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Thursday, April 14, 2016

Louisiana Chronic Wasting Disease CWD TSE Prion Surveillance and Testing Program?

>>>Louisiana Chronic Wasting Disease CWD TSE Prion Surveillance and Testing Program?
 
LOL!!!
 
 
LDWF monitoring for CWD in state’s white-tailed deer population Disease has been found in Texas and Arkansas; plans already in place if detected here From News Reports

 

 The Louisiana Department of Wildlife and Fisheries is actively monitoring the state's deer herd for chronic wasting disease, a fatal brain infection that has already been found in both Arkansas and Texas. The Louisiana Department of Wildlife and Fisheries is actively monitoring the state's deer herd for chronic wasting disease, a fatal brain infection that has already been found in both Arkansas and Texas.

 

Even though no cases of chronic wasting disease have been found in Louisiana, the state is stepping up preventive efforts to monitor Louisiana’s native white-tailed deer population for the incurable brain infection.

 

According to the Louisiana Department of Wildlife and Fisheries, the disease has already entered both Texas and Arkansas, and the state has developed a plan in the event it eventually is found here.

 

“We’ve been monitoring for CWD statewide for more than 10 years, and have checked 7,000-plus deer and have not discovered it,” said Dr. Jim LaCour, the state wildlife veterinarian who updated the Louisiana Wildlife and Fisheries Commission on the disease during its meeting today in Baton Rouge. “We are being proactive because it’s in our neighboring states, and it’s close enough that we need to be on guard.’’

 

CWD is a neurodegenerative disease found in most deer species, including moose, elk and mule deer, as well as white-tailed deer. It is infectious and always fatal. It’s part of a group of diseases known as transmissible spongiform encephalopathies (TSEs) and is similar to BSE (mad cow disease) in cattle and scrapie in sheep. The diseases cause irreversible damage to brain tissue which leads to salivation, neurological symptoms, emaciation and death of the animal, according to a press release.

 

CWD is caused by prions, which are proteins normally found in the body that have mutated. These prions kill nerve cells and cause holes to develop in the brain tissue. They are spread through direct deer-to-deer contact or through contact with urine, feces, saliva and body parts of infected deer or infectious materials in the soil. It’s most commonly found in deer pens and captive facilities, the release states.

 

It is different from hemorrhagic disease (epizootic hemorrhagic disease virus and/ or bluetongue virus), which is a virus spread by bites from infected insects.

 

Deer infected with CWD can spread the disease even before symptoms develop, and it can take one to two years for infected animals to become symptomatic. When symptoms appear they can include emaciation, lethargy, abnormal behavior and loss of bodily functions. Other signs include excessive salivation, loss of appetite, progressive weight loss, excessive thirst and urination, teeth grinding and drooping ears.

 

According to the Centers for Disease Control and Prevention, there is no evidence that CWD can infect humans. However, the CDCP recommends caution in handling venison in the infected region and that deer be tested for CWD before consuming.

 

The prions remain for years in the environment and there has not been a method discovered to eradicate them.

 

“Once the infected deer die, after they decompose, those particles go into the soil and they stay there indefinitely,’’ LaCour said.

 

CWD has been documented in 23 states and two Canadian provinces.

 

Though Louisiana has yet to see a case of CWD, LaCour and Jimmy Ernst, the Deer Management Assistance Program coordinator, said the LDWF has developed a plan should the disease be found here.

 

Once it is discovered, there will be feeding and baiting restrictions in the geographic area where the disease is initially found. It may also be necessary to reduce and maintain a lower deer density in that area, the release states.

 

There also will be movement restrictions placed on deer body parts, and the creation of a CWD management zone — the size of which will depend on the location and distribution of infected deer.

 

“Hunters won’t be able to bring a whole deer out from property within that radius,’’ Ernst said. “They’ll be able to bring out the deboned meat, a clean skull plate with the antlers, and the cape, which is the skin of the head and shoulders.

 

“The goal is to take an area around the initial case and maintain intensive surveillance. We will liberalize the season locally and we will test those harvested animals as they come out. By stopping baiting and feeding, which congregates animals, and by reducing the population, there isn’t as much deer-to-deer interaction. That will slow the spread of the disease. We will continue surveillance and control in that area for an indefinite period of time. Hopefully, working with hunters and landowners, we can minimize the spread of the disease with these measures.’’

