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About Me

T E R R Y S .S I N G E L T A R Y S R .

My mother was murdered bywhat I call corporate andpolitical homicide i.e. FORPROFIT! she died from a rarephenotype of CJD i.e. theHeidenhain Variant ofCreutzfeldt Jakob Disease i.e.sporadic, simply meaning fromunknown route and source. Ihave simply been trying tovalidate her death DOD12/14/97 with the truth. Thereis a route, and there is asource. There are many herein the USA. WE must make CJDand all human TSE, of all agegroups 'reportable' Nationallyand Internationally, with awritten CJD questionnaireasking real questionspertaining to route and sourceof this agent. Friendly fire hasthe potential to play a huge rolein the continued transmissionof this agent via the medical,dental, and surgical arena. Wemust not flounder any longer....TSSView my complete profile

T U E S D A Y , J U L Y 1 2 , 2 0 1 6

Chronic Wasting Disease CWD, Scrapie, BovineSpongiform Encephalopathy BSE, TSE, PrionZoonosis Science HistoryNIH may destroy human brain collection

http://www.washtimes.com/upi-breaking/20050323-053919-8481r.htm

Washington Times - Washington,DC,USA

NIH may destroy human brain collection

By Steve Mitchell Medical Correspondent

Washington, DC, Mar. 24 (UPI) -- The National Institutes of Health maydiscard part or all of a rare collection that includes hundreds of humanbrain samples from patients that suffered from a disorder similar to madcow disease -- unless another researcher or institution takes them on,United Press International has learned.

Several scientists said the collection, which is held by the NIH's NationalInstitute for Neurological Disorders and Stroke in Bethesda, Md. -- andincludes brains and other tissue samples from people afflicted with thebrain-wasting illness Creutzfeldt Jakob disease -- is irreplaceable andcould even provide insight into treatments for the fatal disorder.

Currently, there is no cure for CJD and patients typically die within a yearafter symptoms begin.

However, NIH officials in control of the collection's fate told UPI theremaining samples are of little scientific value and may be disposed of ifresearchers outside the agency do not claim it. That position stands insharp contrast with CJD experts who thought the collection should bepreserved.

"It's invaluable," said Dr. Paul Brown, former medical director of the NIH'sLaboratory for Central Nervous System Studies, whose expertise is in CJDand mad cow disease (also known as bovine spongiform encephalopathy,or BSE).

The collection is badly in need of organization and no one is certain howmany brains or other tissue samples it contains, said Brown, who workedwith the collection since its inception in the 1960's until his retirement lastyear. There could be brains, blood, spinal fluid and various other tissuesfrom 1,000 people or more, he said. Some of the specimens would be ofscientific use today, he said.

"This collection has the unique value of stretching back to the beginningof when these diseases were discovered," Brown told UPI, noting that the

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first samples were obtained in 1963. "It would be as though you had inyour hands the possibility of finding out when AIDS started."

Bruce Johnson, a former technician at the CNSS lab who workedextensively with the collection before he retired in 2003, told UPI he wastold "in two years they (NIH officials)are going to destroy it, if nobodywants it."

Eugene Major, acting director of the basic neuroscience program at theNIH, said no specific timeframe had been established.

"We have not set a firm deadline date," Major told UPI. "We are workingvery hard with investigators that we know in order to be able to make surethat whatever we deem is valuable is potentially kept here." Somesamples already have been determined not to have any research value andhave been "removed and disposed of," he said.

Others samples have been given out to Dr. David Asher at the Food andDrug Administration and Pierluigi Gambetti at the National Prion DiseasePathology Surveillance Center in Cleveland, Ohio.

Major maintained the remaining collection was not particularly valuable forresearch. "Whatever had been collected here that has not already beendistributed to responsible investigators who could use them really has verylittle remaining value," he said.

Neither Asher nor Gambetti returned phone calls from UPI, but Brownsaid he thought Asher had received only a dozen or two samples at mostand Gambetti had not received much at all.

Neil Cashman, a brain-disease researcher at the University of Toronto'sCenter for Research in Neurodegenerative Diseases -- who has tried toobtain the collection from the NIH -- said it was priceless.

"It would be like destroying an art museum," Cashman told UPI. "There'sall this information and insight that's locked up in these tissues and if it'sdestroyed it will be lost forever."

The Memorial Institute for Neurodegenerative Diseases Inc., a non-profitorganization consisting of more than 40 university and instituteresearchers from the United States, Canada, United Kingdom and France,also thinks the brain collection is invaluable.

"It is the opinion of the Board of Directors ... of The MIND Inc., that the ...brain bank should not be broken up nor destroyed," said Harry E. Peery,MIND's executive director, in a letter to UPI. "We believe that thiscollection is of inestimable research value and should be kept intact."

The institute, at the University of Saskatchewan in Saskatoon, applied forpossession of the collection in early 2004, but received a letter from theNINDS indicating the fate of the collection had not yet been determined.

"We have heard nothing further since that time" and continue to beinterested in acquiring the complete collection, Peery said.




CJD belongs to a group of rare, brain-wasting disorders that are littleunderstood, incurable and fatal. This includes mad cow disease in cows,chronic wasting disease in deer and elk. The most infamous of theseillnesses in humans is variant CJD, which people can contract from eatingbeef products infected with the mad-cow pathogen.

Although vCJD has infected more than 154 people worldwide, only onecase has ever been detected in the United States -- in a Florida womanwho is thought to have contracted the disease while living in the UnitedKingdom. However, the NIH brain samples have never been screened forvCJD -- something Johnson thinks is critically important.

"No one has ever looked to see if any American (in the collection) in thepast had variant CJD," Johnson said. "You think it would be required thatthey do that. You think it would be a Congressional mandate that they testthese brains: 'Let's see if we've got this disease in our country.'"

Johnson noted at least one brain in the collection he personally hadexamined -- from a French woman collected in 1971 -- showed evidence ofpossible vCJD infection, but the sample needed further study to be sure.

Other samples in the collection include the brains of patients who wereonly 16 years old when they were diagnosed with CJD. This would beunusual for sporadic CJD, because generally it strikes those over age 60.Variant CJD, on the other hand, typically occurs in patients in their 20s oryounger.

"I thought it was absolutely vital (to test these brains)," Johnson said."Maybe there's a dozen cases in there of variant CJD."

Major disagreed. "There's really no reason to do that," he said. "The effortit would take to screen those samples ... would not give us any newinsights into variant CJD beyond what it is we already know."

Johnson said he was frustrated with the NIH administration's lack ofinterest in preserving the collection or testing for vCJD. "They don'tunderstand," he said, "they honest-to-god don't understand what it's allabout."

Patient advocates also objected to the possible destruction of the brains.

Terry Singeltary, whose mother died of a type of CJD called Heidenhainvariant in 1997, said he is outraged and families of other CJD victimsprobably will be, too.

"A lot of these families went through a lot of heartache and a lot of troubleto get these brain samples to the NIH," Singeltary told UPI. "Now they'rejust going to discard them because they're not of scientific use? That'sjust asinine. That stuff is valuable information."

Graham Steel, vice-chair of the Human BSE Foundation in the UnitedKingdom, told UPI, "The potential loss of such important tissue sampleswould be a massive blow for TSE (the group of diseases that includes CJDand BSE) research in the United States. This should not be allowed tohappen."

Singeltary noted there currently is no cure for these diseases. "If you




don't have any answers yet, why would you throw these specimensaway?" he asked.

He added that more sensitive tests are just becoming available and couldhelp determine the origin of some of the CJD cases. "We've all been sittingaround waiting for more sensitive tests to get validated because we wantanswers," he said.

"You know, it must be an embarrassment," Johnson said. "Some Senatoris going to eventually say 'What is NIH doing about mad cow disease?'And people are going to scratch their heads and say 'not much'." Headded, "What's going to happen (is) one of these senators or their wife isgoing to develop spontaneous CJD one day and ... there's going to be hellraised and they're going to ask, 'Why isn't NIH working on this?'"

--

E-mail [email protected]


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

I will first post the beginning of my letter to these officials asking for help.

I will then post the letters from the Honorable Senator Cornyn and wouldlike to thank him for pursuing this for us, and getting this in writing. Itmeant a lot to all of us.

Thanks to Steve Mitchell of UPI for his continued efforts to find the truthabout all human and animal TSEs, and his continued efforts in trying tokeep the USDA/APHIS/FDA/CDC/NIH Federal Officials honest and forthcoming. However, it's kinda like pulling teeth sometimes, all for the safetyand security of US citizens i am sure.

IN the reply from NIH back to Senator Cornyn on this issue, there weresome concerns of mine that i will bring up and comment on laterbelow...TSS

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

Subject: NIH to destroy our loved ones brain tissues, WE NEED YOURHELP PLEASE

Date: Fri, 25 Mar 2005 16:04:57 –0600

From: "Terry S. Singeltary Sr."

To: [email protected]





CC: [email protected], [email protected],[email protected],[email protected], [email protected],[email protected], [email protected], [email protected], [email protected] References: <422ca640.3030108="" wt.net="">

Greetings again Honorable Senator Hutchison and otherHonorableMembers of Texas Office,

My name is Terry S. Singeltary Sr. I lost my Mother to hvCJD aka madcow.THE Heidenhain Variant of Creutzfeldt Jakob Disease.(there is morethan one strain of mad cow disease and i will reference last)I am onceagain writing to you on a matter of extreme importance. I would appreciateyour assistance in writing to the National Institutes of Health requestingthat the brain tissue collected over the years at NINDS from familymembers of Creutzfeldt-Jakob Disease victims be preserved and recordedand not discarded. [See attached articles]

THE WASHINGTON TIMES UNITED PRESS INTERNATIONAL

NIH may destroy human brain collection

snip...same as above...tss

[email protected]://www.washtimes.com/upi-breaking/20050323-053919-8481r.htm

SNIP...END...TSS

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

JOHN CORNYN

TEXAS

UNITED STATES SENATE

WASHINGTON, DC 20510-4305

April 26,2005

Mr. Terry SingeltaryP.O. Box 42Bacliff, Texas 77518

Dear Mr. Singeltary:

In response to your recent request for my assistance, I have contacted theNational Institutes ofHealth. I will write you again as soon as I receive a


mailto:[email protected]://www.washtimes.com/upi-breaking/20050323-053919-8481r.htm



reply.

