, chronic wasting disease has been making its way into the Southeast. This disease could pose a much greater threat to deer populations than hemorrhagic disease. There is still a lot we do not understand about this disease, but it could be a game changer.

Chronic wasting disease, a neurological disease in deer, elk, moose and other members of the deer family, is similar to scrapie of sheep and mad cow disease of cattle. The infectious agents are called prions, which are abnormal cellular proteins synthesized in the brain, spinal cord and lymph tissues. They are highly resistant to heat and disinfectants. In fact, even after captive facilities/deer farms have been depopulated after deer tested positive for chronic wasting disease, there is no guarantee that they can ever be completely disinfected.

Chronic wasting disease can be transmitted directly from animal to animal or indirectly through exposure to prions that persist in the environment. Prions can be passed in saliva, urine or feces, which is the main reason most biologists and some hunters have negative views of supplemental feeding and baiting of deer for harvest. These practices will not introduce the disease, but they greatly increase the risk of spreading it.

While there is no convincing evidence that this disease can affect humans, the science is not 100 percent settled.

Chronic wasting disease is thought to have originated in the Colorado-Wyoming region. For many years, it seemed to be limited to deer and elk in that area. Today, 23 states have had documented cases of the disease. Texas and Arkansas are the latest. The threat of this disease to our state’s deer herd is very real.

The wasting disease was most likely spread by a combination of factors. Moving deer and related animals -- both legally and illegally -- from states affected by the disease is one cause. Other culprits are hunters who unknowingly brought infected deer or elk carcasses back to their home states. This problem prompted the Mississippi Department of Wildlife, Fisheries and Parks to pass regulations in 2016 making it unlawful to import, transport or possess any portion of a deer or related species from any state, territory or foreign country where chronic wasting disease has been confirmed. Once those prions are here, they are most likely here forever.

Whether we can keep Mississippi free of this disease is questionable. It is possible the disease is already here, and we just have not found it yet. In the meantime, all we can do is take all preventative measures and hope we keep it out of Mississippi and other unaffected states. 

For more information on chronic wasting disease, visit

Extension Outdoors logoEditor’s Note: Extension Outdoors is a column authored by several different experts in the Mississippi State University Extension Service. 

Released: May 12, 2017 Contacts: Mr. Chad M. Dacus, Mr. Bill Hamrick



Sen. Tommy Gollott Mississippi proposes another bill to allow CWD in Mississippi via Game Farms

This is very, very concerning imo. 

IF this ruling is upheld as such ;

''The Iowa Supreme Court upheld the district court ruling — saying the law gives the DNR only the authority to quarantine the deer — not the land. The ruling says if the Iowa Legislature wants to expand the quarantine powers as suggested by the DNR, then it is free to do so.''

IF a 'precedent' is set as such, by the Legislature not intervening to expand quarantine powers to the DNR for CWD TSE Prion, and the precedent is set as such that the cervid industry and land there from, once contaminated with the CWD TSE Prion, are free to repopulate, sell the land, etc, imo, this will blow the lid off any containment efforts of this damn disease CWD TSE Prion. The Iowa Supreme Court did not just pass the cwd buck down the road, the Supreme Court of Iowa just threw the whole state of Iowa under the bus at 100 MPH. this makes no sense to me, if this is set in stone and the Legislation does not stop it, and stop if fast, any containment of the cwd tse prion will be futile, imo...terry


Iowa DNR issues statement on Iowa Supreme Court Ruling


PENNSYLVANIA Third Case of CWD Discovered in a Captive Deer Farm in Four Months

Wednesday, February 10, 2016

Wisconsin Two deer that escaped farm had chronic wasting disease CWD


South central Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease 

MONDAY, MAY 15, 2017 

Pennsylvania 25 more deer test positive for CWD TSE PRION in the wild


"Four days after the sentencing (January 21, 2017) an EF3 tornado bisected the property in question and destroyed thousands of linear feet of fencing that enclosed the 420 acre parcel owned by defendant or his family," Starrett wrote in his restitution order earlier this month. "Because of the terrain and other special circumstances, the fencing was on the ground and destroyed for a number of months.

