Michigan-sportsman.com without warning bans terry singeltary sr. for posting peer review sound science on CWD TSE Prion after 16 years
terry
from Bacliff, TEXAS USA
Profile Page Member Since: Sep 13, 2002
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BANNED FOR TROLLING FORUMS AND POSTING UNSUBSTANTIATED CLAIMS ABOUT CWD
Greetings Michigan-Sportsman.com et al hunters (if you read this somewhere), ask yourself, why after 16 years of posting science about chronic wasting disease cwd tse prion, on Michigan-sportsman.com, why without warning, i get banned for passing along sound and peer review science about the cwd tse prion, and could sponsors and the captive game farm industry have been the problem??? the only one that was trolling anyone about anything had been bioactiveTornado Jim Jim Brauker, Ph.D
see ;
this is when things started changing, someone had hacked into michigan-sportsman.com and claimed to be my DAD. hell, my dad had been dead. but what was going on here, then this person was gone???
bioactive said: ↑
Posted On December 20, 2003
AFTER THE FIRST CASE OF MAD COW DISEASE IN THE USA WAS DOCUMENTED
" Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. "
http://www.consumerfreedom.com/article_detail.cfm/a/138-mad-cow-scaremongers
SO, just who are The Center for Consumer Freedom ;
http://www.consumerfreedom.com/index.cfm
let's take a closer look shall we ;
The Center for Consumer Freedom (CCF) (formerly called the "Guest Choice Network (GCN)") is a front group for the restaurant, alcohol and tobacco industries. It runs media campaigns which oppose the efforts of scientists, doctors, health advocates, environmentalists and groups like Mothers Against Drunk Driving, calling them "the Nanny Culture -- the growing fraternity of food cops, health care enforcers, anti-meat activists, and meddling bureaucrats who 'know what's best for you.'"
CCF is registered as a tax-exempt, non-profit organization under the IRS code 501(c)(3). Its advisory board is comprised mainly of representatives from the restaurant, meat and alcoholic beverage industries.
http://www.sourcewatch.org/index.php?title=Center_for_Consumer_Freedom
http://en.wikipedia.org/wiki/Center_for_Consumer_Freedom
SNIP...SEE FULL TEXT AND MORE HERE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
http://madcowusda.blogspot.com/2014/09/mad-cow-scaremongers-consumerfreedomcom.html
AFTER THE FIRST CASE OF MAD COW DISEASE IN THE USA WAS DOCUMENTED
" Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. "
http://www.consumerfreedom.com/article_detail.cfm/a/138-mad-cow-scaremongers
SO, just who are The Center for Consumer Freedom ;
http://www.consumerfreedom.com/index.cfm
let's take a closer look shall we ;
The Center for Consumer Freedom (CCF) (formerly called the "Guest Choice Network (GCN)") is a front group for the restaurant, alcohol and tobacco industries. It runs media campaigns which oppose the efforts of scientists, doctors, health advocates, environmentalists and groups like Mothers Against Drunk Driving, calling them "the Nanny Culture -- the growing fraternity of food cops, health care enforcers, anti-meat activists, and meddling bureaucrats who 'know what's best for you.'"
CCF is registered as a tax-exempt, non-profit organization under the IRS code 501(c)(3). Its advisory board is comprised mainly of representatives from the restaurant, meat and alcoholic beverage industries.
http://www.sourcewatch.org/index.php?title=Center_for_Consumer_Freedom
http://en.wikipedia.org/wiki/Center_for_Consumer_Freedom
SNIP...SEE FULL TEXT AND MORE HERE
http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html
http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html
http://madcowusda.blogspot.com/2014/09/mad-cow-scaremongers-consumerfreedomcom.html
this is when things started changing, someone had hacked into michigan-sportsman.com and claimed to be my DAD. hell, my dad had been dead. but what was going on here, then this person was gone???
Tuesday at 11:16 PM#18 terry terry I Like It a Lot Charter Member 15 season die hard!
Messages:1,446 Likes Received:51 Location:Bacliff, TEXAS USA
FLOUNDERSDAD ???
Greetings Michigan-Sportsman Forum, Floundersdad,and Moderators et al,
i see this long lost thread recently had a few hits.
two from ;
bioactiveTornado Jim
and also i see, who is this new member, joined today, 'Floundersdad' and why do they have my profile picture on their page here i.e. Floundersdad ???
PLEASE SEE; i see at the bottom of this post, just today, a LIKE was hit that was from ;
Today [IMG] Floundersdad liked your post in the thread DNR view of CWD. 2:15 AM
see at bottom of this message the like from Floundersdad; ↑ Terry, I believe that more of us would read your information if you could put it into a synopsis. The above posts, as are some others by you, are a long technical read. I believe that you sincerely want to pass helpful information to us and I am just trying to make a suggestion that would get the most folks on here reading it.
yes sir, i get that from some folks, but then i have others that want the science. then you have the ones that say my posts are too long. i thought by posting a short sentence or two and then posting the science in blogs (no advertisements and have made no money from them, just for education), i thought that would work. but then you have folks that says it's junk science coming from blogs, claiming i am sitting here in my tin foil hat making this stuff up. bottom line, it does not matter what i say, it's the science, show me the transmission studies, i have said that from day one, show me the science. i think that what folks need. the old science that was, and what has happened along the way, all of it, to the latest science. then they can make their own minds up, without just taking my word for it...or not.
kind regards, terry
Floundersdad, 357Maximum, mbrewer and 2 others like this.
IF you go to the profile page Floundersdad, you will see a comment section, with MY profile picture...
see ;
Floundersdad Male, from Kawkawlin
Floundersdad was last seen:
Viewing thread Best knife?, Today at 2:31 AM
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IF you go to the profile page Floundersdad, you will see a comment section, with MY profile picture...
any thoughts???
terry
Sunday, February 25, 2018
PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW
see full thread here;
So after 16 years or so, what happened?
why no warning at all?
did i not deserve at least that much respect?
has it come to just sticking our head in the sand, letting the captive game farming industry junk science rule for the day?
wow, just wow, i am very disappointed to say the least, i had lot of respect for Michigan-Sportsman.com up until now, but looks like the captive game farm industry has won over in most all these working groups on CWD. looks like money and the industry has won out over sound science, imo$$$
i only hope that my 16 years at Michigan-sportsman.com did not go totally wasted trying to educate some about cwd tse prion. GOOD LUCK!...terry
Chronic Wasting Disease CWD TSE Prion RoundUp
February 18, 2018 Discussion in 'Wildlife Diseases'
started by terry, Feb 18, 2018.
Michigan-Sportsman.com who is trolling who? and why are not these trolls banned? they bring no science to the table, just word of mouth junk science by the industry...looks like Michigan-sportsman.com is going to go with the industry and junk science there from, and let it ride...very sad for the state of Michigan...now i was banned from Michigan-sportsman.com after 16 years of posting sound science about cwd tse prion, for what they said was 'trolling forums and posting unsubstantiated claims about cwd'. NOW, if this is not trolling here by otcarcher (who does not even have enough stones to show is name), yet does not get banned, should be disturbing to the free and fair chase hunters of the great state of Michigan that still are there at Michgan-sportsman.com. these are just a few, please see for yourself.
otcarcher
Male, 45
January 14, 2018
Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases
Michigan UPDATE, see also ;
Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan
Contact: Dwayne Etter (DNR), 517-284-4725 or David Williams (MSU), 517-917-0716 Agency: Natural Resources
Jan. 30, 2018
Michigan State University and the Michigan Department of Natural Resources will be placing location-tracking collars on white-tailed deer in south-central Michigan as part of a multiyear study of deer disease, including chronic wasting disease.
SATURDAY, MARCH 03, 2018
WISCONSIN CHRONIC WASTING DISEASE TSE Prion DNR Study Finds CWD-Infected Deer Die At 3 Times Rate Of Healthy Animals
SATURDAY, MARCH 03, 2018
Minnesota CWD All seven of the remaining white-tailed deer on farm Positive
WEDNESDAY, FEBRUARY 21, 2018
TEXAS TPWD CWD TSE PRION 2 MORE FROM BREEDER RELEASE SITE TOTALS 81 CASES TO DATE
Sunday, February 25, 2018
PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW
ANYONE INTERESTED, SEE A BIT OF HISTORY OF MY POSTINGS ON MICHIGAN-SPORTSMAN.COM SINCE 2002 ON CWD TSE PRION...
Chronic Wasting Disease A Time Bomb For Agriculture? | Michigan ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
Jan 30, 2018 - 6 posts - 4 authors
Is chronic wasting disease (CWD) a potential time bomb for the agriculture industry? A silent killer stalking deer and elk, CWD ..... BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW ''I have a neighbor who is a dairy farmer.Interesting CWD nees | Michigan Sportsman - Online Michigan ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
http://www.wideopenspaces.com/cwd-has-jumped-the-species-barrier/CWD TSE PRION DISEASE Singeltary submission to Scottish Parliament ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
Dec 31, 2013 - 1 post - 1 author
Friday, November 22, 2013 *** Wasting disease is threat to the entire UK deer population CWD TSE PRION DISEASE Singeltary submission to Scottish...Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018 ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
Feb 18, 2018 - 14 posts - 5 authors
Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018 FRIDAY, FEBRUARY 16, 2018 Wisconsin Deer from Now-Quarantined PA ... Texas Deer Breeders Continue fight against the state's wildlife agency and its regulations trying to contain CWD TSE Prion .... Terry S. Singeltary Sr.Michigan Whitetail Deer Hunting | Michigan Sportsman - Online ...
