Cwd

Murray said:

https://www.youtube.com/watch?v=buyiCU8TlwQ

I feel like there is a better approach than killing all the older age class. Older bucks are more reclusive and loners. The problem is when deer congregate and does do that the most in their family groups. This is a very good video on CWD. I do believe we need to monitor and manage it the best as possible yet I also feel there is somewhat of a hysteria over it.

Click to expand...

I could only make it about halfway through that presentation. He lost me when he started referring to TB disease data, but extrapolating that to somehow being justification for how the state should change their management of CWD. He's basically trying to compare apples to elephants there. I have no idea who that guy is, but he knows absolutely nothing about disease.

Seems like some voo-doo biology on how the state can "manage" CWD by growing more older bucks? What meeting was this?

After all I have read and all the speeches are listened too, I must say that it bothers me that all the management of this problem has been done based on what boils down to speculation and a possibility of causes and more importantly, guessing at how it is contracted and spread.
There is a real chance that animals create this disease (CWD) inside their bodies because of a complex combination of chemical changes that only minutely involves their environment. More genetic testing between fawn and parents may be needed, but it's like trying to find a problem that isn't always there. Like an electric short in a cars wire harness. Only a problem when the wire gets hot or when the wire touches grounded metal, etc.... not easy to identify.
But, burning or crushing the car will get rid of the problem with about as much resolve as shooting all the deer!
We hunters are financing this feasco , so how about some hard scientific proof about something before we bet the farm and drink the cool aid!
Killing deer only 100% ensures that those dead deer won't be a problem any more. Most all deer shot in the name of testing did not test positive. As many as 1% might have been a carrier, but far less were actually positively identified as having the disease.
Spending millions on guesses and maybes ,and putting laws in place just because someone thinks it is necessary, is less than poor judgement.
We should stop all this now and envest in scientific study to get answers that are backed up by varifiable facts.

Millsworks said:

After all I have read and all the speeches are listened too, I must say that it bothers me that all the management of this problem has been done based on what boils down to speculation and a possibility of causes and more importantly, guessing at how it is contracted and spread.
There is a real chance that animals create this disease (CWD) inside their bodies because of a complex combination of chemical changes that only minutely involves their environment. More genetic testing between fawn and parents may be needed, but it's like trying to find a problem that isn't always there. Like an electric short in a cars wire harness. Only a problem when the wire gets hot or when the wire touches grounded metal, etc.... not easy to identify.
But, burning or crushing the car will get rid of the problem with about as much resolve as shooting all the deer!
We hunters are financing this feasco , so how about some hard scientific proof about something before we bet the farm and drink the cool aid!
Killing deer only 100% ensures that those dead deer won't be a problem any more. Most all deer shot in the name of testing did not test positive. As many as 1% might have been a carrier, but far less were actually positively identified as having the disease.
Spending millions on guesses and maybes ,and putting laws in place just because someone thinks it is necessary, is less than poor judgement.
We should stop all this now and envest in scientific study to get answers that are backed up by varifiable facts.

Click to expand...

Really? There has been a lot of scientific research done to this point, and more continues as we speak. That's how we have come to learn how the disease is spread, how prevalence increases over time, and are learning more now about how it impacts populations long term. What scientific evidence makes you think all of this is speculation?

Have not seen anything that proofs exactly how it is spread or specifically how the deer species aguire it.
Only what is stated as probable.
Saliva transfer can't explain how deer species that have had no contact with each other contract the deasease and more importantly why deer that live in areas that are highly considered as centers for outbrakes never get it.
If I am wrong than it is because of a lack or oversight on my part, just haven't seen it.
It's obvious it exists, it will be ongoing, sure. But too many important questions need answering to properly manage this.