I appreciate having the opportunity to represent you in the United StatesSenate and to be of service in this matter.

Sincerely,

JOHN CORNYN United States Senator JC:djl

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

JOHN CORNYN

TEXAS

UNITED STATES SENATE

WASHINGTON, DC 20510-4305

May 18,2005

Mr. Terry Singeltary P.O. Box 42 Bacliff, Texas 77518

Dear Mr. Singeltary:

Enclosed is the reply I received from the Department of Health and HumanServices in response to my earlier inquiry on your behalf. I hope this willbe useful to you. I appreciate having the opportunity to represent you inthe United States Senate.

Thank you for taking time to contact me. Sincerely,

JOHN CORNYN

United States Senate

JC:djl

Enclosure

DEPARTMENT OF HEALTH & HUMAN SERVICES

National Institutes of Health National Institute of Neurological Disorders




and Stroke NINDS

Building 31, Room 8A52

31 Center Dr., MSC 2540

Bethesda, Maryland 20892-2540

Phone: 301-496-9746

Fax: 301-496-0296

Email: [email protected]

May 10, 2005

The Honorable John CornynUnited States SenatorOccidental Tower5005LBJ Freeway, Suite 1150Dallas, Texas 75244-6199

Dear Senator Cornyn:

Your letter to the National Institutes of Health (NIH) forwardingcorrespondence from Mr. Terry S. Singeltary, Sr., has been forwarded tome for reply. Mr. Singeltary is concerned about the preservation ofCreutzfeldt-Jakob disease (CJD) brain samples that have been maintainedby the National Institute of Neurological Disorders and Stroke (NINDS)Intramural Research programfor many years.

I am sorry to learn that Mr. Singeltary's mother died of CJD and cancertainly understand hisdesire that any tissues that could helpinvestigators unravel the puzzle of this deadly disease are preserved. Ihope he will be pleased to learn that all the brains and other tissues withpotential to help scientists learn about CJD are, and will continue to be,conserved. (The tissues that are discarded are those that have eitherdecayed to an extent that renders them no longer appropriate for researchor those for which we do not have sufficient identification.)

The purpose of gathering these brains and tissues is to help scientistslearn about CJD.

To that end, some of the NINDS-held samples are distributed toinvestigators who can demonstrate that they have a compelling researchor public health need for such materials. For example, samples have beentransferred to NIH grantee Dr. Pierluigi Gambetti, who heads the NationalPrion Diseases Pathology Surveillance Center at Case Western ReserveUniversity in Ohio and works with the Centers for Disease Control andPrevention to monitor all cases of CJD in the United States. Dr. Gambettistudies the tissues to learn about the formation, physical and chemicalproperties, and pathogenic mechanisms of prion proteins, which arebelieved to be involved in the cause of CJD. Samples have also beentransferred to Dr. David Asher, at the U.S. Food and Drug Administration,for use in assessing a potential diagnostic test for CJD.




Page 2 - The Honorable John Cornyn

in closing, we know that donating organs and tissue from loved ones is avery difficult and personal choice that must often be made at the moststressful of times. We at the NINDS are grateful to those stalwart familymembers who make this choice in the selfless hope that it will help othersafflicted with CJD. We also know the invaluable contribution suchdonations make to the advancement of medical science, and we arededicated to the preservation of all of the tissue samples that can help inour efforts to overcome CJD.

I hope this information is helpful to you in responding to Mr. Singeltary.

Sincerely,

Story C. Landis, Ph.D.

Director, National Institute ofNeurological Disorders and Stroke

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

Greetings,

THE concerns i wanted to mention are ;

A. The distribution of those tissue samples and how they are distributed.

I think more people researching this agent (especially sporadic CJD)should be able to obtain the tissue samples. THE political crap belowmust stop, or what i like to call BSeee ;

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

Major previously said, however, that efforts to inform researchers of theavailability of the collection were already underway and included informingNIH grantees. He added he had personally notified researchers atscientific meetings, but no TSE researcher contacted by UPI was aware ofthis."I was never informed," said Laura Manuelidis, an expert on thesediseases and section chief of surgery in the neuropathology department atYale University. She said the first she had heard of the situation was inUPI's March 24 report. Manuelidis also said she contacted Major,expressing interest in the specimens, but so far has not received aresponse. "I sent a letter to (Major) on (March 25) about our interest inthese specimens, but he has not replied," she told UPI in an e-mail.NeilCashman, a TSE expert at the University of Toronto, who said he was notaware the samples might be destroyed, has lobbied colleagues at theUniversity of British Columbia -- where Cashman is scheduled to move tothis summer -- to help draft a letter requesting the collection.The MemorialInstitute for Neurodegenerative Diseases Inc., a non-profit organizationconsisting of more than 40 university and institute researchers from theUnited States, Canada, the United Kingdom and France, requested thecollection in January, 2004. So far, the institute has not been informed of adecision by the NIH.Asked if Major had told him whether the collectionwould be preserved, MIND Executive Director Harry Peery said, "We haveheard nothing further from Eugene Major or anyone else at the NIHregarding the brain collection."




http://washtimes.com/upi-breaking/20050407-110535-2570r.htm

MORE FUNDING TO DR.Frank Bastian! The only funding he gets is fromNIH, and they are on the verge of shutting him down. give him a biggergrant. believe me, all the answers to this agent are not answered yet, andmany many humans and animals have been exposed, with more to follow.There is not enough money being funded/granted to the research ofhuman/animal TSE compared to other diseases and this will come back atus by many more due to incubation period and everyone just ignoring itover the years, and there just might be more to this nightmare than aprion.

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

Dr. Pierluigi Gambetti, who heads the National Prion Diseases PathologySurveillance Center at Case Western Reserve University in Ohio andworks with the Centers for Disease Control and Prevention to monitor allcases of CJD in the United States. Dr. Gambetti studies the tissues tolearn about the formation, physical and chemical properties, andpathogenic mechanisms of prion proteins, which are believed to beinvolved in the cause of CJD.

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

HOW CAN YOU monitor all cases of CJD when it is not reportable in everystate of all age groups? WITH all the animal TSEs in the USA for over 2decades rendered and fed back to each other for human and animalconsumption, with TSE in cattle that we know of in the USA and someothers rendered without TSE test, how can all sporadic CJD in the USA besporadic? I hate that word. its just an excuse or lie.

FINALLY, a kind thank you to Dr. Landis et al at NINDS, and there'confirmation letter' that our loved ones brain and tissues samples will bepreserved and used for CJD research.ALSO, a kind tribute to the late Dr.Joe Gibbs whom we all miss and respected so much. HE would have beenvery upset if those brain and tissue samples would have been destroyed.

with kindest regards, I am sincerely,

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

Groups seek to save NIH brain collection

By STEVE MITCHELL, Medical Correspondent | April 1, 2005 at 4:48 PM

WASHINGTON, April 1 (UPI) -- Scientists, consumer groups and patient-advocates have embarked upon efforts -- including petitioning members ofCongress and seeking storage space at a Canadian university -- to preventthe National Institutes of Health from destroying an irreplaceable collectionof human brains from patients afflicted with a condition similar to mad cowdisease.

As United Press International reported last week, the NIH has begunshopping for a new home for its collection of brains, spinal fluid and othertissues from hundreds of patients around the world who died from





Creutzfeldt Jakob disease -- an incurable, fatal, brain-wasting illness. Thecollection dates back to 1963 and the consensus among scientists in thisfield is it is invaluable for research and could provide insights that might aidin developing diagnostic tests, treatments or cures for CJD.

NIH officials, however, maintain the remaining samples in the collection --stored in some 30 freezers by the National Institute for NeurologicalDisorders and Stroke in Bethesda, Md. -- are of little value and may bedisposed of if researchers or institutions do not come forward to claimthem.

Families of patients who died of CJD have reacted with outrage, concernedthat the effort mounted to collect the brains in the first place has been allfor naught. Several have contacted their respective members of Congressand urged them to step in.

"The brains and brain tissue were sent to NIH in good faith for futureresearch and destroying them is an outrage," Terry Singeltary, a patientadvocate in Bacliff, Texas, wrote in a letter to Sen. Kay Bailey Hutchinson,R-Texas, and several other members of the state's congressionaldelegation. Singeltary's mother died of a type of CJD called Heidenhainvariant in 1997.

Hutchinson's office did not return a call from UPI.

Eugene Major, who serves as acting director of the NINDS and isresponsible for the fate of the brain collection, did not return a call fromUPI.

"The patients these brains were taken from suffered greatly before theydied of CJD," Heather Larson of Phoenix, whose mother succumbed toCJD last year at the age of 56, wrote in a letter to Arizona RepublicanSens. John McCain and Jon Kyl, and Republican Rep. John Shadegg."Their brains hold answers that can save human lives. Destroying thebrains at Bethesda would greatly hinder the research being done to fightthis disease and would cost many their lives."

The offices of McCain and Kyl did not return UPI's calls.

"The ravages of this disease, and the toll it takes not only on its victimsbut on family and loved ones, cannot easily be described to someone whohas not witnessed it personally," Patty Cook of Kansas City, Kan., wrotein a letter to Kansas Republican Sens. Sam Brownback and Pat Roberts,and Democratic Rep. Dennis Moore.

"I urge you to do whatever you can to ensure these brains are notdestroyed," added Cook, whose mother died of CJD in 1982.

Brownback's office did not return a call from UPI.

CJD belongs to a group of diseases -- called transmissible spongiformencephalopathies or TSEs -- that includes mad cow disease, chronicwasting disease in deer and elk, scrapie in sheep and several types ofCJD in humans. There is no cure for CJD and it typically results in deathwithin a year after the onset of symptoms.

Consumer groups also are concerned and are considering taking steps to




ensure the brain collection will be preserved.