"The result is that native deer are free to move on and off of the subject property and the formerly enclosed deer and exposed native deer are free to move on and off of the property."

The restitution order states than none of the deer tested before the fence was damaged were found to carry CWD. However, the remaining deer that came from Texas, which is a CWD-positive state, are on the loose.

***However, the remaining deer that came from Texas, which is a CWD-positive state, are on the loose.



Texas New Exotic CWD Susceptible Species Rules Now in Effect

MONDAY, MAY 15, 2017 

TEXAS New CWD TSE PRION Case Discovered at Fifth Captive Deer Breeding Facility

SUNDAY, MAY 14, 2017 

85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play

FRIDAY, MARCH 31, 2017 

TPWD UPDATE CWD TSE Prion 49 confirmed cases and unwanted firsts for Texas 

Wednesday, July 01, 2015
*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
Thursday, July 09, 2015
TEXAS Chronic Wasting Disease (CWD) Herd Plan for Trace-Forward Exposed Herd with Testing of Exposed Animals
Tuesday, July 21, 2015
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
Wednesday, July 22, 2015
Texas Certified Chronic Wasting Disease CWD Sample Collector, like the Wolf Guarding the Henhouse
Thursday, August 06, 2015
Friday, August 07, 2015
*** Texas CWD Captive, and then there were 4 ?
***raw and uncut***
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas
Saturday, October 03, 2015
Friday, October 09, 2015
Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015
Thursday, September 24, 2015
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing
*** I cannot stress enough to all of you, for the sake of your family and mine, before putting anything in the freezer, have those deer tested for CWD. ...terry
Thursday, November 05, 2015
*** TPW Commission Adopts Interim Deer Breeder Movement Rules
Saturday, November 14, 2015
Monday, November 16, 2015
*** Chronic Wasting Disease (CWD) immediate danger to the white-tailed deer and mule deer resources of Texas
Texas Chronic Wasting Disease Response Update and Interim Deer Management Permit Rules Recommended Adoption of Proposed Rules
Friday, February 05, 2016
Saturday, April 02, 2016
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer
Wednesday, May 04, 2016
TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission
SUNDAY, MAY 22, 2016
 Friday, July 01, 2016
*** TEXAS Thirteen new cases of chronic wasting disease (CWD) were confirmed at a Medina County captive white-tailed deer breeding facility on June 29, 2016
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Confucius ponders...
Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?
Epidemiology of Scrapie in the United States 1977
Scrapie Field Trial Experiments Mission, Texas
A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.
The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. The station was divided into 2 areas: (1) a series of pastures and-pens occupied by male animals only, and (2) a series of pastures and pens occupied by females and young progeny of both sexes. ...
snip...see full text ;
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Texas Intrastate – within state movement of all Cervid or Trucking Chronic Wasting Disease CWD TSE Prion Moratorium
Monday, July 18, 2016
Texas Parks Wildlife Dept TPWD HIDING TSE (CWD) in Deer Herds, Farmers Sampling Own Herds, Rapid Testing, False Negatives, a Recipe for Disaster
TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas with CWD Rule Terry S. Singeltary Sr. comment submission
Wednesday, September 28, 2016
TPWD CWD Sample Collector Trainings in the Trans Pecos and Panhandle
Wednesday, November 09, 2016
Chronic Wasting Disease (CWD) Program Standards - Review and Comment By Terry S Singeltary Sr. November 9, 2016
Friday, November 18, 2016
Thursday, December 08, 2016
TEXAS TAHC confirmed Chronic Wasting Disease (CWD) in a free-ranging elk Dallam County
Saturday, December 03, 2016
The Chronic Wasting Disease Rule Proposal Republished for Comment January 20, 2017
Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry
Texas First Case of CWD Detected in Free-Ranging Texas Whitetail Surveillance Zone 3 in Medina County
Texas CWD Discovered Free-Ranging Whitetail DEER Houston Chronicle Shannon Tompkins PLEASE, CAN YOU HEAR ME NOW?

