Thursday, March 17, 2016

Preliminary Diagnosis Creutzfeldt-Jakob Disease Confirmed in Patient that had Lumbar Puncture at Washington Regional Medical Center

National Laboratory Reports Possible Diagnosis of Creutzfeldt-Jakob Disease


A national laboratory in Chantilly, Va., has confirmed a preliminary diagnosis of an extremely rare condition known as Creutzfeldt-Jakob Disease (CJD) following a Feb. 15, 2016, diagnostic lumbar puncture of a patient at Washington Regional Medical Center. The preliminary lab results were received by WRMC the afternoon of March 15, 2016.

 
WRMC infectious disease specialist James Newton, M.D., emphasized the extreme unlikelihood of any other patients being affected by this rare condition. The Centers for Disease Control and Prevention in Atlanta (CDC) advises that there has not been a single reported case of CJD transmitted by surgical instruments in the four decades since 1976 and the widespread adoption of modern surgical sterilization techniques by the nation’s hospitals. Those sterilization techniques have been standard procedure at WRMC for all operations for 40 years.

 
Out of an abundance of caution and a desire to ensure the safety of patients and staff, upon receiving the lab results WRMC immediately shut all operating rooms. WRMC conducted a thorough sterilization and replaced certain surgical instruments, in adherence with recommendations of the World Health Organization.

 
CJD, a degenerative brain disease, occurs in the population worldwide at the rate of about one person per million per year for reasons that are usually unknown. The illness is not the variant condition known popularly as “mad cow disease.”

 
WRMC will resume surgical cases later today. Dr. Newton stressed that there is no risk to patients currently at WRMC, medical center staff or the general public.

 
Despite the possibility being remote that any other patients of WRMC have been exposed to the protein that causes CJD, WRMC is collaborating with the CDC and Arkansas Department of Health (ADH) to identify and advise those patients who received care at WRMC during the relevant period whether they may be at risk. While medical literature states that the chance that any other patient has been exposed to the CJD protein through surgical instrumentation is extremely small, WRMC believes it important to ensure that patients are appropriately advised as it cannot guarantee that there is absolutely no risk.

 
“We continue to seek the best available guidance and information from the CDC, the Arkansas Department of Health and the medical literature,” said Dr. Newton. “The extreme rarity of this disease and the nature of the potential exposure, which is so small it cannot be quantified, make it a challenge to find published guidelines that are applicable to our situation. Nevertheless, we are committed to finding and sharing with our patients the best available advice.”

 
http://www.wregional.com/main/news/national-laboratory-reports-possible-diagnosis-of-48.aspx

 
Washington Regional postpones Fayetteville surgeries following rare brain disorder discovery

 
By Christie Swanson

 
Posted: March 17, 2016 at 1:13 a.m.

 
FAYETTEVILLE -- Washington Regional Medical Center didn't use its operating rooms Wednesday morning after officials learned a patient was preliminarily diagnosed with a rare degenerative brain disease.

 
Hospital officials learned Tuesday a patient undergoing a diagnostic lumbar puncture Feb. 15 was diagnosed with Creutzfeldt-Jakob Disease by a national laboratory in Chantilly, Va.

 
A news release from the Fayetteville hospital said surgical cases resumed Wednesday afternoon after workers thoroughly sterilized and replaced certain surgical instruments, in adherence with recommendations of the World Health Organization.

 
The disease occurs at the rate of about one person per million each year worldwide and about 300 cases in the United States each year, according to the National Institute of Health. Dr. Gary Wheeler, branch chief of infectious diseases at the Arkansas Department of Health, said there isn't a full explanation for what causes the disorder, it can be traced to abnormal proteins in the brain called prions.

 
He said there hasn't been a case of Creutzfeldt-Jakob Disease being transmitted in a hospital since 1976, before much was known about the disorder and modern surgical sterilization techniques were adopted by hospitals.

 
"There is never a zero chance, but the chances of transmitting this disease are really, really tiny," Wheeler said.

 
Dr. James Newton, Washington Regional infectious disease specialist, also stressed in the release there's an extreme unlikelihood of any other patients being affected and patients, workers and the public are at no risk. He said Washington Regional adopted the recommended sterilization techniques for all operations 40 years ago.

 
"We continue to seek the best available guidance and information from the CDC, the Arkansas Department of Health and the medical literature," Newton stated. "The extreme rarity of this disease and the nature of the potential exposure, which is so small it cannot be quantified, make it a challenge to find published guidelines that are applicable to our situation. Nevertheless, we are committed to finding and sharing with our patients the best available advice."

