CWD- again and forever.

KS does very little testing which is disappointing. CWD is likely very widespread in KS but the testing isn’t significant enough to capture disease distribution. I suspect many other states are in the same boat.
 
Does the QDMA's agenda correlate into AR cwd? I ask, because I know in the early 2000s when WI first "discovered" CWD; is right when Dane, Richland, amd Sauk counties started to really push the QDM ideas of letting bucks mature and growing "trophy deer" became a big deal. Back when my dad was young and my grandpa was early into hunting they shot every deer they saw, which was few, amd hardly any deer lived past 2yo. Now we are the only farm (about 900acres) that shoot doe, the surround farms (about 3000acres combined) won't shoot any doe. And the bucks that get shot in that same area probably average 4.5-5.5 years old. So was CWD not around because the deer weren't getting old enough to contract it and or show signs?
There's long been speculation...not proof...that Wi issues began with importing of infected deer that were released into the wild (not captive) by QDMA types...so if there's a link that is more likely than age or sex management.

Interesting you mention that time. I'll never forget what some of QDMA leaders said when they held a meeting I attended to try and get money and support for their org and ideas. They did talk about some doe harvest but openly said "Does are for women and children".

CWD has...the new info from out west is disconcerting ...traditionally been more prevalent in older deer regardless of sex.

In our testing we don't sample fawns unless a hunter insists on it...because the chance of infection is so low.

One of our more productive decisions has been to pay taxidermists who are trained in taking nodes for testing. Productive because it's more prevalent in older deer, and their business primarily takes in older deer. The percentage of big bucks that have it...many of them looking perfectly healthy to the hunter...is higher.

Until some surprise unknowns in recent years, MN's problems have almost all been traced to captive cervid farms.
 
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One of our more productive decisions has been to pay taxidermists who are trained in taking nodes for testing. Productive because it's more prevalent in older deer, and their business primarily takes in older deer. The percentage of big bucks that have it...many of them looking perfectly healthy to the hunter...is higher.
I know with mule deer and elk it's a totally different story but with whitetails in the midwest, the reason why I think people just don't care much about cwd is simply just because very few deer actually die of the disease before getting harvested. This is why our populations here are still doing so great even though the doom and gloom of cwd continues to hang over us for now almost 20 years.
 
I know with mule deer and elk it's a totally different story but with whitetails in the midwest, the reason why I think people just don't care much about cwd is simply just because very few deer actually die of the disease before getting harvested. This is why our populations here are still doing so great even though the doom and gloom of cwd continues to hang over us for now almost 20 years.
It's true that the average harvested deer is younger...but we should stress that we will have fewer prime age large bucks due to CWD.

I am pretty sure the WI results coming soon will be sobering...but with CWD as big with deniers as it is...some pushed along with political agendas...will enough people care to believe them?
 
In our testing we don't sample fawns unless a hunter insists on it...because the chance of infection is so low.
To add on to this, or perhaps provide some context to my earlier statements. Testing fawns is not typically done. In fact, many states won’t even take fawns for testing.

In regards to testing fetuses, this was done as a research effort, specific to exploring vertical transmission. Of the positive does, it was a smaller portion of fetuses that have been confirmed positive so far. So, it appears vertical transmission is not happening in every pregnancy. This work has not been published yet, as they are waiting for the rest of the mouse bioassays to be completed. These bio assays are necessary for certain uses of amplification assays like RT-quic and PMCA(both of which were used for this project), to confirm that prions are infectious and not a false positive or non-infectious.

The standard testing protocol used by game and fish agencies, is ELISA and IHC to confirm. The results of those tests are much more concrete and clear, in terms of infectious disease and what a positive means in terms of biological relevancy.
 
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One that I find particularly interesting is the genetics side of this discussion. And I caution you here because some of that discussion gets a little complex and is beyond my ability to fully understand or convey.

But one of the simpler ideas is that there would likely be signs in the genetic make up of the herds. Since it affects different genotypes differently, we would likely see that reflected in the populations. Instead, the animals that are the least susceptible(but they still get it and it still kills them because they aren’t “resistant”) are a minority of the animals in the wild. This is unlikely to be the case if it had been around say, twice, or three times as long. They would likely be the dominate genotype.
Yup, over my pea brain. Thank you for the detailed response though.
 
What is the consensus on this having been around forever/ or being relatively new from what you are seeing or hearing? know you are deeply involved on this.
There was CWD experts at the MT Mule Deer CAC. I can not remember her exact words, but the Lab leak is looking a little less likely as the source. She also talked about evidence that protein spontaneously folded in some cases.
 
