January 14, 2018

Texas TPWD CWD positive Panhandle Roadkill Whitetail

http://chronic-wasting-disease.blogspot.com/2018/01/texas-tpwd-cwd-positive-panhandle.html


kind regards, terry

Old news. But, the sky is definitely falling. Thanks for the heads up. I’m gonna go invest in Reynolds wrap.

Yep, all the deer in Texas will soon be gone. Maybe they can figure out a way to get rid of anthrax which is the real threat in certain areas of west Texas.

Terry Singletary — A retired machinist and high school dropout, Terry Singletary suffered the tragic loss of his mother to “sporadic” Creutzfeldt-Jakob disease (CJD) in 1997. Desperate to find an explanation for his mother’s death, he has devoted himself to the sad and fruitless task of connecting her death to her diet. Various reports confirm that Mrs. Singletary’s life was claimed by the most common sub-type of CJD (one that accounts for 70 percent of “sporadic” cases). Sporadic CJD, unlike its newer “variant,” is not linked to meat.

As the self-appointed international coordinator of CJD Watch, an organization he co-founded with social worker Deborah Oney, Singletary is cited in media reports as an apparent expert on tracking mad cow disease. This despite his lack of formal education and the absence for support from any credible academic, medical or scientific authority. His sensationalist allegations about the safety of U.S. beef have found their way into hundreds of newspapers and broadcasts. Singletary moderates a mad-cow discussion forum run by a vegetarian activist group; his contributions account for more than half the traffic on the “BSE-L” mailing list, which is generally read by real scientists. Animal rights activists and other food-scare artists frequently refer to him as “Dr. Terry Singletary,” apparently an honorary degree as he has yet to finish high school.

Like many activists, Singletary ignores overwhelming epidemiological and laboratory evidence that rules out a connection between sporadic CJD and beef. Relying entirely on shallow circumstantial evidence and frequent repetition of claims which have been publicly refuted as false, he also blindly insists upon a mad-cow with Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease. His specific allegations have been clearly refuted by Centers for Disease Countrol and Prevention scientists in the journal Neurology.

I heard that deep frying backstrap prohibits the spread of cwd to humans, but to make sure if you cover with your grandma's gravy there would be no way to contract!

Never let facts or the life's work of hundreds of actual scientists and medical research professionals get in the way of a good story.

LMAO! getting desperate now are ya


i just love it when folks are grasping for straws and fake news trying to cover up the truth. this old article has been proven so terribly wrong, and they just don't get it, still. every thing i said back then has come true...sadly.

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

snip...SEE FULL TEXT HERE ;

http://betaamyloidcjd.blogspot.com/2010/12/alimentary-prion-infections-touch-down.html

Mad Cow Scaremongers by Terry S. Singeltary Sr. a review of the TSE prion agent 2003-2011

http://transmissiblespongiformencephalopathy.blogspot.com/2011/09/mad-cow-scaremongers.html

TUESDAY, DECEMBER 12, 2017

*** Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017 ***

(zoonosis and environmental risk factors towards the bottom, after state by state reports)

http://chronic-wasting-disease.blogspot.com/2017/12/chronic-wasting-disease-cwd-tse-prion.html

FRIDAY, DECEMBER 15, 2017

Canada CFIA updating its national CWD TSE PRION efforts to eradicate disease farmed cervid NOT successful December 14, 2017

http://chronic-wasting-disease.blogspot.com/2017/12/canada-cfia-updating-its-national-cwd.html

TUESDAY, DECEMBER 12, 2017

Bovine Spongiform Encephalopathy BSE TSE Prion (aka mad cow disease) Report December 14, 2017 2017

http://bovineprp.blogspot.com/2017/12/bovine-spongiform-encephalopathy-bse.html

MONDAY, JANUARY 1, 2018

PRESIDENT TRUMP KILLS PROPOSED RULE THAT WOULD HAVE PROHIBITED THE USE OF COW BYPRODUCTS IN THE MANUFACTURING OF DRUGS WARNING TO ALL COUNTRIES

http://bseusa.blogspot.com/2018/01/president-trump-kills-proposed-rule.html

TUESDAY, DECEMBER 12, 2017

SCRAPIE TSE PRION UPDATE USA DECEMBER 14, 2017

http://scrapie-usa.blogspot.com/2017/12/scrapie-tse-prion-update-usa-december.html