 
Wheeler said the surgical instruments used on the infected patients likely had to undergo more stringent soaking using stronger agents such as undiluted chlorine bleach and additional time in an autoclave.

 
The hospital is collaborating with the Centers for Disease Control and Prevention and the Arkansas Department of Health to identify and advise patients who received hospital care since the Feb. 15 procedure. Less than 1 percent of cases nationwide are classified as acquired, meaning the disease is transmitted by exposure to brain or nervous system tissue, usually through certain medical procedures.

 
The disease usually appears later in life and progresses rapidly, according to the National Institute of Health. Symptoms typically start around age 60 and about 90 percent of people die within a year.

 
Early stages of the disease cause failing memory, behavioral changes, lack of coordination and visual disturbances. As the disease progresses, mental deterioration becomes pronounced and involuntary movement, blindness, weakness of the extremities and coma may occur.

 
Wheeler said testing for Creutzfeldt-Jakob Disease is advancing, and there are some labs that can test spinal fluid. The best way to diagnosis the disease is by a brain biopsy, he said.

 
Washington Regional stated in its news release the disease wasn't a variant condition known as bovine spongiform encephalopathy, or "mad cow" disease.

 
Wheeler said he also heard people worried the Washington Regional case could be tied to chronic wasting disease, a similar brain disorder found in deer and elk. He said the disorder has never been transmitted from an animal to a person.

 
"Hopefully it will stay that way," he said. "Fear of the unknown is what people have to deal with."

 
NW News on 03/17/2016

 
http://www.nwaonline.com/news/2016/mar/17/washington-regional-postpones-fayettevi/?news-arkansas-nwa

 

 TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE AKA MAD COW TYPE DISEASE ARE IN ALL HOSPITALS, WE HAVE ALL BEEN EXPOSED ONE WAY OR THE OTHER, EXPOSURE FROM DEER, ELK, CATTLE, SHEEP, EXPOSURE FROM SECOND HAND TRANSMISSION, IATROGENIC, FRIENDLY FIRE.

 

 PLEASE REMEMBER, ALL IATROGENIC CJD IS, IS SPORADIC CJD UNTIL THE ROUTE, SOURCE, THE IATROGENIC EVENT IS TRACED BACK, THEN DOCUMENTED, THEN PUT INTO THE ACADEMIC DOMAIN, AND FINALLY THE PUBLIC DOMAIN, WHICH VERY SELDOM HAPPENS DO TO THE LONG INCUBATION PERIOD, SURVEILLANCE, AND LACK OF ANY TRACE BACK EFFORTS.

 

 PLEASE REMEMBER ALSO, 85%+ OF ALL HUMAN TSE PRION DISEASE I.E. THE SPORADIC CJD IS NOT A SINGLE STRAIN FROM A TWISTED UP PROTEIN, WITH NO ROUTE AND SOURCE. THIS HAS NEVER BEEN PROVEN. THERE ARE MANY STRAINS TO THE SPORADIC CJD, ALL OF WHICH THE ROUTE AND SOURCE HAS NOT BEEN DOCUMENTED.

 

 > Washington Regional stated in its news release the disease wasn't a variant condition known as bovine spongiform encephalopathy, or "mad cow" disease.

 

 ABSOLUTELY, THEY DO NOT KNOW THIS FOR SURE. IT VERY WELL COULD BE TIED TO EITHER ATYPICAL OR TYPICAL BSE OR ATYPICAL OR TYPICAL SCRAPIE, PLUS, NEW SCIENCE IS SHOWING THAT THE SPECIES BARRIER FOR CWD TO HUMANS IS NOT AS ROBUST AS ONCE THOUGHT, PLEASE SEE PRION2015 REFERENCES BELOW.

 

 >Wheeler said he also heard people worried the Washington Regional case could be tied to chronic wasting disease, a similar brain disorder found in deer and elk. He said the disorder has never been transmitted from an animal to a person.

 

 AGAIN, WHEELER HAS NO CLUE THAT THIS IS TRUE, JUST MORE WISHFUL THINKING.

 

 LET’S EVALUATE THE LATEST SCIENCE AND SOME OLD CONFIDENTIAL DATA, AND ALSO, LET US SEE WHAT THE PRION GODS AT CDC NIH SAID ABOUT CWD TO HUMAN RISK FACTOR, LET’S LOOK AT THE REST OF THE SCIENCE AND THE FACTS, THEN THE LAY PUBLIC CAN MAKE A BETTER DECISION. ...

