CWD research

Point being, many of these "models" are doomsday type modeling and IMO, very damaging when those models fall way short of the reality on the ground. I also think that prevalence is over-stated as well. I won't go into many details, but I know of a cwd prevalence in a deer herd in Wyoming that stated it was 67% via sampling 3 deer. Again, I think the researchers and GF agencies need to be cautious and transparent with their modeling, prevalence rates, etc. etc. If you want people to support your CWD management, it has to be reliable and solid factually. Some of what I've seen has given me pause in regard to CWD research techniques and models.
I can't find the raw data in a quick search but, "...five-year averages were calculated to ensure a significant sample size,” the WGFD wrote. “The Project herd in the Lander Region continues to have the highest CWD prevalence in the state at 66.3%. The Shoshone River herd in the Cody Region is second at 47.6%.”

I don't think it was 3 deer over five years.
 
I can't find the raw data in a quick search but, "...five-year averages were calculated to ensure a significant sample size,” the WGFD wrote. “The Project herd in the Lander Region continues to have the highest CWD prevalence in the state at 66.3%. The Shoshone River herd in the Cody Region is second at 47.6%.”

I don't think it was 3 deer over five years.
Yeah, see that's the issue I have. Why not just publish the sample size? I pushed back pretty hard on the sample size in a deer herd near me and again, not surprisingly, when more deer were sampled, prevalence declined pretty sharply from what I was told initially.

The other case I mentioned with the 3 deer and 67% prevalence, they are going to be killing more deer as obviously 3 deer isn't a big enough sample to determine jack diddly.

Its not like I'm anti CWD Management, and like I told those I met with from the GF, I would absolutely give up hunting mule deer the rest of my life to make sure they stay healthy over time. But, being in the Science field myself, I need to see the facts. I need to see controls, I need to see sampling methods, I need to see sample size, and everything else that goes into management decisions. In particular when its calling for hammering the older age class males in a population.

I'm not unreasonable but I need to be convinced.
 
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I'm not unreasonable but I need to be convinced.
I don't think you are being unreasonable. I tend to believe the experts (WGFD, in this case) unless they give me reason to doubt them. Perhaps you have reason(s) to doubt them or you're just less trusting in general?
 
I don't think you are being unreasonable. I tend to believe the experts (WGFD, in this case) unless they give me reason to doubt them. Perhaps you have reason(s) to doubt them or you're just less trusting in general?
Yeah, I'm a bit less trusting because according to the "experts" elk in the Laramie Range should be at a minimum double digit prevalence by now according to the early modeling they presented 10-15 years ago. I find it hard to believe that elk will ever be extinct anytime soon there when: 1. cow/calf ratios are in the 30/100 plus range 2. we're issuing OTC unlimited cow permits. 3. We've hired people to kill elk to help control their numbers. 4. Prevalence hasn't changed over that time in spite of the modeling predictions and hovers in that 3-5% range.

I will grant a bit of graciousness that from what I've seen CWD doesn't appear to NOT happen in a one-size fits all scenario. I think there's still a lot of unknowns as well, so I don't want to be overly critical and/or skeptical. I've also heard that there is mounting evidence that CWD does not impact elk nearly as much as deer.

That said, when its declared that prevalence is 67% based on sampling 3 deer, I'm told that elk will be extinct in the Laramie Range, etc. its hard for me to fully get behind some of the management recommendations. I'm all about starting with the low hanging fruit, don't allow baiting, try to disperse animals as much as possible, concentrate efforts on hot spots, etc.

But, where I start to balk is when the discussion starts about late season hunting of mature mule deer bucks to kill them off, drastic population reductions, and even how those are conducted. One thing that I totally disagreed with was that proposed late seasons near me, there was not going to be any teeth behind mandatory testing. IMO, if we're going to conduct a 10 year plus reduction in mature buck mule deer, at the very least there should be MANDATORY, as in if you don't submit a sample you're heavily fined and/or lose you license for a couple years, mandatory. I see no value in killing off a segment of the population if we're not going to test 100% of the deer killed. It has to be worth it.