The idea that the agent itself is a prion is as of I can find, a theary, a widely believed one ,but nun the less a theary.
The prion desease ,or TSE (transmissible spongiform encephalopathic) may be on the right train of thought, but if it is there still remains big questions about the way it's spread.
Pion diseases (TSEs) are rare degenerative brain disorders characterized by tiny holes found in the brain when seen under a microscope. Tuff to test live subjects. Furthermore, the accuracy of state to state testing could be highly questionable. False positives and negatives happen.
cJD is the most well known of the rare human form of this type of disease (Creutzfeldt Jakobs Disease).
More rare and less known are (FFI) and (GSS). Which are human TSEs that have been found to be hereditary and only exists in a few families around the world.
If this disease is hereditary and past on from mother to young or father to young ,it may jump and skip generations and even not affect all that receive it.
Shooting deer won't likely fix the issue if any of the above is true..
So, yes really.

I haven't been on here in a long time and am sorry for that just always busy it seems like. The way I look at it is you will never stop cwd without an actuall cure or killing off every animal. Banning baiting and shooting the majority of the deer will not help! These animals breed and will travel many miles to find a mate it will not stop spreading by simple things like mentioned earlier a much less slow it down.

Just let it run its course is what is what I say.

Can't say I think nothing should be done, but killing hundreds of thousands of deer just because someone said that might help is not acceptable.
There could be a solution waiting to be discovered some day. There could also be a real chance that this disease is a complex and naturally​ forming thing that has existed for thousands of years and can not be contained, much less controlled.
In reality very few deer have been killed buy the disease when you look at the vast numbers of deer species that have been affected. A loss, sure, but nothing compared to the slautered numbers across the country in the name of good ideas that have not been substantiated thoroughly.

Wish I had the answer. Mass killing can't be the best we can do, is it?
Especially when the sportsman that now have less game to hunt are paying for this management plan that will certainly take a decade or more to level out. If it stops that is.

Millsworks said:

The idea that the agent itself is a prion is as of I can find, a theary, a widely believed one ,but nun the less a theary.
The prion desease ,or TSE (transmissible spongiform encephalopathic) may be on the right train of thought, but if it is there still remains big questions about the way it's spread.
Pion diseases (TSEs) are rare degenerative brain disorders characterized by tiny holes found in the brain when seen under a microscope. Tuff to test live subjects. Furthermore, the accuracy of state to state testing could be highly questionable. False positives and negatives happen.
cJD is the most well known of the rare human form of this type of disease (Creutzfeldt Jakobs Disease).
More rare and less known are (FFI) and (GSS). Which are human TSEs that have been found to be hereditary and only exists in a few families around the world.
If this disease is hereditary and past on from mother to young or father to young ,it may jump and skip generations and even not affect all that receive it.
Shooting deer won't likely fix the issue if any of the above is true..
So, yes really.

Click to expand...

One more response before I bow out, because I have a thing against misinformation. There is very little debate about how CWD is spread. Prions being the causative agent is a hypothesis backed up by both captive and field studies since the 1970s carried out by disease ecologists, epidemiologists, veterinarians, molecular biologists, and others. No other causative agent has ever been implicated despite extensive research.

There is an ante mortem test. It has been in use for nearly a decade. We can watch animals turn from negative to positive during repeated sampling events. Geneticists have been sequencing and researching the cervid genome for over a decade as well, including extensive sequencing and study of the gene that codes for the protein involved in CWD. There is no evidence of a genetic basis for CWD, again despite extensive study to find such.

There is likely very little variation in testing between states when it comes to CWD because most states use the same few national labs to do the testing. Currently there are17 approved labs in the US. Labs must be certified to test for CWD, which involves meeting rigorous standards to ensure accuracy and adherence to testing procedures, and standardisation between labs.

I could go on, but I won't because I don't think it will make any difference. You haven't cited a single source to support your ideas, though someone could literally get a Master's degree writing up the literature review of all the primary literature that exists that directly refutes your suppositions. I personally don't have the time to do that.

If sportsmen are really that concerned with having more game to hunt, they shouldn't latch on to pseudo science and water cooler conjecture just because it tells them what they want to hear. The states are by and large managing CWD according to the best available science. Unfortunately there is no simple, pretty way to address it. If there was, we'd be doing that.

