Sunday, October 18, 2015

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

Pennsylvania Game Commission Law and Law Makers Forum bans Singeltary from speakng and trying to warn them about CWD Chronic Wasting Disease CWD TSE prion 2002

Outdoors with Tom Venesky: A smelly situation

 
First Posted: 8:26 am - October 18th, 2015

 
By Tom Venesky - tvenesky@timesleader.com

 
Six years ago Dr. Walter Cottrell presented an important recommendation to the Pennsylvania Game Commission board, and he urged they follow his advice.

 
Cottrell practically begged.

 
Pleaded.

 
But he couldn’t convince.

 
Cottrell, who was the PGC’s wildlife veterinarian at the time, gave a presentation to the commissioners during the October 2009 board meeting about chronic wasting disease. The disease had yet to be detected in Pennsylvania, but Cottrell urged the commissioners to take a step to reduce the risk.

 
He recommended the commissioners vote to ban the use of deer urine. Cottrell reasoned that since infected deer shed CWD prions in their urine, and there is no way to certify it’s safe, it would be best if the commissioners take a proactive approach and prohibit the use of deer lure.

 
They didn’t, and now the disease is present in the state.

 
In all fairness, the board’s lack of action regarding a ban on the use of deer urine back in 2009 didn’t lead to the current CWD outbreak in Pennsylvania, where the disease has surfaced in captive and wild deer in three areas across the state.

 
Still, I can’t help but feel that the board, in 2009, missed an opportunity to be truly proactive on the CWD front when they didn’t vote to ban the use of deer urine.

 
Especially considering another state has now listened to Cottrell.

 
In May, the Vermont Fish and Wildlife Board voted to ban the use of deer urine-based lures, effective in 2016.

 
Like Pennsylvania, Vermont shares a border with another state – New York, where CWD has been found. Vermont doesn’t want the disease to cross the border, and banning the use of deer urine is one safeguard they felt needed to be taken.

 
While the PGC board has yet to act on a deer urine ban in 2009, apparently the topic is generating some renewed interest. It was discussed at the board’s working group meeting in August and again at the September meeting.

 
The roadblock to instituting a ban on the use of deer urine by hunters is the impact such a move could have on the lure industry. The PGC will be meeting with industry representatives, who are looking at ways to certify the deer used to produce urine-based lures are free of CWD.

 
Maybe a compromise can be reached but right now, as far as I know, there isn’t a way to certify that a particular urine-based lure is free of CWD prions. And while we wait for such a test to materialize there is a chance that hunters may be in inadvertently pouring contaminated lure on the ground.

 
That’s unsettling.

 
I don’t know how a lure company can claim its product is free of prions when there is no non-lethal way to test a deer for CWD.

 
Just because a captive herd has not had any diseased animals for several years doesn’t mean CWD isn’t present, or won’t show up. It can take a year or more for symptoms to appear, and considering that captive deer operations frequently buy, sell and trade animals with other facilities, from other states, how can anyone say with certainty that a facility is CWD-free?

 
Consider this: According to a news release issued by the Vermont Fish and Wildlife Department regarding the ban, the first CWD case in Pennsylvania was from a captive deer operation that was considered “CWD-free” and was also selling urine-based lure.

 
Was that lure contaminated with CWD prions? Where was it used? Is it still out there?

 
We’ll never know, and until there’s a indisputable means to test urine-based lure before it is sold, a ban is the only answer.

 
I know that prohibiting the use of deer lure in Pennsylvania will be a big financial hit to the industry. That’s unfortunate, and for the lure industry’s sake I hope they do find a way to test and certify their product.

 
But how much of a financial hit would a widespread outbreak of CWD be to Pennsylvania’s deer hunting industry? Our deer hunting tradition is far too great to risk losing to a little bottle of urine.

 
Some contend that there isn’t any evidence the use of deer lure can spread CWD, but I don’t think it’s very proactive to wait until proof is discovered and then react.

 
We do know that infected deer shed CWD prions in their urine. The disease has been found in captive deer farms in Pennsylvania and many other states. And the urine used to make lure comes from deer farms.

 
If urine-based lure wasn’t a risk factor for spreading CWD, then why does the PGC ban its use in the three Disease Management Areas in the state?

 
Vermont did the right thing by prohibiting the use of urine-based deer lure. It’s a proactive, preventative step that has been supported by Cottrell and several other scientists with extensive CWD research under their belts.

 
Vermont listened to what Cottrell tried to tell Pennsylvania years ago.

 
The PGC board turned a deaf ear to his recommendation in 2009, but it’s still not to late to listen and act.

 
I’m convinced.

 
timesleader

 
Reach Tom Venesky at 570-991-6395 or on Twitter @TLTomVenesky

 
http://timesleader.com/sports/489445/outdoors-with-tom-venesky-a-smelly-situation

 
Pennsylvania Game Commission Law and Law Makers Forum bans Singeltary from speakng and trying to warn them about CWD Chronic Wasting Disease CWD TSE prion 2002

 

POSTED 8/31/07 HUNTING PA, but was banned again for speaking about CWD. ...TSS

 

Terry, Once banned always banned.

 


 

for posting this ;

 

From: "Terry S. Singeltary Sr." Subject: CWD UPDATE 88 AUGUST 31, 2007

 


 


 

greertings again huntingpa,

 

i do try though. i have bcc'd this to a few friends in Pa for there files.

 

sadly, once PA does finally document CWD (i do hope this never happens), i will be able to say i tried to tell you so, and then show the world _whom_ banned whom, for speaking the truth, and _whom_ tried to cover it up i.e. CWD. i will let the world know about that for sure.

 

ill keep a close on on ya via a few oldtimers there that keep contact with me about CWD, rest assured on that too.

 

it's very suspicious to ban someone simply for speaking about CWD, when there has been no violations of proper etiquette i.e. cussing, etc.

 

i could have stayed silent till the cows come home, and stayed as a silent one, but thought the data there was too important for the hunters in PA, so i went ahead and finally posted (had been signed up and will sign up again soon via another computer), knowing i would probably be banned again for posting important CWD data. but i took a shot anyway. hopefully, someone was able to download and silently passed it on. i dont give up easy, especially when one tries to ban someone from speaking out on the truth about CWD.

 

i was mad the first time you banned me for speaking about CWD, but now i am on sad, i am sad for the hunters in PA.