"This is outrageous," Michael Hansen, a biologist and senior researchassociate with Consumers Union in Yonkers, N.Y., told UPI. "Thosebrains are a critical resource for CJD science and they must be at aresearch facility."

Hansen added that his late friend, Joe Gibbs, the former chief of NINDS'sLaboratory of Central Nervous System Studies, told him the brain of famedchoreographer George Balanchine, who died of CJD in 1983, resides in thecollection.

"How can we claim to be a scientific country if we're going to be throwingaway an irreplaceable repository of the first evidence of these diseases?"asked Felicia Nestor, who serves as a consultant to Public Citizen.

There may be hope yet for the collection, however.

Neil Cashman, an expert on TSEs at the University of Toronto's Center forResearch in Neurodegenerative Diseases, told UPI he has beenattempting to drum up support for acquiring the collection with hiscolleagues at the University of British Columbia in Vancouver -- where heplans to move this summer.

"I'm trying to organize support for an official letter from UBC to NIH torequest the collection," Cashman said.

The letter will probably go out in about a month, he said.

"The goal would be to make it a resource for the world and make thetissues available to scientists who had a reasonable request," he added.

Singeltary said he has heard from at least one other prominent scientist inthis field who said they planned to contact the NIH and urge it toreconsider the fate of the collection.

One brain in the collection, that of a French woman who died in 1971, mayhelp provide clues about the origins of variant CJD -- a condition similar toCJD that humans can contract from eating beef products contaminatedwith the mad-cow pathogen. The first recognized case of vCJD occurred in1995 in the United Kingdom, but an NIH scientist said he tested theFrench woman's brain in 2000 and found signs consistent with vCJD -- notCJD.

French researchers currently are re-examining specimens from the caseto determine if the woman was indeed infected with vCJD. If she was, itwould suggest the disease began infecting people more than 20 yearsearlier than previously thought.

Cashman said the case underscores the value of the NIH brain collection.

"There is information locked up in these freezers that will be lost forever ifthis collection is destroyed," he said.




--

E-mail: [email protected]

http://www.upi.com/Science_News/2005/04/01/Groups-seek-to-save-NIH-brain-collection/72961112392131/

NIH sends mixed signals on CJD brains

By STEVE MITCHELL, Medical Correspondent | April 7, 2005 at 3:30 PM

http://www.upi.com/Science_News/2005/04/07/NIH-sends-mixed-signals-on-CJD-brains/25701112902231/

NIH sends mixed signals on CJD brains

By Steve Mitchell Medical Correspondent


Questions linger in U.S. CJD cases

By STEVE MITCHELL, Senior Medical Correspondent | Oct. 21, 2005 at9:49 PM

http://www.upi.com/Questions-linger-in-US-CJD-cases/65761129945790/

From: TSS

Subject: CJD TISSUE DONATIONS FROM OUR LOVED ONES UP FORSALE TO HIGHEST BIDDERS

Date: June 14, 2006 at 6:40 am PST

Greetings CJD VOICE,

IF i would have been aware of all this greed, i would have never everdonated my mother's brain for research. NIH AND PFIZER SHOULD BEHELD ACCOUNTABLE for there disgraced actions. you cant tell me theydid not know. ...TSS

US scientist accused of selling tissue samples Deal said to earn $285,000for vials that cost millions By Diedtra Henderson, Globe Staff | June 14,2006


http://www.upi.com/Science_News/2005/04/01/Groups-seek-to-save-NIH-brain-collection/72961112392131/

http://www.upi.com/Science_News/2005/04/07/NIH-sends-mixed-signals-on-CJD-brains/25701112902231/


http://www.upi.com/Questions-linger-in-US-CJD-cases/65761129945790/



WASHINGTON -- A senior government scientist pocketed hundreds ofthousands of dollars as a drug company consultant in exchange for humantissue samples that cost the federal government millions to acquire,congressional investigators said yesterday .

The House Energy and Commerce Committee report, the culmination of aone-year inquiry, was released hours before a two-day hearing began toexplore the government's practices for procuring human tissue samples.According to congressional investigators, the National Institutes ofHealth's Dr. Trey Sunderland agreed to collaborate with Pfizer Inc. , theworld's largest drug company. Sunderland, chief of the geriatric psychiatrybranch of the National Institute for Mental Health , sent Pfizer 3,200 tubesof spinal fluid and 388 tubes of plasma collected for Alzheimer's research.

The government spent $6.4 million to obtain the 3,500 samples thatshowed how Alzheimer's disease progressed in 538 subjects.

Pfizer paid Sunderland $285,000 in consulting fees related to the samples,investigators said. In total, Pfizer paid him more than $600,000 from 1998to 2004 for outside consulting and speaking fees. Sunderland is scheduledto testify today at the hearing.

`̀ Contrary to the House committee report, Dr. Sunderland did not receiveany payments from Pfizer for human tissue samples," said Robert F.Muse, the scientist's Washington, D.C., attorney. `̀ He acted properly,ethically, and legally in his relationship with Pfizer."

Pfizer spokeswoman Kate Robins said the company had a transferagreement endorsed by the NIH that permitted Sunderland to sendcerebrospinal fluid from research participants with Alzheimer's, theparticipant's relatives who were at higher risk of developing the neurologicaldisease, and elderly adults with normal Alzheimer's risk.

Sunderland's consulting role tapped his Alzheimer's disease expertise tolook for signals in the samples that could help identify and diagnose thedisease.

`̀ The payments over a six-year period were reasonable and customary foran expert of Dr. Sunderland's stature, and reflect the fair-market value ofhis consulting services," Robins said.

The report said the tissue transfers, reported by a governmentwhistleblower, raised serious questions about how the governmentensures its scientists do not abuse their positions and about the agency'sability to track the valuable samples.

`̀ NIH tells us it has no centralized inventory system that could tell the NIHdirector how many vials of tissues are in freezers at a particular institute,"said Representative Joe Barton , Republican of Texas and House Energyand Commerce Committee chairman . `̀ It would really be a shame if wefind out that the National Institutes of Health has more control over itspaper clips and trash cans than it has over its human tissue samples."

John T. Burklow , a NIH spokesman, said the agency shares `̀ thecommittee's concerns in regard to the ethical management of humantissue samples."

Sunderland's arrangement with the drug maker -- made without NIHknowledge, according to Burklow -- occurred after the agency relaxed its




ethics policy covering scientists' outside activities and ended before theagency enacted more stringent rules.

The NIH, pressured by Barton's committee, on Aug. 25 curbed outsideconsulting deals between its scientists and pharmaceutical andbiotechnology companies.

Diedtra Henderson can be reached at [email protected].

© Copyright 2006 Globe Newspaper Company.

http://www.boston.com/business/globe/articles/2006/06/14/us_scientist_accused_of_selling_tissue_samples/

FOR IMMEDIATE RELEASE Tuesday, June 13, 2006

CONTACT: OD Office of Communications and Public Liaison 301-496-5787

NIH Statement Regarding House Hearing on Human Tissue SamplesAttribution: John Burklow, NIH spokesman

NIH’s position on ethics is clear: any conflict of interest resulting in anindividual personally profiting from official government research activitiescannot be tolerated. We are committed to maintaining the public’s trust inNIH and its scientists as an unbiased source of biomedical researchguidance and advice. The case under consideration concerns events thatbegan in 1998 — after the NIH ethics rules concerning outside activitieswere relaxed — and that ended before the new rules were put in place.NIH has previously referred this case to the relevant authorities forappropriate action.

It is important to note that the specific consulting arrangements inquestion, had they been known to NIH, would not have been approvedunder the present or previous ethics regulations. Outside consultingconnected to an NIH employee’s official government duties has alwaysbeen prohibited at NIH.

NIH has undertaken a comprehensive review of its activities and conflict ofinterest policies in the last few years. As a result of that process, onAugust 25, 2005, NIH implemented comprehensive ethics rules that makeit clear what NIH scientists can and cannot do in regard to outsideactivities. These new rules removed any ambiguity about what is allowedor not allowed. Here are two important points:

Under new NIH regulations, all NIH employees are now prohibited fromengaging in outside employment with pharmaceutical companies andbiotechnology companies in their private capacities — period.Collaboration and partnership with industry can nonetheless be veryvaluable in scientific pursuits and NIH rules allow such activities, as longas they are undertaken through an officially approved CooperativeResearch and Development Agreement (CRADA). Although we cannotdiscuss this particular case because it remains under investigation, wecan speak to the relevant issues that it raises.

Collaborations among scientists that involve human tissue samples arecommon and essential for science. There are, however, stringent rules in


http://www.boston.com/business/globe/articles/2006/06/14/us_scientist_accused_of_selling_tissue_samples/



place to protect the participants who donated their samples, and to ensurethat there is full informed consent.

We share the Committee’s concerns in regard to the ethical managementof human tissue samples and the development of rigorous and uniformpolicies to protect the public’s trust and interests, while advancing scienceto address important public health problems. The thousands of scientistswho work at NIH have always been and remain committed to theseprinciples.

The Office of the Director, the central office at NIH, is responsible forsetting policy for NIH, which includes 27 Institutes and Centers. Thisinvolves planning, managing, and coordinating the programs and activitiesof all NIH components. The Office of the Director also includes programoffices which are responsible for stimulating specific areas of researchthroughout NIH. Additional information is available athttp://www.nih.gov/icd/od/.

The National Institutes of Health (NIH) — The Nation's Medical ResearchAgency — includes 27 Institutes and Centers and is a component of theU.S. Department of Health and Human Services. It is the primary federalagency for conducting and supporting basic, clinical and translationalmedical research, and it investigates the causes, treatments, and curesfor both common and rare diseases. For more information about NIH andits programs, visit www.nih.gov.

http://www.nih.gov/news/pr/jun2006/od-13.htm

2016 BSE, Scrapie, CWD, Zoonosis CJD human TSE Prion disease

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 AgentsPathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologieMolécuIaires, Jouy-en-Josas. France


http://www.nih.gov/icd/od/

http://www.nih.gov/news/pr/jun2006/od-13.htm



Dietary exposure to bovine spongiform encephalopathy (BSE)contaminated bovine tissues is considered as the origin of variantCreutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is theonly recognized zoonotic prion. Despite the variety of TransmissibleSpongiform Encephalopathy (TSE) agents that have been circulating forcenturies in farmed ruminants there is no apparent epidemiological linkbetween exposure to ruminant products and the occurrence of other formof TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD).However, the zoonotic potential of the diversity of circulating TSE agentshas never been systematically assessed. The major issue in experimentalassessment 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, micegenetically engineered to express normal forms of the human prion proteinhas proved essential in studying human prions pathogenesis and modelingthe 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 humanPrPC (HuPrP-Tg). Two lines of mice expressing different forms of thehuman PrPC (129Met or 129Val) are used to determine the role of theMet129Val dimorphism in susceptibility/resistance to the different agents.

