Monday, February 12, 2018

Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties

Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties

Chronic Wasting Disease found in 2 more Pa. deer 

Updated 10:02 AM; Posted 10:02 AM 

Chronic Wasting Disease has been found in more Pennsylvania deer. 

By Matt Miller mmiller@pennlive.com 

The state Department of Agriculture reported Monday that Chronic Wasting Disease has been found in captive deer in Huntingdon and Lancaster counties.

The discoveries bring to 46 the number of cases of the fatal disease that have been detected in Pennsylvania since the first case was reported in Adams County 2012, the agency said.

Officials did not name the deer farm sites where the latest cases were found. One animal at each site was afflicted, they said, and both deer were born and raised at the facilities. Both farms are under quarantine.

CWD attacks the brain of infected deer, elk and moose, producing small lesions that eventually result in death. Animals can get the disease through direct contact with saliva, feces and urine from an infected animal or contaminated environment.

Signs of the disease include weight loss, excessive salivation, increased drinking and urination, and abnormal behavior like stumbling, trembling, and depression. Infected deer and elk may also allow unusually close approach by humans or natural predators. There is no known treatment.

Officials said the latest cases of CWD were discovered through mandatory state testing programs for Pennsylvania's 860 deer breeding and hobby farms and hunting preserves.

http://www.pennlive.com/news/2018/02/chronic_wasting_disease_found.html


02/12/2018

Deer on Bedford County Hunting Preserve, Lancaster County Breeding Farm Test Positive for Chronic Wasting Disease

Harrisburg, PA - The Pennsylvania Department of Agriculture today announced that two additional captive deer have tested positive for Chronic Wasting Disease (CWD) in Pennsylvania, bringing the total to 46 since the disease was discovered in Pennsylvania in 2012.

The disease was confirmed in one white-tailed deer on a hunting preserve in Bedford County, and one at a Lancaster County breeding operation. Both deer were born and raised on their respective premises, and these are the first CWD-positives discovered on either farm. Both operations are now under quarantine. This is the first CWD-positive test result in a Lancaster County captive deer.

“The Department of Agriculture takes the emergence and spread of CWD in Whitetail Deer in Pennsylvania very seriously,” said State Veterinarian Dr. David Wolfgang. ”Farmers with captive deer and other CWD-susceptible species must participate in one of two programs and follow specific procedures outlined for their program. The department is committed to cooperating with deer farmers, the Game Commission, and foresters to keep deer populations in Pennsylvania healthy and at viable population levels.” 

The department’s Pennsylvania Veterinary Laboratory in Harrisburg tested the deer, which were later confirmed positive at the National Veterinary Services Laboratories in Ames, Iowa. The deer were tested as required by the department’s CWD program. Deer cannot be moved on or off these properties without permission from the department.

The Centers for Disease Control and Prevention report no strong evidence that humans or livestock can contract CWD.

CWD attacks the brain of infected deer, elk and moose, producing small lesions that eventually result in death. Animals can get the disease through direct contact with saliva, feces and urine from an infected animal or contaminated environment.

Clinical signs include weight loss, excessive salivation, increased drinking and urination, and abnormal behavior like stumbling, trembling, and depression. Infected deer and elk may also allow unusually close approach by humans or natural predators. The disease is fatal and there is no known treatment or vaccine.

The infectious agent, known as a prion, tends to concentrate in the brain, spinal column, eyes, spleen, and lymph nodes. These high-risk parts must be properly handled and disposed of at the harvest location to prevent disease spread. Low-risk parts such as deboned meat, clean skull caps and capes present little risk and may be taken home.

The first cases of CWD in Pennsylvania were detected in white-tailed deer that died in 2012 on an Adams County deer farm, and wild, white-tailed deer in Blair and Bedford Counties.

The Pennsylvania Department of Agriculture coordinates a mandatory surveillance program for the disease for 860 breeding farms, hobby farms and hunting preserves across the state. Since 1998, accredited veterinarians and certified CWD technicians have tested 27,000 captive deer in Pennsylvania. The Pennsylvania Game Commission collects samples from hunter-harvested deer and elk and wild deer that appear sick or behave abnormally.

Find more information about Pennsylvania’s captive deer CWD programs, and the department’s broader efforts to safeguard animal health at agriculture.pa.gov.