TUESDAY, DECEMBER 12, 2017

Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017

http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html

Tuesday, December 12, 2017

Neuropathology of iatrogenic Creutzfeldt–Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology

http://tauopathies.blogspot.com/2017/12/neuropathology-of-iatrogenic.html


kind regards, terry

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

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

RION 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

"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

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

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

BSE INQUIRY REPORT


kind regards, terry

I hunt the panhandle. This will not change anything for me.

If I'm gonna worry about something killing me, that would be cancer, heart disease etc.... Correct me if I'm wrong Terry, but to this date the data shows I have a much greater chance of dying in a commercial plane crash than I do of CWD. I still use commercial flights anyway.....so I'm certainly not gonna stop eating the venison I kill or pay to have it tested before I do.

Going by your logic of a scorched earth solution for CWD, we should ground all commercial airliners from this day forward.

Man, I really enjoyed the break we have had from these idiotic posts. Guess Mr Singletary was on vacation (or in jail) or something, whatever it was is now over, & now it back to [censored].

Haha. You cited Wikipedia as a source. Hilarious

1. I’d rather die almost any other way.
2. The incubation periods in deer are around two years from infection to death, but in the monkey study, they “sacrificed” the monkeys at 4-7yrs from the date of infection. CWD has been detected in TX for only six years, and until recently it was only a handful of cases. There could be a substantial number people infected with CWD before we ever know it. I’m not saying they actually are, but how would we know? Have you been tested?
3. If you read the scrapie studies, and that’s almost certainly where it started, you’ll find that scrapie is contagious to sheep even through skin contact with a cleaned metal post that had been in contact with diseased sheep MONTHS earlier. Other documentation suggests scrapie can survive for up to 16yrs in the environment.

This is not the deer flu where we might suffer some economic loss if X percent of our heard dies. This is a very very scary disease with very high transmission rates, and 100% mortality rates once infected. On top of that, the impact is very long term. If it ever makes the jump to humans, it may be turn out to be much more transmissible than BSE. This is not just a “don’t eat raw brains” situation.

The sky may not be falling, but the people saying this has been around forever and it won’t infect a human are taking a very irresponsible stance with absolutely no science backing it up. It hasn’t been in Texas long enough for us to know if humans can get it, and I’m not aware of humans being tested for it. The best thing about it is that it has been in CO for quite a few years and currently we don’t have a lot of evidence that it has jumped in CO, even if it can’t be ruled out. I’m for maintaining the mandatory checks inside the surveillance zones, testing any roadkill found, testing any deer volunteered to be tested even outside the zones, and continuing to look for a way to stop its spread.

A less far fetched scenario would be that it makes the jump to cattle. Given it’s easy transmission amoung deer via saliva, fecal matter, food sources etc. If it ever did jump to cattle the problem would be crazy.

You and flounder should meet and have lunch.

Maybe. Here are the questions. With a disease that could have a 10+ year incubation time, isn’t regularly tested for by doctors, and was only detected in Texas in 2012, and that was just one animal, how many years will it be before the guy that ate the first one gets diagnosed? How many people will be infected by the time that first guy gets diagnosed? How far will it have spread by then? Will it be in livestock by then?

I’m not saying the sky is falling. We don’t know if it is or not. But I’m not going to bury my head in the sand and say that until we have proof that it will spread to people we should ignore it. We don’t have proof that it will, but we do have evidence that it can, and we certainly don’t have proof that it can’t. Why not research it before it’s out of control?

At least CO has had it for a while and we still don’t see confirmed human cases.

Yes you did imply the “sky is falling” by saying “this is a very scary disease with very high transmission rates”.