There was CWD experts at the MT Mule Deer CAC. I can not remember her exact words, but the Lab leak is looking a little less likely as the source. She also talked about evidence that protein spontaneously folded in some cases.
I’d be curious who that was. I would agree that no one can prove the “lab leak”, but when the first positive case in the wild happens not far from the first case observed in a captive facility, the statistical odds of that being purely coincidental seems unlikely. But again, can’t prove it, and will never be able to.

To the spontaneously folding portion. I would agree that I would not be surprised to hear this happens once in a while. There seems to be some indication that this can happen in the genome and in moose.

However, I think it would be irresponsible to perpetuate this as a theory for the cause of outbreaks at this point. I say that because to my knowledge, there has not been a single instance in deer, elk, or moose in North America where a spontaneous case has been found.

Dr. Chris Seabury, who is the leader in some of this controversial genetics research thinks spontaneous cases are possible based on his breeding program. However, he has access to I believe hundreds of thousands of tests and genetic profiles and he can’t find or prove a single one has happened. So if they do happen they are incredibly rare.

Additionally, spontaneous cases of scrapie did happen in sheep. This was called “Atypical” scrapie. This is known and proven. However, sheep that got it spontaneously were not really contagious in the horizontal sense like we think for contagious diseases. This is partially believed to be because the prions didn’t accumulate in their bodies the same way it did with the contagious version which was called classical scrapie.

So again, if there is a wildlife health professional out there perpetuating this as a source of disease, I would find that a bit surprising. They either know something no one else does, or they’re flat out irresponsible for suggesting it without providing context to that discussion.
1719582453158.png
 
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I live in Cheyenne Wyoming, right near "ground zero" for CWD. I have noticed that deer populations in this area have stopped declining and have begun "leveling off", according to the WY Fish and Game records. I also read an article that recorded some deer that were taking about twice as long as others to succumb to the disease. I am optimistic that we are seeing natural selection resulting in a deer herd that is more resistant to the disease.
 
Bam Bam we hunt and work for a rancher that shares a fence with Sybille. We have had very few cwd positive deer or elk come off the property and we take mature bucks of 4+ yrs every year, oldest taken was 101 /2 yrs old.
We are some of the sportspersons that pushes back on their cwd plan for that area. I simply don't believer their data that says there are no mature bucks in that area. When I brought up at meeting we have 25 + years of tooth age data to show that they got real quiet.
G&F stated then that they need to try something. Well don't try what has not worked would be my comment.

They have a cow elk in the pens at Sybille that has the cwd resistant gene. Not sure if she is still alive but she lived for years in those pens when nothing else survives for very long.
 
If mortality rate of whitetails in WI due to CWD was high, I would be significantly more worried about it. I have a very hard time believing that the mortality rate from the disease is more than .01% or something super low like that. Cars, hunters and predators are all much more significant threats to the population by 10 fold than CWD is. I could care less about "prevalence rates". They are just something to make it look bad.
 
It's here. It's spreading.

I would be way more interested in an exponential increase in funding to research to see if it's transmissible to humans vs. continuing on a path of seeing if it's controllable.
 
Bam Bam we hunt and work for a rancher that shares a fence with Sybille. We have had very few cwd positive deer or elk come off the property and we take mature bucks of 4+ yrs every year, oldest taken was 101 /2 yrs old.
We are some of the sportspersons that pushes back on their cwd plan for that area. I simply don't believer their data that says there are no mature bucks in that area. When I brought up at meeting we have 25 + years of tooth age data to show that they got real quiet.
G&F stated then that they need to try something. Well don't try what has not worked would be my comment.

They have a cow elk in the pens at Sybille that has the cwd resistant gene. Not sure if she is still alive but she lived for years in those pens when nothing else survives for very long.
Wytex, what is their cwd plan for that area? There have been no CWD related changes in the Snowy Range where I usually hunt. I just found and read an article on the cow elk (Lucky) that was wonderful to find out. I would hope would she is being used to raise other CWD immune elk.
 
If mortality rate of whitetails in WI due to CWD was high, I would be significantly more worried about it. I have a very hard time believing that the mortality rate from the disease is more than .01% or something super low like that. Cars, hunters and predators are all much more significant threats to the population by 10 fold than CWD is. I could care less about "prevalence rates". They are just something to make it look bad.
The Arkansas research project has shown that 34% of positive, GPS collared deer, reach clinical end-stage disease. That 34% represents only end stage CWD. If it was CWD positive but died from a predator, it didn’t go into the CWD column but into the predator column.

IMG_7730.jpeg
 
The Arkansas research project has shown that 34% of positive, GPS collared deer, reach clinical end-stage disease. That 34% represents only end stage CWD. If it was CWD positive but died from a predator, it didn’t go into the CWD column but into the predator column.