I want to do the right thing, but the problem is, I don't think anyone really knows what that is with CWD. My hope is that as more research is conducted, more things tried, perhaps doing the right thing will be clear. That's my take.
 
from MT's CWD 2024 report. Its interesting that in some units the modeled results closely match the observed rates, while in others they grossly overestimate compared to the observed rates.
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What is that they say about models- they are never right, and only sometimes useful?

Models are only as good as the info and knowledge you have when you build them, so obviously imperfect knowledge makes imperfect models. However, they give us a measuring stick- do observations fit the model? If not, why not? What are we missing?

Plus sample sizes and sampling strategies are hugely influential. That likely accounts for some differences between model predictions and observed conditions, and I’m sure there are other factors that aren’t even on the radar yet at play. But we won’t know if we quit trying to figure it out.
 
The simple fact is, some transmissible animal TSE’s DO transmit to humans. Why? What mechanism is it about that strain that confers that ability? Is it a character that is malleable in other TSE’s that could render them transmissible? If so, what types of exposures or conditions need to be present for that to happen? If it happens, what types of things might we do about it?

I don’t see anyone making any sky is falling statements. I see researchers still trying to understand something that has been elusive, and pulling threads trying to figure it out. That’s what science does. I’m not sure why this article generated this big of a reaction honestly.
I might take a more nuanced view than the OP, but I have some problems with its presentation.

I might have some bias, as the same group has been working on a live test for CWD for which IMO claims have been stretched -- and their work has been grabbed by deniers and captive deer folks as reason to attack measures to limit its spread and eliminate restrictions on captive herds...which have been clearly shown to be a major factor in CWD spread.

The research is interesting and worthwhile.

But fanning the flame of transfer to humans without mentioning the length of time humans have been known to have consumed meat from affected animals and the lack of any tie to transmission from doing so rubs me wrong.

Even if it is intentionally designed to generate fear supported funding/support for work that I support....
 
What CWD am I preventing by boiling this Kansas deer skull right now? It’s not hot enough to kill it. Has the spread of CWD been linked to harvested animals being moved? Seems logical, but not sure it’s been proven.
 
I don't know jack about CWD. So if an animal has CWD and you cook the meat-- is the CWD then considered "dead" or illiminated?
 
I don't know jack about CWD. So if an animal has CWD and you cook the meat-- is the CWD then considered "dead" or illiminated?

Can I cook CWD out of my deer meat?​

No. Unlike bacteria and parasites that can be killed through the cooking process, CWD prions cannot be cooked hot enough at home to make them un-infectious. Incineration is necessary to render these prions un-infectious, which leaves no meat to consume.
https://www.ncwildlife.gov/connect/...ked-questions#CanIcookCWDoutofmydeermeat-1013
 
What CWD am I preventing by boiling this Kansas deer skull right now? It’s not hot enough to kill it. Has the spread of CWD been linked to harvested animals being moved? Seems logical, but not sure it’s been proven.

I expect you're just removing the vast majority of potential source material. By boiling your getting rid of 99.something percent of brain, therefore reducing the potential infected material to as close to zero as possible.

Probably best to not let any of the local bucks use the skull cap as a salt lick though.
 
I've included a link below for the CWD study that mentions Wyo deer will go virtually extinct in 41 years.

The sample size of deer captured was 143 which is extremely small. It mentions in the report that the majority of collared deer deaths in this study were from mountain lions and CWD was possibly the 2nd most common cause of death. My guess is that it is difficult to determine if death was truly from CWD or from natural causes (winterkill, drought, poor nutrition/habitat, age, etc.). Death may have been the result of a combination of several factors.

It has been over 10 years since this study was conducted. If deer decline at a rate of -19%/year (as mentioned in the report) there should be a significant decline in the deer population in the study area by 2025?

