CWD TSE PRION UPDATE

[flounder9]

Greetings PAFOA et al,
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Seasons Greetings,
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I thought I might update you all on a bit of CWD TSE Prion science for some here that might still be interested. Please use the information as you wish. I know it’s a thorny issue, just thought some might be interested…Happy Trails……..terry
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***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
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P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion
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Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD
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In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible. ***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
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PRION 2016 CONFERENCE TOKYO
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http://prion2016.org/dl/newsletter_03.pdf
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*** Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission ***
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https://www.ars.usda.gov/research/pu...eqNo115=328261
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PLEASE SEE DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE
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Volume 22, Number 12—December 2016 Dispatch Horizontal Transmission of Chronic Wasting Disease in Reindeer
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http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article
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Saturday, May 28, 2016
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*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***
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http://chronic-wasting-disease.blogs...prpcwd-in.html
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Sunday, December 11, 2016
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Clay Components in Soil Dictate Environmental Stability and Bioavailability of Cervid Prions in Mice
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http://chronic-wasting-disease.blogs...l-dictate.html
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Chronic Wasting Disease (CWD) Susceptibility of Several North American Rodents That Are Sympatric with Cervid CWD Epidemics▿
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http://jvi.asm.org/content/84/1/210.full
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*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
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Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
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http://jgv.sgmjournals.org/content/87/12/3737.full
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***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD.
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Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
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http://www.wda2016.org/uploads/5/8/6...gs_low_res.pdf
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PRION 2016 TOKYO
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Zoonotic Potential of CWD Prions: An Update
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Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6 1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. 4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, 2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
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Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.
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PRION 2016 TOKYO In Conjunction with Asia Pacific Prion Symposium 2016 PRION 2016 Tokyo Prion 2016
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http://prion2016.org/dl/newsletter_03.pdf
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http://grantome.com/grant/NIH/R01-NS088604-01A1

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Monday, May 02, 2016
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*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
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http://chronic-wasting-disease.blogs...ns-update.html
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http://chronic-wasting-disease.blogspot.com/

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Saturday, April 23, 2016
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PRION 2016 TOKYO Saturday, April 23, 2016
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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
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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.
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http://www.tandfonline.com/doi/abs/1...nalCode=kprn20
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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
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http://collections.europarchive.org/...9/23001001.pdf
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Title: Transmission of scrapie prions to primate after an extended silent incubation period)
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*** 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.
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*** 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.
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*** 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.
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http://www.ars.usda.gov/research/pub..._NO_115=313160
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SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

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http://scrapie-usa.blogspot.com/2016...n-animals.html
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http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article
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http://scrapie-usa.blogspot.com/


Wednesday, December 21, 2016
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*** TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH ***
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http://transmissiblespongiformenceph...ation-and.html
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Wednesday, December 14, 2016
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Diagnosis of Human Prion Disease Using Real-Time Quaking-Induced Conversion Testing of Olfactory Mucosa and Cerebrospinal Fluid Samples
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http://creutzfeldt-jakob-disease.blo...ase-using.html
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Terry S. Singeltary Sr.

[gghbi]

Terry, would it be possible to get an executive summary in plain language?? Can we get it?

[Gunsnwater]

I understand why your posting this and I am sorry for your loss. Do you think you could write a bit with out all the alphabet soup stuff and pass on the state of the problem. Is it spreading? Is it in the food supply still? Any way to avoid it? Thanks for the information.

[flounder9]

I understand why your posting this and I am sorry for your loss. Do you think you could write a bit with out all the alphabet soup stuff and pass on the state of the problem. Is it spreading? Is it in the food supply still? Any way to avoid it? Thanks for the information.

Terry, would it be possible to get an executive summary in plain language?? Can we get it?

Greetings Gunsnwater and gghbi et al, I wish I could dumb it down some, but it's really not rocket science. for those that are interested, you are going to have to read the sound tse prion science, ignore the corporate junk science there from, and make your own decisions about these pesky prions. you don't want your families eating them that's for sure, tse prions can kill you. once exposed, if you live long enough to go clinical, there is no cure, it's 100% fatal once clinical. do all people exposed to the tse prion go clinical and die, NO, but do you want to take that chance with your loved ones?

Is it spreading? yes Sir

Any way to avoid it? not really, it's in the food, in the cosmetics, supplements, hospitals surgical/medical/dental, environment, soil, water, the list is endless, but it does not mean to just ignore it then. we must all get on the same page from state to state, country to country, or it will be futile, as we have found out with Korea and Norway with CWD.