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Whitetail Deer Disease. Discussions: 356. Messages: 6,718. Latest: CWD-
Missing: singeltary
cwd transmitted to macaque orally muscle material | Michigan ...
https://www.michigan-sportsman.com › ... › Whitetail Deer Disease
Jun 5, 2017 - 11 posts - 6 authors
The initial results of the study indicate that macaque monkeys (genetically similar to humans) can be infected with Chronic Wasting Disease (CWD) after eating deer that is infected with CWD. CWD is a prion disease, which are fatal, transmissible diseases characterized by abnormal proteins in the brain and ...TEXAS 85th Legislative Session 2017, CWD, AND PAYING TO PLAY
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
Likes Received: 21. Location: Bacliff, TEXAS USA. SUNDAY, MAY 14, 2017 85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play http://chronic-wasting-disease.blogspot.com/More CWD for Michigan | Michigan Sportsman
https://www.michigan-sportsman.com › Deer Hunting
Dec 6, 2015 - Chronic Wasting Disease, which is also referred to as CWD, is bad news in the deer community. CWD affects all members of the cervid family and has been making appearances inMichigan deer, the fourth of which was killed less than a month ago.
Missing: singeltary
8/27/15 CWD Deer Forum | Page 3 | Michigan Sportsman - Online ...
https://www.michigan-sportsman.com › ... › Whitetail Deer Disease
Aug 28, 2015 - 16 posts - 7 authors
I don't believe that is true. A dead deer cannot contract cwd from a dead deer. The dnr said in theforum that there are many false rumors floating around and they have been in contact with most processors from the area and have been explaining the regs. They had a meeting with processors last week.CWD Question? | Michigan Sportsman - Online Michigan Hunting ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
If a CWD infected deer was to die along a watershed, couldn't the prions be dispersed into that watershed simply by erosion, and then infect more deer...Minnesota CWD DNR, Can CWD jump from deer to humans? yes, maybe ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
Mar 21, 2012 - 2 posts - 1 author
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 .... Terry S. Singeltary Sr. Bacliff, Texas USA 77518. MARCH 1, 2011. UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. ...Susceptibility of Domestic Cats to CWD Infection | Michigan ...
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Aug 8, 2011 - 7 posts - 2 authors
Although this is interesting, I'm not quite sure how this would effect anything. We already know that several species are capable of obtaining the disease but only a few are capable of transmitting it. It appears as though cats only fall into the former category. BTW- Thanks for the continued updatesTerry.Chronic Wasting Disease CWD cervids interspecies transmission ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
Terry S. Singeltary Sr. Bacliff, Texas USA 77518. MARCH 1, 2011. UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBYCwd suspect false positive ? | Michigan Sportsman - Online ...
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Nov 19, 2010 - 3 posts - 1 author
Original Message -------- Subject: USA BIO-RADs INCONCLUSIVEs. Date: Fri, 17 Dec 2004 15:37:28 -0600. From: "Terry S. Singeltary Sr." To: susan_berg@bio-CWD to tighten taxidermy rules Hunters need to understand ...
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Jan 7, 2009 - 9 posts - 7 authors
http://www.michigan-sportsman.com/forum/showthread.php?t=250638 ... Investigations in New York indicate that the infection could have been spread by a taxidermist who accepted specimens fromCWD-positive states, allowed rehabilitated fawns access to the taxidermy workshop and spread potentially ...CWD Prions in Elk Antler Velvet (Nutritional Supplements and CJD ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
Mar 19, 2009 - 2 posts - 1 author
Our finding of prions in antler velvet of CWD-affected elk suggests that this tissue may play a role in disease transmission among cervids. .... Subject: METABOLIFE AND TSEs GAO-03-494 ''URGENT DATA'' Date: Thu, 01 May 2003 11:23:01 -CWD MICHIGAN UPDATE September 5, 2008 | Michigan Sportsman ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
Sep 9, 2008 - 2 posts - 1 author
The Indiana DNR (Department of Natural Resources) has tight restrictions on transporting deer, elk, and other cervids into the state. For information go to
TUESDAY, SEPTEMBER 09, 2008 CWD MICHIGAN UPDATE September 5, 2008
chronic-wasting-disease.blogspot.com/.../cwd-michigan-update-september-5-2008.ht...
CWD MICHIGAN UPDATE September 5, 2008
Discussion in 'Whitetail Deer Disease' started by terry, Sep 9, 2008.
Fears Grow Over ''mad Elk Disease'' | Michigan Sportsman - Online ...
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Subject: Fears grow over 'mad elk disease' Date: Thu, 3 Apr 2003 08:15:12 -0600 From: "Terry S.Singeltary Sr." Monitoring Cwd To Humans Hunter Registry Wyoming | Michigan ...
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Aug 30, 2007 - 1 post - 1 author
Atlanta, GA. Background: Chronic wasting disease (CWD) occurs among North American .... http://www.biggamehunt.net/forums/viewtopic.php?p=62733#62733 ... MARCH 26, 2003. RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States EmailTerry S. Singeltary:Mad Cow Question? | Michigan Sportsman - Online Michigan ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
Volume 3, Number 8 01 August 2003. Tracking spongiform encephalopathies in North America Xavier Bosch My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the ...CWD Question? | Michigan Sportsman - Online Michigan Hunting ...
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If a CWD infected deer was to die along a watershed, couldn't the prions be dispersed into that watershed simply by erosion, and then infect more deer...Monitoring Cwd To Humans Hunter Registry Wyoming | Michigan ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
Aug 30, 2007 - 1 post - 1 author
Background: Chronic wasting disease (CWD) occurs among North American deer and elk and has been identified ... purchased from 1996 through 2004, representing 266,535 individual hunters; 175,130 were not Wyoming .... ''Cwd Subclinical Rocky Mountain Elk | Michigan Sportsman - Online ...
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Sep 6, 2004 - 1 post - 1 author
PrPCWD in the brain and nodes of the elk was more variable and unrelated to their PrP genotype. One hundred ... of the Geographical BSE-Risk (GBR III) of USA 2004 ''extremely/very unstable BSE/cattle system'' USA ... From: Terry S. Singeltary Sr. [flounder@wt.net] Sent: Tuesday, July 29, 2003 1:03 PMMad Cow Question? | Michigan Sportsman - Online Michigan ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
Xavier Bosch My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem. 49-year-old Singeltary is ...Game Commission Notified Of Cwd-positive Deer In West Virginia ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
terry. Messages: 1,354. Likes Received: 18. Location: Bacliff, TEXAS USA. ----- Original Message ----- From: "Terry S. Singeltary Sr." Second Case Of Cwd Found In Ny Oneida County Deer | Michigan ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
SECOND CASE OF CWD FOUND IN ONEIDA COUNTY DEER State's Trace Back Finds Second PositiveCWD in Herd Directly Linked to Index Herd *** NOTE TO... ... From: "Terry S. Singeltary Sr." First Ever Study To Investigate Impact Of Cwd On Humans | Michigan ...
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Nov 28, 2005 - 1 post - 1 author
From: TSS () Subject: First ever study to investigate impact of chronic wasting disease on humans Date: November 26, 2005 at 6:06 pm PST First...CWD to tighten taxidermy rules Hunters need to understand ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
Jan 7, 2009 - 9 posts - 7 authors
http://www.michigan-sportsman.com/forum/showthread.php?t=250638 ... Investigations in New York indicate that the infection could have been spread by a taxidermist who accepted specimens fromCWD-positive states, allowed rehabilitated .... 14 OCTOBER 2005 VOL 310 SCIENCE www.sciencemag.orgDNR view of CWD | Michigan Sportsman - Online Michigan Hunting ...
https://www.michigan-sportsman.com › ... › Whitetail Deer Disease
Since I refer to this literature on a semi-regular basis I am posting it as a sticky to aid in the understanding of the current science on CWD. From. ... From http://wwwDeer Scents Banned Due To Cwd Transmission - Michigan Sportsman
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
also, what is TEXAS stance on feeding deer and CWD risk? but before that, lets look at a few things; Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus ) Christina J. Sigurdson1, Elizabeth S. Williams2, Michael W. Miller3, Terry R. Spraker1,4, Katherine ...Deer Scents Banned Due To Cwd Transmission - Michigan Sportsman
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
Subject: DEER SCENTS BANNED DUE TO CWD TRANSMISSION Date: April 25Supplemental Feeding | Michigan Sportsman - Online Michigan ...