I have to respect your view and opinions hunting wife, but the facts are what science is about.
Not everyone will agree with each other on any topic. Sometimes that is what helps fix a problem by pushing others to search for info and adding the facts up to get an answer.
If it is so clear how this disease is contracted and spread than I'm sure it will be eradicated next week.
Obviously, not. Much more info is needed to make accurate management decisions.
Accepting popular theories as facts is too comon in science and life sometimes. When we challenge an idea it must have fact evidence to back it up.
Not enough hard facts yet on CWD. That is the facts.
Thanks for posting your veiw and pushing people to look for the information themselves to find the truth about what is known. The national center for the study of CWD clearly states that this current info is a popularly accepted theory and that not much is known about how it is created and little more is known about how it is spread.
That kinda sums it up for me.

Also check USGS.gov, National wildlife health center. Again, clearly states it is still unknown as to how animals contract or spread CWD. There's some good idea that it is a mutated prion, sure, but that's about it.
Recently it has been proven that prions of the disease can be stored and transmitted through plants. Again I don't see eradication of deer a fix if the soil and plants will affect any new resident deer that will engest plants years later and then be affected.
Guess I'm crazy to think you need to know how the process of CWD is spread in order to stop it spreading.

New research just released has shown some Old World Monkeys are susceptible to contracting CWD.

This is important and alarming news as it was previously believed that there was a species barrier at this level which offered hope that Humans were most likely safe from being able to contract this disease.

While there is no evidence that a person HAS contracted CWD,
there is also no evidence that NO Person has contracted the disease.

If you hunt in a known in a CWD area, please have the animal tested before eating it.

Chronic Wasting Disease: CFIA Research Summary Embargoed until May 23, 2017
(OCR of a scanned original)


Research Findings


Chronic Wasting Disease (CWD) is a progressive, fatal disease of the nervous system of cervids including deer, elk, moose, and reindeer that is caused by abnormal proteins called prions. It is known as a transmissible spongiform encephalopathy (TSE). Other TSEs include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, and Creutzfeldt-Jakob disease (CJD) in humans.

A limited number of experimental studies have demonstrated that non-human primates, specifically squirrel monkeys, are susceptible to CWD prions. An ongoing research study has now shown that CWD can also be transmitted to macaques, which are genetically closer to humans.


The study led by Dr. Stefanie Czub, a scientist at the Canadian Food Inspection Agency (CFIA), and funded by the Alberta Prion Research institute has demonstrated that by orally administering material under experimental conditions from cervids (deer and elk) naturally infected with CWD, the disease can be transmitted to macaques.


in this project, which began in 2009, 18 macaques were exposed to CWD in a variety of ways: by injecting into the brain, through contact with skin, oral administration, and intravenously (into the bloodstream through veins).
So far, results are available from 5 animals. At this point, two animals that were exposed to CWD by direct introduction into the brain, one that was administered infected brain material by oral administration and two that were given infected muscle by oral administration have become infected with CWD. The study is ongoing and testing continues in the remaining animals. The early results will be presented at PRlON 2017, the annual international conference on prion diseases, in Edinburgh, Scotland, May 23 to 26, 2017.


Potential impacts of the new finding

Since 2003 Canada has a policy that recommends that animals and materials known to be infected with prions be removed from the food chain and from health products. Although no direct evidence of CWD prion transmission to humans has ever been recorded, the policy advocates a precautionary approach to managing CWD and potential human exposure to prions. These initial findings do not change Health Canada’s Health Products and Food Branch (HPFB) position on food and health products. A precautionary approach is still recommended to manage the potential risks of exposure to prions through food and health products. Measures are in place at federal, provincial and territorial levels to reduce human exposure to products potentially contaminated by CWD by preventing known infected animals from entering the marketplace.