 

ignorance is bless, but to intentionally stop people from speaking on such an important topic, and passing credible data, important data, should be regarded with great suspicion, and when the time is right, we will let the hunters of PA decide for themselves, on just how serious your cover-up was at Hunting PA. ...TSS

 

HISTORY ON BANNING TSS OF SPEAKING ABOUT CWD ON PA HUNTING

 

Subject: Pennsylvania Game Commission Law and Law Makers Message Board HUNTING PA.COM BANS SPEAKING ABOUT CWD Date: December 21, 2005 at 8:37 am PST

 

Greetings State of PA hunters et al,

 

SEEMS Big Brother is working everywhere these days. after 8 years of trying to warn hunters about CWD on many boards in many states, i find a new low in the state of PA. Banning and deleting postings TSS or anyone from speaking about CWD evidently. the only thing i ever posted was the latest on CWD from some of the top peer review papers to date, and some old confidential data (with references and sources pdf files) for all to see. but evidently, after just trying to warn these hunters, and have been since Sept. 2002 with not one complaint waged against me that i am aware of, the Pennsylvania Game Commission Law and Law Makers board has banned me from speaking about CWD. NOT only on that board, but any board at ;

 


 

i suppose if they just bury there heads in the sand and don't speak about it, it will go away.

 

good luck. ...TSS

 

Welcome Terry S. Singeltary Sr.. [Logout]

 

Law and Law Makers Message Board >> Pennsylvania Game Commission

 

 Pages: 1 Terry S. Singeltary Sr. member

 

Reged: Sep 17 2002 Posts: 129 Loc: TEXAS CWD IMPORTATION OF CERTAIN CARCASS PARTS BAN #513483 - Mon Dec 19 2005 03:59 PM

 

Release #143-05

 

GAME COMMISSION BANS IMPORTATION OF CERTAIN CARCASS PARTS FROM STATES WITH CWD

 

Using newly-granted emergency powers, Pennsylvania Game Commission Executive Director Vern Ross today issued an order banning the importation of specific carcass parts from states and Canadian provinces where CWD had been identified in free-ranging cervid populations.

 

The ban closely mirrors a similar ban issued on Sept. 21 by the state Department of Agriculture, with the support of the Game Commission. Agriculture Secretary Dennis Wolff used his emergency powers to issue the ban pending action by the Board of Game Commissioners to grant similar emergency powers to the agency's executive director.

 

"With chronic wasting disease (CWD) present in free-ranging and captive wildlife populations in 14 states and two Canadian provinces, we must act responsibly and clearly to protect our wild and captive populations of deer and elk, as well as other cervid family members," Ross said. "This ban applies to carcass parts from deer, elk or other cervids susceptible to CWD taken from the wild or from captive facilities in those states where CWD has been found in wild herds.

 

"There are many scientific unknowns about CWD, so this order may need to be altered in the future based on new discoveries, as well as new states that find CWD within their borders or other species that prove susceptible to the disease."

 

For more information, please visit the Pennsylvania Game Commission - State Wildlife Management Agency website: http://www.pgc.state.pa.us/pgc/cwp/view.asp?a=11&Q=166946

 

TSS

 

Terry S. Singeltary Sr. member

 

Reged: Sep 17 2002 Posts: 129 Loc: TEXAS

 

Greetings Samuel and Hunters of PA,

 

i will no longer be able to post here for reasons posted below. sorry for making the posting above. i had not seen this yet. ... good luck...tss

 

Welcome Terry S. Singeltary Sr.. [Logout] My Home · Main Index · Search · Active Topics Who's Online · FAQ · User List · Calendar

 

CWD Postings.

 

From: Samuel

 

Terry,

 

I have to request that you discontinue from posting information on CWD. I have received concerns from individuals on the validity of your information. Since I am not educated on the subject, I cannot validate that the information is correct and or factual. As time moves on, this subject will become quite a "touchy subject" and any information, factual or not, will be scrutinized. From now on, we will have to rely on the PGC to educate the residents here in PA on the subject.

 

Thank you for your concern in this matter and keeping a close vigil on the topic.

 

Samuel

 

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

 

Reged: Sep 17 2002

 

Posts: 132 Loc: TEXAS

 

POSTINGS AND DISCUSSIONS ON CWD HERE #514778 - Wed Dec 21 2005 11:26 AM

 

Greetings PA Hunters,

 

I have been ask not to post anymore here about CWD. SO, i will adhere to there request. i really have no other alternative. i would like to say, this is very disturbing to me, and should be very concerning for you hunters. i have been researching this for almost 8 years and this is the only state that has banned me from posting about TSE. Big Brother is working everywhere, including this board. ...TSS

 

From: Samuel Your post was deleted due to it being a double post. The press release is posted in the PGC Press Release Thread.

 

Like I had asked you, please refrain from posting information on CWD.

 

Thank you.

 

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

 

Pennsylvania Game Commission Law and Law Makers Message Board HUNTING PA.COM

 

TSS

 

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

 

From: TSS Subject: Pennsylvania Game Commission Law and Law Makers Message Board HUNTING PA.COM BANS SPEAKING ABOUT CWD Date: December 21, 2005 at 8:37 am PST

 

Greetings State of PA hunters et al,

 

SEEMS Big Brother is working everywhere these days. after 8 years of trying to warn hunters about CWD on many boards in many states, i find a new low in the state of PA. Banning and deleting postings TSS or anyone from speaking about CWD evidently. the only thing i ever posted was the latest on CWD from some of the top peer review papers to date, and some old confidential data (with references and sources pdf files) for all to see. but evidently, after just trying to warn these hunters, and have been since Sept. 2002 with not one complaint waged against me that i am aware of, the Pennsylvania Game Commission Law and Law Makers board has banned me from speaking about CWD. NOT only on that board, but any board at ;

 


 

i suppose if they just bury there heads in the sand and don't speak about it, it will go away. good luck. ...TSS

 

Welcome Terry S. Singeltary Sr.. [Logout]

 

Law and Law Makers Message Board >> Pennsylvania Game Commission

 

Pages: 1 Terry S. Singeltary Sr. member

 

Reged: Sep 17 2002 Posts: 129 Loc: TEXAS CWD IMPORTATION OF CERTAIN CARCASS PARTS BAN #513483 - Mon Dec 19 2005 03:59 PM

 

Release #143-05

 

GAME COMMISSION BANS IMPORTATION OF CERTAIN CARCASS PARTS FROM STATES WITH CWD

 

Using newly-granted emergency powers, Pennsylvania Game Commission Executive Director Vern Ross today issued an order banning the importation of specific carcass parts from states and Canadian provinces where CWD had been identified in free-ranging cervid populations.

