Buck Hollow Sporting Goods - click or touch to visit their website Midwest Habitat Company

Flounder9 can you explain this article

I don’t think flounder will have a reply. The article does discuss him- not favorably so, out of respect & hearing his point of view.... I wish he’d respond with some bullet points & common sense replies & sure welcome it.

Here’s one thing that jumps out at me..... “mad cow is wide spread, crisis & could do XYZ & is or could be a total disaster to wildlife, humans, etc”. Article clearly looks to debunk & discredit that line of thinking. They are claiming the “scare mongering” is just that - unfound panic & unknowns that have no true answers, understandings or may be motivated by deeper reasons. Whatever. Whether u agree with article or not.... if folks don’t see that a parallel argument could be made with cwd- u missing this. Most of the article could be applied to the “CWD CRISIS”. Not saying which position is correct. This article is obviously a major case against mad cow & prion panic BUT it sure could be a pertinent argument on the “cwd crisis” as well
 
This article was printed in 2003. Who cares if you believe Terry or not. The studies are out there for you to decide on your own. A lot of the time terry links studies (that he didn’t author). Some of you plain and simply put get mad at the idea that growing 6+ year old bucks and having 50+ deer in a field might not be the right thing to do. I’m not here to tell you that CWD is a risk or not (because I have no idea myself), but I don’t have my head so far in the sand that I can’t fathom the idea.


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I know it’s an old article that was initially focused on cattle/beef but then moved onto deer/venison.... I can assure you my head isn’t in the sand on this topic but I will say that I’m skeptical of the true agenda. As always, I’ll continue to research CWD from multiple sources.


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SO, just who are The Center for Consumer Freedom

http://www.consumerfreedom.com/index.cfm

let's take a closer look shall we;

The Center for Consumer Freedom (CCF) (formerly called the "Guest Choice Network (GCN)") is a front group for the restaurant, alcohol and tobacco industries. It runs media campaigns which oppose the efforts of scientists, doctors, health advocates, environmentalists and groups like Mothers Against Drunk Driving, calling them "the Nanny Culture -- the growing fraternity of food cops, health care enforcers, anti-meat activists, and meddling bureaucrats who 'know what's best for you.'"

CCF is registered as a tax-exempt, non-profit organization under the IRS code 501(c)(3). Its advisory board is comprised mainly of representatives from the restaurant, meat and alcoholic beverage industries.

http://www.sourcewatch.org/index.php?title=Center_for_Consumer_Freedom

http://en.wikipedia.org/wiki/Center_for_Consumer_Freedom

SEE FULL TEXT AND MORE HERE

http://madcowusda.blogspot.com/2014/09/mad-cow-scaremongers-consumerfreedomcom.html

Alzheimer's disease

let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...

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

http://journals.plos.org/plosone/ar...notation/933cc83a-a384-45c3-b3b2-336882c30f9d

http://journals.plos.org/plosone/article/comments?id=10.1371/journal.pone.0111492

http://journals.plos.org/plosone/ar...notation/933cc83a-a384-45c3-b3b2-336882c30f9d

https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full

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

IN CONFIDENCE

5 NOVEMBER 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

[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.]

https://web.archive.org/web/2017012...einquiry.gov.uk/files/yb/1992/11/04001001.pdf

https://web.archive.org/web/2004031...einquiry.gov.uk/files/yb/1992/12/16005001.pdf

https://web.archive.org/web/20040315075058/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf

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)

https://www.nature.com/articles/nature15369

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.

snip...

http://web.archive.org/web/20040315...quiry.gov.uk:80/files/yb/1992/12/16005001.pdf

https://web.archive.org/web/2017012...einquiry.gov.uk/files/yb/1992/11/04001001.pdf

https://journals.plos.org/plosone/a...notation/933cc83a-a384-45c3-b3b2-336882c30f9d

please see more of this history and references there from (these blogs are for educational use, I do not advertise or make money from this. just made a promise to mom dod 12/14/97 hvCJD, never forget, and never let them forget.) human transmission of amyloid-β pathology and cerebral amyloid angiopathy, Singeltary Submission to Nature

https://betaamyloidcjd.blogspot.com/2015/10/alzheimergate-re-evidence-for-human.html

P132 Aged cattle brain displays Alzheimer’s-like pathology that can be propagated in a prionlike manner

snip...