 

Ernst said the LDWF will remain vigilant in testing and enacting preventative measures against CWD introduction into Louisiana. Working with Louisiana Department of Agriculture and Forestry to prevent importation of potential CWD-infected animals into the state through the LDAF-licensed deer pen program is a continuing effort of LDWF.

 

For more information about chronic wasting disease, click here.

 


 


 

What to Know About Chronic Wasting Disease

 

The Louisiana Department of Wildlife and Fisheries continues to monitor and test the state’s white-tailed deer population for chronic wasting disease (CDW). It has not been found in Louisiana but Texas and Arkansas have documented it. Here are some facts about the disease:

 

CWD FACT SHEET

 

What is Chronic Wasting Disease?

 

CWD is a neurodegenerative disease found in most deer species, including moose, elk, mule deer and white-tailed deer. It is infectious, always fatal and there is no known cure. It’s part of a group of diseases known as transmissible spongiform encephalopathies (TSEs) and is similar to BSE (mad cow disease) of cattle and scrapie in sheep. These diseases cause irreversible damage to brain tissue which leads to salivation, neurological symptoms, emaciation and death of the animal.

 

Has it been found in Louisiana’s white-tailed deer population?

 

No. But Texas and Arkansas have recorded it. The disease has been documented in 23 states and two Canadian provinces. The Louisiana Department of Wildlife and Fisheries has been monitoring and testing for CWD for more than 10 years and has checked more than 7,000 deer during that time period. The state has yet to test positive for it.

 

What causes CWD and how is it spread?

 

CWD is caused by prions, which are proteins normally found in the body that have mutated. These prions kill nerve cells and cause holes to develop in the brain tissue. They are spread through direct deer-to-deer contact or through contact with urine, feces, saliva and body parts of infected deer or infectious materials in the soil. It’s most commonly found in deer pens and captive facilities. It is different from hemorrhagic disease (epizootic hemorrhagic disease virus and/ or bluetongue virus), which is a virus spread by bites from infected insects.

 

What signs do deer with CWD display?

 

It can take one to two years for CWD to incubate and exhibit outward symptoms in the infected animal. When symptoms appear they can include emaciation, lethargy, abnormal behavior and loss of bodily functions. Other signs include excessive salivation, loss of appetite, progressive weight loss, excessive thirst and urination, teeth grinding and drooping ears.

 


 


 


 

MAYBE LOUISIANA HAS NOT FOUND CWD TO DATE, BECAUSE THEY ARE NOT TESTING FOR CWD ENOUGH. see pitiful PITIFUL cwd test figures of recent years ;

 

2014 – 2015 LOUISIANA ONLY TESTED 18 SAMPLES STATEWIDE FOR CWD...TSS

 

WILDLIFE DISEASE

 

The statewide Wildlife Disease Program was administered by the State Wildlife Veterinarian and the Assistant State Wildlife Veterinarian. Chronic Wasting Disease (CWD) surveillance continued as 18 samples were submitted from all regions of the state to the Southeastern Cooperative Wildlife Disease Study laboratory. Due to cessation of federal funding for this program, only target animals such as neurological or emaciated deer, deer hit by cars, deer harvested adjacent to captive cervid facilities, and escaped exotic cervids were tested.

 


 

2012 – 2013 LOUISIANA ON 21 SAMPLES STATEWIDE FOR CWD...TSS

 

WILDLIFE DISEASE The statewide Wildlife Disease Program was administered by the State Wildlife Veterinarian. An assistant state wildlife veterinarian began work for LDWF this year.

 

Chronic Wasting Disease (CWD) surveillance continued as 21 samples were submitted from all regions of the state to the Southeastern Cooperative Wildlife Disease Study laboratory. Due to cessation of federal funding for this program, only target animals such as neurological or emaciated deer, deer hit by cars, deer harvested adjacent to captive cervid facilities, and escaped exotic cervids were tested.

 


 

2011 – 2012 LOUISIANA CWD SAMPLE TESTING FIGURES

 

WILDLIFE DISEASE

 

The statewide Wildlife Disease Program was administered by the State Wildlife Veterinarian.

 

Chronic Wasting Disease (CWD) surveillance continued as 517 samples were submitted from all regions of the state to the Southeastern Cooperative Wildlife Disease Study laboratory. Samples were collected from hunter-killed deer which are considered low probability samples, as well as from road-killed, pen- killed, and taxidermy specimens which are considered high probability samples. All samples tested negative for CWD.