 

The ban closely mirrors a similar ban issued on Sept. 21 by the state Department of Agriculture, with the support of the Game Commission. Agriculture Secretary Dennis Wolff used his emergency powers to issue the ban pending action by the Board of Game Commissioners to grant similar emergency powers to the agency's executive director.

 

"With chronic wasting disease (CWD) present in free-ranging and captive wildlife populations in 14 states and two Canadian provinces, we must act responsibly and clearly to protect our wild and captive populations of deer and elk, as well as other cervid family members," Ross said. "This ban applies to carcass parts from deer, elk or other cervids susceptible to CWD taken from the wild or from captive facilities in those states where CWD has been found in wild herds.

 

"There are many scientific unknowns about CWD, so this order may need to be altered in the future based on new discoveries, as well as new states that find CWD within their borders or other species that prove susceptible to the disease."

 

For more information, please visit the Pennsylvania Game Commission - State Wildlife Management Agency website: http://www.pgc.state.pa.us/pgc/cwp/view.asp?a=11&Q=166946

 

TSS

 

Terry S. Singeltary Sr. member

 

Reged: Sep 17 2002 Posts: 129 Loc: TEXAS

 

Greetings Samuel and Hunters of PA,

 

i will no longer be able to post here for reasons posted below. sorry for making the posting above. i had not seen this yet. ... good luck...tss

 

Welcome Terry S. Singeltary Sr.. [Logout] My Home · Main Index · Search · Active Topics Who's Online · FAQ · User List · Calendar

 

CWD Postings.

 

From: Samuel

 

Terry,

 

I have to request that you discontinue from posting information on CWD. I have received concerns from individuals on the validity of your information. Since I am not educated on the subject, I cannot validate that the information is correct and or factual. As time moves on, this subject will become quite a "touchy subject" and any information, factual or not, will be scrutinized. From now on, we will have to rely on the PGC to educate the residents here in PA on the subject.

 

Thank you for your concern in this matter and keeping a close vigil on the topic.

 

Samuel

 

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

 

Reged: Sep 17 2002 Posts: 132 Loc: TEXAS POSTINGS AND DISCUSSIONS ON CWD HERE #514778 - Wed Dec 21 2005 11:26 AM

 

Greetings PA Hunters,

 

I have been ask not to post anymore here about CWD.

 

SO, i will adhere to there request. i really have no other alternative. i would like to say, this is very disturbing to me, and should be very concerning for you hunters. i have been researching this for almost 8 years and this is the only state that has banned me from posting about TSE. Big Brother is working everywhere, including this board. ...TSS

 

From: Samuel

 

Your post was deleted due to it being a double post. The press release is posted in the PGC Press Release Thread.

 

Like I had asked you, please refrain from posting information on CWD.

 

Thank you.

 

 =========================

 

Pennsylvania Game Commission Law and Law Makers Message Board HUNTING PA.COM

 

 TSS

 

 =========================

 

----- Original Message ----- From: "Terry S. Singeltary Sr." To: "Terry S. Singeltary Sr." ; "GM, PGCNEWS"

 

Cc: "Jerry Feaser" Sent: Wednesday, December 21, 2005 5:31 PM Subject: Re: Pennsylvania Game Commission - State Wildlife Management Agency eAlert: Newsroom

 

> By the way, Joe Neville said he will see if he can find out why your info > was deleted

 

thank you!

 

i still cannot figure it out. i have posted nothing obscene, abusive, just data on TSEs, all with references. i don't think i even ranted much. there were many things deleted? the second round of deletions was nothing but cwd postings from PA and NM and recent data on CJD from gambetti et al here in the USA, the latest from Aguzzi et al i also posted. i can't believe it was deleted??? please advise, is the board there just off limits for me posting about CWD and or everyone? what about the other boards, cant post about CWD there either? how else are hunters going to learn about this agent if we cannot speak of it??? i have wasted daily, 8 years of my life trying to educate hunters and cattleman, and most of the time they appreciate it. i have failed with the FDA/USDA et al to the most extent. but this is unbelievable. again, a new low..................

 

kind regards, terry

 

----- Original Message ----- From: "GM, PGCNEWS" To: "Terry S. Singeltary Sr." Sent: Wednesday, December 21, 2005 11:20 AM Subject: RE: Pennsylvania Game Commission - State Wildlife Management Agency eAlert: Newsroom

 

By the way, Joe Neville said he will see if he can find out why your info was deleted.

 

-----Original Message----- From: Terry S. Singeltary Sr. [mailto:flounder9@verizon.net] Sent: Wednesday, December 21, 2005 12:16 PM To: Jerry Feaser Cc: Jerry Feaser Subject: Re: Pennsylvania Game Commission - State Wildlife Management Agency eAlert: Newsroom

 

Greetings Jerry,

 

whether you know about this or not, or even care. i have done nothing wrong to be banned from posting about cwd. this is very disturbing?

 

kind regards, terry

 

Subject: Pennsylvania Game Commission Law and Law Makers Message Board HUNTING PA.COM BANS SPEAKING ABOUT CWD Date: December 21, 2005 at 8:37 am PST

 

Greetings State of PA hunters et al,

 

SEEMS Big Brother is working everywhere these days. after 8 years of trying to warn hunters about CWD on many boards in many states, i find a new low in the state of PA. Banning and deleting postings TSS or anyone from speaking about CWD evidently. the only thing i ever posted was the latest on CWD from some of the top peer review papers to date, and some old confidential data (with references and sources pdf files) for all to see. but evidently, after just trying to warn these hunters, and have been since Sept. 2002 with not one complaint waged against me that i am aware of, the Pennsylvania Game Commission Law and Law Makers board has banned me from speaking about CWD. NOT only on that board, but any board at ;

 


 

i suppose if they just bury there heads in the sand and don't speak about it, it will go away. good luck. ...TSS

 

Welcome Terry S. Singeltary Sr.. [Logout]

 

Law and Law Makers Message Board >> Pennsylvania Game Commission

 

Pages: 1 Terry S. Singeltary Sr. member

 

Reged: Sep 17 2002 Posts: 129 Loc: TEXAS CWD IMPORTATION OF CERTAIN CARCASS PARTS BAN #513483 - Mon Dec 19 2005 03:59 PM

 

Release #143-05

 

GAME COMMISSION BANS IMPORTATION OF CERTAIN CARCASS PARTS FROM STATES WITH CWD

 

Using newly-granted emergency powers, Pennsylvania Game Commission Executive Director Vern Ross today issued an order banning the importation of specific carcass parts from states and Canadian provinces where CWD had been identified in free-ranging cervid populations.

