Wednesday, August 23, 2023

CWD TSE PRION OF CERVID, ZOONOSIS, don't let history repeat itself!

CWD TSE PRION OF CERVID, ZOONOSIS, don't let history repeat itself!


sporadic sCJD, Farmers and Farmers Wife with BSE Herds

ignorance is bliss is it not, when you procrastinate with TSE Prion disease, humans and animals can die, so why not let history repeat itself. COME ON PEOPLE! Do you really want to risk death for your children, your wife, your family and friends, when i promised Mom, never forget, and never let them forget, i included even the ones that don't want to know...GET THOSE DEER TESTED FOR CWD!

with relations to the CWD debacle, let me show you how that works sometimes, just an example of zoonosis of BSE and the just say no to science crowd, what can happen. now this is with BSE aka mad cow disease, CWD in cervid has shown to be more of a risk factor to humans, but with BSE in cows, it was first thought that only very young people can contract nvCJD there from, but that theory went out the door a long time ago, and that all sporadic CJD is spontaneous happening...NOT! this is what ignorance of the scientific facts can do to you, your, wife, your kids, your family...please, let's not repeat this ignorance (well, we already have really imo)...

SPORADIC CJD, farmer with bse herd LANCET ARTICLE FIRST CASE CJD FARMER


The first farmer’ – August 1992

5.7 At the beginning of August 1992, Dr Will confidentially informed Dr Ailsa Wight (DH, senior medical officer with responsibility for TSEs), that a probable case of CJD had occurred in a 60-year-old farmer whose farm, in the Manchester area, had a history of BSE. Dr Wight passed on this information to Sir Kenneth Calman (CMO) on 13 August 1992, stating that the CJD patient was alive and had been visited by the CJDSU.188 Although unconfirmed, the diagnosis was considered likely to be CJD on clinical grounds. Dr Wight advised that: There is no direct evidence that the two events (BSE and CJD) are linked and Dr Will feels they are probably a coincidence. Despite the rarity of CJD, it was perhaps only a matter of time before this situation arose, given the large numbers of people employed in the agricultural and related industries, and the fact that BSE cases now total over 65,000.189

5.8 This ‘first case’ of CJD in a cattle farmer was discussed by SEAC190 at their 13th meeting on 15 October 1992.191 Dr Will informed the meeting that one of the farmer’s cows had confirmed BSE in 1989 and that the farmer had developed CJD two years later.192 


IN CONFIDENCE

SECOND CASE OF CJD IN A DAIRY-FARMER

''DH is aware of a second case of CJD in a Dairy Farmer who has BSE in his herd.''


‘The third farmer’ – December 1994 5.33 A ‘third case’ associated with farming where cattle in the herd had contracted BSE concerned a farm worker from Cornwall who had died in early December 1994, aged 54. There had been two confirmed cases of BSE on the farm, in August 1991 and October 1992. Additionally, a cow sold off the farm in December 1987 had been diagnosed with BSE in September 1988.224 5.34 On 1 December 1994, the case was reported in the local newspaper, The Cornishman, while the patient was still in hospital.225 5.35 On 19 December 1994, Mr Charles Lister, DH, minuted the private secretary to Baroness Cumberlege with information about this possible ‘third case in farmers/ farm workers who have had BSE cases in their herds’.226 This minute enclosed the article from The Cornishman and was copied to DH officials and to Mr Eddy at  
MAFF. He noted that diagnosis would not be confirmed until post mortem, but the Surveillance Unit thought it highly likely to be CJD.


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


cover-up of 4th farm worker ??? 


CONFIRMATION OF CJD IN FOURTH FARMER 


now story changes from; 

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

to; 

This is not unexpected...

was another farmer expected? 


4th farmer, and 1st teenager 


2. snip...

Over a 5 year period, which is the time period on which the advice from Professor Smith and Dr. Gore was based, and assuming a population of 120,000 dairy farm workers, and an annual incidence of 1 per million cases of CJD in the general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an individual in the general population to develop CJD. Using the actual current annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5 TIMES.

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


CJD FARMERS WIFE 1989 


''When first mentioning the case, he claimed she was only 36, but after a few more glasses of wine he became less certain of that and thought she could have been older. Locally, they made quite an association with BSE, since she was a farmers wife on a farm that, atypically for that area of S Yorkshire, had several BSE cases. I was told the clinical and pathological pictures were typical of CJD.'' 

BSE11/1 0006

DEPARTMENT OF HEALTH Eilecn House Room 80-94 Newington Causeway

IN CONFIDENCE

Dr RG Will

Consultant Neurologist

Western General Hospital

Crewe Road

EDINBURGH

EH4 2XU 13 October 1989

Dear Bob

An otherwise enjoyable dinner last night as quest of the Association of Clinical Pathology was marred by a ca with a neuropathologist who was just about to write to details of a case of CJD he had just seen. When first mentioning the case, he claimed she was only 36, but after a few more glasses of wine he became less certain of that and thought she could have been older. Locally, they made quite an association with BSE, since she was a farmers wife on a farm that, atypically for that area of S Yorkshire, had several BSE cases. I was told the clinical and pathological pictures were typical of CJD. The brain is now preserved in Sheffield, but fresh material was sent to Newcastle for animal inoculation. I suggested the NPU might be interested in molecular biology studies at some time so asked them to retain any other material they may still have in the freezer.