There is absolutely no data supporting the lie that it has a high transmission rate. Its been known to be in existence in Colorado and Wyoming for decades and hasn’t decimated any populations.

You also imply that it’s ONLY been in Texas for a few years when in fact no one knows how many years it’s been in ANY state. We just know when cases were found.

1) A lot of things can make something scary other than their likelihood. There are all kinds of snakes, spiders and diseases in South America that are scary, yet very uncommon.
2) 10%-12% disease prevalence in a wild population is a high transmission rate to me. There are some areas where it is that prevalent.
3) how bout I change my position to say “it probably has not been prevelant in TX too much prior to 2012”? Better? Since it’s been known since 1968, I doubt there were very many deer in TX that had it and that far back without anyone noticing till 2012. Obviously they probably didn’t notice the very first one, or even the very first year.
4) None of this means the sky is falling, but you won’t catch me saying we shouldn’t test any more deer or research the disease any further. I think there should be more check stations for VOLUNTARY checks all over the state so that it’s more convenient. I would like to get a deer tested next time I kill one, but since I’m outside the zone, I won’t be driving two hours to drop off a sample. Did you notice that, I won’t drive two hours to have a deer tested. If I thought the sky was falling I’d probably either make the drive or quit hunting all together.

I know squatt about CWD. What I don't understand is that the WT Deer population of Texas is very large. Yet there have been very few confirmed cases of CWD reported.And other than those reported at Deer breeders the supposedly confirmed cases have been many miles apart. They say that Deer will show signs of having it. I have not heard of anyone saying they have observed these signs in Deer while hunting. I hope this CWD scare is not something like global warming where the dire predictions of how bad it is keeps changing when those predictions don't happen each year.

If you're actually worried about deer health/mortality, work on anthrax, internal parasites, hemorrhagic disease, blue tongue, bovine tuberculosis & tick born disease's.
You scientific types know, the things that are easily 'picked up' & actually do kill deer in numbers.

Brain abscesses caused by pedicule injury or by problems associated with abnormal antler shedding probably kill more bucks every year in a handful of Tx counties than CWD does nationwide.
How many have seen a buck or any deer with brain abscess, overload of internal parasites, anthrax or any other fatal ailment.

Do we want to turn a blind eye to CWD, no not at all, but there is no need or advantage to using unsubstantiated overly hyped scare tactics and humongous leaps in relevance wrapped up in a sensationalist 'fake' news/media format most of which is a manipulated BS tidbits version of sound reasonable scientific method.

It certainly could become prevalent in the future, with a little help from its friends.
And if you don't think that happens frequently by those whose funding & entire life's work depends on it, I've got some ocean front property in Kansas to sell.

Dang there are some world class googlers on this thread!

It takes years to incubate, and deer don’t show symptoms till the end of its course. They can transmit it before that. Because it kills slowly, a lot of deer that get it will die of something else(hunting) before they show symptoms, but not before they transmit it to other deer. The cases that pop up many many miles from any other cases problem come from killing a deer with CWD(that you didn’t realize had it) in or near a known CWD area, and transporting that carcass home to a CWD free area. Because the infectious agent can live in the soil for many years, it is almost inevitable that a deer will eventually come into contact with soil where that carcass was dumped if it was dumped out in the open somewhere that deer actually exist.

I hope all it is, is a global warming type scare that never amounts to anything.

So that's where you draw the line on non sense theories? Lose your mind over CWD, but global warming is just crazy. Gotcha.

The globe hadn’t warmed since 1998 until they started revising data and using temps in the wakes of ships which ALWAYS register higher than temps from bouyes. Global warming is a political tool with scientists on both sides of the issue, but politicians on only one side.