MEDIA CONTACT: Shannon Powers - 717.783.2628

# # #



01/19/2018

CWD TEST RESULTS CONTINUE TO COME IN HARRISBURG, PA - Pennsylvania’s statewide deer seasons have come to a close, and within the next several weeks, final chronic wasting disease test results will return from deer harvested by hunters in the 2017-18 seasons.

snip...

At this time, 51 deer from the 2017-18 hunting seasons have tested positive for CWD. All have been within the DMAs. Forty-eight were within DMA 2, in southcentral Pennsylvania; and three were within DMA 3 in northcentral Pennsylvania.

But the majority of samples collected still are being analyzed.

snip...end



02/12/2018

Deer on Bedford County Hunting Preserve, Lancaster County Breeding Farm Test Positive for Chronic Wasting Disease

Harrisburg, PA - The Pennsylvania Department of Agriculture today announced that two additional captive deer have tested positive for Chronic Wasting Disease (CWD) in Pennsylvania, bringing the total to 46 since the disease was discovered in Pennsylvania in 2012.

snip...

01/19/2018 CWD TEST RESULTS CONTINUE TO COME IN HARRISBURG, PA - Pennsylvania’s statewide deer seasons have come to a close, and within the next several weeks, final chronic wasting disease test results will return from deer harvested by hunters in the 2017-18 seasons.

snip...

At this time, 51 deer from the 2017-18 hunting seasons have tested positive for CWD. All have been within the DMAs. Forty-eight were within DMA 2, in southcentral Pennsylvania; and three were within DMA 3 in northcentral Pennsylvania.

is it 51 or 46 ???

terry


-----Original Message-----
From: Terry Singeltary
To: bse-l
Cc:
Sent: Mon, Feb 12, 2018 9:02 am
Subject: Pennsylvania Deer found near Jefferson County elementary school tests positive for CWD TSE Prion


Pennsylvania Deer found near Jefferson County elementary school tests positive for CWD TSE Prion

3. Deer found near Jefferson County elementary school tests positive for CWD [PA] 

By Ron Musselman WJACtv.com February 8, 2018 

BROOKVILLE - An adult doe found found near a Jefferson County elementary school has tested positive for chronic wasting disease. 

"We did detect a CWD-positive (deer) 0.6 miles from the school," Pennsylvania Game Commission spokesman Travis Lau said Thursday. 

Officials said the deer was located along a stretch of Route 322 near Pinecreek Elementary School. 

As of Jan. 19, the Game Commission said 51 deer from the 2017-18 hunting season had tested positive for CWD in the Disease Management Areas. 

Jefferson County is located in DMA 3. 

Source: 




 Deer tests positive for CWD in Pine Creek Township

By Patti Slaughter Feb 8, 2018 0

BROOKVILLE — The body of a deer killed along Route 322, near Pine Creek Elementary School, has tested positive for Chronic Wasting Disease.

According to Jefferson County Treasurer Jim “Moon” VanSteenberg, the deer was found along the stretch of highway between the school and the Bob Olsen farm In Pine Creek Township.

Route 322 in Jefferson County is included in the Pennsylvania Game Commission’s Disease Management Area (DMA) 3. The most recent report from the Game Commission says that 51 deer from the 2017-18 hunting seasons have tested positive for CWD. All have been within the DMAs. Forty-eight were within DMA 2, in southcentral Pennsylvania, and three were within DMA 3, which covers northcentral Pennsylvania...snip...end



Pennsylvania Managing the Spread and Prevalence of Chronic Wasting Disease CWD TSE Prion 


Managing the Spread and Prevalence of Chronic Wasting Disease

The Pennsylvania Game Commission collects samples from deer harvested across the state and tests them for chronic wasting disease (CWD), as part of the agency’s ongoing CWD surveillance. Within the state’s Disease Management Areas — where the disease has been detected in captive and free-ranging deer — intensified sampling occurs.

During the 2017-18 deer hunting seasons, the Game Commission offered free CWD testing for hunters harvesting deer within Disease Management Areas (DMAs). Free testing offered hunters a way to have their deer tested prior to consuming it, and it provides the Game Commission with additional samples to better pinpoint areas where the disease exists, so specific problem spots might be addressed. Successful hunters within DMAs dropped off heads from more than 1,500 deer in head-collection containers. Game Commission staff collected more than 3,000 other samples within DMAs. In total, nearly 8,000 samples were collected statewide. Slightly more than 5,700 whitetails were tested for CWD in 2016; 25 tested positive, all were in or near DMA 2, the only area of the state where CWD has been detected in the wild.