The report mentions that genotypes play a major role in life expectancy of CWD positive deer. It is possible that deer with desirable DF or FF genes live longer and it's extremely hard to predict if deer with resilient genotypes will live just as long as deer that do not contract CWD.

Generally speaking, deer live short lives and may not contract CWD until they are relatively old. How many truly sick CWD deer are going to make it through a rough Wyo winter with coyotes and mtn lions on the prowl? It makes sense that over time the poor genetic and sick deer will be replaced by those with the very best genetics in the herd! It would be interesting to know how quickly this actually happens. I imagine there will always be poor genes even in the healthiest environment and herd, but the proportions should change over time. The turnover rate depends on a lot of different factors..... the proportion of DF or FF genes in the herd, predation numbers, winterkill, drought, habitat condition, other diseases, etc. This is a prime example of the old-school conception of "survival of the fittest" and "natural selection."

Habitat condition plays a vital role in fawn recruitment and deer survival. I've been seeing healthy twin fawns born in sites where we've conducted cheatgrass improvement projects in the epi-center of where CWD was first reported here in Colorado since the 1980's. Yes, CWD has been around for 45+ years, and the deer are doing fantastic on these sites with healthy habitat! According to the report they should be extinct?

Bottom line......Culling operations and harvesting older age class bucks may actually do more harm than good from a genotype standpoint if it is desirable to preserve the best genetic material in the herds.

Here is a link to the entire report. The report also includes info on CWD in deer vs elk.


Chronic Wasting Disease will cause a Wyoming deer herd to go virtually extinct in 41 years, a five-year study predicts.

The investigation, which relied on the capture of 143 deer, examined the dynamics in the Southern Converse County Mule Deer Herd that lives southwest of Douglas near Laramie Peak. There, a population that once numbered some 14,000 in the early 2000s dwindled to half that size in about a decade.

The Chronic Wasting Disease study is one of only three that have been conducted on wild deer, elk or moose herds, none of which have yet seen print. While wildlife managers have long suspected CWD as a principle agent in the ravaged Converse herd, the study puts numbers on the problem, calculating a 19 percent decline annually.

University of Wyoming doctoral student Melia DeVivo spent four years of fieldwork and another year crunching numbers before defending her PhD thesis on the herd. She calculated the herd would go extinct in 41 years, without taking into account genetic differences that make some deer more resistant to CWD, or accounting for deer migration into the area. Even when taking in those factors, the herd will decline dramatically, she said.

“I estimated that CWD was causing a 19 percent annual reduction in the population, which is pretty significant,” she said. “Potentially, in 41 years, it would be locally extinct.”

The number-one cause of mortality was mountain lions, the study found.

“I was already on the lookout for that,” DeVivo said. “This has also been shown in CWD studies in Colorado. We did see that CWD-positive deer were more susceptible to mountain-lion predation.”

The second leading cause of death was CWD itself.

Genotypes make a difference

Researchers have found that deer with different genes react differently to CWD exposure. The key gene at a location known as codon 225 can have one of three combinations of alleles respectively named SS, SF or FF, DeVivo said. All three are represented in the Converse herd.

The majority of mule deer today are SS, and they get infected at a higher rate, the study showed. “They are 30 times more likely to be CWD-positive compared to deer that had SF or FF,” she said.

Although DeVivo’s mathematical model predicted the herd would go extinct in 41 years, without accounting for genetic variations, that won’t actually happen because new deer are expected to move into the herd’s home range. When accounting for genetic variation, the study predicts the genetic mix of a surviving population will change over time.

“What I found was within a 100-year period we do see a significant increase in those less-susceptible genotype — where the FF becomes the dominant genotype,” she said. “I still model a significant decline in the population.”
 
The report mentions that genotypes play a major role in life expectancy of CWD positive deer. It is possible that deer with desirable DF or FF genes live longer and it's extremely hard to predict if deer with resilient genotypes will live just as long as deer that do not contract CWD.