Is it in the food supply still? yes Sir, and the hospitals and that's what I am most concerned with, once consumed and exposed, then you go to the hospital for some procedure, then that complete surgical unit is exposed to 'pass if forward' i.e. iatrogenic exposure. I am always amazed at this old study ;

*** 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.

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


***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD.
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Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
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http://www.wda2016.org/uploads/5/8/6...gs_low_res.pdf


Wednesday, December 21, 2016

TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH

http://transmissiblespongiformenceph...ation-and.html


Thursday, December 08, 2016

USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie

http://scrapie-usa.blogspot.com/2016...adication.html

http://scrapie-usa.blogspot.com/2016...s-mission.html

I wish I had all the answers, but I don't. I do know that by ignoring it, it will not go away. it will mutate, and it will continue to spread.

we must remove the industry from the scientific and decision policy making, that's what the problem has been all along, and that's why we are in this mess.

Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
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Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
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snip...
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The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
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http://collections.europarchive.org/.../m09/tab05.pdf
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http://collections.europarchive.org/...m09a/tab01.pdf
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http://collections.europarchive.org/...6/10004001.pdf
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In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells
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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. ...
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http://web.archive.org/web/200603070...m11b/tab01.pdf
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”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.
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http://collections.europarchive.org/...m11b/tab01.pdf
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*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
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http://collections.europarchive.org/...m11b/tab01.pdf
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http://bse-atypical.blogspot.com/201...pongiform.html
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SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
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***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.***
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http://www.nature.com/articles/srep11573


Primate Biol., 3, 47–50, 2016 www.primate-biol.net/3/47/2016/ doi:10.5194/pb-3-47-2016 © Author(s) 2016. CC

Attribution 3.0 License.

Prions

Walter Bodemer German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany Correspondence to: Walter Bodemer (wbodemer@dpz.eu)

Received: 15 June 2016 – Revised: 24 August 2016 – Accepted: 30 August 2016 – Published: 7 September 2016

Abstract.

Prions gained widespread public and scientific interest in the year 2000. At that time, the human neurological Creutzfeldt–Jakob disease (CJD) was known. However, new CJD cases were diagnosed but they could not be ascribed to one of the classical CJD categories i.e. sporadic (sCJD), hereditary or acquired. Hence, they were classified as variant CJD (vCJD). Later on, experimental evidence suggested that vCJD was caused by prions postulated as unique novel infectious agents and, for example, responsible for bovine spongiform encephalopathy (BSE) also known as mad cow disease. The infection of humans by transmission of BSE prions also defined vCJD as a zoonotic disease. Prions, especially those associated with scrapie in sheep had been known for quite some time and misleadingly discussed as a slow virus. Therefore, this enigmatic pathogen and the transmission of this unusual infectious agent was a matter of a controversial scientific debate. An agent without nucleic acid did not follow the current dogma postulating DNA or RNA as inheritable information encoding molecules. Although numerous experimental results clearly demonstrated the infectious capacity of prions in several animal species, a model close to human was not readily available. Therefore, the use of rhesus monkeys (Macaca mulatta) served as a non-human primate model to elucidate prion infection under controlled experimental conditions. Not the least, transmission of BSE, human vCJD, and sCJD prions could be confirmed in our study. Any prion infection concomitant with progression of disease in humans, especially vCJD, could be analyzed only retrospectively and at late stages of disease. In contrast, the prion-infected rhesus monkeys were accessible before and after infection; the progression from early stage to late clinical stages – and eventually death of the animal–could be traced. Because of the phylogenetic proximity to humans, the rhesus monkey was superior to any rodent or other animal model. For these reasons an experimental approach had been conceived by J. Collinge in London and A. Aguzzi in Zurich and performed in a cooperative study with both research groups in the pathology unit of the German Primate Center (DPZ). The study in the DPZ lasted from 2001 until 2012. Our research in the pathology unit provided a temporal monitoring of how an initial prion infection develops eventually into disease; an approach that would have never been possible in humans since the time point of infection with prions from, for example, BSE is always unknown. Telemetry revealed a shift in sleep– wake cycles early on, long before behavioral changes or clinical symptoms appeared. Pathology confirmed nonneuronal tissue as hidden places where prions exist. The rhesus model also allowed first comparative studies of epigenetic modifications on RNA in peripheral blood and brain tissue collected from uninfected and prion infected animals. To conclude, our studies clearly demonstrated that this model is valid since progression to disease is almost identical to human CJD.

Published by Copernicus Publications on behalf of the Deutsches Primatenzentrum GmbH (DPZ).


SNIP...