TUESDAY, JUNE 13, 2017

Pennsylvania Chronic Wasting Disease CWD TSE PRION Senate Joint Hearing Tuesday, June 13, 2017

MONDAY, JUNE 05, 2017 

Arkansas CWD Management Zone expands to include Van Buren County 213 cases to date 

SUNDAY, MAY 21, 2017 

Arkansas Chronic Wasting Disease CWD TSE Prion Roundup 212 Cases Confirmed To Date 

 THURSDAY, MAY 18, 2017
Minnesota Four more farmed white-tailed deer test positive for Chronic Wasting Disease CWD TSE Prion

MONDAY, MARCH 27, 2017 

Wyoming CWD Postive Mule Deer Doe Near Pinedale 

MONDAY, MARCH 20, 2017 

Wisconsin CWD TSE Prion Annual Roundup 441 positive 

TUESDAY, MARCH 14, 2017 

Iowa 12 deer test positive for chronic wasting disease from 2016-17 hunting seasons 

MONDAY, MARCH 13, 2017 


FRIDAY, MARCH 10, 2017 

Nebraska Tests confirm spread of CWD to Lancaster County 

SATURDAY, MAY 20, 2017

Missouri CWD TSE PRION Surveillance and Monitoring




Maryland DNR Six Deer Test Positive for Chronic Wasting Disease 

MONDAY, MARCH 13, 2017 





CWD, TSE, PRION, Cattle, Pigs, Sheep, and Humans aka Mad Cow Disease


CWD of deer and elk is spreading across North America and cannot be stopped.

The tse prion aka mad cow type disease is not your normal pathogen.

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.

You cannot cook the TSE prion disease out of meat. you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.

The TSE prion agent also survives Simulated Wastewater Treatment Processes.

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.

You can bury it and it will not go away.

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.

it’s not your ordinary pathogen you can just cook it out and be done with.

that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?

i strenuously urge you all to rethink this cutting of funds for research of the TSE Prion disease. 




Potential sources of infectivity for direct contact animals include urine, feces, and saliva from their CWDwtd-challenged pen-mates, as has been shown for CWD-affected white-tailed deer (6,8,9). Pinpointing the source of infectivity in the indirect contact group is more difficult. Infectious prions can travel at least 30 m in airborne particulate (10), but because the negative control reindeer in the pen adjacent to the indirect contact reindeer did not become positive, a more direct route of transmission is likely in this case. Penning, feeding, and watering protocols were designed to prevent exposure of negative control and indirect contact reindeer to potential infectivity on feed and water buckets, bedding, or fencing (6,11). However, reindeer might have had access to bedding from adjacent pens that had spread into the central alleyway.

During the 5-year course of this study, reindeer were moved between pens several times to maintain an optimal number of animals per pen (Technical Appendix[PDF - 251 KB - 7 pages] Figure 1). Prolonged persistence of prion infectivity in the natural environment has been documented for both CWD (2 years [5]) and scrapie (up to 16 years [12]). In addition, thorough cleaning and disinfection might not be sufficient to remove all infectivity from the environment, leading to persistence of infectivity under experimental housing conditions (13).

In reindeer challenged orally with the agent of CWD, the SS138 genotype (serine/serine at PRNP codon 138) has been associated with susceptibility to disease and the NS138 (asparagine/serine) genotype with resistance (1). In the study we report, disease developed in reindeer with the NS138 genotype after intracranial inoculation, although the extent of lymphoreticular system involvement was significantly lower than in NN138 and SS138 reindeer. The potential association of the NN138 polymorphism with shorter survival times is interesting. However, as with all potential genotype versus phenotype interactions, care should be taken not to over-interpret these results given the small group sizes and the large number of PRNP genotype groups in this study.

Our results demonstrate that reindeer are susceptible to the agent of CWD from white-tailed deer, mule deer, and elk sources after intracranial inoculation. Furthermore, naive reindeer are susceptible to the agent of CWD after direct and indirect exposure to CWD-infected reindeer, suggesting a high potential for horizontal transmission of CWD within and between farmed and free-ranging reindeer (and caribou) populations.