By mid-January 2018, 51 deer from 2017 had tested positive for CWD; all have been within the DMAs. Forty-eight were within DMA 2, in southcentral Pennsylvania; and three were within DMA 3 in northcentral Pennsylvania. The majority of samples collected had yet to be analyzed at the time of this report.

The agency continues to assess test results to evaluate the best response to confront CWD where it exists. DMA boundaries regularly have been adjusted in relation to newly detected CWD-positive animals. During 2017, the Game Commission partnered with the U.S. Department of Agriculture’s APHIS’s Wildlife Services on a CWD surveillance effort where 30 deer were removed by sharpshooters, one of which tested positive for chronic wasting disease.

Attempting to control hot spots and remove animals with a greater likelihood of carrying the disease is the agency’s best chance at managing CWD on a larger scale, while minimizing the impact on the larger deer population or diminishing deer hunting opportunities. CWD is not a new disease, and other states have decades of experience dealing with CWD in the wild. It first was detected in Pennsylvania in 2012 at a captive deer facility, and it was detected in free-ranging deer soon after. By January 2018, in Pennsylvania, CWD had been detected in 98 free-ranging deer.

CWD is spread from deer to deer through direct and indirect contact. The disease attacks the brains of infected deer, elk, and moose, and will eventually result in the death of the infected animal. There is no live test for CWD and no known cure. There also is no evidence CWD can be transmitted to humans, however, it is recommended the meat of infected deer — or deer thought to be sick — not be consumed.

For more information on CWD, the rules applying within DMAs, or what hunters can do to have harvested deer tested for CWD, visit the Game Commission’s website, www.pgc.pa.gov. Information can be found by clicking on the button titled “CWD Information” near the top of the homepage.




DMAP permits in DMA 2 and DMA 3 have sold out for the 2017-18 seasons. The Game Commission created DMAP (Deer Management Assistance Program) units in DMA 2 and DMA 3 to focus hunter effort in areas where CWD-positive deer have been found. Hunters can apply for antlerless deer permits in those DMAP units through the automated license sales system. Although these DMAP permits can be used on public and private lands within the appropriate DMAP unit, hunters must receive permission from private landowners prior to hunting. Although these DMAP permits can be used on public and private lands within the appropriate DMAP unit, hunters must receive permission from private landowners prior to hunting. The North Unit #2874, of DMA 2 contains portions of southern Blair County and northwestern Bedford County. The South Unit, #2875, of DMA 2 contains eastern Bedford County and most of Fulton County. DMAP Unit 3045 encompasses DMA 3 in totality.






MONDAY, FEBRUARY 12, 2018 

Pennsylvania Deer found near Jefferson County elementary school tests positive for CWD TSE Prion



SATURDAY, JANUARY 20, 2018

Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have tested positive for CWD majority of samples collected still are being analyzed

http://chronic-wasting-disease.blogspot.com/2018/01/pennsylvania-cwd-tse-prion-cases.html


FRIDAY, DECEMBER 15, 2017 

Pennsylvania Four Deer Test Positive for Chronic Wasting Disease on Franklin, Fulton County Quarantined Hunting Preserves



THURSDAY, SEPTEMBER 28, 2017

Pennsylvania GAME COMMISSION OFFERS FREE CWD TESTS FOR DMA-HARVESTED DEER



 THURSDAY, SEPTEMBER 21, 2017

Pennsylvania Game Commission has scheduled a series of public meetings to ensure Pennsylvanians remain informed about chronic wasting disease CWD TSE Prion



 SATURDAY, AUGUST 12, 2017

*** Pennsylvania 27 deer from Bedford County farm test positive for chronic wasting disease ***



 WEDNESDAY, JULY 12, 2017

PENNSYLVANIA CWD FOUND IN THE WILD IN CLEARFIELD COUNTY



THURSDAY, JUNE 01, 2017

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



 Chronic wasting disease research becomes more crucial as cases grow in Pa. deer With fatal deer disease on the rise, Penn State researchers hunt for answers to help limit CWD's spread 

 Jeff Mulhollem May 23, 2017 

 UNIVERSITY PARK, Pa, — The recent announcement by the Pennsylvania Game Commission that it found 25 more wild deer with chronic wasting disease last year underlines the importance of studies being conducted by a team of researchers in Penn State's College of Agricultural Sciences.