View attachment 331057
What would explain the huge difference in predation between positive and not detected? I would expect those numbers to remain the same due to the fact that predators aren't going to differentiate between the two. In fact, maybe even predation is a bit higher in Positive is what I would expect. Is this just because the sample size is too small?

Also, where is car fatalities? That under abnormal or other?
 
Yup, over my pea brain. Thank you for the detailed response though.
Think of it along basic Darwin natural selection lines.

Those that are naturally resistant should die less often, and over the time they will dominate more and more of the breeding--so their progeny will be more resistant and so on. Over time the "winners" --those less likley to get it and die--start to dominate, and we'd see more deer that are exposed but don't die from CWD.

He's saying that takes some time.

And we can't document the dominance of those that are more resistant yet--they still die. So given that, it's unlikey it was around a long time before first being discovered.

I would take a different road based on what I know, which may well not be up to date--that is that there is very little evidence any that get it don't eventually die from it. Same principal applies though--if it had been around for a long time we'd assume selection processes would have started to show some resistance somewhere.
 
I’d be curious who that was. I would agree that no one can prove the “lab leak”, but when the first positive case in the wild happens not far from the first case observed in a captive facility, the statistical odds of that being purely coincidental seems unlikely. But again, can’t prove it, and will never be able to.

To the spontaneously folding portion. I would agree that I would not be surprised to hear this happens once in a while. There seems to be some indication that this can happen in the genome and in moose.

However, I think it would be irresponsible to perpetuate this as a theory for the cause of outbreaks at this point. I say that because to my knowledge, there has not been a single instance in deer, elk, or moose in North America where a spontaneous case has been found.

Dr. Chris Seabury, who is the leader in some of this controversial genetics research thinks spontaneous cases are possible based on his breeding program. However, he has access to I believe hundreds of thousands of tests and genetic profiles and he can’t find or prove a single one has happened. So if they do happen they are incredibly rare.

Additionally, spontaneous cases of scrapie did happen in sheep. This was called “Atypical” scrapie. This is known and proven. However, sheep that got it spontaneously were not really contagious in the horizontal sense like we think for contagious diseases. This is partially believed to be because the prions didn’t accumulate in their bodies the same way it did with the contagious version which was called classical scrapie.

So again, if there is a wildlife health professional out there perpetuating this as a source of disease, I would find that a bit surprising. They either know something no one else does, or they’re flat out irresponsible for suggesting it without providing context to that discussion.
View attachment 331053
I agree as well with the skepticism about a wildlife disease expert speculating on origin--unless it was done in a private conversation.

What I hear and prefer to do in such discussions is say that's immaterial.

Who cares how it developed?

Now we have to deal with it--doing that doesn't have to be influenced by how it started at all and wasting energy talking about that isn't productive.

You could say knowing how it started can help prevent the spread in the future--except we know how it spreads, we know captive cervid operations role in the spread--state after state has followed this closely, we know a great deal about it. And while it's interesting to focus on the science for some what we should be focusing on is how to decrease it's presence and manage it where it is too far along to eradicate--how we can eradicate it where new infestations start up--and how we can keep if from spreading.
 
I live in Cheyenne Wyoming, right near "ground zero" for CWD. I have noticed that deer populations in this area have stopped declining and have begun "leveling off", according to the WY Fish and Game records. I also read an article that recorded some deer that were taking about twice as long as others to succumb to the disease. I am optimistic that we are seeing natural selection resulting in a deer herd that is more resistant to the disease.
Maybe--are you in an area where populations are relatively isolated? Whitetails move a lot but I've long been told in the west with elevation and terrain there is a greater chance of the disease avoiding just rolling across the landscape because deer are more isolated from each other at a local level in some places.
 
What would explain the huge difference in predation between positive and not detected? I would expect those numbers to remain the same due to the fact that predators aren't going to differentiate between the two. In fact, maybe even predation is a bit higher in Positive is what I would expect. Is this just because the sample size is too small?

Also, where is car fatalities? That under abnormal or other?
It's not specific to CWD. Stressed or compromised health deer are more easily ID'd and taken down by predators. The sick die at a higher rate.

Wish more hunters made that connection...when a predator kills something, there's a higher than average likelihood something was wrong with it that would have eventually killed it had the predator not been there first.

Despite asking for reports we don't get many of sick deer just before they die, but we know even if outwardly they look OK their behavior changes and they become less wary.

I also don't think its easy to ID a deer had CWD based on what's left at a predator kill site. The tissues used to ID it's presence by labs are usually places where it's more pronounced, like lymph nodes. Not much of them if any left at predator kill sites.
 

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