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Chronic Wasting Disease CWD TSE Prion 2019 Where The Rubber Meets The Road

Greetings BigGameHunt et al, 

 

it's been a while since i have posted here about chronic wasting disease cwd tse prion, and there is a great deal of science that has come forth that some of you may not be aware of, of which you should imo, please educate yourselves, because only you can make the proper decisions for your family. this is one of my end of year reports on the tse prion disease, 21st year since 12/14/97. lot has changed. and some has not. so, there is a lot here to ingest, and i did not want to flood this board with a lot of different post, so this should rap it up for now...GOOD LUCK!

 

2019 prepare for the storm

 

WITH the recent findings that Scrapie will transmit to Macaque by oral route, that Scrapie and CWD TSE Prion will transit to pigs orally, recent outbreak documented of TSE Prion Disease in Dromedary Camels, Algeria, atypical TSE Prion still being documented, and again just recently in the USA, of another atypical BSE case, and this discovery was only documented by testing 20k head of cattle from some 100M head of cattle in any given year in the USA, the continued denial that atypical BSE and atypical Scrapie are a transmissible disease (science has shown otherwise) this is concerning to me. 

 

Science and scientific policy makers have forgotten what Gibbs, Gajdusek, Hadlow, Alper, Zigas, even Gordon with the infamous Scrapie vaccine blunder, a discovery of valuable importance, and so many others i am failing to remember now, what some found long ago, like Dr. Gibbs, he tried to warn us about scrapie zoonosis potential, yet that went ignored for decades and decades. 

 

we/scientist/officials/the world, knows the USA FDA PART 589 TSE PRION FEED ban has failed terribly, the BSE testing has failed terribly, and the surveillance there from has failed, SRM removal breaches, all proven by the OIG or the GAO, and others. 

 

But yet, we find ourselves now debating the issue of these same risk factors for scrapie, the same risk factors that we all knew were there, with science staring us in the face, we still deny scientific facts all in the name of corporate interest. 

 

let's not continue to make these same mistakes. human and animal life is at stake here. we must remove corporate/government/lobbyist interest from the scientific policy making and regulations there from for the TSE Prion, all of them. I urge you all to take a good look at the most recent science i have put together here for you. this is a free full course of the tse prion disease.

 

cwd tse prion

 

cwd and scrapie has now been documented to transmit to pigs BY ORAL ROUTE, this is terrible news. FEED, FEED, FEED!

 

I KINDLY WISH TO SUBMIT THE FOLLOWING LATEST SCIENCE ON THE CHRONIC WASTING DISEASE CWD TSE PRION. 

 

THE TSE PRION aka mad cow type disease is not your normal pathogen. 

 

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. 

 

you cannot cook the TSE prion disease out of meat. 

 

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. 

 

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

 

the TSE prion agent also survives Simulated Wastewater Treatment Processes. 

 

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. 

 

you can bury it and it will not go away. 

 

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. 

 

it’s not your ordinary pathogen you can just cook it out and be done with. 

 

***> that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.

 

this old study next always stuns me. think of this the next time you clean your tools you use to gut and bone out your kill, and then feeding it to your family and friends...tss 

 

1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 

 

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

 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. 

 

Laboratory of Central Nervous System Studies, National Institute of 

 

Neurological Disorders and Stroke, National Institutes of Health, 

 

Bethesda, MD 20892. 

 

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

 

PMID: 8006664 [PubMed - indexed for MEDLINE]

 

 

https://www.ncbi.nlm.nih.gov/pubmed/8006664?dopt=Abstract

 

 

***> NORWAY CWD UPDATE December 2018

 

Report from the Norwegian Scientific Committee for Food and Environment (VKM) 2018: 16

 

Factors that can contribute to spread of CWD – an update on the situation in Nordfjella, Norway

 

Opinion of Panel on biological hazards of the Norwegian Scientific Committee for Food and Environment 13.12.2018 ISBN: 978-82-8259-316-8 ISSN: 2535-4019 Norwegian Scientific Committee for Food and Environment (VKM) Po 222 Skøyen 0213 Oslo Norway FRIDAY, DECEMBER 14, 2018 

 

Norway, Nordfjella VKM 2018 16 Factors that can contribute to spread of CWD TSE Prion UPDATE December 14, 2018

 

https://vkm.no/download/18.696229a71677d983532c0c11/1544792739325/CWD%20...

 

https://chronic-wasting-disease.blogspot.com/2018/12/norway-nordfjella-v...

 

THURSDAY, OCTOBER 25, 2018

 

 

***> Norway New additional requirements for imports of hay and straw for animal feed from countries outside the EEA due to CWD TSE Prion

 

 

https://www.mattilsynet.no/dyr_og_dyrehold/dyrehelse/nye_tilleggskrav_ve...

 

 

https://chronic-wasting-disease.blogspot.com/2018/10/norway-new-addition...

 

 

***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018 

 

P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer 

 

Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) 

 

(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. 

 

Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer. 

 

Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection. 

 

Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD. 

 

https://prion2018.org/

 

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

 

***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. 

 

Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3

 

Correspondence

 

Gudmundur Georgsson [email protected]

 

1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland

 

2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland

 

3 Bethesda, Maryland, USA

 

Received 7 March 2006 Accepted 6 August 2006

 

In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.

 

http://www.microbiologyresearch.org/docserver/fulltext/jgv/87/12/3737.pd...

 

TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 

 

https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261

 

*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 

 

http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article

 

SEE;

 

Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;

 

Some unofficial information from a source on the inside looking out -

 

Confidential!!!!

 

As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

 

---end personal email---end...tss

 

http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-ora... ***> cwd scrapie pigs oral routes

 

***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***

 

>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***

 

***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).

 

***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period.

 

***> This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.

 

***> Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.

 

>>>> The successful transmission of pig-passaged CWD to Tg40 mice reported here suggests that passage of the CWD agent through pigs results in a change of the transmission characteristics which reduces the transmission barrier of Tg40 mice to the CWD agent. If this biological behavior is recapitulated in the original host species, passage of the CWD agent through pigs could potentially lead to increased pathogenicity of the CWD agent in humans.

 

https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091

 

https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017

 

https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105

 

SNIP...SEE FULL TEXT, MUCH MORE

 

FRIDAY, DECEMBER 28, 2018 

 

Chronic Wasting Disease CWD TSE Prion 2019 Where The Rubber Meets The Road 

 

https://chronic-wasting-disease.blogspot.com/2018/12/chronic-wasting-dis...

 

 

kindest regards, terry