 


 

 FISCAL YEAR 2009-2010

 

Wildlife Disease

 

The statewide Wildlife Disease Program was administered by the State Wildlife Veterinarian. Chronic Wasting Disease (CWD) surveillance continued as 600 samples were submitted from all regions of the state to the Southeastern Cooperative Wildlife Disease Study laboratory. Samples were collected from hunterkilled deer which are considered low probability samples, as well as from road-killed, pen- killed and taxidermy specimens which are considered high probability samples. All samples tested negative for CWD.

 


 



update;


Tuesday, July 12, 2016

Louisiana Notice of Intent Cervid Carcass Importation (LAC XIX.V.1.119) CWD TSE PRION

http://chronic-wasting-disease.blogspot.com/2016/07/louisiana-notice-of-intent-cervid.html
 


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.

 


 

United States v. Billy Powell, No. 6:11-CR-00059 (E.D. Tex.), AUSA Jim Noble.

 

On September 22, 2011, licensed deer breeder Billy Powell was sentenced to serve six months’ home confinement as a condition of a three-year term of probation. Powell was also ordered to pay a $1 million fine, to be deposited into the Fish and Wildlife Lacy Act Reward Fund, as well as pay $500,000 in restitution to Texas Parks and Wildlife. During the term of probation, Powell will be prohibited from participating in any manner of commercial deer breeding. Additionally, Powell must

 

ECS Monthly Bulletin October 2011 17

 

forfeit any illegally imported deer, any progeny of those deer, and any biological material derived from the deer, including antlers, mounts, semen, and cloned deer. Powell has already forfeited more than 1,300 straws of frozen semen valued at approximately $961,500.

 

After a four-year investigation, Powell pleaded guilty to smuggling approximately 37 whitetail deer in violation of the Lacey Act (16 U.S.C. §§ 3372 (a)(2)(A), 3373 (d)(2)) from Indiana, Illinois, and Ohio into Texas over a three-year period. Powell also admitted that he made a false statement and submitted a false document (18 U.S.C. § 1001) to a United States Fish and Wildlife agent.

 

On at least four separate occasions between October 2006 and June 2008, Powell illegally imported the deer, many of which came from captive deer farms in Indiana, to his deer breeding facility in Texas. Powell was aware that Texas law prohibits any person from possessing a deer acquired from an out-of-state source. The fair market value of these deer exceeded approximately $800,000, with the additional value of the semen and the progeny estimated to exceed $1.25 million. The defendant also lied to a Fish and Wildlife agent regarding the actual number of deer that he had brought into the state.

 

As an unfortunate consequence of Powell’s actions, all 334 deer at his facility had to be euthanized to facilitate testing for chronic wasting disease (CWD) and bovine tuberculosis (BT), as there currently is no live-animal test for CWD. This was necessary to ensure that neither disease was present in Powell's deer breeding facility or in any deer breeding facility that had received deer from Powell's facility since October 2004. Once these diseases become established in wild populations, they are extremely difficult, if not impossible, to eradicate.

 

This case was investigated by the Special Operations Unit of the Texas Parks and Wildlife and United States Fish and Wildlife Service.

 


 

 Louisiana Business, 3 Associates Charged With Smuggling Deer Into Mississippi

 

featured-miss-deer-smuggling

 

Posted by Matt Alpert

 

February 14, 2014

 

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A Louisiana business, its CEO and two associates have been indicted on charges of illegally smuggling deer into Mississippi.

 

The Sun Herald reported that the accused men smuggled whitetail deer from Louisiana to wildlife enclosures they managed in Mississippi for the purposes of breeding and trophy buck hunting, which is illegal under the Federal Lacey Act.

 

Both federal and state law prohibits smuggling deer into Mississippi from out of state to prevent the spread of chronic wasting disease and bovine tuberculosis. Both diseases can wreak havoc on deer populations.

 

More Stories About CWD More Stories About CWD Check out these articles about the threat of chronic wasting disease in deer populations throughout the US.

 

Omni Pinnacle, an emergency response services company that responds to natural disasters throughout the US, is the company at the center of the criminal charges. Its CEO, Brian R. Reine, and his associates Ronald W. Reine and Bruce A. Swilley, Jr. are the three men accused of smuggling deer. They were arraigned on Wednesday, and released on bonds of $25,000 each.