These results may contribute to uncover a previously unsuspected etiology surrounding some cases of sporadic AD. However, the early and controversial stage of the field of prion-like transmission in non-prion diseases added to the artificial nature of the animal models utilized for these studies, indicate that extrapolation of the results to humans should not be done without further experiments.

P75 Determining transmissibility and proteome changes associated with abnormal bovine prionopathy
Dudas S (1,2), Seuberlich T (3), Czub S (1,2)

In the first passage, cattle were intra-cranially challenged with brain homogenate from 2 Swiss animals with abnormal prionopathy. The challenged cattle incubated for 3 years and were euthanized with no clinical signs of neurologic disease. Animals were negative when tested on validated diagnostic tests but several research methods demonstrated changes in the prion conformation in these cattle, including density gradient centrifugation and immunohistochemistry. Currently, samples from the P1 animals are being tested for changes in protein levels using 2-D Fluorescence Difference Gel Electrophoresis (2D DIGE) and mass spectrometry. It is anticipated that, if a prionopathy is present, this approach should identify pathways and targets to decipher the source of altered protein conformation. In addition, a second set of cattle have been challenged with brain material from the first passage. Ideally, these cattle will be given a sufficient incubation period to provide a definitive answer to the question of transmissibility.

=====prion 2018===

https://prion2018.org/wp-content/uploads/2018/05/program.pdf

https://prion2018.org/

however in 1 C-type challenged animal, Prion 2015 Poster Abstracts

S67 PrPsc was not detected using rapid tests for BSE.

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

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

Posted by Terry S. Singeltary Sr. on 03 Jul 2015 at 16:53 GMT

http://www.plosone.org/annotation/listThread.action?root=86610

Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan.

This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada.

It also suggests a similar cause or source for atypical BSE in these countries.

see page 176 of 201 pages...tss

http://www.neuroprion.org/resources/pdf_docs/conferences/prion2009/prion2009_bookofabstracts.pdf

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

http://www.plosone.org/annotation/l...id=635CE9094E0EA15D5362B7D7B809448C?root=7143

http://bovineprp.blogspot.com/2018/02/

THURSDAY, FEBRUARY 7, 2019

In Alzheimer's Mice, Decades-Old Human Cadaveric Pituitary Growth Hormone Samples Can Transmit and Seed Amyloid-Beta Pathology

https://betaamyloidcjd.blogspot.com/2019/02/in-alzheimers-mice-decades-old-human.html

kind regards, terry
 
The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock.

https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article

***> IMPORTS AND EXPORTS <***

***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***

http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html

USA MAD COW CASE 2018 FLORIDA

WEDNESDAY, SEPTEMBER 26, 2018

JAVMA In Short Update USDA announces detection of atypical BSE

http://bovineprp.blogspot.com/2018/09/javma-in-short-update-usda-announces.html

ZOONOSIS OF SCRAPIE TSE PRION

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.
==============

https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf

***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.

http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

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

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a

Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

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.

http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20

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.

http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160

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

Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation

SNIP...

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.

snip...

https://www.nature.com/articles/srep11573


kind regards, terry
 
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.

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

***> 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. <***
Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research

2017 Annual Report

1a. Objectives (from AD-416):

snip...

4. Accomplishments

1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. 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.

2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, 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.

snip...