These transmission experiments confirm the ability of BSE prions topropagate in 129M- HuPrP-Tg mice and demonstrate that Met129homozygotes may be susceptible to BSE in sheep or goat to a greaterdegree than the BSE agent in cattle and that these agents can conveymolecular properties and neuropathological indistinguishable from vCJD.However homozygous 129V mice are resistant to all tested BSE derivedprions independently of the originating species suggesting a highertransmission barrier for 129V-PrP variant.

Transmission data also revealed that several scrapie prions propagate inHuPrP-Tg mice with efficiency comparable to that of cattle BSE. While theefficiency of transmission at primary passage was low, subsequentpassages resulted in a highly virulent prion disease in both Met129 andVal129 mice. Transmission of the different scrapie isolates in these miceleads to the emergence of prion strain phenotypes that showed similarcharacteristics to those displayed by MM1 or VV2 sCJD prion. Theseresults demonstrate that scrapie prions have a zoonotic potential and raisenew questions about the possible link between animal and human prions.

http://www.tandfonline.com/na101/home/literatum/publisher/tandf/journals/content/kprn20/2016/kprn20.v010.sup01/19336896.2016.1163048/20160418/19336896.2016.1163048.fp.png_v03

Research Project: TRANSMISSION, DIFFERENTIATION, ANDPATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORMENCEPHALOPATHIES

Title: Transmission of scrapie prions to primate after an extended silentincubation period

Authors

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


http://www.tandfonline.com/na101/home/literatum/publisher/tandf/journals/content/kprn20/2016/kprn20.v010.sup01/19336896.2016.1163048/20160418/19336896.2016.1163048.fp.png_v03



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

Interpretive Summary: The transmissible spongiform encephalopathies(also called prion diseases) are fatal neurodegenerative diseases thataffect animals and humans. The agent of prion diseases is a misfoldedform of the prion protein that is resistant to breakdown by the host cells.Since all mammals express prion protein on the surface of various cellssuch as neurons, all mammals are, in theory, capable of replicating priondiseases. One example of a prion disease, bovine spongiformencephalopathy (BSE; also called mad cow disease), has been shown toinfect cattle, sheep, exotic undulates, cats, non-human primates, andhumans when the new host is exposed to feeds or foods contaminatedwith the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent ofsheep scrapie. After an incubation period of approximately 10 years amacaque developed progressive clinical signs suggestive of neurologicdisease. Upon postmortem examination and microscopic examination oftissues, there was a widespread distribution of lesions consistent with atransmissible spongiform encephalopathy. This information will have ascientific impact since it is the first study that demonstrates thetransmission of scrapie to a non-human primate with a close geneticrelationship to humans. This information is especially useful to regulatoryofficials and those involved with risk assessment of the potentialtransmission of animal prion diseases to humans. Technical Abstract:Classical bovine spongiform encephalopathy (c-BSE) is an animal priondisease that also causes variant Creutzfeldt-Jakob disease in humans.Over the past decades, c-BSE's zoonotic potential has been the drivingforce in establishing extensive protective measures for animal and humanhealth.

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

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

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

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160

Scrapie to Humans USA?

1: Neuroepidemiology. 1985;4(4):240-9. Related Articles,

Links

Sheep consumption: a possible source of spongiform encephalopathy inhumans.


http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160



Davanipour Z, Alter M, Sobel E, Callahan M.

A fatal spongiform encephalopathy of sheep and goats (scrapie) sharesmany characteristics with Creutzfeldt-Jakob disease (CJD), a similardementing illness of humans. To investigate the possibility that CJD isacquired by ingestion of contaminated sheep products, we collectedinformation on production, slaughtering practices, and marketing of sheepin Pennsylvania. The study revealed that sheep were usually marketedbefore central nervous system signs of scrapie are expected to appear;breeds known to be susceptible to the disease were the most commonbreeds raised in the area; sheep were imported from other states includingthose with a high frequency of scrapie; use of veterinary services on thesheep farms investigated and, hence, opportunities to detect the diseasewere limited; sheep producers in the area knew little about scrapie despitethe fact that the disease has been reported in the area, and animal organsincluding sheep organs were sometimes included in processed food.Therefore, it was concluded that in Pennsylvania there are some 'weaklinks' through which scrapie-infected animals could contaminate humanfood, and that consumption of these foods could perhaps account forspongiform encephalopathy in humans. The weak links observed areprobably not unique to Pennsylvania.

PMID: 3915057 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract

2015

O.05: Transmission of prions to primates after extended silent incubationperiods: Implications for BSE and scrapie risk assessment in humanpopulations

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

Prion diseases (PD) are the unique neurodegenerative proteinopathiesreputed to be transmissible under field conditions since decades. Thetransmission of Bovine Spongiform Encephalopathy (BSE) to humansevidenced that an animal PD might be zoonotic under appropriateconditions. Contrarily, in the absence of obvious (epidemiological orexperimental) elements supporting a transmission or geneticpredispositions, PD, like the other proteinopathies, are reputed to occurspontaneously (atpical animal prion strains, sporadic CJD summing 80%of human prion cases). Non-human primate models provided the firstevidences supporting the transmissibiity of human prion strains and thezoonotic potential of BSE. Among them, cynomolgus macaques broughtmajor 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 PDfrom bovine, ovine and cervid origins even after very long silent incubationperiods.

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

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


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3915057&dopt=Abstract



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

***thus questioning the origin of human sporadic cases. We will presentan updated panorama of our different transmission studies and discuss theimplications of such extended incubation periods on risk assessment ofanimal PD for human health.

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

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

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

***our findings suggest that possible transmission risk of H-type BSE tosheep and human. Bioassay will be required to determine whether thePMCA products are infectious to these animals.

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

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

Tuesday, December 16, 2014

*** Evidence for zoonotic potential of ovine scrapie prions

Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1,Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5,Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & OlivierAndréoletti1, Affiliations Contributions Corresponding author Journal name:Nature Communications Volume: 5, Article number: 5821 DOI:doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10November 2014 Published 16 December 2014 Article tools CitationReprints Rights & permissions Article metrics

Abstract

Although Bovine Spongiform Encephalopathy (BSE) is the cause of variantCreutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential ofscrapie prions remains unknown. Mice genetically engineered tooverexpress the human prion protein (tgHu) have emerged as highlyrelevant models for gauging the capacity of prions to transmit to humans.These models can propagate human prions without any apparenttransmission barrier and have been used used to confirm the zoonoticability of BSE. Here we show that a panel of sheep scrapie prions transmitto several tgHu mice models with an efficiency comparable to that of cattleBSE.

***The serial transmission of different scrapie isolates in these mice led tothe propagation of prions that are phenotypically identical to those causingsporadic CJD (sCJD) in humans.


https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf



***These results demonstrate that scrapie prions have a zoonotic potentialand raise new questions about the possible link between animal andhuman prions.

Subject terms: Biological sciences• Medical research At a glance

http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html

see more here ;

http://www.nature.com/ncomms/2014/141216/ncomms6821/extref/ncomms6821-s1.pdf

***The serial transmission of different scrapie isolates in these mice led tothe propagation of prions that are phenotypically identical to those causingsporadic CJD (sCJD) in humans.***

***These results demonstrate that scrapie prions have a zoonotic potentialand raise new questions about the possible link between animal andhuman prions.***

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

5. A positive result from a chimpanzee challenged severly would likelycreate alarm in some circles even if the result could not be interpreted forman. I have a view that all these agents could be transmitted provided alarge enough dose by appropriate routes was given and the animals keptlong enough. Until the mechanisms of the species barrier are more clearlyunderstood it might be best to retain that hypothesis.

snip...

R. BRADLEY

http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf

1: J Infect Dis 1980 Aug;142(2):205-8

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie tononhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease ofsheep and goats were transmitted to squirrel monkeys (Saimiri sciureus)that were exposed to the infectious agents only by their nonforcedconsumption of known infectious tissues. The asymptomatic incubation


http://www.nature.com/ncomms/2014/141216/ncomms6821/full/ncomms6821.html

http://www.nature.com/ncomms/2014/141216/ncomms6821/extref/ncomms6821-s1.pdf




period in the one monkey exposed to the virus of kuru was 36 months;that in the two monkeys exposed to the virus of Creutzfeldt-Jakob diseasewas 23 and 27 months, respectively; and that in the two monkeysexposed to the virus of scrapie was 25 and 32 months, respectively.Careful physical examination of the buccal cavities of all of the monkeysfailed to reveal signs or oral lesions. One additional monkey similarlyexposed to kuru has remained asymptomatic during the 39 months that ithas been under observation.

snip...

The successful transmission of kuru, Creutzfeldt-Jakob disease, andscrapie by natural feeding to squirrel monkeys that we have reportedprovides further grounds for concern that scrapie-infected meat mayoccasionally give rise in humans to Creutzfeldt-Jakob disease.

PMID: 6997404


Recently the question has again been brought up as to whether scrapie istransmissible to man. This has followed reports that the disease has beentransmitted to primates. One particularly lurid speculation (Gajdusek 1977)conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob diseaseand transmissible encephalopathy of mink are varieties of a single "virus".The U.S. Department of Agriculture concluded that it could "no longerjustify or permit scrapie-blood line and scrapie-exposed sheep and goatsto be processed for human or animal food at slaughter or rendering plants"(ARC 84/77)" The problem is emphasised by the finding that some strainsof scrapie produce lesions identical to the once which characterise thehuman dementias"

Whether true or not. the hypothesis that these agents might betransmissible to man raises two considerations. First, the safety oflaboratory personnel requires prompt attention. Second, action such asthe "scorched meat" policy of USDA makes the solution of the acrapieproblem urgent if the sheep industry is not to suffer grievously.

snip...

