Chronic Wasting Disease

Long kills controversial fenced hunting bill INDIANA

2012-02-03T16:38:00.002-06:00

Long kills controversial fenced hunting bill

February 1, 2012 | Filed under: Issues,Top stories | Posted by: Lesley Weidenbener

By Lesley Weidenbener

The Statehouse File

INDIANAPOLIS – An effort to legalize fenced deer hunting is dead for this session.

Senate President Pro Tem David Long, R-Fort Wayne, said he will use a procedural move to kill House Bill 1265 and won’t allow it to be considered in the Senate in the 2012 session.

“I think it is a terrible bill,” Long said. “It’s something that first of all it’s not real hunting. It fences in these animals.”

Fenced deer preserves allow hunters to pay money – sometimes thousands of dollars – to shoot deer that are sometimes bred to have larger antlers. Proponents say the preserves are large enough to give the deer plenty of opportunity to escape but critics say they violate the fair chase doctrine that dictates ethical hunting.

In 2006, the Department of Natural Resources passed rules – signed by Gov. Mitch Daniels – that made the preserves illegal. But a lawsuit essentially stopped the enforcement. The suit is still pending and four preserves are operating.

HB 1265 – approved 56-40 by the House this week – would have legalized the preserves and created a licensing process for new businesses.

The bill’s author, Rep. Matt Ubelhor, R-Linton, said the preserves and the farms that provide them with deer already have a $50 million annual economic impact on the state. Ubelhor says that could increase if more preserves are permitted to operate.

But Long said Wednesday he prefers to maintain the status quo.

“The bill as it currently exists would open it wide open,” Long said. “I thought we had an understanding (in the General Assembly) that we weren’t going down that path again.”

Lesley Weidenbener is managing editor of TheStatehouseFile.com, a news website powered by Franklin College journalism students.

http://thestatehousefile.com/long-kills-controversial-fenced-hunting-bill/2937/

Move to expand Ind. fenced deer hunting shelved

1:38 PM, Feb. 2, 2012

INDIANAPOLIS (WTW) — An attempt to legalize hunting deer and elk that are kept inside high fences has been shelved by the state Senate's leader.

The House voted 56-40 this week to approve a bill allowing the fenced hunting, but Senate President Pro Tem David Long said he thought it was a "terrible idea" and will use a procedural move to kill the proposal for this year's legislative session.

The bill would have legalized four existing shooting preserves that are now operating under an injunction issued in a lawsuit against state Department of Natural Resources rules adopted in 2006 to ban captive hunting. The bill also would have allowed more similar preserves to operate.

Long, R-Fort Wayne, said Wednesday that he believed legislators reached a tacit agreement several years ago not to intercede.

"It's not real hunting," he said. "It fences in these animals. Almost every real hunter that I talk to says it's a terrible idea and they don't support it."

Supporters say legalizing the fenced hunting preserves would be an economic boon and would provide Indiana's 400 deer farms with a place to sell their animals.

Rick Miller, president of the Indiana Deer and Elk Farmers Association, told The Journal Gazette in Fort Wayne (http://bit.ly/z2oSiH) that deer farmers are now selling their deer out of state, but he expects that chronic wasting disease, which is fatal to deer and elk, will eventually hit Indiana and force an end to such sales. He said Indiana's existing preserves wouldn't be enough to keep the farms in business.

"They're killing us," Miller said of the Senate action. "We are begging lawmakers to help us put it to bed one way or another."

Eleven states have full bans on captive hunting and 15 states have partial prohibitions. States surrounding Indiana do not have a ban, and shooting preserves and deer farming have boomed there.

Bill sponsor Rep. Matt Ubelhor, R-Bloomfield, said Indiana's existing preserves are large — akin to 80 city blocks — and allow deer the opportunity to elude hunters.

"It's certainly fair chase," Ubelhor said.

___

Copyright 2012 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

http://www.indystar.com/usatoday/article/38486835?odyssey=mod

Senate President Pro Tem David Long, R-Fort Wayne, said he will use a procedural move to kill House Bill 1265 and won’t allow it to be considered in the Senate in the 2012 session.

“I think it is a terrible bill,” Long said. “It’s something that first of all it’s not real hunting. It fences in these animals.”

BRILLIANT MOVE BY Senate President Pro Tem David Long, R-Fort Wayne, even though he is a Republican ;-)

I could not agree more. ...tss

With CWD spreading, and CJD rising in the USA and Canada, with rise in pcsCJD i.e. pending classification sporadic CJD i.e. they don’t know what or where in the world this strain came from, and refuse to investigate further, ignoring updated science that not only has CWD mutated into a second strain i.e. Wisconsin Strain of CWD, and the fact that many scientist around the globe are very concerned for the potential of CWD being a zoonosis disease. Also ignoring recent updated science that shows a link between atypical BSE and atypical Scrapie with sporadic CJD. All this moved me to dig a bit deeper into these game farms that raise deer and or elk to enhance their natural size and antler spread and circumference i.e. farmed ‘straw’ bred bucks. in my opinion, there is no ethics in hunter farmed 'straw' bred bucks. I wanted to find out just how dangerous these game farms are to the wild, considering for the captives, most are nothing more than a petri dish for disease i.e. CWD.

What I found was interested, and concerning. the close proximity from cwd infected game farm to cwd infected game farm, and the CWD infection in the wild surrounding those said game farms. I wrote the Wisconsin DNR and division of animal health asking ;

‘‘Could you please tell me where I can locate the information on each CWD infected game farm in Wisconsin (all nine to date), dates they became infected, infection rate, etc. ???’’

They were very kind in replying and supplied the following information ;

Friday, February 03, 2012

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

http://chronic-wasting-disease.blogspot.com/2012/02/wisconsin-farm-raised-deer-farms-and.html

From: Terry S. Singeltary Sr.

Sent: Friday, January 27, 2012 2:06 PM

To: h57@in.gov

Cc: h51@in.gov; h75@in.gov; h53@in.gov; h46@in.gov; h30@in.gov; h54@in.gov; h62@in.gov; h69@in.gov; h64@in.gov; h17@in.gov; h42@in.gov; h56@in.gov

Subject: re-Indiana game farming cervids and CHRONIC WASTING DISEASE THERE FROM

From: Terry S. Singeltary Sr.

Sent: Friday, January 27, 2012 1:56 PM

To: info@indianawildlife.org

Cc: dnrwebmaster@dnr.IN.gov; s1@iga.in.gov; s4@iga.in.gov; h57@in.gov; simpson@indianawildlife.org; twardy@indianawildlife.org; watson@indianawildlife.org

Subject: Re: re-Indiana game farming cervids and CHRONIC WASTING DISEASE THERE FROM House Bill 1265

snip...

From: Terry S. Singeltary Sr.

Sent: Friday, January 27, 2012 2:06 PM

To: h57@in.gov

Cc: h51@in.gov; h75@in.gov; h53@in.gov; h46@in.gov; h30@in.gov; h54@in.gov; h62@in.gov; h69@in.gov; h64@in.gov; h17@in.gov; h42@in.gov; h56@in.gov

Subject: re-Indiana game farming cervids and CHRONIC WASTING DISEASE THERE FROM

From: Terry S. Singeltary Sr.

Sent: Friday, January 27, 2012 1:56 PM

To: info@indianawildlife.org

Cc: dnrwebmaster@dnr.IN.gov; s1@iga.in.gov; s4@iga.in.gov; h57@in.gov; simpson@indianawildlife.org; twardy@indianawildlife.org; watson@indianawildlife.org

Subject: Re: re-Indiana game farming cervids and CHRONIC WASTING DISEASE THERE FROM House Bill 1265

SEE FULL TEXT ;

http://www.prpsc.proboards.com/index.cgi?board=prpsccwd&action=display&thread=2

http://www.prpsc.proboards.com/index.cgi

Comment from Terry Singeltary Document ID: APHIS-2011-0032-0002Document

Type: Public Submission

This is comment on Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals:

Chronic Wasting Disease Herd Certification Program Docket ID: APHIS-2011-0032RIN:

Topics: No Topics

associated with this document View Document: Show Details Document Subtype:

Public Comment Status: Posted Received Date: January 24 2012, at 12:00 AM Eastern Standard Time Date Posted: January 25 2012, at 12:00 AM Eastern Standard Time Comment Start Date: January 24 2012, at 12:00 AM Eastern Standard Time Comment Due Date: March 26 2012, at 11:59 PM Eastern Daylight

Time Tracking Number: XXXXXXXXX

First Name: Terry

Middle Name: S.

Last Name: Singeltary

City: Bacliff

Country: United States State or Province: TX

Organization Name: LAYPERSON

Submitter's Representative: CJD TSE PRION VICTIMS

Comment: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001) I believe that any voluntary program for CWD free herd certification from game farms will be futile, as was the partial and voluntary mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary ban. Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin having documented 9 CWD infected game farms, with one having the highest CWD infection rate in the world, 80% CWD infection rate. I believe that all game farms should be SHUT DOWN PERMANENTLY. CWD TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. you cannot cook the CWD 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 CWD TSE Prion agent will survive in the environment for years, if not decades. you can bury it and it will not go away. CWD 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.

Tuesday, December 20,

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

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

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

additional data submission ; Name: Terry S. Singeltary

Address: Bacliff, TX,

Submitter's Representative: CJD TSE PRION VICTIMS

Organization: LAYPERSON

-----------------------------------------------------

General Comment Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001)

I believe that any voluntary program for CWD free herd certification from game farms will be futile, as was the partial and voluntary mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary ban.

Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin having documented 9 CWD infected game farms, with one having the highest CWD infection rate in the world, 80% CWD infection rate.

I believe that all game farms should be SHUT DOWN PERMANENTLY.

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

you cannot cook the CWD 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 CWD TSE Prion agent will survive in the environment for years, if not decades.

you can bury it and it will not go away.

CWD 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.

Tuesday, December 20, 2011

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

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

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

http://www.regulations.gov/#!documentDetail;D=APHIS-2011-0032-0002

=======================END...TSS=====================

Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al

2012-02-03T11:49:00.000-06:00

Greetings Wisconsin hunters et al,

With CWD spreading, and CJD rising in the USA and Canada, with rise in pcsCJD i.e. pending classification sporadic CJD i.e. they don’t know what or where in the world this strain came from, and refuse to investigate further, ignoring updated science that not only has CWD mutated into a second strain i.e. Wisconsin Strain of CWD, and the fact that many scientist around the globe are very concerned for the potential of CWD being a zoonosis disease. Also ignoring recent updated science that shows a link between atypical BSE and atypical Scrapie with sporadic CJD. All this moved me to dig a bit deeper into these game farms that raise deer and or elk to enhance their natural size and antler spread and circumference i.e. farmed ‘straw’ bred bucks. in my opinion, there is no ethics in hunter farmed 'straw' bred bucks. I wanted to find out just how dangerous these game farms are to the wild, considering for the captives, most are nothing more than a petri dish for disease i.e. CWD.

What I found was interested, and concerning. the close proximity from cwd infected game farm to cwd infected game farm, and the CWD infection in the wild surrounding those said game farms.

I wrote the Wisconsin DNR and division of animal health asking ;

‘‘Could you please tell me where I can locate the information on each CWD infected game farm in Wisconsin (all nine to date), dates they became infected, infection rate, etc. ???’’

They were very kind in replying and supplied the following information ;

Farm CWD first Detected Incidence

Hall 09-04-2002 82 1 hunted in 2002, 6 hunted in 2003, 10 hunted in 2004, 4 in breeding herd 2005, 61 in breeding herd 2006 (60 of 76 at depop)

Hirschboeck 09-20-2002 6 2 in 2002 & 4 of 122 at depopulation

Sperber 03-05-2003 1 197 remaining depoped

Hetzel 10-03-2003 1 2 remaining depoped

Breber 05-01-2004 1 15 remaining depoped

Kuhnke 07-28-2004 3 1 in July, 1 in Aug, 1 of 23 at depop

Christensen 01-07-2005 2 1 in 2007, owner killed and buried remaining 33

Landwer 09-22-2008 2 1 of 66 at depop

Hookstead 10-01-2008 1 2 remaining depoped

---------

99 total positives

Dr Bourie

CWD Program Manager

Div of Animal Health

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

From: Ryan, Tamara M - DNR

Sent: Wednesday, February 01, 2012 4:11 PM

To: Terry S. Singeltary Sr. ; Bourie, Richard D - DATCP Cc: Thiede, Kurt A - DNR ; Ross, Laurie J - DNR ; Hauge, Tom M - DNR Subject: RE: Singeltary request re cwd game farms Wisconsin

Hello Terry –

Thanks for checking in. Please know that attempts have been made to respond to your request. Dr. Bourie of DATCP responded on Monday which was the same date your email was forwarded to him. However, I received an email from him advising that his email communications to your email address were bouncing back & he requested additional contact information. I looked into this and determined we only had your email address. I’m certain that he will be getting in contact with you once he sees this email chain. In the interim, please respond to all with your phone number & address just in case.

Thank you.

P Tami Ryan

Wildlife Health Section Chief Bureau of Wildlife Management Wisconsin Department of Natural Resources Phone: 608-266-3143 Fax: 608-267-7857 Email: tamara.ryan@wi.gov

From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]

Sent: Wednesday, February 01, 2012 3:52 PM

To: Ryan, Tamara M - DNR; Bourie, Richard D - DATCP Cc: Thiede, Kurt A - DNR; Ross, Laurie J - DNR; Hauge, Tom M - DNR

Subject: Re: Singeltary request re cwd game farms Wisconsin

Greetings again WDNR et al,

I have still yet to get any answer about my questions below.

‘‘Could you please tell me where I can locate the information on each CWD infected game farm in Wisconsin (all nine to date), dates they became infected, infection rate, etc. ???’’

this is important information, and the public should be able to acquire this information, you would think ?

thank you,

kind regards,

terry

From: Ryan, Tamara M - DNR

Sent: Monday, January 30, 2012 8:10 AM

To: Bourie, Richard D - DATCP

Cc: Thiede, Kurt A - DNR ; Ross, Laurie J - DNR ; Hauge, Tom M - DNR ; flounder9@verizon.net

Subject: FW: Singeltary request re cwd game farms Wisconsin

Mr. Singeltary – This information can be obtained from the Wisconsin Department of Agriculture, Trade and Consumer Protection (DATCP). I’ve copied Dr. Bourie from DATCP who is the best person to respond to your request.

Dr. Bourie – Please respond to Mr. Singeltary on the email request below. Thank you.

Tami

P Tami Ryan Wildlife Health Section Chief Bureau of Wildlife Management Wisconsin Department of Natural Resources Phone: 608-266-3143 Fax: 608-267-7857 Email: tamara.ryan@wi.gov

--------------------------------------------------------------------------------

From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net]

Sent: Wednesday, January 25, 2012 02:15 PM

To: Ross, Laurie J - DNR Subject: cwd game farms Wisconsin

Greetings WDNR et al,

Could you please tell me where I can locate the information on each CWD infected game farm in Wisconsin (all nine to date), dates they became infected, infection rate, etc. ???

many thanks,

kind regards,

terry

===============end...TSS===============

strange this comes out after two weeks of me asking questions ???

Bourie and Deer Farmers Weather the CWD Storm

By lsiekmann | Published: February 2, 2012

http://wfbf.com/ag-newswire/bourie-and-deer-farmers-weather-the-cwd-storm/

HOW could one call 9 infected CWD game farms, weathering the storm ???

MOST disturbing about the 9 CWD infected game farms in Wisconsin in report above, was the ‘Christensen’ farm, where the ‘owner killed and buried remaining 33’ deer. what’s disturbing to me is not the fact that 33 potentially CWD infected deer were buried, apparently before any CWD testing was done on those remaining 33 suspect CWD exposed deer. that could be one heck of a hot spot for years, decades to come. seems the officials could have dug those deer up, incinerated the remains, then dug up the soil around that pit where all those dead, suspect deer were buried at, and then treat all that soil some how. seems the ‘Christensen’ farm was trying to hide something. ...just my take...tss

A review of those 9 CWD infected game farms in Wisconsin ;

Hirschboeck 09-20-2002 6 2 in 2002 & 4 of 122 at depopulation

Wisconsin : DNR Hunting Deer That Escaped From Farm Now Under Quarantine

Date: October 24, 2002 Source: Milwaukee Journal Sentinel

Contacts: Lee Bergquist lbergquist@journalsentinel.com

State officials said Wednesday they recently learned that several deer escaped in March from a northern Walworth County deer farm that is known to have harbored at least one deer with chronic wasting disease.

The DNR has dispatched wardens to a game farm owned by James Hirschboeck of the Town of Troy in the hope of finding and killing the deer, which are believed to be roaming in the wild.

Hirschboeck is also under investigation, accused of trying to sell deer that had been quarantined and could not be moved, an affidavit filed for a search warrant in Dane County says.

The affidavit also says Hirschboeck is suspected in the past four weeks of trying to entice another deer farm operator with whom he had done business to falsify records.

In an interview, Hirschboeck denied any wrongdoing. "None of that is true," he said.

Warden Karl Brooks said the escapes of "several" deer took place in March - shortly after the fatal deer disease was first reported in the wild deer population near Mount Horeb in Dane County.

This is the first admission by state officials that deer have escaped from a game farm tainted by the disease.

The escaped deer are believed to have tags in their ears. Neighbors have reported seeing deer with ear tags near Hirschboeck's 80-acre farm, Brooks said.

In addition to efforts to kill the tagged deer, Brooks said, an estimated 500 deer that will be killed and tested this hunting season in Walworth County will help determine whether the fatal brain disease has moved to a new part of the state.

Officials Monitor Farm

Hirschboeck's farm came under scrutiny by the DNR after it was discovered that he bought deer from another Walworth County deer farm that is suspected to have sold a deer to a third farm in Portage County that later tested positive for the disease. That buck, sold to deer farmer Stan Hall, tested positive for the disease in September.

The buck was the first of two captive deer in Wisconsin to have tested positive. So far, 40 wild deer from a 411-square-mile region of Dane, Iowa and Sauk counties have been found with the disease.

The first finding in captive deer last month prompted the state agriculture department to quarantine the two farms in Walworth County and a third farm in Portage County. A fourth game farm in Dane County has been quarantined, as well.

On Oct. 16, it was learned that a deer on the Hirschboeck farm also tested positive after state investigators found deer there appearing to be in poor health.

As the DNR began investigating Hirschboeck's business dealings, they recently learned that some of his deer had escaped. Brooks said the DNR believes the deer that tested positive on his farm was there long enough to have intermingled with the escaped deer.

"This is extremely significant because it confirms our fears that CWD might not be as easily contained as we initially had hoped," Brooks said.

Source Uncertain

Wisconsin officials are not sure how the disease showed up in Wisconsin, but one theory points to the possibility of an infected game farm. Game farms routinely moved deer in and out of the state until the agriculture department effectively banned such shipments in March.

When the presence of chronic wasting disease was reported Feb. 28, it was the first time deer with chronic wasting disease - captive or wild - had been found east of the Mississippi River.

The finding has thrust deer hunting in Wisconsin into tumult as hunters wonder how widely the disease has spread and whether venison is safe to eat. One effect: License sales are down about 23% from the same time last year.

The DNR has said it believed the disease is contained in and around the 411-square-mile region, where it wants to kill as many as 25,000 deer this hunting season.

Experts also have indicated that venison should be safe to eat, and as recently as last week, Dennis Maki, an infectious disease expert at the University of Wisconsin-Madison, said finding the abnormal protein that is believed to cause the disease in meat was remote.

The World Health Organization advises people not to eat any part of a deer suspected of having the disease or the brain, eyes, spleen, tonsils, lymph nodes or spinal cord of any deer.

As part of its investigation, the DNR said that Hirschboeck:

* Asked Hall to alter his deer farm records twice in the past four weeks. * Tried to convince another game farm operator, Michael E. Bischel of Helenville in Jefferson County, to subvert the quarantine. Bischel told the DNR that Hirschboeck suggested that he buy a large buck from Hirschboeck, kill it, bind its front and back hooves, and then saw off its antlers so wardens would not recognize it.

Hirschboeck denied both allegations and said he has cooperated fully with the DNR and the agriculture department.

* Sold six does to Bischel in January but did not provide any receipts. Hirschboeck said he sold deer to Bischel but was never paid. Bischel could not be reached for comment. * Was not registered to operate a game farm in 2001 and faces forfeitures totaling $1,033. * Was issued five citations totaling $1,002.50 for feeding wild game and failing to cleaning up the feed after being ordered to do so.

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

436 deer have escaped from farms to wild; State finds violations, lax record keeping at many sites, report says

March 19, 2003 Milwaukee Journal-Sentinel (Wisconsin) by Lee Bergquist lbergquist@journalsentinel.com

A state inspection of private deer farms, prompted by the discovery of chronic wasting disease, found that 436 white-tailed deer escaped into the wild, officials said Tuesday. The Department of Natural Resources found that captive deer have escaped from one-third of the state's 550 deer farms over the lifetime of the operations. The agency also uncovered hundreds of violations and has sought a total of 60 citations or charges against deer farm operators.

These and other findings come as state officials say they are still no closer to understanding how the fatal deer disease got to Wisconsin.

Since the discovery a little more than a year ago, chronic wasting disease has thrown both deer hunting and management of Wisconsin's 1.4 million deer herd into tumult. Fewer hunters went into the woods last year, and a booming deer population has the DNR worried that the number of whitetails could grow out of control.

Tuesday's findings were presented to the state Department of Agriculture, Trade and Consumer Protection. The DNR had regulated deer farms, but the authority was transferred to the Agriculture Department on Jan. 1. Now agriculture regulators oversee elk, deer and other captive cervids.

Stricter regulations -- and closer attention to the operations of game farms -- should cut down on future violations, officials from the two agencies said. Tougher reporting requirements also will help authorities keep better track of the movement of animals, they said.

Permanent rules take effect in June, and include tighter controls on moving animals and requiring the reporting of escaped animals within 48 hours. There will be mandatory testing of every deer age 16 months or older that dies.

Almost from the start of the state's battle against chronic wasting disease, game farm operators came under scrutiny because their business involves the buying and selling of captive deer and elk across state lines. When the disease was first discovered here Feb. 28, 2002, Wisconsin became the first state to have the disease east of the Mississippi River.

A representative of the deer industry said Tuesday that the DNR is trying to shift blame for chronic wasting disease to his industry.

"The state of Wisconsin has spent a year chasing chronic wasting disease, and they have made zero progress," said Gary Nelson, president of Whitetails of Wisconsin. "In the past, they have essentially collected our fees and ignored us. Now that they have discovered CWD, they are looking for someone to blame."

A DNR representative agreed that the agency could have done a better job keeping tabs on deer farms.

"We're not pointing fingers," said Karl Brooks, a conservation warden with the DNR. "But two things that we know for sure is that there is CWD in the wild deer population, and we have found CWD on game farms."

CWD found on 2 farms

Seven deer have tested positive for the disease on game farms -- one on a Portage County farm and six on a Walworth County farm -- since the disease was discovered in three wild deer killed near Mount Horeb in western Dane County. One deer that tested positive on the Walworth County farm escaped and roamed free for six months.

Regulations have only begun to catch up to the captive deer industry, and "unfortunately, it took CWD to get us there," said agriculture secretary Rod Nilsestuen at a news briefing in Madison.

As the DNR prepared to hand over authority for overseeing game farms to the agriculture department, it sent 209 conservation wardens to 550 farms to collect information, attempt to pinpoint the source of the disease and to learn whether other deer had been exposed to it.

The audit found that most farms were in compliance, but the DNR found many violations and instances of poor record keeping. Also in numerous instances, fences did not stop wild and captive deer from intermingling.

At least 227 farms conducted part of their business on a cash basis, making it hard to track animal movement with financial records.

For example, both the Internal Revenue Service and the state Department of Revenue have been contacted about a deer farm near Wild Rose in Waushara County that is suspected of selling six large bucks for $45,000 in cash and not using live deer shipping tags as required.

The DNR found that game farm operators have more deer in captivity than their records show, which is "due in part because the owners of a number of large deer farm operations were unable to accurately count the number of deer within their fences," the audit found.

Hundreds of deer escape

The DNR found a total of 671 deer that escaped farms -- 436 of which were never found -- because of storm-damaged fences, gates being left open or the animals jumping over or through fences.

In one example in Kewaunee County, a deer farmer's fence was knocked down in a summer storm. Ten deer escaped, and the farmer told the DNR he had no intention of trying to reclaim them. The DNR found five of the deer, killed them and cited the farmer for violation of a regulation related to fencing.

Another deer farmer near Mishicot, in Manitowoc County, released all nine of his whitetails last summer after he believed the discovery of chronic wasting disease was going to drive down the market for captive deer.

The DNR found 24 instances of unlicensed deer farms and issued 19 citations.

===============end...tss===============

Sperber 03-05-2003 1 197 remaining depoped

Wisconsin : Diseased Elk Found in Manitowoc County

Date: March 25, 2003 Source: Milwaukee Journal Sentinel

Contacts: Dennis Chaptman dchaptman@journalsentinel.com

Game-farm animal is first ill non-deer discovered here

Madison - Chronic wasting disease has been found in a farm-raised elk in Manitowoc County, marking the first time in Wisconsin that the ailment has been found in an animal other than a deer, state officials said Tuesday.

A 6-year-old female elk, one of 20 imported by Valders elk farmer Eugene Sperber from Stearns County, Minn., tested positive for the the fatal brain disease after dying in a fight with another elk.

Sperber's herd was quarantined by state agriculture officials in September, when state animal health officials discovered that it may have been exposed to the disease, which has been found in the state's white-tailed deer population.

The Minnesota Board of Animal Health reported in August that an elk from an Aitkin County farm in northern Minnesota tested positive for the disease. That animal had also spent time on two other farms, including the one in Stearns County.

That prompted Wisconsin officials to track other animals from those farms that may have entered Wisconsin game farms. They found 32 animals on six farms, and all were quarantined, including those on Sperber's farm.

Sperber, who could not be reached for comment Tuesday, imported the 20 elk in December 2000 and January 2001.

One of the imported elk died earlier and was not tested for the disease, and all of the remaining 18 imported elk were killed for testing Friday, before the National Veterinary Services Laboratory in Ames, Iowa, reported Monday that one elk tested positive for the disease.

Test results on the other animals are pending, said Donna Gilson, a spokeswoman for the state agriculture department.

The fate of Stearns' other 180 elk, which did not come from Minnesota but are under quarantine, has not been decided.

"We're concerned for the deer and elk industry, and for this particular farmer," Gilson said. "It's a really tough situation to be in after a year that's been difficult for deer and elk farmers in general. It's been hard for them economically and emotionally."

First in the region

Tuesday's news marked the first time that chronic wasting disease has been discovered in the northeastern part of the state. A total of 80 diseased deer have been found in Dane, Iowa, Sauk and Richland counties; and seven infected deer were discovered on game farms in Walworth and Portage counties.

Sarah Shapiro Hurley, a Department of Natural Resources veterinarian, said wildlife officials are monitoring the situation in Manitowoc County closely, but don't believe it poses a threat to the deer population there.

"Free-ranging and captive animals do have areas of interface, but we don't have any reason to believe that we have anything going on in the wild herd that is connected with that situation in the captive herd," she said.