 

From Jan. 2011 to Dec. 2012, the Reines smuggled whitetail deer from Louisiana, Kentucky, Illinois and Pennsylvania into wildlife enclosures in Mississippi’s Pearl River and Lamar Counties. The deer were used for breeding and trophy hunts for some of Omni Pinnacle’s business gatherings and public relations meetings.

 

If convicted, Omni Pinnacle faces a $500,000 fine, and the men face up to five years in prison and $250,000 fines for each charge. They are scheduled on March 17 for a hearing in a U.S. District Court in Gulfport, Miss.

 

RELATED: Big Game Outfitter Charged With Wounding Mountain Lions To Make Them Easier To Hunt

 

Chronic wasting disease is a deadly disease that affects the nervous system of deer. Both the federal and state governments throughout the US have strict laws intended to prevent the spread of the disease among deer populations. Smuggling deer across state lines can spread the disease to untainted deer populations.

 


 

Open season on escaped exotic deer near Delhi

 

Daily Comet - www.dailycomet.com 13 Nov 2009

 

Location: Delhi, Richland Parish, Louisiana -

 

. . . Up to 14 fallow deer and an unknown number of sika deer escaped through a broken fence at High Delta Exotics, a wildlife park and hunting ranch, John Hanks, a biologist with the Louisiana Department of Wildlife and Fisheries, said Thursday.

 

He said the deer might have diseases they could spread to native whitetails. "The biggest we're worried about is chronic wasting disease," he said. The disease has not been found in Louisiana deer.

 


 

 

NORTH AMERICA IS ALREADY RESPONSIBLE FOR SHIPPING CWD TO KOREA, HOW MANY MORE COUNTRIES MUST FALL DUE TO THE OIE AND THE USDA $$$

 

 

Friday, May 13, 2011

 

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

 


 

Tuesday, April 12, 2016

 

The first detection of Chronic Wasting Disease (CWD) in Europe

 


 

Sunday, April 10, 2016

 

Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer (Rangifer tarandus tarandus)

 


 

Saturday, April 9, 2016

 

The Norwegian Veterinary Institute (NVI, 2016) has reported a case of prion disease Cervid Spongiform Encephalopathy detected in free ranging wild reindeer (Rangifer tarandus tarandus)

 

Department for Environment, Food and Rural Affairs

 


 

Monday, April 11, 2016

 

***DECLARATION OF EXTRAORDINARY EMERGENCY DUE TO A FOREIGN ANIMAL DISEASE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION CHRONIC WASTING DISEASE CWD IN THE UNITED STATES AND NORTH AMERICA ?

 


 

 Thursday, April 07, 2016

 

What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016

 

Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008).

 

***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...

 

For the purpose of the qualitative risk assessment developed here it is necessary to estimate the probability that a 30-ml bottle of lure contains urine from an infected deer. This requires an estimate of the proportion of deer herds in the USA which are infected with CWD together with the within herd prevalence.

 

The distribution map of CWD in US shows it is present mainly in central states (Figure 1). However, Virginia in the east of the country has recorded seven recent cases of CWD (Anon 2015a). Some US manufacturers claim to take steps to prevent urine being taken from infected animals eg by sourcing from farms where the deer are randomly tested for CWD (Anon 2015a). However, if disease is already present and testing is not carried out regularly, captive populations are not necessarily disease free (Strausser 2014). Urine-based deer lures have been known to be collected from domestic white-tailed deer herds and therefore there is a recognised risk. This is reflected by 6 US States which have

 

14

 

banned the use of natural deer urine for lures, as the deer urine may be sourced from CWD-endemic areas in the USA as well as from areas free of CWD. For example, the US State of Virginia is banning the use of urine-based deer lures on July 2015 and Vermont from 2016 due to the risk of spread of CWD. Alaska banned their use in 2012 (Anon 2015a). Pennsylvania Game Commission has banned urine-based deer lures and acknowledged that there is no way to detect their use (Strausser 2014). On the basis of unpublished data (J. Manson, Pers. Comm.) it appears that up to 50% of deer herds can be infected with 80-90% of animals infected within some herds.

 

*** It is therefore assumed that probability that a 30-ml bottle of deer urine lure imported from the USA is sources from an infected deer is medium.

 

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 cannot be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the very low tonnage of non-fish origin processed animal proteins that were imported from US into GB.

 

*** Overall, therefore, it is considered there is a greater than negligible risk that (non-ruminant) 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...