While Federal and P/T government’s animal disease control policies continue to divert known CWD-infected animals away from entering the food and feed supply, research and development of sensitive detection methods including live-animal sampling techniques remain crucial for ensuring an accurate diagnosis. In addition, consistent federal, provincial and territorial communications of appropriate precautionary measures for hunters and indigenous communities are required.


Next Steps

The CFlA will continue to collaborate with national and international partners to develop and validate new diagnostic techniques. The CFlA will also continue to offer confirmatory testing services and reference laboratory expertise to provincial and territorial partners on demand.


Currently, CFlA laboratories are leading or collaborating on several research projects to understand the potential for CWD to infect humans. These projects use non‐human primates, genetically modified mice, and cell-free amplification approaches. Given the present findings, CFiA encourages continued research into TSEs.


The results of this study reinforce the need to redesign the federal program to foster greater adoption of risk mitigation measures for farmed cervids. Federal and provincial government collaboration will continue as new program options are assessed.


The results of Dr. Czub’s research into CWD will be of interest to scientists, governments, industry and people who consume cervid products. After the presentation at PRION 2017, the research will follow the normal steps of completion, peer review and publication. The Government of Canada will monitor the response to this research and determine whether further review of the science is required. Other studies underway by other researchers may also become public as a result of the presentation of Dr. Czub’s research.


The Public Health Agency of Canada, Health Canada, CFlA and other Federal partners are working together to assess what policies or programs need further review as well as preparing other communications about the research and health policy and advice to Canadian.
2017/04/28

Click to expand...

Notice to Members Regarding Chronic Wasting Disease (CWD)

Posted on: May 31st, 2017

To: MNA Members

From: Métis Nation of Alberta

Date: Wednesday, May 31, 2017
Métis Nation of Alberta (MNA) was made aware of a recent Canadian research study examining the transmission of Chronic Wasting Disease. The initial results of the study indicate that macaque monkeys (genetically similar to humans) can be infected with Chronic Wasting Disease (CWD) after eating deer that is infected with CWD. CWD is a prion disease, which are fatal, transmissible diseases characterized by abnormal proteins in the brain and nervous system. To date no research has shown that CWD can be passed on to humans, and no human cases of CWD have ever been identified. However, this new research indicates that it is a possibility. The Deputy Chief Medical Officer of Health has reached out to us to share with our Métis harvesters this important information.

For more information you can visit:

http://aep.alberta.ca/fish-wildlife...onic-wasting-disease/cwd-updates/default.aspx

and

www.nwhc.usgs.gov/disease_information/chronic_wasting_disease/index.jsp.

What the Alberta Government knows:

CWD is present in southeastern Alberta, with the area slowly spreading westward over time (introduced into Alberta from Saskatchewan) – see map for more information at http://aep.alberta.ca/fish-wildlife...uments/HuntersCWD-HarvestedDeerHeads-2016.pdf
CWD circulates in deer populations, particularly mule deer; it has been found in about 4% of deer tested in 2016;
Elk can be infected in areas where CWD has been present in deer for a long period of time;
Moose can also be infected, but this would be fairly rare.
Necessary Precautions for Harvesters:

Hunters and others who handle carcasses follow basic handling precautions (available here http://aep.alberta.ca/fish-wildlife...DeerCarcassTransportationHandling-Oct2009.pdf

All deer, moose and elk harvested from CWD mandatory submission wildlife management units (WMUs) be tested for CWD; and
A negative result (no CWD detected by the test) must be obtained before any part of an animal is eaten.

For more information, contact:
Amy Quintal
Métis Nation of Alberta
Métis Harvesting Liaison
Tel: (780) 455 – 2200
[email protected]

http://albertametis.com/2017/05/notice-members-regarding-chronic-wasting-disease-cwd/

FRIDAY, JUNE 02, 2017

Alberta Canada Chronic Wasting Disease (CWD) Surveillance Update: 2016/17 Final

http://chronic-wasting-disease.blogspot.com/2017/06/alberta-canada-chronic-wasting-disease.html

Chronic Wasting Disease: CFIA Research Summary

Embargoed until May 23, 2017

(OCR of a scanned original)

Research Findings

Chronic Wasting Disease (CWD) is a progressive, fatal disease of the nervous system of cervids including deer, elk, moose, and reindeer that is caused by abnormal proteins called prions. It is known as a transmissible spongiform encephalopathy (TSE). Other TSEs include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, and Creutzfeldt-Jakob disease (CJD) in humans.