DNR and state agriculture officials will continue to evaluate the case and monitor information from Manitowoc County, Hurley added. There were no immediate plans to shoot and test any more wild deer in response to the latest finding, she said.

"We took a very adequate sample in Manitowoc County this fall," she said, referring to the more than 200 samples - none of them showing infection - taken during the annual hunt.

Game farms under scrutiny

Wisconsin imposed emergency restrictions on moving animals to and from game farms in April 2002 to curb the spread of the disease. Chronic wasting disease attacks the brains of the animals, causing them to become emaciated, act abnormally and eventually die.

Dan Gunderson, spokesman for the Wisconsin Commercial Elk and Deer Farmers Association, said the discovery is a difficult one for the Sperbers.

"This is not only a financial loss, but it's almost like losing part of your family, and the loss is taken personally," said Gunderson, in a telephone interview after he visited the farm.

Gunderson said the discovery also shows that farmers, working in tandem with state agriculture officials, have established an effective monitoring plan.

"It's a bad-news, good-news story," he said. "All of their elk, even though they didn't all come from Minnesota, are quarantined until 2006. It's a business tragedy, but the good news is the system under which the department of agriculture is regulating it works."

Gilson said agency officials were not surprised that the disease turned up in a farm-raised elk here, especially considering the animal's history in Minnesota.

"It's been primarily a disease of elk out west and, in the wild, in mule deer, but on farms it's been an elk disease there," she said. "We weren't as surprised as we were disappointed."

Gunderson said the finding means that farmers need to be watchful and keep working with state officials.

Gilson added that animal health investigators now will attempt to trace the movements of elk from the Valders farm to other locations, she added.

"The DNR found chronic wasting disease because it went looking for it," she said.

==============================end...tss==========================

Hetzel 10-03-2003 1 2 remaining depoped

Wisconsin : Whitetail On Sauk County Farm Tests Positive For CWD

Date: October 21, 2003 Source: Wisconsin Department of Agriculture, Trade and Consumer Protection

Contacts: Donna Gilson 608-224-5130

MADISON -- A whitetail deer from a Sauk County farm has tested positive for chronic wasting disease, State Veterinarian Dr. Robert Ehlenfeldt said today.

The 2-year-old buck, owned by William Hetzel, Hillpoint in Bear Creek Township, died of digestive problems Oct. 1 and was tested routinely as the law requires. The National Veterinary Services Laboratory in Ames, Iowa, reported Monday, Oct. 20, that the test was positive.

The buck was one of only four deer on the farm. The others are a doe and her two fawns. The farm has been quarantined, which prohibits any live animals from being moved off the property. The herd is enrolled in the CWD monitoring program.

Agriculture officials are checking herd records to find out where the infected animal originated.

The Wisconsin Department of Agriculture, Trade and Consumer Protection's policy is to kill and test herds where CWD is found, as well as herds where infected animals originated. There is no approved CWD test for live animals.

This is the 10th farm-raised animal in Wisconsin to test positive for CWD and the fourth farm where the disease has been found. One of the infected animals was an elk; the rest have been whitetail deer. Currently 13 herds are under quarantine: four connected with on-farm CWD cases in Portage and Walworth counties; two that received animals from a herd in Minnesota later found to be infected; and seven that are within the Department of Natural Resources CWD eradication zone.

=====================end...tss=======================

Breber 05-01-2004 1 15 remaining depoped

Wisconsin : CWD-Positive Deer Found on Racine County Farm

Date: May 25, 2004 Source: Wisconsin Department of Agriculture, Trade, and Consumer Protection

Contacts: Donna Gilson 608-224-5130

MADISON -- A whitetail deer that died on a Racine County farm has tested positive for chronic wasting disease, State Veterinarian Dr. Robert Ehlenfeldt announced today.

The National Veterinary Services Laboratory in Ames, Iowa, reported the test results Friday, May 21. According to the farm's records on file with the Wisconsin Department of Agriculture, Trade and Consumer Protection, the doe was 9 years old. She had died of natural causes and a sample for CWD testing was collected May 1. Department rules require that all farm-raised deer and elk 16 months or older must be tested when they die, go to slaughter or are killed.

The deer was owned by Colin Breber, of Raymond, and was one of a small herd of about 10 whitetails. The herd is enrolled in the state's CWD monitoring program.

Breber's farm was quarantined Saturday, May 22, because the remaining animals have been exposed to CWD. The quarantine stops movement of live deer off the farm. Department staff are tracing movements of deer onto and from the farm, to find the source of the CWD-positive deer as well as other herds that may have been exposed.

Department policy calls for destroying herds in which CWD has been found, as well as source herds where CWD positive animals originated.

In all, 15 herds in Wisconsin are under quarantines related to CWD. Only two of those herds actually have had animals test positive. The rest are herds that may have been exposed to CWD, either because of contact with infected animals or because they are within the Department of Natural Resources disease eradication zone.

To date, 16 farm-raised animals in Wisconsin have tested positive for CWD on five farms. One of the infected animals was an elk; the rest have been whitetail deer.

==============end...tss========================

Kuhnke 07-28-2004 3 1 in July, 1 in Aug, 1 of 23 at depop

Wisconsin : CWD-Infected Herd Destroyed On Walworth County Farm

Date: November 04, 2004 Source: Wisconsin Department of Agriculture, Trade and Consumer Protection

Contacts: Contact: Donna Gilson 608-224-5130

MADISON -- A Walworth County herd of farm-raised deer and elk was destroyed Wednesday, Nov. 3, because it was infected with chronic wasting disease.

The herd of 12 white-tailed deer and 9 elk owned by Wayne Kuhnke, Delavan, was killed by gunshot by wildlife specialists from the U.S. Department of Agriculture Wildlife Services. They worked under contract with the Department of Agriculture, Trade and Consumer Protection, which regulates farm-raised deer in Wisconsin.

The Kuhnke herd had been under quarantine since September 2002 because Wisconsin animal health officials linked it to animals in two CWD-infected herds. Recently two animals from the Kuhnke herd also tested positive for CWD.

Brain stem samples were removed from each animal and shipped to the National Veterinary Services Laboratory in Ames, Iowa, for testing. Test results are expected within three weeks. Carcasses were sent to the Wisconsin Veterinary Diagnostic Laboratory for chemical digestion.

Kuhnke will be required to burn or bury all feed, bedding, manure and wooden feed troughs used by the deer. He also must clean all organic material from metal, concrete or plastic items that came in contact with the animals. DATCP staff will then disinfect those articles with a strong chlorine bleach solution. In areas of heavy animal traffic, the owner will need to scrape off and bury 2 inches of topsoil and replace it.

Kuhnke may not re-introduce farm-raised deer or elk to the property for five years. He may use the property for other species.

Kuhnke will receive federal and state indemnity payments for the animals. The indemnity amounts have not been determined yet. The U.S. Department of Agriculture will pay disposal costs.

To date, 19 CWD-positive animals have been found on six Wisconsin farms. All have been white-tailed deer except for one elk imported from a Minnesota herd later found to be infected. More than 8,000 farm-raised deer and elk have been tested in Wisconsin, and about 540 herds are enrolled in the CWD monitoring program.

Currently 17 herds are under quarantine because there has been at least one CWD-positive animal found in them, because they are linked to infected herds, or because they are inside the Department of Natural Resources CWD eradication zones.

===================end...tss=================

Christensen 01-07-2005 2 1 in 2007, owner killed and buried remaining 33

Wisconsin : CWD-Positive Whitetail Found On Crawford County Farm

Date: January 26, 2005 Source: Wisconsin Department of Agriculture, Trade and Consumer Protection

Contacts: Donna Gilson 608-224-5130

MADISON -- A white-tailed deer that died on a Crawford County farm has tested positive for chronic wasting disease, State Veterinarian Dr. Robert Ehlenfeldt announced today.

The National Veterinary Services Laboratory in Ames, Iowa, reported the test results Friday, Jan. 21. The 19-month-old buck died from respiratory causes, according to the laboratory report, and was sampled for CWD testing Jan. 12. Wisconsin Department of Agriculture, Trade and Consumer Protection rules require that all farm-raised deer and elk 16 months or older must be tested when they die, go to slaughter or are killed.

The deer was owned by Curtis Christenson, Eastman, and was one of a herd of about 40 animals. The herd is enrolled in the state’s CWD monitoring program.

Christenson’s herd was quarantined Jan. 21, because the remaining animals have been exposed to CWD. The quarantine stops movement of live deer off the farm. Department staff are tracing movements of deer onto and from the farm, to find out if other herds may have been exposed.

In an unrelated case, Ehlenfeldt announced he has quarantined a deer herd owned by Don Schnell, Rosholt. The Portage County deer herd was quarantined because a deer sold from it to an Almond hunting preserve tested positive after being shot on the preserve. No other animals on Schnell's farm have tested positive.

In all, 20 herds in Wisconsin are under quarantines related to CWD. Ten of those herds are related to on-farm CWD cases. The rest are herds that may have been exposed to CWD, because they are within the Department of Natural Resources disease eradication zone.

To date, 28 farm-raised animals in Wisconsin have tested positive for CWD on seven farms, out of more than 10,000 tested. One of the infected animals was an elk; the rest have been white-tailed deer.

================end...tss===================

Landwer 09-22-2008 2 1 of 66 at depop

PUBLIC HEARINGS

Robert Landwer, Owner, and Kathy Landwer, Agent (R10-06) – Request to Amend the Portage County Zoning Ordinance by Changing the Zoning Classification of an Area Approximately 8.59 Acres From A4, General Agricultural Zoning District to C4, Highway Commercial Zoning District – Part of Parcel #016-25-0718-06.01 – Town of Eau Pleine.

Piesik read the public hearing notice. Lucht provided a report stating the requested change is to locate a wood chipping and asphalt grinding facility. The Land Conservation Division (LCD) and Wisconsin Department of Natural Resources (DNR) will be working with the site on stormwater issues.

The site is on the location of a former deer farm. Approximately one year ago, the deer tested positive for chronic wasting disease (CWD) and had to be destroyed. Department of Agriculture, Trade, and Consumer Protection (DATCP) ordered the fence surrounding the property to remain for five years in order to keep wild deer, elk, and other animals out of the area to prevent the spreading of CWD. The site will be accessed by a new driveway built through the wooded portion of the site; a gate will be opened and closed as the site is accessed. Petitioner states there will be approximately 8-10 trucks per day traveling on and off the site during the peak season. Portage County Planning and Zoning Department staff recommends approval of the request.

http://www.co.portage.wi.us:8080/APPS/committees/committees.nsf/a31acf8e580f5f9186257475006d61cf/335c85b6575f2d458625774b005430eb?OpenDocument

====================end...tss==========================

Hookstead 10-01-2008 1 2 remaining depoped

Buck at Jefferson County preserve had chronic wasting disease e-mail print By Lee Bergquist of the Journal Sentinel Dec. 19, 2008 |(0) Comments

A 7-year-old buck from a Jefferson County hunting preserve has tested positive for chronic wasting disease, state agriculture officials reported Friday.

The white-tailed deer was killed Dec. 1 as part of an effort by the owner of the 53-acre preserve to cull his herd and repopulate it with new stock, said Donna Gilson, a spokeswoman for the Department of Agriculture, Trade and Consumer Protection.

Two deer remain on the preserve and will be killed. They have been quarantined by State Veterinarian Robert Ehlenfeldt.

Gilson said the agriculture department will trace any possible movement of deer from the preserve to other captive facilities.

The hunting preserve, Maple Hill Whitetails, is owned by Steve Hookstead of Helenville. According to the preserve's Web site, the business offers hunts, and breeding and genetics services. Hookstead was unavailable for comment.

Hookstead's breeding herd will not be killed because the deer are separated from the hunting preserve by a fence, Gilson said.

Chronic wasting disease was discovered in wild deer in Wisconsin in 2002. Since then, 98 deer and one elk have tested positive from nine captive facilities. More than 22,500 farm-raised deer and elk have been tested.

Chronic wasting disease is always fatal and affects deer, elk and moose.

The disease is a transmissible spongiform encephalopathy, a class of diseases that includes mad cow disease in cattle, scrapie in sheep and Creutzfeldt-Jakob disease in humans.

According to the World Health Organization, any tissue that may have come from deer with CWD should not be eaten, but there is no evidence the disease can be transmitted to humans.

http://www.jsonline.com/news/wisconsin/36473349.html

=================end...tss===============

NOW, if you look at the map that shows these game farms in relations to surround CWD infection rate in the wild, you will see the close proximity from one to the other i.e. CWD infected game farms, to CWD infection in the wild.

please see map here, and you will see that this phenominum is NOT only unique to Wisconsin, but with most all other game farms in other states. see map here ;

http://www.nwhc.usgs.gov/disease_information/chronic_wasting_disease/index.jsp

MORE INFORMATION ON FARMED DEER IN WISCONSIN ;

Information for Farm-Raised Deer Keepers in Wisconsin

Wisconsin Administrative Rules for Farm-Raised Deer Keepers (see sections 10.45 to 10.58)

http://docs.legis.wisconsin.gov/code/admin_code/atcp/10.pdf

General Requirements

General Requirements Summary Brochure (2 page PDF)

New Farm-Raised Deer Keeper Application (4 page PDF)

CWD Sampling Reimbursement (1 page Word doc)

General Fencing Requirements

Herds With White-tailed Deer (see section 90.21)

Herds With No White-tailed Deer (see section 90.20)

Premises Within 5 Miles of Multiple CWD Positive

http://docs.legis.wisconsin.gov/code/admin_code/atcp/10.pdf

CWD Herd Status Program

CWD Herd Status Program Summary Brochure (2 page PDF)

CWD Herd Status Program Application Packet (5 page PDF)

Census Documents (for CWD Herd Status Program)

Census Instructions (1 page Word doc)

Inventory Census Form (3 page PDF)

Purchased Additions (1 page PDF)

Live Subtractions (1 page PDF)

Deaths (1 page PDF)

Newborn Summary (1 page PDF)

Request for Electronic Census Form (1 page Word doc)

Hunting Preserves

Hunting Preserves in Wisconsin Summary Brochure (2 page PDF)

Hunting Preserve Certificate Application (2 page PDF)

Moving Requirements

In-State Movement Requirements (1 page Word doc)

In-State Shipping Permit (2 page Word doc)

Importing Into Wisconsin

Exporting to Other States

Useful Information

To Purchase a CD List of Registered Farm-Raised Deer Keepers

Wisconsin Department of Natural Resources - Wild deer testing positive for CWD

United States Geological Survey - Chronic Wasting Disease in North America

Laboratories that are certified by the United States Department of Agriculture

Deer Keeper Organizations

Whitetails of Wisconsin

Wisconsin Commercial Deer and Elk Farmer’s Association

Reindeer Owners and Breeders Association

North American Elk Breeder Association

For more information or to sign up for updates contact:

Dr. Richard Bourie, Program Manager

(608) 224-4886

Richard.Bourie@wisconsin.gov

Karen Torvell, Program Associate

(608) 224-4896

Karen.Torvell@wisconsin.gov

http://datcp.wi.gov/Farms/Deer_Farming/index.aspx

Useful Information To Purchase a CD List of Registered Farm-Raised Deer Keepers

How To Order

Ordering Documents over the Phone using a Credit Card

Call the Document Sales Office at (800) 362-7253 or (608) 266-3358 to place an order using Visa or MasterCard.

http://www.doa.state.wi.us/subcategory.asp?linksubcatid=525&linkcatid=266&linkid=49&locid=2

http://datcp.wi.gov/Farms/Deer_Farming/index.aspx

Additionally, the last day for APHIS funding for CWD testing of farmed cervids would be December 31, 2011. After that day, APHIS-approved laboratories and the National Veterinary Services Laboratories (NVSL) would be using established user fees, and producers would be charged directly for routine CWD testing...

see full text letter here ;

http://www.wcdefa.org/ECM_USDA_CWD_letter_101411.pdf

Greetings Wisconsin Hunters outdoorsman/woman et al ,

I will quote something from another deer hunting forum in another state, that was well said ;

“Ironic that one can operate a game farm to pose such a threat to wildlife and not only avoid responsibility for mitigating the danger (maintaining fences) but also get the state to buy your failed business.”

kind regards,

terry

Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm

Delwyn P. Keane1⇓ Daniel J. Barr1 Philip N. Bochsler1 S. Mark Hall2 Thomas Gidlewski3 Katherine I. O'Rourke4 Terry R. Spraker5 Michael D. Samuel6 1University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory, Madison, WI 2The U.S. Department of Agriculture, Animal Plant Health Inspection Service, National Veterinary Services Laboratories, Pathobiology Laboratory, Ames, IA 3The U.S. Department of Agriculture, Animal Plant Health Inspection Service, Veterinary Services, Fort Collins, CO 4The U.S. Department of Agriculture, Agricultural Research Service, Animal Disease Research Unit, Pullman, WA 5The Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 6The U.S. Geological Survey, Wisconsin Cooperative Wildlife Research Unit, University of Wisconsin, Madison, WI. ↵University of Wisconsin, Wisconsin Veterinary Diagnostic Laboratory, 445 Easterday Lane, Madison, WI 53706. Delwyn.Keane@wvdl.wisc.edu Next Section

Abstract In September 2002, chronic wasting disease (CWD), a prion disorder of captive and wild cervids, was diagnosed in a white-tailed deer (Odocoileus virginianus) from a captive farm in Wisconsin. The facility was subsequently quarantined, and in January 2006 the remaining 76 deer were depopulated. Sixty animals (79%) were found to be positive by immunohistochemical staining for the abnormal prion protein (PrPCWD)in at least one tissue; the prevalence of positive staining was high even in young deer. Although none of the deer displayed clinical signs suggestive of CWD at depopulation, 49 deer had considerable accumulation of the abnormal prion in the medulla at the level of the obex. Extraneural accumulation of the abnormal protein was observed in 59 deer, with accumulation in the retropharyngeal lymph node in 58of 59 (98%), in the tonsil in 56 of 59 (95%), and in the rectal mucosal lymphoid tissue in 48 of 58 (83%). The retina was positive in 4 deer, all with marked accumulation of prion in the obex. One deer was considered positive for PrPCWD in the brain but not in the extraneural tissue, a novel observation in white-tailed deer. The infection rate in captive deer was 20-fold higher than in wild deer. Although weakly related to infection rates in extraneural tissues, prion genotype was strongly linked to progression of prion accumulation in the obex. Antemortem testing by biopsy of rectoanal mucosal-associated lymphoid tissue (or other peripheral lymphoid tissue) may be a useful adjunct to tonsil biopsy for surveillance in captive herds at risk for CWD infection.

http://vdi.sagepub.com/content/20/5/698.long

Monday, January 16, 2012

9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD

http://chronic-wasting-disease.blogspot.com/2012/01/9-game-farms-in-wisconsin-test-positive.html

Tuesday, December 20, 2011

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

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

SNIP...SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

*** 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.

(PLEASE NOTE SOME OF THESE OLD UK GOVERNMENT FILE URLS ARE SLOW TO OPEN, AND SOMETIMES YOU MAY HAVE TO CLICK ON MULTIPLE TIMES, PLEASE BE PATIENT, ANY PROBLEMS PLEASE WRITE ME PRIVATELY, AND I WILL TRY AND FIX OR SEND YOU OLD PDF FILE...TSS)

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

Wednesday, November 16, 2011

Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wisconsin-creutzfeldt-jakob-disease-cwd.html

Saturday, December 31, 2011

Depopulation Plan Being Developed for Captive Deer Facility in Macon County after second CWD positive confirmation

http://chronic-wasting-disease.blogspot.com/2011/12/depopulation-plan-being-developed-for.html

Monday, November 14, 2011 WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wyoming-creutzfeldt-jakob-disease-cwd.html

Sunday, November 13, 2011

COLORADO CWD CJD TSE PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/colorado-cwd-cjd-tse-prion-reporting.html

Wednesday, January 04, 2012

CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND HOLT COUNTIES DURING NOVEMBER HUNT

http://chronic-wasting-disease.blogspot.com/2012/01/cwd-nebraska-ngpc-26-deer-carcasses.html

Wednesday, December 21, 2011

CWD UTAH San Juan deer hunting unit

http://chronic-wasting-disease.blogspot.com/2011/12/cwd-utah-san-juan-deer-hunting-unit.html

Thursday, December 29, 2011

Aerosols An underestimated vehicle for transmission of prion diseases?

PRION www.landesbioscience.com please see more on Aerosols and TSE prion disease here ;. ...

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/aerosols-underestimated-vehicle-for.html

Wednesday, January 18, 2012

BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE

February 1, 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html

Thursday, January 26, 2012

The Risk of Prion Zoonoses

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/risk-of-prion-zoonoses.html

Thursday, January 26, 2012

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

Science 27 January 2012:

Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/facilitated-cross-species-transmission.html

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html

SEE FULL TEXT ;

Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

http://scrapie-usa.blogspot.com/2011/02/environmental-sources-of-scrapie-prions.html

Monday, January 05, 2009

CWD, GAME FARMS, BAITING, AND POLITICS

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html

Thursday, August 28, 2008

cwd, feeding, and baiting piles

http://chronic-wasting-disease.blogspot.com/2008/08/cwd-feeding-and-baiting-piles.html

UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html

Monday, February 14, 2011

THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER

NO, NO, NOT NO, BUT HELL NO !

Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html

http://www.thewildlifenews.com/2011/11/03/jackson-hole-newsguide-retired-biologist-stop-feeding-make-elk-migrate/

more concern here ;

Saturday, November 12, 2011

Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease

Fri, 22 Sep 2006 09:05:59 –0500

http://chronic-wasting-disease.blogspot.com/2011/11/human-prion-disease-and-relative-risk.html

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

PRION 2010

International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria

SNIP...

PPo4-4:

Survival and Limited Spread of TSE Infectivity after Burial

Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK

Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried. The authors gratefully acknowledge funding from DEFRA

SEE MORE HERE ;

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html

PRION 2011

Envt.16: Soil Properties as a Factor in CWD Spread in Western Canada

Alsu Kuznetsova,† Tariq Siddique and Judd Aiken

University of Alberta; Edmonton, AB Canada†Presenting author; Email: alsu@ualberta.ca

Soil can serve as a stable reservoir for infectious prion proteins (PrPSc). Soils are diverse and complex, varying in clay, silt, sand and organic components. We have shown that PrPSc binds clay minerals avidly, an interaction that considerably enhances prion infectivity. Conversely quartz sand bound PrPSc less avidly. These studies would suggest that soils with lower clay and higher sand content bind prions less avidly and do not enhance infectivity to the same level as clay-rich soils. We hypothesize that clay content of a soil plays an integral role in the spread of CWD. In this study, we present the soil properties in the western Canada. Soils of the CWD-region generally are similar in texture, clay mineralogy and soil organic matter content. In total these soils can be characterized as clay loamy, montmorillonite (smectite) with 6–10 % organic carbon. The major soils in the CWD-region are Chernozems, present in 60% of total area. These soils have a humic horizon in which organic matter has accumulated (1–17% organic C). Solonetzic soils are also common to Alberta and Saskatchewan. We suggest that the greatest risk of CWD spread in western Canada is restricted to clay loamy, montmorillonite soils with humus horizon. Such soils are predominant in the southern region of Alberta, Saskatchewan and Manitoba, but are less common in northern regions of the provinces.

Envt.28: High Survival Rates of TSE Infectivity Buried in Two Soil Types Allister J. Smith The Roslin Insitute; Roslin, UK Email: allister.smith@roslin.ed.ac.uk Two field experiments nearing completion are investigating the migration and/or persistence of TSE infectivity in the soil environment, either buried within bovine heads or buried without containment. In the first experiment five pairs of bovine heads, spiked with mouse-passaged BSE (301V) macerate, were buried within lysimeters containing either clay or sandy soil. A pair of unspiked bovine heads was also buried to act as controls. Pairs of heads have been exhumed annually during which a corer is used to take soil samples above, surrounding and below the head. Any brain material within the head is recovered during dissection. The soil samples have undergone protein extraction, and the extracts along with the brain material have been assayed for infectivity by bioassay in VM mice. Bioassay results from the first experiment show that for all four years most of the intracranial brain samples have been positive for TSE infectivity in both the clay and sandy soil. There is little change in the survival curves between years 1 and 4 indicating little reduction in the amounts of infectivity over time. There has been very limited infectivity found in samples surrounding the heads buried in the sandy soil, but infectivity has been found in the soil samples surrounding the clay heads and the levels increase slightly from years one to four, presumably as the heads have decomposed. In a parallel experiment a bolus of infectivity (301V) was placed in the centre of two large lysimeters, containing either clay or sandy soil. Over the course of four years, core samples have been taken at eight time points, on the vertical and at 3 distances from the centre. These samples have been assayed for infectivity and to date only one sample from the sandy soil has produced pathological evidence of TSE disease in one mouse. In order to ascertain whether any of the bolus remained at the end of the experiment, we collected a much larger central core (d = 16 cm) and extracted samples for bioassay, concentrating on the core portions that correlated to the original bolus location. The samples from these core portions caused disease in a high proportion of mice (bioassay still in progress), with apparently higher infectivity levels in the clay soil, so far. This result indicates that there has been very little migration of TSE infectivity without containment in either clay or sandy soil and that there has been little reduction in titre with time.

Envt.29: Time-Dependent Decline in PrPTSE Desorption from Soil Particles Christen B. Smith,1,† Clarissa J. Booth,2 Kartik Kumar2 and Joel A. Pedersen1–3 1Environmental Chemistry and Technology Program; 2Molecular and Environmental Toxicology Center; 3Department of Soil Science, University of Wisconsin; Madison, WI USA †Presenting author, Email: cmbell@wisc.edu Environmental routes of transmission are implicated in epizootics of sheep scrapie and chronic wasting disease in deer, elk, and moose. Strong evidence suggests that soil may serve as an environmental reservoir of prions, which can persist in the environment for years. The disease-associated form of the prion protein (PrPTSE) readily attaches to soil particle surfaces. Prior studies reported reduced PrPTSE recovery from experimentally spiked soils after longer contact times, which in some cases has been interpreted as degradation of PrPTSE. Here, we investigate PrPTSE desorption from sterilized and untreated soil particles as a function of protein-soil contact time. Soil particles were sterilized by autoclaving or g-irradiation. Desorption of PrPTSE from whole soils, montmorillonite clay, and quartz sand was analyzed by immunoblotting following 1-, 7-, and 14-day contact times. We found that PrPTSE recovery from both sterile and untreated soil samples declined significantly with contact time suggesting the strengthening of protein-particle interactions over time. Recovery of PrPTSE from whole soils declined to a larger extent than did that from montmorillonite and quartz sand possibly reflecting the contribution of particle-associated natural organic matter to the mechanisms of PrPTSE attachment. The influence of PrPTSE-soil particle attachment on oral disease transmission warrants investigation.

www.landesbioscience.com PRION

http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf

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

Friday, February 20, 2009

Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2009/02/both-sides-of-fence-strategic-review-of.html

ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html

2009 CWD SYMPOSIUM UTAH

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf

Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area

65

Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area

Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- tracy.a.nichols@aphis.usda.gov

Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.

snip...