76/10.12/4.6

http://web.archive.org/web/20010305223125/www.bseinquiry.gov.uk/files/yb/1976/10/12004001.pdf

snip...see full text ;

http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html

Monday, May 02, 2016

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




http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html



http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html

PRION 2016 TOKYO

Zoonotic Potential of CWD Prions: An Update

Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, DianeKofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5,Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6

1Department of Pathology, 3National Prion Disease PathologySurveillance Center, 5Department of Neurology, 6National Center forRegenerative Medicine, Case Western Reserve University, Cleveland, OH44106, USA.

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

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

Chronic wasting disease (CWD) is a widespread and highly transmissibleprion disease in free-ranging and captive cervid species in North America.The zoonotic potential of CWD prions is a serious public health concern,but the susceptibility of human CNS and peripheral organs to CWD prionsremains largely unresolved. We reported earlier that peripheral and CNSinfections were detected in transgenic mice expressing human PrP129Mor PrP129V. Here we will present an update on this project, includingevidence for strain dependence and influence of cervid PrP polymorphismson CWD zoonosis as well as the characteristics of experimental humanCWD prions.

PRION 2016 TOKYO

In Conjunction with Asia Pacific Prion Symposium 2016

PRION 2016 Tokyo

Prion 2016

http://prion2016.org/dl/newsletter_03.pdf

Prion 2016

Purchase options Price * Issue Purchase USD 198.00

http://www.tandfonline.com/toc/kprn20/10/sup1



http://prion2016.org/dl/newsletter_03.pdf

http://www.tandfonline.com/toc/kprn20/10/sup1



Cervid to human prion transmission

Kong, Qingzhong

Case Western Reserve University, Cleveland, OH, United States

Abstract

Prion disease is transmissible and invariably fatal. Chronic wastingdisease (CWD) is the prion disease affecting deer, elk and moose, and itis a widespread and expanding epidemic affecting 22 US States and 2Canadian provinces so far. CWD poses the most serious zoonotic priontransmission risks in North America because of huge venisonconsumption (>6 million deer/elk hunted and consumed annually in theUSA alone), significant prion infectivity in muscles and other tissues/fluidsfrom CWD-affected cervids, and usually high levels of individual exposureto CWD resulting from consumption of the affected animal among oftenjust family and friends. However, we still do not know whether CWD prionscan infect humans in the brain or peripheral tissues or whetherclinical/asymptomatic CWD zoonosis has already occurred, and we haveno essays to reliably detect CWD infection in humans. We hypothesizethat:

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

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

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

(4) CWD transmission to humans has already occurred. We will test thesehypotheses in 4 Aims using transgenic (Tg) mouse models andcomplementary in vitro approaches.

Aim 1 will prove that the classical CWD strain may infect humans in brainor peripheral lymphoid tissues at low levels by conducting systemicbioassays in a set of "humanized" Tg mouse lines expressing commonhuman PrP variants using a number of CWD isolates at varying doses androutes. Experimental "human CWD" samples will also be generated forAim 3.

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

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




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

Public Health Relevance There are significant and increasing humanexposure to cervid prions because chronic wasting disease (CWD, awidespread and highly infectious prion disease among deer and elk inNorth America) continues spreading and consumption of venison remainspopular, but our understanding on cervid-to-human prion transmission isstill very limited, raising public health concerns. This proposal aims todefine the zoonotic risks of cervid prions and set up and apply essays todetect CWD zoonosis using mouse models and in vitro methods. Thefindings will greatly expand our knowledge on the potentials andcharacteristics of cervid prion transmission in humans, establish reliableessays for such infections and may discover the first case(s) of CWDinfection in humans.

Funding Agency Agency National Institute of Health (NIH)

Institute National Institute of Neurological Disorders and Stroke (NINDS)

Type Research Project (R01)

Project # 1R01NS088604-01A1

Application # 9037884

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

Program Officer Wong, May

Project Start 2015-09-30

Project End 2019-07-31

Budget Start 2015-09-30

Budget End 2016-07-31

Support Year 1

Fiscal Year 2015




Total Cost $337,507

Indirect Cost $118,756

Institution

Name Case Western Reserve University

Department Pathology

Type Schools of Medicine

DUNS # 077758407

City Cleveland

State OH

Country United States

Zip Code 44106

http://grantome.com/grant/NIH/R01-NS088604-01A1

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

We hypothesize that:

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

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

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

(4) *** CWD transmission to humans has already occurred. *** We willtest these hypotheses in 4 Aims using transgenic (Tg) mouse models andcomplementary in vitro approaches.

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


http://grantome.com/grant/NIH/R01-NS088604-01A1



=======

Key Molecular Mechanisms of TSEs

Zabel, Mark D.

Colorado State University-Fort Collins, Fort Collins, CO, United StatesAbstract Prion diseases, or transmissible spongiform encephalopathies(TSEs), are fatal neurodegenerative diseases affecting humans, cervids,bovids, and ovids. The absolute requirement of PrPC expression togenerate prion diseases and the lack of instructional nucleic acid defineprions as unique infectious agents. Prions exhibit species-specifictropism, inferring that unique prion strains exist that preferentially infctcertain host species and confront transmission barriers to heterologoushost species. However, transmission barriers are not absolute. Scientificconsensus agrees that the sheep TSE scrapie probably breached thetransmission barrier to cattle causing bovine spongiform encephalopathythat subsequently breached the human transmission barrier and likelycaused several hundred deaths by a new-variant form of the human TSECreutzfeldt-Jakob disease in the UK and Europe. The impact to humanhealth, emotion and economies can still be felt in areas like farming, bloodand organ donations and the threat of a latent TSE epidemic. Thisprecedent raises the real possibility of other TSEs, like chronic wastingdisease of cervids, overcoming similar human transmission barriers. Agroundbreaking discovery made last year revealed that mice infected withheterologous prion strains facing significant transmission barriersreplicated prions far more readily in spleens than brains6. Furthermore,these splenic prions exhibited weakened transmission barriers andexpanded host ranges compared to neurogenic prions. These dataquestion conventional wisdom of avoiding neural tissue to avoid prionxenotransmission, when more promiscuous prions may lurk in extraneuraltissues. Data derived from work previously funded by NIH demonstrate thatComplement receptors CD21/35 bind prions and high density PrPC anddifferentially impact prion disease depending on the prion isolate or strainused. Recent advances in live animal and whole organ imaging have led usto generate preliminary data to support novel, innovative approaches toassessing prion capture and transport. We plan to test our unifyinghypothesis for this proposal that CD21/35 control the processes ofperipheral prion capture, transport, strain selection and xenotransmissionin the following specific aims. 1. Assess the role of CD21/35 in splenicprion strain selection and host range expansion. 2. Determine whetherCD21/35 and C1q differentially bind distinct prion strains 3. Monitor theeffects of CD21/35 on prion trafficking in real time and space 4. Assessthe role of CD21/35 in incunabular prion trafficking

Public Health Relevance Transmissible spongiform encephalopathies, orprion diseases, are devastating illnesses that greatly impact public health,agriculture and wildlife in North America and around the world. The impactto human health, emotion and economies can still be felt in areas likefarming, blood and organ donations and the threat of a latent TSEepidemic. This precedent raises the real possibility of other TSEs, likechronic wasting disease (CWD) of cervids, overcoming similar humantransmission barriers. Early this year Canada reported its first case ofBSE in over a decade audits first case of CWD in farmed elk in threeyears, underscoring the need for continued vigilance and research.Identifying mechanisms of transmission and zoonoses remains anextremely important and intense area of research that will benefit humanand other animal populations.


Institute National Institute of Allergy and Infectious Diseases (NIAID)

Type High Priority, Short Term Project Award (R56)




Project # 1R56AI122273-01A1



Program Officer Beisel, Christopher E

Project Start 2016-02-16




Support Year 1

Fiscal Year 2016

Total Cost

Indirect Cost Institution Name Colorado State University-Fort Collins

Department Microbiology/Immun/Virology

Type Schools of Veterinary Medicine

DUNS # 785979618 City Fort Collins

State CO


Zip Code 80523

http://grantome.com/grant/NIH/R56-AI122273-01A1

PMCA Detection of CWD Infection in Cervid and Non-Cervid Species


http://grantome.com/grant/NIH/R56-AI122273-01A1



Hoover, Edward Arthur

Colorado State University-Fort Collins, Fort Collins, CO, United StatesAbstract Chronic wasting disease (CWD) of deer and elk is an emerginghighly transmissible prion disease now recognized in 18 States, 2Canadian provinces, and Korea. We have shown that Infected deer harborand shed high levels of infectious prions in saliva, blood, urine, and feces,and in the tissues generating those body fluids and excreta, therebyleading to facile transmission by direct contact and environmentalcontamination. We have also shown that CWD can infect some non-cervidspecies, thus the potential risk CWD represents to domestic animalspecies and to humans remains unknown. Whether prions borne in blood,saliva, nasal fluids, milk, or excreta are generated or modified in theproximate peripheral tissue sites, may differ in subtle ways from thosegenerated in brain, or may be adapted for mucosal infection remain openquestions. The increasing parallels in the pathogenesis between priondiseases and human neurodegenerative conditions, such as Alzheimer'sand Parkinson's diseases, add relevance to CWD as a transmissibleprotein misfolding disease. The overall goal of this work is to elucidate theprocess of CWD prion transmission from mucosal secretory and excretorytissue sites by addressing these questions: (a) What are the kinetics andmagnitude of CWD prion shedding post-exposure? (b) Are excreted prionsbiochemically distinct, or not, from those in the CNS? (c) Are peripheralepithelial or CNS tissues, or both, the source of excreted prions? and (d)Are excreted prions adapted for horizontal transmission via natural/trans-mucosal routes? The specific aims of this proposal are: (1) To determinethe onset and consistency of CWD prion shedding in deer and cervidizedmice; (2); To compare the biochemical and biophysical properties ofexcretory vs. CNS prions; (3) To determine the capacity of peripheraltissues to support replication of CWD prions; (4) To determine theprotease- sensitive infectious fraction of excreted vs. CNS prions; and (5)To compare the mucosal infectivity of excretory vs. CNS prions.Understanding the mechanisms that enable efficient prion disseminationand shedding will help elucidate how horizontally transmissible prionsevolve and succeed, and is the basis of this proposal. Understanding howinfectious misfolded proteins (prions) are generated, trafficked, shed, andtransmitted will aid in preventing, treating, and managing the risksassociated with these agents and the diseases they cause.