 

The ban closely mirrors a similar ban issued on Sept. 21 by the state Department of Agriculture, with the support of the Game Commission. Agriculture Secretary Dennis Wolff used his emergency powers to issue the ban pending action by the Board of Game Commissioners to grant similar emergency powers to the agency's executive director.

 

"With chronic wasting disease (CWD) present in free-ranging and captive wildlife populations in 14 states and two Canadian provinces, we must act responsibly and clearly to protect our wild and captive populations of deer and elk, as well as other cervid family members," Ross said. "This ban applies to carcass parts from deer, elk or other cervids susceptible to CWD taken from the wild or from captive facilities in those states where CWD has been found in wild herds.

 

"There are many scientific unknowns about CWD, so this order may need to be altered in the future based on new discoveries, as well as new states that find CWD within their borders or other species that prove susceptible to the disease."

 

For more information, please visit the Pennsylvania Game Commission - State Wildlife Management Agency website: http://www.pgc.state.pa.us/pgc/cwp/view.asp?a=11&Q=166946

 

TSS

 

Terry S. Singeltary Sr. member

 

Reged: Sep 17 2002 Posts: 129 Loc: TEXAS

 

Greetings Samuel and Hunters of PA,

 

i will no longer be able to post here for reasons posted below. sorry for making the posting above. i had not seen this yet. ... good luck...tss

 

Welcome Terry S. Singeltary Sr.. [Logout] My Home · Main Index · Search · Active Topics Who's Online · FAQ · User List · Calendar

 

CWD Postings.

 

From: Samuel

 

Terry,

 

I have to request that you discontinue from posting information on CWD. I have received concerns from individuals on the validity of your information. Since I am not educated on the subject, I cannot validate that the information is correct and or factual. As time moves on, this subject will become quite a "touchy subject" and any information, factual or not, will be scrutinized. From now on, we will have to rely on the PGC to educate the residents here in PA on the subject.

 

Thank you for your concern in this matter and keeping a close vigil on the topic.

 

Samuel ===========================

 

Reged: Sep 17 2002 Posts: 132 Loc: TEXAS POSTINGS AND DISCUSSIONS ON CWD HERE #514778 - Wed Dec 21 2005 11:26 AM

 

Greetings PA Hunters,

 

I have been ask not to post anymore here about CWD. SO, i will adhere to there request. i really have no other alternative. i would like to say, this is very disturbing to me, and should be very concerning for you hunters. i have been researching this for almost 8 years and this is the only state that has banned me from posting about TSE. Big Brother is working everywhere, including this board. ...TSS

 

From: Samuel Your post was deleted due to it being a double post. The press release is posted in the PGC Press Release Thread.

 

Like I had asked you, please refrain from posting information on CWD.

 

Thank you.

 

 =========================

 

Pennsylvania Game Commission Law and Law Makers Message Board HUNTING PA.COM

 

TSS

 

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

 

##################### Bovine Spongiform Encephalopathy #####################

 

New Mexico Department of Game and Fish Media contact: Dan Williams, (505) 476-8004 Public contact: (505) 476-8000 dan.williams@state.nm.us

 

FOR IMMEDIATE RELEASE, DEC. 9, 2005:

 

TWO NEW MEXICO ELK TEST POSITIVE FOR CHRONIC WASTING DISEASE

 

snip...end

 

************2015 OCTOBER CWD TSE PRION**************

 

TEXAS PRICE OF CWD TSE PRION POKER GOES UP $$$

 

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

 

Title: Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus)

 

Authors

 

item Moore, S - item Kunkle, Robert item Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin

 

Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A

 

Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of North American cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, but CWD has not been reported in free-ranging caribou (Rangifer tarandus caribou) or farmed reindeer. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWD-wtd), mule deer (Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWD-wtd, CWD-md, or CWD-elk. Two years after challenge of inoculated reindeer, non-inoculated control reindeer were introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a pen adjacent to the CWD-md inoculated reindeer (n=2). Reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrP-CWD). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (MPI). ***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 and="" are="" both="" can="" cervid="" cwd="" directly="" div="" from="" have="" indirectly.="" mpi="" naive="" reindeer="" shown="" sources="" susceptible="" that="" to="" transmit="" various="" we="">
 


 

***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 and="" are="" both="" can="" cervid="" cwd="" directly="" div="" from="" have="" indirectly.="" mpi="" naive="" reindeer="" shown="" sources="" susceptible="" that="" to="" transmit="" various="" we="">
 

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

 

snip...see more here;

 

Tuesday, September 29, 2015

 

*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly

 

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

 


 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

*** 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.

 


 

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

 

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

 

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

 

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

 

SUMMARY:

 


 

For Immediate Release Thursday, October 2, 2014

 

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

 

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

 

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

 


 

*** see history of this CWD blunder here ;

 


 

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

 


 

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

 

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

 


 

CWD, spreading it around...

 

for the game farm industry, and their constituents, to continue to believe that they are _NOT_, and or insinuate that they have _NEVER_ been part of the problem, will only continue to help spread cwd. the game farming industry, from the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet mills, shooting pens, to large ranches, are not the only problem, but it is painfully obvious that they have been part of the problem for decades and decades, just spreading it around, as with transportation and or exportation and or importation of cervids from game farming industry, and have been proven to spread cwd. no one need to look any further than South Korea blunder ;

 

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

 

spreading cwd around...

 

Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.

 

***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.

 


 

spreading cwd around...

 

Friday, May 13, 2011

 

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

 

Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea

 

Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.

 

On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.

 

All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.

 

Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.

 

Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.

 

Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).

 

In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.

 

Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.

 

All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.

 

Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.

 

In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.

 

In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.

 


 


 


 


 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES

 

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

 

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

 

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

 

SUMMARY:

 


 

For Immediate Release Thursday, October 2, 2014

 

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

 

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

 

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

 


 

*** see history of this CWD blunder here ;

 


 

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

 


 

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

 

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

 


 

CWD, spreading it around...