A limited number of experimental studies have demonstrated that non-human primates, specifically squirrel monkeys, are susceptible to CWD prions. An ongoing research study has now shown that CWD can also be transmitted to macaques, which are genetically closer to humans.

The study led by Dr. Stefanie Czub, a scientist at the Canadian Food Inspection Agency (CFIA), and funded by the Alberta Prion Research institute has demonstrated that by orally administering material under experimental conditions from cervids (deer and elk) naturally infected with CWD, the disease can be transmitted to macaques.

in this project, which began in 2009, 18 macaques were exposed to CWD in a variety of ways: by injecting into the brain, through contact with skin, oral administration, and intravenously (into the bloodstream through veins). So far, results are available from 5 animals. At this point, two animals that were exposed to CWD by direct introduction into the brain, one that was administered infected brain material by oral administration and two that were given infected muscle by oral administration have become infected with CWD. The study is ongoing and testing continues in the remaining animals. The early results will be presented at PRlON 2017, the annual international conference on prion diseases, in Edinburgh, Scotland, May 23 to 26, 2017.

Potential impacts of the new finding

Since 2003 Canada has a policy that recommends that animals and materials known to be infected with prions be removed from the food chain and from health products. Although no direct evidence of CWD prion transmission to humans has ever been recorded, the policy advocates a precautionary approach to managing CWD and potential human exposure to prions. These initial findings do not change Health Canada’s Health Products and Food Branch (HPFB) position on food and health products. A precautionary approach is still recommended to manage the potential risks of exposure to prions through food and health products. Measures are in place at federal, provincial and territorial levels to reduce human exposure to products potentially contaminated by CWD by preventing known infected animals from entering the marketplace.

While Federal and P/T government’s animal disease control policies continue to divert known CWD-infected animals away from entering the food and feed supply, research and development of sensitive detection methods including live-animal sampling techniques remain crucial for ensuring an accurate diagnosis. In addition, consistent federal, provincial and territorial communications of appropriate precautionary measures for hunters and indigenous communities are required.

Next Steps

The CFlA will continue to collaborate with national and international partners to develop and validate new diagnostic techniques. The CFlA will also continue to offer confirmatory testing services and reference laboratory expertise to provincial and territorial partners on demand.

Currently, CFlA laboratories are leading or collaborating on several research projects to understand the potential for CWD to infect humans. These projects use non‐human primates, genetically modified mice, and cell-free amplification approaches. Given the present findings, CFiA encourages continued research into TSEs.

The results of this study reinforce the need to redesign the federal program to foster greater adoption of risk mitigation measures for farmed cervids. Federal and provincial government collaboration will continue as new program options are assessed.

The results of Dr. Czub’s research into CWD will be of interest to scientists, governments, industry and people who consume cervid products. After the presentation at PRION 2017, the research will follow the normal steps of completion, peer review and publication. The Government of Canada will monitor the response to this research and determine whether further review of the science is required. Other studies underway by other researchers may also become public as a result of the presentation of Dr. Czub’s research.