With the overarching goal of determining how the always-fatal-to-cervids disease will disburse through the state's free-ranging white-tailed deer herd, the research is aimed at informing the commission's efforts to slow or limit the spread of the disease, according to David Walter, adjunct assistant professor of wildlife ecology. 

Often referred to as CWD, chronic wasting disease infects the brain and nervous system of cervids. The illness, which belongs to a group of diseases known as transmissible spongiform encephalopathies, or prion diseases, eventually produces enough damage to the brains of affected animals to result in death. While CWD is similar to so-called mad cow disease in cattle and scrapie in sheep, there is no known relationship between them.

There is no strong evidence, either, that humans can contract CWD, according to the U.S. Centers for Disease Control and Prevention, although the disease is similar to Creutzfeldt-Jakob disease, a rare, fatal syndrome that afflicts people.

Walter, who is assistant unit leader of the Pennsylvania Cooperative Fish and Wildlife Research Unit at Penn State, conducted research from 2007 to 2011 on the spread of the disease in Colorado and Nebraska in free-ranging mule deer and white-tailed deer. Since coming to Penn State in 2012, he has concentrated on the CWD outbreak spreading through deer herds in Virginia, West Virginia, Maryland and Pennsylvania.

Working under Walter's guidance in 2013-14, master's degree student Tyler Evans, now a wildlife biologist with the West Virginia Department of Natural Resources, investigated the geographic coordinates where deer testing positive for CWD were found, and he modeled the likely future spread of the disease in Pennsylvania.

Miller and a deer head Chronic wasting disease infects the brain and nervous system of cervids, and animals cannot be tested while they are alive. Here, researcher Will Miller (left) samples a deer head for the disease.

Image: Penn State "That research looked at what environmental variables were associated with the presence or absence of chronic wasting disease in the Northeast," Walter said. "We obtained the geographic coordinates of hunter-killed deer that tested positive for CWD and overlaid them on a map showing a variety of habitat and landscape features. The analysis showed a high prevalence of CWD in deer sampled from low-lying open and developed landscapes."

Now, Walter's advisee Will Miller, a doctoral degree candidate in the Intercollege Graduate Degree Program in Ecology, is continuing to study the spread of CWD in Pennsylvania. But he is focusing on whether some deer might be susceptible to the disease because of their genes, and how genetic variation in deer might influence where and how fast the disease spreads.

"It appears that deer in Pennsylvania's Northern Tier are less related to those in Maryland and in southern Pennsylvania," Walter said. "That may well have implications for how CWD spreads."

Walter and Miller are slated to travel to Edinburgh, Scotland, in late May to attend an international conference focused on prions and diseases the mysterious proteins cause. At the conference, Miller will present findings of his research focusing on genetic susceptibility of some deer in Pennsylvania to chronic wasting disease.

Detected in captive and free-ranging deer and elk in 23 states and two Canadian provinces, CWD was found last year in reindeer in Norway, Walter pointed out. "The Europeans are eager to learn what we know about the disease, based on our experience in North America," he said. "But despite all that we are learning about the disease, there is much we still don't know."

In the case of the outbreak in Pennsylvania's wild deer, that includes how the disease infected free-ranging deer in Pennsylvania. Among the possible sources, two include captive deer and wild deer moving from Maryland. Although researchers have seen evidence that deer may carry the disease over the border with Maryland, the Pennsylvania counties of Blair and Bedford, where CWD originally was found in 2012, also had the highest inventories of captive cervids in Pennsylvania.

map showing CWD outbreaks Genetics research focusing on "microsatellite markers" in white-tailed deer in Pennsylvania and surrounding states has indicated four clusters within deer herds with animal movement more likely within a cluster than between clusters.

Image: Penn State The location of the original outbreak, which was more than 40 miles from the Maryland border, makes it difficult to confirm the actual source of infection.

"In southern Fulton and Bedford counties, we have seen more CWD-positive deer along the border," Walter said. "We have seen over time that it is likely the disease is moving into this area from the West Virginia-Maryland outbreak."

The Game Commission tests both hunter-killed deer and animals killed on highways in parts of the state for CWD to assess the dimensions of the outbreak, Walter noted. The dual approach addresses sampling bias built into testing hunter harvests.