 

for the game farm industry, and their constituents, to continue to believe that they are _NOT_, and or insinuate that they have _NEVER_ been part of the problem, will only continue to help spread cwd. the game farming industry, from the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet mills, shooting pens, to large ranches, are not the only problem, but it is painfully obvious that they have been part of the problem for decades and decades, just spreading it around, as with transportation and or exportation and or importation of cervids from game farming industry, and have been proven to spread cwd. no one need to look any further than South Korea blunder ;

 

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

 

spreading cwd around...

 

Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.

 

***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.

 


 

spreading cwd around...

 

Friday, May 13, 2011

 

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

 

Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea

 

Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.

 

On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.

 

All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.

 

Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.

 

Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.

 

Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).

 

In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.

 

Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.

 

All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.

 

Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.

 

In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.

 

In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.

 


 


 


 


 

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

 

The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.

 


 

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

 

Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.

 


 

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

 

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.

 


 

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

 

Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE

 

In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.

 


 

PL1

 

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

 

Claudio Soto

 

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

 

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

 

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

 

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

 

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

 

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

 


 

see ;

 


 


 


 


 


 

98 | Veterinary Record | January 24, 2015

 

EDITORIAL

 

Scrapie: a particularly persistent pathogen

 

Cristina Acín

 

Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’

 

From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).

 

Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.

 

Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.

 

The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).

 

In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.

 

Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).

 

In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.

 

The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).

 

Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).

 

So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?

 

What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.

 

References

 

snip...

 

98 | Veterinary Record | January 24, 2015

 


 

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

 

Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C. Maddison, BSc, PhD3 + Author Affiliations

 

1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and chronic wasting disease of deer/elk are contagious prion diseases where environmental reservoirs are directly implicated in the transmission of disease. In this study, the effectiveness of recommended scrapie farm decontamination regimens was evaluated by a sheep bioassay using buildings naturally contaminated with scrapie. Pens within a farm building were treated with either 20,000 parts per million free chorine solution for one hour or were treated with the same but were followed by painting and full re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue. All animals became infected over an 18-month period, even in the pen that had been subject to the most stringent decontamination process. These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.

 

SNIP...

 

Discussion

 

Thorough pressure washing of a pen had no effect on the amount of bioavailable scrapie infectivity (pen B). The routine removal of prions from surfaces within a laboratory setting is treatment for a minimum of one hour with 20,000 ppm free chlorine, a method originally based on the use of brain macerates from infected rodents to evaluate the effectiveness of decontamination (Kimberlin and others 1983). Further studies have also investigated the effectiveness of hypochlorite disinfection of metal surfaces to simulate the decontamination of surgical devices within a hospital setting. Such treatments with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous treatment of the pen surfaces did not effectively remove the levels of scrapie infectivity over that of the control pens, indicating that this method of decontamination is not effective within a farm setting. This may be due to the high level of biological matrix that is present upon surfaces within the farm environment, which may reduce the amount of free chlorine available to inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had also became scrapie positive within nine months, with all animals in this pen being RAMALT positive by 18 months of age. Pen D was no further away from the control pen (pen A) than any of the other pens within this barn. Localised hot spots of infectivity may be present within scrapie-contaminated environments, but it is unlikely that pen D area had an amount of scrapie contamination that was significantly different than the other areas within this building. Similarly, there were no differences in how the biosecurity of pen D was maintained, or how this pen was ventilated compared with the other pens. This observation, perhaps, indicates the slower kinetics of disease uptake within this pen and is consistent with a more thorough prion removal and recontamination. These observations may also account for the presence of inadvertent scrapie cases within other studies, where despite stringent biosecurity, control animals have become scrapie positive during challenge studies using barns that also housed scrapie-affected animals (Ryder and others 2009). The bioassay data indicate that the exposure of the sheep to a farm environment after decontamination efforts thought to be effective in removing scrapie is sufficient for the animals to become infected with scrapie. The main exposure routes within this scenario are likely to be via the oral route, during feeding and drinking, and respiratory and conjunctival routes. It has been demonstrated that scrapie infectivity can be efficiently transmitted via the nasal route in sheep (Hamir and others 2008), as is the case for CWD in both murine models and in white-tailed deer (Denkers and others 2010, 2013). Recently, it has also been demonstrated that CWD prions presented as dust when bound to the soil mineral montmorillonite can be infectious via the nasal route (Nichols and others 2013). When considering pens C and D, the actual source of the infectious agent in the pens is not known, it is possible that biologically relevant levels of prion survive on surfaces during the decontamination regimen (pen C). With the use of galvanising and painting (pen D) covering and sealing the surface of the pen, it is possible that scrapie material recontaminated the pens by the movement of infectious prions contained within dusts originating from other parts of the barn that were not decontaminated or from other areas of the farm.

 

Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity. This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.

 

The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.

 

Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014

 


 

Monday, November 3, 2014

 

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

 


 

PPo3-22:

 

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

 

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

 

Key words: scrapie, evironmental persistence, sPMCA

 

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

 


 

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

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

Contamination of Plants with Prions Excreted in Urine and Feces

 

Under natural conditions, it is likely that the main source of prions in the environment comes from secretory and excretory fluids, such as saliva, urine, and feces. We and others have shown that PrPSc is released in these fluids and excretions in various animal species (Gonzalez-Romero et al., 2008; Haley et al., 2009, 2011; Maddison et al., 2010; Terry et al., 2011; Moda et al., 2014). It has been estimated that the amount of infectious prions spread by excreta during the animals’ lifespan could match or even surpass the quantity present in the brain of a symptomatic individual (Tamgu¨ ney et al., 2009). To study whether plant tissue can be contaminated by waste products excreted from prion-infected hamsters and deer, leaves and roots were incubated with samples of urine and feces and the presence of PrPSc analyzed by serial rounds of PMCA. For these experiments, plant tissues were incubated for 1 hr with urine or feces homogenates obtained either from 263K-infected hamsters or CWD-affected cervids. This time was chosen because longer incubation with these biological fluids affected the integrity of the plant tissue. After being thoroughly washed and dried, PrPSc attached to leaves and roots was detected by PMCA. The results clearly show that PrPSc was readily detectable after three or four rounds of PMCA in samples of wheat grass leaves and roots exposed to both urine and feces from 263K sick hamsters (Figure 3A) and CWD-affected cervids (Figure 3B). Comparing these results with studies of the direct detection of PrPSc in urine and feces (Figures 3A and 3B), it seems that the majority of PrPSc present in these waste products was effectively attached to leaves and roots. No signal was observed in plant tissue exposed to urine or feces coming from non-infected hamsters.