The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels. snip...end...full text at ;

http://www.landesbioscience.com/

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html

http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html

Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-to-tighten-taxidermy-rules-hunters.html

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

Form 1100-001

(R 2/11)

NATURAL RESOURCES BOARD AGENDA ITEM

SUBJECT: Inf01mation Item: Almond Deer Fatm Update

FOR: DECEIVIBER 2011 BOARD MEETING

SNIP...

These laboratory results show that 60 of the 76 animals tested positive for chronic wasting disease. The 76 deer constituted the breeding herd on Hall’s farm. He also operated a hunting preserve on the property until 2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWD was not detected in those animals. The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

SNIP...

Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years. However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil. Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. Evidence of environmental transmission also was documented in a Colorado research facility where mule deer became infected with CWD in two of three paddocks where infected deer carcasses had decomposed on site 1.8 years earlier, and in one of three paddocks where infected deer had last resided 2.2 years earlier (Miller et al. 2004).

SNIP...

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

FULL TEXT AND MORE HERE ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

with 9 infected game farms documented to date in Wisconsin, with one of them having the highest infection rate ever in the world i.e. 80%, I think it’s time for all of these game farms to be shut down. just my opinion. ...TSS

Comment from Terry Singeltary Document ID: APHIS-2011-0032-0002Document

Type: Public Submission This is comment on Notice: Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program Docket ID: APHIS-2011-0032RIN:

Topics: No Topics associated with this document View Document: Show Details

Document Subtype: Public Comment Status: Posted Received Date: January 24 2012, at 12:00 AM Eastern Standard Time Date Posted: January 25 2012, at 12:00 AM Eastern Standard Time Comment Start Date: January 24 2012, at 12:00 AM Eastern Standard Time Comment Due Date: March 26 2012, at 11:59 PM Eastern Daylight Time Tracking Number: 80fa2c68 First Name: Terry Middle Name: S. Last Name: Singeltary City: Bacliff Country: United States State or Province: TX Organization Name: LAYPERSON Submitter's Representative: CJD TSE PRION VICTIMS

Name: Terry S. Singeltary

Address:

Bacliff, TX,

Submitter's Representative: CJD TSE PRION VICTIMS

Organization: LAYPERSON

--------------------------------------------------------------------------------

General Comment

Agency Information Collection Activities; Proposals, Submissions, and Approvals: Chronic Wasting Disease Herd Certification Program (Document ID APHIS-2011-0032-0001)

I believe that any voluntary program for CWD free herd certification from game farms will be futile, as was the partial and voluntary mad cow feed ban of August 4, 1997. That failed terribly, with some 10,000,000 of banned blood laced MBM being fed out in 2007, a decade post August 4, 1997 partial and voluntary ban.

Game farms are a petri dish for CWD TSE Prion disease, with Wisconsin having documented 9 CWD infected game farms, with one having the highest CWD infection rate in the world, 80% CWD infection rate.

I believe that all game farms should be SHUT DOWN PERMANENTLY.

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

you cannot cook the CWD 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 CWD TSE Prion agent will survive in the environment for years, if not decades.

you can bury it and it will not go away.

CWD 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.

Tuesday, December 20, 2011

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

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

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

full submission here ;

http://www.regulations.gov/#!documentDetail;D=APHIS-2011-0032-0002

Friday, February 25, 2011

Soil clay content underlies prion infection odds

http://chronic-wasting-disease.blogspot.com/2011/02/soil-clay-content-underlies-prion.html

Monday, August 8, 2011

Susceptibility of Domestic Cats to CWD Infection

Oral.29: Susceptibility of Domestic Cats to CWD Infection

see also ;

Enzymatic Digestion of Chronic Wasting Disease Prions Bound to Soil

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

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

see this and more here ;

http://felinespongiformencephalopathyfse.blogspot.com/2011/08/susceptibility-of-domestic-cats-to-cwd.html

layperson

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net

Nebraska Fish and Game Association Censors Singeltary from speaking about Chronic Wasting Disease (CWD) again

2012-01-25T12:16:00.000-06:00

Nebraska Fish and Game Association Censors Singeltary from speaking about Chronic Wasting Disease (CWD) again

You have been banned for the following reason: Voted to ban.

Date the ban will be lifted: Never

http://www.nefga.org/forum/forumdisplay.php?11-Nebraska-Hunting-Forum

The director and the moderators of this forum came together and voted to ban you from this forum. We had a lot of members complain about the way you wet about posting your threads.

I personally would like to say thanks for helping some of our members realize the importance of CWD and the affects. Thank you for your time.

Best regards, xxxx

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

Terry,

First off, I would like to apologize for the harsh manner in which you have been greeted on this site. As you said, I'm sure you are used to it but that is no excuse. I know there have been problems in the past of people registering on this forum to simply blow their own horn and promote their own cause. One guy was trying to convince people common carp were the best game fish and threatened to stock them into every public body of water he could reach! Notwithstanding, the greeting you received was unnecessarily harsh and a poor representation of the majority of people on this site.

Regarding CWD, I am not too familiar with the disease but I do try to keep up on the current state it. I too am puzzled why the people with the largest interest in deer are so resistant to learn more about this major issue. It certainly seems like you know what you are talking about and as you have said you have spent many years learning about and researching this topic.

One small piece of advice I may offer you is to introduce yourself and give some background information about yourself. Where are you from? Do you hunt or fish? Why are you interested in CWD/TSE? Do you work professionally with this topic? Just some ideas. I understand you are trying to provide a large amount of information and are unable to post links to articles, but the large blocks of text pasted in your posts comes off as impersonal and abrasive to some, especially from a new member.

I hope you stick around, I am always eager to learn especially when the issue is something as large as this.

Regards xxxxxxx

***************

I was waaaay too far down the food chain to know him! The only vets I knew were the IIC's (inspector in charge) if whatever establishment I was working at. With the game and parks pushing increased white tail doe harvest in our state as a result of politically motivated legislation (Senator Lautenbaugh's deer depredation bill) passed 2 years ago, your information and "sounding the alarm" is falling on deaf ears with those who have the clout to do anything about it. It's your right to do what you're doing, but in my opinion it's a waste of time. Where are you from, and do you eat the deer you kill?

***************

You're proceeding on the wrong assumption. A little background info. would be in order. I'm a retired Federal Meat and Poultry Inspector for the USDA. I've educated myself on the CWD issue, and have made my decision in regards to the consumption (or lack thereof) of venison. You have obviously educated yourself on this issue, and are free to divulge your information in this forum. I honestly feel the vast majority of the members of this forum have already made their decision in regards to this matter; and it is my personal opinion you are, for lack of a better description, "beating a dead horse". Out of curiosity, have you had any contact with our states game and parks commission with your concerns, and if so, what has been their response? xxxx

***************

nobody's trolling here. i asked to come here to speak about CWD. CWD in Nebraska is mounting, it's spreading, and humans are being exposed to the CWD agent. if it was just the people that eat meat, were the only ones that were exposed, that is one thing. but this is about your cervids and environment, and, when you become exposed with the CWD agent, or any other TSE, and then have medical or dental or donate blood, you then expose others. so, it's just not about consumption. i knew there would be some that do not want to hear it, that's o.k., your entitled to your opinion, but others here may want to hear some of this, and try and do something to prevent the further exposure and spreading of the CWD TSE agent. i assure you i am here to promote awareness about CWD, to promote discussion and debate, nothing else. i am vested in nothing but the truth, and have been all along. i don't advertise on any of my blogs i post this CWD TSE science to. it's there for educational purposes. you need to educate yourself folks, with all the science. and yes, i am anti, i am anti stupid. i am anti corporate and political science. and the cut and paste are just facts, they have links. when i can post the links, the posts will be much shorter. but if it will make you feel better, i will go jump in a lake too, if you just become more aware to what you are dealing with i.e. CWD TSE prion disease. i had chicken last night, and a steak last week. oh, and yes somebody does just show up out of no where, from another state, and talk about CWD. i did, i do, and i have done it for years, from state to state as they fall with CWD, or any other TSE in a species. i was asked to be moderator of one State that fell, after being there for years, and i said the same thing, i can't moderate a state that i don't live in. but they freely accept the science and discussion and debate that comes from it. there are a few states that i have had trouble with, simply because they did not want to hear it, and did not want there hunters to hear it, because of the financial fallout. one of those states has recently let me back in to speak and share science about CWD. look, this is about more than money here, it's about your cervids, and your people. i have been in the pits for years doing this, debated folks and scientist all over the world, there is nothing you can say that will hurt my feelings. i am just the messenger folks, you can hate me, throw all the stones you wish, but read the science and educate yourself all you can. CWD and TSEs are here. they have even now linked the TSE agent to Alzheimer's, ALS, Parkinson's disease. and there is science now showing that Alzheimer's is transmissible. course there was science showing that a decade ago i.e. transmission studies. what does all this mean? i cannot answer that. i can tell you this, continue to ignore the CWD TSE agent and you risk your herd and people. shoot the messenger if you must, (i am full of holes), but don't ignore the science. ...

kind regards,

terry

http://www.nefga.org/forum/showthread.php?43539-Chronic-Wasting-Disease-CWD-TSE-Prion-Disease-Nebraska

***************

Greetings Nebraska Hunters et al,

I kind greetings from Bacliff Texas. I signed up again here after a very long absence, to monitor what appears to be an increasing spread of CWD in Nebraska.

I am interested in what you hunters in Nebraska think about this CWD prion agent, and what your concerns might be, especially since it seems that CWD has mutated into a second strain. A disturbing factor indeed. also, new and emerging science has shown that the risk factor for transmission to humans is very real, and increasing with every new strain of CWD found.

ALSO, recently, a stern warning from Prof. Aguzzi about Aerosol and the TSE prion agent, in relations with CWD ;

In Chronic Wasting disease (CWD) of deer several careful studies have been performed that, together with our present finding, depose in favor of airborne transmission in this naturally occurring disease. Indeed, CWD prions can be transmitted experimentally via aerosol and the nasal route to transgenic cervidized mice.33 Although no anecdotal or epidemiological evidence has come forward that airborne transmission may be important for the spread of CWD, several lines of thought suggest that this possibility is not implausible. In deer, prions have been detected in urine, saliva, feces and blood of diseased animals. Moreover, it was claimed that pathological prion protein could be recovered from the environmental water in an endemic area.34 Since all fluids can act as sources for the generation of aerosols, any of the body fluids mentioned above may represent the point of origin for airborne transmission of CWD prions.

ALSO, recently science shows ;

Accelerated shedding of prions following damage to the olfactory epithelium

In this study we investigated the role of damage to the nasal mucosa in the shedding of prions into nasal fluids as a pathway for prion transmission. Here we demonstrate that prions can replicate to high levels in the olfactory sensory epithelium (OSE) in hamsters and that induction of apoptosis in olfactory receptor neurons (ORNs) in the OSE resulted in sloughing off of the OSE from nasal turbinates into the lumen of the nasal airway. In the absence of nasotoxic treatment olfactory marker protein (OMP), which is specific for ORNs, was not detected in nasal lavages. However, after nasotoxic treatment that leads to apoptosis of ORNs both OMP and prion proteins were present in nasal lavages. The cellular debris that was released from the OSE into the lumen of the nasal airway was positive for both OMP and the disease-specific isoform of the prion protein, PrPSc. Using the real time quaking-induced conversion assay to quantify prions, a 100- to 1,000-fold increase in prion seeding activity was observed in nasal lavages following nasotoxic treatment. Since neurons replicate prions to higher levels than other cell types and ORNs are the most environmentally exposed neurons, we propose that an increase in ORN apoptosis or damage to the nasal mucosa in a host with a pre-existing prion infection of the OSE could lead to a substantial increase in the release of prion infectivity into nasal fluids. This mechanism of prion shedding from the olfactory mucosa could contribute to prion transmission.

AS far as human risk factor from CWD, either from consumption, and or friendly fire or the pass it forward mode ‘iatrogenic’ , this risk factor is very real ;

EFSA Journal 2011 The European Response to BSE: A Success Story

This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential. ...end

I have followed this BSE TSE prion saga daily since December 14, 1997, when I watched my mother die from the Heidenhain Variant of Creutzfeldt Jakob Disease. I never did accept the UKBSEnvCJD only theory, and now science does not agree with it either. I don’t want to over state my concern here, but I am very concerned for Nebraska and the CWD ramifications there from, to animals, livestock, and humans.

I want to know how you as hunters are concerned with CWD, not only concern for yourself, but your family as well, your wife, your children, are you concerned for them as well, or not? remember, this is a disease that can incubate for decades, and more and more scientist seem to be very concerned for the potential transmission of CWD to humans, if it has not happened already and being masked as sporadic CJD.

ARE you concerned about the deer herd, or do you think CWD will just kill itself out?

OR, do you think CWD might kill the deer herds out?

WHAT are your concerns about CWD and GAME FARMS, and the environmental factors there from?

some of which have proven to be nothing more than a petri dish for TSE prion contamination. Some of these game farms use, or have used in the past high protein pellets containing SRMs (specified risk materials) i.e. ANIMAL TISSUE. oral transmission of CWD TSE tainted tissue is easily transmitted to deer. just this December the final report about the closing of a game farm in Wisconsin, and the purchase there from by the state, due to the incredible CWD infection rate there, and ramifications there from for years, if not decades to come. are you pro game farms, or not, and why?

WHAT about baiting and feeding? do you bait or feed, and if so, why, and if not, why not?

THESE are some of many of my questions I am curious about here.

I hope you don’t mind me asking these questions. I follow CWD from state to state, as it emerges.

I am NOT anti-hunter, I don’t care what you eat, I am a carnivore.

so please don’t shoot the messenger.

I will be glad to share some recent science with you as soon as I can post a few links here.

Nebraska has a CWD problem, it’s spreading, and I am just curious, what concerns the hunters have for it.

thank you,

kind regards, terry

LAYPERSON

http://www.nefga.org/forum/showthread.php?43539-Chronic-Wasting-Disease-CWD-TSE-Prion-Disease-Nebraska&p=416422#post416422

***************

Join Date Jan 2012 Location 77518 Posts 0 Thanks 0 Thanked 0 Times in 0 Posts Nebraska cwd forum ??? hello there,

i was wondering if it is possible to speak about cwd here, and pass along some science links on the topic? i have been following CWD and other TSE since 1997 and am very concerned about the spread of CWD, and it looks like Nebraska is going to be another hot spot. i went to make a post with a few links, but i don't think that's possible to post links now. it would not be the first time i have been shut down about speaking about CWD, but i was wanting to know before making a post, just so i did not waste your time or mine. there is just some new science emerging on CWD i think everyone should know about. i am not anti-hunter, i am pro-hunter, i am a carnivore.

would it be possible to make a forum here for CWD or Animal disease ???

If not, can i post some scientific study links about cwd TSE prion disease to the hunting forum ???

thank you, kind regards, terry

http://www.nefga.org/forum/private.php?do=showpm&pmid=338298

***************

Terry,

Thank you for your inquiry on this matter. We don't see a problem with you posting or discussing the topic on CWD but we do ask you that you keep it under the Hunting section of the forum and just post a new thread. Also please take a look at the forum guidelines before posting so that you know what type of topics will be tolerated. Another thing you can find in the guidelines is that you can not post links, images, and attachments until you reach a minimum of 10 posts.

Guidelines: http://www.nefga.org/forum/showthread.php?28199-Forum-Guidelines-12-01-2009

Thank you xxxxx

***************

Terry,

When you asked me if you could talk about CWD here I was under the impression you wanted to discuss the issue with other forum members. We don't have a problem with you discussing the issue with other member but just posting facts about it is just going to get other members upset with you and deter them from reading any of your posts. The long and lengthy posts you have made are to most people are very drawn out and will not get read. Please keep it a discussion or we may just have to pull the plug.

***************

You have been banned for the following reason: Voted to ban.

Date the ban will be lifted: Never

http://www.nefga.org/forum/forumdisplay.php?11-Nebraska-Hunting-Forum

The director and the moderators of this forum came together and voted to ban you from this forum. We had a lot of members complain about the way you wet about posting your threads. I personally would like to say thanks for helping some of our members realize the importance of CWD and the affects. Thank you for your time.

Best regards, xxxx

==============================end================================

> > > but just posting facts about it is just going to get other members upset

scientific facts are hard to digest sometimes. ignore them at your own, and others, peril. ...tss

2006

Chronic Wasting Disease 2006 Update Nebraska

My last posting before being banned due to discussing CWD in Nebraska the first time, in 2006 (I was trying to warn them back then, they shot the messenger then too) ;

posted August 09, 2006 09:17 PM

--------------------------------------------------------------------------------

Chronic Wasting Disease 2006 Update Nebraska

Summary of Chronic Wasting Disease in Nebraska

Chronic Wasting Disease testing during the 2005 deer hunting season produced 15 positives from 7,381 samples collected. Since testing began in 1997 there have been 65 positive mule deer and 29 positive white-tailed deer, out of 24,849 tested.

The locations of free ranging deer testing positive for the years 2002 - 2005 are shown below.

http://www.agr.state.ne.us/footmouth/cwd_update.htm

Captive Elk Herds Positive for CWD in Nebraska

http://www.agr.state.ne.us/footmouth/necwd1.jpg

Subject: SCRAPIE and CWD USA UPDATE July 19, 2006

Date: July 19, 2006 at 12:06 pm PST

SCRAPIE USA UPDATE MAY 31, 2006

Infected and Source Flocks

snip...end

http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=next_topic;f=12;t=000490;

AND THAT ENDED THAT. that was my last post before they banned me from speaking about CWD back then. ...

Due to a decision by the Commission, public posts to the Outdoor Forum are no longer allowed.

xxxx xxxxxxx

Information Systems Analyst Sr.

Nebraska Game and Parks Commission

2200 N. 33rd St.

(402) 471-5646

XXXXXXXXXXXXX

http://www.ngpc.state.ne.us

***************

2012

NOW, let me be perfectly clear. this time, it was the Nebraska Fish and Game Association that allowed me back on board, to post about CWD, after I had asked them to do so. what happened was, I got to speaking the truth about game farms, and CWD spreading there from, and a certain few complained, and kept complaining, they did not want anymore information (valid scientific peer review journals) that might hurt their industry. SO, I thank NFGC again for giving me a chance to try and educate hunters on CWD and the TSE prion disease. I think I supplied enough information to help educate, the ones that wanted to be educated, however, it’s the other folks I am concerned about. the ones that don’t want to be educated on this CWD, the ones that don’t want to speak about it, or learn about, and they don’t want others to either. these few folks are the ones that will help continue the spread of CWD. these folks caused the surpressing of CWD TSE prion information. to be good stewards of the woods and hunt, you cannot stick your head in the sand. these few folks did, and in doing so, they want everyone else’s head in the sand. and that’s been the problem all along. ...good luck!

so much for freedom of speech. can’t say I did not try. ... TSS

Don’t Forget CWD

Sunday, January 22nd, 2012 | Posted by Dr. Dave Samuel

Nebraska just announced the finding of Chronic Wasting Disease in several counties in the center of the state. This shows the continued spread from western Nebraska. So what you say, “It’s obvious that CWD can’t spread to humans and it sure doesn’t seem to be hurting our deer herds.”

Maybe. Maybe on both counts. The release of information showing the spread of CWD in Nebraska (where I hunt every fall in the eastern part of the state) caused me to check out the website, http://transmissiblespongiformencephalopathy.blogspot.com/ . That blog lists a lot of other website with tons of information on CWD. CWD is not spread by bacteria but rather by prions that invade and destroy the brain. One very similar disease of humans is Creutzfeldt-Jacob Disease. This blog presents a lot of information on that disease relative to whether humans can get CWD from diseased deer or elk.

Bottom line is that we don’t know a lot about prions. We do know that prions survive in soil for years. We know that deer can be placed in an area where CWD lived and after being removed for over a year, deer placed there again get CWD.

We don’t know how long prions stay viable in the soil. My guess is . . . many, many years. Maybe decades. We know that deer have prions in nervous tissue but also in lymph tissue and even muscles. We know that prions are spread via saliva and urine. (In fact that is why many states are concerned about baiting for deer.) We don’t think prions can be spread via eating deer meat but we aren’t positive. Scary because another prion disease ‘mad cow disease’ can be spread from cows to humans leading to death.

I don’t want to play the ‘what if’ game, but ‘what if’ one hunter got CWD from eating deer meat and that hunter died? Let’s not go there. The ramifications are beyond comprehension.

Another aspect of this problem is found on the above website as well as http://chronic-wasting-disease.blogspot.com/ . I invite you to go to this website and after you peruse it you will see the relationship of CWD and deer farms. They discuss the Almond deer farm in Wisconsin. A buck shot there in 2002 had CWD and this led to all deer there being killed in 2006. Sixty of the 76 deer killed were CWD positive. In order to keep control of this situation and make sure the fence separating the contaminated farm from wild deer remained intact, the DNR bought the farm in 2011. Remember, this farm probably has CWD prions in the soil, so the potential for spread to wild deer is real. However, 1200 deer outside the farm have been tested and no CWD was found. The DNR wants to make sure the fences stay intact, so they bought it and will do research on CWD there. Seems like a good idea.

A total decontamination of the farm was conducted, but there is no way to know whether prions are still in the soil. They probably are. All timber along the fence is being cut to protect the fence. A second fence 12 feet from the first is being constructed. Apparently the Wisconsin DNR is very concerned about the spread of CWD.

If baiting for deer has been shown to exacerbate the spread of CWD then why do we find baiting being legalized in more and more states? The reason is simple. Hunters want baiting and they apply political pressure to keep baiting if they have it or to get baiting if they do not have it. The DNR in my home state of West Virginia would love to stop baiting for deer to prevent, or slow the spread of CWD from the eastern panhandle of the state, but the hunters won’t let that happen. A political hot potato.

Again, check out the above two web sites then tell me that CWD is not a potential problem for hunters and deer. This ain’t your average disease. So far, humans eating venison are OK and so far deer herds are OK too. But packing large numbers of deer in small areas is an experiment and only time will tell if ‘it’s not nice to fool with Mother Nature.’

http://bowhunting.net/2012/01/dont-forget-cwd/

Wednesday, January 04, 2012

CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND HOLT COUNTIES DURING NOVEMBER HUNT

http://chronic-wasting-disease.blogspot.com/2012/01/cwd-nebraska-ngpc-26-deer-carcasses.html

Friday, February 25, 2011

Soil clay content underlies prion infection odds

http://chronic-wasting-disease.blogspot.com/2011/02/soil-clay-content-underlies-prion.html

Monday, August 8, 2011

Susceptibility of Domestic Cats to CWD Infection

Oral.29: Susceptibility of Domestic Cats to CWD Infection

http://felinespongiformencephalopathyfse.blogspot.com/2011/08/susceptibility-of-domestic-cats-to-cwd.html

Tuesday, January 24, 2012

CWD found in two free-ranging deer from Macon County Missouri

http://chronic-wasting-disease.blogspot.com/2012/01/cwd-found-in-two-free-ranging-deer-from.html

Monday, January 16, 2012

9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD

http://chronic-wasting-disease.blogspot.com/2012/01/9-game-farms-in-wisconsin-test-positive.html

> > > similar if less acute concerns exist for all nine deer farms in Wisconsin that have tested positive for CWD. < < <

WISCONSIN DEPT. OF NATURAL RESOURCES

NEWS RELEASE

Wisconsin Department of Natural Resources

West Central Region

1300 W. Clalremont Ave., PO Box 4001, Eau Claire, WI 54702-2786 Phone: (715) 839-3715 TDD: 711 dnr.wi.gov www.wisconsin.gov

DATE: Monday, July 18,2011

CONTACTS: Davin Lopez, ONR CWO coordinator, Madison. 608-267-2948 Kris Belling, DNR regional wildlife supervisor, Eau Claire, 715-839-3736

SUBJECT: Public input sought on future of CWO-tainted deer farm

BAD CLAlRE - Neighbors and others interested ill the deer farm formerly known as Buckhorn Flats are invited to a public meeting on the future ofthe property, now owned by the state Department of Natural Resources.

The open house meeting will mil 6-8 p.m. Thursday, July 28, in the auditorium at the Almond- Bancroft School at 1336 Elm Street in Almond, Background on the property, now called the Almond Deer Farm, will be provided, and the public is invited to ask questions and offer input 011 the management of the site,

The first case of CWD, 01' chronic wasting disease, among Wisconsin farm-raised deer was discovered on this property in September 2002. CWD, which affects deer and elk, is a contagious and always fatal brain disease for which there is no cure. The discovery o.f CWD on this property led .to the . depopulation of the entire deer herd on the farm.

In the end, 82 of the deer killed and removed tested positive for CWD. This is an 80 percent infection rate, the highest rate ofCWD infection recorded in North America, and possibly in the world.

The property is located along the east side of3rd Street, about one mile north and west of the Village of Almond in Portage County. The DNR purchased the 80~acre property this past spring for $465,000. There are 25 acres of cropland and 55 acres of woodland. About 65 acres are fenced, the area previously used as a deer farm. The property includes a single-family residence and a storage shed located outside of the fence.

Research indicates prions, proteins associated with the disease, can persist in soil for a minimum of three years and perhaps much longer. Prions that cause scrapie, a CWD-Iike disease in sheep and goats, have remained available and infectious for up to 16 years. DNR officials believe there is all unacceptable risk that CWD prions would infect wild white-tailed deer around this site if the fences would be removed. Since the previous owners were selling the property, and there is no continuing obligation to maintain the fence, wildlife officials concluded the best available option was to acquire the property.

similar if less acute concerns exist for all nine deer farms in Wisconsin that have tested positive for CWD. Because the question of how long a contaminated site is a risk to deer is of national and international 'interest there will be a number of opportunities for research at the Almond farm. Plans include building a second fence, if funding is available, to provide a secondary barrier and further reduce the risk of disease transmission to the wild deer herd. In addition, DNR officials must decide whether to maintain ownership of the house and lot.

The primary reason for DNR purchase ofthe property is to ensure that the deel-,fence remains intact, preventing wild deer from accessing the property and becoming infected. The pNR has an ethical and financial responsibility to maintain the fences until science offers a solution for assessing the risk 01' remediating the site. The fence will be inspected frequently.

-30-

The following counties are In the Wast Central Region: Adams, Buffalo, Chippewa, Clark, Dunn, Eau Claire, Jackson, Juneau, La Crosse, Marathon, Monroe, Pepin. Pierce, Portage, st. Croix, Trempealeau, Varnon and Wood. The Public Affairs Manager for DNR West Central Region Is Ed Culhane, 715-839-3715.

Tuesday, December 20, 2011

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

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

SNIP...SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html

TSS

CWD found in two free-ranging deer from Macon County Missouri

2012-01-24T10:11:00.000-06:00

CWD found in two free-ranging deer from Macon County

Statewide

Published on: Jan. 24, 2012

Posted by Joe Jerek

JEFFERSON CITY Mo – The Missouri Department of Conservation (MDC) received two positive test results for Chronic Wasting Disease (CWD) from 1,077 tissue samples taken from free-ranging deer harvested by hunters in north-central Missouri during the 2011 fall firearms deer season. Both positive test results were from adult bucks harvested by Missouri hunters in Macon County, and are the first CWD-positive results for free-ranging deer in Missouri.

MDC plans to obtain more tissue samples for CWD testing by harvesting additional deer in the immediate area where the two infected deer were harvested.