Because hunters are restricted by antler regulations from killing young male deer, and they mostly pass on taking young females and button bucks, some reached the mistaken conclusion that the disease primarily infects older deer. But road kills show that is not the case, Walter explained.

"It is a chronic disease, so it takes a while for the animal to succumb, but there is a fallacy out there that young deer can't get it — but they do, and we are detecting it now. Wisconsin has found CWD in fawns," he said.

"Most of the road kills with CWD are yearling males and females. We don't see that in hunter harvests, so our data from across the country has been skewed. Collecting and testing road kills has been a great investment of resources, and it has proved to be very valuable in finding this disease in areas we wouldn't find it otherwise."

Chronic wasting disease is not established in Pennsylvania yet, the way it is in Wisconsin and West Virginia, Walter believes, and he would like to see the Game Commission and state Department of Agriculture take steps, such as targeted culling of deer in CWD hotspots, to keep it at bay.

MEDIA CONTACTS: Jeff Muhollem jjm29@psu.edu Work Phone: 814-863-2719



MONDAY, MAY 15, 2017 

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



 WEDNESDAY, MARCH 01, 2017 

South central Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease 



FRIDAY, JANUARY 13, 2017 

Pennsylvania Deer Tests Positive for Chronic Wasting Disease four-year-old white-tailed deer Franklin County Hunting Preserve



Wednesday, May 11, 2016 

PENNSYLVANIA TWELVE MORE CASES OF CWD FOUND: STATE GEARS UP FOR ADDITIONAL CONTROL MEASURES 



Sunday, October 18, 2015

*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans Singeltary 2002 from speaking A smelly situation UPDATED 2015



Saturday, November 07, 2015

PENNSYLVANIA CHRONIC WASTING DISEASE CWD TSE PRION RULES EXPAND
Saturday, November 07, 2015

Pennsylvania 2015 September Minutes CWD Urine Scents

Tuesday, May 05, 2015

Pennsylvania CWD DETECTED IN SIX MORE FREE-RANGING DEER Disease Management Area 2 again expanded due to new cases Release #030-15



Sunday, July 13, 2014

Louisiana deer mystery unleashes litigation 6 does still missing from CWD index herd in Pennsylvania Great Escape

http://chronic-wasting-disease.blogspot.com/2014/07/louisiana-deer-mystery-unleashes.html


Saturday, June 29, 2013

PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA


Tuesday, June 11, 2013

*** CWD GONE WILD, More cervid escapees from more shooting pens on the loose in Pennsylvania


Tuesday, May 28, 2013

Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013
*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.

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


 Sunday, January 06, 2013

USDA TO PGC ONCE CAPTIVES ESCAPE

*** "it‘s no longer its business.”

”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.


ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;

''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end


Wednesday, November 14, 2012

PENNSYLVANIA 2012 THE GREAT ESCAPE OF CWD INVESTIGATION MOVES INTO LOUISIANA and INDIANA



Tuesday, October 23, 2012

PA Captive deer from CWD-positive farm roaming free
Thursday, October 11, 2012

Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests Positive


 *** 2017-2018 CWD TSE Prion UPDATE






Decontaminating Equipment Personal protective equipment (PPE), such as boots, gloves, clothing, etc., supplies, facilities, and vehicles exposed to potentially CWD infected tissues and environments should be properly cleaned and disinfected after each use. 


***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 ***

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



TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 


*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 



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

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 


Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;

Some unofficial information from a source on the inside looking out -

Confidential!!!!

As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

---end personal email---end...tss

http://chronic-wasting-disease.blogspot.com/

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...
TSE Scrapie, CWD, BSE, Prion, Soil


Clay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern Illinois

Sheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-Pinilla

Scientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-x

Download Citation

Ecological epidemiology Ecological modelling Infectious diseases Prions

Received: 21 August 2017

Accepted: 08 December 2017

Published online: 22 December 2017


Abstract


Environmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.