 


 

Summary and MORE HERE ;

 

What is the risk of chronic wasting disease being introduced into Great Britain? An updated Qualitative Risk Assessment March 2016

 


 

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

 

31 Jan 2015 at 20:14 GMT

 

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

 

31 Jan 2015 at 20:14 GMT

 

see Singeltary comment ;

 


 

*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***

 

Sunday, March 20, 2016

 

Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission

 


 

 It is clear that the designing scientists must also have shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

it is clear that the designing scientists must have also shared Mr Bradleys surprise at the results because all the dose levels right down to 1 gram triggered infection.

 


 

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle

 

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

 

snip...

 

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

 


 

Monday, April 04, 2016

 

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

 


 

Thursday, March 31, 2016

 

Chronic Wasting Disease CWD TSE Prion Roundup USA April 1, 2016

 


 

Tuesday, March 15, 2016

 

Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated with Pathogens from Produce Grown in Fields Amended with Untreated Biological Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and Information Singeltary Submission

 


 

Friday, April 08, 2016

 

Arkansas AGFC Chronic Wasting Disease CWD TSE Prion Confirms 23 Additional Cases Total At 79 To Date

 


 

Friday, April 01, 2016

 

ARKANSAS CHRONIC WASTING DISEASE CWD TSE PRION CASES EXPLODE BY 27 NEW CASES WITH 50 CASES TOTAL TO DATE

 


 

TEXAS TAHC BREAKS IT'S SILENCE WITH TWO MORE CASES CWD CAPTIVE DEER BRINGING TOTAL TO 10 CAPTIVES REPORTED TO DATE

 

April 1, 2016

 

New CWD Cases Discovered at Captive Deer Breeding Facilities

 

AUSTIN – Two new cases of chronic wasting disease (CWD) in Texas captive deer, including the first confirmed from a live test tonsillar biopsy sample, have been validated. The Texas Parks and Wildlife Department (TPWD) and Texas Animal Health Commission (TAHC) are conducting an epidemiological investigation into these new cases.

 

One case involves a 3 1/2-year-old captive raised white-tailed doe that was born and raised on-site and died on-site of natural causes at a deer breeding facility in Medina County where the disease had not previously been found. Test samples were submitted in compliance with TAHC herd plan requirements.

 

The live test finding is from a 2 ½-year-old captive white-tailed buck in the Uvalde- Medina County deer breeding facility that was the source of a CWD positive white-tailed buck harvested by a hunter from a release site on the same ranch.

 

With these new confirmations, 10 white-tailed deer in or originating from deer breeding facilities have been confirmed positive for CWD in the state since the original detection in June 2015.

 

Tissue samples revealed the presence of CWD prions during testing at the Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) in College Station. The samples were submitted to the National Veterinary Services Laboratory in Ames, Iowa, which validated the suspect findings Friday evening.

 

The disease was first recognized in 1967 in captive mule deer in Colorado. CWD has also been documented in captive and/or free-ranging deer in 24 states and 2 Canadian provinces. In Texas, the disease was first discovered in 2012 in free-ranging mule deer along a remote area of the Hueco Mountains near the Texas-New Mexico border, and last summer was detected in two, separate captive white-tailed deer breeding facilities in Medina and Lavaca counties.

 

CWD among cervids is a progressive, fatal disease that commonly results in altered behavior as a result of microscopic changes made to the brain of affected animals. An animal may carry the disease for years without outward indication, but in the latter stages, signs may include listlessness, lowering of the head, weight loss, repetitive walking in set patterns and a lack of responsiveness. To date there is no evidence that CWD poses a risk to humans or non-cervids. However, as a precaution, the U.S. Centers for Disease Control and the World Health Organization recommend not to consume meat from infected animals.

 

More information on CWD can be found on TPWD’s website, http://www.tpwd.texas.gov/CWD or at the Chronic Wasting Disease Alliance website, http://www.cwd-info.org.

 

More information about the TAHC CWD program may be found at http://www.tahc.state.tx.us/animal_health/cwd/cwd.html

 

###

 


 

>>>One case involves a 3 1/2-year-old captive raised white-tailed doe that was born and raised on-site and died on-site of natural causes at a deer breeding facility in Medina County where the disease had not previously been found. <<<

 

which came first, the chicken or the egg. that would be like you dying from CJD or Asbestosis, yet your death certificate says congestive heart failure for cause of death. you must then get the death certificate changed to read the actual cause of death. ...