The Public Health Agency of Canada, Health Canada, CFlA and other Federal partners are working together to assess what policies or programs need further review as well as preparing other communications about the research and health policy and advice to Canadian. 2017/04/28

===end...UNOFFICIAL...NO URL LINK...TSS===

see much more here on cwd zoonosis;

0:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada

http://prion2017.org/programme/


WEDNESDAY, MAY 03, 2017

*** First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques

http://chronic-wasting-disease.blogspot.com/2017/05/first-evidence-of-intracranial-and.html

Wednesday, May 24, 2017

PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1

Subject: PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh

*see archives of previous Prion Conferences, the ones that are still available, scroll down towards bottom in this link.

http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html

WEDNESDAY, MAY 31, 2017

Texas New Exotic CWD Susceptible Species Rules Now in Effect

http://chronic-wasting-disease.blogspot.com/2017/05/texas-new-exotic-cwd-susceptible.html


Wednesday, May 24, 2017

PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1

Subject: PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh

*see archives of previous Prion Conferences, the ones that are still available, scroll down towards bottom in this link.

http://prionprp.blogspot.com/2017/05/prion2017-conference-video-update-23-26.html

WEDNESDAY, MAY 31, 2017

Texas New Exotic CWD Susceptible Species Rules Now in Effect

http://chronic-wasting-disease.blogspot.com/2017/05/texas-new-exotic-cwd-susceptible.html

WEDNESDAY, MAY 17, 2017

CWD, TSE, PRION, Cattle, Pigs, Sheep, and Humans aka Mad Cow Disease

http://chronic-wasting-disease.blogspot.com/2017/05/cwd-tse-prion-cattle-pigs-sheep-and.html


kind regards, terry

TUESDAY, JUNE 06, 2017

CHRONIC WASTING DISEASE CWD TSE PRION ZOONOSIS ZOONOTIC INSIDIOUS AND DIRE CONSEQUENCES AHEAD

http://chronic-wasting-disease.blogspot.com/2017/06/chronic-wasting-disease-cwd-tse-prion.html

PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1

University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen

This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.

Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.

At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.

PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS

TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

http://chronic-wasting-disease.blogspot.com/2017/06/prion-2017-conference-abstract-first.html

I posted a few months ago about a talk I heard at one of the wildlife conferences regarding CWD in elk. I tracked down their project report from this past fall - this is from ongoing research at Wind Cave National Park, and is a joint undertaking by USGS and the National Park Service. I got the impression at the meeting that this was being prepared for publication in one of the primary journals, but I could be wrong. I have not seen any articles yet.

https://www.nps.gov/wica/learn/nature/upload/USGS-Elk-Population-Mgmt-Report.pdf

From the paper, here is one of the conclusions presented in that talk that caught my attention:

In context with typically high survival rates and typically low prevalence of CWD in elk, annual mortality of elk at WICA during 2011–14 and mortality associated with
confirmed or presumptive CWD were exceptional and present substantial long-term challenges for elk management. In combination with low pregnancy rates and high perinatal
losses, adult mortality rates were not sustainable. Vital rates were indicative of a population decline that may not be alleviated by compensatory responses to falling elk density.
In particular, studies in adjacent Custer State Park have implicated cougar predation as the cause of similar neonatal losses (Chad P. Lehmann, SDGFP, oral communication).
Mortality from cougar predation probably is not proportional to population size, hence is likely to increase, rather then decrease, as elk numbers decline. Likewise, reduced density
may not alleviate adult mortality from accidents or hunting. Persistent environmental contamination, the gregarious nature of elk, and the long course of disease from infection
to mortality are all likely to diminish effects of density on CWD infection; hence, reducing elk densities may not reverse the increase in prevalence that occurred during ca. 2000
to 2015. If survival and fecundity do not increase, the population will continue declining at similar or greater rates after population objectives have been reached.

Click to expand...

Now, keep in mind that this herd is at least partially range-restricted so it is unclear how things may play out in a totally free-ranging, more or less unmanipulated population. However, looking at this scenario where you have range restriction of an artificially inflated population, the unusually high prevalence of disease under those circumstances, and the apparent population trend that is beginning to emerge, I can't help but wonder how this might compare to what CWD will look like in western Wyoming elk once it hits the feedgrounds. It will be interesting to see what the population does over the next decade or two at WICA.