When I hear more, I will pass on the details to you, but you may hear from your own grapevine contacts in any case. Lets hope Dr Timperley got the age wrong by several decades. And lets also hope the media do not hype it up before we have a chance: to investigate in adequate detail.

I presume all is going well with your plans for the monitoring study and that my lack of news on that at this end only means that you and Dr Dastgir are still sorting it out between you. Still no news of when the "Tyrrell" report will be published. With best wishes.

Yours sincerely

Dr Hilary Pickles Principal Medical Officer

vd: leer ty Qe Tenspeeny

89/10.13/3.1 


20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A 19 year old died from sCJD in France in 1985. There is no evidence of an iatrogenic cause for those cases.... 


zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm 

***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116*** 


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

Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.ukReceived. August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002.


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

Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.


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. 

============== 

PRION 2015 CONFERENCE


***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. 

***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

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


PRION 2016 TOKYO

Saturday, April 23, 2016

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis

Prion 2016 Animal Prion Disease Workshop Abstracts

WS-01: Prion diseases in animals and zoonotic potential

Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. 

These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. 


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

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

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

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


The L-type BSE prion is much more virulent in primates and in humanized mice than is the classical BSE prion, which suggests the possibility of zoonotic risk associated with the L-type BSE prion


Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.


Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.


Atypical L-type bovine spongiform encephalopathy (L-BSE) transmission to cynomolgus macaques, a non-human primate

Fumiko Ono 1, Naomi Tase, Asuka Kurosawa, Akio Hiyaoka, Atsushi Ohyama, Yukio Tezuka, Naomi Wada, Yuko Sato, Minoru Tobiume, Ken'ichi Hagiwara, Yoshio Yamakawa, Keiji Terao, Tetsutaro Sata

Affiliations expand

PMID: 21266763

Abstract

A low molecular weight type of atypical bovine spongiform encephalopathy (L-BSE) was transmitted to two cynomolgus macaques by intracerebral inoculation of a brain homogenate of cattle with atypical BSE detected in Japan. They developed neurological signs and symptoms at 19 or 20 months post-inoculation and were euthanized 6 months after the onset of total paralysis. Both the incubation period and duration of the disease were shorter than those for experimental transmission of classical BSE (C-BSE) into macaques. Although the clinical manifestations, such as tremor, myoclonic jerking, and paralysis, were similar to those induced upon C-BSE transmission, no premonitory symptoms, such as hyperekplexia and depression, were evident. Most of the abnormal prion protein (PrP(Sc)) was confined to the tissues of the central nervous system, as determined by immunohistochemistry and Western blotting. The PrP(Sc) glycoform that accumulated in the monkey brain showed a similar profile to that of L-BSE and consistent with that in the cattle brain used as the inoculant. PrP(Sc) staining in the cerebral cortex showed a diffuse synaptic pattern by immunohistochemistry, whereas it accumulated as fine and coarse granules and/or small plaques in the cerebellar cortex and brain stem. Severe spongiosis spread widely in the cerebral cortex, whereas florid plaques, a hallmark of variant Creutzfeldt-Jakob disease in humans, were observed in macaques inoculated with C-BSE but not in those inoculated with L-BSE.


see full text;


''H-TYPE BSE AGENT IS TRANSMISSIBLE BY THE ORONASAL ROUTE''

This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.


Wednesday, May 24, 2023 

WAHIS, WOAH, OIE, United States of America Bovine spongiform encephalopathy Immediate notification



CWD TO HUMANS, What If, has it already happened?

PART 2. TPWD CHAPTER 65. DIVISION 1. CWD

31 TAC §§65.82, 65.85, 65.88

The Texas Parks and Wildlife Commission in a duly noticed meeting on May 25, 2023 adopted amendments to 31 TAC §§65.82, 65.85, and §65.88, concerning Disease Detection and Response, without changes to the proposed text as published in the April 21, 2023, issue of the Texas Register (48 TexReg 2048). The rules will not be republished.

***> Currently, there is scientific evidence to suggest that CWD has zoonotic potential; however, no confirmed cases of CWD have been found in humans.


17 DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.

Rebeca Benavente1, Francisca Bravo1,2, Paulina Soto1,2, J. Hunter Reed3, Mitch Lockwood3, Rodrigo Morales1,2

1Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, USA. 2Universidad Bernardo O’Higgins, Santiago, Chile. 3Texas Parks and Wildlife, Austin, USA

Abstract

The zoonotic potential of chronic wasting disease (CWD) remains unknown. Currently, there are no known natural cases of CWD transmission to humans but increasing evidence suggests that the host range of CWD is not confined only to cervid species. Alarmingly, recent experimental evidence suggests that certain CWD isolates can induce disease in non-human primates. While the CDC strongly recommends determining CWD status in animals prior to consumption, this practice is voluntary. Consequently, it is plausible that a proportion of the cervid meat entering the human food chain may be contaminated with CWD. Of additional concern is that traditional diagnostic techniques used to detect CWD have relatively low sensitivity and are only approved for use in tissues other than those typically ingested by humans. In this study, we analyzed different processed meats derived from a pre-clinical, CWD-positive free-ranging elk. Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. 

