Son of a gun...

http://www.ksat.com/content/pns/ksat/new...ina-county.html

Gracias STXRM

How many deer have died because of cwd in Texas breeding pens?

Directly---To date zero

In directly as a political tool... Hundreds

I believe the deer in question in Medina County didn't even die from cwd. Apparently he jumped into the fence and broke his neck.

This is a very serious problem. 40 animal transfers have been made in Texas from what is now an identified CWD infected site. It is unclear as to whether any of those 40 locations made any animal transfers afterwards. Given the persistance of CWD in the environment (outside the host), and considering the large number of now suspected locations, it is likely that CWD will have a continuing presence in Texas. The ramifications of this would be quite extensive. Millions of dollars of deer will probably be killed, and if any evidence that the disease has spread beyond high fenced ranches in the whitetail population is found, then it is likely that we may see a ban on any kind of baiting for whitetail hunting in those regions (as is the case with Wisconsin).Not to mention the loss of whitetail deer as a food source in those areas.

I disagree. EHD is much more prevelant in the state. It kills thousands of deer a year, and has been around forever, and no one is freaking out over that. Colorado spent $80 million on how to stop CWD, and they figured out that it wasn't that big of a deal. Colorado now has 0 regulations on CWD. Heck, there are scientist at A&M that say CWD may not even be transferable to other deer.I think TPWD will try to use this as a way of getting more control of the deer breeding industry. Just do a little research for yourself on CWD, and try not to get your information from The Outdoor Channel.

I'm a Dr and I have a reasonably good understanding of prions, EHD, and CWD. There is certainly no shortage of literature and studies that demonstrate that CWD is definitely infectious among other deer and cloven hooved ungulates, but it is also being discovered that it can infect an ever growing list of other species. It has a larger reservoir that EHD, represented by these other species (including agriculture), and that is why there is increasing concern over it. Yes, EHD may be more virulent than CWD. But mortality with CWD is 100%. That coupled with it's persistance in the environment make it a serious concern.

Then how did this one have it?

So where exactly has there been a massive die of deer from CWD? From the disease, not from a state coming in and massacring hundreds or thousands of animals because one was sick.

CWD is a slow and horrible death that takes years. Many (maybe most) that have it were killed by humans in an attempt to stop it from spreading.

So your saying there have been 0 massive die offs from CWD? Sounds like state wildlife departments have killed about 100X more deer than CWD. So we are suppose to loose our minds over something that hasn't even shown it kills in large numbers. All this is, is a case of tpwd wanting to take down a multi billion dollar deer industry that it is envious of.

Mk . . .

What has killed more deer in North America, CWD or wildlife agencies?

I sure hope your info on the 40 numbers is correct and what I have been told is false since my redneck contacts are saying different.

Humor me then since I am just a dumb redneck. Do you have a link(s) and pics of this 100% mortality from CWD so I can see it? I have looked and looked without any luck. I can't find one pic of a dead animal that died from CWD. I can find info on slaughters of large numbers of deer with a small % testing postive in wild deer. I can also find examples of the slaughter of deer in breeding pens that were suspected of CWD and killed for that reason, but none of them ever tested postive for CWD. If CWD is being found in more than just deer then why stop at the slaughter of just deer in the pens or in the wild then? I would think every species of animal within that ranch or those counties should be slaughtered that might be a carrier at this point, correct?

So does CWD occur only in locations where all the animals that have it are killed or are you are saying that there are animals deaths from CWD 100% the time before the slaughter starts? If so can you provide links to clarify. Again sorry just a redneck so I need more detailed info at to this 100% mortality.
I consider any disease to humans, wildlife or livestock serious. This first case of WT with CWD is serious, but to me how it got to Central Texas is even more serious at this point. Since other animals stand the same chance of getting it just as this deer has until we find out how it got here. I do not always take what is written on any forum 100% truthful without asking questions.

First let me separate what I am certain of from what I am not certain of. I am NOT certain that 40 is the exact number of animal transfers from the infected site, since I did not hear this directly from the ranchers themselves. It was an estimation for a 3 year period given by someone who worked with TWIMS.

What I do know is that CWD and similar diseases in this class, are always fatal (Kreuzfeld-Jakob, and "Mad cow disease"). The exception may be Scrapie, and just today I came across some literature that said some sheep seem to show resistance. But whether they are simply able to delay the symptoms by a few years, or actually avoid infection is not known to me. If you want documentation that it is 100% fatal, follow this link:
https://tpwd.texas.gov/huntwild/wild/diseases/cwd/media/tpwd_cwd_factsheet.pdf

In regard to how many animals should be killed, that is still a contested issue because biologists are still determining how it is transmitted, and how likely each of those transmission methods are to infect other animals. They also don't know exactly how many other species can be affected by this prion. Right now, I believe the protocol is to kill and test cloven hooved ungulates that would have been in the same area that this infected deer was confined to. It is also important to remember that when it comes to testing, animals in the beginning stages of infection have a good chance of not registering positive on the test. CWD is slow to progress.
Killing all animals in a county would be quite extreme and would receive overwhelming resistance and backlash. There would have to be unfaltering scientific documentation proving it was necessary.

Regarding this question: "So does CWD occur only in locations where all the animals that have it are killed or are you are saying that there are animals deaths from CWD 100% the time before the slaughter starts?"
Understand that I said this:"CWD is a slow and horrible death that takes years. Many (maybe most) that have it were killed by humans in an attempt to stop it from spreading." Because someone else was saying that there had not been a large scale "die off" caused by CWD. So the point I was making was that many of the infected deer were killed before they had a chance to die from the disease. But earlier today I came across an article saying that in Colorado or Wyoming they were witnessing a 50% reduction from CWD in some wild Mule Deer herds. Again, it is slow, but unwavering.

How this particular deer contracted the disease is the million dollar question. Maybe some whitetail deer were brought to the ranch from outside the state illegally. Or, maybe they bought infected exotic deer from out of state (Whitetail cannot be imported from out of state, but exotics still can). Maybe from other livestock. Maybe even from deer attractant scent used on the property. A few days ago Virginia outlawed the use of urine based scent attractants, specifically because it can be a means of spreading CWD. This is the mess the epidemiologists have to deal with.

Oh wow. Linking a tpwd "fact" sheet to support your arguments. Exactly what are tpwd "facts"on spikes today.

Facts are facts though. Your statement that "there would have to be 'unfaltering' evidence before they tried to kill all deer in a county" is bogus since in Wisconsin they tried just that. Based on their flawed belief that it would have an impact.

As long as DNR's are listening to "Drs" like you, I guess they'll keep getting it wrong.

Again, DNR's have and will continue to kill vastly higher numbers than CWD has or will. Until the public rises up and tells them to go pound sand.

what about CWD infection rates on some of these game farms ???

CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) FarmUpdate DECEMBER 2011The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80acres of land for $465,000 for the Statewide Wildlife Habitat Program inPortage County and approve the restrictions on public use of the site.SUMMARY:

http://dnr.wi.gov/about/nrb/2011/december/12-11-2b2.pdf

For Immediate Release Thursday, October 2, 2014

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship,which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS)National Veterinary Services Lab in Ames, IA confirmed that a male whitetail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD. -30-

http://www.iowaagriculture.gov/press/2014press/press10022014.asp

*** see history of this CWD blunder here ;

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/070313_consent_order.pdf

On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had beencut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/060613_consent_order.pdf

Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

snip...

In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

Animals considered at high risk for CWD include:

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

snip...

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

snip...

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

snip...

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

snip...

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

snip...

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

snip...

http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf

Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

http://chronic-wasting-disease.blogspot.com/2012/12/defra-uk-what-is-risk-of-chronic.html

CHRONIC WASTING DISEASE CWD TSE PRION, how much does it pay to find CWD $$$

CWD, spreading it around...

for the game farm industry, and their constituents, to continue to believe that they are _NOT_, and or insinuate that they have _NEVER_ been part of the problem, will only continue to help spread cwd. the game farming industry, from the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet mills, shooting pens, to large ranches, are not the only problem, but it is painfully obvious that they have been part of the problem for decades and decades, just spreading it around, as with transportation and or exportation and or importation of cervids from game farming industry, and have been proven to spread cwd. no one need to look any further than South Korea blunder ;

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

spreading cwd around...

Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.

***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2081988/

spreading cwd around...

Friday, May 13, 2011

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea

Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea

Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.

On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.

All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.

Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.

Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.

Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).

In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.

Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.

All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.

Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.

In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.

In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.

http://www.prion2011.ca/files/2011TSEBookletV6Final.pdf

http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf

http://www.cwd-info.org/index.php/fuseaction/news.detail/ID/c792d0e56e0cb3ee3a6517e754729cac

http://chronic-wasting-disease.blogspot.com/2011/05/chronic-wasting-disease-cwd-outbreaks.html


Terry S. Singeltary Sr.

Still ignorantly criticizing I see.
One deer in Texas vs a population of infected deer in Wisconsin is not the same situation. Likewise, scientists did not know then what we know now.

First a doctor, now a scientist. Impressive.

