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#6259811 - 04/14/16 10:56 AM The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer
flounder Offline
Woodsman

Registered: 10/29/11
Posts: 174
Loc: 77518
While Rome Burns, price of cwd prion poker goes up globally, it’s started to look like the early days of the BSE epidemic, except with cwd tse prion, it will be much worse...terry

Tuesday, April 12, 2016

The first detection of Chronic Wasting Disease (CWD) in Europe

http://chronic-wasting-disease.blogspot.com/2016/04/the-first-detection-of-chronic-wasting.html


with sad regards, terry

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#6259939 - 04/14/16 11:57 AM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: flounder]
stxranchman Offline
Obie Juan Kenobi

Registered: 08/04/10
Posts: 52092
Are the dang Norway HF Reindeer Breeders to blame?
_________________________


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#6259988 - 04/14/16 12:27 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: stxranchman]
BenBob Online   content
THF Trophy Hunter

Registered: 01/27/06
Posts: 5827
Loc: Undercover
Originally Posted By: stxranchman
Are the dang Norway HF Reindeer Breeders are to blame?


That right there is funny and I don't care who you are.
_________________________
Tired, Wired, and Uninspired

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#6260100 - 04/14/16 01:34 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: flounder]
aeb Offline
THF Celebrity

Registered: 06/06/10
Posts: 16185
Loc: West Texas
Santa, we have a problem! eeks333
_________________________



You sure you want to poach on our place?

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#6260180 - 04/14/16 02:19 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: stxranchman]
kdkane1971 Online   content
Pro Tracker

Registered: 01/30/14
Posts: 1805
Loc: Mesopotamia
Originally Posted By: stxranchman
Are the dang Norway HF Reindeer Breeders are to blame?

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#6260221 - 04/14/16 02:39 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: flounder]
jshouse Offline
THF Trophy Hunter

Registered: 01/24/10
Posts: 6238
Loc: Rockwall
should we all just take up fishing Terry?
_________________________

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#6260875 - 04/14/16 10:00 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: flounder]
bp3 Offline
Tracker

Registered: 08/06/11
Posts: 848
Obummer will say it's climate change rifle

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#6262925 - 04/16/16 04:32 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: flounder]
Grizz Online   content
THF Trophy Hunter

Registered: 02/28/08
Posts: 5845
Loc: Granbury, TX
_________________________

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#6262978 - 04/16/16 05:15 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: stxranchman]
SniperRAB Online   content
GRAMPS!!!

Registered: 03/26/12
Posts: 21128
Loc: Nurturing Biosphere Mothership
Originally Posted By: stxranchman
Are the dang Norway HF Reindeer Breeders to blame?



It's a refuge roflmao
_________________________

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#6263030 - 04/16/16 06:05 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: bp3]
don k Offline
THF Trophy Hunter

Registered: 08/27/08
Posts: 9282
Loc: Bandera, Tx
Originally Posted By: bp3
Obummer will say it's climate change rifle
Actually you are probably right. Since the Earth is now warming at an alarming rate WT from Texas can now walk all the way to Norway without having to go through the snow and ice. Won't be long before we will have a Moose season here in Texas.
_________________________
http://www.ibexgoats.com/home.html

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#6263408 - 04/16/16 10:55 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: flounder]
Erathkid Offline
THF Celebrity

Registered: 01/19/11
Posts: 14616
Loc: Dollas,Taxes Bluff Dale Tx
Terry, I have to ask, what is it that is so alarming to you? This has probably been around since cervids have roamed the earth. Why the "Chicken little", attitude?
_________________________
Life is too short, as is. Don't chance it.
Don't text and drive.

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#6263740 - 04/17/16 09:48 AM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: flounder]
BubRay Online   content
Tracker

Registered: 08/26/08
Posts: 674
Loc: McKinney/Albany
You know Dasher and Dancer and Prancer and Vixen,
you know Comet and Cupid and Donner and Blitzen,
But do you recall
The prion that took out them all.........
_________________________
Take Care,
Bub

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#6263765 - 04/17/16 10:15 AM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: Erathkid]
flounder Offline
Woodsman

Registered: 10/29/11
Posts: 174
Loc: 77518
Originally Posted By: Erathkid
Terry, I have to ask, what is it that is so alarming to you? This has probably been around since cervids have roamed the earth. Why the "Chicken little", attitude?



it’s about much more than cwd in deer or elk, it’s about TSE in all species, exposure, and friendly fire there from. you only have to see it once. I don’t do this because of my choosing. I simply made a promise, never forget, and never let them forget.

I just don’t want any of you folks or your loved ones to go though this. none of us should have to go through this. it’s been a colossal global cover up thanks to the USDA and the OIE $$$

Sunday, January 17, 2016

Heidenhain Variant Creutzfeldt Jakob Disease autopsy case report 'MOM'

Based on this finding, the present case corresponds to the Heidenhain variant. It is not uncommon for Creutzfeldt-Jakob disease to present with visual symptoms as the initial manifestation of the disease. Vargas et al (3) has reported three cases with these characteristics. FINAL AUTOPSY DIAGNOSIS I. Brain: Creutzfeldt-Jakob disease, Heidenhain variant.