 

 >The Centers for Disease Control and Prevention in Atlanta (CDC) advises that there has not been a single reported case of CJD transmitted by surgical instruments in the four decades since 1976 and the widespread adoption of modern surgical sterilization techniques by the nation’s hospital

 

 THE ABSOLUTELY DO NOT KNOW THIS AS FACT. AGAIN, WISHFUL THINKING.

 

 WHAT’S GOOD ABOUT NOT LOOKING, NO TRACE BACKS WITH SPORADIC CJD, IF YOU DON’T LOOK, YOU DON’T FIND, LIKE BSE IN CATTLE.

 

 I WILL GIVE YOU THE FACTS THAT DISPUTE EVERYTHING THE CDC NIH USDA FDA STATES WITH SOUND SCIENCE, and you will not print it because you can’t. this is just the way it is $$$

 

 they call it, USDA INC.

 

 just saying, carry on with this charade $$$

 

 p.s. for Gods sake, look at the recent science about Alzheimer’s and the potential it may be a Transmissible Spongiform Encephalopathy TSE Prion and that it may be iatrogenic...

 

 p.s.s. one more think, if you think our fine federal friends will not lie to you, will not cover something up that kills you, another disease of long incubation, covered up for 100 years, all one has to do is look back at tobacco and asbestos.

 

 NOW ON TO THE FACTS AND THE SCIENCE ;

 

 Terry S. Singeltary Sr. said:

 

 re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

 

 2015-12-07 02:27 AM

 

 Terry S. Singeltary Sr. said: re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

 

 Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)

 

 I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.

 

 First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.

 

 Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.

 

 where have we all heard this before? it’s been well documented via the BSE Inquiry. have they not learned a lesson from the last time?

 

 we have seen this time and time again in England (and other Country’s) with the BSE mad cow TSE Prion debacle.

 

 That ‘anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.

 

 The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients who got pooled extracts injected from thousands of cadavers were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.

 

 That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find ‘alarming’ is pathetic.

 

 Sounds like the journalists had it right in the first place: ‘Alzheimer’s may be a transmissible infection’ in The Independent to ’You can catch Alzheimer’s’ in The Daily Mirror or ‘Alzheimer’s bombshell" in The Daily Express.

 

 if not for the journalist, the layperson would not know about these important findings.

 

 where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?

 

 when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.

 

 to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer’s, the price of poker goes up drastically.

 

 so, who makes that final decision, and how many more decades do we have to wait?

 

 the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?

 

 Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.

 

 FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.

 

 in my opinion, it’s one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.

 

 greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it’s bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.

 

 my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer’s of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.

 

 I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...

 

 [9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]

 


 


 

 snip...see full Singeltary Nature comment here;

 


 

 see Singeltary comments to Plos ;

 

 Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN

 

 BSE101/1 0136

 

 IN CONFIDENCE

 

 CMO

 

 From: . Dr J S Metiers DCMO

 

 4 November 1992

 

 TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

 

 1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.

 

 2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible.

 

 what are the implications for public health?

 

 3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.

 

 1

 

 92/11.4/1.1

 

 BSE101/1 0137

 

 4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.

 

 J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2

 


 

 >>> The only tenable public line will be that "more research is required’’ <<<

 

 >>> possibility on a transmissible prion remains open<<<

 

 O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?

 

 Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

 

 *** Singeltary comment PLoS ***

 

 Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

 

 Posted by flounder on 05 Nov 2014 at 21:27 GMT

 


 

 Sunday, November 22, 2015

 

 *** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis Abstract

 

 Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.

 

 Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00

 


 


 

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

 

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

 

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

 


 

 PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS

 

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

 

 O18

 

 Zoonotic Potential of CWD Prions

 

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

 

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

 

 ==================

 

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

 

 ==================

 

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

 

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

 

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

 

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

 

 ================

 

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

 

 ================

 


 

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

 

 Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

 

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

 

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

 


 


 

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

 


 

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

 


 

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

 

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

 

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

 

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

 

 From: "Belay, Ermias"

 

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

 

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

 

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

 

 Dear Sir/Madam,

 

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

 

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

 

 -----Original Message-----

 

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

 

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

 

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

 

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

 

 Thursday, April 03, 2008

 

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

 

 snip...

 

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

 

 snip... full text ;

 


 

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

 

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

 


 

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

 

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

 


 

 Envt.07:

 

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

 

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

 


 

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

 

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

 


 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

 snip...