I do like how flounder cited all his information. Those were some interesting reads for sure.

I would question any scientist or doctor on what they know now, and that's reading this latest prion gathering post. They are still grasping at straws to say the least.

And let me state clearly I have no skins in the ranching or breeding game. I think at this point it would be fair to say everyone with a theory or opinion is ignorant to truly understanding this disease and what causes it. And that's why you don't just kill healthy acting deer on a wide spread scale until your understand more of what you dealing with. Especially basing their lives on a test that could be extremely flawed to begin with.

This could be genetic as well as environmental just like many researchers believe Alzheimers is. And logically when you see a high occurance of positive tests on deer farms would logically make sense of a genetic trait that the test identifies.

There is not enough factually supported data to be calling anybody ignorant except the supposed experts record of treating this problem that they claim to understand more than we do.

Couldn't agree more. Jumping to conclusions with incomplete data is no platform to be calling people ignorant from.

I'll note he didn't explain how the "correct data" has had "biologists" changing their stories for decades.

I'm sure as a doctor, and a scientist, he will set it all straight before long.

The Ranch with the CWD Case offered to donate all of the deer to the A&M Research team where animals are sent for testing. That way they would be able to see if rectal and blood testing could be used in accordance with testing with the brain stem and TPWD refused. The unknown is what is somewhat scary about CWD and TPWD and TAHC should be working with the owners and take advantage of the situation to learn more about CWD and help them get through this for everyone's benefit. Instead, TPWD is treating them like criminals and only seem to care about destroying the herd (EVIDENCE) and any linkage to it, that's what's more criminal in my opinion!

I'm willing to bet all these breeders in Texas, most of whom are probably some of the wealthiest people in Texas, aren't going to take this lying down. I bet before too long we will be talking about TPWD getting sued over this.

This has been an on going problem, no live test has been validated, yet they destroy herds whithout letting researchers take samples that could possibly lead to a live test.

TPWD is tracking all deer movement into, and out of that ranch in Medina County for the last 5 years. That will pretty much connect every breeder in Texas to this deer in some way. So instead of testing a couple hundred animals on one ranch, they will be able to claim who knows how many animals on who knows how many ranches to test. The breeding industry is about to get hammered.
I don't own a breeding facility, or even work on one is these ranches. I sure will hate to see how many deer are going to be killed in the name of "containment" in the coming months. I'm sure only a few of the most profitable breeders will be the only ones left after all this.
I blame these HF ranches and breeders for a lot of things in today's hunting world. The prices for leases, and basically the price of hunting in general has gone through the roof in recent years in part, what I believe, to these whitetail ranches. That being said, I hate to see the government come in and tell people what to do with their private property. The next few weeks will be very interesting in how the state will handle all this

The wealthiest hunters I know (the kind that can afford to hunt places where legitimate Boone and Crockett caliber deer can be harvested) find the practice of shooting pen raised deer detestable.

I'm not saying shooting pen raised deer is my thing. But a person ought to be able to decide what to do on their own land don't you think?

Cool but that's not what the thread is about.

for what's it's worth, I will ggive the owners a thumbs up for ;


>>>The Ranch with the CWD Case offered to donate all of the deer to the A&M Research team where animals are sent for testing. That way they would be able to see if rectal and blood testing could be used in accordance with testing with the brain stem<<<


but not knowing the rest of the story, I won't comment about TPWD or TAHC and any reasoning they might have for not wanting use the herd for research

I do hope they test all of the deer for cwd, and the results are published to the public?

however, I will say this. I know of another situation with captives with cwd, that if I am not mistaken, after cwd was discovered, there was a time period where the situation was set into limbo, either for litigations, courts, the government, the owners, whatever, those perfectly healthy deer that everyone was so concerned about, all those healthy looking deer, after the final testing was done after much delay, a long time after, there was an 79.8% CWD infection rate documented. I'm just saying, you let this cwd linger, the chances of the cwd agent spreading grows and grows. so dammed if they do, danged if they don't. all I am saying, if you snooze, you loose. this is why ;


For Immediate Release Thursday, October 2, 2014

Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov

TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).

http://www.iowaagriculture.gov/press/2014press/press10022014.asp

*** see history of this CWD blunder here ;

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/070313_consent_order.pdf

On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.

http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/060613_consent_order.pdf



***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentallyrelevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.

https://prion2015.files.wordpress.com/2015/05/programguide1.pdf

Wednesday, June 10, 2015

Zoonotic Potential of CWD Prions

LATE-BREAKING ABSTRACTS

http://chronic-wasting-disease.blogspot.com/2015/06/zoonotic-potential-of-cwd-prions.html

Wednesday, April 22, 2015

Circulation of prions within dust on a scrapie affected farm

http://transmissiblespongiformencephalop...in-dust-on.html

Friday, January 30, 2015

*** Scrapie: a particularly persistent pathogen ***

http://transmissiblespongiformencephalop...t-pathogen.html

2012

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

snip...

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.

*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

http://www.landesbioscience.com/journals/prion/03-Prion6-2-Transmission-and-strains.pdf

2011

*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.

http://www.usaha.org/Portals/6/Reports/2011/report-cwal-2011.pdf

*** We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

*** The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

PRION 2014 CONFERENCE

CHRONIC WASTING DISEASE CWD

A FEW FINDINGS ;

Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.

We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.

Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.

Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.

Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.

Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.

see full text and more ;

Monday, June 23, 2014

*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD

https://www.landesbioscience.com/journal...n%20Animals.pdf

http://chronic-wasting-disease.blogspot.com/2014/06/prion-2014-chronic-wasting-disease-cwd.html

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

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

http://jgv.sgmjournals.org/content/87/12/3737.full

New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication

http://www.pnas.org/content/97/7/3418.full

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

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/

Detection of protease-resistant cervid prion protein in water from a CWD-endemic area

http://www.landesbioscience.com/journals/prion/NicholsPRION3-3.pdf

A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing

http://onlinelibrary.wiley.com/doi/10.1111/j.1539-6924.2012.01922.x/abstract

Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals

http://transmissiblespongiformencephalop...spongiform.html

98 | Veterinary Record | January 24, 2015

EDITORIAL

Scrapie: a particularly persistent pathogen

Cristina Acín

Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’

From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).

Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.

Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.

The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).

In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.

Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).

In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.

The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).

Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).

So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?

What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.

References

snip...

98 | Veterinary Record | January 24, 2015

http://veterinaryrecord.bmj.com/content/176/4/97.extract

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C. Maddison, BSc, PhD3 + Author Affiliations

1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and chronic wasting disease of deer/elk are contagious prion diseases where environmental reservoirs are directly implicated in the transmission of disease. In this study, the effectiveness of recommended scrapie farm decontamination regimens was evaluated by a sheep bioassay using buildings naturally contaminated with scrapie. Pens within a farm building were treated with either 20,000 parts per million free chorine solution for one hour or were treated with the same but were followed by painting and full re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue. All animals became infected over an 18-month period, even in the pen that had been subject to the most stringent decontamination process. These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.

SNIP...

Discussion

Thorough pressure washing of a pen had no effect on the amount of bioavailable scrapie infectivity (pen B). The routine removal of prions from surfaces within a laboratory setting is treatment for a minimum of one hour with 20,000 ppm free chlorine, a method originally based on the use of brain macerates from infected rodents to evaluate the effectiveness of decontamination (Kimberlin and others 1983). Further studies have also investigated the effectiveness of hypochlorite disinfection of metal surfaces to simulate the decontamination of surgical devices within a hospital setting. Such treatments with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous treatment of the pen surfaces did not effectively remove the levels of scrapie infectivity over that of the control pens, indicating that this method of decontamination is not effective within a farm setting. This may be due to the high level of biological matrix that is present upon surfaces within the farm environment, which may reduce the amount of free chlorine available to inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had also became scrapie positive within nine months, with all animals in this pen being RAMALT positive by 18 months of age. Pen D was no further away from the control pen (pen A) than any of the other pens within this barn. Localised hot spots of infectivity may be present within scrapie-contaminated environments, but it is unlikely that pen D area had an amount of scrapie contamination that was significantly different than the other areas within this building. Similarly, there were no differences in how the biosecurity of pen D was maintained, or how this pen was ventilated compared with the other pens. This observation, perhaps, indicates the slower kinetics of disease uptake within this pen and is consistent with a more thorough prion removal and recontamination. These observations may also account for the presence of inadvertent scrapie cases within other studies, where despite stringent biosecurity, control animals have become scrapie positive during challenge studies using barns that also housed scrapie-affected animals (Ryder and others 2009). The bioassay data indicate that the exposure of the sheep to a farm environment after decontamination efforts thought to be effective in removing scrapie is sufficient for the animals to become infected with scrapie. The main exposure routes within this scenario are likely to be via the oral route, during feeding and drinking, and respiratory and conjunctival routes. It has been demonstrated that scrapie infectivity can be efficiently transmitted via the nasal route in sheep (Hamir and others 2008), as is the case for CWD in both murine models and in white-tailed deer (Denkers and others 2010, 2013). Recently, it has also been demonstrated that CWD prions presented as dust when bound to the soil mineral montmorillonite can be infectious via the nasal route (Nichols and others 2013). When considering pens C and D, the actual source of the infectious agent in the pens is not known, it is possible that biologically relevant levels of prion survive on surfaces during the decontamination regimen (pen C). With the use of galvanising and painting (pen D) covering and sealing the surface of the pen, it is possible that scrapie material recontaminated the pens by the movement of infectious prions contained within dusts originating from other parts of the barn that were not decontaminated or from other areas of the farm.

Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity. This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.

The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.

Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014

http://veterinaryrecord.bmj.com/content/early/2014/10/31/vr.102743.abstract

Monday, November 3, 2014

Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination

http://transmissiblespongiformencephalopathy.blogspot.com/2014/11/persistence-of-ovine-scrapie.html

PPo3-22:

Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie

Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK

Key words: scrapie, evironmental persistence, sPMCA

Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.

http://www.prion2010.org/bilder/prion_20...00b77af81be3099

Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

snip...

In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

Animals considered at high risk for CWD include:

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

snip...

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011). The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE). Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

snip...

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

snip...

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

snip...

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

snip...

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

snip...

http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf


kind regards, terry

You posted an abstract elsewhere that was pretty disconcerting. However I cannot find the full article anywhere online. If you come across it, please post it. Here was the abstract:

"Zoonotic Potential of CWD Prions

Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA

Chronic wasting disease (CWD) is a widespread and expanding prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern. Current literature generated with in vitro methods and in vivo animal models (transgenic mice, macaques and squirrel monkeys) reports conflicting results. The susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. In our earlier bioassay experiments using several humanized transgenic mouse lines, we detected protease-resistant PrPSc in the spleen of two out of 140 mice that were intracerebrally inoculated with natural CWD isolates, but PrPSc was not detected in the brain of the same mice. Secondary passages with such PrPSc-positive CWD-inoculated humanized mouse spleen tissues led to efficient prion transmission with clear clinical and pathological signs in both humanized and cervidized transgenic mice. Furthermore, a recent bioassay with natural CWD isolates in a new humanized transgenic mouse line led to clinical prion infection in 2 out of 20 mice. ***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection."

Are they're any articles published on any die offs of wild deer? There have been a number posted on penned deer getting it, but what about wild herds?

Sure they should but not if it affects the health of other wildlife.

Only Mass die offs you will find on wild deer or elk is EHD, toxins, starvation.... The quick killers

It's quick enough to be observed...example the 100 plus elk that died in NM in 2013.

You have to remember CWD wasn't discovered until migrating Elk and Mule deer stopped migrating via a fence research enclosure. Yotes, Bears etc have done a good job covering up CWD deaths. Note no CWD has been found in Yotes or Bears or other animals that ate CWD carcasses. Also Note that I'm not a doctorate

Open season in West Texas border on all free range hoofed animals..... Have fun.. You're a few years late though.

It's scary. I own a HF ranch with only native deer on it and I don't maintain the fence very well. I know deer can come and go. If one of my HF neighbors imported a deer from that facility, TPWD will want to cull all of their deer AND mine too.

Which brings me to my question. I see TPWD compensated the landowner for the deer. Is there a standard $ figure per deer or do pen raised deer get more $ compared to my puny hill country deer??

So if it is such a slow acting disease, chances are we've all shot a wild deer caring it and consumed it.

Since it seems to be the norm to post links about CWD...here is one that has not been posted that seems interesting.
Link

Good article, Darwinism at work.

But I thought CWD was a deer version of Ebola. Something that could wipe out every deer in Texas? According to this article, it may not be all that big of a deal. This article makes too much sense, we better get back on topic.

Sweet Geezus. Would you please get with the program?! Mr tx_biologist has already established that Alzheimer's is caused by CWD.

You have a better chance of winning the Texas lottery according to TPWD and biologist. But yes you are correct

the abstract you speak of are papers in progress, and were presented at the Prion2015 conference as abstracts. the finished product will come out soon after (months usually). there was another paper that was interesting as well, and then others from the prion2014 conference. see ;




P.105: RT-QuIC models trans-species prion transmission

Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious. Studies of the effects of primary or tertiary prion protein structures on trans-species prion transmission have relied primarily upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect. As an alternative strategy, we used real-time quakinginduced conversion (RT-QuIC) to investigate trans-species prion conversion.

To assess trans-species conversion in the RT-QuIC system, we compared chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions, as well as feline CWD (fCWD) and feline spongiform encephalopathy (FSE). Each prion was seeded into each host recombinant PrP (full-length rPrP of white-tailed deer, bovine or feline). We demonstrated that fCWD is a more efficient seed for feline rPrP than for white-tailed deer rPrP, which suggests adaptation to the new host.

Conversely, FSE maintained sufficient BSE characteristics to more efficiently convert bovine rPrP than feline rPrP. Additionally, human rPrP was competent for conversion by CWD and fCWD. ***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.

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

***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***

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

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


old data from the BSE Inquiry way back ;


In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...

snip...

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)

snip...see full report ;

http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf

Thursday, October 10, 2013

*************CJD REPORT 1994 increased risk for consumption of veal and venison and lamb**************

http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html

CJD9/10022

October 1994

Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ

Dear Mr Elmhirst,

CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT

Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.

The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.

The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.

The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.

I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.

http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf

Thursday, October 10, 2013

*** CJD REPORT 1994 increased risk for consumption of veal and venison and lamb

http://creutzfeldt-jakob-disease.blogspot.com/2013/10/cjd-report-1994-increased-risk-for.html

PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;

Thursday, May 26, 2011

Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007

FoodNet Population Survey Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.

http://transmissiblespongiformencephalop...nd-venison.html

NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;

Wednesday, March 18, 2009

Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II

http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html

now, let’s see what the authors said about this casual link, personal communications years ago. 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

*** 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). ***

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249

*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf

Bingo.... a fact that these scientists and doctors don't seem to wanna talk about

*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent

*** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,

*** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.

PPo2-27:

Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

*** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.

PPo2-7:

Biochemical and Biophysical Characterization of Different CWD Isolates

*** The data presented here substantiate and expand previous reports on the existence of different CWD strains.

https://www.landesbioscience.com/journals/prion/Prion4-3-PPo2.pdf

Envt.07:

Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease

***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.

http://www.landesbioscience.com/journals/prion/Prion5-Supp-PrionEnvironment.pdf?nocache=1333529975

>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<

*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***

Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

Wednesday, January 01, 2014

Molecular Barriers to Zoonotic Transmission of Prions

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein.

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.

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

http://chronic-wasting-disease.blogspot.com/2014/01/molecular-barriers-to-zoonotic.html


kind regards, terry

I have heard the same thing about testing and year amount being bumped for 2yrs out to 5yrs now. Also found it interesting that last week the day after the story leaked that 2 ranches who got deer from this breeding ranch offered to kill those deer for testing. Called Austin and they were told to wait. Told to wait????? I guess "they" want to make sure that if any other ranches have CWD that it gets a running head start to make sure it spreads into those deer herds thoroughly. I guess it makes the validation of the impending slaughter more valid to the public eye.....
Sad thing for me is there is more whizzing on corner posts and tires right now than than there is trying to channel our efforts find out the source of what or how CWD got into that deer in that facility. IMO what will happen is the "sky will fall", deer will be slaughtered in very high numbers, compiling info will be used to this to drag this out as long as it can be to allow as many more deer to get CWD...just so that the slaughter can be validated in the uniformed public eye, then the "sky will fall" again, more deer will be slaughtered, sometime in the future while deer are being slaughtered CWD will be found again in another area not even related to this one or any other one...sadly when the real emphasis should be on research to find the source(s) of how it got to those pens....all the emphasis right now is being directed to stopping the deer breeding industry instead of all sides focusing on our real problem- CWD.
CWD was in Texas already in wild free ranging deer before it was found in Central Texas. It did not seem to be to much of a problem since deer were still being allowed to be moved from breeding pens to other breedrs or released on any ranch(LF or HF) or being moved via TTT permits from any ranch in Texas to another ranch. All that was required was a CWD test on a minimum number of or % of deer being moved to qualify. Today, that is much different with CWD now in WT deer in Texas.
I don't think this particular ranch woke up one morning to say "I am going to introduced CWD into Texas". Sadly, they are being convicted in the publics eye of that right now. I do not know of one single ranch or landowner that wanted CWD to be found in Texas but it had been. Those same people to a person never wanted it found in WT deer in Texas. But it happened. It is here and now we have to deal with it. We need to work on find the source of how it got into Central Texas before it shows up again and again.
I had a noted wildlife biologist tell me 12 yrs ago that in his opinion CWD had been or was in Texas already. Pretty sad that I can now tell him...you were right.
Texas has alway been looked at as the leader in wildlife management and research, now is our chance to show why we are the leader.