2 Methods and results

2.1 Animals The reason to perform prion research in rhesus monkeys was to monitor infection and the temporal progression of prion infection in the rhesus monkey. In contrast to studies of human CJD cases, we could decide on the infectious dose. We also could control behavior immediately after prion inoculation and during the rather long time until animals died from the prion infection. Hidden places where prions might exist were found. Even epigenetic modifications on RNA could be detected. Taken together, these experimental approaches depended on animals. Using rhesus monkeys as a model system required thorough ethic reasoning and consultation with authorities before we actually turned to conduct the experiments. The Number of animals was limited just to fulfill statistical conditions. The individual health status was obtained and health care was provided throughout the study. The animals underwent daily inspection to monitor any changes in health and behavior. The experiments were conceived with the aim of reducing pain, suffering, and harm. Groups of animals were preferred in order to keep them in a social environment. The animals were originally kept in Vienna at Baxter and transferred to the German Primate Center (DPZ) in 2001. J. Collinge, A. Aguzzi, and C. Weissmann were the scientists who recommended this well-controlled prion infection study, and financial support was provided by an EU grant.To ensure statistical significance four groups consisting of four rhesus macaques each were formed: one uninfected control group, one group infected with BSE prions, one with vCJD prions, and one with sCJD prions. Health of animals, infection, and progression to disease was looked at in our pathology department and in cooperation with W. Schulz-Schaeffer at the UMG (University Medicine, Göttingen). Besides, neurologists from the UMG also observed the animals whenever clinical symptoms seemed to appear. This close observation and comparison with human CJD cases demonstrated how close clinical progression of human disease resembles the experimental infection in the non-human primate.

2.2 Infection Infectious prions from brain tissue of one sCJD and one vCJD case (provided by J. Collinge) as well as BSE prions (from a “German” madcow case and provided by W. Schulz Schaeffer) were intraperitoneally administered into the rhesus monkeys.

2.3 Monitoring of behavior and telemetry Early behavioral monitoring was carried out by the ethologists I. Machatschke and J. Dittami from Vienna University. Transmitters were used to record changes in the circadian rhythms. Body temperature, sleep–wake cycles, and activity profiles could be obtained over a time span of 2 years. Up to half a year after infection animals did not show any signs of prion infection. However, after 6 months and persisting for another few months some animals had some disturbances in circadian rhythms which disappeared and then never appeared again(I. Machatschke, personal communication,2006).For a rather long time of about 4–5 years animals seemed to be healthy. But then, almost all animals rapidly progressed to symptoms. Symptoms were highly similar or even identical to those seen in human CJD.

2.4 Pathology Blood and necropsy specimens from the animals served as a valuable source to detect pathologically associated prion protein even in non-neuronal skeletal and cardiac tissue. These “hidden places” of prion pathology and replication were clearly demonstrated and extended our view where prions might spread within an organism. Not only leukocytes and neuronal tissue harbor abnormal prion protein isoforms but also other tissues can propagate prion protein isoforms leading to toxicity, cell degeneration, and eventually transmissible prions (Krasemann et al., 2010, 2013).


SNIP...


3 Conclusion

Most importantly, early signs of an altered circadian rhythm, sleep–wake cycle, and activity and body temperature were recorded in prion-infected animals. This experimental approach would have never been feasible in studies with human CJD cases. After 4–6 years animals developed clinical symptoms highly similar to those typical for CJD. Clinicians confirmed how close the animal model and the human disease matched. Non-neuronal tissue like cardiac muscle and peripheral blood with abnormal, disease-related prion protein were detected in rhesus monkey tissues.*

Molecular changes in RNA from repetitive Alu and BC200 DNA elements were identified and found to be targets of epigenetic editing mechanisms active in prion disease. To conclude, our results with the rhesus monkey model for prion disease proved to be a valid model and increased our knowledge of pathogenic processes that are distinctive to prion disease.


SEE FULL TEXT ;


http://www.primate-biol.net/3/47/2016/pb-3-47-2016.pdf

[flounder9]

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.

FRIDAY, JANUARY 20, 2017

MICHIGAN CHRONIC WASTING DISEASE IDENTIFIED IN TWO MECOSTA COUNTY FARMED DEER

http://chronic-wasting-disease.blogs...g-disease.html

FRIDAY, JANUARY 20, 2017

Minnesota Chronic Wasting Disease investigation traces exposure to Meeker County farm

http://chronic-wasting-disease.blogs...g-disease.html

SUNDAY, JANUARY 22, 2017

Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry

http://chronic-wasting-disease.blogs...sion-2017.html

FRIDAY, JANUARY 13, 2017

Pennsylvania Deer Tests Positive for Chronic Wasting Disease four-year-old white-tailed deer Franklin County Hunting Preserve

http://chronic-wasting-disease.blogs...itive-for.html

SATURDAY, JANUARY 14, 2017

CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017

http://chronic-wasting-disease.blogs...tse-prion.html

kind regards, terry

[Qtrborecrazy]

Looks like a lot of the disease comes from captive herds.