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Nov 10, 2002 - 15 posts - 4 authors
Sewing the seeds of CWD through. Animal Protein.... you can search the archives here, or here is part of the thread (see below)... kind regards, terry. Subject: MAD DEER/ELK DISEASE AND POTENTIAL SOURCES Date: Sat, 25 May 2002 18:41Sewing The Seeds Of Cwd Mad Deer/elk Through Feeding ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
terry. Subject: SEWING THE SEEDS OF CWD MAD DEER/ELK THROUGH FEEDING, ESPECIALLY FROM ANIMAL PROTEIN !!! Date: Thu, 12 Sep 2002 12:Monitoring Cwd To Humans Hunter Registry Wyoming | Michigan ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
Aug 30, 2007 - 1 post - 1 author
From: "Terry S. Singeltary Sr." Subject: CWD NEW MEXICO RECORDS IT'S 19 CASE (near Texas border again) http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=Cwd 2003 Gain Report E23101 | Michigan Sportsman - Online ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
Original Message -------- Subject: European Union Sanitary/Phytosanitary/Food Safety Chronic Wasting Disease 2003 GAIN REPORT E23101 Date: Sat, 25 Sep 2004 13:24:28 -0500. From: "Terry S. SingeltarySr." Reply-To
Mad Cow Question?
Michigan Sportsman - Online Michigan ...
https://www.michigan-sportsman.com › Forums › Michigan Hunting › Wildlife Diseases
2002 12:07:02 -0700 >>From: Terry S. Singeltary Sr. Reply-To: BSE-L >> >>so ... how many dead road-kill CWD infected carcasses >>were rendered into ... Cached - 68k LegaI Basis for Animal-Derived Legal Basis for Animal-Derived ... From: Sent: To: Subject: Terry S. Singeltary Sr. [flounder@wt.net] Monday ... easilyCWD EXPERT LIES TO PUBLIC, or is just plain stupid - Michigan ...
https://www.michigan-sportsman.com › ... › Michigan Hunting › Wildlife Diseases
CWD EXPERT LIES TO PUBLIC, or is just plain stupid??? Posted Oct. 05, 2002. CWD expert to lead Waupaca session snip... Shull, director of the Wisconsin Veterinary Diagnostic Laboratory in Madison .... Four years ago, Terry Singeltary watched his .... quoted or in any other forum is limited to the patients we investigated.
SATURDAY, MARCH 03, 2018
Michigan-Sportsman.com Bans Terry S. Singeltary Sr. For Speaking about Chronic Wasting Disease CWD TSE Prion
*** 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 ***
https://histodb11.usz.ch/Images/videos/video-004/video-004.html
Sterling Heights MICHIGAN, sporadic CJD, WE WANT ANSWERS!
-------- Original Message --------
Subject: [CJDVoice] Case Researchers Head National Search for Human Version of Mad Cow Disease
Date: Mon, 22 Mar 2004 09:22:15 -0600
From: "Terry S. Singeltary Sr."
Reply-To: cjdvoice@YAHOOGROUPS.COM
To: bse-l CC: CJDVOICE
Case Researchers Head National Search for Human Version of Mad Cow Disease
Karen Johnson
Jeffrey Schwan of Sterling Heights, Michigan was a healthy young man – a 26 year old electrical design engineer with six-pack abs and a penchant for softball. But, over a period of five months, his health rapidly declined, beginning with misspellings, irritability, forgetfulness, and poor vision, until he died, September 27, 2001, a shadow of his former self. “He was basically a skeleton with skin stretched across. His brain was decimated by the disease. He couldn't remember where he went to high school. Couldn't even write his name. He wrote it worse than a kindergartener,” said his mother, Theresa Schwan. The cause of Jeffrey’s failing health was unknown until researchers at Case were able to make the diagnosis. Jeffrey Schwan died of Creutzfeldt-Jakob disease (CJD), a brain wasting disease in humans caused by proteins called prions that are misfolded, allowing them to clump and form plaques on the brain. CJD is similar to mad cow disease, and has received a lot of attention in recent years because, while many cases occur sporadically or in family lines, a particular variant (vCJD) is caused by eating mad cow infected beef...SNIP...END...TSS
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...END...TSS
*** WDA 2016 NEW YORK ***
*** We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf
Volume 23, Number 9—September 2017
Research Letter Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion
***Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.
https://wwwnc.cdc.gov/eid/article/23/9/16-1474_article
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
* Strongly consider having the deer or elk tested for CWD before you eat the meat.
* If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals.
* If your animal tests positive for CWD, do not eat meat from that animal.
https://www.cdc.gov/prions/cwd/prevention.html
Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
https://www.youtube.com/embed/Vtt1kAVDhDQ
http://prion2017.org/programme/
TUESDAY, JUNE 13, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
snip...
Two transmission experiments using squirrel monkeys have been able to show prion disease after intracerebral and oral inoculation with CWD prions.
The systematic review also summarized two transmission experiments using macaques (a non-human primate species considered genetically closer to humans than squirrel monkeys) which, at the time of review, had not caused prion disease after inoculation with CWD prions by several modes (e.g., intracerebral, oral) up to 10 years of observation since exposure to CWD prions.
Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle.
These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle.
SATURDAY, JULY 29, 2017 Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC Health Products and Food Branch (HPFB)
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease
Prepared by: Bureau of Microbial Hazards (BMH), Food Directorate, Health Products and Food Branch, Health Canada
Date: April 26, 2017 Issue: Chronic Wasting Disease (CWD) is a progressive, fatal, transmissible neurological disease that naturally infects cervids, and has been identified in deer, elk, moose, and reindeer.
To date there is no direct evidence that CWD has been or can be transmitted from animals to humans.
However, initial findings from a laboratory research project funded by the Alberta Prion Research Institute (APRI) and Alberta Livestock Meat Agency (ALMA), and led by a Canadian Food Inspection Agency (CFIA) scientist indicate that CWD has been transmitted to cynomolgus macaques (the non-human primate species most closely related to humans that may be used in research), through both the intracranial and oral routes of exposure.
Both infected brain and muscle tissues were found to transmit disease.
Health Canada’s Health Products and Food Branch (HPFB) was asked to consider the impact of these findings on the Branch’s current position on CWD in health products and foods.
Summary and Recommendation:
Health Canada’s Health Products and Food Branch (HPFB) is responsible for assessing risks to human health from diseases of animal origin that may be transmitted through health products and food, and for developing regulations and policies to mitigate risks from products regulated under the Food and Drug Act as well as various associated regulations.
While extensive disease surveillance in Canada and elsewhere has not provided any direct evidence that CWD has infected humans, the potential for CWD to be transmitted to humans cannot be excluded. In exercising precaution, HPFB continues to advocate that the most prudent approach is to consider that CWD has the potential to infect humans.
This position has been aligned with that of the World Health Organization (WHO) since the late 1990s, and remains consistent with the WHO’s 2012 position that “No tissue that is likely to contain the bovine spongiform encephalopathy (BSE) agent, nor part or product of any animal which has shown signs of a TSE should enter the (human or animal) food chain.”
This precautionary position on TSEs is also consistent with the conclusions documented by the Transmissible Spongiform Encephalopathy (TSE) Secretariat in 2003, and a systematic literature review conducted by the Public Health Agency of Canada (PHAC) in 2017.
The findings of the macaque experiment do not change HPFB’s current position with respect to the safety of food and health products and CWD, which considers that a precautionary approach to the management of the potential risks of exposure through food and health products is warranted.
Background: Chronic Wasting Disease (CWD) is a fatal disease that has been detected in cervids. To date, the disease has been identified in deer, elk, moose, and reindeer. CWD belongs to a class of diseases called transmissible spongiform encephalopathies (TSEs).
Along with other well-known TSEs, such as bovine spongiform encephalopathy (BSE) in cattle, scrapie in sheep and goats and Creutzfeldt–Jakob disease (CJD) and variant CJD (vCJD) in humans, CWD is characterized by the accumulation of abnormal misfolded proteins (called prions) in multiple organs and tissues, including lymphatic, muscle and neural tissues.
CWD was first recognized as a fatal wasting disease of captive deer in the United States in the late 1960s, and was later identified as a TSE in 1980. In Canada, CWD was first detected in the Toronto Zoo in the 1970s and diagnosed in farmed elk in 1996.
The first Canadian case in a wild cervid was confirmed in a mule deer in Saskatchewan in November 2000.
The disease has now been detected in cervids in 24 US states and two Canadian provinces (Alberta and Saskatchewan).
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The exact routes and mechanisms of CWD transmission between animals remain unclear. There is evidence that infection is transmitted directly from animal to animal during close contact with saliva, urine and feces, and indirectly through the environment.
While incubation periods may be variable, once the disease is contracted, the time to presentation of clinical symptoms is about 16 to 36 months.
It is only in the later, clinical stages that CWD is typified by the chronic weight loss and behavioral changes that eventually lead to death.
In 2003, Health Canada’s TSE secretariat assessed the potential for CWD to pose a hazard to human health.
It was noted at that time that there was no evidence to indicate that CWD had ever infected a human.
Given the lack of scientific evidence of the potential for CWD to become a human pathogen, it was stated that the most prudent course of action was to consider that CWD could have the potential to infect humans, and thus take a precautionary approach to its management, which was consistent with the position taken by the World Health Organization (WHO).