Public Health Relevance Chronic wasting disease (CWD) of deer and elkis an emergent highly transmissible prion disease now recognizedthroughout the USA as well as in Canada and Korea. We have shown thatinfected deer harbor and shed high levels of infectious prions in saliva,blood, urine, and feces thereby leading to transmission by direct contactand environmental contamination. In that our studies have also shown thatCWD can infect some non-cervid species, the potential risk CWD mayrepresents to domestic animal species and humans remains unknown.The increasing parallels in the development of major humanneurodegenerative conditions, such as Alzheimer's and Parkinson'sdiseases, and prion diseases add relevance to CWD as a model of atransmissible protein misfolding disease. Understanding how infectiousmisfolded proteins (prions) are generated and transmitted will aid ininterrupting, treating, and managing the risks associated with theseagents and the diseases they cause.


Institute National Institute of Neurological Disorders and Stroke (NINDS)

Type Research Project (R01)

Project # 4R01NS061902-07






Program Officer Wong, May Project Start 2009-09-30




Support Year 7

Fiscal Year 2016

Total Cost $409,868

Indirect Cost $134,234 Institution Name Colorado State University-FortCollins

Department Microbiology/Immun/Virology

Type Schools of Veterinary Medicine

DUNS # 785979618 City Fort Collins

State CO


Zip Code 80523

http://grantome.com/grant/NIH/R01-NS061902-07

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 havezoonotic potential, at least as judged by the compatibility of CWD prionsand their human PrPC target. Furthermore, extrapolation from this simplein vitro assay suggests that if zoonotic CWD occurred, it would most likelyeffect those of the PRNP codon 129-MM genotype and that the PrPrestype would be similar to that found in the most common subtype of sCJD(MM1).***


http://grantome.com/grant/NIH/R01-NS061902-07



https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249

PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TOHUMANS

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

O18

Zoonotic Potential of CWD Prions

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, DianeKofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1CaseWestern Reserve University, Cleveland, Ohio, USA, 2Second University ofNaples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

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

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

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

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

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

Kristen Davenport, Davin Henderson, Candace Mathiason, and EdwardHoover Prion Research Center; Colorado State University; Fort Collins, COUSA

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

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

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

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





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

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

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

Transmissible Spongiform Encephalopathy TSE PRION update January 2,2014

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

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

http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm

http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html

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


*** The potential impact of prion diseases on human health was greatlymagnified by the recognition that interspecies transfer of BSE to humansby beef ingestion resulted in vCJD. While changes in animal feedconstituents and slaughter practices appear to have curtailed vCJD, thereis concern that CWD of free-ranging deer and elk in the U.S. might alsocross the species barrier. Thus, consuming venison could be a source ofhuman prion disease. Whether BSE and CWD represent interspeciesscrapie transfer or are newly arisen prion diseases is unknown. Therefore,the possibility of transmission of prion disease through other food animalscannot be ruled out. There is evidence that vCJD can be transmittedthrough blood transfusion. There is likely a pool of unknown size ofasymptomatic individuals infected with vCJD, and there may beasymptomatic individuals infected with the CWD equivalent. Thesecircumstances represent a potential threat to blood, blood products, andplasma supplies.

http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf

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

CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITEDKINGDOM THIRD ANNUAL REPORT AUGUST 1994


https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

http://wwwnc.cdc.gov/eid/article/20/1/13-0858_article.htm

http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html


http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf



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

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

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

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

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

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

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

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

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

snip...

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

snip...

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

snip...

In the study in the USA, a range of foodstuffs were associated with anincreased risk of CJD, including liver consumption which was associated




with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. Bycomparing the data from 3 studies in relation to this particular dietaryfactor, the risk of liver consumption became non-significant with an oddsratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN.ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;

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 LodgeSpencers 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 thirdannual report from the CJD Surveillance Unit. I am sorry that you aredissatisfied with the way in which this report was published.

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

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

The statistical results reqarding the consumption of venison was put intoperspective in the body of the report and was not mentioned at all in thepress release. Media attention regarding this report was low key but gavea realistic presentation of the statistical findings of the Unit. This approachto publication was successful in that consumption of venison washighlighted only once by the media ie. in the News at one televisionproqramme.

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

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







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


Wednesday, May 25, 2016

USDA APHIS National Scrapie TSE Prion Eradication Program April 2016Monthly Report Prion 2016 Tokyo Update

http://scrapie-usa.blogspot.com/2016/05/usda-aphis-national-scrapie-tse-prion.html

***Moreover, sporadic disease has never been observed in breedingcolonies or primate research laboratories, most notably among hundredsof animals over several decades of study at the National Institutes ofHealth25, and in nearly twenty older animals continuously housed in ourown facility.***

http://www.nature.com/articles/srep11573

Thursday, March 29, 2012

*** atypical Nor-98 Scrapie has spread from coast to coast in the USA2012

NIAA Annual Conference April 11-14, 2011San Antonio, Texas

http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html


APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee onAnimal Health; Meeting May 2, 2016, and June 16, 2016 SingeltarySubmission

http://animalhealthreportpriontse.blogspot.com/2016/04/aphis-docket-no-aphis-2016-0029.html

Thursday, September 10, 2015

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



http://scrapie-usa.blogspot.com/2016/05/usda-aphis-national-scrapie-tse-prion.html

http://www.nature.com/articles/srep11573

http://nor-98.blogspot.com/2012/03/atypical-nor-98-scrapie-has-spread-from.html




http://tseac.blogspot.com/2015/09/25th-meeting-of-transmissible.html

Thursday, June 9, 2016

Advisory Committee; Transmissible Spongiform EncephalopathiesAdvisory Committee; Termination

http://tseac.blogspot.com/2016/06/advisory-committee-transmissible.html

Sent: Monday, January 08,2001 3:03 PM

TO: [email protected]

FDA CJD BSE TSE Prion Scientific Advisors and Consultants StaffJanuary 2001 Meeting Singeltary Submission

2001 FDA CJD TSE Prion Singeltary Submission

http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf

15 November 1999

British Medical Journal

vCJD in the USA * BSE in U.S.

http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us

2 January 2000


U.S. Scientist should be concerned with a CJD epidemic in the U.S., aswell

http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February14, 2001 JAMA


http://tseac.blogspot.com/2015/09/25th-meeting-of-transmissible.html

http://tseac.blogspot.com/2016/06/advisory-committee-transmissible.html







To the Editor: In their Research Letter, Dr Gibbons and colleagues1reported that the annual US death rate due to Creutzfeldt-Jakob disease(CJD) has been stable since 1985. These estimates, however, are basedonly on reported cases, and do not include misdiagnosed or preclinicalcases. It seems to me that misdiagnosis alone would drastically changethese figures. An unknown number of persons with a diagnosis ofAlzheimer disease in fact may have CJD, although only a small number ofthese patients receive the postmortem examination necessary to makethis diagnosis. Furthermore, only a few states have made CJD reportable.Human and animal transmissible spongiform encephalopathies should bereportable nationwide and internationally.

Terry S. Singeltary, Sr Bacliff, Tex

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

http://jama.jamanetwork.com/article.aspx?articleid=1031186

26 March 2003

Terry S. Singeltary, retired (medically) CJD WATCH

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like tocomment on the CDC's attempts to monitor the occurrence of emergingforms of CJD. Asante, Collinge et al [1] have reported that BSEtransmission to the 129-methionine genotype can lead to an alternatephenotype that is indistinguishable from type 2 PrPSc, the commonestsporadic CJD. However, CJD and all human TSEs are not reportablenationally. CJD and all human TSEs must be made reportable in everystate and internationally. I hope that the CDC does not continue to expectus to still believe that the 85%+ of all CJD cases which are sporadic areall spontaneous, without route/source. We have many TSEs in the USA inboth animal and man. CWD in deer/elk is spreading rapidly and CWDdoes transmit to mink, ferret, cattle, and squirrel monkey by intracerebralinoculation. With the known incubation periods in other TSEs, oraltransmission studies of CWD may take much longer. Every victim/familyof CJD/TSEs should be asked about route and source of this agent. Toprolong this will only spread the agent and needlessly expose others. Inlight of the findings of Asante and Collinge et al, there should be drasticmeasures to safeguard the medical and surgical arena from sporadic CJDsand all human TSEs. I only ponder how many sporadic CJDs in the USAare type 2 PrPSc?

http://www.neurology.org/content/60/2/176/reply#neurology_el_535

re-Human Prion Diseases in the United States

Posted by flounder on 01 Jan 2010 at 18:11 GMT

http://www.plosone.org/annotation/listThread.action?root=363







Sent: Monday, January 08,2001 3:03 PM

TO: [email protected]

FDA CJD BSE TSE Prion Scientific Advisors and Consultants StaffJanuary 2001 Meeting Singeltary Submission

2001 FDA CJD TSE Prion Singeltary Submission


15 November 1999


vCJD in the USA * BSE in U.S.