SMH

Genetic resistance to Scrapie in sheep, is well known and described, it's not a huge leap to think that some lines of deer will also be naturally resistant. The trans species barrier between humans and CWD is significant, but understanding how the barrier was breached, with BSE is important. The process of virulence amplification created by processing sick cattle and sheep into cattle feed is cautionary. Basically, each generation that got directly infused in to cattle through feed, without being exposed to environmental degradation, got a little more infectious until it breached the species barrier.

That is not impossible. Although other prions are more likely. We won't know until people actually start getting tested

Is this suppose to mean something? Mice experiments? You guys are way out in lala land if you think this latest research is going to make me or anybody like me stop eating venison because it might have CWD. If it does indeed turn out to be factual that this disease takes years to show the symptoms of the disease you are delusional to believe that deer haven't already been killed and eaten that would of tested positive.

They aren't normal mice. They're transgenic mice. They have been genetically altered, most likely to have proteins like that of humans, so that researchers can see if the prions can induce changes in human proteins. I have no doubt that people in CWD infected regions have eaten CWD infected meat. But Texas has not yet been identified as on of those regions. So, the question being addressed now is whether it is wise to stop eating wild game before CWD spreads throughout Texas.

It's incredibly depressing. I don't want to give it up. But I don't want dementia even more.

Evolution can overcome some pretty big hurdles. But in the most CWD saturated zones, CWD is definitely having some dramatic effects. The South Converse Mule Deer Herd in Wyoming has been reduced in population by 60% due to this disease, and the mortality rate isn't showing signs of slowing down.

Parts of West Texas ARE identified as part of those regions. 7 wild free ranging animals so far have been found POSITIVE for CWD in the transpecos area.

That's not solely due to CWD.

What about the ORGINAL CWD detection area of CO how are those populations?

Yes I am aware, but it wasn't significant enough to count the whole state as a CWD region

Here is an interesting read...notice the live testing results and the factual replies to the unknowns listing a lot of factors that could be the reasons for the decline...also the deaths number or how they died...interesting to see actual research being done on live deer and live deer testing.
http://billingsgazette.com/news/state-an...07ea837cde.html

The South Converse Herd was part of the original cwd detection area

That because most maps are NOT putting whole states as a region. They are put geographic areas as regions with in states. On top of that most maps haven't been update since 2013. Let's not forget the geographical size of Texas on top of that

That number alone suggest 10-15% CWD rate on that range.

And so was the CO side and it has rebounded some years and stayed steady others. I find it humors that now CWD is the overall culprit for historic mulie deer decline nation wide...What about elk population growth?

Come on Doc keep googling!!!! We need more pitchforks

If this herd has the highest CWD infection rate of any population, and their population is declining faster than any other population . . . then there is probably an obvious logical connection there.

It's funny how people describe hunting. I guided the wealthiest people in the world, including a King while on the King Ranch, which is low fence, and every time I am the one who knew where the deer was and took the hunter to the location and all they did was pull the trigger or release the arrow. Same thing while guiding Elk in Colorado and Canada. I did the scouting and I knew where the Elk were and again, all the hunter did was pull the trigger. I have also had guests that think High Fence hunting is something that they would never do until they couldn't get the animal that they were after and then would go to a neighboring High Fence place to look around and almost always ended up going back to hunt.
I love how we are fast to judge. This is America, let folks hunt as they will. A true trophy is in the eye of the Hunter! If you don't like it then don't do it but don't tell landowners what they can or can't do on their own property or else you are communist and just haven't accepted it yet.
TPWD should be working these folks to better the entire state. All they are about is Power, period. The corrupt and powerful always feel the need for more Power, no matter who they destroy to get it.

Mule Deer populations have been going down for decades now. Drought is a big culprit, habitat destruction, other species taking over. But, sure lets just say it's all CWD. After all, there can only be one reason for anything that happens in nature right?

http://www.texashunting411.com/mule-deer-population-boosted-at-black-gap-wma/

Sorry, my last response was for JMalin. Again, sorry THF, I just really get frustrated with Communism thinking.

Well said

What I find interesting is your ignoring the other 30 plus areas with CWD. Some one such as your self that is highly interested in CWD as of a few THF days ago...would exclude non CWD type morality , expecially in a state that has a 90% migration rate, or a desert area that's also fighting Feds over sage grouse regulations and habitat conservation.

With out the historical environmental tends in front of you I guess:
1)it's easy to say yelp it's all CWD
2) CWD explains low recruitment in sage grouse also... No other reseasonable explanation.
3) don't know why all the other CWD hot spots are holding population numbers and/or swing with envorimental trends but this one should be used as an example of what's going to for sure happen....

Fact of the matter is we are now 67 years into the classification of CWD being a clinical disease. That particular area in Wyoming is now 36 years into the discovery of CWD there( which no one still knows if it was imported or finally identified).... We still have deer, we still have elk.

How is Wisconsin deer herd doing now?

I agree whole hearty!!! But this is about CWD in Texas and America not so much HF, LF or No fence.

CWD really might be more serious than we all believe. Think about all these decisions that have happened in DC recently. Is it possible that CWD has infected the grounds of the White House and the Supreme Court? I mean that would explain a lot right??

CWD is a serious disease with out a doubt!!!!!

It's just not the apocalypse. You have to remember they identified it in 60's. They have mapped it back almost as far as the early 1900's they just now if it was already here or transferred/morphed from sheep some how.

Nature has a funny way of covering stuff up and also working its self out.

to date, officials claim it to be the normal (their normal) one in a million i.e. sporadic CJD.


but ;


*** 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).

https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249


so there goes the neighborhood...


terry

That was just my attempt at a little comic relief for this thread.

Thursday, January 15, 2015

41-year-old Navy Commander with sporadic Creutzfeldt–Jakob disease CJD TSE Prion: Case Report

http://creutzfeldt-jakob-disease.blogspot.com/2015/01/41-year-old-navy-commander-with.html

Subject: *** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease aka mad cow type disease

what is CJD ? just ask USDA inc., and the OIE, they are still feeding the public and the media industry fed junk science that is 30 years old.

why doesn’t some of you try reading the facts, instead of rubber stamping everything the USDA inc says.

sporadic CJD has now been linked to BSE aka mad cow disease, Scrapie, and there is much concern now for CWD and risk factor for humans.

My sincere condolences to the family and friends of the House Speaker Becky Lockhart. I am deeply saddened hear this.

with that said, with great respect, I must ask each and every one of you Politicians that are so deeply saddened to hear of this needless death of the Honorable House Speaker Becky Lockhart, really, cry me a friggen river. I am seriously going to ask you all this...I have been diplomatic for about 17 years and it has got no where. people are still dying. so, are you all stupid or what??? how many more need to die ??? how much is global trade of beef and other meat products that are not tested for the TSE prion disease, how much and how many bodies is this market worth?

Saturday, January 17, 2015

*** Becky Lockhart 46, Utah’s first female House speaker, dies diagnosed with the extremely rare Creutzfeldt-Jakob disease

http://creutzfeldt-jakob-disease.blogspot.com/2015/01/becky-lockhart-46-utahs-first-female.html

*** Human Mad Cow Video

http://zoomify.uzh.ch:8080/zoomify/videos/video-009/video-009.html

*** USA sporadic CJD MAD COW DISEASE HAS HUGE PROBLEM Video

http://zoomify.uzh.ch:8080/zoomify/videos/video-004/video-004.html

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

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

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

Laboratory of Central Nervous System Studies, National Institute of

Neurological Disorders and Stroke, National Institutes of Health,

Bethesda, MD 20892.

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

PMID: 8006664 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query...p;dopt=Abstract

PLEASE NOTE *

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

snip...

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf

IATROGENIC TSE PRION

all iatrogenic cjd is, is sporadic CJD, until route and source of the iatrogenic event that took place, is detected, documented, placed in the academic domain as fact, and recorded, which happens very seldom due to a lot of factors, besides the incubation period, and that be mainly industry. kind of like asbestos and tobacco and the industry there from, they knew in the early 1900’s that they both were killing, and they both had long incubation, and somebody chose not to do anything about if for decades and decades. kind of like what we have here with the TSE prion disease. $$$

> In 12 of 15 hospitals with neurosurgical incidents, a decision was made to notify patients of their potential exposure.