Of Grave Concern Heidenhain Variant Creutzfeldt Jakob Disease

http://creutzfeldt-jakob-disease.blogspot.com/2016/01/of-grave-concern-heidenhain-variant.html

Saturday, February 13, 2016

The Risk of Prion Infection through Bovine Grafting Materials in dentistry

http://bovineprp.blogspot.com/2016/02/the-risk-of-prion-infection-through.html

Thursday, August 13, 2015

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

http://creutzfeldt-jakob-disease.blogspot.com/2015/08/iatrogenic-cjd-due-to-pituitary-derived.html

Saturday, April 16, 2016

More infections from dirty scopes than estimated, what about CJD TSE Prion aka mad cow type disease?

I tried warning OLYMPUS in 1999 about this risk factor from CJD TSE.

Report: More infections from dirty scopes than estimated

http://creutzfeldt-jakob-disease.blogspot.com/2016/04/more-infections-from-dirty-scopes-than.html

Thursday, April 14, 2016

*** Arizona 22 year old diagnosed with Creutzfeldt Jakob Disease CJD ***

http://creutzfeldt-jakob-disease.blogspot.com/2016/04/arizona-22-year-old-diagnosed-with.html

all iatrogenic cjd is, is sporadic cjd, until the iatrogenic event is discovered, traced back, documented in the Academic domain, and then put into the public domain and documented as an iatrogenic CJD event. that’s why 85%+ of all human TSE prion disease is still sporadic CJD. problem solved $$$ 85%+ of all human TSE prion i.e. sporadic CJD just happens, a spontaneous event. not in your life. this has never been proven in the field naturally for humans or animals.

Saturday, April 16, 2016

APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission

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

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

07 02:27 AM

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)

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

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.]

http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf

http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf

snip...see full Singeltary Nature comment here;

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

see Singeltary comments to Plos ;

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

BSE101/1 0136

IN CONFIDENCE

CMO

From: . Dr J S Metiers DCMO

4 November 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

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

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

what are the implications for public health?

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

1

92/11.4/1.1

BSE101/1 0137

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

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

http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf

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

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

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

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

*** Singeltary comment PLoS ***

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

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

http://www.plosone.org/annotation/listThread.action?root=82860

Sunday, November 22, 2015

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

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

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

http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20

http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html

*** 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.

http://www.ncbi.nlm.nih.gov/entrez/query...p;dopt=Abstract

Saturday, April 16, 2016

APHIS [Docket No. APHIS-2016-0029] Secretary's Advisory Committee on Animal Health; Meeting May 2, 2016, and June 16, 2016 Singeltary Submission

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

Transmissible Spongiform Encephalopthy TSE Prion Disease

*** Kuru Video

Kuru: The Science and The Sorcery

https://www.youtube.com/watch?v=vw_tClcS6To

*** Scrapie Video

http://zoomify.uzh.ch:8080/zoomify/videos/video-011/video-011.html

*** Human Mad Cow Video

http://zoomify.uzh.ch:8080/zoomify/videos/video-009/video-009.html

*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video

http://zoomify.uzh.ch:8080/zoomify/videos/video-004/video-004.html

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

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

http://zoomify.uzh.ch:8080/zoomify/videos/video-004/video-004.html


Terry S. Singeltary Sr.

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#6263780 - 04/17/16 10:22 AM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: flounder]
BOBO the Clown Online   content
decoy

Registered: 04/19/07
Posts: 41114
Loc: Metroplex
Terry has there ever been one case of CWD transmitted to humans?

By your own admission we should stop hunting and eating deer due to CWD. When you are on a hunting forum and publically express the mass extermination of a deer and elk, it doesn't bode well.

Top
#6264124 - 04/17/16 03:26 PM Re: The first detection of Chronic Wasting Disease (CWD) in Europe, Norway Wild Reindeer [Re: BOBO the Clown]
flounder Offline
Woodsman

Registered: 10/29/11
Posts: 174
Loc: 77518
Originally Posted By: BOBO the Clown
Terry has there ever been one case of CWD transmitted to humans?

By your own admission we should stop hunting and eating deer due to CWD. When you are on a hunting forum and publically express the mass extermination of a deer and elk, it doesn't bode well.




I don't care what you eat Sir. it's when that starts to risk others via iatrogenic mode, then it becomes a problem for all of us. you have missed my whole point. it was wasteful attempt to try and educate you...my bad.



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.***

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

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 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.

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 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).***

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

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

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


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

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

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

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

From: "Belay, Ermias"

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

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

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

Dear Sir/Madam,

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

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

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

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

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

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

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

Thursday, April 03, 2008

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

snip...

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

snip... full text ;

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

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.

https://www.organicconsumers.org/old_articles/madcow/killer123103.php

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 ***

http://zoomify.uzh.ch:8080/zoomify/videos/video-004/video-004.html

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.

http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975

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.

http://www.sciencemag.org/content/311/5764/1117.long

***********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 ;

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf

CJD9/10022

October 1994

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

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

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

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

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

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

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

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

*** 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).***

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


carry on here...terry

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