 

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

 

 snip...

 

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

 

 snip...

 

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

 

 snip...see full report ;

 


 

 CJD9/10022

 

 October 1994

 

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

 

 Dear Mr Elmhirst,

 

 CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

 

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

 

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

 

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

 

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

 

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

 


 

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

 


 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

 ===============

 

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

 

 ===============

 

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

 

 ==============

 


 

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

 

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

 

 Authors

 

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

 

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

 

 Interpretive Summary: The transmissible spongiform encephalopathies (also called prion diseases) are fatal neurodegenerative diseases that affect animals and humans. The agent of prion diseases is a misfolded form of the prion protein that is resistant to breakdown by the host cells. Since all mammals express prion protein on the surface of various cells such as neurons, all mammals are, in theory, capable of replicating prion diseases. One example of a prion disease, bovine spongiform encephalopathy (BSE; also called mad cow disease), has been shown to infect cattle, sheep, exotic undulates, cats, non-human primates, and humans when the new host is exposed to feeds or foods contaminated with the disease agent. The purpose of this study was to test whether non-human primates (cynomologous macaque) are susceptible to the agent of sheep scrapie. After an incubation period of approximately 10 years a macaque developed progressive clinical signs suggestive of neurologic disease. Upon postmortem examination and microscopic examination of tissues, there was a widespread distribution of lesions consistent with a transmissible spongiform encephalopathy. This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans. Technical Abstract: Classical bovine spongiform encephalopathy (c-BSE) is an animal prion disease that also causes variant Creutzfeldt-Jakob disease in humans. Over the past decades, c-BSE's zoonotic potential has been the driving force in establishing extensive protective measures for animal and human health.

 

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

 

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

 

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

 


 

 ***This information will have a scientific impact since it is the first study that demonstrates the transmission of scrapie to a non-human primate with a close genetic relationship to humans. This information is especially useful to regulatory officials and those involved with risk assessment of the potential transmission of animal prion diseases to humans.

 

 ***This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

 


 

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

 

 5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

 

 snip...

 

 R. BRADLEY

 


 

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

 


 

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

 

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

 


 

 MAD COW DISEASE HAS BEEN IN THE USA FOR DECADES, AND I BELIEVE IT WAS IN THE USA FIRST, PLEASE SEE ;

 

 Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

 

 snip...

 

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

 


 


 


 

 The agreement reached reflects the U.S.’ negligible risk classification for bovine spongiform encephalopathy (BSE) by the World Organization for Animal Health (OIE).

 


 

 LMAO...who’s kidding whom $$$ OIE!

 

 Saturday, February 6, 2016

 

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

 


 

 Tuesday, March 15, 2016

 

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

 


 

 Thursday, December 17, 2015

 

 Annual report of the Scientific Network on BSE-TSE 2015 EFSA-Q-2015-00738 10 December 2015

 


 

 Sunday, October 18, 2015

 

 World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research

 


 

 Wednesday, March 2, 2016

 

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

 


 

 Thursday, March 10, 2016

 

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

 

 *** CHRONIC WASTING DISEASE: The Final Epidemic ***

 


 

 Friday, August 14, 2015

 

 *** Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation ***

 


 

 Saturday, January 31, 2015

 

 European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route

 


 

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

 

 ======

 

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

 

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

 

 ======

 

 31 Jan 2015 at 20:14 GMT

 

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

 

 31 Jan 2015 at 20:14 GMT

 


 

 infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et al TRIPLE MAD COW FIREWALL, 10 YEARS AFTER ;

 

 10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007

 

 Date: March 21, 2007 at 2:27 pm PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.

 

 Firm initiated recall is ongoing. REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.

 

 VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI

 

 ___________________________________

 

 PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007 CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified. RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.

 

 Firm initiated recall is complete. REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.

 

 VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV

 

 END OF ENFORCEMENT REPORT FOR MARCH 21, 2007

 


 

 *** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

 infamous august 4, 1997 BSE TSE prion mad cow feed ban, part of usda fda et al TRIPLE MAD COW FIREWALL, 16 YEARS AFTER ;

 

 Sunday, December 15, 2013

 

 FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE

 


 

 Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE)

 

 Date: June 21, 2007 at 2:49 pm PST

 

 Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program

 

 An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services.

 

 In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE),

 

 *** the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle.

 

 As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.

 

 snip...