Generally speaking, deer live short lives and may not contract CWD until they are relatively old. How many truly sick CWD deer are going to make it through a rough Wyo winter with coyotes and mtn lions on the prowl? It makes sense that over time the poor genetic and sick deer will be replaced by those with the very best genetics in the herd! It would be interesting to know how quickly this actually happens. I imagine there will always be poor genes even in the healthiest environment and herd, but the proportions should change over time. The turnover rate depends on a lot of different factors..... the proportion of DF or FF genes in the herd, predation numbers, winterkill, drought, habitat condition, other diseases, etc. This is a prime example of the old-school conception of "survival of the fittest" and "natural selection."
One issue that gets glossed over by folks that start getting excited about “desireable” genotypes and natural selection is that these more resistant genotypes are present at very low levels in populations before CWD. This really suggests that those genotypes are not advantageous and have been under negative selection pressure- the more abundant genotype being more advantageous.

So while CWD may exert higher selection pressure that would increase those low-frequency genotypes in the population, that doesn’t necessarily mean they are superior genotypes when it comes to overall survival, or that that change in frequency would be good for the population at large.

Let’s pretend that FF genotype causes some kind of nutrient absorption problem in the gut. Well, that genotype would likely be selected against, and be present at low levels in the population. Now CWD comes in, and those malabsorbing deer might live with CWD for an extra 6 months. That might be enough to increase that genotype in the population. But is that actually good for the population overall? Maybe not.

At the end of the day, no one knows what that gene actually does, so there is no way to say whether this genotype or that genotype is “superior”. Without actually knowing the selection pressures on that gene outside of CWD, it is also impossible to say whether the model accurately predicts change in genotype frequency over time.
 
I would agree that there is a reason why particular genotypes are low in a population and not all genotypes are good. However, what is the alternative? All of the predictions of massive CWD die-offs have never happened. Deer have proven their resilience to battle this disease in the wild.

Chronic Wasting Disease is one in a group of diseases called the transmissible spongiform encephalopathies (TSEs), such as scrapie in domestic sheep and goats. One thing that is known is that domestic sheep struggled with scrapies. Sheep are a prime example of a resistance genotype success story. I'm not aware of any negative side-effects compared to the benefits gained by using resistant genotypes by the sheep industries to battle scrapies? Someone that knows more about domestic sheep genotypes may chime in whether there are any negative side-affects?

With that said, it's an unknown what proportion of SS, SF and FF genotypes are in deer populations across the West. The statement that SF and DF genotypes are low in the above document is really meaningless since it was such a small sample.

Most G&F agencies are slowly collecting data for CWD prevalence and from what I understand likely haven't made the next step to test CWD genotypes when sampling? Are SF and DF genotypes increasing in areas infested with CWD prions. Are SF and DF proportions the same across the West? No one knows?

You raise a very good question....Do deer with SF and DF genotypes have side-affects that may impact their health.....no one knows? Overall, do deer with SF and DF genotypes in live longer in wild herds across the West....no one knows?

All of us muley fanatics ought to be excited that even though CWD prions have existed and have been building in soils for over 4 centuries there has never been 1 catastrophic die-off! Whether this is from resistant deer is unknown. If resistant genes have increased, I'm certain that natural selection with continue to benefit the species.
 
Here's an interesting publication article comparing 2005 with 2025 CWD genotype and mtn lion data...spanning 20ish years. It highlights another good reason for not harvesting older age class bucks.

 
I expect you're just removing the vast majority of potential source material. By boiling your getting rid of 99.something percent of brain, therefore reducing the potential infected material to as close to zero as possible.

Probably best to not let any of the local bucks use the skull cap as a salt lick though.
Removing it to where? If you're dumping it on the ground when you're done, then it didn't help. Do we know that municipal water treatment effectively destroys CWD?
 
Removing it to where? If you're dumping it on the ground when you're done, then it didn't help. Do we know that municipal water treatment effectively destroys CWD?

I assume he's removing the material from the skull and dumping the water in Kansas before bringing it back to Mississippi.

This doesn't seem like that hard a concept to me.
 
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