The Public Health Agency of Canada (PHAC) recently published a systematic review summarizing the evidence in the scientific literature on the transmissibility of CWD prions to humans (2017).
This review summarized available epidemiological evidence, as well as evidence on CWD infectivity using experimental models, including non-human primates, transgenic mice, and in vitro experiments.
The review showed that animal models using humanized transgenic mice did not demonstrate transmission.
Two transmission experiments using squirrel monkeys have been able to show prion disease after intracerebral and oral inoculation with CWD prions.
The systematic review also summarized two transmission experiments using macaques (a non-human primate species considered genetically closer to humans than squirrel monkeys) which, at the time of review, had not caused prion disease after inoculation with CWD prions by several modes (e.g., intracerebral, oral) up to 10 years of observation since exposure to CWD prions.
Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle.
These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle.
While the study is ongoing, and findings have yet to be subjected to formal peer review, the initial results will be presented at PRION 2017, an annual international conference on TSE diseases (Edinburgh May 23-26, 2017).
In advance of this conference, a multi-departmental working group (including CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC) has been established to coordinate risk management and risk communication activities.
As the lead in managing the potential human health risks related to health products and food that could contain cervid materials, Health Canada’s HPFB has considered the initial findings of this research within the context of known and accepted science and evidence related to the transmissibility of CWD to cervids, other animals, transgenic mice, and its potential to be transmissible to humans, to provide an updated advisory opinion of the potential risk to human health.
This opinion is provided to the working group to inform the assessment of current CWD control policies in Canada as well as the advice related to the potential risks posed by CWD through the consumption of cervid food products.
Health Canada’s Current Position on TSEs in Health Products and Food: HPFB has previously addressed concerns regarding human exposure to BSE, and remains alert to the possibility that other animal TSEs such as scrapie and CWD may also pose risks to human health.
HPFB maintains a precautionary stance in relation to human exposure to TSEs through health products and food.
In 2003, HPFB adopted the position that no material derived from an animal known to be infected with any TSE (including CWD) should be used or consumed by humans or animals.
This position was, and continues to be, consistent with the position of the WHO.
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HPFB requires pre-market review and approval of all human therapeutics, biologics and genetic therapies, veterinary drugs and natural health products intended for sale in Canada.
This includes a requirement for license holders of these products to maintain documentation and provide information for any materials of animal origin that may be used within their products, including therapeutic substances, reagents and excipients.
This documentation can include letters of attestation, Certificates of Suitability or Veterinary Certificates.
While there are no specific federal regulations related to the use(s) of cervids in foods, current federal animal disease control policies support the diversion of known CWD-infected farmed animals away from the food and feed supply.
Outreach, communications, and monitoring programs related to wild cervids, as well as disease surveillance for farmed cervids, fall within the jurisdiction of the Provincial and/or Territorial governments.
Hazard Characterization In 2003, Health Canada’s TSE secretariat assessed the potential for CWD to pose a hazard to human health.
Given the lack of scientific evidence of the potential for CWD to become a human pathogen, it was stated that the most prudent course of action was to consider that CWD could have the potential to infect humans, and thus take a precautionary approach to its management.
Following nearly two decades of ongoing human prion disease surveillance and retrospective review by PHAC and the Centers for Disease Control and Prevention (CDC), there have been no identified cases of human prion disease or any other outcome attributed to CWD in Canada, the USA, or elsewhere.
In 2017, PHAC published a systematic literature review of the evidence for the transmissibility of CWD to humans, which included evidence of successful transmission of CWD intracranially and orally to squirrel monkeys.
From this review, it was concluded that CWD transmission to humans has not been recorded.
In five epidemiological studies no association between CWD exposure and human prion disease was identified.
Some cases of CJD had a history of exposure to cervids and venison in CWD affected regions, but no definitive link to CWD could be found.
The assessment of the evidence captured in this systematic review does not support the hypothesis that CWD is readily transmitted to humans; however, the positive evidence of interspecies transmission from in vivo and in vitro experiments indicates that the species barrier is not absolute.
The initial findings from the APRI/ALMA-funded macaque experiment are consistent with this conclusion.
Potential Sources of Exposure to Cervids and Cervid-derived Materials:
Canadians may be exposed to cervids, and materials derived from cervids through a variety of sources, and routes of exposure, including in their diet and through the use of natural health products that contain antler velvet.
There is also the potential for Canadians to be exposed to cervids through farming (including veterinary services), slaughter, velvet harvest, as well as through field dressing of hunted animals, preparing trophies and/or the use of cervid-derived materials (e.g., urine) as hunting lures.
While monitoring and control programs are in place to reduce the likelihood that animals known to be infected with CWD reach the marketplace, the possibility cannot be excluded that some of these sources of exposure may be derived from animals with CWD.
Cervid meat (venison) is available in many of the same cuts and processed meat products as for other meat products.
While consumption survey estimates for the general Canadian population (2004 Canadian Community Health Survey, Cycle 2.2) indicate that overall venison consumption is quite low, there are known subpopulations, including rural and Indigenous populations that have higher dietary exposures to this food.
In addition, populations that rely on cervids as an important source of protein are more likely to hunt and/or consume wild cervids.
There are no human biologics or genetic therapies licensed in Canada that contain ingredients of cervid origin, and it is considered unlikely that cervid materials or ingredients would be used in the manufacture
Page 4 of 5
of these human therapeutic products, including medical devices.
There are approximately 200 licenced natural health products (NHPs) that contain ingredients of cervid origin such as antler velvet.
Impact of New Findings on Human Health Risk Assessment:
There have been no known cases of human prion disease or any other outcome attributable to CWD identified to date.
National surveillance of all forms of CJD by PHAC has yielded no direct evidence that CWD has infected humans in Canada.
However, in the absence of definitive information related to the transmissibility of CWD to humans, and in light of the evidence that BSE can be transmitted to humans, HPFB has maintained a precautionary position with respect to CWD that is in agreement with the WHO’s 2012 recommendation that “No tissue that is likely to contain the BSE agent, nor part or product of any animal which has shown signs of a TSE should enter the (human or animal) food chain.”.
The initial findings from the experimental non-human primate transmission study do not change HPFB’s position with respect to food and health products, and a continued precautionary approach to the management of the potential risks of exposure through food and health products is warranted.
HPFB continues to recommend avoiding consumption of foods from known infected or any diseased animals, and taking precautions when handling cervid carcasses.
In addition, in areas where CWD is known to occur in wild cervids, continued consistent Federal and P/T communications, warning and precautions should be provided to groups who may be expected to have higher exposures to cervids through hunting and diet (e.g., rural and Indigenous populations).
While current animal disease control policies support the diversion of known CWD-infected animals away from the food and feed supply, research and development of sensitive detection methods and antemortem sampling techniques remain crucial for ensuring accurate diagnoses.
Continued research into TSEs and continued epidemiologic surveillance for human prion diseases are required. HPFB will continue to review and monitor scientific literature related to CWD, as well as these initial findings and other emerging research related to the potential transmissibility of CWD to humans.
The Branch will continue to update its position on animal TSEs as new scientific evidence indicates the need for further protection of public health.
Reviewed by: Veterinary Drugs Directorate, HPFB Natural and Non-Prescription Health Products Directorate, HPFB Biologics and Genetics Therapies Directorate, HPFB Therapeutic Products Directorate, HPFB Marketed Health Products Directorate, HPFB Approved by: Denise MacGillivray, Director – Bureau of Microbial Hazards, FD, HPFB Date: April 26, 2017
Page 5 of 5
References Waddell, L., Greig, J., Mascarenhas, M., Otten, A., Corrin, T., Hierlihy, K. Current evidence on the transmissibility of chronic wasting disease prions to humans - A systematic review. Transbound Emerg Dis. 2017 Jan 30. doi: 10.1111/tbed.12612. [Epub ahead of print] World Health Organization - Variant Creutzfeldt-Jakob disease - Fact sheet N°180: Revised February 2012. (http://www.who.int/mediacentre/factsheets/fs180/en/) World Health Organization - Bovine spongiform encephalopathy - Fact Sheet N°113 Revised November 2002 (http://www.wiredhealthresources.net/resources/NA/WHOFS_BovineSpongiformEncephalopathy.pdf) Chronic Wasting Disease - What to expect if your animals may be infected. (http://www.inspection.gc.ca/animals/terrestrial-animals/diseases/reportable/cwd/if-your-animals-may-beinfected/eng/1330188848236/1330189018195) Chronic Wasting Disease of Deer and Elk: A Canadian Perspective. TSE Secretariat, Health Canada January 2003. Chronic Wasting Disease of Cervids: A Human Health Concern? TSE Secretariat, Health Canada March 2003. Chronic Wasting Disease: A Review for Health Canada; prepared by Dr Terry Spraker, University of Colorado for the TSE Secretariat, Health Canada, March 2006.
https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.pdf
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
PRION 2017 CONFERENCE VIDEO
https://www.youtube.com/embed/Vtt1kAVDhDQ
WEDNESDAY, MARCH 07, 2018
Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan
http://chronic-wasting-disease.blogspot.com/2018/03/addressing-deer-disease-dnr-msu.html
SATURDAY, MARCH 03, 2018
Minnesota CWD All seven of the remaining white-tailed deer on farm Positive
TUESDAY, NOVEMBER 22, 2016
Minnesota Tests confirm 2 CWD-positive deer near Lanesboro
Thursday, September 19, 2013
Chronic Wasting Disease CWD surveillance, deer feeding ban continues in southeastern Minnesota
Friday, September 28, 2012
Stray elk renews concerns about deer farm security Minnesota
Friday, May 25, 2012
Chronic Wasting Disease CWD found in a farmed red deer from Ramsey County Minnesota
SATURDAY, MARCH 17, 2012
Minnesota CWD DNR, Can chronic wasting disease jump from deer to humans? yes, maybe some day YOUTUBE
Tuesday, January 25, 2011
Minnesota, National Veterinary Services Laboratory in Ames, Iowa, has confirmed CWD case near Pine Island
Friday, January 21, 2011
MINNESOTA HIGHLY SUSPECT CWD POSITIVE WILD DEER FOUND NEAR PINE ISLAND
Saturday, October 31, 2009
Elk from Olmsted County herd depopulated to control CWD Three additional elk from the 558-head herd tested positive
Tuesday, January 27, 2009
Chronic Wasting Disease found in a farmed elk from Olmsted County ST. PAUL, Minn.