 

TEXAS CWD TESTING TOTAL FIGURES ??? anyone’s guess to date. TAHC et al should take up Arkansas reporting of test results to the public and open discussion. ...

 

>>>One case involves a 3 1/2-year-old captive raised white-tailed doe that was born and raised on-site and died on-site of natural causes at a deer breeding facility in Medina County where the disease had not previously been found. <<<

 

which came first, the chicken or the egg. that would be like you dying from CJD or Asbestosis, yet your death certificate says congestive heart failure for cause of death. you must then get the death certificate changed to read the actual cause of death. ...

 

TEXAS CWD TESTING TOTAL FIGURES ??? anyone’s guess to date. TAHC et al should take up Arkansas reporting of test results to the public and open discussion. ...

 

Friday, February 26, 2016

 

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

 


 

Friday, February 05, 2016

 

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

 


 

CWD ROUNDUP

 

Tuesday, March 29, 2016

 

Maryland Department of Natural Resources Five Deer Test Positive for Chronic Wasting Disease ONE OUTSIDE CWD MANAGEMENT ZONE

 


 

Friday, March 18, 2016

 

Michigan confirms additional CWD-positive free-ranging, white-tailed deer, bringing the total to seven

 


 

Wednesday, March 16, 2016

 

Wisconsin CWD sample survey 2015 confirms 290 cases of Chronic Wasting Disease TSE Prion

 


 

Thursday, March 10, 2016

 

WYOMING RIDE EM COWBOY HELICOPTER WRANGLING RAMBO STYLE DEER BULLDOGGING RODEO FOR CWD VIDEO

 

CHRONIC WASTING DISEASE: The Final Epidemic

 


 

Tuesday, March 08, 2016

 

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

 


 

Wednesday, March 02, 2016

 

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

 


 

Sunday, March 06, 2016

 

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

 


 

TEXAS CWD TESTING TOTAL FIGURES ??? anyone’s guess to date. TAHC et al should take up Arkansas reporting of test results to the public and open discussion. ...

 

Friday, February 26, 2016

 

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

 


 

Friday, February 26, 2016

 

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

 


 

Friday, February 05, 2016

 

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

 


 

Tuesday, February 02, 2016

 

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

 


 

Friday, February 05, 2016

 

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

 


 

Friday, January 29, 2016

 

NEBRASKA Three Positives for CWD Found in Recent Testing of Deer

 


 

Friday, November 20, 2015

 

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

 


 

Friday, October 23, 2015

 

Ohio Wildlife Council Passes Rule to Help Monitor CWD

 


 

Wednesday, August 05, 2015

 

Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed cases to date

 


 

Wednesday, February 11, 2015

 

World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with two counts of tampering with evidence

 


 

Thursday, October 23, 2014

 

*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE

 


 

Monday, June 11, 2012

 

*** OHIO Captive deer escapees and non-reporting ***

 


 

Thursday, March 31, 2016

 

Chronic Wasting Disease CWD TSE Prion Roundup USA April 1, 2016

 


 

Friday, February 05, 2016

 

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

 


 

Saturday, February 6, 2016

 

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

 


 

Friday, March 18, 2016 CFSAN

 

Constituent Update: FDA Announces Final Rule on Bovine Spongiform Encephalopathy BSE MAD COW TSE PRION Center for Food Safety and Applied Nutrition - Constituent Update

 


 

Monday, March 28, 2016

 

National Scrapie Eradication Program February 2016 Monthly Report

 


 

*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***

 

Monday, November 16, 2015

 

*** Docket No. APHIS-2007-0127 Scrapie in Sheep and Goats Terry Singeltary Sr. Submission ***

 


 


 

Wednesday, March 2, 2016

 

RANCHO He did not know that they were placing healthy cow heads next to suspect carcasses BSE TSE Prion

 


 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 


 

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

 

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

 

Authors

 

item Comoy, Emmanuel - item Mikol, Jacqueline - item Luccantoni-Freire, Sophie - item Correia, Evelyne - item Lescoutra-Etchegaray, Nathalie - item Durand, Valérie - item Dehen, Capucine - item Andreoletti, Olivier - item Casalone, Cristina - item Richt, Juergen item Greenlee, Justin item Baron, Thierry - item Benestad, Sylvie - item Hills, Bob - item Brown, Paul - item Deslys, Jean-Philippe -

 

Submitted to: Scientific Reports Publication Type: Peer Reviewed Journal Publication Acceptance Date: May 28, 2015 Publication Date: June 30, 2015 Citation: Comoy, E.E., Mikol, J., Luccantoni-Freire, S., Correia, E., Lescoutra-Etchegaray, N., Durand, V., Dehen, C., Andreoletti, O., Casalone, C., Richt, J.A., Greenlee, J.J., Baron, T., Benestad, S., Brown, P., Deslys, J. 2015. Transmission of scrapie prions to primate after an extended silent incubation period. Scientific Reports. 5:11573.