SO, X number of patients, from 3 hospitals, where

''exposure to potentially CJD-contaminated instruments ''

took place on these patients, the final decision NOT to tell those folks about the potential exposure to the CJD TSE prion

insane, thus, the TSE prion agent continues to spread. ...please see further comments here ;

http://creutzfeldt-jakob-disease.blogspot.com/2013/11/management-of-neurosurgical-instruments.html

Tuesday, February 11, 2014

Novant Health Forsyth Medical Center Information on potential CJD exposure

http://creutzfeldt-jakob-disease.blogspot.com/2014/02/novant-health-forsyth-medical-center.html

Thursday, June 04, 2015

Catholic Medical Center v. Civil No. 14-cv-180-JL Opinion No. 2015 DNH 110 Fireman’s Fund Insurance Company Creutzfeldt Jakob Disease TSE Prion tainted medical instruments

UNITED STATES DISTRICT COURT DISTRICT OF NEW HAMPSHIRE

http://creutzfeldt-jakob-disease.blogspot.com/2015/06/catholic-medical-center-v-civil-no-14.html

Sunday, March 09, 2014

A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease

FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES

http://creutzfeldt-jakob-disease.blogspot.com/2014/03/a-creutzfeldt-jakob-disease-cjd.html

Tuesday, March 11, 2014

Science and Technology Committee Oral evidence: Blood, tissue and organ screening, HC 990 Wednesday 5 March 2014 SPORADIC CJD

Actually, it is nearer 2 per million per year of the population will develop sporadic CJD, but your lifetime risk of developing sporadic CJD is about 1 in 30,000. So that has not really changed. When people talk about 1 per million, often they interpret that as thinking it is incredibly rare. They think they have a 1-in-a-million chance of developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of developing it.

http://creutzfeldt-jakob-disease.blogspot.com/2014/03/science-and-technology-committee-oral.html



terry

Let me translate, with sufficient forced amplification, one strain of the CWD prion can be forced to convert human prions. That conversion is most likely to occur in to individuals carrying one out of three possible gene variants. What can't be quantified is the possibility of that amplification occurring outside of a lab. There is no definitive evidence that CWD has crossed the species barrier but there are five cases were, it's unlikely to be the cause of vCJD, but it can't be completely ruled out.

Terry spare us the stories about Sporadic CJD it has a very different clinical presentation to vCJD or Mad Cow Disease. Let's confine the discussion to CWD or allied TSE diseases. On the larger scale all prion diseases are related, but the focus of this forum is hunting, lets stick with game animals and their relatives.

I, and I'm sure others, are interested in information pertaining to propabilites of human infection by CWD. If in the coming weeks we find out that deer test positive for CWD in multiple locations in Texas, then deciding whether or not to continue eating wild game meat will be on most hunters' minds. And, everyone should make informed decisions for themselves based on the current data available. I'm glad I read one of the articles Terry posted yesterday, because it has changed my perspective on things and made me ask more questions.

Describing the effects of CWD in the most infected deer population doesnt mean I'm ignoring other CWD locations. It just means I'm describing how bad it can get. I am aware that mule deer populations are declining in other areas as well, including areas where CWD is not prevalent. But, nowhere else are populations dropping as quickly as the South Converse Herd. And I don't think it is a coincidence that they have the highest rate of infection.

I'm not sure where you got 67 and 36 years. CWD was first identified there 48 years ago near the Colorado/ Wyoming border. That was when it was first identified and named.

CWD in Wisconsin is getting worse. Next month they are adding three more counties to the bait ban list due to increasing spread of CWD in those counties.

Here is an article I think I posted in the other thread yesterday. But I'll post it here too because I think it gives a good overview of the situation.
https://www.hcn.org/blogs/goat/chronic-wasting-disease-forgotten-but-not-gone

I ment to write 48, 67 was the year.

Regardless if it truly was epidemic we would already be wiped out in Wyoming and especially CO. That's hasn't happened. Drought and winter kills have been much more effective in limiting recruitment then CWD.

I didn't say anything about not linking to information about CWD or vCJD linked to meat. I was referring to Sporadic CJD that has a different clinical presentation. I'm just trying to keep things reasonably on topic not all prion diseases are transmitted through meat.

Informed decisions? This info you lab guys keep posting is suppose to give me an informed decision to make based on people splicing human genes in mice and forcing prions into them? With this type of decision making logic you shouldn't be eating any processed food or meat from the grocery store. Is that the way you guys roll?

we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease

2005

DEFRA Department for Environment, Food & Rural Affairs

Area 307, London, SW1P 4PQ Telephone: 0207 904 6000 Direct line: 0207 904 6287 E-mail: h.mcdonagh.defra.gsi.gov.uk

GTN: FAX:

Mr T S Singeltary P.O. Box 42 Bacliff Texas USA 77518

21 November 2001

Dear Mr Singeltary

TSE IN HOUNDS

Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.

As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.

Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.

Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less

critical. For more details see- http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf

As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.

Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK

You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.

I hope this is helpful

Yours sincerely 4

HUGH MCDONAGH BSE CORRESPONDENCE SECTION

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

HOUND SURVEY

I am sorry, but I really could have been a co-signatory of Gerald's minute.

I do NOT think that we can justify devoting any resources to this study, especially as larger and more important projects such as the pathogenesis study will be quite demanding.

If there is a POLITICAL need to continue with the examination of hound brains then it should be passed entirely to the VI Service.

J W WILESMITH Epidemiology Unit 18 October 1991

Mr. R Bradley

cc: Mr. G A H Wells

http://collections.europarchive.org/tna/20081106102318/http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf

3.3. Mr R J Higgins in conjunction with Mr G A Wells and Mr A C Scott would by the end of the year, indentify the three brains that were from the ''POSITIVE'' end of the lesion spectrum.

http://collections.europarchive.org/tna/20080103034308/http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf

TSE in dogs have not been documented simply because OF THE ONLY STUDY, those brain tissue samples were screwed up too. see my investigation of this here, and to follow, later follow up, a letter from defra, AND SEE SUSPICIOUS BRAIN TISSUE SAF's. ...TSS

http://www.mad-cow.org/00/aug00_late_news.html#ggg

TSE & HOUNDS

GAH WELLS (very important statement here...TSS)

HOUND STUDY

*** AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.

snip...

http://web.archive.org/web/20060307063542/http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf



terry


p.s.


Monday, February 14, 2011

THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER

NO, NO, NOT NO, BUT HELL NO !

Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011

http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html

OR-09: Canine spongiform encephalopathy—A new form of animal prion disease

Monique David, Mourad Tayebi UT Health; Houston, TX USA

It was also hypothesized that BSE might have originated from an unrecognized sporadic or genetic case of bovine prion disease incorporated into cattle feed or even cattle feed contaminated with prion-infected human remains.1 However, strong support for a genetic origin of BSE has recently been demonstrated in an H-type BSE case exhibiting the novel mutation E211K.2 Furthermore, a specific prion protein strain causing BSE in cattle is believed to be the etiological agent responsible for the novel human prion disease, variant Creutzfeldt-Jakob disease (vCJD).3 Cases of vCJD have been identified in a number countries, including France, Italy, Ireland, the Netherlands, Canada, Japan, US and the UK with the largest number of cases. Naturally occurring feline spongiform encephalopathy of domestic cats4 and spongiform encephalopathies of a number of zoo animals so-called exotic ungulate encephalopathies5,6 are also recognized as animal prion diseases, and are thought to have resulted from the same BSE-contaminated food given to cattle and humans, although and at least in some of these cases, a sporadic and/or genetic etiology cannot be ruled out. The canine species seems to display resistance to prion disease and no single case has so far been reported.7,8 Here, we describe a case of a 9 week old male Rottweiler puppy presenting neurological deficits; and histological examination revealed spongiform vacuolation characteristic of those associated with prion diseases.9 Initial biochemical studies using anti-PrP antibodies revealed the presence of partially proteinase K-resistant fragment by western blotting. Furthermore, immunohistochemistry revealed spongiform degeneration consistent with those found in prion disease and displayed staining for PrPSc in the cortex.

Of major importance, PrPSc isolated from the Rottweiler was able to cross the species barrier transmitted to hamster in vitro with PMCA and in vivo (one hamster out of 5). Futhermore, second in vivo passage to hamsters, led to 100% attack rate (n = 4) and animals displayed untypical lesional profile and shorter incubation period.

In this study, we show that the canine species might be sensitive to prion disease and that PrPSc isolated from a dog can be transmitted to dogs and hamsters in vitro using PMCA and in vivo to hamsters.

If our preliminary results are confirmed, the proposal will have a major impact on animal and public health and would certainly lead to implementing new control measures for ‘canine spongiform encephalopathy’ (CSE).

References 1. Colchester AC, Colchester NT. The origin of bovine spongiform encephalopathy: the human prion disease hypothesis. Lancet 2005; 366:856-61; PMID:16139661; http:// dx.doi.org/10.1016/S0140-6736(05)67218-2.

2. Richt JA, Hall SM. BSE case associated with prion protein gene mutation. PLoS Pathog 2008; 4:e1000156; PMID:18787697; http://dx.doi.org/10.1371/journal. ppat.1000156.

3. Collinge J. Human prion diseases and bovine spongiform encephalopathy (BSE). Hum Mol Genet 1997; 6:1699-705; PMID:9300662; http://dx.doi.org/10.1093/ hmg/6.10.1699.

4. Wyatt JM, Pearson GR, Smerdon TN, Gruffydd-Jones TJ, Wells GA, Wilesmith JW. Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Vet Rec 1991; 129:233-6; PMID:1957458; http://dx.doi.org/10.1136/vr.129.11.233.

5. Jeffrey M, Wells GA. Spongiform encephalopathy in a nyala (Tragelaphus angasi). Vet Pathol 1988; 25:398-9; PMID:3232315; http://dx.doi.org/10.1177/030098588802500514.