“Teamwork among landowners, hunters and MDC staff allowed us to detect this infection early,” said MDC Deer Biologist Jason Sumners. “We will be working with local landowners to harvest additional deer for tissue sampling. This is a first step and one of our best hopes for containing, and perhaps even eliminating, what we believe to be a recent localized event.”

MDC staff have contacted the two Missouri hunters who harvested the CWD-positive bucks to inform them of the situation and answer questions.

CWD is a neurological disease that is limited to deer, elk, moose and other members of the deer family, known as “cervids.” CWD is spread by animal-to-animal contact or by animal contact with soil that contains prions from urine, feces or the decomposition of an infected animal. Deer and other cervids with signs of CWD show changes in natural behavior and can exhibit extreme weight loss, excessive salivation, stumbling and tremors. CWD can spread through natural movements of infected animals, transportation of infected live captive animals, or the transportation of infected carcasses.

The Missouri Department of Agriculture (MDA) says there is no evidence from existing research that CWD can spread to domestic livestock, such as sheep or cattle. The Missouri Department of Health and Senior Services (MDHSS) says there is no scientific evidence that CWD is transmissible to humans through contact with or the consumption of deer meat.

MDC conducted its tissue-sampling effort during the fall firearms season in November in response to two cases of CWD found in captive white-tailed deer at two private, captive-hunting preserves in Linn and Macon counties. A third captive deer at one of the preserves tested positive for CWD in December. The two earlier cases of CWD found at the private hunting preserves were detected in February 2010 and October 2011. The two free-ranging bucks that tested positive were harvested within two miles of the Macon County preserve.

CWD in deer can only be confirmed by laboratory testing of the brain stem or lymph tissue. Tissue samples collected by MDC were tested by the Southeast Cooperative Wildlife Disease Study Laboratory of the University of Georgia, Athens, with confirmation by the National Veterinary Services Laboratory in Ames, Iowa.

The disease was first recognized in 1967 in captive mule deer in Colorado. CWD has also been documented in both captive and free-ranging deer in neighboring Kansas and Nebraska. It has been documented in free-ranging deer in neighboring Illinois. CWD has also been documented in both captive and free-ranging members of the deer-family in Colorado, Minnesota, New York, South Dakota, Wisconsin and the Canadian provinces of Alberta and Saskatchewan. Maryland, New Mexico, North Dakota, Utah, Virginia, West Virginia and Wyoming also have documented cases of CWD in free-ranging members of the deer family. Michigan and Montana have documented cases of CWD in captive members of the deer family.

CWD is transmitted through prions, which are abnormal proteins that attack the nervous systems of these species. These prions accumulate in the brain, spinal cord, eyes, spleen, and lymph nodes of infected animals. While there is no scientific evidence that CWD is transmissible to humans or animals other than deer and other cervids, health officials caution that consumption of these parts is not recommended. They also advise people to not eat meat from animals known to be infected with CWD or that exhibit signs of any disease.

While CWD is new to free-ranging deer in Missouri, MDC has been testing for it for years. With the help of hunters, MDC has tested more than 34,000 free-ranging deer for CWD from all parts of the state since 2002.

Missouri also has a Cervid Health Committee to address the threat of CWD to Missouri’s free-ranging and captive cervids. The Committee is composed of wildlife biologists, veterinarians and other animal-health experts from MDC, MDA, MDHSS and the USDA.

http://mdc.mo.gov/newsroom/cwd-found-two-free-ranging-deer-macon-county

Friday, October 21, 2011

Chronic Wasting Disease Found in Captive Deer Missouri

http://chronic-wasting-disease.blogspot.com/2011/10/chronic-wasting-disease-found-in.html

Friday, February 26, 2010

Chronic wasting disease found in Missouri deer

http://chronic-wasting-disease.blogspot.com/2010/02/chronic-wasting-disease-found-in.html

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html

TSS

Chronic Wasting Disease CWD cervids interspecies transmission

2012-01-22T21:27:00.000-06:00

Chronic Wasting Disease CWD cervids interspecies transmission

Wednesday, January 5, 2011

ENLARGING SPECTRUM OF PRION-LIKE DISEASES Prusiner Colby et al 2011 Prions

David W. Colby1,* and Stanley B. Prusiner1,2

+ Author Affiliations

1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu

SNIP...

Greetings,

I believe the statement and quote below is incorrect ;

"CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."

Please see ;

Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089

"although the infection rate was low (4 of 13 animals [Hamir et al. 2001])."

shouldn't this be corrected, 86% is NOT a low rate. ...

kindest regards,

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

MARCH 1, 2011

UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;

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

From: David Colby

To: flounder9@verizon.net

Cc: stanley@XXXXXXXX

Sent: Tuesday, March 01, 2011 8:25 AM

Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

Dear Terry Singeltary,

Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter.

Warm Regards, David Colby

David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware

====================END...TSS==============

SNIP...SEE FULL TEXT ;

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html

UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html

Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies Location: Virus and Prion Diseases of Livestock

Title: TRANSMISSION OF CHRONIC WASTING DISEASE AGENT OF MULE DEER (CWD**MD) TO SUFFOLK SHEEP BY INTRACEREBRAL ROUTE

Authors

Hamir, Amirali Kunkle, Robert Cutlip, Randall - ARS RETIRED Miller, Janice - ARS RETIRED Williams, Elizabeth - UNIVERSITY OF WYOMING Richt, Juergen

Submitted to: European Society of Veterinary Pathology Publication Type: Abstract Publication Acceptance Date: June 5, 2006 Publication Date: August 31, 2006 Citation: Hamir, A., Kunkle, R., Cutlip, R., Miller, J., Williams, E., Richt, J. 2006. Transmission of chronic wasting disease agent of mule deer (CWD**md) to Suffolk sheep by intracerebral route [abstract]. European Society of Veterinary Pathology 24th Annual Meeting. Paper No. P63. p. 171-172.

Technical Abstract: Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) that has been identified in captive and free-ranging cervids in the U.S. since 1967. To determine the transmissibility of CWD to sheep, 8 Suffolk lambs [4 QQ and 4 QR at codon 171 of prion protein (PRNP) gene] were inoculated intracerebrally with a pooled brain suspension from 28 mule deer naturally affected with CWD (CWD**md). Two other lambs (1 QQ and 1 QR at codon 171 of the PRNP gene) were kept as non-inoculated controls. Within 36 months post inoculation (MPI), 2 animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in the sheep with the clinical signs of TSE and its tissues were positive for the abnormal prion protein (PrP**res) by immunohistochemistry and Western blot. Between 36 and 60 MPI, 3 other sheep were euthanized because of conditions unrelated to TSE. The remaining 3 sheep remained non-clinical at the termination of the study (72 MPI) and were euthanized at that time. One of the 3 animals revealed SE and its tissues were positive for PrP**res. Both sheep positive for PrP**res were homozygous QQ at codon 171. Retrospective examination of the PRNP genotype of the 2 TSE-positive animals revealed that the sheep with clinical prion disease (euthanized at 35 MPI) was heterozygous (AV) and the sheep with the sub-clinical disease (euthanized at 72 MPI) was homozygous (AA) at codon 136 of the PRNP. These findings demonstrate that transmission of the CWD**md agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a significant part in successful transmission and incubation period of CWD**md.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194075

Transmission of chronic wasting disease of mule deer to Suffolk sheep following intracerebral inoculation

Amir N. Hamir,1 Robert A. Kunkle, Randall C. Cutlip, Janice M. Miller, Elizabeth S. Williams, Juergen A. Richt

Abstract. To determine the transmissibility of chronic wasting disease (CWD) to sheep, 8 Suffolk lambs of various prion protein genotypes (4 ARQ/ARR, 3 ARQ/ARQ, 1 ARQ/VRQ at codons 136, 154, and 171, respectively) were inoculated intracerebrally with brain suspension from mule deer with CWD (CWDmd). Two other lambs were kept as noninoculated controls. Within 36 months postinoculation (MPI), 2 inoculated animals became sick and were euthanized. Only 1 sheep (euthanized at 35 MPI) showed clinical signs that were consistent with those described for scrapie. Microscopic lesions of spongiform encephalopathy (SE) were only seen in this sheep, and its tissues were determined to be positive for the abnormal prion protein (PrPres) by immunohistochemistry and Western blot. Three other inoculated sheep were euthanized (36 to 60 MPI) because of conditions unrelated to TSE. The 3 remaining inoculated sheep and the 2 control sheep did not have clinical signs of disease at the termination of the study (72 MPI) and were euthanized. Of the 3 remaining inoculated sheep, 1 was found to have SE, and its tissues were positive for PrPres. The sheep with clinical prion disease (euthanized at 35 MPI) was of the heterozygous genotype (ARQ/VRQ), and the sheep with subclinical disease (euthanized at 72 MPH) was of the homozygous ARQ/ARQ genotype. These findings demonstrate that transmission of the CWDmd agent to sheep via the intracerebral route is possible. Interestingly, the host genotype may play a notable part in successful transmission and incubation period of CWDmd.

snip...

Thus far, among domestic animals, CWDmd has been transmitted by the intracerebral route to a goat18 and cattle.5–7 The present findings demonstrate that it is also possible to transmit CWDmd agent to sheep via the intracerebral route. However, the only sheep to develop clinical TSE within 35 MPI was genotypically AV at PRNP codon 136, suggesting that host genotype may play a notable part in successful transmission of the disease in this species. Although in Suffolk sheep the AV variant at codon 136 is very rare,17 selective breeding of Suffolk sheep with this codon has begun in the hope of testing this differential susceptibility hypothesis in a future study of CWDmd transmission to sheep.

Key words: Chronic wasting disease; immunohistochemistry; intracerebral transmission; prion protein; sheep; spongiform encephalopathy.

http://vdi.sagepub.com/content/18/6/558.long

Research Project: Transmission, Differentiation, and Pathobiology of Transmissible Spongiform Encephalopathies Location: Virus and Prion Diseases of Livestock

Title: EXPERIMENTAL SECOND PASSAGE OF CHRONIC WASTING DISEASE (CWD(MULE DEER)) AGENT TO CATTLE

Authors

Hamir, Amirali Kunkle, Robert Miller, Janice - ARS RETIRED Greenlee, Justin Richt, Juergen

Submitted to: Journal of Comparative Pathology Publication Type: Peer Reviewed Journal Publication Acceptance Date: July 25, 2005 Publication Date: January 1, 2006 Citation: Hamir, A.N., Kunkle, R.A., Miller, J.M., Greenlee, J.J., Richt, J.A. 2006. Experimental second passage of chronic wasting disease (CWD(mule deer)) agent to cattle. Journal of Comparative Pathology. 134(1):63-69.

Interpretive Summary: To compare the findings of experimental first and second passage of chronic wasting disease (CWD) in cattle, 6 calves were inoculated into the brain with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but the CWD agent was detected in their CNS tissues by 2 laboratory techniques (IHC and WB). These findings demonstrate that inoculated cattle amplify CWD agent but also develop clinical CNS signs without manifestation of microscopic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, namely, sheep scrapie. The current study confirms previous work that indicates that the diagnostic tests currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of microscopic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB. Technical Abstract: To compare clinicopathological findings of first and second passage of chronic wasting disease (CWD) in cattle, a group of calves (n=6) were intracerebrally inoculated with CWD-mule deer agent previously (first) passaged in cattle. Two other uninoculated calves served as controls. Beginning 10-12 months post inoculation (PI), all inoculates lost appetite and lost weight. Five animals subsequently developed clinical signs of central nervous system (CNS) abnormality. By 16.5 months PI, all cattle had been euthanized because of poor prognosis. None of the animals showed microscopic lesions of spongiform encephalopathy (SE) but PrPres was detected in their CNS tissues by immunohistochemistry (IHC) and Western blot (WB) techniques. These findings demonstrate that intracerebrally inoculated cattle not only amplify CWD PrPres but also develop clinical CNS signs without manifestation of morphologic lesions of SE. This situation has also been shown to occur following inoculation of cattle with another TSE agent, scrapie. The current study confirms previous work that indicates the diagnostic techniques currently used for confirmation of bovine spongiform encephalopathy (BSE) in the U.S. would detect CWD in cattle, should it occur naturally. Furthermore, it raises the possibility of distinguishing CWD from BSE in cattle due to the absence of neuropathologic lesions and a unique multifocal distribution of PrPres, as demonstrated by IHC, which in this study, appears to be more sensitive than the WB.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=178318

Wednesday, September 21, 2011

Evidence for distinct CWD strains in experimental CWD in ferrets

http://chronic-wasting-disease.blogspot.com/2011/09/evidence-for-distinct-cwd-strains-in.html

Wednesday, October 12, 2011

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

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

Wednesday, July 06, 2011

Swine Are Susceptible to Chronic Wasting Disease by Intracerebral Inoculation

http://chronic-wasting-disease.blogspot.com/2011/07/swine-are-susceptible-to-chronic.html

see incredible infection rate at one of these game farms Wisconsin shut down and bought out. 86% infection rate...

Monday, January 16, 2012

9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD

http://chronic-wasting-disease.blogspot.com/2012/01/9-game-farms-in-wisconsin-test-positive.html

Tuesday, December 20, 2011

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

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

SNIP...SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

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

CWD END OF YEAR REVIEW 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

This is an interesting editorial about the Mad Cow Disease debacle, and it’s ramifications that will continue to play out for decades to come ;

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip…

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as “sporadic” CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip…

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html

http://transmissiblespongiformencephalopathy.blogspot.com/

Chronic Wasting Disease Susceptibility of Four North American Rodents

Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu

We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html

please see ;

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf

Oral.29: Susceptibility of Domestic Cats to CWD Infection

Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason† Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu

Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness. Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.

www.landesbioscience.com Prion

http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf

see more recent science abstracts from the Prion 2011 on CWD here ;

http://felinespongiformencephalopathyfse.blogspot.com/2011/08/susceptibility-of-domestic-cats-to-cwd.html

PAGE 25

Transmission Studies

Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculam (?saline).

Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in all of these species with the shortest incubation period in the ferret.

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

Generation of a New Form of Human PrPScin Vitro by Interspecies Transmission from Cervid Prions*

Marcelo A. Barria‡, Glenn C. Telling§, Pierluigi Gambetti¶, James A. Mastrianni‖ and Claudio Soto‡,1

+ Author Affiliations

From the ‡Mitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, University of Texas Medical School at Houston, Houston, Texas 77030,

the §Departments of Microbiology, Immunology, and Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky Medical Center, Lexington, Kentucky 40506,

the ¶Institute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, and

the ‖Department of Neurology, The University of Chicago, Chicago, Illinois 60637

1 To whom correspondence should be addressed: University of Texas Medical School at Houston, 6431 Fannin St., Houston, TX 77030. Tel.: 713-500-7086; Fax: 713-500-0667; E-mail: claudio.soto@uth.tmc.edu.

Abstract

Prion diseases are infectious neurodegenerative disorders that affect humans and animals and that result from the conversion of normal prion protein (PrPC) into the misfolded prion protein (PrPSc). Chronic wasting disease (CWD) is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. Determining the risk of transmission of CWD to humans is of utmost importance, considering that people can be infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the misfolded form by CWD PrPSc, we performed experiments using the protein misfolding cyclic amplification technique, which mimics in vitro the process of prion replication. Our results show that cervid PrPSc can induce the conversion of human PrPC but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, the newly generated human PrPSc exhibits a distinct biochemical pattern that differs from that of any of the currently known forms of human PrPSc. Our results also have profound implications for understanding the mechanisms of the prion species barrier and indicate that the transmission barrier is a dynamic process that depends on the strain and moreover the degree of adaptation of the strain. If our findings are corroborated by infectivity assays, they will imply that CWD prions have the potential to infect humans and that this ability progressively increases with CWD spreading.

snip...

Interestingly, when the Western blot profile of this newly generated form of human PrPSc (termed CWD-huPrPSc) was compared with known strains of human prions, it was clear that CWD-huPrPSc exhibited a different pattern (Fig. 4A). The electrophoretic migration of this protein after PK-digestion is similar to the type 1 strain of sCJD, but its glycosylation profile is clearly different, showing a highly predominant diglycosylated form (Fig. 4A and B). This result suggests that CWD hu-PrPSc corresponds to a new human prion strain. Interestingly, a detailed previous study from Gambetti’s group comparing the biochemical characteristics of PrPSc from cervids and humans showed that CWD PrPSc is similar to sCJDMM1 in terms of electrophoretic mobility (6). However, the misfolded protein associated with CWD is predominantly di-glycosylated, whereas PrPSc from type 1 sCJD is mostly monoglycosylated (6). Based on the fact that transmission of BSE prions to humans resulted in a new form of PrPSc very similar to the one in cattle (6;27), these authors predicted that if humans were infected by CWD it is likely that PrPSc would be of type 1 and with a predominance of the diglycosylated isoform (6). Our results agree with that prediction and suggest that the newly generated CWD-huPrPSc acquires the biochemical properties of the cervid infectious material (Fig. 4A and B).

snip...

Our results have far-reaching implications for human health, since they indicate that cervid PrPSc can trigger the conversion of human PrPC into PrPSc, suggesting that CWD might be infectious to humans. Interestingly our findings suggest that unstable strains from CWD affected animals might not be a problem for humans, but upon strain stabilization by successive passages in the wild, this disease might become progressively more transmissible to man.

Reference List

snip...

please see full text and many thanks to the Professor Soto and the other Authors of this study AND to The Journal Of Biological Chemistry for the free full text !!!

Amyloid Neurodegeneration Neurological Diseases Prions Protein Conformation Prion Diseases

http://www.jbc.org/content/286/9/7490.abstract

http://www.jbc.org/content/early/2011/01/04/jbc.M110.198465.long

see full text and more here ;

http://chronic-wasting-disease.blogspot.com/2011/01/generation-of-new-form-of-human-prpsc.html

PLEASE NOTE ;

there are now two documented strains of CWD, and science is showing that indeed CWD could transmit to humans via transmission studies ;

P35

ADAPTATION OF CHRONIC WASTING DISEASE (CWD) INTO HAMSTERS, EVIDENCE OF A WISCONSIN STRAIN OF CWD

Chad Johnson1, Judd Aiken2,3,4 and Debbie McKenzie4,5 1 Department of Comparative Biosciences, University of Wisconsin, Madison WI, USA 53706 2 Department of Agriculture, Food and Nutritional Sciences, 3 Alberta Veterinary Research Institute, 4.Center for Prions and Protein Folding Diseases, 5 Department of Biological Sciences, University of Alberta, Edmonton AB, Canada T6G 2P5

The identification and characterization of prion strains is increasingly important for the diagnosis and biological definition of these infectious pathogens. Although well-established in scrapie and, more recently, in BSE, comparatively little is known about the possibility of prion strains in chronic wasting disease (CWD), a disease affecting free ranging and captive cervids, primarily in North America. We have identified prion protein variants in the white-tailed deer population and demonstrated that Prnp genotype affects the susceptibility/disease progression of white-tailed deer to CWD agent. The existence of cervid prion protein variants raises the likelihood of distinct CWD strains. Small rodent models are a useful means of identifying prion strains. We intracerebrally inoculated hamsters with brain homogenates and phosphotungstate concentrated preparations from CWD positive hunter-harvested (Wisconsin CWD endemic area) and experimentally infected deer of known Prnp genotypes. These transmission studies resulted in clinical presentation in primary passage of concentrated CWD prions. Subclinical infection was established with the other primary passages based on the detection of PrPCWD in the brains of hamsters and the successful disease transmission upon second passage. Second and third passage data, when compared to transmission studies using different CWD inocula (Raymond et al., 2007) indicate that the CWD agent present in the Wisconsin white-tailed deer population is different than the strain(s) present in elk, mule-deer and white-tailed deer from the western United States endemic region.

http://www.istitutoveneto.it/prion_09/Abstracts_09.pdf

PPo3-7:

Prion Transmission from Cervids to Humans is Strain-dependent

Qingzhong Kong, Shenghai Huang,*Fusong Chen, Michael Payne, Pierluigi Gambetti and Liuting Qing Department of Pathology; Case western Reserve University; Cleveland, OH USA *Current address: Nursing Informatics; Memorial Sloan-Kettering Cancer Center; New York, NY USA

Key words: CWD, strain, human transmission

Chronic wasting disease (CWD) is a widespread prion disease in cervids (deer and elk) in North America where significant human exposure to CWD is likely and zoonotic transmission of CWD is a concern. Current evidence indicates a strong barrier for transmission of the classical CWD strain to humans with the PrP-129MM genotype. A few recent reports suggest the presence of two or more CWD strains. What remain unknown is whether individuals with the PrP-129VV/MV genotypes are also resistant to the classical CWD strain and whether humans are resistant to all natural or adapted cervid prion strains. Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP, indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains. Preliminary results on CWD transmission in transgenic mice expressing human PrP-129V will also be discussed.

Acknowledgement Supported by NINDS NS052319 and NIA AG14359.

PPo2-27:

Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

Marcelo A. Barria,1 Glenn C. Telling,2 Pierluigi Gambetti,3 James A. Mastrianni4 and Claudio Soto1 1Mitchell Center for Alzheimer's disease and related Brain disorders; Dept of Neurology; University of Texas Houston Medical School; Houston, TX USA; 2Dept of Microbiology, Immunology & Molecular Genetics and Neurology; Sanders Brown Center on Aging; University of Kentucky Medical Center; Lexington, KY USA; 3Institute of Pathology; Case western Reserve University; Cleveland, OH USA; 4Dept of Neurology; University of Chicago; Chicago, IL USA

Prion diseases are infectious neurodegenerative disorders affecting humans and animals that result from the conversion of normal prion protein (PrPC) into the misfolded and infectious prion (PrPSc). Chronic wasting disease (CWD) of cervids is a prion disorder of increasing prevalence within the United States that affects a large population of wild and captive deer and elk. CWD is highly contagious and its origin, mechanism of transmission and exact prevalence are currently unclear. The risk of transmission of CWD to humans is unknown. Defining that risk is of utmost importance, considering that people have been infected by animal prions, resulting in new fatal diseases. To study the possibility that human PrPC can be converted into the infectious form by CWD PrPSc we performed experiments using the Protein Misfolding Cyclic Amplification (PMCA) technique, which mimic in vitro the process of prion replication. Our results show that cervid PrPSc can induce the pathological conversion of human PrPC, but only after the CWD prion strain has been stabilized by successive passages in vitro or in vivo. Interestingly, this newly generated human PrPSc exhibits a distinct biochemical pattern that differs from any of the currently known forms of human PrPSc, indicating that it corresponds to a novel human prion strain. Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.

PPo2-7:

Biochemical and Biophysical Characterization of Different CWD Isolates

Martin L. Daus and Michael Beekes Robert Koch Institute; Berlin, Germany

Key words: CWD, strains, FT-IR, AFM

Chronic wasting disease (CWD) is one of three naturally occurring forms of prion disease. The other two are Creutzfeldt-Jakob disease in humans and scrapie in sheep. CWD is contagious and affects captive as well as free ranging cervids. As long as there is no definite answer of whether CWD can breach the species barrier to humans precautionary measures especially for the protection of consumers need to be considered. In principle, different strains of CWD may be associated with different risks of transmission to humans. Sophisticated strain differentiation as accomplished for other prion diseases has not yet been established for CWD. However, several different findings indicate that there exists more than one strain of CWD agent in cervids. We have analysed a set of CWD isolates from white-tailed deer and could detect at least two biochemically different forms of disease-associated prion protein PrPTSE. Limited proteolysis with different concentrations of proteinase K and/or after exposure of PrPTSE to different pH-values or concentrations of Guanidinium hydrochloride resulted in distinct isolate-specific digestion patterns. Our CWD isolates were also examined in protein misfolding cyclic amplification studies. This showed different conversion activities for those isolates that had displayed significantly different sensitivities to limited proteolysis by PK in the biochemical experiments described above. We further applied Fourier transform infrared spectroscopy in combination with atomic force microscopy. This confirmed structural differences in the PrPTSE of at least two disinct CWD isolates. The data presented here substantiate and expand previous reports on the existence of different CWD strains.

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

Saturday, November 12, 2011

Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease

Fri, 22 Sep 2006 09:05:59 –0500

http://chronic-wasting-disease.blogspot.com/2011/11/human-prion-disease-and-relative-risk.html

Tuesday, May 31, 2011

Chronic Wasting Disease

DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011

Top Curr Chem (2011) DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011

Chronic Wasting Disease

Sabine Gilch, Nandini Chitoor, Yuzuru Taguchi, Melissa Stuart, Jean E. Jewell, and Hermann M. Schatzl

Abstract

Chronic wasting disease (CWD) is a prion disease of free-ranging and farmed ungulates (deer, elk, and moose) in North America and South Korea. First described by the late E.S. Williams and colleagues in northern Colorado and southern Wyoming in the 1970s, CWD has increased tremendously both in numerical and geographical distribution, reaching prevalence rates as high as 50% in freeranging and >90% in captive deer herds in certain areas of USA and Canada. CWD is certainly the most contagious prion infection, with significant horizontal transmission of infectious prions by, e.g., urine, feces, and saliva. Dissemination and persistence of infectivity in the environment combined with the appearance in wildliving and migrating animals make CWD presently uncontrollable, and pose extreme challenges to wild-life disease management. Whereas CWD is extremely transmissible among cervids, its trans-species transmission seems to be restricted, although the possible involvement of rodent and carnivore species in environmental transmission has not been fully evaluated. Whether or not CWD has zoonotic potential as had Bovine spongiform encephalopathy (BSE) has yet to be answered. Of note, variant Creutzfeldt–Jakob disease (vCJD) was only detected because clinical presentation and age of patients were significantly different from classical CJD. Along with further understanding of the molecular biology and pathology of CWD, its transmissibility and species restrictions and development of methods for preclinical diagnosis and intervention will be crucial for effective containment of this highly contagious prion disease.

snip...

8 Zoonotic Potential Deer hunting is a popular sport in the USA; venison is usually consumed by hunters and their families, and this raises reasonable concerns about the transmissibility of CWD to humans, as exemplified by the zoonotic transmission of BSE. Epidemiological studies have not revealed an increased incidence of CJD in CWD endemic areas. Suspicious case reports about persons having consumed venison and succumbed to neurological disorders turned out to be classical or familial CJD and a causal link to the consumption of contaminated meat could not be proven [109]. In vitro conversion assays were performed to assess the convertibility of human PrPc into PK resistant PrP using CWD derived from elk, mule deer, and white-tailed deer as a template. Only a very low conversion rate could be demonstrated, indicative of a considerable species barrier [110]. In a very recent study employing protein misfolding cyclic amplification (PMCA), a highly sensitive method for in vitro amplification conversion of human PrPc was successful, albeit with the restriction that CWD prions had to be adapted by PMCA or in vivo passage through cervidized tg mice. Passaged CWD template gave rise to a new form of human PrPSc, and its infectivity is currently under investigation. Of note, when field isolates of CWD Chronic Wasting Disease brains were used as a template, no conversion of human PrPc was achieved, which again questions the relevance of the in vitro data [111]. Studies using humanized tg mouse inoculated with CWD furthermore argue against transmissibility to humans since mice did not develop prion disease [112–114]. The best possible animal models to study transmission of animal prion diseases to humans probably are non-human primates. For instance, inoculation of BSE prions into Cynomolgus macaques provided the first hints that BSE might be transmissible to humans [115]. However, oral or i.c. challenge with CWD of macaques did not cause disease [116]. On the other hand, squirrel monkeys (Saimiri sciureus) were susceptible to i.c. inoculation with CWD prions [116, 117], and after oral exposure PrPSc was detectable in brain, spleen, and lymph nodes of 2/15 squirrel monkeys [116]. This shows that CWD can be transmitted to certain non-human primates, although results in Cynomolgus macaques might be of higher relevance since they are evolutionary closer relatives of humans than squirrel monkeys. Overall, there is no compelling evidence that CWD can be transmitted to humans with high efficiency.

snip...end

http://chronic-wasting-disease.blogspot.com/2011/05/chronic-wasting-disease-doi.html

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html

CJD9/10022

October 1994

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

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

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

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

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

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

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

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

PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html

NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

Wednesday, March 18, 2009

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

http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD

Accepted 15 November 2010. Abstract Full Text PDF References .