Dr. Moore is a postdoctoral research associate at the National Animal Disease Center, US Department of Agriculture, Ames, Iowa. Her research interests include pathogenesis and pathology of animal diseases with a special interest in neuropathology and prion diseases.



In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.

Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission 

Submitted to: Emerging Infectious Diseases 

Publication Type: Peer Reviewed Journal 

Publication Acceptance Date: 8/29/2016 

Publication Date: 12/1/2016 

Citation: Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi: 10.3201/eid2212.160635.

Interpretive Summary: Chronic wasting disease (CWD) is a fatal neurodegenerative disease that occurs in farmed and wild cervids (deer and elk) of North America and was recently diagnosed in a single free-ranging reindeer (Rangifer tarandus tarandus) in Norway. CWD is a transmissible spongiform encephalopathy (TSE) that is caused by infectious proteins called prions that are resistant to various methods of decontamination and environmental degradation. Little is known about the susceptibility of or potential for transmission amongst reindeer. In this experiment, we tested the susceptibility of reindeer to CWD from various sources (elk, mule deer, or white-tailed deer) after intracranial inoculation and tested the potential for infected reindeer to transmit to non-inoculated animals by co-housing or housing in adjacent pens. Reindeer were susceptible to CWD from elk, mule deer, or white-tailed deer sources after experimental inoculation. Most importantly, non-inoculated reindeer that were co-housed with infected reindeer or housed in pens adjacent to infected reindeer but without the potential for nose-to-nose contact also developed evidence of CWD infection. This is a major new finding that may have a great impact on the recently diagnosed case of CWD in the only remaining free-ranging reindeer population in Europe as our findings imply that horizontal transmission to other reindeer within that herd has already occurred. Further, this information will help regulatory and wildlife officials developing plans to reduce or eliminate CWD and cervid farmers that want to ensure that their herd remains CWD-free, but were previously unsure of the potential for reindeer to transmit CWD. Technical 

Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal prion disease of cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, and CWD was recently reported in a free-ranging reindeer of Norway. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer, non-inoculated negative control reindeer were introduced into the same pen as the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to the CWDmd inoculated reindeer (indirect contact; n=2). Experimentally inoculated reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrPcwd). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (months PI). PrPcwd was detected in 5 out of 6 sentinel reindeer although only 2 out of 6 developed clinical disease during the study period (< 57 months PI). We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naïve reindeer both directly and indirectly.

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. 

***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. 

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

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

Wednesday, December 16, 2015 

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

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

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 

with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion...tss
 Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
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.
>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<
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.
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

MONDAY, JUNE 12, 2017

Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?

TUESDAY, JUNE 20, 2017

Norway Confirms 6th Case of Skrantesjuke CWD TSE Prion Disease


Subject: PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 

University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 

This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 

Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 

At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 


 Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?

IF human transmission studies are unethical and will never take place, how much evidence is enough, and how much exposure do we allow, before a call is made. 

HOW many humans do we expose before enough is enough?

How many body bags now are enough, for a very long incubating disease that the body bags will for sure mount later, if something is NOT finally done NOW.

the public must know.

Now, i will tell you all how this will be interpreted by our fine federal friends, and their lobbyist et al from corporate America, and Doctors there from, here is how this will still read, rubber stamped ;

''There is no direct evidence that CWD can transmit to humans, and CWD has never been identified in humans anywhere in the world, including in areas where CWD has been present in animal populations for decades.''

this is absurd, and fake news at it's finest.

what is 'direct evidence', if human transmission is not possible?

there is more than enough evidence to make that call now. 

with that, who will finally make that judgement call, knowing that if cwd transmits to humans, it will look like the most common human tse prion i.e. sporadic cjd?

who makes that final call, when, and how many more humans must die before that decision is made and put in the public domain so we can go on with this and try to implement rules and regulations that might finally turn the tide, or do just let corporate science run rampant? 

or, will they continue to run with the infamous UKBSEnvCJD only theory$

with cwd now being documented to transmit macaque, AND TO PIGS orally (lot of human medicine made from pigs), the price of continuing to play TSE Prion Poker with humans goes up drastically. 