Hunting Wife said:

I see what you are saying, and I don't completely disagree with you. We do know that prions are capable of arising spontaneously in some circumstances. And we do know they've been around for at least centuries. Scrapie, which is the domestic sheep version, has been known since the early 1700s. But I think what we are seeing today with these infectious prion diseases likely has more to do with the rise of domestication and animal husbandry practices altering the way prions circulate within populations. I do not think it is a coincidence that every animal prion disease we know about seems to have arisen in captive animals first. Here's an article with an interesting overview of prion diseases.
https://virologyj.biomedcentral.com/articles/10.1186/1743-422X-8-493

I doubt we will ever have evidence to either support or refute prion disease role in pre-modern extinctions. But I think somehow, we are responsible for CWD being what it is today.

Click to expand...

spontaneous transmissible spongiform encephalopathy has never been proven to be spontaneous, naturally, in any species. 85%+ of all human tse prion disease i.e. sporadic cjd, has never, ever, been proven to be a spontaneous disease. sporadic simply means unknown. ...

SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY

***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

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

O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

***is the third potentially zoonotic PD (with BSE and L-type BSE),

***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

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

***thus questioning the origin of human sporadic cases***

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

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

Saturday, April 23, 2016

PRION 2016 TOKYO

Saturday, April 23, 2016

SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

Taylor & Francis

Prion 2016 Animal Prion Disease Workshop Abstracts

WS-01: Prion diseases in animals and zoonotic potential

Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,

Natalia Fernandez-Borges a. and Alba Marin-Moreno a

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

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

To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.

These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.

Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

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

why do we not want to do TSE transmission studies on chimpanzees $

5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

snip...

R. BRADLEY

http://collections.europarchive.org...einquiry.gov.uk/files/yb/1990/09/23001001.pdf

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

*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

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

just the other day efsa admitted that the additional 'spontaneous' BSE cases were caused by feed, and that my friends, is where the 'elephant in the room' lay. all the officials, lobbyist, industry, that kept saying atypical bse, atypical scrapie, were a spontaneous disease of old folks, old cattle, well, they all are eating crow now...

THURSDAY, JULY 13, 2017

EFSA BSE Sixty cases of mad cow disease since 2001 breached feed ban likely the cause

Scientists investigate origin of isolated BSE cases

http://bovineprp.blogspot.com/2017/07/efsa-bse-sixty-cases-of-mad-cow-disease.html


continued...terry

even Alzheimer's is not spontaneous, and scientist are finally seeing the writing on the wall there now.

Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ???

>>> The only tenable public line will be that "more research is required’’ <<<

>>> possibility on a transmissible prion remains open<<<

O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?

[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]

http://collections.europarchive.org...einquiry.gov.uk/files/yb/1992/11/04001001.pdf

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

http://web.archive.org/web/20030714222309/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf

http://collections.europarchive.org...einquiry.gov.uk/files/yb/1992/11/04001001.pdf

snip...see full Singeltary Nature comment here;

http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments

see Singeltary comments to Plos ;

Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN

BSE101/1 0136

IN CONFIDENCE

CMO

From: . Dr J S Metiers DCMO

4 November 1992

TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES

1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.

2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible.

what are the implications for public health?

3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk. However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed.

1

92/11.4/1.1

BSE101/1 0137

4. The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion. The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.

J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2

http://collections.europarchive.org...einquiry.gov.uk/files/yb/1992/11/04001001.pdf

>>> The only tenable public line will be that "more research is required’’ <<<

>>> possibility on a transmissible prion remains open<<<

O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?

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

Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)

snip...see full Singeltary Nature comment here;

http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments

Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

*** Singeltary comment PLoS ***

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT

http://www.plosone.org/annotation/listThread.action?root=82860

Sunday, November 22, 2015

*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis Abstract

Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.

Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00

http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20

http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html

*** 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.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract


kind regards, terry

Why is game fencing to keep game animals captive allowed?

Serious issue, yes. Sky falling? No. Game farms bad? yes.