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



cwd tse prion and soil, see more ;




CWD TSE Prion Update
SATURDAY, FEBRUARY 10, 2018
Chronic wasting disease management in ranched elk using rectal biopsy testing Research Paper 09 Feb 2018 http://chronic-wasting-disease.blogspot.com/2018/02/chronic-wasting-disease-management-in.html


FRIDAY, FEBRUARY 09, 2018 Mississippi Chronic Wasting Disease confirmed in a White-tailed Deer http://chronic-wasting-disease.blogspot.com/2018/02/mississippi-chronic-wasting-disease.html


WEDNESDAY, JANUARY 24, 2018

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE

2017 7/6/17 Breeder Deer Medina Facility #5 White-tailed Deer M 4

2017 9/13/17 Breeder Deer Uvalde Facility #3 White-tailed Deer F 5

2017 10/6/17 Release Site Medina Facility #3 Elk F 4

2017 10/6/17 Breeder Deer Uvalde Facility #3 White-tailed Deer F 1

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer M 7

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 9

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 9

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 6

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer M 4

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2017 10/11/17 Breeder Deer Medina Facility #4 White-tailed Deer F 4

2017 10/25/17 Breeder Deer Medina Facility #5 White-tailed Deer F 3

2017 11/27/17 Breeder Release Site Medina Facility #4 White-tailed Deer M 4.5

2017 11/29/17 Breeder Release Site Medina Facility #3 White-tailed Deer M 4.5

2017 12/18/17 Free Range El Paso Mule Deer M 5.5

2017 12/22/17 Free Range Hartley Mule Deer M 2.5

2017 12/22/17 Free Range Hartley Mule Deer M 4.5

2017 12/29/17 Free Range Hartley White-tailed Deer M 2.5

2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 3.5

2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 3.5

2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 6.5

2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 5.5

2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 4.5

2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 4.5

2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 8.5

2017 1/8/18 Breeder Deer Uvalde Facility #3 White-tailed Deer F 3.5

2017 1/8/18 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 5.5

2017 1/8/18 Breeder Release Site Uvalde Facility #3 White-tailed Deer F 4.5

snip...see more here, you will have to hit the EXPAND button and go page by page to get all CWD postives;



 WEDNESDAY, JANUARY 24, 2018

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE



SUNDAY, MAY 14, 2017 

85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play, a lesson on how political and corporate science helps spread a deadly disease 



TEXAS HISTORY OF CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD COW TYPE DISEASE



 WEDNESDAY, FEBRUARY 07, 2018 

New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.



THURSDAY, FEBRUARY 08, 2018 

Utah Chronic Wasting Disease CWD TSE Prion Update to date from 2017 Hunting Season



 MONDAY, FEBRUARY 05, 2018 

Nebraska Chronic Wasting Disease CWD TSE Prion 2017 Survey Confirms 203 Positives From 1,807 Deer Sampled



FRIDAY, JANUARY 26, 2018 

WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE



 SATURDAY, FEBRUARY 03, 2018 

Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018



 TUESDAY, JANUARY 30, 2018 

Colorado Chronic Wasting Disease CWD TSE Prion 7/2015-6/2016 Results (2017?)



 THURSDAY, JANUARY 25, 2018 

Ohio Chronic Wasting Disease CWD TSE Prioin aka mad deer update 2016-2017 SEASON SUMMARY



 SATURDAY, JANUARY 20, 2018

Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have tested positive for CWD majority of samples collected still are being analyzed



 WEDNESDAY, JANUARY 24, 2018 

Illinois Chronic Wasting Disease CWD TSE Prion cases mounting with 75 confirmed 2017 and 685 total to date



 THURSDAY, FEBRUARY 08, 2018

Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season



 THURSDAY, DECEMBER 07, 2017 

Montana Chronic Wasting Disease Found in Deer north of Chester



 TUESDAY, DECEMBER 05, 2017 

Montana Fish, Wildlife and Parks testing has identified two more cases of chronic wasting disease in Carbon County deer



 FRIDAY, DECEMBER 08, 2017 

Minnesota Chronic wasting disease update: second deer tests positive on Winona County farm



FRIDAY, NOVEMBER 24, 2017 

Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting CWD TSE PRION DISEASE risk factors



 WEDNESDAY, NOVEMBER 22, 2017 

Minnesota Chronic Wasting Disease discovered in Winona County farm



 WEDNESDAY, NOVEMBER 15, 2017 

Minnesota DNR 7 deer test presumptive positive in southeast’s CWD management zone



 THURSDAY, NOVEMBER 09, 2017 

Minnesota CWD TSE Prion Disease not detected in latest round of CWD tests on farmed deer herd in Crow Wing County?