CHRONIC WASTING DISEASE UPDATE September 6, 2002
Minnesota has announced the finding of CWD in a captive elk in Aitkin County. The animal was a five-year-old male. It had been purchased from a captive facility in Stearns County in August of 2000. The herd where the elk was found has been placed under quarantine as has two additional facilities where the infected elk had resided prior to it coming to the farm in Aitkin County. Minnesota DNR officials will test wild deer in the area to determine if there is any sign of CWD in the free-ranging population. This is the first case of CWD in either captive or freeranging cervids in Minnesota. Several more states have passed bans on the importation of deer and elk carcasses from states where CWD has been found in wild animals. Previously the states of Colorado, Illinois and Iowa and the province of Manitoba had passed such bans. The states of Vermont, Oregon and Missouri have enacted similar bans. Numerous states have issue voluntary advisories to their out-of-state hunters encouraging them not to bring the carcass or carcass parts of deer and elk into their state. The bans do permit the importation of boned out meat, hides or cape with no meat attached, clean skull cap with antler attached, finished taxidermy heads or the ivories of elk. The state of Georgia has recently banned the importation of live cervids into that state also. Some citizens of Colorado have formed a new political action group called Colorado Wildlife Defense (just happens that the acronym is CWD). The stated goal of this group are; Elimination of big game diseases, especially CWD; promotion of healthy wildlife habitat; promotion of scientifically sound wildlife research; promotion of a discussion of the ethics of hunting and wildlife management; education of the hunting and non hunting public. Their action plan calls for; requiring double fencing of all game farms at owners expense; all game farmers provide annual proof of bonding; prohibit new licenses for deer and elk farms; prohibit expansion in acreage of existing game farms; prohibit the transfer of game farm licenses; prohibit charging for hunting behind high wire; prohibit blocking of traditional migratory paths by high fences; requiring game farms to maintain environmental controls and prohibit the escape of contaminated water or soil; requiring immediate reporting of missing deer or elk from game farms; and requiring all game farm deer and elk to be tested for brucellosis and TB. Wisconsin has announced that 7 more free-ranging deer have tested positive for CWD. They have expanded their eradication zone by an additional 15 square miles to cover these findings. The total number of free-ranging CWD positive in Wisconsin is now 31 white-tail deer.
In 2000, a elk farmer in Wisconsin received elk from a CWD exposed herd in Colorado. At that time, the farmer advised the Wisconsin Department of Agriculture that both animals from the exposed herd in Colorado were dead. He has now advised Wisconsin Ag. that he was mistaken and that one of the animals is still alive in his herd. The second draft of the implementation documents for the National CWD Plan was distributed to committee members and others on Friday, August 30. The final documents are due to APHIS and USFWS on Friday, September 13. The herd of captive elk in Oklahoma that had been exposed to CWD will be destroyed this week. This herd had an elk test positive for CWD in 1997 but the depopulation of the herd was not agreed to by the owners and federal representatives until this week. Since the discovery of CWD in the herd, the remaining animals have been under quarantine, however, in the meantime the herd has dropped from 150 animals to 74. Due to a lack of communication, not all of the 76 animals that died in the interim were tested for CWD. All remaining animals will be tested but the true degree of infection rate of the herd will never be known.
The owners of the facility will not be permitted to restock the area with cervids for a period of five years. A New York based organization, BioTech Research Fund I LLC has committed a $1 million line of credit to fund commercialization of tests for brain-wasting disorders and production of various vaccines to Gene-Thera of Wheat Ridge, Colorado. Gene-Thera has spent three years developing new ways not only to diagnose CWD, but create vaccines for mad cow disease, E. coli contaminants and foot-and-mouth disease. Its tests for CWD have been successful in more than 100 samples from Colorado and Wisconsin according to company officials. Gene-Thera plans to license and market some o fits disease test kits by the end of the year, then begin volume distribution by mid-2003. The abstracts of the presentations from the CWD Conference in Denver August 6 and 7 have been posted on the Colorado Division of Wildlife web site. You will need adobe acrobat reader to read them.
The Division web site is: http://wildlife.state.co.us/CWD/Symposium_booklet.pdf
Minnesota: Second case in a game farmed elk discovered in Stearns Co.
This is a trace forward from the previously affected game farm in Aitkins Co. An additional game farm in Benton Co is under quarantine.
snip...
Supporting Documents: Colorado: CWD-Exposed Elk Used in 1990 Study- Wildlife officials call W. Slope move a mistake
Date: January 17, 2003 Source: Denver Post Contacts: Theo Stein Environment Writer
The Colorado Division of Wildlife knowingly used a herd of captive elk exposed to chronic wasting disease in a grazing study on the Western Slope in January 1990, possibly introducing the disease to the elk-rich area. "It was a bad call," said Jeff Ver Steeg, the division's top game manager. "I can't deny it." About 150 wild elk were allowed to graze in the same pens near Maybell after the research herd was removed and may have picked up the abnormal protein that causes the disease from the feces and urine left by the captive elk. While the Division of Wildlife has expressed concern before that its animals might have helped spread CWD, this is the first time the agency has acknowledged it knowingly moved elk exposed to CWD deep into an area where the disease was not known to already exist. Studies that could help determine the source of CWD on the Western Slope are incomplete, and officials say what data that do exist are so new and so spotty they may not provide all the answers. So far, it appears that less than 1 percent of deer and elk in the area are infected, compared with as much as 15 to 20 percent in hotspots in northeastern Colorado. But as wildlife officials grapple with CWD's appearance in northwestern Colorado, officials now admit the decision to continue the grazing study over the objections of some biologists was an error. At the time, biologists wanted to see whether elk grazing on winter range depleted forage that ranchers wanted for fattening cattle in spring. "I think in hindsight a lot of good people probably did some dumb things, myself included," said Bruce Gill, a retired wildlife manager who oversaw research efforts and remembers the debate over the project. "Had we known CWD would explode into such a potentially volatile ecologic and economic issue, we wouldn't have done it." Elk ranchers, who have been blamed for exporting the disease from its stronghold on the Colorado and Wyoming plains to seven states and two Canadian provinces, say the agency's belated disclosure smacks of a coverup. "It's pure negligence," said Jerry Perkins, a Delta banker and rancher who is now demanding a legislative inquiry. "If I'd have moved animals I knew to be infected around like that, I'd be in jail." Grand Junction veterinarian and sportsman Dick Steele said he faults the agency for not disclosing information about CWD-exposed research animals before October, when information was posted on the Division of Wildlife website. "This went way beyond poor judgment," he said. "My main concern is that this has been hidden for the last 12 years. It would have been real important to our decision-making process on how to deal with CWD." While the Maybell information is new, Perkins and other ranchers have long suspected Division of Wildlife research facilities near Meeker and Kremmling, which temporarily housed mule deer kept in heavily infected pens at the Fort Collins facility, have leaked CWD to the wild. Fear of an outbreak led the agency to sample 450 deer around the Meeker and Kremmling facilities. None tested positive, but the sample size was only large enough to detect cases if the infection rate was greater than 1 percent. This fall, tests on 23,000 deer and elk submitted by hunters statewide have revealed 48 CWD cases north of Interstate 70 and west of the Continental Divide. Biologists believe the infection rate in that area, which includes the Maybell, Meeker and Kremmling sites, is still well below 1 percent. But CWD has never been contained in a wild population, so experts fear the problem will grow worse.
The Division of Wildlife says it will be months before a statistical analysis of the fall's sampling results can be completed, an exercise that may shed light on the disease's origin on the Western Slope. "We're just not going to speculate at this point," said Ver Steeg of the possible Maybell connection. "This is one possibility, but certainly not the only possibility." Some biologists think a defunct elk ranch near Pagoda, which had dozens of unexplained deaths in the mid-'90s, is another, a suggestion Perkins rejects. "It may be inconclusive to them," said Perkins. "It isn't inconclusive to us."