***> Our results show positive prion detection in all products. 

***>To confirm the resilience of CWD-prions to traditional cooking methods, we grilled and boiled the meat products and evaluated them for any remnant PMCA seeding activity. Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking. 

***> Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products. 

***> Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. 

***> CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. 

***> Our results show positive prion detection in all products. 

***> Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking.

***> Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products. 

=====

Transmission of prion infectivity from CWD-infected macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.

Samia Hannaoui1,2, Ginny Cheng1,2, Wiebke Wemheuer3, Walter Schulz-Schaeffer3, Sabine Gilch1,2, Hermann Schatzl1,2 1University of Calgary, Calgary, Canada. 2Calgary Prion Research Unit, Calgary, Canada. 3Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany

***> Further passage to cervidized mice revealed transmission with a 100% attack rate. 

***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one. 

****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism. 

***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease

=====


Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD

Aims: Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we aimed to determine the zoonotic potential of CWD using a mouse model for human prion diseases.

Material and Methods: Transgenic mice overexpressing human PrPChomozygous for methionine at codon 129 (tg650) were inoculated intracerebrally with brain homogenates of white-tailed deer infected with Wisc-1/CWD1 or 116AG CWD strains. Mice were monitored for clinical signs and were euthanized at terminal disease. Brains were tested by RT-QuIC, western blot upon PK digestion, and immunohistochemistry; fecal homogenates were analyzed by RT-QuIC. Brain/spinal cord and fecal homogenates of CWD-inoculated tg650 mice were inoculated into tg650 mice or bank voles. Brain homogenates of bank voles inoculated with fecal homogenates of CWD-infected tg650 mice were used for second passage in bank voles.

Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650 mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.

Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.

Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.


U of M expert warns of increasing likelihood of CWD transmission to humans

Cathy Wurzer and Gretchen BrownJune 5, 2023 1:30 PM

Minnesota scientists have watched chronic wasting disease (CWD) — a fatal, neurological illness — kill deer and elk.

Now, they’re studying its potential to jump to humans.

The University of Minnesota’s Center for Infectious Disease Research and Policy has received more than $1.5 million in state money to start prepping for the possibility of CWD spreading to cows, pigs and possibly humans.

He said transmission to humans has not yet been confirmed, but research suggests it is increasingly likely — especially as the disease continues to spread among deer and elk.

“None of us want to believe this could happen,” he told MPR News host Cathy Wurzer. “But you know, as much as you hope it isn't going to happen, hope is not a strategy.”

Current testing can be done only if animals die or are killed, and lymph nodes or brain matter is removed for testing to verify the disease.

That means captive deer often aren’t tested until they die or show symptoms of the disease, and that’s often too late to stop the spread of the disease.

And there aren’t yet adequate tests for humans, Osterholm said — let alone protocols in place if a human were to test positive for the disease.

Michael Osterholm, Ph.D. is a world-renowned epidemiologist who heads the center.


PLoS One. 2020; 15(8): e0237410. Published online 2020 Aug 20. doi: 10.1371/journal.pone.0237410 PMCID: PMC7446902 PMID: 32817706 

Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease 

Abstract 

While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.

snip...

The results demonstrate: (a) that the minimum CWD oral infectious dose is vastly lower than historical studies used to establish infection; (b) that a direct relationship exists between dose and incubation time to first prion replication detection in tonsils, irrespective of genotype; (c) that a difference was not discernible between brain vs. saliva source prions in ability to establish infection or in resultant disease course; and (d) that the CWD infection process appears to conform more to a threshold dose than an accumulative dose dynamic. 


*** now, let’s see what the authors said way back about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE. 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 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 



> However, to date, no CWD infections have been reported in people. 

sporadic, spontaneous CJD, 85%+ of all human TSE, did not just happen. never in scientific literature has this been proven. if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way; 

sporadic = 54,983 hits 

 
spontaneous = 325,650 hits 

 

key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. 

SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***

> However, to date, no CWD infections have been reported in people.

key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry

*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***

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




CWD TSE PRION AND ZOONOTIC, ZOONOSIS, POTENTIAL

Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY 

Date: Fri, 18 Oct 2002 23:12:22 +0100 

From: Steve Dealler 

Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member 

To: BSE-L@ References: 

Dear Terry,

An excellent piece of review as this literature is desperately difficult to get back from Government sites.

What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!

Steve Dealler 

=====

''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).''

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 ;


MONDAY, DECEMBER 16, 2019 

Chronic Wasting Disease CWD TSE Prion aka mad cow type disease in cervid Zoonosis Update

***> ''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II) <***

What if?


ZOONOSIS OF CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE, who makes the final call?

HAS it already happened?

zoonosis of chronic wasting disease cwd tse prion to humans, as sporadic CJD, what if?


Terry S. Singeltary Sr.

posted by Terry S. Singeltary Sr. at 1:19 PM

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