I haven’t lost my mind on CWD, I’m just saying we should keep an eye on it. There are a few things about the disease that make it different from others. 100% mortality, long incubation times, persistence in the environment, and a particularly slow uncomfortable death. The long incubation time makes it hard to track, the persistence in the environment make it hard to stop, and the other factors make it bad to get. It’s the perfect hoax disease. I hope it’s a hoax. If it’s not a hoax, what’s wrong with gaining some knowledge about now, instead of when it’s all over? If it’s the worst case scenario, it will probably be a 10-30 years before we know it. What’s wrong with doing a little research now instead of waiting? It is real. No one argues that. What’s wrong with doing a little research on it?

You understand that research has been going on don't you? Just because it "showed up" in Texas recently doesn't mean that it's this brand new diseases that we know nothing about. And if you see global warming as a political stunt, how could you possibly not see that's exactly what is going on with CWD?

Yes I know that it is being studied. Some comments in this thread suggest that it shouldn’t be. I think that it should continue to be studied and that, as with any serious disease steps should be taken to contain it until we know that it doesn’t need to be contained. I like that NM will not allow you to leave a CWD zone with anything but meat, hide and a cleaned and bleached skull plate. I like that Texas requires testing inside of CWD monitoring zones and tests roadkill outside the zones. I wish there were more voluntary testing stations, and those will probably come on their own in time.

I never said that it definitely wasn’t a political stunt. I hope that it is just a political stunt for funding, but I don’t think we really know the answer to that yet. There are two big factions in this debate. The people that think it’s the near inescapable zombie apocalypse, and the people that think it’s all made up crap. A few features of the disease allow it to fit nicely in either category. The long incubation time means that it does not rapidly decimate populations. Many infected deer die of something else before we know they were infected, and because they would have died anyway, their death removed the disease’s impact on the population(compensatory mortality). It also results in a spreading rate that is not only low, but seems even lower than it is. These features make the unbelieving side assume it’s not spreading and isn’t serious. They also make the apocalypse side freak out about how it’s already all over and everything has it. The next feature is the mode of transmission. The disease persists in the environment and seems highly contagious. BSE pretty much required someone/something to eat infected tissue. We stopped feeding cows the leftovers of processed cows and BSE pretty much went away. This disease seems more like scrapie. It lasts a long time in the environment, isn’t destroyed by rendering, and is taken up by plants, so the deer doesn’t have to eat an infected deer. It may have to near an infected deer’s waste, or it may simply have to eat grass where an infected deer’s carcass was disposed of two years ago. So the nay sayers say that deer don’t eat deer, and the fact that it pops up in places isolated from other known areas is proof that it’s been around forever and we’re just now finding it, while the zombie freak outs say that it’s inescapable and going to slowly sweep across the world. I personally think that most of the spreading probably comes from carcass disposal. You shoot a deer in CO, and dump it Medina and bingo. Some probably comes from migration. Those mountain muleys will cover some serious territory from time to time.

I don’t think I fall in either camp, but am certainly closer to the alarmists than the other side. There is some evidence that it can jump species more easily than BSE, and that unlike BSE, which remains BSE even in other hosts, CWD adapts slightly when they infect a new host species with it. That means that if I do shoot a deer in a CWD zone, I will not be eating it until the test comes back negative. I don’t think it has infected hunters yet or we would see more CJD in CO. It hasn’t really been known to be in TX long enough to know, but I bet plenty of people in CO have eaten deer with CWD. It’s been known in CO for 50yrs, so it’s probably not infecting humans. One reason could well be how deer are processed. Beef animals are sawn in half down the center of the spine getting spinal fluid and tissue right on all your good steaks. Most people don’t split a deer like that. I’m not sure how processors do it. I’ve sawn deer in half down the spine, but I won’t be anymore. I do think that that it is spreading from hunters not being careful. I think that it would be wise for states to eliminate carcass movement from areas known to contain CWD(allow only boned out meat, hides and skull plates). But that’s up to individual states. I’m not for eradicating herds, or stoping hunting until we know more, but I’m not for ignoring it either. I think the studies should focus on whether it can be transmitted to other species from eating meat(the macaque study includes that) and then if it can be transmitted from animal to animal without the consumption of meat.