This is criminal negligence now, imo...terry


Notice to Members Regarding Chronic Wasting Disease (CWD)

Posted on: May 31st, 2017 

To: MNA Members From: Métis Nation of Alberta 

Date: Wednesday, May 31, 2017 

*** Métis Nation of Alberta (MNA) was made aware of a recent Canadian research study examining the transmission of Chronic Wasting Disease. The initial results of the study indicate that macaque monkeys (genetically similar to humans) can be infected with Chronic Wasting Disease (CWD) after eating deer that is infected with CWD. CWD is a prion disease, which are fatal, transmissible diseases characterized by abnormal proteins in the brain and nervous system. To date no research has shown that CWD can be passed on to humans, and no human cases of CWD have ever been identified. However, this new research indicates that it is a possibility. The Deputy Chief Medical Officer of Health has reached out to us to share with our Métis harvesters this important information. For more information you can visit:


What the Alberta Government knows: 

CWD is present in southeastern Alberta, with the area slowly spreading westward over time (introduced into Alberta from Saskatchewan) – see map for more information at 

CWD circulates in deer populations, particularly mule deer; it has been found in about 4% of deer tested in 2016; Elk can be infected in areas where CWD has been present in deer for a long period of time; Moose can also be infected, but this would be fairly rare. Necessary Precautions for Harvesters: Hunters and others who handle carcasses follow basic handling precautions (available here 

All deer, moose and elk harvested from CWD mandatory submission wildlife management units (WMUs) be tested for CWD; and A negative result (no CWD detected by the test) must be obtained before any part of an animal is eaten. 

For more information, contact: Amy Quintal Métis Nation of Alberta Métis Harvesting Liaison Tel: (780) 455 – 2200

Chronic Wasting Disease: CFIA Research Summary 

 Embargoed until May 23, 2017 

(OCR of a scanned original) 

Research Findings 

Chronic Wasting Disease (CWD) is a progressive, fatal disease of the nervous system of cervids including deer, elk, moose, and reindeer that is caused by abnormal proteins called prions. It is known as a transmissible spongiform encephalopathy (TSE). Other TSEs include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, and Creutzfeldt-Jakob disease (CJD) in humans.

A limited number of experimental studies have demonstrated that non-human primates, specifically squirrel monkeys, are susceptible to CWD prions. An ongoing research study has now shown that CWD can also be transmitted to macaques, which are genetically closer to humans. 

The study led by Dr. Stefanie Czub, a scientist at the Canadian Food Inspection Agency (CFIA), and funded by the Alberta Prion Research institute has demonstrated that by orally administering material under experimental conditions from cervids (deer and elk) naturally infected with CWD, the disease can be transmitted to macaques. 

in this project, which began in 2009, 18 macaques were exposed to CWD in a variety of ways: by injecting into the brain, through contact with skin, oral administration, and intravenously (into the bloodstream through veins). So far, results are available from 5 animals. At this point, two animals that were exposed to CWD by direct introduction into the brain, one that was administered infected brain material by oral administration and two that were given infected muscle by oral administration have become infected with CWD. The study is ongoing and testing continues in the remaining animals. The early results will be presented at PRlON 2017, the annual international conference on prion diseases, in Edinburgh, Scotland, May 23 to 26, 2017. 

Potential impacts of the new finding

Since 2003 Canada has a policy that recommends that animals and materials known to be infected with prions be removed from the food chain and from health products. Although no direct evidence of CWD prion transmission to humans has ever been recorded, the policy advocates a precautionary approach to managing CWD and potential human exposure to prions. These initial findings do not change Health Canada’s Health Products and Food Branch (HPFB) position on food and health products. A precautionary approach is still recommended to manage the potential risks of exposure to prions through food and health products. Measures are in place at federal, provincial and territorial levels to reduce human exposure to products potentially contaminated by CWD by preventing known infected animals from entering the marketplace. 