Abstract

The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.

http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract

"These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent."

Potential Venison Exposure Among FoodNet Population Survey Respondents, 2006-2007

Ryan A. Maddox1*, Joseph Y. Abrams1, Robert C. Holman1, Lawrence B. Schonberger1, Ermias D. Belay1 Division of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Centers for Disease Control and Prevention, Atlanta, GA *Corresponding author e-mail: rmaddox@cdc.gov

The foodborne transmission of bovine spongiform encephalopathy to humans, resulting in variant Creutzfeldt-Jakob disease, indicates that humans can be susceptible to animal prion diseases. However, it is not known whether foodborne exposure to the agent causing chronic wasting disease (CWD) in cervids can cause human disease. The United States Foodborne Diseases Active Surveillance Network (FoodNet) conducts surveillance for foodborne diseases through an extensive survey administered to respondents in selected states. To describe the frequency of deer and elk hunting and venison consumption, five questions were included in the 2006-2007 FoodNet survey. This survey included 17,372 respondents in ten states: California, Colorado, Connecticut, Georgia, Maryland, Minnesota, New Mexico, New York, Oregon, and Tennessee. Of these respondents, 3,220 (18.5%) reported ever hunting deer or elk, with 217 (1.3%) reporting hunting in a CWD-endemic area (northeastern Colorado, southeastern Wyoming, and southwestern Nebraska). Of the 217 CWD-endemic area hunters, 74 (34.1%) were residents of Colorado. Respondents reporting hunting were significantly more likely to be male than female (prevalence ratio: 3.3, 95% confidence interval: 3.1-3.6) and, in general, older respondents were significantly more likely to report hunting than younger respondents. Venison consumption was reported by more than half (67.4%) of the study population, and most venison consumers (94.1%) reported that at least half of their venison came from the wild. However, more than half (59.1%) of the consumers reported eating venison only one to five times in their life or only once or twice a year. These findings indicate that a high percentage of the United States population engages in hunting and/or venison consumption. If CWD continues to spread to more areas across the country, a substantial number of people could potentially be exposed to the infectious agent.

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf

now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????

“Our conclusion stating that we found no strong evidence of CWD transmission to humans”

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

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

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

From: "Belay, Ermias"

To:

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

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

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

Dear Sir/Madam,

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.

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

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

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

From:

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

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

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

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

Thursday, April 03, 2008

A prion disease of cervids: Chronic wasting disease

2008 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

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

snip...

full text ;

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

Monday, November 14, 2011

WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wyoming-creutzfeldt-jakob-disease-cwd.html

Wednesday, November 16, 2011

Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wisconsin-creutzfeldt-jakob-disease-cwd.html

Sunday, November 13, 2011

COLORADO CWD CJD TSE PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/colorado-cwd-cjd-tse-prion-reporting.html

Monday, May 23, 2011 CDC

Assesses Potential Human Exposure to Prion Diseases Travel Warning

Public release date: 23-May-2011

Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences

CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or "Mad Cow Disease"), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.

"While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases," commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta."But it's also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents."

Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.

CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.

Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.

The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.

The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.

According to Abrams, "The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health."

###

The article is "Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey" by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.

In an accompanying podcast CDC's Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast.

http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php

Thursday, December 29, 2011

Aerosols An underestimated vehicle for transmission of prion diseases?

PRION http://www.landesbioscience.com

please see more on Aerosols and TSE prion disease here ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/aerosols-underestimated-vehicle-for.html

Sunday, July 27, 2008

DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

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

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

Date: Fri, 16 May 2003 11:47:37 -0500

From: "Terry S. Singeltary Sr."

To: fdadockets@oc.fda.gov

Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

Several factors on this apparent voluntary proposal disturbs me greatly, please allow me to point them out;

1. MY first point is the failure of the partial ruminant-to-ruminant feed ban of 8/4/97. this partial and voluntary feed ban of some ruminant materials being fed back to cattle is terribly flawed. without the _total_ and _mandatory_ ban of all ruminant materials being fed back to ruminants including cattle, sheep, goat, deer, elk and mink, chickens, fish (all farmed animals for human/animal consumption), this half ass measure will fail terribly, as in the past decades...

2. WHAT about sub-clinical TSE in deer and elk? with the recent findings of deer fawns being infected with CWD, how many could possibly be sub-clinically infected. until we have a rapid TSE test to assure us that all deer/elk are free of disease (clinical and sub-clinical), we must ban not only documented CWD infected deer/elk, but healthy ones as well. it this is not done, they system will fail...

3. WE must ban not only CNS (SRMs specified risk materials), but ALL tissues. recent new and old findings support infectivity in the rump or ass muscle. wether it be low or high, accumulation will play a crucial role in TSEs.

4. THERE are and have been for some time many TSEs in the USA. TME in mink, Scrapie in Sheep and Goats, and unidentified TSE in USA cattle. all this has been proven, but the TSE in USA cattle has been totally ignored for decades. i will document this data below in my references.

5. UNTIL we ban all ruminant by-products from being fed back to ALL ruminants, until we rapid TSE test (not only deer/elk) but cattle in sufficient numbers to find (1 million rapid TSE test in USA cattle annually for 5 years), any partial measures such as the ones proposed while ignoring sub-clinical TSEs and not rapid TSE testing cattle, not closing down feed mills that continue to violate the FDA's BSE feed regulation (21 CFR 589.2000) and not making freely available those violations, will only continue to spread these TSE mad cow agents in the USA. I am curious what we will call a phenotype in a species that is mixed with who knows how many strains of scrapie, who knows what strain or how many strains of TSE in USA cattle, and the CWD in deer and elk (no telling how many strains there), but all of this has been rendered for animal feeds in the USA for decades. it will get interesting once someone starts looking in all species, including humans here in the USA, but this has yet to happen...

6. IT is paramount that CJD be made reportable in every state (especially ''sporadic'' cjd), and that a CJD Questionnaire must be issued to every family of a victim of TSE. only checking death certificates will not be sufficient. this has been proven as well (see below HISTORY OF CJD -- CJD QUESTIONNAIRE)

7. WE must learn from our past mistakes, not continue to make the same mistakes...

snip...

Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine I. O'Rourke5 and Edward A. Hoover1

Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523- 1671, USA1 Department of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, University of Wyoming, Laramie, WY 82070, USA 2 Colorado Division of Wildlife, Wildlife Research Center, 317 West Prospect Road, Fort Collins, CO 80526-2097, USA3 Colorado State University Veterinary Diagnostic Laboratory, 300 West Drake Road, Fort Collins, CO 80523-1671, USA4 Animal Disease Research Unit, Agricultural Research Service, US Department of Agriculture, 337 Bustad Hall, Washington State University, Pullman, WA 99164-7030, USA5

Author for correspondence: Edward Hoover.Fax +1 970 491 0523. e-mail ehoover@lamar.colostate.edu

Mule deer fawns (Odocoileus hemionus) were inoculated orally with a brain homogenate prepared from mule deer with naturally occurring chronic wasting disease (CWD), a prion-induced transmissible spongiform encephalopathy. Fawns were necropsied and examined for PrP res, the abnormal prion protein isoform, at 10, 42, 53, 77, 78 and 80 days post-inoculation (p.i.) using an immunohistochemistry assay modified to enhance sensitivity. PrPres was detected in alimentary-tract-associated lymphoid tissues (one or more of the following: retropharyngeal lymph node, tonsil, Peyer's patch and ileocaecal lymph node) as early as 42 days p.i. and in all fawns examined thereafter (53 to 80 days p.i.). No PrPres staining was detected in lymphoid tissue of three control fawns receiving a control brain inoculum, nor was PrPres detectable in neural tissue of any fawn. PrPres-specific staining was markedly enhanced by sequential tissue treatment with formic acid, proteinase K and hydrated autoclaving prior to immunohistochemical staining with monoclonal antibody F89/160.1.5. These results indicate that CWD PrP res can be detected in lymphoid tissues draining the alimentary tract within a few weeks after oral exposure to infectious prions and may reflect the initial pathway of CWD infection in deer. The rapid infection of deer fawns following exposure by the most plausible natural route is consistent with the efficient horizontal transmission of CWD in nature and enables accelerated studies of transmission and pathogenesis in the native species.

snip...

These results indicate that mule deer fawns develop detectable PrP res after oral exposure to an inoculum containing CWD prions. In the earliest post-exposure period, CWD PrPres was traced to the lymphoid tissues draining the oral and intestinal mucosa (i.e. the retropharyngeal lymph nodes, tonsil, ileal Peyer's patches and ileocaecal lymph nodes), which probably received the highest initial exposure to the inoculum. Hadlow et al. (1982) demonstrated scrapie agent in the tonsil, retropharyngeal and mesenteric lymph nodes, ileum and spleen in a 10-month-old naturally infected lamb by mouse bioassay. Eight of nine sheep had infectivity in the retropharyngeal lymph node. He concluded that the tissue distribution suggested primary infection via the gastrointestinal tract. The tissue distribution of PrPres in the early stages of infection in the fawns is strikingly similar to that seen in naturally infected sheep with scrapie. These findings support oral exposure as a natural route of CWD infection in deer and support oral inoculation as a reasonable exposure route for experimental studies of CWD.

snip...

http://vir.sgmjournals.org/cgi/content/full/80/10/2757

snip...see full text ;

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

Subject: DOCKET-- 03D-0186 -- FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

Date: Fri, 16 May 2003 11:47:37 -0500

From: "Terry S. Singeltary Sr."

To: fdadockets@oc.fda.gov

Greetings FDA,

i would kindly like to comment on;

Docket 03D-0186

FDA Issues Draft Guidance on Use of Material From Deer and Elk in Animal Feed; Availability

http://madcowfeed.blogspot.com/2008/07/docket-03d-0186-fda-issues-draft.html

Article

Experimental oral transmission of chronic wasting disease to red deer

(Cervus elaphus elaphus): Early detection and late stage distribution

of protease-resistant prion protein

Aru Balachandran, Noel P. Harrington, James Algire, Andrei Soutyrine, Terry R. Spraker,

Martin Jeffrey, Lorenzo González, Katherine I. O'Rourke

Abstract - Chronic wasting disease (CWD), an important emerging prion disease of cervids, is readily transmitted by intracerebral or oral inoculation from deer-to-deer and elk-to-elk, suggesting the latter is a natural route of exposure. Studies of host range susceptibility to oral infection, particularly of those species found in habitats where CWD currently exists are imperative. This report describes the experimental transmission of CWD to red deer following oral inoculation with infectious CWD material of elk origin. At 18 to 20 months post-inoculation, mild to moderate neurological signs and weight loss were observed and animals were euthanized and tested using 3 conventional immunological assays. The data indicate that red deer are susceptible to oral challenge and that tissues currently used for CWD diagnosis show strong abnormal prion (PrPCWD) accumulation. Widespread peripheral PrPCWD deposition involves lymphoreticular tissues, endocrine tissues, and cardiac muscle and suggests a potential source of prion infectivity, a means of horizontal transmission and carrier state.

SNIP...

There is a strong correlation between the presence of PrPTSE and infectivity in prion diseases. Although the epidemiologic evidence strongly suggests that CWD is not transmissible to humans, this study and others suggest caution in this regard. The finding of PrPCWD in various organs, albeit in clinical CWD, suggests that humans who consume or handle meat from CWD-infected red deer may be at risk of exposure to CWD prions. This study found that red deer tissues other than nervous and lymphoid tissue can support CWD prion replication and accumulation. As a result, the consumption or handling of meat from CWD-infected red deer will put humans at risk of exposure to CWD prions. In spite of a well-documented species barrier, a cautious approach would involve preventing such tissues from entering the animal and human food chains. Future studies will require sensitive and quantitative techniques such as bioassays in transgenic mice that assess tissue infectivity and quantitative immunoassays adapted to PrPCWD detection in peripheral tissues.

SNIP...

The exact mode of transmission of CWD in nature remains unclear but is believed to involve direct animal-to-animal contact or environmental contamination. As TSE agents are extremely resistant in the environment (39), oral exposure is the most plausible pathway by which the CWD prion may be introduced to deer in nature and represents a significant obstacle to eradication of CWD from either farmed or free-ranging cervid populations. The distribution of PrPCWD in gut-associated lymphoid tissues, salivary glands, and nasal mucosa in the red deer of this study suggests potential routes of PrPCWD shedding into the environment via fluids such as saliva or feces. However, this study did not identify the point at which an animal may become infectious during the course of infection. An improved understanding of the mechanisms of shedding and transmission will be important in the future management of CWD.

SNIP...

In summary, this study demonstrates the potential for oral transmission of CWD to red deer and describes the pattern of PrPCWD accumulation for this species. The current surveillance testing regime for cervids would be expected to identify CWD-infected red deer should it occur in North America. These results confirm the usefulness of rapid tests such as ELISA but with generally slightly lower sensitivity when compared with IHC when testing tissues with patchy or sporadic PrPCWD deposition. The finding of PrPCWD in several extraneural tissues including cardiac muscle and the endocrine system suggests that further investigation and monitoring of the potential transmissibility to other species including humans is warranted.

SNIP...

(Traduit par Isabelle Vallières)

Can Vet J 2010;51:169-178

Ottawa Laboratory - Fallowfield, Canadian Food Inspection Agency, Ottawa, Ontario (Balachandran, Harrington, Algire,

Soutyrine); Veterinary Diagnostic Laboratory, Colorado State University, Fort Collins, Colorado, USA (Spraker); Veterinary

Laboratory Agency, Department for the Environment, Food & Rural Affairs, Lasswade, Midlothian, Scotland, United Kingdom

(Jeffrey, González); Animal Disease Research Unit, Agricultural Research Service, United States Department of Agriculture, Pullman,

Washington, USA (O'Rourke).

Address all correspondence to Dr. Aru Balachandran; e-mail: BalachandranA@inspection.gc.ca

http://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1109&context=zoonoticspub

Saturday, November 6, 2010

TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU Berne, 2010 TAFS

INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation

http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html

Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>

Prion disease update 2010 (11)

PRION DISEASE UPDATE 2010 (11)

http://www.promedmail.org/direct.php?id=20101206.4364

Wednesday, January 18, 2012

BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE

February 1, 2012

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/bse-in-goats-can-be-mistaken-for.html

Friday, January 6, 2012

OIE 2012 Training Manual on Wildlife Diseases and Surveillance and TSE Prion disease

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/oie-2012-training-manual-on-wildlife.html

Tuesday, January 17, 2012

Annual report of the Scientific Network on BSE-TSE EFSA-Q-2011-01110 Issued: 20 December 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/annual-report-of-scientific-network-on.html

http://transmissiblespongiformencephalopathy.blogspot.com/

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

2011 Monday, September 26, 2011

L-BSE BASE prion and atypical sporadic CJD

http://bse-atypical.blogspot.com/2011/09/l-bse-base-prion-and-atypical-sporadic.html

http://creutzfeldt-jakob-disease.blogspot.com/

TSS

9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD

2012-01-16T22:31:00.000-06:00

9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD

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

Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years.

However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil.

Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. < < <

SEEMS Wisconsin may have to have a 5 year CWD plan of quarantine and disinfection for the whole state of Wisconsin, and that probably is not near long enough. it may take decades, if Wisconsin can ever be cleaned up at all. Wisconsin has 9 _documented_ CWD infected game farms to date. Wisconsin should close every one of those CWD infected game farms down, and do the same thing with them, as they did the Almond Buckhorn Farm. just my opinion. ...TSS

> > > similar if less acute concerns exist for all nine deer farms in Wisconsin that have tested positive for CWD. < < <

WISCONSIN DEPT. OF NATURAL RESOURCES

NEWS RELEASE

Wisconsin Department of Natural Resources

West Central Region

1300 W. Clalremont Ave., PO Box 4001, Eau Claire, WI 54702-2786 Phone: (715) 839-3715 TDD: 711 dnr.wi.gov www.wisconsin.gov

DATE: Monday, July 18,2011

CONTACTS: Davin Lopez, ONR CWO coordinator, Madison. 608-267-2948 Kris Belling, DNR regional wildlife supervisor, Eau Claire, 715-839-3736

SUBJECT: Public input sought on future of CWO-tainted deer farm

In the end, 82 of the deer killed and removed tested positive for CWD. This is an 80 percent infection rate, the highest rate ofCWD infection recorded in North America, and possibly in the world.

-30-

Tuesday, December 20, 2011

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

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

SNIP...SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

TSS

Rapid Detection of CWD PrP: Comparison of Tests Designed for the Detection of BSE or Scrapie

2012-01-11T14:05:00.000-06:00

ORIGINAL ARTICLE

Rapid Detection of CWD PrP: Comparison of Tests Designed for the Detection of BSE or Scrapie

T. Blasche1,†, E. v. Schenck2,‡, A. Balachandran3, M. W. Miller4, J. Langenberg5,§, K. Frölich6, F. Steinbach7Article first published online: 28 DEC 2011 DOI: 10.1111/j.1865-1682.2011.01294.x

Keywords: CWD; deer; ELISA; rapid test; Western blot

Summary

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) mainly affecting cervids in North America. The accumulation of an abnormal form of host-encoded prion protein (PrPCWD) in the CNS and lymphoid tissues is characteristic of the disease and known to be caused by pathogenic prion proteins (PrPres), which are thought to be transmitted mainly by contact with body fluids, such like saliva. Species known to be naturally infected by CWD include Rocky Mountain elk (Cervus elaphus nelsoni), white-tailed deer (Odocoileus virginianus) and mule deer (Odocoileus hemionus). Recently, large-scale disease eradication or control programs have been attempted to curtail the spread of disease. But reports of diseased free-ranging and farmed cervids in many locations in the USA and Canada are still continuing. The goal of this study was to find sensitive rapid test systems that are reliably able to detect CWD-associated PrPCWD in cervids, thereby reviewing an important control tool in case the disease spreads further and reaches Europe. Seven tests, originally developed for the detection of other TSE diseases such as Scrapie and bovine spongiform encephalopathy, including two Western blots, four enzyme-linked immunosorbent assays (ELISAs), and one lateral flow device, were included in this study. All seven tests evaluated were able to detect pathogenic prion proteins (PrPCWD) in Northern American infected animals and distinguish physiologic prion protein (PrPc) in brainstem (obex region) and lymph node samples from North American and European cervids, respectively. However, the specificity and sensitivity of the tests differed significantly. Highly sensitive tests for the detection of prion proteins are an important tool both for the design of effective disease surveillance and control strategies and the safety of the food chain. Thus, this study contributes to the emergency preparedness against CWD.

http://onlinelibrary.wiley.com/doi/10.1111/j.1865-1682.2011.01294.x/abstract

Prion Disease Blood Test Using Immunoprecipitation and Improved Quaking-Induced Conversion

Christina D. Orrúa, Jason M. Wilhama, Lynne D. Raymonda, Franziska Kuhnb, Björn Schroederb, Alex J. Raeberb, and Byron Caugheya

+ Author Affiliations

Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA,a and Prionics AG, Zurich, Switzerlandb Address correspondence to Byron Caughey, bcaughey@nih.gov. Editor Reed Wickner, National Institutes of Health

Next Section

ABSTRACT

A key challenge in managing transmissible spongiform encephalopathies (TSEs) or prion diseases in medicine, agriculture, and wildlife biology is the development of practical tests for prions that are at or below infectious levels. Of particular interest are tests capable of detecting prions in blood components such as plasma, but blood typically has extremely low prion concentrations and contains inhibitors of the most sensitive prion tests. One of the latter tests is quaking-induced conversion (QuIC), which can be as sensitive as in vivo bioassays, but much more rapid, higher throughput, and less expensive. Now we have integrated antibody 15B3-based immunoprecipitation with QuIC reactions to increase sensitivity and isolate prions from inhibitors such as those in plasma samples. Coupling of immunoprecipitation and an improved real-time QuIC reaction dramatically enhanced detection of variant Creutzfeldt-Jakob disease (vCJD) brain tissue diluted into human plasma. Dilutions of 1014-fold, containing ~2 attogram (ag) per ml of proteinase K-resistant prion protein, were readily detected, indicating ~10,000-fold greater sensitivity for vCJD brain than has previously been reported. We also discriminated between plasma and serum samples from scrapie-infected and uninfected hamsters, even in early preclinical stages. This combined assay, which we call “enhanced QuIC” (eQuIC), markedly improves prospects for routine detection of low levels of prions in tissues, fluids, or environmental samples.

IMPORTANCE Transmissible spongiform encephalopathies (TSEs) are largely untreatable and are difficult to diagnose definitively prior to irreversible clinical decline or death. The transmissibility of TSEs within and between species highlights the need for practical tests for even the smallest amounts of infectivity. A few sufficiently sensitive in vitro methods have been reported, but most have major limitations that would preclude their use in routine diagnostic or screening applications. Our new assay improves the outlook for such critical applications. We focused initially on blood plasma because a practical blood test for prions would be especially valuable for TSE diagnostics and risk reduction. Variant Creutzfeldt-Jakob disease (vCJD) in particular has been transmitted between humans via blood transfusions. Enhanced real-time quaking-induced conversion (eRTQ) provides by far the most sensitive detection of vCJD to date. The 15B3 antibody binds prions of multiple species, suggesting that our assay may be useful for clinical and fundamental studies of a variety of TSEs of humans and animals.

http://mbio.asm.org/content/2/3/e00078-11.full

Title: Investigation of the effects of experimental autolysis on the detection of abnormal prion protein in lymphoid and central nervous system tissues from elk and sheep using the Western blotting method

Authors

Huang, H - CANADIAN FOOD INSPECTION Soutyrine, A - Rendulich, J - CANADIAN FOOD INSPECTION OROURKE, KATHERINE Balachandran, A - CANADIAN FOOD INSPECTION

Submitted to: Canadian Journal of Veterinary Research Publication Type: Peer Reviewed Journal Publication Acceptance Date: January 17, 2010 Publication Date: January 3, 2011 Citation: Huang, H., Soutyrine, A., Rendulich, J., Orourke, K.I., Balachandran, A. 2011. Investigation of the effects of experimental autolysis on the detection of abnormal prion protein in lymphoid and central nervous system tissues from elk and sheep using the Western blotting method. Canadian Journal of Veterinary Research. 75(1)69-72.

Interpretive Summary: Tissues unsuitable for standard microscopic examination for evidence of chronic wasting disease of elk or scrapie of sheep are often submitted for testing in Canada. In this investigation, a method for testing these tissues using an enrichment step was evaluated. The study showed that the amount of the disease marker PrP-Sc in lymph nodes and brain from prion-positive elk and sheep decreased gradually but was still detectable after 5 and 15 days incubation at body temperature. This assay is therefore a useful screening and confirmatory test for PrP-Sc in these tissues. Technical Abstract: Chronic wasting disease CWD is a transmissible spongiform encephalopathy of cervid ruminants, including white tailed deer, mule deer, black tailed deer, moose, and elk. The disease is related to the scrapie of sheep. In both diseases, diagnosis is typically made by detection of the disease associated prion protein PrP-Sc using histology, immunohistochemistry, or enzyme-linked immunosorbent assays. CWD in farmed elk and scrapie in domestic sheep are endemic in some regions of Canada. Surveillance of fallen stock is a component of the control program. However, these samples show varying levels of autolysis and bacterial overgrowth. The resulting loss of morphology complicates diagnosis by histology and immunohistochemistry. In this study, the investigators evaluated a sensitive western blot with enrichment of the marker protein PrP-Sc using phosphotungstate acid precipitation. A simulated autolysis trial using tissues held at 37C for 0, 5, or 15 days was conducted, using a commercial enzyme linked immunosorbent assay as a reference test for quantitative measurements. The investigation demonstrated that although the PrP-Sc signal was reduced by autolysis, the western blot analysis could correctly identify the PrP-Sc positive cases. Validation of the method for elk and sheep will allow the Canadian Food Inspection Agency to use a single western blot diagnostic method for all small and wild ruminant species in the prion surveillance programs.

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=202285

better hurry up. ...tss

CWD END OF YEAR REVIEW 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

This is an interesting editorial about the Mad Cow Disease debacle, and it’s ramifications that will continue to play out for decades to come ;

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip…

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as “sporadic” CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip…

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html

http://transmissiblespongiformencephalopathy.blogspot.com/

Tuesday, May 31, 2011

Chronic Wasting Disease

DOI: 10.1007/128_2011_159 # Springer-Verlag Berlin Heidelberg 2011

http://chronic-wasting-disease.blogspot.com/2011/05/chronic-wasting-disease-doi.html

Saturday, November 12, 2011

Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease

Fri, 22 Sep 2006 09:05:59 –0500

http://chronic-wasting-disease.blogspot.com/2011/11/human-prion-disease-and-relative-risk.html

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html

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

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

PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey

Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html

NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

Wednesday, March 18, 2009

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

http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html

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

UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html

CWD to cattle figures CORRECTION

Greetings,

I believe the statement and quote below is incorrect ;

Please see ;

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089

" although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "

shouldn't this be corrected, 86% is NOT a low rate. ...

kindest regards,

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

Thank you!

Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.

http://cshperspectives.cshlp.org/letters/submit

re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html

Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures.

snip...

http://cshperspectives.cshlp.org/content/3/1/a006833.full.pdf+html

please see CWD potential to humans here ;

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html

Greetings,

I believe the statement and quote below is incorrect ;

Please see ;

http://www.ars.usda.gov/research/publications/publications.htm?seq_no_115=194089

"although the infection rate was low (4 of 13 animals [Hamir et al. 2001])."

shouldn't this be corrected, 86% is NOT a low rate. ...

kindest regards,

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

MARCH 1, 2011

UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;

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

From: David Colby

To: flounder9@verizon.net

Cc: stanley@XXXXXXXX

Sent: Tuesday, March 01, 2011 8:25 AM

Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

Dear Terry Singeltary,

Warm Regards, David Colby

David Colby, PhDAssistant ProfessorDepartment of Chemical EngineeringUniversity of Delaware

====================END...TSS==============

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html

Thursday, December 29, 2011

Aerosols An underestimated vehicle for transmission of prion diseases?