 

Prions Bind to Living Plants

 

To investigate a more natural scenario for prion contamination of living plants, we sprayed the leaves of wheat grass with a preparation containing 1% 263K hamster brain homogenate. Plants were let to grow for different times after exposure, and PrPSc was detected in the leaves by PMCA in duplicates for each time point. The results show that PrPSc was able to bind to leaves and remained attached to the living plants for at least 49 days after exposure (Figure 4). Considering that PrPSc signal was detectable normally in the second or third round of PMCA without obvious trend in relation to time, we conclude that the relative amount of PrPSc present in leaves did not appear to change substantially over time. These data indicate that PrPSc can be retained in living plants for at least several weeks after a simple contact with prion contaminated materials, and PrPSc remains competent to drive prion replication.

 

DISCUSSION

 

This study shows that plants can efficiently bind prions contained in brain extracts from diverse prion infected animals, including CWD-affected cervids. PrPSc attached to leaves and roots from wheat grass plants remains capable of seeding prion replication in vitro. Surprisingly, the small quantity of PrPSc naturally excreted in urine and feces from sick hamster or cervids was enough to efficiently contaminate plant tissue. Indeed, our results suggest that the majority of excreted PrPSc is efficiently captured by plants’ leaves and roots. Moreover, leaves can be contaminated by spraying them with a prion-containing extract, and PrPSc remains detectable in living plants for as long as the study was performed (several weeks). Remarkably, prion contaminated plants transmit prion disease to animals upon ingestion, producing a 100% attack rate and incubation periods not substantially longer than direct oral administration of sick brain homogenates. Finally, an unexpected but exciting result was that plants were able to uptake prions from contaminated soil and transport them to aerial parts of the plant tissue. Although it may seem farfetched that plants can uptake proteins from the soil and transport it to the parts above the ground, there are already published reports of this phenomenon (McLaren et al., 1960; Jensen and McLaren, 1960; Paungfoo-Lonhienne et al., 2008). The high resistance of prions to degradation and their ability to efficiently cross biological barriers mayplay a role in this process. The mechanism by which plants bind, retain, uptake, and transport prions is unknown. Weare currently studying the way in which prions interact with plants using purified, radioactively labeled PrPSc to determine specificity of the interaction, association constant, reversibility, saturation, movement, etc.

 

Epidemiological studies have shown numerous instances of scrapie or CWD recurrence upon reintroduction of animals on pastures previously exposed to prion-infected animals. Indeed, reappearance of scrapie has been documented following fallow periods of up to 16 years (Georgsson et al., 2006), and pastures were shown to retain infectious CWD prions for at least 2 years after exposure (Miller et al., 2004). It is likely that the environmentally mediated transmission of prion diseases depends upon the interaction of prions with diverse elements, including soil, water, environmental surfaces, various invertebrate animals, and plants.

 

However, since plants are such an important component of the environment and also a major source of food for many animal species, including humans, our results may have far-reaching implications for animal and human health. Currently, the perception of the risk for animal-to-human prion transmission has been mostly limited to consumption or exposure to contaminated meat; our results indicate that plants might also be an important vector of transmission that needs to be considered in risk assessment.

 


 

SNIP...SEE FULL TEXT ;

 

Saturday, October 03, 2015

 

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015

 


 

***S P O N T A N E O U S***S P O R A D I C***

 

spontaneous atypical BSE ???

 

if that's the case, then France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE, problem solved $$$

 

As of December 2011, around 60 atypical BSE cases have currently been reported in 13 countries, *** with over one third in France.

 


 

so 20 cases of atypical BSE in France, compared to the remaining 40 cases in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+ cases per country, besides Frances 20 cases. you cannot explain this away with any spontaneous BSe. ...TSS

 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

*** spontaneous TSE prion, that's wishful thinking. on the other hand, if spontaneous did ever happen (never once documented in the field), it would be our worst nightmare, due to feed. just saying.

 

*** We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. ***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

 

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

 


 


 

PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS

 

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

 

O18

 

Zoonotic Potential of CWD Prions

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 


 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

HD.13: CWD infection in the spleen of humanized transgenic mice

 

Liuting Qing and Qingzhong Kong

 

Case Western Reserve University; Cleveland, OH USA

 

Chronic wasting disease (CWD) is a widespread prion disease in free-ranging and captive cervid species in North America, and there is evidence suggesting the existence of multiple CWD strains. The susceptibility of human CNS and peripheral organs to the various CWD prion strains remains largely unclear. Current literature suggests that the classical CWD strain is unlikely to infect human brain, but the potential for peripheral infection by CWD in humans is unknown. We detected protease-resistant PrpSc in the spleens of a few humanized transgenic mice that were intracerebrally inoculated with natural CWD isolates, but PrpSc was not detected in the brains of any of the CWD-inoculated mice. ***Our ongoing bioassays in humanized Tg mice indicate that intracerebral challenge with such PrpSc-positive humanized mouse spleen already led to prion disease in most animals. ***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.

 

Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system

 

Marcelo A.Barria,1 Aru Balachandran,2 Masanori Morita,3 Tetsuyuki Kitamoto,4 Rona Barron,5 Jean Manson,5 Richard Kniqht,1 James W. lronside1 and Mark W. Head1

 

1National CJD Research and Surveillance Unit; Centre for Clinical Brain Sciences; School of Clinical Sciences; The University of Edinburgh; Edinburgh, UK; 2National and OIE Reference Laboratory for Scrapie and CWD; Canadian Food Inspection Agency; Ottawa Laboratory; Fallowfield. ON Canada; 3Infectious Pathogen Research Section; Central Research Laboratory; Japan Blood Products Organization; Kobe, Japan; 4Department of Neurological Science; Tohoku University Graduate School of Medicine; Sendai. Japan; 5Neurobiology Division; The Roslin Institute and R(D)SVS; University of Edinburgh; Easter Bush; Midlothian; Edinburgh, UK

 

Background. Bovine spongiform encephalopathy (BSE) is a known zoonotic prion disease, resulting in variant Creurzfeldt- Jakob disease (vCJD) in humans. In contrast, classical scrapie in sheep is thought to offer little or no danger to human health. However, a widening range of prion diseases have been recognized in cattle, sheep and deer. The risks posed by individual animal prion diseases to human health cannot be determined a priori and are difficult to assess empirically. The fundamemal event in prion disease pathogenesis is thought to be the seeded conversion of normal prion protein (PrPC) to its pathological isoform (PrPSc). Here we report the use of a rapid molecular conversion assay to test whether brain specimens from different animal prion diseases are capable of seeding the conversion of human PrPC ro PrPSc.