 Friday, August 05, 2016

MINNESOTA CHRONIC WASTING DISEASE SURVEILLANCE AND TESTING CWD TSE PRION UPDATE



 January 14, 2018

Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases




 Michigan UPDATE, see also ;

Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan 

Contact: Dwayne Etter (DNR), 517-284-4725 or David Williams (MSU), 517-917-0716 Agency: Natural Resources

Jan. 30, 2018 

Michigan State University and the Michigan Department of Natural Resources will be placing location-tracking collars on white-tailed deer in south-central Michigan as part of a multiyear study of deer disease, including chronic wasting disease.



 January 14, 2018

Missouri MDC REPORTS 15 NEW CASES OF CWD TSE Prion in Deer



 MONDAY, JANUARY 29, 2018 

Wyoming, Hanna, WGFD diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 161



 MONDAY, JANUARY 29, 2018 

North Dakota CWD Confirmed whitetail buck and a mule deer doe 2017 deer gun season from unit 3F2




 TUESDAY, DECEMBER 12, 2017 

*** Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017 ***

(zoonosis and environmental risk factors towards the bottom, after state by state reports)



 MONDAY, MARCH 13, 2017 

CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017



 SATURDAY, JANUARY 14, 2017 

CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017



 FRIDAY, DECEMBER 15, 2017

Canada CFIA updating its national CWD TSE PRION efforts to eradicate disease farmed cervid NOT successful December 14, 2017



TUESDAY, DECEMBER 12, 2017 

Bovine Spongiform Encephalopathy BSE TSE Prion (aka mad cow disease) Report December 14, 2017 2017



TUESDAY, DECEMBER 12, 2017 

SCRAPIE TSE PRION UPDATE USA DECEMBER 14, 2017



TUESDAY, DECEMBER 12, 2017 

Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017



Tuesday, December 12, 2017 

Neuropathology of iatrogenic Creutzfeldt–Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology



 TUESDAY, JANUARY 30, 2018 

Chronic Wasting Disease A Time Bomb For Agriculture? 

WOW, i am shocked, this came from the PORK farm journal...nice article!



CWD TO PIGS

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

Location: Virus and Prion Research

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

Author item Moore, Sarah 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.



CONFIDENTIAL

EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

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 ;


WEDNESDAY, APRIL 05, 2017

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



WEDNESDAY, APRIL 05, 2017

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



 cattle are highly susceptible to white-tailed deer CWD and mule deer CWD

***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.

SNIP...



 price of prion poker goes up for cwd to cattle;


 Monday, April 04, 2016

*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***



 *** 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. 




 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?



WEDNESDAY, MAY 17, 2017

*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***



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

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



 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.



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.


2011

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


TUESDAY, MARCH 28, 2017 

*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***


SHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...


*** 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. 


COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?

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


IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989



ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;

''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end


MONDAY, SEPTEMBER 25, 2017

Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis



FRIDAY, NOVEMBER 24, 2017 

Brain Tanning Hides and CWD Transmissible Spongiform Encephalopathy TSE Prion Disease Risk Factors Warning



SUNDAY, AUGUST 06, 2017 

USA Chronic Wasting Disease CWD TSE Prion Emergency Response Plan Singeltary et al



ZOONOSIS OF TSE PRION DISEASE


O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

***is the third potentially zoonotic PD (with BSE and L-type BSE),

***thus questioning the origin of human sporadic cases. 

We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
 Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.


PRION 2016 TOKYO

Saturday, April 23, 2016

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis

Prion 2016 Animal Prion Disease Workshop Abstracts

WS-01: Prion diseases in animals and zoonotic potential

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 


why do we not want to do TSE transmission studies on chimpanzees $

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

snip...

R. BRADLEY


Title: Transmission of scrapie prions to primate after an extended silent incubation period) 

*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. 



Volume 23, Number 9—September 2017 

Research Letter Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion


***Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.


2017

Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 

Chronic Wasting Disease (CWD) 

Prevention 

* Strongly consider having the deer or elk tested for CWD before you eat the meat. 

* If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. 

* If your animal tests positive for CWD, do not eat meat from that animal. 
 > However, to date, no CWD infections have been reported in people. 

key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** 
TUESDAY, SEPTEMBER 12, 2017 

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 


SATURDAY, JANUARY 27, 2018 

CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018



Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018

CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE. 

THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$

BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.

SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.

SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.

SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***



CDC CWD TSE PRION UPDATE USA JANUARY 2018

As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk.
CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand.
Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd.
As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids.
 Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018
snip... 
Prion 2017 Conference Abstracts CWD

 2017 PRION CONFERENCE 

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

Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 

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

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

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

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

PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 

Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO 

PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS 

*** PRION 2017 CONFERENCE VIDEO 



 TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT 

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


TUESDAY, JULY 04, 2017

*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***


TUESDAY, JUNE 13, 2017

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


Wednesday, May 24, 2017 

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


SATURDAY, JULY 29, 2017 

Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC 


***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.*** 


SATURDAY, JULY 29, 2017 
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC 


Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿ 

Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations

 In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.



Prions in Skeletal Muscles of Deer with Chronic Wasting Disease 

Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.



*** WDA 2016 NEW YORK *** 

 We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. 

 Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders 


Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo Zoonotic Potential of CWD Prions: An Update 

Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6 

1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. 

4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, 

2Encore Health Resources, 1331 Lamar St, Houston, TX 77010 

Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions. 

PRION 2016 TOKYO 

In Conjunction with Asia Pacific Prion Symposium 2016 

PRION 2016 Tokyo 

Prion 2016 


Cervid to human prion transmission 

Kong, Qingzhong 

Case Western Reserve University, Cleveland, OH, United States 

Abstract 

Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. We hypothesize that: 

(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues; 

(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence; 

(3) Reliable essays can be established to detect CWD infection in humans;and 

(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches. 

Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3. 

Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1. 

Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions. 

Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans. 

Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans. 

Funding Agency Agency National Institute of Health (NIH) 

Institute National Institute of Neurological Disorders and Stroke (NINDS) 

Type Research Project (R01) 

Project # 1R01NS088604-01A1 

Application # 9037884 

Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND) 

Program Officer Wong, May 

Project Start 2015-09-30 

Project End 2019-07-31 

Budget Start 2015-09-30 

Budget End 2016-07-31 

Support Year 1 

Fiscal Year 2015 

Total Cost $337,507 

Indirect Cost $118,756 

Institution 

Name Case Western Reserve University 

Department Pathology 

Type Schools of Medicine 

DUNS # 077758407 

City Cleveland 

State OH 

Country United States 

Zip Code 44106 


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

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

you cannot cook the TSE prion disease out of meat. 

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. 

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

the TSE prion agent also survives Simulated Wastewater Treatment Processes. 

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

you can bury it and it will not go away. 

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

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

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

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. 

Laboratory of Central Nervous System Studies, National Institute of 

Neurological Disorders and Stroke, National Institutes of Health, 

Bethesda, MD 20892. 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. 

PMID: 8006664 [PubMed - indexed for MEDLINE] 


New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication 


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


Detection of protease-resistant cervid prion protein in water from a CWD-endemic area 


A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing 


Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals 


PPo4-4: 

Survival and Limited Spread of TSE Infectivity after Burial 



URINE

SUNDAY, JULY 16, 2017

*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***


Discussion

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

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

This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.

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

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

Wednesday, December 16, 2015

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

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

Singeltary submission ;

Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose

*** DOCUMENT ID: APHIS-2006-0118-0411



FRIDAY, NOVEMBER 24, 2017 

Norwegian Food Safety Authority makes changes to measures to limit the spread of disease Skrantesjuke (CWD) in deer wildlife



TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 


*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 


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

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 


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. 

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

Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;

Some unofficial information from a source on the inside looking out -

Confidential!!!!

As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

---end personal email---end...tss
http://chronic-wasting-disease.blogspot.com/


MONDAY, JANUARY 29, 2018 

Assessment of Chronic Wasting Disease Prion Shedding in Deer Saliva with Occupancy Modeling



SATURDAY, FEBRUARY 03, 2018 

Dehydration of prions on environmentally relevant surfaces protects them from inactivation by freezing and thawing



SATURDAY, JANUARY 27, 2018 

CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018

http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html




Diagnosis and Reporting of Creutzfeldt-Jakob Disease 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob Disease 

To the Editor: 

In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally. 

Terry S. Singeltary, Sr Bacliff, Tex 

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323. 




Terry S. Singeltary Sr.



posted by Terry S. Singeltary Sr. at 10:20 AM

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