PRION http://www.landesbioscience.com

please see more on Aerosols and TSE prion disease here ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/aerosols-underestimated-vehicle-for.html

Saturday, December 31, 2011

Depopulation Plan Being Developed for Captive Deer Facility in Macon County after second CWD positive confirmation

http://chronic-wasting-disease.blogspot.com/2011/12/depopulation-plan-being-developed-for.html

please see this game farm that was shut down, and the incredible infection rate ;

Tuesday, December 20, 2011

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

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

Wednesday, December 21, 2011

CWD UTAH San Juan deer hunting unit

http://chronic-wasting-disease.blogspot.com/2011/12/cwd-utah-san-juan-deer-hunting-unit.html

Monday, November 14, 2011

WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wyoming-creutzfeldt-jakob-disease-cwd.html

Wednesday, November 16, 2011

Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wisconsin-creutzfeldt-jakob-disease-cwd.html

Sunday, November 13, 2011

COLORADO CWD CJD TSE PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/colorado-cwd-cjd-tse-prion-reporting.html

Wednesday, January 04, 2012

CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND HOLT COUNTIES DURING NOVEMBER HUNT

http://chronic-wasting-disease.blogspot.com/2012/01/cwd-nebraska-ngpc-26-deer-carcasses.html

Friday, December 23, 2011

Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model

Volume 18, Number 1—January 2012 Dispatch

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/oral-transmission-of-l-type-bovine.html

Saturday, December 3, 2011

Isolation of Prion with BSE Properties from Farmed Goat

Volume 17, Number 12—December 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/isolation-of-prion-with-bse-properties.html

Monday, January 2, 2012

EFSA Minutes of the 6th Meeting of the EFSA Scientific Network on BSE-TSE Brussels, 29-30 November 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2012/01/efsa-minutes-of-6th-meeting-of-efsa.html

Wednesday, January 11, 2012

Bucks for brains on offer to cattle and sheep producers Queensland TSE PRION TESTING

http://usdameatexport.blogspot.com/2012/01/bucks-for-brains-on-offer-to-cattle-and.html

Thursday, November 18, 2010

UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS

http://bse-atypical.blogspot.com/2010/11/united-states-of-america-vs-galen-j.html

Friday, February 18, 2011

UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS ''PLEADS GUILTY"

http://bse-atypical.blogspot.com/2011/02/united-states-of-america-vs-galen-j.html

BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992

IN CONFIDENCE

The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".

http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html

http://madcowtesting.blogspot.com/

tss

CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND HOLT COUNTIES DURING NOVEMBER HUNT

2012-01-04T09:44:00.002-06:00

CWD Found in Buffalo, Custer, Holt Counties

January 3, 2012

LINCOLN, Neb. – Chronic wasting disease (CWD) in deer has appeared for the first time in Buffalo, Custer and Holt counties, according to the Nebraska Game and Parks Commission.

There were 1,565 lymph node samples collected from deer taken during the 2011 November firearm deer season, with 26 samples testing positive for CWD. In addition, samples were taken from 37 culled deer that showed clinical symptoms for CWD, with one male mule deer from Garden County testing positive. Those symptoms include a rough, emaciated appearance and a lack of fear of humans.

There were a record 51 positives from 3,645 samples in Nebraska in 2010. However, the surveillance effort was reduced in 2011 due to a lack of funds. The 2011 effort focused on central Nebraska, the leading edge of the disease as it spreads from west to east.

Game and Parks confirmed CWD in the state’s deer population in 2000. CWD is a disease that can affect deer and elk and always is fatal to the affected animal. Humans have never been known to contract CWD.

http://outdoornebraska.ne.gov/search_results.asp?cx=004642562441590118981%3A_8s8njxre5k&cof=FORID%3A10&ie=UTF-8&q=news&sa=Search&siteurl=outdoornebraska.ne.gov%2FNews%2Fradio%2Fradio.asp

Chronic wasting disease found in deer killed in central Nebraska, game officials say

LINCOLN, Neb. — The Nebraska Game and Parks Commission says chronic wasting disease has been found in three central Nebraska counties for the first time.

The commission says a total of 26 deer carcasses tested positive for the disease in Buffalo, Custer and Holt counties during the November firearm hunting season. Nearly 1,600 lymph node samples were taken. One mule deer carcass in Garden County tested positive.

In 2010, 51 positives were found in the more than 3,600 test samples.

The 2011 testing was curtailed by budget issues, so it was concentrated on central Nebraska, which the commission says is the leading edge of the disease as it spreads from west to east.

The disease affects deer and elk and is always fatal. No human cases have ever been recorded.

http://www.therepublic.com/view/story/bb5b706b581a49d2b0276bc25aa64e77/NE--Diseased-Deer/

Nebraska Chronic Wasting Disease

http://outdoornebraska.ne.gov/wildlife/guides/cwd/cwd.asp

http://outdoornebraska.ne.gov/wildlife/guides/cwd/cwdresults.asp

http://outdoornebraska.ne.gov/wildlife/guides/cwd/pdf/management.pdf

CWD IN NEBRASKA IS INCREASING WITH 51 POSITIVE CASES IN 2010

Posted Mar 02 2011 9:31pm

Fifty-One Deer Test Positive for CWD

March 1, 2011 News

LINCOLN, Neb. – Nebraska is experiencing an increase in the number of deer testing positive for chronic wasting disease (CWD), as well as a wider distribution, according to the Nebraska Game and Parks Commission. There were a record 51 positives in 2010.

CWD is a disease that can affect deer and elk and is always fatal to the affected animal. Humans have never been known to contract CWD.

There were 3,645 lymph node samples collected from deer harvested during the November firearm season. The 51 positives were the most in Nebraska in one year.

The counties with the highest number of positives were: Sioux, 11; Sheridan, 7; Dawes, 6; Garden, 6; Box Butte, 4; Scotts Bluff, 4; and Morrill, 3. There were two positives each in Banner and Hitchcock counties and one each in Hooker, Keith, Lincoln, Loup, Cherry, and Hall counties. The counties in which CWD was found for the first time are: Hitchcock, Hooker, Lincoln, and Loup.

No elk tested positive for CWD in 2010.

http://outdoornebraska.ne.gov/blogs/2011/03/fifty-one-deer-test-positive-cwd/

Can Humans Be Infected with CWD? There is currently no scientific evidence that CWD has or can spread to humans, either through contact with infected animals or by eating the meat of infected animals. The Centers for Disease Control and Prevention has conducted an exhaustive study of CWD and human risk and has stated: "The risk of infection with the CWD agent among hunters is extremely small, if it exists at all." However, as we are still learning about this disease, the Commission recommends that hunters take precautions to limit risks. First and foremost, do not harvest any animal that appears sick or is acting strange.

Note the animal's location and contact the Commission. Avoid cutting or puncturing the spinal cords or brains of animals taken in the areas where CWD occurs. Do not use household utensils to field dress or process your deer. Wear rubber or latex gloves when handling any harvested animal.

Can the Disease Spread to Other Animals, Such As Cattle? Again, there is no indication or scientific evidence that the disease can spread to species other than deer or elk, but research in this area continues. Studies have shown that cattle placed in close and confined proximity with infected deer and elk have not developed the disease after living with them for over seven years.

http://outdoornebraska.ne.gov/wildlife/guides/CWD/cwd.asp

http://outdoornebraska.ne.gov/blogs/

Wednesday, March 02, 2011

CWD IN NEBRASKA IS INCREASING WITH 51 POSITIVE CASES IN 2010

http://chronic-wasting-disease.blogspot.com/2011/03/cwd-in-nebraska-is-increasing-with-51.html

Wednesday, February 04, 2009

Nebraska reports 22 cases of CWD in deer

http://chronic-wasting-disease.blogspot.com/2009/02/nebraska-reports-22-cases-of-cwd-in.html

Tuesday, December 18, 2007

NEBRASKA CWD tested 3,400 deer, with 17 testing positive 2007

http://chronic-wasting-disease.blogspot.com/2007/12/nebraska-cwd-tested-3400-deer-with-17.html

http://chronic-wasting-disease.blogspot.com/2007_12_01_archive.html

http://wildlifedisease.nbii.gov/documents/CWD%20Updates/Update%2089.pdf

CHRONIC WASTING DISEASE CWD END OF YEAR REVIEW 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html

http://transmissiblespongiformencephalopathy.blogspot.com/

Thursday, December 29, 2011

Aerosols An underestimated vehicle for transmission of prion diseases?

PRION www.landesbioscience.com

please see more on Aerosols and TSE prion disease here ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/aerosols-underestimated-vehicle-for.html

Saturday, December 31, 2011

Depopulation Plan Being Developed for Captive Deer Facility in Macon County after second CWD positive confirmation

http://chronic-wasting-disease.blogspot.com/2011/12/depopulation-plan-being-developed-for.html

please see this game farm that was shut down, and the incredible infection rate ;

Tuesday, December 20, 2011

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

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

Wednesday, December 21, 2011

CWD UTAH San Juan deer hunting unit

http://chronic-wasting-disease.blogspot.com/2011/12/cwd-utah-san-juan-deer-hunting-unit.html

Monday, November 14, 2011

WYOMING Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wyoming-creutzfeldt-jakob-disease-cwd.html

Wednesday, November 16, 2011

Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wisconsin-creutzfeldt-jakob-disease-cwd.html

Sunday, November 13, 2011

COLORADO CWD CJD TSE PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/colorado-cwd-cjd-tse-prion-reporting.html

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html

Friday, December 23, 2011

Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model

Volume 18, Number 1—January 2012 Dispatch

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/oral-transmission-of-l-type-bovine.html

Saturday, December 3, 2011

Isolation of Prion with BSE Properties from Farmed Goat

Volume 17, Number 12—December 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/isolation-of-prion-with-bse-properties.html

TSS

Wednesday, January 04, 2012

CWD NEBRASKA NGPC 26 DEER CARCASSES TESTED POSITIVE BUFFALO, CUSTER AND HOLT COUNTIES DURING NOVEMBER HUNT

http://chronic-wasting-disease.blogspot.com/2012/01/cwd-nebraska-ngpc-26-deer-carcasses.html

Depopulation Plan Being Developed for Captive Deer Facility in Macon County after second CWD positive confirmation

2011-12-31T10:39:00.000-06:00

December 30, 2011

Depopulation Plan Being Developed for Captive Deer Facility in Macon County

The Missouri Department of Agriculture is finalizing a depopulation and management plan for an approximately 3,000 acre captive wildlife hunting facility in northern Missouri following two positive tests for Chronic Wasting Disease. The facility, operated by Heartland Wildlife Ranches, LLC, is home to white-tail deer, elk and red deer.

The plan includes a requirement to depopulate and test all remaining animals for CWD, as well as restrictions on the future movement of animals into the facility. The plan follows multiple positive CWD tests indentified through random surveillance and extends the facility's current quarantine until all animals have been depopulated and tested for the disease.

In October, MDA received results from the USDA National Veterinary Services Laboratory in Ames, Iowa indicating that a captive white-tail deer harvested in the Macon County facility tested positive for CWD. The animal that tested positive was inspected as part of the State's CWD surveillance and testing program. A second positive test result on a captive white-tail deer within the same facility was verified late this week.

"This plan is an important step forward as we continue working to ensure that this situation is addressed quickly and effectively and that the health of Missouri's cervids is protected from this disease," said State Veterinarian Dr. Linda Hickam.

The State's CWD Contingency Plan was developed in 2002 and revised in 2003 by the Cervid Health Committee, a task force comprised of industry representatives, veterinarians and staff from the departments of Agriculture, Conservation and Health and Senior Services and the U.S. Department of Agriculture.

In February 2010 a case of CWD was confirmed in Linn County on a captive hunting preserve operated by the same entity, Heartland Wildlife Ranches, LLC. The Linn County facility was depopulated and no further infection was identified at that facility.

CWD is transmitted by live animal to animal contact or soil to animal contact. The disease was first recognized in 1967 in captive mule deer in the Colorado Division of Wildlife captive wildlife research facility in Fort Collins, Colorado. CWD has been documented in deer and/or elk in Colorado, Illinois, Kansas, Maryland, Michigan, Minnesota, Montana, Nebraska, New Mexico, New York, North Dakota, Oklahoma, South Dakota, Utah, Virginia, West Virginia, Wisconsin, and the Canadian Provinces of Alberta and Saskatchewan. There has been no evidence that the disease can be transmitted to humans.

CWD is a neurological disease found in deer, elk and moose; it has not been reported in humans or non-cervid animals.

For more information on CWD, contact Missouri's State Veterinarian Dr. Linda Hickam at (573) 751-3377 or visit the Department online at http://www.mda.mo.gov.

http://mda.mo.gov/news/2011/Depopulation_Plan_Being_Developed_for_Captive_Deer_Facility_in_Macon_County

Friday, October 21, 2011 Chronic Wasting Disease Found in Captive Deer Missouri October 20, 2011

http://chronic-wasting-disease.blogspot.com/2011/10/chronic-wasting-disease-found-in.html

please see this game farm that was shut down, and the incredible infection rate ;.

Tuesday, December 20, 2011.

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

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

Thursday, December 29, 2011.

Aerosols An underestimated vehicle for transmission of prion diseases?

PRION www.landesbioscience.com

please see more on Aerosols and TSE prion disease here ;. ...

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/aerosols-underestimated-vehicle-for.html

Monday, June 27, 2011.

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates.

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html

kind regards, terry

Chronic Wasting Disease discovered on game farm Saskatchewan Wednesday Dec. 21, 2011

2011-12-22T12:43:00.000-06:00

Chronic Wasting Disease discovered on game farm

CTV Saskatoon

Date: Wednesday Dec. 21, 2011 5:55 PM CST

Chronic wasting disease has been discovered on another game farm in Saskatchewan. It is the fourth case in the province so far this year.

The latest case involves a white tail deer from a farm in the Prince Albert area. The animal was discovered to be carrying the disease through a mandatory testing program for all animals over the age of 12 months that die on farms.

Canada Food Inspection Agency scientists say the disease poses very little risk to humans.

However, they say to prevent the spread of CWD to other animals or farms it is necessary to slaughter the entire herd.

Alex McIsaac, from CIFA, says slaughter is the only way to do an accurate test. "Unfortunately we don't have a live animal test at this time so that's the only way we can determine how far it has spread, unfortunately it's by destroying animals and using this post-mortem sample."

http://saskatoon.ctv.ca/servlet/an/local/CTVNews/20111221/sas-cwd-111221/20111221/?hub=Saskatoon

Saskatchewan deer tests positive for fatal disorder

CWD case doesn't raise concern with CFIA

Reported by Brent Bosker First Posted: Dec 20, 2011 8:46am

Chronic Wasting Disease (CWD) has resurfaced in Saskatchewan.

According to the Canadian Food Inspection Agency (CFIA), a white tail deer tested positive for the fatal disorder last month on a farm in the Prince Albert district.

The farm where the deer tested positive has been quarantined and the remainder of the herd will be destroyed.

The case isn’t raising any concern with the CFIA who monitors and investigates cases.

“Basically this is about what we would expect to see,” said Alex McIsaac, veterinarian disease control specialist with CFIA.

“We find these cases through surveillance … it’s a mandatory requirement for cervid producers in Saskatchewan to submit heads from animals over 12 months of age that die unexpectedly,” McIssac said.

CWD is a degenerative disease that affects the central nervous system of cervids such as elk, moose and deer.

The disease is a spongy type of legion on the brain that McIssac said causes a number of symptoms.

“We would see a lack of coordination, difficulty walking, separation from herd (so now they don’t feel they’re a part of the herd they’re a little nervous about where they are), excess of salivation (so they drool a lot), depression … and unusual behavior.”

This case comes six months after the last case was reported and is the fourth one this year.

Since surveillance began in 1996 there have been 66 cases across Canada, predominantly in Saskatchewan.

Saskatchewan had five cases in 2010 and two in 2009.

Edited by News Talk Radio's Karin Yeske.

http://cjme.com/story/saskatchewan-deer-tests-positive-fatal-disorder/37094

Herds infected with Chronic Wasting Disease in Canada in 2011

The CFIA works with provincial governments and industry to conduct regular CWD surveillance. Ongoing provincial surveillance for CWD varies with each particular province's perceived threat and infection status. Testing is mandatory in Manitoba, Saskatchewan, Alberta and the Yukon; it is voluntary elsewhere.

In addition, CWD is a reportable disease under the Health of Animals Regulations. This means that all suspected cases must be reported to the CFIA.

The following table lists domestic cervid herds confirmed to be infected with CWD in Canada in 2011.

Current as of: 2011-11-30

Date confirmed Location Animal type infected

November 22 Saskatchewan Deer

May 15 Saskatchewan Elk

January 19 Saskatchewan Deer

January 4 Saskatchewan Deer

http://www.inspection.gc.ca/english/anima/disemala/rep/2011cwdmdce.shtml

CWD ALBERTA CANADA STATISTICS 2011

http://www.srd.alberta.ca/FishWildlife/WildlifeDiseases/ChronicWastingDisease/CWDUpdates/documents/CWD-PositiveStats-WildDeerAlberta-Dec2011.pdf

http://www.environment.gov.sk.ca/cwd

http://www.environment.gov.sk.ca/Default.aspx?DN=2634b531-ef3e-43da-9dc4-2c7e9cb36cf5

http://www.agriculture.gov.sk.ca/Default.aspx?DN=4aa45d0a-145a-44ad-b970-0e749381af14

http://www.inspection.gc.ca/english/anima/disemala/cwdmdc/cwdmdce.shtml

ALBERTA

http://www1.agric.gov.ab.ca/$department/deptdocs.nsf/all/rsb7193

YUKON

http://www.emr.gov.yk.ca/agriculture/disease_monitoring.html

Wednesday, June 01, 2011

Management of CWD in Canada: Past Practices, Current Conditions, Current Science, Future Risks and Options

http://chronic-wasting-disease.blogspot.com/2011/06/management-of-cwd-in-canada-past.html

see the incredible infection rate from cwd at this game farm in Wisconsin ;

Tuesday, December 20, 2011

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

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

Monday, January 05, 2009

CWD, GAME FARMS, BAITING, AND POLITICS

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html

http://chronic-wasting-disease.blogspot.com/2008/08/cwd-feeding-and-baiting-piles.html

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

http://transmissiblespongiformencephalopathy.blogspot.com/

Saturday, November 12, 2011

Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease

Fri, 22 Sep 2006 09:05:59 –0500

http://chronic-wasting-disease.blogspot.com/2011/11/human-prion-disease-and-relative-risk.html

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html

Friday, March 4, 2011

Alberta dairy cow found with mad cow disease

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/alberta-dairy-cow-found-with-mad-cow.html

Wednesday, August 11, 2010

REPORT ON THE INVESTIGATION OF THE SIXTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

http://bse-atypical.blogspot.com/2010/08/report-on-investigation-of-sixteenth.html

Thursday, August 19, 2010

REPORT ON THE INVESTIGATION OF THE SEVENTEENTH CASE OF BOVINE SPONGIFORM ENCEPHALOPATHY (BSE) IN CANADA

http://bseusa.blogspot.com/2010/08/report-on-investigation-of-seventeenth.html

Thursday, February 10, 2011

TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY REPORT UPDATE CANADA FEBRUARY 2011 a nd how to hide mad cow disease in Canada Current as of: 2011-01-31

http://madcowtesting.blogspot.com/2011/02/transmissible-spongiform-encephalopathy.html

Thursday, August 19, 2010

SCRAPIE CANADA UPDATE Current as of 2010-07-31

The following table lists sheep flocks and/or goat herds confirmed to be infected with scrapie in Canada in 2010.

Current as of: 2010-07-31

http://nor-98.blogspot.com/2010/08/scrapie-canada-update-current-as-of.html

Increased Atypical Scrapie Detections

Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.

http://gain.fas.usda.gov/Recent%20GAIN%20Publications/This%20Week%20in%20Canadian%20Agriculture%20%20%20%20%20Issue%2028_Ottawa_Canada_11-6-2009.pdf

The most recent assessments (and reassessments) were published in June 2005 (Table I; 18), and included the categorisation of Canada, the USA, and Mexico as GBR III. Although only Canada and the USA have reported cases, the historically open system of trade in North America suggests that it is likely that BSE is present also in Mexico.

http://www.oie.int/boutique/extrait/06heim937950.pdf

http://nor-98.blogspot.com/2011/06/usda-scrapie-report-for-april-2011-new.html

Wednesday, February 16, 2011

IN CONFIDENCE

SCRAPIE TRANSMISSION TO CHIMPANZEES

IN CONFIDENCE

http://scrapie-usa.blogspot.com/2011/02/in-confidence-scrapie-transmission-to.html

Sunday, April 18, 2010

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

http://scrapie-usa.blogspot.com/2010/04/scrapie-and-atypical-scrapie.html

Monday, April 25, 2011

Experimental Oral Transmission of Atypical Scrapie to Sheep

Volume 17, Number 5-May 2011

http://nor-98.blogspot.com/2011/04/experimental-oral-transmission-of.html

Monday, November 30, 2009

USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE

http://nor-98.blogspot.com/2009/11/usda-and-oie-collaborate-to-exclude.html

I strenuously urge the USDA and the OIE et al to revoke the exemption of the legal global trading of atypical Nor-98 scrapie TSE. ...TSS

Friday, February 11, 2011

Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues

http://nor-98.blogspot.com/2011/02/atypicalnor98-scrapie-infectivity-in.html

PRICE OF MAD COW TSE PRION POKER GOES UP $$$

NATURAL FIELD CASE OF BSE TO A GOAT ;

Saturday, December 3, 2011

Isolation of Prion with BSE Properties from Farmed Goat Volume 17, Number 12—December 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/isolation-of-prion-with-bse-properties.html

Wednesday, August 18, 2010

Incidence of CJD Deaths Reported by CJD-SS in Canada as of July 31, 2010

http://creutzfeldt-jakob-disease.blogspot.com/2010/08/incidence-of-cjd-deaths-reported-by-cjd.html

Thursday, August 4, 2011

Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011 (SEE VIDEO)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html

Sunday, August 21, 2011

The British disease, or a disease gone global, The TSE Prion Disease (SEE VIDEO)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/british-disease-or-disease-gone-global.html

Saturday, March 5, 2011

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/mad-cow-atypical-cjd-prion-tse-cases.html

TSS

CWD UTAH San Juan deer hunting unit

2011-12-21T11:13:00.003-06:00

Posted Friday, 23 December 2011 14:49

Chronic Wasting Disease in new area

Disease doesn't affect people, but it's fatal to deer

A deer infected with chronic wasting disease has been found in a new area in Utah. That's not a surprise, though — the new area is next to an area where the disease has been for years.

An elk afflicted with chronic wasting disease.

Photo by Dr. Beth Williams 1,200 samples taken this fall

Technicians at the Utah Veterinary Diagnostic Laboratory in Logan have finished testing tissue samples taken from more than 1,200 deer, elk and moose this fall.

Hunters across Utah took the animals, and biologists with the Division of Wildlife Resources collected the samples.

One of the deer that was taken on the San Juan deer hunting unit in southeastern Utah tested positive for the disease. This is the first time a deer from the unit has tested positive for chronic wasting disease (CWD).

Leslie McFarlane, wildlife disease coordinator for the DWR, says she's not surprised that a deer from the San Juan unit tested positive for CWD. "We've found deer with CWD on the La Sal Mountains," she says. "The La Sal Mountains are just north of the San Juan unit."

Most deer are disease free

Fortunately for Utah's deer herds, CWD is not widespread in Utah.

Since 2002, almost 19,000 deer have been tested in the state. Of the nearly 19,000 deer, only 54 tested positive for CWD.

The 54 deer came from three major areas in Utah:

Area Number of deer

Southeastern Utah 38

Central Utah 10

Northeastern Utah 6

One elk, no moose

To date, only one elk — a cow taken on the La Sal Mountains in November 2009 — has tested positive for the disease.

CWD has never been found in a moose in Utah.

http://wildlife.utah.gov/dwr/news/42-utah-wildlife-news/691-chronic-wasting-disease-found-in-new-area.html

http://wildlife.utah.gov/dwr/news.html

Chronic Wasting Disease Found in New Area in Utah

by Outdoor Hub on December 20, 2011

species: Mule Deer location(s): Utah

A deer infected with chronic wasting disease has been found in a new area in Utah. That’s not a surprise, though—the new area is next to an area where the disease has been for years. 1,200 samples taken this fall Technicians at the Utah Veterinary Diagnostic Laboratory in Logan have finished testing tissue samples taken from more than 1,200 deer, elk and moose this fall. Hunters across Utah took the animals, and biologists with the Division of Wildlife Resources collected the samples. One of the deer that was taken on the San Juan deer hunting unit in southeastern Utah tested positive for the disease. This is the first time a deer from the unit has tested positive for chronic wasting disease (CWD). Leslie McFarlane, wildlife disease coordinator for the DWR, says she’s not surprised that a deer from the San Juan unit tested positive for CWD. “We’ve found deer with CWD on the La Sal Mountains,” she says. “The La Sal Mountains are just north of the San Juan unit.” Most deer are disease free Fortunately for Utah’s deer herds, CWD is not widespread in Utah. Since 2002, almost 19,000 deer have been tested in the state. Of the nearly 19,000 deer, only 54 tested positive for CWD. The 54 deer came from three major areas in Utah:

Area Number of deer

Southeastern Utah 38

Central Utah 10

Northeastern Utah 6

One elk, no moose To date, only one elk—a cow taken on the La Sal Mountains in November 2009—has tested positive for the disease. CWD has never been found in a moose in Utah. Learn more CWD is fatal to deer, elk and moose. But there’s no evidence that it can be transmitted to humans. More information about CWD is available at http://go.usa.gov/5d8.

http://www.outdoorhub.com/news/chronic-wasting-disease-found-in-new-area-in-utah/

http://wildlife.utah.gov/diseases/cwd/update2011.pdf

http://wildlife.utah.gov/diseases/cwd/cwd_positives_map.jpg

http://wildlife.utah.gov/diseases/cwd/11sampleunits.jpg

http://wildlife.utah.gov/diseases/cwd/

http://wildlife.utah.gov/dwr/news.html

http://go.usa.gov/5d8

Friday, March 12, 2010

Elk tests positive for CWD UTAH Posted Thursday, 11 March 2010

http://chronic-wasting-disease.blogspot.com/2010/03/elk-tests-positive-for-cwd-utah.html

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

TSS

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

2011-12-20T22:10:00.004-06:00

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

Form 1100-001

(R 2/11)

NATURAL RESOURCES BOARD AGENDA ITEM

SUBJECT: Inf01mation Item: Almond Deer Fatm Update

FOR: DECEIVIBER 2011 BOARD MEETING

TUESDAY

TO BE PRESENTED BY I TITLE: Tami Ryan, Wildlife Health Section Chief

SUMMARY:

2.8.2

Item No.

In April 20 II, the Natural Resources Board approved the Department purchase of a former deer farm known as Buckhorn Flats in Portage County. Following acquisition the property officially became a Bureau of Wildlife Management program property. Staff in the Bureau's Wildlife Health Section, the West Central District, and Northeast District have taken steps towards public outreach with the local community, developed a property managment plan and biosecurity protocols, are working towards the installation of a secondary fence, and are awaiting research proposals that will advance the scientific understanding of Chronic Wasing Disease.

SNIP...