 

Material and Methods. Classical BSE (C-type BSE), H-type BSE, L-type BSE, classical scrapie, atypical scrapie, chronic wasting disease and vCJD brain homogenates were tested for their ability to seed conversion of human PrPC to PrPSc in protein misfolding cyclic amplification (PMCA) reactions. Newly formed human PrPSc was detected by protease digestion and western blotting using the antibody 3F4.

 

Results. C-type BSE and vCJD were found to efficiently convert PrPC to PrPSc. Scrapie failed to convert human PrPC to PrPSc. Of the other animal prion diseases tested only chronic wasting disease appeared to have the capability ro convert human PrPC to PrPSc. The results were consistent whether the human PrPC came from human brain, humanised transgenic mouse brain or from cultured human cells and the effect was more pronounced for PrPC with methionine at codon 129 compared with that with valine.

 

Conclusion. Our results show that none of the tested animal prion disease isolates are as efficient as C-type BSE and vCJD in converting human prion protein in this in vitro assay. ***However, they also show that there is no absolute barrier ro conversion of human prion protein in the case of chronic wasting disease.

 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

 


 

cwd to humans ???

 

there has been no official documentation of cwd to humans on paper, to date.

 

cwd transmission studies on humans are illegal.

 

cwd transmits freely to the squirrel monkey, but not yet to the macaque, and the macaque is a bit closer to humans than the squirrel monkey.

 

still, with cwd freely transmitting to the squirrel monkey, scientist are very concerned about the cwd to human risk factor, exposure, and potential iatrogenic transmission there from.

 

85% of human TSE is sporadic cjd, and each and every one of them are up for debate as to route and source. I believe that friendly fire (iatrogenic) or the pass it forward mode of the TSE prion will be a large portion of that. all iatrogenic cjd is, is sporadic cjd until the iatrogenic event is discovered, documented, put into the academic and then the public domain, which very seldom happens due to lack of trace back efforts.

 

see what the authors said about this casual link with cwd to human with the case of Jeffrey Schwan 26 year old, and personal communications years ago with cdc about that case. 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: Terry S. Singeltary Sr.

 

Sent: Saturday, November 15, 2014 9:29 PM

 

To: Terry S. Singeltary Sr.

 

Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984

 

THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE

 

R. G. WILL

 

1984

 

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

 

snip...

 


 

July's Milwaukee Journal Sentinel article did prod state officials to ask CDC to investigate the cases of the three men who shared wild game feasts. The two men the CDC is still investigating were 55 and 66 years old. But there's also Kevin Boss, a Minnesota hunter who ate Barron County venison and died of CJD at 41. And there's Jeff Schwan, whose Michigan Tech fraternity brothers used to bring venison sausage back to the frat house. His mother, Terry, says that in May 2001, Jeff, 26, began complaining about his vision. A friend noticed misspellings in his e-mail, which was totally unlike him. Jeff began losing weight. He became irritable and withdrawn. By the end of June, he couldn't remember the four-digit code to open the garage door or when and how to feed his parents' cats. At a family gathering in July, he stuck to his parents and girlfriend, barely talking. "On the night we took him to the hospital, he was speaking like he was drunk or high and I noticed his pupils were so dilated I couldn't see the irises," his mother says. By then, Jeff was no longer able to do even simple things on his computer at work, and "in the hospital, he couldn't drink enough water." When he died on September 27, 2001, an autopsy confirmed he had sporadic CJD.

 

In 2000, Belay looked into three CJD cases reported by The Denver Post, two hunters who ate meat from animals killed in Wyoming and the daughter of a hunter who ate venison from a plant that processed Colorado elk. All three died of CJD before they were 30 years old. The CDC asked the USDA to kill 1,000 deer and elk in the area where the men hunted. Belay and others reported their findings in the Archives of Neurology, writing that although "circumstances suggested a link between the three cases and chronic wasting disease, they could find no 'causal' link." Which means, says Belay, "not a single one of those 1,000 deer tested positive for CWD. For all we know, these cases may be CWD. What we have now doesn't indicate a connection. That's reassuring, but it would be wrong to say it will never happen."

 

So far, says NIH researcher Race, the two Wisconsin cases pinpointed by the newspaper look like spontaneous CJD. "But we don't know how CWD would look in human brains. It probably would look like some garden-variety sporadic CJD." What the CDC will do with these cases and four others (three from Colorado and Schwan from Upper Michigan), Race says, is "sequence the prion protein from these people, inject it into mice and wait to see what the disease looks like in their brains. That will take two years."

 

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

 

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

 


 

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

 

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

 


 

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

 


 

*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. ***

 


 

*** IF CWD is not a risk factor for humans, then I guess the FDA et al recalled all this CWD tainted elk tenderloin (2009 Exotic Meats USA of San Antonio, TX) for the welfare and safety of the dead elk. ...tss

 

Exotic Meats USA Announces Urgent Statewide Recall of Elk Tenderloin Because It May Contain Meat Derived From An Elk Confirmed To Have Chronic Wasting Disease

 

Contact: Exotic Meats USA 1-800-680-4375

 

FOR IMMEDIATE RELEASE -- February 9, 2009 -- Exotic Meats USA of San Antonio, TX is initiating a voluntary recall of Elk Tenderloin because it may contain meat derived from an elk confirmed to have Chronic Wasting Disease (CWD). The meat with production dates of December 29, 30 and 31, 2008 was purchased from Sierra Meat Company in Reno, NV. The infected elk came from Elk Farm LLC in Pine Island, MN and was among animals slaughtered and processed at USDA facility Noah’s Ark Processors LLC.

 

Chronic Wasting Disease (CWD) is a fatal brain and nervous system disease found in elk and deer. The disease is caused by an abnormally shaped protein called a prion, which can damage the brain and nerves of animals in the deer family. Currently, it is believed that the prion responsible for causing CWD in deer and elk is not capable of infecting humans who eat deer or elk contaminated with the prion, but the observation of animal-to-human transmission of other prion-mediated diseases, such as bovine spongiform encephalopathy (BSE), has raised a theoretical concern regarding the transmission of CWD from deer or elk to humans. At the present time, FDA believes the risk of becoming ill from eating CWD-positive elk or deer meat is remote. However, FDA strongly advises consumers to return the product to the place of purchase, rather than disposing of it themselves, due to environmental concerns.