6. Kirkwood JK, Wells GA, Wilesmith JW, Cunningham AA, Jackson SI. Spongiform encephalopathy in an arabian oryx (Oryx leucoryx) and a greater kudu (Tragelaphus strepsiceros). Vet Rec 1990; 127:418-20; PMID:2264242.

7. Bartz JC, McKenzie DI, Bessen RA, Marsh RF, Aiken JM. Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. J Gen Virol 1994; 75:2947-53; PMID:7964604; http://dx.doi.org/10.1099/0022-1317- 75-11-2947.

8. Lysek DA, Schorn C, Nivon LG, Esteve-Moya V, Christen B, Calzolai L, et al. Prion protein NMR structures of cats, dogs, pigs, and sheep. Proc Natl Acad Sci U S A 2005; 102:640-5; PMID:15647367; http://dx.doi.org/10.1073/pnas.0408937102.

9. Budka H. Neuropathology of prion diseases. Br Med Bull 2003; 66:121-30; PMID:14522854; http://dx.doi.org/10.1093/bmb/66.1.121.

http://www.landesbioscience.com/journals/prion/01-Prion6-2-OralPresentations.pdf

Monday, March 26, 2012

CANINE SPONGIFORM ENCEPHALOPATHY: A NEW FORM OF ANIMAL PRION DISEASE

http://caninespongiformencephalopathy.blogspot.com/2012/03/canine-spongiform-encephalopathy-new.html

Monday, March 8, 2010

Canine Spongiform Encephalopathy aka MAD DOG DISEASE

http://caninespongiformencephalopathy.blogspot.com/


terry

I agree. But, the folks who want to ban high fences are going to do their best to tie CWD to "pens" regardless of how big. Everyone with an agenda will use it for their personal favorite, we've already seen it tied to Alzheimer's and sage grouse etc.

All logic is tossed out when a good crisis presents itself.

By comparing the amount of PK-resistant prion protein in the two substrates, an assessment of the host’s species barrier can be made. We show that the CER assay correctly predicts known prion species barriers of laboratory mice and, as an example, show some preliminary results suggesting that bobcats (Lynx rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting disease agent.

http://www.jove.com/video/52522/assessing-transmissible-spongiform-encephalopathy-species-barriers


>>> show some preliminary results suggesting that bobcats (Lynx rufus) may be susceptible to white-tailed deer (Odocoileus virginianus) chronic wasting disease agent.


AD.63: Susceptibility of domestic cats to chronic wasting disease

Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1

1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA

Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD. These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.

http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf

www.landesbioscience.com

PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)

http://www.landesbioscience.com/journals/prion/04-Prion6-2-Pathogenesis-and-pathology.pdf

http://chronic-wasting-disease.blogspot.com/2012/05/chronic-wasting-disease-cwd-prion2012.html

http://www.prion2011.ca/files/PRION_2011_-_Posters_(May_5-11).pdf

http://felinespongiformencephalopathyfse...ats-to-cwd.html

PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)

http://www.landesbioscience.com/journals/prion/04-Prion6-2-Pathogenesis-and-pathology.pdf

http://chronic-wasting-disease.blogspot.com/2012/05/chronic-wasting-disease-cwd-prion2012.html

Thursday, May 31, 2012

CHRONIC WASTING DISEASE CWD PRION2012 Aerosol, Inhalation transmission, Scrapie, cats, species barrier, burial, and more

http://chronic-wasting-disease.blogspot.com/2012/05/chronic-wasting-disease-cwd-prion2012.html

Monday, August 8, 2011

Susceptibility of Domestic Cats to CWD Infection

http://felinespongiformencephalopathyfse...ats-to-cwd.html

Sunday, August 25, 2013

Prion2013 Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

http://chronic-wasting-disease.blogspot.com/2013/08/prion2013-chronic-wasting-disease-cwd.html

Feline Spongiform Encephalopathy (FSE) FSE was first identified in the UK in 1990. Most cases have been reported in the UK, where the epidemic has been consistent with that of the BSE epidemic. Some other countries (e.g. Norway, Liechtenstein and France) have also reported cases.

Most cases have been reported in domestic cats but there have also been cases in captive exotic cats (e.g. Cheetah, Lion, Asian leopard cat, Ocelot, Puma and Tiger). The disease is characterised by progressive nervous signs, including ataxia, hyper-reactivity and behavioural changes and is fatal.

The chemical and biological properties of the infectious agent are identical to those of the BSE and vCJD agents. These findings support the hypothesis that the FSE epidemic resulted from the consumption of food contaminated with the BSE agent.

The FSE epidemic has declined as a result of tight controls on the disposal of specified risk material and other animal by-products.

References: Leggett, M.M. et al.(1990) A spongiform encephalopathy in a cat. Veterinary Record. 127. 586-588

Synge, B.A. et al. (1991) Spongiform encephalopathy in a Scottish cat. Veterinary Record. 129. 320

Wyatt, J. M. et al. (1991) Naturally occurring scrapie-like spongiform encephalopathy in five domestic cats. Veterinary Record. 129. 233.

Gruffydd-Jones, T. J.et al.. (1991) Feline spongiform encephalopathy. J. Small Animal Practice. 33. 471-476.

Pearson, G. R. et al. (1992) Feline spongiform encephalopathy: fibril and PrP studies. Veterinary Record. 131. 307-310.

Willoughby, K. et al. (1992) Spongiform encephalopathy in a captive puma (Felis concolor). Veterinary Record. 131. 431-434.

Fraser, H. et al. (1994) Transmission of feline spongiform encephalopathy to mice. Veterinary Record 134. 449.

Bratberg, B. et al. (1995) Feline spongiform encephalopathy in a cat in Norway. Veterinary Record 136. 444

Baron, T. et al. (1997) Spongiform encephalopathy in an imported cheetah in France. Veterinary Record 141. 270-271

Zanusso, G et al. (1998) Simultaneous occurrence of spongiform encephalopathy in a man and his cat in Italy. Lancet, V352, N9134, OCT 3, Pp 1116-1117.

Ryder, S.J. et al. (2001) Inconsistent detection of PrP in extraneural tissues of cats with feline spongiform encephalopathy. Veterinary Record 146. 437-441

Kelly, D.F. et al. (2005) Neuropathological findings in cats with clinically suspect but histologically unconfirmed feline spongiform encephalopathy. Veterinary Record 156. 472-477.

http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/bse/othertses/index.htm#fse

3 further cheetah cases have occured, plus 1 lion, plus all the primates, and 20 additional house cats. Nothing has been published on any of these UK cases either. One supposes the problem here with publishing is that many unpublished cases were _born_ long after the feed "ban". Caught between a rock and a hard place: leaky ban or horizontal transmission (or both).

http://www.mad-cow.org/may99_zoo_news.html

http://www.mad-cow.org/00/aug00_late_news.html#ggg

YOU explained that imported crushed heads were extensively used in the petfood industry...

http://web.archive.org/web/20060303042720/http://www.bseinquiry.gov.uk/files/yb/1989/04/14001001.pdf

In particular I do not believe one can say that the levels of the scrapie agent in pet food are so low that domestic animals are not exposed...

http://web.archive.org/web/20040301231838/http://www.bseinquiry.gov.uk/files/yb/1989/04/24003001.pdf

http://web.archive.org/web/20060303042732/http://www.bseinquiry.gov.uk/files/yb/1989/04/25001001.pdf

on occassions, materials obtained from slaughterhouses will be derived from sheep affected with scrapie or cattle that may be incubating BSE for use in petfood manufacture...

http://web.archive.org/web/20060303042739/http://www.bseinquiry.gov.uk/files/yb/1989/05/03007001.pdf

*** Meldrum's notes on pet foods and materials used

http://web.archive.org/web/20060303042745/http://www.bseinquiry.gov.uk/files/yb/1989/05/16001001.pdf

*** BSE & Pedigree Petfoods ***

http://web.archive.org/web/20060303042725/http://www.bseinquiry.gov.uk/files/yb/1989/05/16002001.pdf



terry

Sunday, June 14, 2015

Larry’s Custom Meats Inc. Recalls Beef Tongue Products That May Contain Specified Risk Materials BSE TSE Prion

http://madcowusda.blogspot.com/2015/06/larrys-custom-meats-inc-recalls-beef.html



terry


terry

I have a better idea. Why don't you and terry start a CJD thread and let this thread stay on topic? Evidently most of us here aren't influenced much by scare tactics, and are much more interested in the facts as they pertain to CWD.... You know, the original subject of this thread?

Go tell someone else somewhere else that the sky is falling.

Thursday, June 25, 2015

Wisconsin CWD-positive white-tailed deer found on Eau Claire County farm

http://chronic-wasting-disease.blogspot.com/2015/06/wisconsin-cwd-positive-white-tailed.html


Wednesday, March 04, 2015

*** Disease sampling results provide current snapshot of CWD in Wisconsin finding 324 positive detections statewide in 2014

http://chronic-wasting-disease.blogspot.com/2015/03/disease-sampling-results-provide.html


Tuesday, October 07, 2014

*** Wisconsin white-tailed deer tested positive for CWD on a Richland County breeding farm, and a case of CWD has been discovered on a Marathon County hunting preserve

http://chronic-wasting-disease.blogspot.com/2014/10/wisconsin-white-tailed-deer-tested.html


see;

‘’It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin. In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.’’

nothing like the wolf guarding the henhouse.