While Federal and P/T government’s animal disease control policies continue to divert known CWD-infected animals away from entering the food and feed supply, research and development of sensitive detection methods including live-animal sampling techniques remain crucial for ensuring an accurate diagnosis. In addition, consistent federal, provincial and territorial communications of appropriate precautionary measures for hunters and indigenous communities are required. 

Next Steps

The CFlA will continue to collaborate with national and international partners to develop and validate new diagnostic techniques. The CFlA will also continue to offer confirmatory testing services and reference laboratory expertise to provincial and territorial partners on demand. 

Currently, CFlA laboratories are leading or collaborating on several research projects to understand the potential for CWD to infect humans. These projects use non‐human primates, genetically modified mice, and cell-free amplification approaches. Given the present findings, CFiA encourages continued research into TSEs. 

The results of this study reinforce the need to redesign the federal program to foster greater adoption of risk mitigation measures for farmed cervids. Federal and provincial government collaboration will continue as new program options are assessed. 

The results of Dr. Czub’s research into CWD will be of interest to scientists, governments, industry and people who consume cervid products. After the presentation at PRION 2017, the research will follow the normal steps of completion, peer review and publication. The Government of Canada will monitor the response to this research and determine whether further review of the science is required. Other studies underway by other researchers may also become public as a result of the presentation of Dr. Czub’s research. 

The Public Health Agency of Canada, Health Canada, CFlA and other Federal partners are working together to assess what policies or programs need further review as well as preparing other communications about the research and health policy and advice to Canadian. 2017/04/28 


0:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 

Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada 

see science to date that the call should be made NOW, that cwd to humans is possible, and all precautions there fore, should be take will great urgency.


*** First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques


*** 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).***

Molecular Barriers to Zoonotic Transmission of Prions

 *** 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.

*** 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). ***

*** 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). ***

*** 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).


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).


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. ...


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 ;

you can see more evidence here ;

Wednesday, May 24, 2017 

PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1


Location: Virus and Prion Research

Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin

Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:

Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.

Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.

Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:

This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.

CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.

Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.



While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...

we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.

 Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....

 snip...see much more here ;


Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease


Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in vitro Conversion Assay

Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR1 1University of British Columbia, Brain Research Centre, Canada; 2Public Health Agency of Canada, National Microbiology Laboratory, Canada; 3Animal Diseases Research Institute, Canada Food Inspection Agency, National Reference Laboratory for Scrapie and CWD, Canada; 4Ontario Cancer Institute and Department of Medical Biophysics, University of Toronto, Canada

Background: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that can affect North American cervids (deer, elk, and moose). Although the risk of CWD crossing the species barrier and causing human disease is still unknown, however, definite bovine spongiform encephalopathy (BSE) transmission to humans as variant CJD (vCJD), it would seem prudent to limit the exposure of humans to CWD.

Aim: In view of the fact that BSE can be readily transmitted to non-bovid species, it is important to establish the species susceptibility range of CWD.

Methods: In vitro conversion system was performed by incubation of prions with normal brain homogenates as described before, and protease K (PK) resistant PrP was determined by immunoblotting with 6H4 monoclonal prion antibody.

Results: Our results demonstrate that PrPC from cervids (including moose) can be efficiently converted to a protease-resistant form by incubation with elk CWD prions, presumably due to sequence and structural similarities between these species. Interestingly, hamster shows a high conversion ratio by PrPCWD. Moreover, partial denaturation of substrate PrPC can apparently overcome the structural barriers between more distant species.