 

Exotic Meats USA purchased 1 case of Elk Tenderloins weighing 16.9 lbs. The Elk Tenderloin was sold from January 16 – 27, 2009. The Elk Tenderloins was packaged in individual vacuum packs weighing approximately 3 pounds each. A total of six packs of the Elk Tenderloins were sold to the public at the Exotic Meats USA retail store. Consumers who still have the Elk Tenderloins should return the product to Exotic Meats USA at 1003 NE Loop 410, San Antonio, TX 78209. Customers with concerns or questions about the Voluntary Elk Recall can call 1-800-680-4375. The safety of our customer has always been and always will be our number one priority.

 

Exotic Meats USA requests that for those customers who have products with the production dates in question, do not consume or sell them and return them to the point of purchase. Customers should return the product to the vendor. The vendor should return it to the distributor and the distributor should work with the state to decide upon how best to dispose. If the consumer is disposing of the product he/she should consult with the local state EPA office.

 

#

 

RSS Feed for FDA Recalls Information11 [what's this?12]

 


 

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.

 


 

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 ;

 


 

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

 

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

 


 

*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

 


 

P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum

 

Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State University; Ames, IA USA

 

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

 


 

PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS

 

THANK YOU PRION 2015 TAYLOR & FRANCIS, Professor Chernoff, and Professor Aguzzi et al, for making these PRION 2015 Congressional Poster and Oral Abstracts available freely to the public. ...Terry S. Singeltary Sr.

 

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

 

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

 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold longe incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), is the third potentially zoonotic PD (with BSE and L-type BSE), ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

 

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

 

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

 

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

 


 

Saturday, May 30, 2015

 

PRION 2015 ORAL AND POSTER CONGRESSIONAL ABSTRACTS

 


 


 

2012

 

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

 

snip... The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like. *** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

 

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

 


 

Wednesday, October 07, 2015

 

***Deer Prion Proteins Modulate the Emergence and Adaptation of Chronic Wasting Disease Strains

 


 

2011

 

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

 


 

Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Title: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease Authors

 

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

 

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

 


 


 

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

 

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In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.

 

***However, this recommendation is guidance and not a requirement by law.

 

======

 

31 Jan 2015 at 20:14 GMT

 

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

 

Singeltary et al

 

31 Jan 2015 at 20:14 GMT

 


 

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

 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

 

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

 


 

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

 


 

Sunday, January 06, 2013

 

USDA TO PGC ONCE CAPTIVES ESCAPE

 

*** "it‘s no longer its business.”

 


 

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

 


 

Sunday, July 13, 2014

 

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

 


 

Saturday, June 29, 2013

 

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

 


 

Tuesday, June 11, 2013

 

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

 


 

Tuesday, May 28, 2013

 

Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd Pennsylvania Update May 28, 2013

 

*** 6 doe from Pennsylvania CWD index herd still on the loose in Louisiana, quarantine began on October 18, 2012, still ongoing, Lake Charles premises.

 


 

Wednesday, November 14, 2012

 

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

 


 

Tuesday, October 23, 2012

 

PA Captive deer from CWD-positive farm roaming free

 


 

Thursday, October 11, 2012

 

Pennsylvania Confirms First Case CWD Adams County Captive Deer Tests Positive

 


 

**********2014 PENNSYLVANIA CWD**********

 

Tuesday, October 21, 2014

 

Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE

 


 

**********2015 PENNSYLVANIA CWD***********

 

Tuesday, May 05, 2015

 

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

 


 

Wednesday, February 11, 2015

 

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

 


 

Saturday, October 03, 2015

 

TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015

 


 

Friday, October 09, 2015

 

Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015

 


 

Thursday, September 24, 2015

 

TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing

 

*** I cannot stress enough to all of you, for the sake of your family and mine, before putting anything in the freezer, have those deer tested for CWD.

 

*** see past warnings about cwd from Shannon Tompkins of the Houston Chronicle

 

*** see video and latest transmission studies and warnings below.

 


 

CENSORED, RAW, UNCUT...it’s getting nasty in the pits...sometimes you can’t fix stupid...wasted days and wasted nights...

 

Sunday, July 26, 2015

 

*** TEXAS IN MELT DOWN MODE OVER CAPTIVE CWD AND THEY ARE PUTTING LIPSTICK ON THAT PIG AND TAKING HER TO THE DANCE LIKE MAD COW DISEASE ***

 


 

Sunday, August 02, 2015

 

TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?

 


 

Tuesday, October 06, 2015

 

*** TAHC 393rd Commission Meeting Chronic Wasting Disease CWD TSE Prion October 6, 2015

 


 

Wednesday, March 25, 2015

 

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

 


 

Wednesday, March 18, 2015

 

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

 


 

Saturday, September 12, 2015

 

*** In utero transmission and tissue distribution of chronic wasting disease-associated prions in free-ranging Rocky Mountain elk ***

 


 

Sunday, September 13, 2015

 

*** urine, feces, and chronic wasting disease cwd tse prion risk factors, loading up the environment ***

 


 

Friday, August 28, 2015

 

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

 


 

Thursday, April 30, 2015

 

Immediate and ongoing detection of prions in the blood of hamsters and deer following oral, nasal, or blood inoculations

 


 

Thursday, September 10, 2015

 

25th Meeting of the Transmissible Spongiform Encephalopathies Advisory Committee Food and Drug Administration Silver Spring, Maryland June 1, 2015

 


 

 Tuesday, August 4, 2015

 

*** FDA U.S. Measures to Protect Against BSE ***

 


 

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

 

*** now, from all the consumption and exposure above, now think iatrogenic cjd tse prion at a hospital near you, what if?

 

TSS

 

Thursday, August 13, 2015

 

Iatrogenic CJD due to pituitary-derived growth hormone with genetically determined incubation times of up to 40 years

 


 


 


 


 

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

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

 

Terry S. Singeltary, Sr Bacliff, Tex

 

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

 


 

 

Terry S. Singeltary Sr.

 


posted by Terry S. Singeltary Sr. at 9:43 AM

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