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

FRIDAY, APRIL 20, 2018

*** Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?

Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies

http://scrapie-usa.blogspot.com/2018/04/scrapie-transmits-to-pigs-by-oral-route.html


kind regards, terry
 
QDM said:
Terry,

I want to be as open minded as anyone about CWD and what to do about it as best I can to protect myself and family.
However, I’m finding info like the link below that leaves me with more questions/concerns.

https://www.consumerfreedom.com/articles/138-mad-cow-scaremongers/



Sent from my iPhone using Tapatalk
Click to expand...


i hope that explains any concerns you may have.

i still eat meat, got my guns, and am pro-hunt. the only problem i have is chewing up my meat, i am long in the tooth, and molars are gone. sucks getting old...


hope ya'll have a great weekend...


kind regards, terry
 
Sligh1 said:
I don’t think flounder will have a reply. The article does discuss him- not favorably so, out of respect & hearing his point of view.... I wish he’d respond with some bullet points & common sense replies & sure welcome it.

Here’s one thing that jumps out at me..... “mad cow is wide spread, crisis & could do XYZ & is or could be a total disaster to wildlife, humans, etc”. Article clearly looks to debunk & discredit that line of thinking. They are claiming the “scare mongering” is just that - unfound panic & unknowns that have no true answers, understandings or may be motivated by deeper reasons. Whatever. Whether u agree with article or not.... if folks don’t see that a parallel argument could be made with cwd- u missing this. Most of the article could be applied to the “CWD CRISIS”. Not saying which position is correct. This article is obviously a major case against mad cow & prion panic BUT it sure could be a pertinent argument on the “cwd crisis” as well
Click to expand...

BSE INQUIRY DFA 15 Monitoring and Enforcement of the SBO Specified Bovine Offal Regulations, MRM, and TSE PRION

one more thing folks, i have followed this circus since 1997, and researched it to the early days of the BSE Inquiry, even made a statement about these snake oil supplements that contained SRMs here in the USA and abroad, i.e. like deer antler velvet in supplements, along with brains, eyes, pituitary and such. even had one company reprocess their manufacturing of some of their products due to the risk factors the tse prion and their products used, much too late though. the fda has been trying to warn of this for decades, but there is little to no regulations for that industry, considering corporate America and it's junk science that is pushed through by lobbyist, and those that believe in ted nugent science. this really is not rocket science. all one has to do is follow the transmission studies. as someone said though, don't believe me or uncle ted, one has to make their own minds up with the science at hand, for their family.

mad cow disease, the typical c-type BSE, supposedly the UK strain, well, that's around the world now, along with all the atypical BSE cases, and don't think for one minute the bullshit that the usda oie want you to believe, i.e. that atypical BSE is a old cow type disease, and is a spontaneous event. this is BSe at it's finest, bought and paid for by the usda inc and the oie. again, all one has to do is look at the science. IF, this was true, then why is places like Poland and France, having an extremely out of the ordinary, spontaneous event. IT'S FEED FOLKS, and i believe this is _part_ of the problem with cervid.

MONDAY, FEBRUARY 04, 2019

POLAND DETECTS BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION

Poland is Proof atypical BSE is NOT an old cow spontaneous disease...tss

https://bse-atypical.blogspot.com/2019/02/poland-detects-bovine-spongiform.html

BUT REMEMBER, BSE IS NOT CWD, CWD IS MUCH WORSE, IN MANY WAYS, to date.

also, this was 25 years ago.this is old science. some of this science, transmission, strains, and such, have changed, for the worse.

but this might give you an idea of the concerns of processing meat with BSE TSE Prion aka mad cow disease. these files are archived in my BSE Inquiry files, some of the BSEInquiry Links may be old and not work. if you see one that you might like to have source link that works, let me know, and i will see if i can update...

kind regards, terry

Subject: BSE INQUIRY EARLY DAYS DFA 15 Monitoring and Enforcement of the SBO Specified Bovine Offal Regulations

(xi.) There was concern about contamination during carcase splitting and, in particular, concern that splitting often caused the spinal cord to be severed which could result in small pieces of cord becoming lodged between vertebrae;[14]
(xii.) There was concern about mechanically recovered meat, particularly that recovered from the spinal column;[15]
(xiii.) There was concern that removal of the specified offals did not fully remove the nervous and lymphatic tissue from the animal leaving some of those tissues in food for human consumption;[16]