Texas just documented another case of CWD, I wonder what the Wisconsin’s Deer Czar (from TEXAS), seems Dr. Dough’s passive approach on CWD is not working out too well.

yep, while the Texas deer czar dr. dough was off to Wisconsin pushing the privately owned shooting pen industry (livestock cervid industry), Texas fell to CWD, and have now documented 7 cases of CWD to date.

IF Texas would test for CWD in the captive industry aggressively, I think we would all be shocked as to what they would find.

for your information...

According to Wisconsin’s White-Tailed Deer Trustee Dr. James Kroll, people who call for more public hunting opportunities are “pining for socialism.” He further states, “(Public) Game management is the last bastion of communism.”

“Game Management,” says James Kroll, driving to his high-fenced, two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.” Kroll, also known as Dr. Deer, is the director of the Forestry Resources Institute of Texas at Stephen F. Austin State University, and the “management” he is referring to is the sort practiced by the State of Texas. The 55-year-old Kroll is the leading light in the field of private deer management as a means to add value to the land. His belief is so absolute that some detractors refer to him as Dr. Dough, implying that his eye is on the bottom line more than on the natural world.

Kroll, who has been the foremost proponent of deer ranching in Texas for more than thirty years, doesn’t mind the controversy and certainly doesn’t fade in the heat. People who call for more public lands are “cocktail conservationists,” he says, who are really pining for socialism. He calls national parks “wildlife ghettos” and flatly accuses the government of gross mismanagement. He argues that his relatively tiny acreage, marked by eight-foot fences and posted signs warning off would-be poachers, is a better model for keeping what’s natural natural while making money off the land.

Dr. Deer Wisconsin Report: Will High-Fence Bias Skew Final Plan?

Categories: Blogs, Daniel Schmidt's Whitetail Wisdom, Deer News, Featured Tags: antler restricitons, dan schmidt, Dr. Deer, james kroll, James Kroll Wisconsin, qdm, quality deer management, texas hunting, wisconsin deer hunting March 29, 2012 According to Wisconsin’s White-Tailed Deer Trustee Dr. James Kroll, people who call for more public hunting opportunities are “pining for socialism.” He further states, “(Public) Game management is the last bastion of communism.”

OPINION BLOG

These are just two insights into the man who has been asked to provide analysis and recommended changes to Wisconsin’s deer management program. Kroll’s insights are from an article entitled “Which Side of the Fence Are You On?” by Joe Nick Patoski for a past edition of Texas Monthly. If nothing more, the article gives an unabashed look into the mind-set that will be providing the Wisconsin DNR with recommendations on how to change their deer management practices. James Kroll (also known as “Deer Dr.”) was appointed to the Wisconsin “deer czar” position last fall. He was hired by the Department of Administration and instructed to complete a review of the state’s deer management program.

Here’s a sample of the article:

“Game Management,” says James Kroll, driving to his high-fenced, two-hundred-acre spread near Nacogdoches, “is the last bastion of communism.” Kroll, also known as Dr. Deer, is the director of the Forestry Resources Institute of Texas at Stephen F. Austin State University, and the “management” he is referring to is the sort practiced by the State of Texas. The 55-year-old Kroll is the leading light in the field of private deer management as a means to add value to the land. His belief is so absolute that some detractors refer to him as Dr. Dough, implying that his eye is on the bottom line more than on the natural world.

Kroll, who has been the foremost proponent of deer ranching in Texas for more than thirty years, doesn’t mind the controversy and certainly doesn’t fade in the heat. People who call for more public lands are “cocktail conservationists,” he says, who are really pining for socialism. He calls national parks “wildlife ghettos” and flatly accuses the government of gross mismanagement. He argues that his relatively tiny acreage, marked by eight-foot fences and posted signs warning off would-be poachers, is a better model for keeping what’s natural natural while making money off the land.

A trip to South Africa six years ago convinced Kroll that he was on the right track. There he encountered areas of primitive, lush wildlife-rich habitats called game ranches. They were privately owned, privately managed, and enclosed by high fences. He noticed how most of the land outside those fences had been grazed to the nub, used up. “Game ranches there derive their income from these animals — viewing them, hunting them, selling their meat,” he says. “There are no losers.” At his own ranch Kroll has set up a smaller version of the same thing. His land is indeed lush, verdant, with pine groves, an abundance of undergrowth, wild orchids, New Jersey tea, jack-in-the-pulpits, and other native plants. He has also set up a full-scale breeding research center and is one of twenty Texas deer breeders using artificial insemination to improve his herd. “We balance sex and age ratio,” he says. “We manage habitat. We control the population and manage for hunting. I want to leave the deer herd better than it was before we came.”

It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin. In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.

“That has given landowners more freedom,” Kroll told Texas Monthly. “(However,) You still have to let the state on your land to get a wildlife-management permit.” The key difference here is that 98 percent of Texas is comprised of private land. Wisconsin, on the other hand, consists of approximately 34.8 million acres of land, and 25.5 percent of the state’s 638,000 gun-hunters reported hunting on public land at some point during the season (2010, Duey, Rees).

According to the Wisconsin Realtors Association, more than 5.7 million acres of this land, or 16.5 percent, is publicly owned and used for parks, forests, trails, and natural resource protection. [Note: these statistics do not include the public land used for roads, government buildings, military bases, and college/school campuses.] This 5.7 million acres of public land is owned as follows:

Federal government owns approximately 1.5 million acres (4.4 percent of the state’s land area). Almost all of the federal forestland in Wisconsin is located in Chequamegon-Nicolet National Forest.

State government owns approximately 1.6 million acres (4.6 percent of the state’s land area). The land is managed by two agencies, the Board of Commissioners of Public Land (who manages lands granted by federal government) and the DNR (managing land owned by the state).

County government owns approximately 2.6 million acres (7.5 percent of the state’s land area).

Public land is located in 71 of Wisconsin’s 72 counties, with the most public land located in Bayfield County (464,673 acres). [Note: Menominee County does not have any public land, but 98 percent of the land is held in trust by the Menominee Tribe.] Twenty counties have more than 100,000 acres of public land, while only 12 counties have fewer than 10,000 acres.

What does this all mean? My initial reaction, which is one that I predicted when Kroll was named to the state’s deer trustee position, is that his team’s final recommendations — if implemented — will be heavily skewed toward the state’s larger landowners (500+ acres) and folks who own small parcels in areas comprised mostly of private land.

It is also my prediction that the final recommendations (again, if implemented) will do little, if anything, to improve deer herds and deer hunting on Wisconsin’s 5.7 million acres of public land.

Where does this leave the public-land hunter? “It will suck to be you,” said one deer manager who asked to remain anonymous out of fear for his job. “The resources and efforts will go toward improving the private land sector. This is all about turning deer hunting away from the Public Land Doctrine and more toward a European-style of management — like they have in Texas.”

I do, of course, hope these assumptions are wrong. As with all things in life, we should maintain an open mind to change. Life is all about change. However, change for the sake of change is usually a recipe for disaster. Especially when that change is driven by something more than a sincere desire to manage public resources for the greater good.

As noted yesterday (Dr. James Kroll Report: Is That All You Get For Your Money), I will provide more of my opinions and interpretation on this important issue in forthcoming installments of this blog. Read his full preliminary report here.

http://www.texasmonthly.com/story/which-side-fence-are-you

http://www.texasmonthly.com/preview/2002-02-01/feature5

http://www.deeranddeerhunting.com/deer-n...skew-final-plan

snip...see full text ;

Thursday, March 29, 2012

TEXAS DEER CZAR SAYS WISCONSIN DNR NOT DOING ENOUGH ABOUT CWD LIKE POT CALLING KETTLE BLACK

http://chronic-wasting-disease.blogspot.com/2012/03/texas-deer-czar-says-wisconsin-dnr-not.html

Friday, June 01, 2012

*** TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS

http://chronic-wasting-disease.blogspot.com/2012/06/texas-deer-czar-to-wisconsin-ask-to.html

Tuesday, July 10, 2012

Dr. James C. Kroll Texas deer czar final report on Wisconsin

http://chronic-wasting-disease.blogspot.com/2012/07/dr-james-c-kroll-texas-deer-czar-final.html

Wednesday, March 18, 2015

Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-confirmed.html

Wednesday, March 25, 2015

Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015

http://chronic-wasting-disease.blogspot.com/2015/03/chronic-wasting-disease-cwd-cases.html



UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;

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

From: David Colby To: flounder9@verizon.net

Cc: stanley@XXXXXXXX

Sent: Tuesday, March 01, 2011 8:25 AM

Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

Dear Terry Singeltary,

Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor Department of Chemical Engineering University of Delaware

===========END...TSS==============

Thursday, July 03, 2014

How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets?

http://chronic-wasting-disease.blogspot.com/2014/07/how-chronic-wasting-disease-is.html



PRION CONFERENCE 2014 HELD IN ITALY RECENTLY CWD BSE TSE UPDATE

> First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)

PRION 2014 - PRIONS: EPIGENETICS and NEURODEGENERATIVE DISEASES – Shaping up the future of prion research

Animal TSE Workshop 10.40 – 11.05 Talk Dr. L. Cervenakova First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)

http://www.prion2014.org/images/Animal_TSE_workshop.pdf

P.126: Successful transmission of chronic wasting disease (CWD) into mice over-expressing bovine prion protein (TgSB3985)

Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1 1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA

Keywords: chronic wasting disease, transmission, transgenic mouse, bovine prion protein

Background. CWD is a disease affecting wild and farmraised cervids in North America. Epidemiological studies provide no evidence of CWD transmission to humans. Multiple attempts have failed to infect transgenic mice expressing human PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal human PrPC in vitro provides additional evidence that transmission of CWD to humans cannot be easily achieved. However, a concern about the risk of CWD transmission to humans still exists. This study aimed to establish and characterize an experimental model of CWD in TgSB3985 mice with the following attempt of transmission to TgHu mice.

Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse (CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD) or elk (CWD/Elk). Animals were observed for clinical signs of neurological disease and were euthanized when moribund. Brains and spleens were removed from all mice for PrPCWD detection by Western blotting (WB). A histological analysis of brains from selected animals was performed: brains were scored for the severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain regions.

Results. Clinical presentation was consistent with TSE. More than 90% of TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres in the brain but only mice in the latter group carried PrPCWD in their spleens. We found evidence for co-existence or divergence of two CWD/ Tga20 strains based on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen by WB. However, on neuropathological examination we found presence of amyloid plaques that stained positive for PrPCWD in three CWD/WTD- and two CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and CWD/Elkinfected mice were similar but unique as compared to profiles of BSE, BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM mice tested positive for PrPCWD by WB or by immunohistochemical detection.

Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.

PRION 2014 CONFERENCE

CHRONIC WASTING DISEASE CWD

A FEW FINDINGS ;

Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.

We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.

Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.

Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.

Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.

Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.

P.28: Modeling prion species barriers and the new host effect using RT-QuIC

Kristen A Davenport, Davin M Henderson, Candace K Mathiason, and Edward A Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious.

Studies of the effects of primary or tertiary prion protein www.landesbioscience.com Prion 37 structures on trans-species prion transmission have relied upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect.

As an alternative strategy, we are using real-time quaking-induced conversion (RT-QuIC) to investigate the propensity for and the kinetics of trans-species prion conversion. RT-QuIC has the advantage of providing more defined conditions of seeded conversion to study the specific role of native PrP:PrPRES interactions as a component of the species barrier.

We are comparing chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions by seeding each prion into its native host recPrP (full-length bovine recPrP, or white tail deer recPrP) vs. into the heterologous species.

Upon establishing the characteristics of intra-species and inter-species prion seeding for CWD and BSE prions, we will evaluate the seeding kinetics and cross-species seeding efficiencies of BSE and CWD passaged into a common new host—feline—shown to be a permissive host for both CWD and BSE.

*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.

https://www.landesbioscience.com/journal...d%20Biology.pdf

Chronic Wasting Disease Susceptibility of Four North American Rodents

Chad J. Johnson1*, Jay R. Schneider2, Christopher J. Johnson2, Natalie A. Mickelsen2, Julia A. Langenberg3, Philip N. Bochsler4, Delwyn P. Keane4, Daniel J. Barr4, and Dennis M. Heisey2 1University of Wisconsin School of Veterinary Medicine, Department of Comparative Biosciences, 1656 Linden Drive, Madison WI 53706, USA 2US Geological Survey, National Wildlife Health Center, 6006 Schroeder Road, Madison WI 53711, USA 3Wisconsin Department of Natural Resources, 101 South Webster Street, Madison WI 53703, USA 4Wisconsin Veterinary Diagnostic Lab, 445 Easterday Lane, Madison WI 53706, USA *Corresponding author email: cjohnson@svm.vetmed.wisc.edu

We intracerebrally challenged four species of native North American rodents that inhabit locations undergoing cervid chronic wasting disease (CWD) epidemics. The species were: deer mice (Peromyscus maniculatus), white-footed mice (P. leucopus), meadow voles (Microtus pennsylvanicus), and red-backed voles (Myodes gapperi). The inocula were prepared from the brains of hunter-harvested white-tailed deer from Wisconsin that tested positive for CWD. Meadow voles proved to be most susceptible, with a median incubation period of 272 days. Immunoblotting and immunohistochemistry confirmed the presence of PrPd in the brains of all challenged meadow voles. Subsequent passages in meadow voles lead to a significant reduction in incubation period. The disease progression in red-backed voles, which are very closely related to the European bank vole (M. glareolus) which have been demonstrated to be sensitive to a number of TSEs, was slower than in meadow voles with a median incubation period of 351 days. We sequenced the meadow vole and red-backed vole Prnp genes and found three amino acid (AA) differences outside of the signal and GPI anchor sequences. Of these differences (T56-, G90S, S170N; read-backed vole:meadow vole), S170N is particularly intriguing due its postulated involvement in "rigid loop" structure and CWD susceptibility. Deer mice did not exhibit disease signs until nearly 1.5 years post-inoculation, but appear to be exhibiting a high degree of disease penetrance. White-footed mice have an even longer incubation period but are also showing high penetrance. Second passage experiments show significant shortening of incubation periods. Meadow voles in particular appear to be interesting lab models for CWD. These rodents scavenge carrion, and are an important food source for many predator species. Furthermore, these rodents enter human and domestic livestock food chains by accidental inclusion in grain and forage. Further investigation of these species as potential hosts, bridge species, and reservoirs of CWD is required.

http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.html


please see ;

http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf


http://chronic-wasting-disease.blogspot.com/


terry

Kristen A Davenport, Davin M Henderson, Candace K Mathiason, and Edward A Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA

The propensity for trans-species prion transmission is related to the structural characteristics of the enciphering and heterologous PrP, but the exact mechanism remains mostly mysterious.

Studies of the effects of primary or tertiary prion protein www.landesbioscience.com Prion 37 structures on trans-species prion transmission have relied upon animal bioassays, making the influence of prion protein structure vs. host co-factors (e.g. cellular constituents, trafficking, and innate immune interactions) difficult to dissect.

As an alternative strategy, we are using real-time quaking-induced conversion (RT-QuIC) to investigate the propensity for and the kinetics of trans-species prion conversion. RT-QuIC has the advantage of providing more defined conditions of seeded conversion to study the specific role of native PrP:PrPRES interactions as a component of the species barrier.

We are comparing chronic wasting disease (CWD) and bovine spongiform encephalopathy (BSE) prions by seeding each prion into its native host recPrP (full-length bovine recPrP, or white tail deer recPrP) vs. into the heterologous species.

Upon establishing the characteristics of intra-species and inter-species prion seeding for CWD and BSE prions, we will evaluate the seeding kinetics and cross-species seeding efficiencies of BSE and CWD passaged into a common new host—feline—shown to be a permissive host for both CWD and BSE.

*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.

I assume this is an ongoing study. It's an important one because it seeks to replicate the process that produced vCJD and is the potential path for CWD to breach the species barrier. It should help quantify the real danger of CWD crossing the trans species barrier.

In one ear and out the other

Folks, just because pathogens share similar transmission vectors does not mean that the pathogen is going to somehow jump species barriers that are in place.

Canine distemper and the flu's have been around for centuries. Flu's effect people as well as canines. But we don't get distemper.

Now, can someone in a lab conjure up some gene combination that would never occur in nature to provide a means of trans specie transmission? Maybe.

But that's not what this thread was supposed to be about.

x2

Wouldn't properly cooking your venison take care of this problem? If you think about it for half a second, there's no telling what hunters have ingested over the years from wild game. I'll take my chances still.

No, it's someone like 900 degrees for 4hours... But is it actually a problem

Looks like this topic has lost its steam.

It's just the lull before the storm. TPWD is designing a strategy that (if rumors are true) will include not only killing all deer in the pen the buck came from, but all pens on the ranch. Even though they are separated by a 30' alley and have never co-mingled. After that, they do have designs on going after all ranches that have had transfers of breeder deer from that ranch (47 is the last number I've heard). Not stocker deer from what I hear, but deer that were put into pens for breeding in licensed breeding facilities.

Also, it's rumored (two different sources) that they have told the landowner that not only can he not take pictures or video the slaughter, but that he can't even be on his own ranch during the slaughter.

I hope that the last rumor above isn't true. For the state's sake. I can assure you it will cost the state more than it can imagine if they try that.

Thank God we've got all the irrelevant links out of the way. Hopefully we can focus on what the test results are from the deer, and use this thread to share relevant information about how the state proceeds.

I'd be working on a federal injunction ASAP. That's some BS. I've heard similar. Something don't smell right and it ain't on the private land owner this time.

I have heard the same about the owner. Also some other things that are very disturbing if true.

CWD in Texas now.......thanks a lot Obama

X100