To date, 19 CWD-positive animals have been found on six Wisconsin farms.
*** All have been white-tailed deer except for one elk imported from a Minnesota herd later found to be infected.
More than 8,000 farm-raised deer and elk have been tested in Wisconsin, and about 540 herds are enrolled in the CWD monitoring program.
CWD disease detected on Lac qui Parle County cervid farm southwestern Minnesota (2006-03-15)
Date: March 15, 2006 at 12:36 pm PST
Chronic wasting disease detected on Lac qui Parle County cervid farm (2006-03-15) The Board of Animal Health announced today that chronic wasting disease (CWD) has been detected in one domestic white-tailed deer on a cervid farm in Lac qui Parle County, which is located in southwestern Minnesota.
Immediately, DNR officials will conduct a local deer survey to determine the number of wild deer in the area. It is expected that not many deer will be found because the area is highly agricultural, with little deer habitat surrounding the farm. DNR will conduct opportunistic sampling of deer, like road kills, in the immediate area now and will conduct intensive hunter-harvested surveillance during the 2006 firearm deer season.
Although this positive animal is a captive deer, DNR has conducted surveillance for CWD in wild deer in the area. The farm is located near the northern boundary of deer permit area 447, where wild deer surveillance for CWD last occurred in 2003.
Lou Cornicelli, DNR big game program coordinator, said, "In 2003, we conducted wild deer CWD surveillance in adjoining permit areas 433, 446 and 447. In total, we collected 392 samples from those permit areas during the regular firearm deer season and CWD was not detected."
The sampling of wild deer was designed statistically to have a 95 percent confidence of detecting a 1 percent infection rate, according to Mike DonCarlos, DNR wildlife programs manager.
"This situation is very similar to the positive elk farm discovered in Stearns County in 2003, which followed the first discovery of CWD in an Aitkin County elk farm," DonCarlos said. “The DNR response will be similar to the Stearns County action and will include an initial assessment of wild deer populations in the area and development of a surveillance program for next fall."
From 2002 to 2004, DNR staff collected nearly 28,000 CWD samples statewide and no disease found in the wild herd.
"The intensive surveillance conducted in 2003 indicated CWD was not present in wild deer," Cornicelli said. “In addition, all indications are that this positive captive deer has not contacted any wild deer, but we will conduct additional surveillance this fall to be sure."
Friday, August 05, 2016
MINNESOTA CHRONIC WASTING DISEASE SURVEILLANCE AND TESTING CWD TSE PRION UPDATE
THURSDAY, NOVEMBER 09, 2017
Minnesota CWD TSE Prion Disease not detected in latest round of CWD tests on farmed deer herd in Crow Wing County?
PRION CONFERENCE 2015, 2016, 2017, ON potential for CWD TSE PRION ZOONOSIS, if it has not happened already...
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
snip...
R. BRADLEY
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
*** WDA 2016 NEW YORK ***
*** We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
Volume 23, Number 9—September 2017
Research Letter Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion
***Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
* Strongly consider having the deer or elk tested for CWD before you eat the meat.
* If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals.
* If your animal tests positive for CWD, do not eat meat from that animal.
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
SATURDAY, JANUARY 27, 2018
CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
https://web.archive.org/web/20170126073306/http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
https://web.archive.org/web/20170126073306/http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
*** I urge everyone to watch this video closely...terry
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
*** 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 ***
https://histodb11.usz.ch/Images/videos/video-004/video-004.html
*** 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.
http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf
''Results: We assessed archived human biopsy tissues from CWD endemic and non-endemic regions for the presence of abnormal PrP by RT-QuIC. Formalin-fixed, paraffin-embedded histology blocks were processed to extract tissue homogenates. Our study focused on analyzing appendix biopsy samples due to their previous use in surveillance studies and accessibility, but we also show the methodology can be applied to additional lymphoreticular tissues such as tonsils, spleen and lymph nodes. We compared 100 appendix biopsies from patients residing within the chronic wasting disease (CWD) endemic region to 100 appendix biopsies from patients residing outside the CWD endemic region.''
???
???
1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of
Neurological Disorders and Stroke, National Institutes of Health,
Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
PMID: 8006664 [PubMed - indexed for MEDLINE]
the tse prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE prion disease out of meat.
you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also survives Simulated Wastewater Treatment Processes.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.
you can bury it and it will not go away.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
it’s not your ordinary pathogen you can just cook it out and be done with.
that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.
snip...
CWD TO PIGS
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.
Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.
Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:
This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.
CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...see much more here ;
WEDNESDAY, APRIL 05, 2017
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
WEDNESDAY, APRIL 05, 2017
*** Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease ***
cattle are highly susceptible to white-tailed deer CWD and mule deer CWD
***In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research, however, suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008). It is apparent, though, that CWD is affecting wild and farmed cervid populations in endemic areas with some deer populations decreasing as a result.
SNIP...
price of prion poker goes up for cwd to cattle;
Monday, April 04, 2016
*** Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle ***
MONDAY, JUNE 12, 2017
Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?
i am thinking of that 10,000,000 POUNDS OF BLOOD LACED MEAT AND BONE MEAL IN COMMERCE WARNING LETTER back in 2007, see;
SATURDAY, NOVEMBER 4, 2017
FDA 589.2000, Section 21 C.F.R. Animal Proteins Prohibited in Ruminant Feed WARNING Letters and FEED MILL VIOLATIONS OBSERVATIONS 2017 to 2006
FRIDAY, NOVEMBER 3, 2017
BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW
''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''
IN CONFIDENCE
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
SHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;
''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
MONDAY, SEPTEMBER 25, 2017
Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis
TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION
*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
URINE
SUNDAY, JULY 16, 2017
*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***
Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20).
Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22).
Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing.
Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building.
Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9).
The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture.
When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep.
Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease.
It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled.
Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases.
Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA.
Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice.
In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals.
In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions).
As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay.
False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28).
This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm.
This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc.
In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc.
Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing.
The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material.
In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12).
A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30).
This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model.
Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
TSE Scrapie, CWD, BSE, Prion, Soil
Clay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern Illinois
Sheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-Pinilla
Scientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-x
Download Citation
Ecological epidemiology Ecological modelling Infectious diseases Prions
Received: 21 August 2017
Accepted: 08 December 2017
Published online: 22 December 2017
Abstract
Environmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.
tse prion soil
cwd tse prion and soil, see more ;
USA MAD DEER ROUNDUP
Feb. 16, 2018
Durkin: Stop private deer industry from trucking CWD across state
Patrick Durkin, For USA TODAY NETWORK-Wisconsin Published 10:13 a.m. CT Feb. 16, 2018
A Waupaca County captive-deer shooting preserve that discovered its first two cases of chronic wasting disease in October found 10 more CWD cases last fall, with 11 of the deer coming from a breeding facility in Iowa County — Wisconsin’s most infected county.
Hunt’s End Deer Ranch near Ogdensburg is one of 376 fenced deer farms in Wisconsin, according to the Department of Agriculture, Trade and Consumer Protection. Hunt’s End bought the diseased deer from Windy Ridge Whitetails, a 15-acre, 110-deer breeding facility south of Mineral Point in Iowa County. Of Wisconsin’s 4,175 CWD cases in wild deer, 2,261 (54 percent) are in Iowa County.
Since CWD’s discovery in three wild deer shot during the November 2001 gun season, CWD has been detected on 18 Wisconsin deer farms, of which 11 were “depopulated.” DATCP has identified 242 CWD cases in captive facilities the past 16 years.
The state’s worst site remains the former Buckhorn Flats Game Farm near Almond in Portage County, where 80 deer tested positive for this always-fatal disease from 2002 to 2006. When the U.S. Department of Agriculture shot out the 70-acre pen in January 2006, 60 of the remaining 76 deer carried CWD, a nearly 80 percent infection rate.
The Department of Natural Resources bought the heavily contaminated site for $465,000 in 2011 and has kept it fenced and deer-free since.
The last time DATCP exterminated a captive herd was November 2015, when it killed 228 deer at Fairchild Whitetails, a 10-acre breeding facility in Eau Claire County, and paid its owner, Richard Vojtik, $298,770 in compensation. Tests revealed 34 of those deer carried CWD (15 percent), but two bucks had escaped earlier. Those bucks roamed five months before being shot and tested. They, too, had CWD.
Both operations were outside the endemic CWD region in southern Wisconsin; Buckhorn Flats by about 60 miles and Fairchild Whitetails by about 120. Wisconsin’s four most active CWD outbreaks on deer farms are north of U.S. 10, and farther away from the endemic region — basically the DNR’s Southern Farmlands district — which had 584 CWD cases 2017-18 and 4,148 since 2001.
Those businesses are:
• Wilderness Whitetails, near Eland in Marathon County: 68 CWD cases, including 43 in 2017-18. DATCP first reported CWD there in December 2013 in a 5-year-old buck shot by a facility client. The operation also found three cases in 2014, nine in 2015 and 12 in 2016.