 

 Topics that will be covered in ongoing or planned reviews under Goal 1 include:

 

 soundness of BSE maintenance sampling (APHIS),

 

 implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),

 

 snip...

 

 The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.

 

 4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half

 


 

 Wednesday, July 15, 2015

 

 Additional BSE TSE prion testing detects pathologic lesion in unusual brain location and PrPsc by PMCA only, how many cases have we missed?

 


 

 ***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.

 

 ***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.

 

 IBNC Tauopathy or TSE Prion disease, it appears, no one is sure

 

 Posted by flounder on 03 Jul 2015 at 16:53 GMT

 


 

 *** Needless conflict ***

 

 Nature 485, 279–280 (17 May 2012) doi:10.1038/485279b

 

 Published online 16 May 2012

 

 Terry S. Singeltary Sr. said:

 

 I kindly wish to submit the following please ;

 


 

 INDICTMENT

 


 

 Wednesday, March 2, 2016

 

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

 


 

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

 

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

 

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

 

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

 

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

 

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

 

 Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

 

 ================

 


 


 

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

 

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

 

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

 

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

 

 Monday, November 16, 2015

 

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

 


 


 

 98 | Veterinary Record | January 24, 2015

 

 EDITORIAL

 

 Scrapie: a particularly persistent pathogen

 

 Cristina Acín

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

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

 

 References

 

 snip...

 

 98 | Veterinary Record | January 24, 2015

 


 

 *** These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils.

 

 *** These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.

 

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

 

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

 


 

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

 

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

 


 

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

 

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

 


 

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

 

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

 

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

 


 

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

 

 Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

 PL1

 

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

 

 Claudio Soto

 

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

 

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

 

 =========================

 

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

 

 ========================

 

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

 


 

 Wednesday, December 16, 2015

 

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

 

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

 

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

 

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

 

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

 

 snip...

 

 Discussion

 

 Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).

 

 Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.

 

 This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.

 

 PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.

 

 In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.

 

 Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification

 


 

 Wednesday, December 16, 2015

 

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

 


 

 Monday, January 4, 2016

 

 Long live the OIE, or time to close the doors on a failed entity?

 


 

 Thursday, October 22, 2015

 

 Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened

 


 

 Thursday, June 04, 2015

 

 Catholic Medical Center v. Civil No. 14-cv-180-JL Opinion No. 2015 DNH 110 Fireman’s Fund Insurance Company Creutzfeldt Jakob Disease TSE Prion tainted medical instruments

 

 UNITED STATES DISTRICT COURT DISTRICT OF NEW HAMPSHIRE

 


 

 Tuesday, February 11, 2014

 

 Novant Health Forsyth Medical Center Information on potential CJD exposure

 


 

 Tuesday, February 11, 2014

 

 Novant Health Forsyth Medical Center Information on potential CJD exposure

 


 

 Monday, February 10, 2014

 

 18 Forsyth Medical Center patients exposed to CJD; apology issued...OOOPS, SORRY, TOO BAD $$$

 


 

 Thursday, January 16, 2014

 

 The Anspach Effort, Inc. RECALL FDA Blackmax motor had been used in a case where the patient was diagnosed with Creutzfeldt-Jacob Disease (CJD) MARYLAND HOSTPITAL

 


 

 Friday, January 10, 2014

 

 vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???

 


 

 Thursday, January 23, 2014

 

 Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) [Docket No. FDA–2013–D–1574]

 


 

 Wednesday, November 27, 2013

 

 NHS failed to sterilise surgical instruments contaminated with 'mad cow' disease

 


 

 Saturday, November 16, 2013

 

 Management of neurosurgical instruments and patients exposed to creutzfeldt-jakob disease 2013 December

 

 Infect Control Hosp Epidemiol.

 


 

 Tuesday, September 24, 2013

 

 NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)

 

 Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15

 


 

 Thursday, September 05, 2013

 

 Possible Patient Exposure to Creutzfeldt-Jakob Disease Announced New Hampshire DHHS

 

 Press Release

 


 

 Friday, July 19, 2013

 

 Beaumont Hospital in Dublin assessing patients for CJD

 


 

 Monday, April 15, 2013

 

 Dr. Stephen B. Thacker Director Centers for Disease Control and Prevention′s Office of Science, Epidemiology and Laboratory Services (OSELS) dies from Creutzfeldt Jakob Disease CJD

 


 

 Thursday, April 12, 2012

 

 Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to 2010

 

 Eurosurveillance, Volume 17, Issue 15, 12 April 2012

 