BSE Inquiry

DFA 15 Monitoring and Enforcement of the SBO Specified Bovine Offal Regulations

http://bseinquiry.blogspot.com/2017/08/dfa-15-monitoring-and-enforcement-of.html

SATURDAY, AUGUST 26, 2017

https://bseinquiry.blogspot.com/2017/08/dfa-14-consideration-of-risk-from.html

BSE INQUIRY DFA 16 MID 1995 TO THE FINAL DAYS

https://bseinquiry.blogspot.com/2017/08/bse-inquiry-dfa-16-mid-1995-to-final.html

Wednesday, January 23, 2019

CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019

https://specifiedriskmaterial.blogspot.com/2019/01/cfia-sfcr-guidance-on-specified-risk.html

THURSDAY, FEBRUARY 07, 2019

CWD TSE Prion, and Processing your own meat

https://chronic-wasting-disease.blogspot.com/2019/02/cwd-tse-prion-and-processing-your-own.html

this is all in the world those 300k+ bovine that died with BSE were consuming, a nutritional supplement with srms, i.e. specified risk materials, the most highest risk tissue for the tse prion.

Sender: "Patricia Cantos" <patricia.cantos at bse.org.uk>

To: "Terry S Singeltary Sr. (E-mail)" <flounder at wt.net>

Subject: Your submission to the Inquiry

Date: Fri, 3 Jul 1998 10:10:05 +0100

3 July 1998 Mr Terry S Singeltary Sr. E-Mail: Flounder at wt.net Ref: E2979

Dear Mr Singeltary,

Thank you for your E-mail message of the 30th of June 1998 providing the Inquiry with your further comments. Thank you for offering to provide the Inquiry with any test results on the nutritional supplements your mother was taking before she died.

As requested I am sending you our general Information Pack and a copy of the Chairman's letter. Please contact me if your system cannot read the attachments.

Regarding your question, the Inquiry is looking into many aspects of the scientific evidence on BSE and nvCJD. I would refer you to the transcripts of evidence we have already heard which are found on our internet site at http://www.bse.org.uk. Could you please provide the Inquiry with a copy of the press article you refer to in your e-mail? If not an approximate date for the article so that we can locate it? In the meantime, thank you for you comments. Please do not hesitate to contact me on 0171 261 8332 should you have any queries.

Yours sincerely Patricia Cantos Families Team Leader Attachments TSS

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

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

Subject: re: METABOLIFE AND TSEs GAO-03-494 ''URGENT DATA''

Date: Thu, 01 May 2003 16:04:35 -0400

From: "Marcia G Crosse" <CrosseM at gao.gov>

To: <flounder at wt.net>

CC: "Charles W Davenport" <DavenportC at gao.gov>, "Carolyn Feis Korman" <FeisKormanC at gao.gov>, "Martin Gahart" <GahartM at gao.gov>

Mr. Singletary,

We were informed by representatives of Metabolife, Inc. that Metabolife 356 was reformulated to remove bovine complex as an ingredient in the product, approximately September 2001. We did not independently verify the contents of the product.

Sincerely, Marcia Crosse Acting Director Health CarePublic Health and Science Issues U.S. General Accounting Office 441 G Street, N.W. Washington, D.C. 20548

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

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

Subject: Re: METABOLIFE AND TSEs GAO-03-494 ''URGENT DATA''

Date: Thu, 01 May 2003 15:48:52 -0500

From: "Terry S. Singeltary Sr." <flounder at wt.net>

To: Marcia G Crosse <CrosseM at gao.gov>

CC: Charles W Davenport <DavenportC at gao.gov>, Carolyn Feis Korman <FeisKormanC at gao.gov>, Martin Gahart <GahartM at gao.gov> References: <seb14599.014 at GAOGWIA1.GAO.GOV>

THANK YOU!