The preserve held about 310 deer in its 351-acre pen last summer. Since beginning tests in 2002, the facility tested 373 deer before finding its first case 11 years later.
• Hunt’s End, Waupaca County: 12 cases, all in 2017-18. The owners, Dusty and Mandy Reid, didn’t detect CWD on the 84-acre shooting facility until two 4-year-old bucks tested positive last fall. DATCP announced those cases Oct. 20, and disclosed 10 additional cases in response to my open-records request in January.
Both Oct. 20 bucks originated from Windy Ridge Whitetails. Nine other bucks from Windy Ridge, owned by Steven and Marsh Bertram, tested positive for CWD after being shot by Hunt’s End clients.
Now DATCP records covering the past five years showed Hunt’s End acquired 31 deer from Windy Ridge, which also sent a combined 67 whitetails to nine other Wisconsin deer farms during that period.
Paul McGraw, DATCP’s state veterinarian and administrator in animal health, quarantined three Hunt’s End properties Oct. 20, but let its owners, continue selling hunts because “properly handled dead animals leaving the premises do not pose a disease risk.”
McGraw also quarantined Windy Ridge, but the specifications let the business move more deer to the Waupaca shooting facility. It made two more shipments to Hunt’s End, the last occurring Nov. 13.
• Apple Creek Whitetails, Oconto County: 11 cases. Since discovering CWD in September 2016 in an 18-month-old doe killed inside the facility near Gillett, DATCP has identified 10 more cases, including three in 2017-18. The preserve held about 1,850 deer on 1,363 acres, and tested 466 in 2016. After first testing for CWD in 2009, the business processed 1,192 deer before finding its first case 18 months ago.
• Three Lakes Trophy Ranch, Oneida County: Nine cases. Since discovering CWD in December 2015 in a 3-year-old buck at Three Lakes, DATCP has identified eight more cases, including two in 2017-18. The preserve held about 545 whitetails on 570 acres.
Although the Hunt’s End outbreak traces to Iowa County deer, Windy Ridge Whitetails sent even more deer, 42, to Vojtik’s American Adventures Ranch near Fairchild with no documented problems. DATCP reports no CWD cases there, and Vojtik, who also owned the 10-acre Fairchild Whitetails breeding facility, said he hasn’t bought Windy Ridge deer the past two years.
Vojtik said Wednesday that he and his clients shoot out his enclosure’s herd of about 200 deer each year to reduce CWD risks. And because he’s not in DATCP’s herd-status program, he must only test 50 percent of deer dying there.
Meanwhile, Wilderness Whitetails tests all of its dead deer. It leads the state with 68 CWD cases, even though it has maintained a “closed herd” since opening its Eland facility in 2004, said its owner, Greg Flees, when reached Wednesday. Flees said all deer in the 351-acre facility were born there or came from his family’s Portage County breeding pen, which began in the 1970s and has never had CWD.
Flees said the jump from 12 CWD cases in 2016 to 43 in 2017 is no mystery or surprise. “We shot more deer to lower our densities, so we found more CWD,” he said. He thinks CWD was in the facility’s soils when they enclosed it with an 8-foot-high fence 14 years ago, or it arrived in alfalfa bales brought in for feed.
Perhaps the bigger mystery is why DATCP allows any deer from Iowa County to be shipped anywhere. Windy Ridge Whitetails is one of eight captive-deer facilities in CWD-infected counties — Sauk, Dane, Iowa, Rock, Walworth and Richland — enrolled in DATCP’s herd-status program, which allows deer transfers if facilities follow specified guidelines.
That won’t change soon, either. In a letter Jan. 30 responding to my open records request, Paul Dedinsky, DATCP’s chief legal counsel, wrote, “The Department is not proposing any rule changes to prohibit movement from CWD endemic areas.”
No doubt Wisconsin’s wild deer provide a vast, mostly undocumented pool for spreading CWD, but sick deer can only carry disease as far as they walk. With DATCP’s approval, privately owned deer could spread CWD wherever they’re trucked.
Patrick Durkin is a freelance writer who covers outdoors for USA TODAY NETWORK-Wisconsin. Email him at patrickdurkin56@gmail.com.
FRIDAY, FEBRUARY 16, 2018
Wisconsin Stop private deer industry from trucking CWD across state
FRIDAY, FEBRUARY 16, 2018
Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion
FRIDAY, JANUARY 26, 2018
WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE
Tuesday, December 20, 2011
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:
captive deer farmers breeders entitlement program, i.e. indemnity program, why?
how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms, and why do tax payers have to pay for it ???
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).
For Immediate Release
Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov Share on facebook Share on twitter Share on email Share on print More Sharing Services 1
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). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
-30-
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). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
INFORM: Cervid Health and States Indemnity FY 2015
USDA Animal and Plant Health Inspection Service sent this bulletin at 09/19/2014 05:22 PM EDT
Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS) received a total of $3 million in appropriated funding to support cervid health activities in fiscal year (FY) 2014, and made approximately $1.0 million of this funding available for indemnity of chronic wasting disease (CWD) positive, suspect, and exposed farmed cervids. All of the available FY2014 indemnity funding was used to depopulate three CWD-infected herds. However, several States have asked about the availability of Federal indemnity funds for CWD-exposed animals in the future.
VS plans to offer Federal indemnity for CWD-exposed cervids beginning in FY2015. Briefly, we will prioritize the highest risk CWD-exposed animals for indemnity based on the availability of funding. Any newly reported CWD-positive herds will be considered for indemnity as they are identified, based first on funding availability and secondly on the risk presented by the herd.
We will reassess our fiscal year funding on a quarterly basis so that providing indemnity for exposed animals does not exhaust available funding early in the fiscal year. By taking this fiscally cautious approach, we hope to provide indemnity for positive herds identified later in the fiscal year while removing high-risk animals from the landscape as soon as possible to minimize the risk for disease spread. Further, removal and testing of these exposed animals will provide a better understanding of the disease risk presented by these animals/herds.
VS plans to work with our State and industry stakeholders on the criteria to assess the risk and on the process through which States can request this indemnity. These will be finalized in a VS Guidance Document in the near future. We look forward to working with you to implement this process in the coming year.
***
FRIDAY, FEBRUARY 23, 2018
Pennsylvania NEW CWD MANAGEMENT AREA TO BE ANNOUNCED
MONDAY, FEBRUARY 12, 2018
Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties
WEDNESDAY, FEBRUARY 21, 2018
Maryland Chronic Wasting Disease CWD TSE Prion Found In Ten Deer Allegany and Washington Counties
SATURDAY, FEBRUARY 17, 2018
Montana Special Hunts 9 more cases CWD TSE Prion to date, more samples still pending
FRIDAY, FEBRUARY 09, 2018
Mississippi Chronic Wasting Disease confirmed in a White-tailed Deer
TUESDAY, FEBRUARY 13, 2018
*** MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations ***
WEDNESDAY, NOVEMBER 22, 2017
Minnesota Chronic Wasting Disease discovered in Winona County farm
FRIDAY, NOVEMBER 24, 2017
Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting CWD TSE PRION DISEASE risk factors
WEDNESDAY, FEBRUARY 21, 2018
TEXAS TPWD CWD TSE PRION 2 MORE FROM BREEDER RELEASE SITE TOTALS 81 CASES TO DATE
WEDNESDAY, JANUARY 24, 2018
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE
FRIDAY, FEBRUARY 16, 2018
Texas Deer Breeders Continue fight against the state’s wildlife agency and its regulations trying to contain CWD TSE Prion
WEDNESDAY, FEBRUARY 07, 2018
New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.
FRIDAY, FEBRUARY 09, 2018
Virginia 2017 Hunt Confirms 16 Cases Chronic Wasting Disease CWD TSE Prion
MONDAY, FEBRUARY 05, 2018
Nebraska Chronic Wasting Disease CWD TSE Prion 2017 Survey Confirms 203 Positives From 1,807 Deer Sampled
SATURDAY, FEBRUARY 03, 2018
Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018
THURSDAY, FEBRUARY 08, 2018
Utah Chronic Wasting Disease CWD TSE Prion Update to date from 2017 Hunting Season
TUESDAY, JANUARY 30, 2018
Colorado Chronic Wasting Disease CWD TSE Prion 7/2015-6/2016 Results (2017?)
THURSDAY, JANUARY 25, 2018
Ohio Chronic Wasting Disease CWD TSE Prioin aka mad deer update 2016-2017 SEASON SUMMARY
SATURDAY, JANUARY 20, 2018
Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have tested positive for CWD majority of samples collected still are being analyzed
WEDNESDAY, JANUARY 24, 2018
Illinois Chronic Wasting Disease CWD TSE Prion cases mounting with 75 confirmed 2017 and 685 total to date
THURSDAY, FEBRUARY 08, 2018
Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season
SATURDAY, FEBRUARY 10, 2018
Chronic wasting disease management in ranched elk using rectal biopsy testing Research Paper 09 Feb 2018
January 14, 2018
Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases
Michigan UPDATE, see also ;
Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan
Contact: Dwayne Etter (DNR), 517-284-4725 or David Williams (MSU), 517-917-0716 Agency: Natural Resources
Jan. 30, 2018
Michigan State University and the Michigan Department of Natural Resources will be placing location-tracking collars on white-tailed deer in south-central Michigan as part of a multiyear study of deer disease, including chronic wasting disease.