2 January 2000


U.S. Scientist should be concerned with a CJD epidemic in the U.S., aswell



Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February14, 2001 JAMA


To the Editor: In their Research Letter, Dr Gibbons and colleagues1reported that the annual US death rate due to Creutzfeldt-Jakob disease(CJD) has been stable since 1985. These estimates, however, are basedonly on reported cases, and do not include misdiagnosed or preclinicalcases. It seems to me that misdiagnosis alone would drastically changethese figures. An unknown number of persons with a diagnosis ofAlzheimer disease in fact may have CJD, although only a small number ofthese patients receive the postmortem examination necessary to makethis diagnosis. Furthermore, only a few states have made CJD reportable.Human and animal transmissible spongiform encephalopathies should bereportable nationwide and internationally.







Terry S. Singeltary, Sr Bacliff, Tex

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


26 March 2003

Terry S. Singeltary, retired (medically) CJD WATCH

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like tocomment on the CDC's attempts to monitor the occurrence of emergingforms of CJD. Asante, Collinge et al [1] have reported that BSEtransmission to the 129-methionine genotype can lead to an alternatephenotype that is indistinguishable from type 2 PrPSc, the commonestsporadic CJD. However, CJD and all human TSEs are not reportablenationally. CJD and all human TSEs must be made reportable in everystate and internationally. I hope that the CDC does not continue to expectus to still believe that the 85%+ of all CJD cases which are sporadic areall spontaneous, without route/source. We have many TSEs in the USA inboth animal and man. CWD in deer/elk is spreading rapidly and CWDdoes transmit to mink, ferret, cattle, and squirrel monkey by intracerebralinoculation. With the known incubation periods in other TSEs, oraltransmission studies of CWD may take much longer. Every victim/familyof CJD/TSEs should be asked about route and source of this agent. Toprolong this will only spread the agent and needlessly expose others. Inlight of the findings of Asante and Collinge et al, there should be drasticmeasures to safeguard the medical and surgical arena from sporadic CJDsand all human TSEs. I only ponder how many sporadic CJDs in the USAare type 2 PrPSc?


Alzheimer-type brain pathology may be transmitted by grafts of dura mater

26/01/2016

http://blog.smw.ch/alzheimer-type-brain-pathology-may-be-transmitted-by-grafts-of-dura-mater/#comment-89016



http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments





http://blog.smw.ch/alzheimer-type-brain-pathology-may-be-transmitted-by-grafts-of-dura-mater/#comment-89016



http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments




http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d


BSE prions propagate as either variant CJD-like or sporadic CJD-like prionstrains in transgenic mice expressing human prion protein

*** Surprisingly, however, BSE transmission to these transgenic mice, inaddition to producing a vCJD-like phenotype, can also result in a distinctmolecular phenotype that is indistinguishable from that of sporadic CJDwith PrPSc type 2.

These data suggest that more than one BSEderived prion strain mightinfect humans;

***it is therefore possible that some patients with a phenotype consistentwith sporadic CJD may have a disease arising from BSE exposure.

snip...

These studies further strengthen the evidence that vCJD is caused by aBSE-like prion strain.

Also, remarkably, the key neuropathological hallmark of vCJD, thepresence of abundant florid PrP plaques, can be recapitulated on BSE orvCJD transmission to these mice.

***However, the most surprising aspect of the studies was the finding thatan alternate pattern of disease can be induced in 129MM Tg35 mice fromprimary transmission of BSE, with a molecular phenotypeindistinguishable from that of a subtype of sporadic CJD. This finding hasimportant potential implications as it raises the possibility that somehumans infected with BSE prions may develop a clinical diseaseindistinguishable from classical CJD associated with type 2 PrPSc. Thisis, in our experience, the commonest molecular sub-type of sporadic CJD.In this regard, it is of interest that the reported incidence of sporadic CJDhas risen in the UK since the 1970s (Cousens et al., 1997)...

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/pdf/cdf653.pdf

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

Subject: re-BSE prions propagate as either variant CJD-like or sporadicCJD

Date: Thu, 28 Nov 2002 10:23:43 -0000

From: "Asante, Emmanuel A" [email protected]


http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/pdf/cdf653.pdf



To: "'[email protected]'" [email protected]

Dear Terry,

I have been asked by Professor Collinge to respond to your request. I ama Senior Scientist in the MRC Prion Unit and the lead author on the paper.I have attached a pdf copy of the paper for your attention.

Thank you for your interest in the paper.

In respect of your first question, the simple answer is, ***yes. As you willfind in the paper, we have managed to associate the alternate phenotypeto type 2 PrPSc, the commonest sporadic CJD. It is too early to be ableto claim any further sub-classification in respect of Heidenhain variant CJDor Vicky Rimmer's version. It will take further studies, which are on-going,to establish if there are sub-types to our initial finding which we are nowreporting. The main point of the paper is that, as well as leading to theexpected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which isindistinguishable from type 2 PrPSc.

I hope reading the paper will enlighten you more on the subject. If I can beof any further assistance please to not hesitate to ask. Best wishes.

Emmanuel Asante

<>

____________________________________

Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. ImperialCollege School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PGTel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email:[email protected] (until 9/12/02) New e-mail: [email protected](active from now)

____________________________________

Thursday, August 12, 2010

Seven main threats for the future linked to prions

First threat

The TSE road map defining the evolution of European policy for protectionagainst prion diseases is based on a certain numbers of hypotheses someof which may turn out to be erroneous. In particular, a form of BSE (calledatypical Bovine Spongiform Encephalopathy), recently identified bysystematic testing in aged cattle without clinical signs, may be the originof classical BSE and thus potentially constitute a reservoir, which may beimpossible to eradicate if a sporadic origin is confirmed.




***Also, a link is suspected between atypical BSE and some apparentlysporadic cases of Creutzfeldt-Jakob disease in humans. These atypicalBSE cases constitute an unforeseen first threat that could sharply modifythe European approach to prion diseases.

Second threat

snip...

http://www.neuroprion.org/en/np-neuroprion.html

Monday, October 10, 2011

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

snip...

EFSA and the European Centre for Disease Prevention and Control(ECDC) recently delivered a scientific opinion on any possibleepidemiological or molecular association between TSEs in animals andhumans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011).This opinion confirmed Classical BSE prions as the only TSE agentsdemonstrated to be zoonotic so far

*** but the possibility that a small proportion of human cases so farclassified as "sporadic" CJD are of zoonotic origin could not be excluded.Moreover, transmission experiments to non-human primates suggest thatsome TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible minkencephalopathy (TME) and chronic wasting disease (CWD) agents) mighthave zoonotic potential.

snip...

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

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

early days BSE and nvCJD UK

5.195 Among occupational groups exposed to BSE, farmers remainunusual in having such an excess over the incidence of CJD for thepopulation as a whole. No cases of CJD have been reported amountveterinarians exposed to BSE. Four people in the meat industry (butchers,abattoirs, rendering plants, etc) have been reported to have vCJD.386 Thepresent evidence has been accepted by some as reassuring in that suchoccupations may not pose as serious a risk as might have been expected.

http://collections.europarchive.org/tna/20080102111737/http://www.bseinquiry.gov.uk/pdf/volume8/chapter5.pdf


http://www.neuroprion.org/en/np-neuroprion.html

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

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

http://collections.europarchive.org/tna/20080102111737/http://www.bseinquiry.gov.uk/pdf/volume8/chapter5.pdf



This was not simply another farmer but the third farmer......


suspect case of CJD in a farmer who has had a case of BSE in his beefsuckler herd.


cover-up of 4th farm worker ???



CONFIRMATION OF CJD IN FOURTH FARMER


now story changes from;

SEAC concluded that, if the fourth case were confirmed, it would beworrying, especially as all four farmers with CJD would have had BSEcases on their farms.

to;

This is not unexpected...

was another farmer expected?


4th farmer, and 1st teenager












2. snip...

Over a 5 year period, which is the time period on which the advice fromProfessor Smith and Dr. Gore was based, and assuming a population of120,000 dairy farm workers, and an annual incidence of 1 per millioncases of CJD in the general population, a DAIRY FARM WORKER IS 5TIMES MORE LIKELY THAN an individual in the general population todevelop CJD. Using the actual current annual incidence of CJD in the UKof 0.7 per million, this figure becomes 7.5 TIMES.

3. You will recall that the advice provided by Professor Smith in 1993 andby Dr. Gore this month used the sub-population of dairy farm workers whohad had a case of BSE on their farms - 63,000, which is approximatelyhalf the number of dairy farm workers - as a denominator. If the abovesums are repeated using this denominator population, taking an annualincidence in the general population of 1 per million the observed rate in thissub-population is 10 TIMES, and taking an annual incidence of 0.7 permillion, IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than that inthe general population...


CJD FARMERS WIFE 1989



20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A19 year old died from sCJD in France in 1985. There is no evidence of aniatrogenic cause for those cases....


THE COVER UP OF MAD COW DISEASE IN FARMERS, FARMERSWIVES, AND VICKY RIMMER, THE DAY MAD COW SCIENCECHANGED $$$


*** SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMSWITH BSE HERD AND ABATTOIRS ***

http://bseinquiry.blogspot.com/2008/05/sporadic-cjd-in-farmers-farmers-wives.html

DOES ANYONE BESIDES ME SEE A PATTERN YET ???

Vickey Rimmer, 16, DID NOT DIE FROM nvCJD, she died from a form of






http://bseinquiry.blogspot.com/2008/05/sporadic-cjd-in-farmers-farmers-wives.html



sporadic CJD, whatever the hell that is. and there have been 16 year olddie from sporadic CJD in the USA as well.

SIMPLY PUT, the ukbsenvcjd only theory was wrong from day one. theelderly are expendable, pets and kids are not.

Science was dictated by 'big buisness' after the Vickey Rimmer case withthe ukbsenvcjd only myth.

and there have been 16 year old die from sporadic CJD in the USA as well.

snip...

I have interviewed Mrs Rimmer at my constituency surgery

IF there is nothing to hide, why is there so much SECRECY? WHY is theGovernment and other Bodies trying to stop any CHANCE OF PEOPLECONNECTING THE TWO DISEASES. The B.S.E. problem is obvious, butif the correct measures are taken, surely the problem could be contained,however, as it stands the lack of investigation and interest of thepossibility of B.S.E. and C.J.D. being linked is open for speculation andsurely someone has to account for peoples lives! WHY is so much troublebeing taken to convice people that B.S.E. and C.J.D. are not linked?Guilty Conscience perhaps ? - or cover up?