 Research articles

 


 

 Tuesday, July 31, 2012

 

 11 patients may have been exposed to fatal disease Creutzfeldt-Jakob Disease CJD Greenville Memorial Hospital

 


 

 Thursday, August 02, 2012

 

 CJD case in Saint John prompts letter to patients Canada CJD case in Saint John prompts letter to patients

 


 

 Tuesday, July 31, 2012

 

 11 patients may have been exposed to fatal disease Creutzfeldt-Jakob Disease CJD Greenville Memorial Hospital

 


 

 Thursday, August 02, 2012

 

 CJD case in Saint John prompts letter to patients Canada CJD case in Saint John prompts letter to patients

 


 

 Saturday, February 12, 2011

 

 Another Pathologists dies from CJD, another potential occupational death ?

 

 another happenstance of bad luck, a spontaneous event from nothing, or friendly fire ???

 


 

 Wednesday, November 30, 2011

 

 First iCJD Death Confirmed in Korea

 


 

 Thursday, December 08, 2011

 

 A case of Iatrogenic Creutzfeldt Jakob Disease (iCJD) in a patient who had received a German-manufactured human dura mater graft 23 years ago

 


 

 Thursday, December 8, 2011

 

 S. Korea confirms second case of iatrogenic Creutzfeldt-Jakob disease 48-year-old man

 

 2011/12/08 11:08 KST

 


 

 Monday, December 12, 2011

 

 Second iatrogenic CJD case confirmed Korea

 


 


 

 Sunday, April 06, 2014

 

 SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date

 


 

 Thursday, April 17, 2014

 

 Novant: Three more may have been exposed to disease CJD

 


 

 Wednesday, September 10, 2014

 

 Creutzfeldt-Jakob disease (CJD) biannual update (August 2014), with updated guidance on decontamination of gastrointestinal endoscopy equipment

 

 Research and analysis

 


 

 Tuesday, August 26, 2014

 

 Blood reference materials from macaques infected with variant Creutzfeldt-Jakob disease agent

 


 

 Sunday, January 17, 2016

 

 Of Grave Concern Heidenhain Variant Creutzfeldt Jakob Disease

 


 

 Monday, August 17, 2015

 

 FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS

 

 I told Olympus 15 years ago about these risk factors from endoscopy equipment, disinfection, even spoke with the Doctor at Olympus, this was back in 1999. I tried to tell them that they were exposing patients to dangerous pathogens such as the CJD TSE prion, because they could not properly clean them. even presented my concern to a peer review journal GUT, that was going to publish, but then it was pulled by Professor Michael Farthing et al... see ;

 


 

 Wednesday, March 02, 2016

 

 Endoscope Maker Olympus Agrees To $646 Million Settlement Over Kickbacks, while still ignoring the elephant in the room, CJD TSE PRIONS

 


 

 2003

 

 Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al

 

 Evidence For CJD/TSE Transmission Via Endoscopes

 

 From Terry S. Singletary, Sr flounder@wt.net 1-24-3

 


 

 Monday, December 26, 2011

 

 Prion Uptake in the Gut: Identification of the First Uptake and Replication Sites

 


 

 Saturday, February 13, 2016

 

 The Risk of Prion Infection through Bovine Grafting Materials in dentistry

 


 

 Saturday, January 16, 2016

 

 Revised Preventive Measures to Reduce the Possible Risk of Transmission of Creutzfeldt-Jakob Disease and Variant Creutzfeldt-Jakob Disease by Blood and Blood Products Guidance for Industry

 


 

 Tuesday, May 26, 2015

 

 Minimise transmission risk of CJD and vCJD in healthcare settings Last updated 15 May 2015

 


 

 Friday, October 09, 2015

 

 An alarming presentation level II trauma center of Creutzfeldt-Jakob disease following a self-inflicted gunshot wound to the head

 


 

 Wednesday, January 06, 2016

 

 CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE U.K. 23rd ANNUAL REPORT 2014 (published 18th November 2015)

 


 

 Saturday, December 12, 2015

 

 CREUTZFELDT JAKOB DISEASE CJD TSE PRION REPORT DECEMBER 14, 2015

 


 

 PLEASE REMEMBER, IN 55 YEARS AND OLDER, THE RATE OF DOCUMENTED CJD JUMPS TO ONE IN 9,000. but officials don’t tell you that either. carry on...

 

 Terry S. Singeltary Sr.

Links to this post:

Create a Link

<< Home