January 14, 2018
Missouri MDC REPORTS 15 NEW CASES OF CWD TSE Prion in Deer
MONDAY, JANUARY 29, 2018
Wyoming, Hanna, WGFD diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 161
MONDAY, JANUARY 29, 2018
North Dakota CWD Confirmed whitetail buck and a mule deer doe 2017 deer gun season from unit 3F2
SUNDAY, FEBRUARY 18, 2018
Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018
TUESDAY, DECEMBER 12, 2017
*** Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017 ***
(zoonosis and environmental risk factors towards the bottom, after state by state reports)
MONDAY, MARCH 13, 2017
CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017
SATURDAY, JANUARY 14, 2017
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper (Document ID APHIS-2012-0105-0001)
***Terry S. Singeltary Sr. submission
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
*** DOCUMENT ID: APHIS-2006-0118-0411
SUNDAY, FEBRUARY 11, 2018
Experimental sheep BSE prions generate the vCJD phenotype when serially passaged in transgenic mice expressing human prion protein
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
Ivett Ackermann, Anne Balkema-Buschmann, Reiner Ulrich, Kerstin Tauscher, James C. Shawulu, Markus Keller, Olanrewaju I. Fatola, Paul Brown and Martin H. GroschupEmail authorView ORCID ID profile
Veterinary Research201748:88
https://doi.org/10.1186/s13567-017-0495-5© The Author(s) 2017
Received: 22 August 2017Accepted: 1 December 2017Published: 19 December 2017
Abstract
In classical bovine spongiform encephalopathy (C-BSE), an orally acquired prion disease of cattle, the ileal Peyer’s patch (IPP) represents the main entry port for the BSE agent. In earlier C-BSE pathogenesis studies, cattle at 4–6 months of age were orally challenged, while there are strong indications that the risk of infection is highest in young animals. In the present study, unweaned calves aged 4–6 weeks were orally challenged to determine the earliest time point at which newly formed PrPBSE and BSE infectivity are detectable in the IPP. For this purpose, calves were culled 1 week as well as 2, 4, 6 and 8 months post-infection (mpi) and IPPs were examined for BSE infectivity using a bovine PrP transgenic mouse bioassay, and for PrPBSE by immunohistochemistry (IHC) and protein misfolding cyclic amplification (PMCA) assays. For the first time, BSE prions were detected in the IPP as early as 2 mpi by transgenic mouse bioassay and PMCA and 4 mpi by IHC in the follicular dendritic cells (FDCs) of the IPP follicles. These data indicate that BSE prions propagate in the IPP of unweaned calves within 2 months of oral uptake of the agent.
snip...
In summary, our study demonstrates for the first time PrPBSE (by PMCA) and prion infectivity (by mouse bioassay) in the ileal Peyer’s patch (IPP) of young calves as early as 2 months after infection. From 4 mpi nearly all calves showed PrPBSE positive IPP follicles (by IHC), even with PrPBSE accumulation detectable in FDCs in some animals. Finally, our results confirm the IPP as the early port of entry for the BSE agent and a site of initial propagation of PrPBSE and infectivity during the early pathogenesis of the disease. Therefore, our study supports the recommendation to remove the last four metres of the small intestine (distal ileum) at slaughter, as designated by current legal requirements for countries with a controlled BSE risk status, as an essential measure for consumer and public health protection.
FRIDAY, DECEMBER 22, 2017
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
Thursday, November 16, 2017
Texas Natural Meats Recalls Beef Products Due To Possible Specified Risk Materials Contamination
*** Subject: USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS 2017
TUESDAY, DECEMBER 12, 2017
Bovine Spongiform Encephalopathy BSE TSE Prion (aka mad cow disease) Report December 14, 2017 2017
TUESDAY, DECEMBER 12, 2017
Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017
FRIDAY, DECEMBER 15, 2017
Canada CFIA updating its national CWD TSE PRION efforts to eradicate disease farmed cervid NOT successful December 14, 2017
TUESDAY, DECEMBER 12, 2017
SCRAPIE TSE PRION UPDATE USA DECEMBER 14, 2017
USAHA 2017 RESOLUTIONS
RESOLUTION NUMBER: 23
APPROVED AS AMENDED SOURCE: COMMITTEE ON WILDLIFE AND CAPTIVE WILDLIFE
SUBJECT MATTER: Annual Reporting on Chronic Wasting Disease Epidemiological Data
BACKGROUND INFORMATION: Chronic wasting disease (CWD) has been recognized in wild cervids since the 1980’s. Availability of complete epidemiological information is critical for evaluating the effectiveness of science-based disease control programs. Access to pertinent information from epidemiological investigations across the country in wild populations is imperative to developing success strategies for managing the disease. More comprehensive information is needed on CWD epidemiology in the affected wild populations. Analysis of data from CWD affected populations across the country will improve risk assessment. Comprehensive epidemiological data evaluation may potentially identify factors contributing to the detection of CWD, enhance mitigation strategies to reduce the likelihood of CWD in new populations, and facilitate its earliest detection when it is present.
RESOLUTION: The United States Animal Health Association (USAHA) requests the United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service, Veterinary Services and other appropriate federal and state agencies to work cooperatively to assemble, analyze, summarize, and make available annually to the Committee on Wildlife and Captive Wildlife at the USAHA meeting all pertinent information from epidemiological investigations of Chronic Wasting Disease (CWD) in cervid populations (including wild, free-ranging, and captive).
Specific information requested may include:
1) Compiled CWD testing data from each state to include:
a) Overall state testing numbers of each susceptible species tested;
b) Number of CWD positive tests found annually in each state;
c) Overall state testing in wild populations;
d) Prevalence of CWD in positive populations;
e) Population totals for each susceptible species of wild herds in each state;
f) Demography of positive and negative animals in infected herds;
g) Results from all tissues that were tested;
h) Duration of monitoring prior to detection of the first case - including numbers of animals in the herd, numbers tested, and numbers not tested;
i) Results of trace-forward and trace-back investigations; and
j) All other pertinent data that will enhance risk assessment of CWD in cervids and identification of effective mitigation measures.
2) Compiled data should also be posted on the USDA website.
http://www.usaha.org/upload/Resolution/2017/Resolution_23_CWD_Data.pdf
RESOLUTION NUMBER: 21 APPROVED SOURCE: COMMITTEE ON SHEEP, GOATS AND CAMELIDS SUBJECT MATTER: National Scrapie Eradication Program Funding
BACKGROUND INFORMATION: Due to the success of the cooperative National Scrapie Eradication Program, no new cases of scrapie have been identified in the United States (US) in the past 18 months. There are key components of the program that have been critical to this success and the effort to have the US be recognized internationally as free from scrapie, which would open new markets to US sheep and goat products. Surveillance and traceability are vital to this eradication program. Program use of sheep and goat official tags have demonstrated that official plastic tags are preferred over metal tags for readability and to reduce safety concerns. Funding for tags that are readable, acceptable to producers and efficient for regulators is essential to continue identification compliance and progress of the program.
RESOLUTION: The United States Animal Health Association urges the United States Secretary of Agriculture to request a congressional appropriation of five million additional dollars of new money to be added to the Equine, Cervid and Small Ruminant health line for the purpose of supporting Small Ruminant Health Programs to complete the eradication of scrapie and assure program success. It is vital that this new funding does not reduce other current United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services program funding lines.
lol, drop in the bucket and a band-aid approach to something that needed a tourniquet decades ago...
TUESDAY, DECEMBER 12, 2017
Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017
THURSDAY, FEBRUARY 15, 2018
Iatrogenic Creutzfeldt-Jakob disease with Amyloid-β pathology: an international study
WEDNESDAY, NOVEMBER 1, 2017
Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies
http://betaamyloidcjd.blogspot.com/2017/11/blood-derived-amyloid-protein-induces.html
Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ???
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
https://web.archive.org/web/20040315075058/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
snip...see full Singeltary Nature comment here;
http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO 4
November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk.
However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed. 1
92/11.4/1.1
BSE101/1 0137 4.
The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion.
The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2
https://web.archive.org/web/20160320084827/http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
snip...see full Singeltary Nature comment here;
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d
https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
http://www.plosone.org/annotation/listThread.action?root=82860
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1982.tb26849.x/abstract
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis
Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00
http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20
http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html
Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies
http://betaamyloidcjd.blogspot.com/2017/11/blood-derived-amyloid-protein-induces.html
Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ???
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
https://web.archive.org/web/20040315075058/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
snip...see full Singeltary Nature comment here;
http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO 4
November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk.
However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed. 1
92/11.4/1.1
BSE101/1 0137 4.
The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion.
The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2
https://web.archive.org/web/20160320084827/http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
snip...see full Singeltary Nature comment here;
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d
https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
http://www.plosone.org/annotation/listThread.action?root=82860
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1982.tb26849.x/abstract
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis
Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00
http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20
http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html
Terry S. Singeltary Sr.
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