HOUSE OF COMMONS

FROM BARRY JONES, M.P.

22 FEBRUARY 1994


Alleged Case of Creutzfeld Jakob Disease: Victoria Rimmer.

(now story changes that biopsy shows she does not have CJD...tss)


now story changes to ;

Advice

7. The Parliamentary Secretary is invited to note the recent statementsmade on __________ and the present position which remains that CJDcannot be confirmed, in this case at this stage.







3. The Medical Director at ___________________ Hospital advised theDepartment on 6 June that the results of ___________________ brainbiopsy had been received and that it showed NO EVIDENCE OF CJD.______________ Hospital subsequently issued a statement to the pressto this effect and this was publicised widely in the press (doc 1). Newscoverage which followed suggested that the statement made by________________ Hospital had been misleading (doc 2). Enquires havebeen made of the Medical Director at _______________ Hospital who hasCONFIRMED THAT THE STATEMENT ISSUED BY THE HOSPITAL WASISSUED IN ERROR. The facts are that two pathology reports on the samepiece of brain tissue were recieved. The first report indicated that CJD wasunlikely, The second report indicated that CJD was possible, PERHAPSEVEN LIKELY, but that no definitive diagnosis could be made before apost mortem was undertaken.


MAD COW MEAL DESTROYED MY DAUGHTERS LIFE

A TEENAGE GIRL may have caught the human form of MAD COWDISEASE by eating a contaminated burger it was claimed last night.

VICKY RIMMER, 16, has the killer Creutzfeldt-Jakob disease (CJD).


GIVE ME BACK MY LIFE

THEY BEGGED ME TO HUSH IT UP – GRAN’S AGONY


HUSH UP! GOVERNMENT TOLD GRAN: ''YOU MUST THINK OF THEECONOMY''


WHY IS MY GIRL DYING ? '' IT WAS LIKE SOMEBODY OLD INSIDE AYOUNG PERSON'S BODY


Wednesday, October 09, 2013










*** WHY THE UKBSEnvCJD ONLY THEORY IS SO POPULAR IN IT'SFALLACY, £41,078,281 in compensation ***

http://creutzfeldt-jakob-disease.blogspot.com/2013/10/why-ukbsenvcjd-only-theory-is-so.html

Friday, October 23, 2015

*** CJD FOUNDATION CREUTZFELDT JAKOB DISEASE TSE PRIONQUESTIONNAIRE UPDATE OCTOBER 2015 ***

http://cjdquestionnaire.blogspot.com/2015/10/cjd-foundation-creutzfeldt-jakob.html

DEATH CERTIFICATES, CJD, AND CODING ERRORS

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m26a/tab01.pdf


routine passive mortality CJD surveillance USA ?

THIS has been proven not to be very useful in the U.K.;

THE EPIDEMIOLOGY OF CJD RG WILL 1984 (182 PAGES)

snip...

One reason for this was the _inaccuracy_ in coding of cases correctlycertified as CJD Coding is carried out by staff who are not medicallyqualified and it is not surprising that coding errors occur in the processingof large numbers of certificates. In 1982, 12,000 certificates per week wereprocessed at the office of population censuses and surveys by 15 codersand 6 checkers (Alderson et al., 1983). The occurrence of both inter- andintra-observer coding errors has been described (Curb et al., 1983) and the_inaccuracies_ of BOTH certification and coding discovered in this study_support_ the introduction of a more accurate system of death certificatesand a more detailed and specific coding system...

snip...

http://web.archive.org/web/20040521215716/http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf

Draft Proposal For The Monitoring of Creutzfeldt-Kakob Disease 1989 Dr.R. Will


http://creutzfeldt-jakob-disease.blogspot.com/2013/10/why-ukbsenvcjd-only-theory-is-so.html

http://cjdquestionnaire.blogspot.com/2015/10/cjd-foundation-creutzfeldt-jakob.html



http://web.archive.org/web/20040521215716/http://www.bseinquiry.gov.uk/files/mb/m26/tab01.pdf



snip...

IDENTIFICATION OF CASES

Cases of CJD may be identified from death certificates, but this alone isunlikely to provide adequate monitoring. ERRORS are made in certificationand diagnosis; in the Oxford study death certificates were obtained on aseries of known confirmed cases and CJD was mentioned in only 66% ofcertificates. In another series of 175 certified cases, 42 patients werejudged not to have suffered from CJD after examination of case notes (7)...

full text;


2001 Deepthroat to Singeltary

The most frightening thing I have read all day is the report of Gambetti'sfinding of a new strain of sporadic cjd in young people.........Dear God,what in the name of all that is holy is that!!! If the US has different strainsof scrapie.....why???? than the UK...then would the same mechanismsthat make different strains of scrapie here make different strains of BSE...ifthe patterns are different in sheep and mice for scrapie.....could not theBSE be different in the cattle, in the mink, in the humans.......I really thinkthe slides or tissues and everything from these young people with the newstrain of sporadic cjd should be put up to be analyzed by many, manyexperts in cjd........bse.....scrapie Scrape the damn slide and put it intomice.....wait.....chop up the mouse brain and and spinal cord........put intosome more mice.....dammit amplify the thing and start the damnedresearch.....This is NOT rocket science...we need to use what we knowand get off our butts and move....the whining about how long everythingtakes.....well it takes a whole lot longer if you whine for a year and thenstart the research!!! Not sure where I read this but it was a recent pressrelease or something like that: I thought I would fall out of my chair when Iread about how there was no worry about infectivity from a histopath slideor tissues because they are preserved in formic acid, or formalin orformaldehyde.....for God's sake........ Ask any pathologist in the UK whatthe brain tissues in the formalin looks like after a year.......it is a big fatsponge...the agent continues to eat the brain ......you can't make slidesanymore because the agent has never stopped........and the old slides thatare stained with Hemolysin and Eosin......they get holier and holier anddegenerate and continue...what you looked at 6 months ago is notthere........Gambetti better be photographing every damned thing he islooking at.....

Okay, you need to know. You don't need to pass it on as nothing willcome of it and there is not a damned thing anyone can do about it. Don'teven hint at it as it will be denied and laughed at.......... USDA is gonna doas little as possible until there is actually a human case in the USA of thenvcjd........if you want to move this thing along and shake the earth....thenwe gotta get the victims families to make sure whoever is doing theautopsy is credible, trustworthy, and a saint with the courage of Joan ofArc........I am not kidding!!!! so, unless we get a human death fromEXACTLY the same form with EXACTLY the same histopath lesions asseen in the UK nvcjd........forget any action........it is ALL gonna besporadic!!!

And, if there is a case.......there is gonna be every effort to link it tointernational travel, international food, etc. etc. etc. etc. etc. They will goso far as to find out if a sex partner had ever traveled to the UK/europe,etc. etc. .... It is gonna be a long, lonely, dangerous twisted journey to the





truth. They have all the cards, all the money, and are willing to threatenand carry out those threats....and this may be their biggest downfall...

Thanks as always for your help.

(Recently had a very startling revelation from a rather senior person ingovernment here..........knocked me out of my chair........you must keeppushing. If I was a power person....I would be demanding that there be aleast a million bovine tested as soon as possible and agressively seekingthis disease. The big players are coming out of the woodwork as there ismoney to be made!!! In short: "FIRE AT WILL"!!! for the very dumb....who's"will"! "Will be the burden to bare if there is any coverup!"

again it was said years ago and it should be taken seriously....BSE willNEVER be found in the US! As for the BSE conference call...I think youdid a great service to freedom of information and making some peoplefeign integrity...I find it scary to see that most of the "experts" areemployed by the federal government or are supported on the "teat" offederal funds. A scary picture! I hope there is a confidential panelorganized by the new government to really investigate this thing.

You need to watch your back........but keep picking at them.......like abuzzard to the bone...you just may get to the truth!!! (You probably havemore support than you know. Too many people are afraid to show you orlet anyone else know. I have heard a few things myself... you ask thequestions that everyone else is too afraid to ask.)

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

U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001

http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html


APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee onAnimal Health; Meeting May 2, 2016, and June 16, 2016 SingeltarySubmission


Evidence That Transmissible Mink Encephalopathy Results from FeedingInfected Cattle

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

snip...

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


http://tseac.blogspot.com/2011/02/usa-50-state-bse-mad-cow-conference.html




http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf



In Confidence - Perceptions of unconventional slow virus diseases ofanimals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A. Robertson gave a brief account of BSE. The US approach wasto accord it a very low profile indeed. Dr. A Thiermann showed the picturein the ''Independent'' with cattle being incinerated and thought this was afanatical incident to be avoided in the US at all costs. ...

http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

”The occurrence of CWD must be viewed against the contest of thelocations in which it occurred. It was an incidental and unwelcomecomplication of the respective wildlife research programmes. Despite it’ssubsequent recognition as a new disease of cervids, therefore justifyingdirect investigation, no specific research funding was forthcoming. TheUSDA veiwed it as a wildlife problem and consequently not their province!”...page 26.

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


A comparison of classical and H-type bovine spongiform encephalopathyassociated with E211K prion protein polymorphism in wild type and EK211cattle following intracranial inoculation

http://bse-atypical.blogspot.com/2016/05/a-comparison-of-classical-and-h-type.html

Monday, June 20, 2016

Specified Risk Materials SRMs BSE TSE Prion Program

http://specifiedriskmaterial.blogspot.com/2016/06/specified-risk-materials-srms-bse-tse.html

to be continued...TSS


http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf



http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

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

http://bse-atypical.blogspot.com/2016/05/a-comparison-of-classical-and-h-type.html

http://specifiedriskmaterial.blogspot.com/2016/06/specified-risk-materials-srms-bse-tse.html



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Terry S. Singeltary Sr. Bacliff, Texas USA 77518 [email protected] by Terry S. Singeltary Sr. at 3:07 PM

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Chronic Wasting Disease CWD, Scrapie, Bovine Spongiform Encephalopathy BSE, TSE, Prion Zoonosis Science History