 

Interpretive Summary: The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie.

 

***After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease.

 

***Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy.

 

***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans.

 

***This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

Technical Abstract:

 

Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health.

 

***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.

 


 

***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***

 

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

 

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan

 

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

 

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

 

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice,

 

***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.

 

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

 

PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS

 

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

 

O18

 

Zoonotic Potential of CWD Prions

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 


 

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

 

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

 

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

 

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.

 


 


 

*** 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).***

 


 

*** 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.

 


 

now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”

 

From: TSS (216-119-163-189.ipset45.wt.net)

 

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

 

Date: September 30, 2002 at 7:06 am PST

 

From: "Belay, Ermias"

 

To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

 

Sent: Monday, September 30, 2002 9:22 AM

 

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Dear Sir/Madam,

 

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

 

Ermias Belay, M.D. Centers for Disease Control and Prevention

 

-----Original Message-----

 

From: Sent: Sunday, September 29, 2002 10:15 AM

 

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

 

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

 

Thursday, April 03, 2008

 

A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.

 

snip...

 

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

 

snip... full text ;

 


 

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

 

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

 


 

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

 

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

 


 

Envt.07:

 

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

 

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

 


 

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

 

Abstract The emergence of chronic wasting disease (CWD) in deer and elk in an increasingly wide geographic area, as well as the interspecies transmission of bovine spongiform encephalopathy to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic potential of CWD. Because meat consumption is the most likely means of exposure, it is important to determine whether skeletal muscle of diseased cervids contains prion infectivity. Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.

 


 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

snip...

 

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

 

snip...

 

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

 

snip...

 

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

 

snip...see full report ;

 


 

CJD9/10022

 

October 1994

 

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

 

Dear Mr Elmhirst,

 

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

 

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

 

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

 

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

 

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

 

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

 


 

*** 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).***

 


 

PRION 2015 CONFERENCE USA

 

***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE. ***

 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***

 

P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification

 

Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan

 

To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).

 

Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.

 

Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice,

 

***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.

 

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

 


 


 

PL1

 

Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.

 

Claudio Soto

 

Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.

 

Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.

 

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

 

***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

 

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

 

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.

 


 

see ;

 

Potential role of soil properties in the spread of CWD in western Canada

 

Alsu Kuznetsova, Debbie McKenzie, Pamela Banser, Tariq Siddique & Judd M. Aiken

 


 

Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted Infectivity from Complex Solutions (BASICS)

 

Estimating Prion Adsorption Capacity of Soil by BioAssay of Subtracted Infectivity from Complex Solutions (BASICS) A. Christy Wyckoff, Krista L. Lockwood, Crystal Meyerett-Reid, Brady A. Michel, Heather Bender, Kurt C. VerCauteren, Mark D. Zabel PLOS x Published: March 4, 2013 http://dx.doi.org/10.1371/journal.pone.0058630

 


 

Behavior of Prions in the Environment: Implications for Prion Biology

 

Shannon L. Bartelt-Hunt1*, Jason C. Bartz2*

 


 

Prion Amplification and Hierarchical Bayesian Modeling Refine Detection of Prion Infection A. Christy Wyckoff1, 2 n1 , Nathan Galloway3 n1 , Crystal Meyerett-Reid1 , Jenny Powers4 , Terry Spraker1 , Ryan J. Monello4 , Bruce Pulford1 , Margaret Wild4 , Michael Antolin3 , Kurt VerCauteren2 […] & Mark Zabel1 - Show fewer authors Scientific Reports 5, Article number: 8358 (2015) doi:10.1038/srep08358 Download Citation

 

Molecular ecology Proteins Statistics Received: 27 June 2014

 


 

CELL REPORTS

 

Report

 

Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions

 


 

PRION UPDATE VIA VEGETABLE PLANTS FROM THE SOIL

 

 56. Members considered that there is no evidence that crops grown on the land which received composted excreta from BSE-challenged animals pose a TSE risk to humans or animals. One member suggested that, as some of these animals are orally challenged with high doses of BSE-infected materials, and the distribution of infectivity in the digestive system is not completely understood, it might be premature to conclude that there is no infective agent in the manure.