MIRACLES DO HAPPEN! ;-)
Thursday, March 19, 2009

Chronic Wasting Disease Prions in Elk Antler Velvet (Nutritional Supplements and CJD)

http://chronic-wasting-disease.blogspot.com/2009/03/chronic-wasting-disease-prions-in-elk.html

terry
 
Terry,
From what I’ve researched. There has been 4 cases of vCJD in the US. There has been a slow uptick in the number of CJD cases in the US. Almost 500 a year now. I haven’t been able to find the reason for that. Or maybe it’s just being diagnosed more than before? I wouldn’t knowingly eat an infected deer, maybe the sky will fall some day and there will be a huge swing in the number of TSE in humans but as of right now that is simply not the case. The numbers do not lie. With the number of CWD positives growing by the day. The number of CWD consumed meat would also be on the rise. Therefor there we should start seeing more cases of vCJD.
 
MN Hunter said:
Terry,
From what I’ve researched. There has been 4 cases of vCJD in the US. There has been a slow uptick in the number of CJD cases in the US. Almost 500 a year now. I haven’t been able to find the reason for that. Or maybe it’s just being diagnosed more than before? I wouldn’t knowingly eat an infected deer, maybe the sky will fall some day and there will be a huge swing in the number of TSE in humans but as of right now that is simply not the case. The numbers do not lie. With the number of CWD positives growing by the day. The number of CWD consumed meat would also be on the rise. Therefor there we should start seeing more cases of vCJD.
Click to expand...

all studies to date shows that cwd transmission to humans WILL NOT look like nvcjd or what they call now as vcjd. it will look like sporadic cjd.


However, we can say with confidence that under the conditions used here, none of the animal isolates tested were as efficient as C-type BSE in converting human PrPC, which is reassuring.

***Less reassuring is the finding that there is no absolute barrier to the conversion of human PrPC by CWD prions in a protocol using a single round of PMCA and an entirely human substrate prepared from the target organ of prion diseases, the brain.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3884726/

*** now, let’s see what the authors said 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 (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

> 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).***

http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys

http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true

https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article


kind regards, terry
 
Michael Osterholm, director for the University of Minnesota's Center for Infectious Disease Research and Policy who sat on a panel of experts tracking the emergence of mad cow disease, or BSE, decades ago, told lawmakers this:

"It is my best professional judgment based on my public health experience and the risk of BSE transmission to humans in the 1980s and 1990s and my extensive review and evaluation of laboratory research studies ... that it is probable that human cases of CWD associated with the consumption of contaminated meat will be documented in the years ahead. It is possible that number of human cases will be substantial and will not be isolated events."

https://www.winonadailynews.com/new...cle_fa49cff4-336f-5e18-9a66-c2248e8df354.html

We hypothesize that:

(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;

(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;

(3) Reliable essays can be established to detect CWD infection in humans; and

(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.

ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE

here is the latest;

PRION 2018 CONFERENCE

Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice

Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).

To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.

After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.

Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.

The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.

The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..

***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***

https://prion2018.org/

READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;

P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States

Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..

SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.

AND ANOTHER STUDY;

P172 Peripheral Neuropathy in Patients with Prion Disease

Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..

IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,

AND

included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),

AND

THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.

snip...

see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry

https://prion2018.org/wp-content/uploads/2018/05/program.pdf

https://prion2018.org/

THURSDAY, OCTOBER 04, 2018

Cervid to human prion transmission 5R01NS088604-04 Update

http://grantome.com/grant/NIH/R01-NS088604-04

http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html


kind regards, terry
 
This is from the National Institute of Health.

creased. These findings are consistent with other studies that indicate a relative excess of cases among females [33], [35]–[38] but a higher incidence of CJD among the male population [35], [39]. The CJD incidence rates varied regionally, with the highest rate in the Northeast region and the lowest rates in the South and West regions. The low rate in the West is of particular interest due to the longstanding presence of chronic wasting disease (CWD) among cervids in parts of the region, particularly in Colorado and Wyoming.
 
A couple short sentence reply’s or little facts would be a lot nicer than 10 links to studies most on here are not going to read. In laymen terms would be nice too, people might take you a little more serious.



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