CORRESPONDENCE/MEMORANDUM-------------

DATE: November 21, 20 ll FILE REF: 2300

TO: Natural Resources Board

FROM: Cathy Stepp

SUBJECT: Almond Deer Farm Update

The first case of Chronic Wasting Disease (CWD) among Wisconsin's farm-raised deer occurred in a white-tailed deer buck shot by a hunter at the property (formerly known as Buckhorn Flats) in September 2002. This situation prompted the eventual depopulation of the entire farm. The deer, a mix of does and yearlings, were destroyed on January 17, 2006- 4 years later- by U.S. Department of Agriculture shooters under a USDA agreement with the farm owner. Sixty of the 76 animals tested positive for CWO. The 76 deer constituted the breeding herd in the breeding facility on the farm. The prope1ty also had a hunting preserve until2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWO was not detected in those animals. The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The nearly 80% prevalence rate discovered on Buckhorn Flats is the highest prevalence recorded in any captive cervid operation in North America.

The DNR acquired the property on April 13, 20 ll. After extensive consideration and pursuit of several options, it was decided that purchasing the property and subsequent management of the property is the only realistic option to keep the fences intact. Wisconsin's wild white-tailed deer herd is one of the state's most valuable natural resources, and those deer are a valuable resource of recreational, economic, and ecological significance to all citizens of the state. CWO is a serious long-term threat to Wisconsin's deer herd and the future of Wisconsin's hunting traditions. Over 1,200 free-ranging deer have been tested since 2002 in Portage County with no detections of CWD. We have ve~y high levels of confidence that CWO does not occur in the free-ranging herd in this area. This is of pmticular significance considering this farm is located 60 miles nmih of any known occurrence of CWO in wild deer.

The Hall farm is the most concerning of the depopulated game farms in Wisconsin because of its potential high level of soil contamination. Similar concerns exist to some degree for all nine positive farms and any future farms in which CWD positive cervids are found. However, Buckhorn Flats is a unique situation due to the nearly 80% prevalence rate that occurred there, which is the highest infection rate in a captive cervid farm in North America and perhaps the world. The property has undergone cleaning and disinfection per USDA guidelines. Under the established premise plan, no species of cervids could be brought onto the property for five years, and fences were to be maintained to keep free-ranging deer from entering the property. The premise plan expired on May 24, 20 ll. Despite this five year premise plan and site decontamination, the department had serious concerns over the bioavailability of infectious prions at this site to free-ranging white-tailed deer should the fences be removed or otherwise compromised.

Based on current scientific knowledge, CWD prions are known to persist in the environment for at least 3 years and potentially much longer. Evidence of environmental transmission was documented in a Colorado research facility where mule deer became infected with CWD. Furthermore, the likely transmission of CWD via soil is corroborated by recent studies that show that prions bind to soil components with high affinity and are not easily removed by water. These findings suggest that soil may contribute more significantly to TSE transmission than previously recognized.

Department Actions to Date

The DNR has taken steps to inform the public regarding the background of the Almond Farm as well as future plans for the property. A secondary fence, research, and occupancy of the house are all topics of interest. A description of each topic is identified below:

A. A Property Management Plan was developed to provide a background and future plans for the property. Chapters within the plan include a description of the property, research opportunities, facilities, public communications, and biosecurity protocols (see attachment).

B. The DNR held a public meeting the evening of July 28th at the Almond-Bancroft School to discuss the recent acquisition of the deer farm formerly known as Buckhorn Flats. Twenty-nine people signed in and stayed for the 2-hour duration including local deer farmers, conservation congress delegates, etc. Following 45 minutes of presentation, the meeting focused on the question and answer period. The DNR also asked for public input regarding how they could help in varying capacities at the Almond Farm (see attachment).

C. The DNR will begin timber removal from outside the fence this winter. Timber removal from inside the fence has begun with hazardous trees removed. The construction of a second fence 10 – 12 feet outside the present fence will begin in the spring. This will add an additional level of security for keeping wild deer from entering the farm and maintain the integrity of the perimeter (see attachment).

D. The DNR plans to use the Almond Farm as a CWD research facility. Because the question of how long a contaminated site is a risk to deer is of national and international interest, there may be opportunities for research and funding at this facility. One way to potentially assess whether there is a risk to deer from the Almond Farm is to conduct bioassays focusing on prions persisting in soil and what role environmental contamination plays in disease transmission. A proposal is pending from the University of Wisconsin – Stevens Point that concerns prion degradation via composting. The group is seeking additional funding from the University of Wisconsin – Madison and representatives in Canada. USGS is also contemplating a proposal contingent on funding from their pending federal budget. Any proposed research that includes bringing captive cervids onto the property will be thoroughly reviewed by the CWD Research Committee consisting of the Wildlife Health Team, the Wildlife Policy Team, and Department administration as well as external CWD experts prior to permission being granted to ensure that the health of the wild deer herd will not be endangered. The double fencing described above will be critical to minimize the risk of ingress of free-ranging and egress of any experimental captive cervids. E. The house is rented and currently occupied by a Northeast district wildlife employee. The Lessee agrees to perform weekly fence inspections to insure that the fence integrity has not been compromised. The Lessee also pays for all utilities, and will provide lawn care, snow removal, gutter cleaning, and other miscellaneous maintenance as needed. In exchange for these services the monthly rental fee has been waived. It is agreed that the Lessor and the Lessee shall review said waiver of the monthly rental charge at the end of every twelve months that this lease is in effect (see attachment).

Attachments

Almond Farm Property Management Plan

Questions/Comments from Almond Farm Public Meeting (07-28-2011)

DNR News Release – Almond Farm Public Meeting Announcement (07/18/2011)

External Fence Aerial Photo

Occupancy Agreement

Natural Resources Board Agenda Item – Land Acquisition of the Almond Farm

(March 2011)

THIS PAGE INTENTIONALLY LEFT BLANK

SNIP...

CHAPTER ONE

BACKGROUND ; SUPPORTING

INFORMATION

Background

The first case of CWD among Wisconsin’s farm-raised deer occurred in a white-tailed deer buck shot by a hunter at Buckhorn Flats in September 2002. This situation prompted the eventual depopulation of the entire farm. The deer, a mix of does and yearlings, were destroyed on January 17, 2006 by U.S. Department of Agriculture shooters under a USDA agreement with the farm owner, Stan Hall. Tissue samples were sent to the Wisconsin Veterinary Diagnostic Laboratory for initial screening tests and to the USDA National Veterinary Services Laboratories in Ames, Iowa, for confirmation.

These laboratory results show that 60 of the 76 animals tested positive for chronic wasting disease. The 76 deer constituted the breeding herd on Hall’s farm. He also operated a hunting preserve on the property until 2005. Four deer, two does and two fawns, the only deer remaining in the former preserve, were killed and tested as well. CWD was not detected in those animals. The total number of deer to test positive from this farm from the initial discovery to final depopulation is 82. The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.

The property has undergone cleaning and disinfection as per USDA guidelines. Under an established premise plan, no species of cervids could be brought onto the property for five years, and fences must be maintained to keep wild deer from entering the property so long as the property remained under current ownership. The premise plan expired on May 24, 2011.

Despite the five year premise plan and site decontamination, The WI DNR has concerns over the bioavailability of infectious prions at this site to wild white-tail deer should these fences be removed. Current research indicates that prions can persist in soil for a minimum of 3 years. However, Georgsson et al. (2006) concluded that prions that produced scrapie disease in sheep remained bioavailable and infectious for at least 16 years in natural Icelandic environments, most likely in contaminated soil. Additionally, the authors reported that from 1978-2004, scrapie recurred on 33 sheep farms, of which 9 recurrences occurred 14-21 years after initial culling and subsequent restocking efforts; these findings further emphasize the effect of environmental contamination on sustaining TSE infectivity and that long-term persistence of prions in soils may be substantially greater than previously thought. Evidence of environmental transmission also was documented in a Colorado research facility where mule deer became infected with CWD in two of three paddocks where infected deer carcasses had decomposed on site 1.8 years earlier, and in one of three paddocks where infected deer had last resided 2.2 years earlier (Miller et al. 2004).

Environmental contamination has been identified as a possible cause of recurrence of CWD-infection on elk farms in Canada, when elk were reintroduced one year after depopulation, clean up and disinfection. To date, 8 CWD infected farms remain under CFIA (government of Canada) quarantine indefinitely and will not be allowed to repopulate with cervids until there is additional research on detection of prions in soils and better understanding of the duration of persistence of disease-causing prion post depopulation of CWD-infected cervid farms (Douglas, CFIA, pers. comm.).

Furthermore, the likely transmission of CWD via soil is corroborated by recent studies showing long-term persistence of prions in soil, that prion binds to soil components with high affinity and is not easily removed by water, and that oral prion disease transmission may be enhanced when bound to soil (Johnson et al. 2006, Schramm et al. 2006, Johnson et al. 2007). These findings suggest that soil may harbor more TSE infectivity and contribute more significantly to TSE transmission than previously recognized. These studies highlight the concerns about the risk of transmission via environmental contamination beyond five years and that efforts should be made to prevent freeranging deer from coming into contact with these contaminated facilities.

SNIP...

CHAPTER TWO

OBJECTIVE FOR PROPERTY

Maintain the Perimeter Deer Fence

The primary reason for DNR purchase of the property is to ensure that the deer fence remains intact, preventing wild deer from accessing the prion infected property. The DNR has an ethical and financial responsibility to maintain the fences until the science offers a solution for assessing the risk of remediating the site. The fence will be inspected frequently and repaired as needed.

It is desired to construct a second deer proof fence outside of the existing fence as further insurance for the property. The land immediately outside of the current fence will be cleared of all trees and brush to prepare of installation of the fence and allow vehicle access between the fences. It is hoped that land clearing will be completed in the fall of 2011 with the new fence being constructed as soon as conditions permit in 2012, however, the timing is contingent on funding.

Research Opportunities

The DNR plans to use the Almond Farm as a CWD research facility. Because the question of how long a contaminated site is a risk to deer is of national and international interest, there may be opportunities for research and funding at this facility. One way to potentially assess whether there is a risk to deer from the Almond Farm is to conduct bioassays, either on site or at an alternate location, to monitor for disease transmission. Any proposed research that includes bringing captive cervids onto the property will be thoroughly reviewed by the CWD Research Committee consisting of the Wildlife Health Team, the Wildlife Policy Team, and Department administration as well as external CWD experts prior to permission being granted to ensure that the health of the wild deer herd will not be endangered. The double fencing described above will be critical to minimize the risk of ingress of free-ranging and egress of any experimental captive cervids.

Facilities

SNIP...

CHAPTER THREE

BIOSECURITY PROTOCOLS

The “Almond Farm” owned by the Wisconsin DNR is a CWD prion contaminated facility, and specific guidelines for apparel and equipment sanitization must be followed to prevent prion contamination outside of the contaminated facility. Sanitization guidelines for equipment and surfaces are based upon recommendations from the American Association of Veterinary Laboratory Diagnosticians: Laboratory Safety and Waste disposal Committee and Pathology Committee 2004 publication, “Best Management Practices for Handling Suspect Biosafety Level 2 Animal Transmissible Spongiform Encephalopathy (TSE) Diagnostic Samples. (Scrapie, Chronic Wasting Disease and Transmissible Mink Encephalopathy) In Animal Health Laboratories” These guidelines are as follows:

General Apparel Guidelines

Facilities should have dedicated PPE (Personal Protective Equipment) that stays on site, and should not be removed under any circumstance. Examples of this are as follows: Boots/overshoes, gloves, eye and ear protection, coveralls, etc.

Anyone entering either facility that chooses to not wear dedicated reusable PPE shall be required to utilize disposable PPE that must be disposed of after each daily use. Examples of acceptable disposable PPE are: Tyvek coveralls, disposable gloves, plastic boot covers, etc.

Any personal footwear not left on site must be sanitized utilizing a 50/50 bleach/water solution*.

Personnel Entry/Exit

Upon entry into contaminated areas, personal footwear should be either removed and replaced by dedicated facility boots, or must be covered with plastic boot covers.

Personal clothing should be covered by putting on disposable Tyvek coveralls to prevent clothing contamination.

If contaminated material will be handled, hands should be covered with latex/nitrile gloves.

Prior to exiting contaminated areas of the facility, all persons must walk through a 50/50* bleach/water solution if boots are worn, or boot covers must be removed and disposed of.

All contaminated disposable apparel must be removed prior to exiting the facility.

Trash receptacles for disposable clothing, gloves, and boot covers should be lined and emptied daily, with liners being tightly sealed and placed directly into closed dumpsters designated for waste disposal in a sanitary landfill.

Equipment Sanitization

All tools, instruments, surfaces, and equipment that have been used in potentially contaminated areas of the facility should be sanitized using a 50/50 bleach/water solution*.

Tools or instruments that come into contact with blood, other bodily fluids, or tissues from potentially positive animals should be soaked in a 50/50 bleach/water solution for 60 minutes to be fully disinfected.

All equipment used on site must be sanitized prior to being transferred to alternate locations (preferably, equipment used on site will be kept on-site).

Equipment that is intended to be moved from the property can only enter on frozen snow covered ground.

Equipment that may be moved between facilities (skid steer, ATV’s, etc.) must be pressure-washed on site prior to movement.

* 50/50 (1:1) Bleach/water solution is a chemically approved and proven method of sanitizing surfaces, sampling/necropsy instruments, and footwear. By using a 50/50 solution, the concentration of chlorine is @20,000 ppm, which is required to neutralize prions to an acceptable level of biosafety. For more information on recommended sanitization procedures, refer to: BEST MANAGEMENT PRACTICES FOR HANDLING SUSPECT BIOSAFETY LEVEL 2 ANIMAL TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY (TSE) DIAGNOSTIC SAMPLES (SCRAPIE, CHRONIC WASTING DISEAS E AND TRANSMISSIBLE MINK ENCEPHALOPATHY) IN ANIMAL HEALTH LABORATORIES: AAVLD BMP CWD scrapie FINAL 18 Feb 2004.pdf

SNIP...

APPROVED:

SNIP...

SEE MAPS

SNIP...SEE FULL TEXT ;

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

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

> > > similar if less acute concerns exist for all nine deer farms in Wisconsin that have tested positive for CWD. < < <

WISCONSIN DEPT. OF NATURAL RESOURCES

NEWS RELEASE

Wisconsin Department of Natural Resources

West Central Region

1300 W. Clalremont Ave., PO Box 4001, Eau Claire, WI 54702-2786 Phone: (715) 839-3715 TDD: 711 dnr.wi.gov www.wisconsin.gov

DATE: Monday, July 18,2011

CONTACTS: Davin Lopez, ONR CWO coordinator, Madison. 608-267-2948 Kris Belling, DNR regional wildlife supervisor, Eau Claire, 715-839-3736

SUBJECT: Public input sought on future of CWO-tainted deer farm

In the end, 82 of the deer killed and removed tested positive for CWD. This is an 80 percent infection rate, the highest rate ofCWD infection recorded in North America, and possibly in the world.

-30-

Tuesday, December 20, 2011

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

http://dnr.wi.gov/org/nrboard/2011/december/12-11-2b2.pdf

SNIP...SEE FULL TEXT ;

http://chronic-wasting-disease.blogspot.com/2011/12/chronic-wasting-disease-cwd-wisconsin.html

Wednesday, November 16, 2011

Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/wisconsin-creutzfeldt-jakob-disease-cwd.html

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

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

http://wildlife.state.co.us/NR/rdonlyres/C82EB818-90C6-4D85-897E-9CE279546CCB/0/JWDEpiCWD.pdf

BSE INQUIRY

THE LANCET VOL 337: FEB 2, 1991

Survival of Scrapie virus after 3 years interment

Paul Brown D. Carleton Gajdusek

http://web.archive.org/web/20060227135818/http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf

Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

SNIP...

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!!!

----------

You can take that with however many grains of salt you wish, and we can debate these issues all day long, but the bottom line, this is not rocket-science, all one has to do is some experiments and case studies. But for the life of me, I don't know what they are waiting on?

Kind regards,

Terry S. Singeltary Sr. Bacliff, Texas USA

More here:

http://collections.europarchive.org/tna/20080102173630/http://www.bseinquiry.gov.uk/files/ws/s018.pdf

SEE FULL TEXT ;

Thursday, February 17, 2011

Environmental Sources of Scrapie Prions

http://scrapie-usa.blogspot.com/2011/02/environmental-sources-of-scrapie-prions.html

see my full posting here ;

Wednesday, October 12, 2011

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

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

Accelerated shedding of prions following damage to the olfactory epithelium

Richard A. Bessen1,*, Jason M. Wilham2, Diana Lowe1, Christopher P. Watschke1, Harold Shearin1, Scott Martinka1, Byron Caughey2 and James A. Wiley1

+ Author Affiliations

1Department of Immunology and Infectious Diseases, Montana State University, Bozeman, Montana, USA 2Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergies and Infectious Diseases, Hamilton, Montana, USA

ABSTRACT

In this study we investigated the role of damage to the nasal mucosa in the shedding of prions into nasal fluids as a pathway for prion transmission. Here we demonstrate that prions can replicate to high levels in the olfactory sensory epithelium (OSE) in hamsters and that induction of apoptosis in olfactory receptor neurons (ORNs) in the OSE resulted in sloughing off of the OSE from nasal turbinates into the lumen of the nasal airway. In the absence of nasotoxic treatment olfactory marker protein (OMP), which is specific for ORNs, was not detected in nasal lavages. However, after nasotoxic treatment that leads to apoptosis of ORNs both OMP and prion proteins were present in nasal lavages. The cellular debris that was released from the OSE into the lumen of the nasal airway was positive for both OMP and the disease-specific isoform of the prion protein, PrPSc. Using the real time quaking-induced conversion assay to quantify prions, a 100- to 1,000-fold increase in prion seeding activity was observed in nasal lavages following nasotoxic treatment. Since neurons replicate prions to higher levels than other cell types and ORNs are the most environmentally exposed neurons, we propose that an increase in ORN apoptosis or damage to the nasal mucosa in a host with a pre-existing prion infection of the OSE could lead to a substantial increase in the release of prion infectivity into nasal fluids. This mechanism of prion shedding from the olfactory mucosa could contribute to prion transmission.

http://jvi.asm.org/content/early/2011/11/23/JVI.06626-11.abstract

Monday, January 05, 2009

CWD, GAME FARMS, BAITING, AND POLITICS

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-game-farms-baiting-and-politics.html

Thursday, August 28, 2008

cwd, feeding, and baiting piles

http://chronic-wasting-disease.blogspot.com/2008/08/cwd-feeding-and-baiting-piles.html

UPDATED DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html

Sunday, January 22, 2012

Chronic Wasting Disease CWD cervids interspecies transmission

http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html

Monday, February 14, 2011

THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER

NO, NO, NOT NO, BUT HELL NO !

Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html

http://www.thewildlifenews.com/2011/11/03/jackson-hole-newsguide-retired-biologist-stop-feeding-make-elk-migrate/

more concern here ;

Saturday, November 12, 2011

Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease

Fri, 22 Sep 2006 09:05:59 –0500

http://chronic-wasting-disease.blogspot.com/2011/11/human-prion-disease-and-relative-risk.html

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html

Wednesday, September 08, 2010

CWD PRION CONGRESS SEPTEMBER 8-11 2010

PRION 2010

International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria

SNIP...

PPo4-4:

Survival and Limited Spread of TSE Infectivity after Burial

Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK

Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.

The authors gratefully acknowledge funding from DEFRA

SEE MORE HERE ;

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html

PRION 2011

Envt.16: Soil Properties as a Factor in CWD Spread in Western Canada

Alsu Kuznetsova,† Tariq Siddique and Judd Aiken

University of Alberta; Edmonton, AB Canada†Presenting author; Email: alsu@ualberta.ca

Soil can serve as a stable reservoir for infectious prion proteins (PrPSc). Soils are diverse and complex, varying in clay, silt, sand and organic components. We have shown that PrPSc binds clay minerals avidly, an interaction that considerably enhances prion infectivity. Conversely quartz sand bound PrPSc less avidly. These studies would suggest that soils with lower clay and higher sand content bind prions less avidly and do not enhance infectivity to the same level as clay-rich soils. We hypothesize that clay content of a soil plays an integral role in the spread of CWD. In this study, we present the soil properties in the western Canada. Soils of the CWD-region generally are similar in texture, clay mineralogy and soil organic matter content. In total these soils can be characterized as clay loamy, montmorillonite (smectite) with 6–10 % organic carbon. The major soils in the CWD-region are Chernozems, present in 60% of total area. These soils have a humic horizon in which organic matter has accumulated (1–17% organic C). Solonetzic soils are also common to Alberta and Saskatchewan. We suggest that the greatest risk of CWD spread in western Canada is restricted to clay loamy, montmorillonite soils with humus horizon. Such soils are predominant in the southern region of Alberta, Saskatchewan and Manitoba, but are less common in northern regions of the provinces.

Envt.28: High Survival Rates of TSE Infectivity Buried in Two Soil Types Allister J. Smith The Roslin Insitute; Roslin, UK Email: allister.smith@roslin.ed.ac.uk Two field experiments nearing completion are investigating the migration and/or persistence of TSE infectivity in the soil environment, either buried within bovine heads or buried without containment. In the first experiment five pairs of bovine heads, spiked with mouse-passaged BSE (301V) macerate, were buried within lysimeters containing either clay or sandy soil. A pair of unspiked bovine heads was also buried to act as controls. Pairs of heads have been exhumed annually during which a corer is used to take soil samples above, surrounding and below the head. Any brain material within the head is recovered during dissection. The soil samples have undergone protein extraction, and the extracts along with the brain material have been assayed for infectivity by bioassay in VM mice. Bioassay results from the first experiment show that for all four years most of the intracranial brain samples have been positive for TSE infectivity in both the clay and sandy soil. There is little change in the survival curves between years 1 and 4 indicating little reduction in the amounts of infectivity over time. There has been very limited infectivity found in samples surrounding the heads buried in the sandy soil, but infectivity has been found in the soil samples surrounding the clay heads and the levels increase slightly from years one to four, presumably as the heads have decomposed. In a parallel experiment a bolus of infectivity (301V) was placed in the centre of two large lysimeters, containing either clay or sandy soil. Over the course of four years, core samples have been taken at eight time points, on the vertical and at 3 distances from the centre. These samples have been assayed for infectivity and to date only one sample from the sandy soil has produced pathological evidence of TSE disease in one mouse. In order to ascertain whether any of the bolus remained at the end of the experiment, we collected a much larger central core (d = 16 cm) and extracted samples for bioassay, concentrating on the core portions that correlated to the original bolus location. The samples from these core portions caused disease in a high proportion of mice (bioassay still in progress), with apparently higher infectivity levels in the clay soil, so far. This result indicates that there has been very little migration of TSE infectivity without containment in either clay or sandy soil and that there has been little reduction in titre with time.

Envt.29: Time-Dependent Decline in PrPTSE Desorption from Soil Particles Christen B. Smith,1,† Clarissa J. Booth,2 Kartik Kumar2 and Joel A. Pedersen1–3 1Environmental Chemistry and Technology Program; 2Molecular and Environmental Toxicology Center; 3Department of Soil Science, University of Wisconsin; Madison, WI USA †Presenting author, Email: cmbell@wisc.edu Environmental routes of transmission are implicated in epizootics of sheep scrapie and chronic wasting disease in deer, elk, and moose. Strong evidence suggests that soil may serve as an environmental reservoir of prions, which can persist in the environment for years. The disease-associated form of the prion protein (PrPTSE) readily attaches to soil particle surfaces. Prior studies reported reduced PrPTSE recovery from experimentally spiked soils after longer contact times, which in some cases has been interpreted as degradation of PrPTSE. Here, we investigate PrPTSE desorption from sterilized and untreated soil particles as a function of protein-soil contact time. Soil particles were sterilized by autoclaving or g-irradiation. Desorption of PrPTSE from whole soils, montmorillonite clay, and quartz sand was analyzed by immunoblotting following 1-, 7-, and 14-day contact times. We found that PrPTSE recovery from both sterile and untreated soil samples declined significantly with contact time suggesting the strengthening of protein-particle interactions over time. Recovery of PrPTSE from whole soils declined to a larger extent than did that from montmorillonite and quartz sand possibly reflecting the contribution of particle-associated natural organic matter to the mechanisms of PrPTSE attachment. The influence of PrPTSE-soil particle attachment on oral disease transmission warrants investigation.

www.landesbioscience.com PRION

http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf

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

Friday, February 20, 2009

Both Sides of the Fence: A Strategic Review of Chronic Wasting Disease

http://chronic-wasting-disease.blogspot.com/2009/02/both-sides-of-fence-strategic-review-of.html

ALSO, NOTE MINERAL LICKS A POSSIBLE SOURCE AND TRANSMISSION MODE FOR CWD

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html

2009 CWD SYMPOSIUM UTAH

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf

Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area

65

Detection of Protease-Resistant Prion Protein in Water from a CWD-Endemic Area

Tracy A. Nichols*1,2, Bruce Pulford1, Christy Wyckoff1,2, Crystal Meyerett1, Brady Michel1, Kevin Gertig3, Jean E. Jewell4, Glenn C. Telling5 and M.D. Zabel1 1Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA 2National Wildlife Research Center, Wildlife Services, United States Department of Agriculture, Fort Collins, Colorado, 80521, USA 3Fort Collins Water and Treatment Operations, Fort Collins, Colorado, 80521, USA 4 Department of Veterinary Sciences, Wyoming State Veterinary Laboratory, University of Wyoming, Laramie, Wyoming, 82070, USA 5Department of Microbiology, Immunology, Molecular Genetics and Neurology, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky, 40536, USA * Corresponding author- tracy.a.nichols@aphis.usda.gov

Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Experimental and epidemiological data indicate that CWD can be transmitted horizontally and via blood and saliva, although the exact mode of natural transmission remains unknown. Substantial evidence suggests that prions can persist in the environment, implicating it as a potential prion reservoir and transmission vehicle. CWD- positive animals can contribute to environmental prion load via biological materials including saliva, blood, urine and feces, shedding several times their body weight in possibly infectious excreta in their lifetime, as well as through decomposing carcasses. Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify minute amounts of CWD prions in spiked water samples at a 1:1 x106 , and protease-resistant prions in environmental and municipal-processing water samples from a CWD endemic area. Detection of CWD prions correlated with increased total organic carbon in water runoff from melting winter snowpack. These data suggest prolonged persistence and accumulation of prions in the environment that may promote CWD transmission.

snip...

The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.

snip...end...full text at ;

http://www.landesbioscience.com/

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html

http://chronic-wasting-disease.blogspot.com/2009/10/detection-of-protease-resistant-cervid.html

Wednesday, January 07, 2009

CWD to tighten taxidermy rules Hunters need to understand regulations

http://chronic-wasting-disease.blogspot.com/2009/01/cwd-to-tighten-taxidermy-rules-hunters.html

DEEP THROAT TO TSS 2000-2001 (take these old snips of emails with how ever many grains of salt you wish. ...tss)

The most frightening thing I have read all day is the report of Gambetti's finding of a new strain of sporadic cjd in young people...Dear God, what in the name of all that is holy is that!!! If the US has different strains of scrapie.....why????than the UK...then would the same mechanisms that make different strains of scrapie here make different strains of BSE...if the patterns are different in sheep and mice for scrapie.....could not the BSE be different in the cattle, in the mink, in the humans.......I really think the slides or tissues and everything from these young people with the new strain of sporadic cjd should be put up to be analyzed by many, many experts in cjd........bse.....scrapie Scrape the damn slide and put it into mice.....wait.....chop up the mouse brain and and spinal cord........put into some more mice.....dammit amplify the thing and start the damned research.....This is NOT rocket science...we need to use what we know and get off our butts and move....the whining about how long everything takes.....well it takes a whole lot longer if you whine for a year and then start the research!!! Not sure where I read this but it was a recent press release or something like that: I thought I would fall out of my chair when I read about how there was no worry about infectivity from a histopath slide or tissues because they are preserved in formic acid, or formalin or formaldehyde.....for God's sake........ Ask any pathologist in the UK what the brain tissues in the formalin looks like after a year.......it is a big fat sponge...the agent continues to eat the brain ......you can't make slides anymore because the agent has never stopped........and the old slides that are stained with Hemolysin and Eosin......they get holier and holier and degenerate and continue...what you looked at 6 months ago is not there........Gambetti better be photographing every damned thing he is looking at.....