 

Furthermore, an unpublished study had indicated low level absorption of PrP from soil by tomato plants although it should be noted that this study had not been repeated. Details of this work would be sent to the SEAC Secretary. Dr Matthews explained that most of the manure from animals challenged with high doses of BSE had already been composted and used for coppicing. Members agreed that the risks from disposal of residual manure from experimental animals would be much less than historic risks of on farm contamination from naturally infected animals at the height of the BSE epidemic. ...SNIP...END

 


 

SRM are certain cattle tissues capable of transmitting BSE. There is no human health risk assessment to indicate the absence of human health concerns associated with use of composted SRM domestically. To date, scientific evidence has not been able to demonstrate that composting destroys prions. Although domestic use would pose a negligible risk to livestock, there is a potential risk to humans via direct ingestion of the compost or of compost particles adhered to skin or plant material (e.g. carrots). Another potential route of exposure is by ingestion of prions that have been taken up by plants. It has been proven that bacteria are readily taken up by some plants (e.g. E. coli in lettuce) thus the uptake of prions by plants cannot be precluded or dismissed at this time. As a science-based regulator, the CFIA cannot change the policy on this issue without a risk assessment demonstrating that the use of composted SRM poses an acceptable risk to humans.

 


 

The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences & Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s Hospital London and William Harvey Hospital Ashford April 1999

 

 snip...

 

 88. Natural decay: Infectivity persists for a long time in the environment. A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep, after they had grazed on land which had previously been grazed by scrapie-infected sheep, even though the land had lain fallow for three years before the healthy sheep were introduced. Brown also quoted an early experiment of his own (1991), where he had buried scrapie-infected hamster brain and found that he could still detect substantial infectivity three years later near where the material had been placed. 89. Potential environmental routes of infection: Brown discusses the various possible scenarios, including surface or subsurface deposits of TSE-contaminated material, which would lead to a build-up of long-lasting infectivity. Birds feeding on animal remains (such as gulls visiting landfill sites) could disperse infectivity. Other animals could become vectors if they later grazed on contaminated land. "A further question concerns the risk of contamination of the surrounding water table or even surface water channels, by effluents and discarded solid wastes from treatment plants. A reasonable conclusion is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge numbers of uncertainties and assumptions that attend each stage of the disposal process". These comments, from a long established authority on TSEs, closely echo my own statements which were based on a recent examination of all the evidence. 90. Susceptibility: It is likely that transmissibility of the disease to humans in vivo is probably low, because sheep that die from scrapie and cattle that die from BSE are probably a small fraction of the exposed population. However, no definitive data are available.

 

 91. Recommendations for disposal procedures: Brown recommends that material which is actually or potentially contaminated by BSE should be: 1) exposed to caustic soda; 2) thoroughly incinerated under carefully inspected conditions; and 3) that any residue should be buried in landfill, to a depth which would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source.

 

 92. This review and recommendations from Brown have particular importance. Brown is one of the world's foremost authorities on TSEs and is a senior researcher in the US National Institutes of Health (NIH). It is notable that such a respected authority is forthright in acknowledging the existence of potential risks, and in identifying the appropriate measures necessary to safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical distribution of variant CJD in the UK (excluding Northern Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41 (02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD (variant CJD) might live closer to rendering factories than would be expected by chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were studied. The incubation period of vCJD is not known but by analogy with other human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure to rendering products, such exposure might plausibly have occurred 8-10 years before the onset of symptoms. The authors were able to obtain the addresses of all rendering plants in the UK which were in production in 1988. For each case of vCJD, the distance from the place of residence on 1st January 1998 to the nearest rendering plant was calculated

 

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 Friday, February 08, 2013

 

*** Behavior of Prions in the Environment: Implications for Prion Biology

 


 


 

 Wednesday, December 16, 2015

 

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

 

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

 

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

 

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

 

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

 

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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 ***

 


 

Circulation of prions within dust on a scrapie affected farm

 

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

 

Abstract

 

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

 

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Discussion

 

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

 

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

 


 

 kind regards, terry

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