Conclusions: Our work correctly predicted the transmission of CWD to a wild moose. We find a species barrier for prion protein conversion between cervids and other species, however, this barrier might be overcome if the PrPC substrate has been partially denatured in a cellular environment. Such an environment might also promote CWD transmission to non-cervid species, *** including humans. Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitro conversion than PrPC treated at physiological pH. This has implications for the process by which the prion protein is converted in disease. Book of Abstracts.pdf

Wednesday, March 18, 2009 

Noah’s Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II 



a) Elk Meat, Elk Tenderloin, Frozen in plastic vacuum packaging. Each package is approximately 2 lbs., and each case is approximately 16 lbs.; Item number 755125, Recall # F-129-9; 

b) Elk Meat, Elk Trim, Frozen; Item number 755155, Recall # F-130-9; 

c) Elk Meat, French Rack, Chilled. Item number 755132, Recall # F-131-9; 

d) Elk Meat, Nude Denver Leg. Item number 755122, Recall # F-132-9; 

e) Elk Meat, New York Strip Steak, Chilled. Item number 755128, Recall # F-133-9; 

f) Elk Meat, Flank Steak Frozen. Item number 755131, Recall # F-134-9; 


Elk Meats with production dates of December 29, 30, and 31 


Recalling Firm: Sierra Meats, Reno, NV, by telephone on January 29, 2009 and press release on February 9, 2009. 

Manufacturer: Noah’s Ark Holding, LLC, Dawson, MN. Firm initiated recall is ongoing. 


Elk products contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). 






TUESDAY, JUNE 20, 2017 

Prion 2017 Conference Transmissible prions in the skin of Creutzfeldt-Jakob disease patients


*** First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques

FRIDAY, JUNE 16, 2017

PRION 2017 P55 Susceptibility of human prion protein to in vitro conversion by chronic wasting disease prions

MONDAY, JUNE 19, 2017 

PRION 2017 P20 Descriptive epidemiology of human prion diseases in Japan: a prospective 16-year surveillance study

Japan Prion Disease Increasing Annually to 2.3 patients per 1 million populations in 2014

TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD


Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?

MONDAY, JUNE 19, 2017 

PRION 2017 CONFERENCE ABSTRACT P61 vCJD strain properties in a Spanish mother and son replicate as those of a young UK case


Amyloid-β accumulation in human growth hormone related iatrogenic CJD patients in the UK

Saturday, June 17, 2017

PRION 2017 P115 α- Synuclein prions from MSA patients exhibit similar transmission properties as PrPSc prions

MONDAY, JUNE 19, 2017 

Transmissible Spongiform Encephalopathies Advisory Committee June 2017 CJD, BSE, Scrapie, CWD, TSE, Prion? 


Docket No. FDA– 2009–N–0505 Agency Information Collection Activities; Proposed Collection; Recordkeeping and Reporting Requirements for Human Food and Cosmetics Manufactured From, Processed With, or Otherwise Containing Material From Cattle

THURSDAY, JUNE 22, 2017 

World Organisation for Animal Health (OIE) to establish liaison office in College Station, Texas


Detection of prions in blood from patients with variant Creutzfeldt-Jakob disease

Tuesday, May 10, 2016

2015 PDA Virus & TSE Safety Forum Meeting Report

>>>Recently transmission of prions from blood of patients with sporadic CJD to humanized mice could be demonstrated.<<<

>>>Further-on, urine samples of a control population (normal and neurological population) showed no signal in the study; *** however, in samples from patients with sporadic CJD and vCJD, a signal was detected in both patient populations.<<<

Meeting Report: 2015 PDA Virus & TSE Safety Forum

Tuesday, March 11, 2014 

Science and Technology Committee Oral evidence: Blood, tissue and organ screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD 

Actually, it is nearer 2 per million per year of the population will develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about 1 in 30,000. So that has not really changed. When people talk about 1 per million, often they interpret that as thinking it is incredibly rare. They think they have a 1-in-a-million chance of developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of developing it. 

Sunday, March 09, 2014 

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease 


Wednesday, December 11, 2013

*** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease ***

Wednesday, October 09, 2013 


THURSDAY, JUNE 22, 2017 

PRION 2017 CONFERENCE P120 Early preclinical detection of prions in blood of macaques peripherally infected with the variant CJD agent

2001 FDA CJD TSE Prion Singeltary Submission


Terry S. Singeltary Sr.


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