Okay, you need to know. You don't need to pass it on as nothing will come of it and there is not a damned thing anyone can do about it. Don't even hint at it as it will be denied and laughed at.......... USDA is gonna do as little as possible until there is actually a human case in the USA of the nvcjd........if you want to move this thing along and shake the earth....then we gotta get the victims families to make sure whoever is doing the autopsy is credible, trustworthy, and a saint with the courage of Joan of Arc........I am not kidding!!!! so, unless we get a human death from EXACTLY the same form with EXACTLY the same histopath lesions as seen in the UK nvcjd........forget any action........it is ALL gonna be sporadic!!!

And, if there is a case.......there is gonna be every effort to link it to international travel, international food, etc. etc. etc. etc. etc. They will go so far as to find out if a sex partner had ever traveled to the UK/europe, etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the truth. They have all the cards, all the money, and are willing to threaten and carry out those threats....and this may be their biggest downfall...

Thanks as always for your help. (Recently had a very startling revelation from a rather senior person in government here..........knocked me out of my chair........you must keep pushing. If I was a power person....I would be demanding that there be a least a million bovine tested as soon as possible and agressively seeking this disease. The big players are coming out of the woodwork as there is money to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's "will"! "Will be the burden to bare if there is any coverup!"

again it was said years ago and it should be taken seriously....BSE will NEVER be found in the US! As for the BSE conference call...I think you did a great service to freedom of information and making some people feign integrity...I find it scary to see that most of the "experts" are employed by the federal government or are supported on the "teat" of federal funds. A scary picture! I hope there is a confidential panel organized by the new government to really investigate this thing.

You need to watch your back........but keep picking at them.......like a buzzard to the bone...you just may get to the truth!!! (You probably have more support than you know. Too many people are afraid to show you or let anyone else know. I have heard a few things myself... you ask the questions that everyone else is too afraid to ask.)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/variably-protease-sensitive-prionopathy.html

http://www.fieldandstream.com/blogs/hunting/2011/02/should-chronic-wasting-disease-scare-you-venison-stock-or-braised-shanks

December 2011, price of TSE Prion Poker Goes Up $$$

Saturday, December 3, 2011

Isolation of Prion with BSE Properties from Farmed Goat

Volume 17, Number 12—December 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/isolation-of-prion-with-bse-properties.html

EFSA Journal 2011 The European Response to BSE: A Success Story

This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;

Monday, October 10, 2011

EFSA Journal 2011 The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html

http://transmissiblespongiformencephalopathy.blogspot.com/

Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque

"BSE-L in North America may have existed for decades"

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html

Sunday, June 26, 2011

Risk Analysis of Low-Dose Prion Exposures in Cynomolgus Macaque

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/risk-analysis-of-low-dose-prion.html

Wednesday, August 24, 2011

There Is No Safe Dose of Prions

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/there-is-no-safe-dose-of-prions.html

Wednesday, August 24, 2011

All Clinically-Relevant Blood Components Transmit Prion Disease following a Single Blood Transfusion: A Sheep Model of vCJD

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/all-clinically-relevant-blood.html

Thursday, August 4, 2011

Terry Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis, Date aired: 27 Jun 2011

(SEE VIDEO)

http://transmissiblespongiformencephalopathy.blogspot.com/2011/08/terry-singeltary-sr-on-creutzfeldt.html

Monday, February 7, 2011

FDA’s Currently-Recommended Policies to Reduce the Possible Risk of Transmission of CJD and vCJD by Blood and Blood Products 2011 ???

http://tseac.blogspot.com/2011/02/fdas-currently-recommended-policies-to.html

Tuesday, September 14, 2010

Transmissible Spongiform Encephalopathies Advisory Committee; Notice of Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)

http://tseac.blogspot.com/2010/09/transmissible-spongiform_14.html

Saturday, October 24, 2009

SaBTO Advisory Committee on the Safety of Blood, Tissues and Organs 2nd Public Meeting 27 October 2009

SaBTO

http://seac992007.blogspot.com/2009/10/sabto-advisory-committee-on-safety-of.html

Meeting of the Transmissible Spongiform Encephalopathies Committee On June 12, 2009 (Singeltary submission)

http://tseac.blogspot.com/2009/05/meeting-of-transmissible-spongiform.html

Sunday, July 27, 2008

Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)

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

Subject: Docket No, 04-047-l Regulatory Identification No. (RIN) 091O-AF46 NEW BSE SAFEGUARDS (comment submission)

Date: Sun, 11 Jul 2004 21:34:22 –0500

From: "Terry S. Singeltary Sr."

To: fdadockets@oc.fda.gov CC: regulations@aphis.usda.gov, burt.pritchett@fda.gov

http://madcowfeed.blogspot.com/2008/07/docket-no-04-047-l-regulatory.html

Response to Public Comments

on the

Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005

INTRODUCTION

The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website: http://www.fsis.usda.gov/Science/Risk_Assessments/index.asp). Comments on technical aspects of the risk assessment were then submitted to FSIS. Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary. This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:

http://www.fsis.usda.gov/PDF/BSE_Risk_Assess_Response_Public_Comments.pdf

Suppressed peer review of Harvard study October 31, 2002.

October 31, 2002 Review of the Evaluation of the Potential for Bovine Spongiform Encephalopathy in the United States Conducted by the Harvard Center for Risk Analysis, Harvard School of Public Health and Center for Computational Epidemiology, College of Veterinary Medicine, Tuskegee University Final Report Prepared for U.S. Department of Agriculture Food Safety and Inspection Service Office of Public Health and Science Prepared by RTI Health, Social, and Economics Research Research Triangle Park, NC 27709 RTI Project Number 07182.024

http://www.fsis.usda.gov/oa/topics/BSE_Peer_Review.pdf

Sunday, February 14, 2010

[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)

http://bseusa.blogspot.com/2010/02/docket-no-fsis-2006-0011-fsis-harvard.html

Thursday, April 9, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed Thursday, April 09, 2009

Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed

mailto:burt.pritchett@fda.hhs.gov

Greetings FDA et al,

I kindly wish to comment on the following ;

[Docket No. FDA-2002-N-0031] (formerly Docket No. 2002N-0273) RIN 0910-AF46

[Federal Register: April 9, 2009 (Volume 74, Number 67)] [Proposed Rules] [Page 16160-16161] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr09ap09-18]

http://madcowfeed.blogspot.com/2009/04/docket-no-fda2002n0031-formerly-docket.html

Owens, Julie

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Monday, July 24, 2006 1:09 PM To: FSIS RegulationsComments

Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98 8/3/2006

Greetings FSIS, I would kindly like to comment on the following ;

http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf

http://www.scribd.com/doc/1490709/USDA-200600111

03-025IFA

03-025IFA-2

Terry S. Singeltary

From: Terry S. Singeltary Sr. [flounder9@verizon.net]

Sent: Thursday, September 08, 2005 6:17 PM

To: fsis.regulationscomments@fsis.usda.gov

Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle

Greetings FSIS,

I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle

http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf

http://www.fda.gov/ohrms/dockets/ac/05/slides/2005-4189oph_1.pdf

Docket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305

Comment Number: EC –254

Accepted - Volume 11

Sources: World Trade Atlas What is the level of passenger traffic arriving in the United States from the affected country? Approximately 185,000 direct flights from Greece arrived to US airports in fiscal year 2000. Also, an unknown number of passengers from Greece arrived via indirect flights. Under APHIS-PPQ's agriculture quarantine inspection monitoring, 584 air passengers from Greece were sampled for items of agricultural interest in fiscal year 2000. Of these passengers, 14 carried meat (non-pork) items that could potentially transmit pathogens that cause BSE; most passengers carried from one to two kilograms (kg) of meat, although one passenger in November 1999 carried 23 kg of meat in a suitcase. Florida, Massachusetts, and New York were the reported destinations of these passengers. None of the passengers with meat items reported plans to visit or work on a ranch or farm while in the US. Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

http://www.aphis.usda.gov/vs/ceah/cei/bse_greece0701.htm

Greetings list members, i just cannot accept this;

> 23 kg of meat in a suitcase (suitcase bomb...TSS)

> The data do not provide a species of origin code for these

> products, therefore they may not contain any ruminant product.

what kind of statement is this? how stupid do they think we are? it could also very well mean that _all_ of it was ruminant based products !

http://www.fda.gov/ohrms/dockets/dockets/02n0276/02N-0276-EC-254.htm

http://creutzfeldt-jakob-disease.blogspot.com/

http://transmissiblespongiformencephalopathy.blogspot.com/

http://bseusa.blogspot.com/

http://bse-atypical.blogspot.com/

http://madcowusda.blogspot.com/

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

http://scrapie-usa.blogspot.com/

http://nor-98.blogspot.com/

Saturday, February 27, 2010

FINAL REPORT OF THE TESTING OF THE BELGIAN (VERMONT) SHEEP February 27, 2010

http://foiamadsheepmadrivervalley.blogspot.com/2010/02/final-report-of-testing-of-belgian.html

http://foiamadsheepmadrivervalley.blogspot.com/

layperson

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net

Transmission of Chronic Wasting Disease Identifies a Prion Strain Causing Cachexia and Heart Infection in Hamsters

2011-12-14T10:36:00.000-06:00

Transmission of Chronic Wasting Disease Identifies a Prion Strain Causing Cachexia and Heart Infection in Hamsters

Richard A. Bessen1*, Cameron J. Robinson2, Davis M. Seelig3, Christopher P. Watschke1, Diana Lowe1, Harold Shearin1, Scott Martinka1, Alex M. Babcock2

1 Department of Immunology and Infectious Diseases, Montana State University, Bozeman, Montana, United States of America,

2 Department of Psychology, Montana State University, Bozeman, Montana, United States of America,

3 Department of Microbiology, Immunology, and Pathology, Colorado State University, Ft. Collins, Colorado, United States of America

Abstract Top

Chronic wasting disease (CWD) is an emerging prion disease of free-ranging and captive cervids in North America. In this study we established a rodent model for CWD in Syrian golden hamsters that resemble key features of the disease in cervids including cachexia and infection of cardiac muscle. Following one to three serial passages of CWD from white-tailed deer into transgenic mice expressing the hamster prion protein gene, CWD was subsequently passaged into Syrian golden hamsters. In one passage line there were preclinical changes in locomotor activity and a loss of body mass prior to onset of subtle neurological symptoms around 340 days. The clinical symptoms included a prominent wasting disease, similar to cachexia, with a prolonged duration. Other features of CWD in hamsters that were similar to cervid CWD included the brain distribution of the disease-specific isoform of the prion protein, PrPSc, prion infection of the central and peripheral neuroendocrine system, and PrPSc deposition in cardiac muscle. There was also prominent PrPSc deposition in the nasal mucosa on the edge of the olfactory sensory epithelium with the lumen of the nasal airway that could have implications for CWD shedding into nasal secretions and disease transmission. Since the mechanism of wasting disease in prion diseases is unknown this hamster CWD model could provide a means to investigate the physiological basis of cachexia, which we propose is due to a prion-induced endocrinopathy. This prion disease phenotype has not been described in hamsters and we designate it as the ‘wasting’ or WST strain of hamster CWD.

snip...

Discussion

A prominent feature of CWD in deer is a progressive loss of body mass and adiposity over a period of weeks to months [1]. This observation is not unique among prion diseases since a wasting phenotype is also found in sheep and goats with scrapie [64]. Despite interspecies transmission of CWD and scrapie to rodents, a similar progressive wasting disease has not been described in SGH except in the terminal stages of disease [31]. In the current study, we describe a progressive loss of body mass and cachexia over several weeks in SGH with CWD that resulted in an average of >50% weight loss at the time of animal sacrifice when hamsters were still active, but not yet moribund. We have termed this progressive disease in SGH the ‘wasting’ phenotype or WST strain of CWD since overt symptoms of neurological symptoms were not prominent for most of the disease phase. The loss of body mass in WST CWD in SGH was distinct from that reported for other natural prion diseases adapted to SGH including transmissible mink encephalopathy (e.g., HY and DY strains) [27], [28], [31], scrapie (e.g., 263K, 22AH, Me7H strains) [44], [65], CWD [16], [17], bovine spongiform encephalopathy [46], [66], and Creutzfeldt-Jakob disease [48] in which changes in body mass were not evident until the late phases of clinical disease or were not described. Changes in body weight have been reported in sheep scrapie that was adapted to SGH, but in these cases there is a preclinical obesity that is characterized by a >25% increase in body mass for the 22CH and 139H scrapie agent strains [30]–[32], [67]. The cellular basis for either prion-induced cachexia or obesity is not completely understood, but an analysis of energy homeostasis in 139H scrapie in SGH revealed a preclinical hyperphagia, non-fasted hyperinsulinemia with hyperglycemia, and fasted hyperleptinemia that is consistent with an anabolic syndrome that had similarities to type II diabetes mellitus [31], [32]. A similar analysis was performed for HY TME in SGH that exhibit a loss of body mass during the late clinical phase of disease and these animals have a different profile that includes hypersecretion of glucagon, increased fasted ß-ketones, fasted hypoglycemia, and suppressed, non-fasted leptin [31]. It was proposed that in HY TME the SGH had a catabolic syndrome and we would predict that WST CWD in SGH would exhibit a more severe catabolic syndrome than found in HY TME since the weight loss was longer in duration and more pronounced. Additional factors that may have also contributed to the severe loss of body mass in WST CWD in SGH include the increased locomotor activity (e.g., distance traveled, average speed, number of rotations) that was first observed at 43 weeks postinfection and hypophagia that was first recorded at 48 weeks postinfection. These preceded the average time of animal sacrifice at 54 weeks postinfection. This data is suggestive of an increased energy expenditure without an increase in energy intake for several weeks. These prion-induced changes resulted in an imbalance between caloric expenditure and intake and could have exacerbated the loss of body mass.

The observed changes in open field behavior in WST CWD-infected SGH, which proceeded the appearance of clinical signs, are consistent with previous studies that reported increased locomotor activity in rodent prion infections [68]–[70]. The present study confirms and extends these findings by demonstrating preclinical hyperactivity in the CWD SGH model. Increased locomotor activity can represent a hyper-reactivity to novel stimuli or impaired novelty-induced exploration. The detailed analysis of open field behavior in the present study revealed no difference in the thigmotaxis between control and infected SGH subjects, which is indicative of normal emotionality [71]. In contrast, WST CWD in SGH resulted in increased rotational behavior that has not been previously reported. The direction (clockwise vs counterclockwise) of increased rotational behavior observed in experimental hamsters was not consistent and may represent differences in the intra-hemispheric deposition of PrPSc in brain structures following CWD infection. Although speculative, the wide spread distribution of PrPSc in structures including the cerebellar white matter, thalamus, hippocampus and substantia nigra can be link to the observed changes in behavior. In addition, abnormal behavior and motor deficits in prion disease models have been associated with changes in the hypothalamo-pituitary-adrenal (HPA) axis [72]. Prion-induced changes in the HPA are also consistent with the wasting syndrome observed in WST CWD in SGH and in cervids with CWD. Irrespective of the origin or mechanism(s), early behavioral markers of prion infection are of epidemiological importance.

Prion-induced endocrinopathies have been proposed to be the primary cause of either obesity or cachexia observed in natural and experimental prion diseases [31], [72]. These can be explained by prion infection of the HPA that results in altered secretion of neuroendocrine hormones or pituitary hormones [31], [72]. These in turn regulate endocrine gland function that can affect body mass and adiposity. Alternatively, prions may directly infect peripheral endocrine glands and alter hormone secretion. Support for these mechanisms can be found in CWD in cervids, sheep scrapie, BSE in cattle, and some human prion diseases in which prion infection has been found in hypothalamic nuclei, the pituitary gland, pancreas, and/or adrenal gland [39], [40], [49], [57], [58], [73]–[76]. In the current study PrPSc deposition was also found in several hypothalamic nuclei, the pancreas, and adrenal gland in WST CWD in SGH. In both the adrenal gland and pancreas, PrPSc deposition was associated with markers for neural structures within these tissues suggesting that prion-induced changes in neural control of these endocrine glands could alter hormone secretion. For example, localization of PrPSc to PGP 9.5-positive structures in the medulla of the adrenal gland could result in a prion effect on sympathetic regulation of adrenaline and noradrenaline, and previous studies have demonstrated increased levels of catecholamines in blood of scrapie infected mice and hamsters [77], [78], and humans with fatal familial insomnia [79]. Similarly, in the pancreas of WST CWD in SGH, PrPSc deposition was associated with synaptophysin-positive structures in the Islet of Langerhans, which is the region containing the hormone producing cells. In several prion diseases infection of the Islet of Langerhans is reported as well as altered levels of pancreatic hormones in serum including insulin and glucagons suggesting that these endocrinopathies are associated with prion infection of the endocrine system [30]–[32]. In other studies, elevated serum levels of leptin, which acts on the hypothalamus to suppress appetite, was described in 139H scrapie in SGH despite evidence of hyperphagia and obesity [31]. These studies suggest that the dysregulation of the endocrine system in prion diseases is complex and could be due to the targeting of prion infection to multiple sites in both the central and peripheral endocrine system. To understand the cellular basis of wasting disease in CWD additional studies are needed to investigate metabolite and hormone serum levels involved in endocrine function and we propose that the WST CWD in SGH can provide a model to investigate the basis of prion-induced cachexia.

Transmission of CWD from white-tailed deer, mule deer, and elk to TgMo-sghPrP and SGH was undertaken in a previous study [16], and our transmission data of CWD from white-tailed deer into the same founder line of TgMo-sghPrP and outbred SGH produced some different findings. Raymond et al [16] demonstrate a very long incubation period on interspecies transmission of white-tailed deer CWD into TgMo-sghPrP (632±73 days with 4 of 9 mice affected, but 8 of 9 mice were PrPSc-positive in brain) that shortened to 272±62 days on second serial passage, and 212±32 and 237±13 days on third serial passage. Our data resulted in a 100% attack rate and a shorter incubation period on interspecies passage (417±23 days) that stabilized to 198±3 days on second serial passage, and did not significantly shorten on third serial passage (189±5 and 198±3 days). Our transmission data on CWD from TgMo-sghPrP into SGH was also distinct from the previous study [16] in which the mean incubation periods ranged from 408 to 462 days, while in the current study they consistently resulted in mean incubation periods ranging from 322 to 379 days on first and second serial passage into SGH. In passage line B we did observe a longer incubation period (477±15 days) that was consistent with the studies by Raymond et al [16], but this occurred after inoculation of brain material from a CWD infected TgMo-sghPrP that had an incubation period that was 157 days while in the earlier study the inocula was from CWD infected TgMo-sghPrP that had incubation periods significantly longer (>270 days). Therefore, the serial passage history of CWD in TgMo-sghPrP was different between these two studies despite a similar incubation period in a subset of SGH. A comparison of the findings from these two studies may suggest that distinct strains of CWD were isolated upon interspecies passage into TgMo-sghPrP and serial passage into SGH, but these conclusions cannot be reached based solely on incubation periods. More extensive analysis of the biological and biochemical phenotypes of hamster adapted CWD isolates would be necessary in order to identify distinct strains of CWD in SGH. Despite intensive efforts to identify CWD strains using TgMo-cervidPrP, which is a more appropriate model for CWD strain identification, only two distinct strains of CWD have been identified and these are strongly influenced by a normal polymorphism in the cervid Prnp [80].

The WST CWD strain in SGH has several similarities to CWD in cervids including a progressive wasting disease, a similar brain distribution of PrPSc, and targeting of prion infection to the neuroendocrine portion of the adrenal gland and pancreas. Additionally, in natural prion diseases of humans and animals, infection of cardiac muscle has only been described in elk and white-tailed deer with CWD [41]. In WST CWD of SGH, PrPSc was also prominent in heart by western blot and cardiac muscle by immunofluoresence. These findings provide another parallel between CWD infection of cervids and WST SGH. Prion infectivity has been described in muscle from CWD deer [15] and PrPSc can also be enriched from the tongue of deer and elk infected with CWD [56]. Although low levels of PrPSc were also described in heart of SGH infected with 263K scrapie and BSE adapted to SGH [66], [81], the levels described in WST CWD appear to be moderately high since more PrPSc was present in heart than in tongue. Previous studies demonstrate that PrPSc is not detected in heart while the tongue has higher levels of prion infectivity than other muscle types in 263K scrapie infected SGH [82]. Prion protein deposition in cardiac tissue has also been described in red deer that were experimentally infected with CWD [83]. Other observations such as altered locomotor activity and the distinct distribution of PrPSc in the olfactory sensory epithelium in WST CWD of SGH have not been directly compared to cervids with CWD in order to determine whether parallel findings are maintained. An advantage of the WST CWD strain in SGH over other rodent models of CWD could be its usefulness in determining the mechanism of prion-induced wasting disease since this key phenotype is maintained for CWD between the deer host and the WST CWD hamster model.

snip...

Citation: Bessen RA, Robinson CJ, Seelig DM, Watschke CP, Lowe D, et al. (2011) Transmission of Chronic Wasting Disease Identifies a Prion Strain Causing Cachexia and Heart Infection in Hamsters. PLoS ONE 6(12): e28026. doi:10.1371/journal.pone.0028026

Editor: Andrew Francis Hill, University of Melbourne, Australia

Received: August 25, 2011; Accepted: October 30, 2011; Published: December 12, 2011

Copyright: © 2011 Bessen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: This work was supported by Public Health Service grants R01 AI055043 and P20 RR020185 from the National Institutes of Health, by the National Research Initiative of the United States Department of Agriculture grant 2006-35201-16626, and The Murphy Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests: The authors have declared that no competing interests exist.

* E-mail: rbessen@montana.edu

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0028026

40,000 human heart valves a year from BSE herds

Sun, 3 Sep 2000.

Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas

Opinion (webmaster): Below are some shocking documents. Here is a British company preparing 40,000 heart valves a year from bovine pericardium, primarily for export, and they are not required to source this material from BSE-free herds even in peak epidemic years. It is amazing to watch health "authorities" grovelling on their bellies to wring petty concessions from middle management at obscure little companies. The main worry is not the practise of using 800 potentially infected cows a week for human heart transplant material but that the press or recipients will get wind of it, hurting business. BSE wasn't the problem, it was awkward queries from importing countries like the US. The cows are stunned using brain penetration -- can't do anything about the chunks of bovine brain blasted into the circulatory system, it's the norm. Can't use younger lower-risk animals either, patch would not be big enough. It is fascinating to see the British government worrying about, but doing nothing, with pigs with BSE 10 years ago. While scrapie was long used as an excuse for continuing with human use of BSE-tainted material, little sheep material was used medically. Bovine transplants, vaccines, insulin doeses, etc. are far more dangerous than dietary material as injections, and are done on a very wide scale. So scrapie was never a valid analogy to BSE, as MAFF knew full well. The British government deferred to the manufacturer's rep for an opinion on how contaminated pericardium might be, just as this appeared showing that this tissue is extremely dangerous:

CJD in a patient who received homograft [was it really?] tissue for tympanic membrane closure.

Eur Arch Otorhinolaryngol 1990;247(4):199-201

Tange RA, Troost D, Limburg M

We report the case history of a 54-year-old man who developed a fatal neurological disorder 4 years after a successful tympanoplasty with homograft pericardium... COMMERCIAL IN CONFIDENCE

snip...see full text ;

http://www.mad-cow.org/00/sep00_news.html#hhh

http://transmissiblespongiformencephalopathy.blogspot.com/2011/01/vaccines-and-transmissible-spongiform.html

http://madcowfeed.blogspot.com/2010/02/import-alert-99-25-detention-without.html

Friday, March 25, 2011

Detection of Prion Protein in Urine-Derived Injectable Fertility Products by a Targeted Proteomic Approach

http://transmissiblespongiformencephalopathy.blogspot.com/2011/03/detection-of-prion-protein-in-urine.html

Sunday, May 1, 2011

W.H.O. T.S.E. PRION Blood products and related biologicals May 2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/who-tse-prion-blood-products-and.html

DATA ON 2ND CWD STRAIN

Wednesday, September 08, 2010CWD PRION CONGRESS SEPTEMBER 8-11 2010

http://chronic-wasting-disease.blogspot.com/2010/09/cwd-prion-2010.html

http://betaamyloidcjd.blogspot.com/2011/01/enlarging-spectrum-of-prion-like.html

Saturday, November 12, 2011

Human Prion Disease and Relative Risk Associated with Chronic Wasting Disease

Fri, 22 Sep 2006 09:05:59 -0500

http://chronic-wasting-disease.blogspot.com/2011/11/human-prion-disease-and-relative-risk.html

Monday, June 27, 2011

Zoonotic Potential of CWD: Experimental Transmissions to Non-Human Primates

http://chronic-wasting-disease.blogspot.com/2011/06/zoonotic-potential-of-cwd-experimental.html

EFSA Journal 2011

The European Response to BSE: A Success Story

This is an interesting editorial about the Mad Cow Disease debacle, and it's ramifications that will continue to play out for decades to come ;

Monday, October 10, 2011

EFSA Journal 2011

The European Response to BSE: A Success Story

snip...

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

snip...

http://www.efsa.europa.eu/en/efsajournal/pub/e991.htm?emt=1

http://www.efsa.europa.eu/en/efsajournal/doc/e991.pdf

see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

http://transmissiblespongiformencephalopathy.blogspot.com/2011/10/efsa-journal-2011-european-response-to.html

Saturday, June 25, 2011

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque

"BSE-L in North America may have existed for decades"

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html

Thursday, June 23, 2011

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/experimental-h-type-bovine-spongiform.html

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

And last but not least, similarities of PrPres between Htype BSE and human prion diseases like CJD or GSS have been put forward [10], as well as between L-type BSE and CJD [17]. These findings raise questions about the origin and inter species transmission of these prion diseases that were discovered through the BSE active surveillance.

full text 18 pages ;

http://www.vetres.org/index.php?option=article&access=standard&Itemid=129&url=/articles/vetres/pdf/2008/04/v07232.pdf

please see full text ;

http://bse-atypical.blogspot.com/2008/06/review-on-epidemiology-and-dynamics-of.html

http://transmissiblespongiformencephalopathy.blogspot.com/2011/11/novel-prion-protein-in-bse-affected.html

R.I.P. MOM DECEMBER 14, 1997 HEIDENHAIN VARIANT OF CREUTZFELDT JAKOB DISEASE

TSS