Doug Duren and Bryan Richards warn of chronic wasting disease (CWD), a fatal, prion-driven deer illness spreading across 25 U.S. states, two Canadian provinces, and South Korea, with Wisconsin’s infected bucks doubling in prevalence since 2008 despite eradication efforts. Prions persist for decades, binding to plants and clay, while experimental models suggest a potential—though unproven—human transmission risk. Norway culled 2,400 reindeer after CWD detection, but U.S. captive cervid facilities (100+ confirmed cases) and hunter resistance to antlerless harvests hinder progress, as seen in Wisconsin’s abandoned "Ernebuck" policy. Science-based solutions like hotspot culling, clay-lined disposal, and education clash with trophy-focused traditions, threatening both wildlife and hunting legacy. [Automatically generated summary]
And Brian Richards, your friend, wildlife biologist.
And, well, we're going to talk about a bunch of things, but one of the things that I wanted to talk about is this scary disease that...
Well, when Ted Nugent was on the podcast, he downplayed the consequences and effects of something called CWD, or chronic wasting disease, which has made it onto your farm.
And you live in Wisconsin, and you have this beautiful place that we visited when we did the meat-eater television show, and this is a new thing, that this chronic wasting disease was just...
It decimates the deer's health and kills them and the suspicion is that some of this at least comes from these high fence operations where people grow deer and treat them like instead of like a wild animal they treat them like a domesticated animal and have them all feeding off of the same Pile of food and they share this disease.
Why would we care about this thing called chronic wasting disease?
And I would argue, and some other scientists have argued, there's two major reasons.
Number one is the impacts of this disease on members of the deer family themselves.
And the other is that we cannot rule out the possibility that CWD could become a human health issue at some point down the road.
Okay, so you kind of nailed those two.
With regard to deer, or members of the deer family, white-tailed deer, mule deer, elk, moose, and most recently it was picked up in reindeer.
In Norway, of all places, we could articulate some reason, some rationale, why this disease might be thought of as being important.
The first we look at would be geographic spread.
So, you know, CWD 20 years ago was thought to be this really novel thing in a very restricted geographic range in southeastern Wyoming, adjacent northeastern Colorado, and maybe a little spillover into Nebraska.
A wildlife biologist, wildlife disease specialist, looked at this disease.
It was interesting.
We didn't know much about it at that point in time, but it seemed to be very isolated there.
With Kuru, which is a human disease, a TSE, likely started when one individual developed Kreutzfeldt-Jakob's disease.
That individual died.
And as was the practice in the Furay tribe in Papua New Guinea, they practiced ritualized cannibalism to honor the dead and to help release the spirits from deceased family members.
So they would feed upon the corpse and the bodies of their deceased.
So when one individual died of probably some variant of Creutzfeldt-Jakob's disease, Then the causative agent, the prion protein, which is concentrated in the central nervous system and lymphatic systems of diseased patients, this was fed back to other members of the family and the extended family.
And so when they got sick and died, fed it again.
So we saw that with Kuru.
In 1960 or around there, it was realized that this cannibalistic behavior was likely the result, you know, or likely the cause of disease transmission.
Cannibalism was outlawed and at that point in time you broke completely the disease transmission cycle.
So no more new cases of Kuru, but they had lingering cases with an extended incubation period up to 40 years later before Kuru finally burned out of that population.
So now with BSE or mad cow disease, We were doing exactly, in essence, the same thing.
Not exactly the same thing, but in essence.
So, in an effort to maximize production and reduce the amount of waste, when they butchered cattle, we would take all the offal, O-F-F-A-L, you know, the hide, the bones, the parts that are inedible, and we would render them, cook them at high temperature and typically, you know, high pressure as well, And it turns into a slurry, a high-protein slurry.
You skim the fat off the top of that and then dehydrate the rest of it, and you have kind of a meat-and-bone meal, a high-protein supplement.
Realizing that cattle grow faster and produce better when they're on a higher-protein diet, it seemed reasonable to use waste material from cows to feed back to cows.
Well, they're a disease-causing agent, but they are incredibly unique.
They're an etiologic agent, like a virus, a bacteria, or, you know, a parasite could be causing disease.
But all these other things have genetic material.
They're alive.
Which allows them to change rapidly to evolve over time.
So the whole concept that you have a protein, a protein that all mammals produce in a normal form, can be converted after production into a disease-associated form that has these radically different characteristics.
One that you mentioned was resistance to heat treatment.
A normal prion protein, and we have billions of them circulating in our bodies right now, have a specific purpose, a cellular purpose.
We don't know exactly what it is, but it's likely involved in some sort of intracellular communication.
It's a string of around 250 amino acids, so a relatively short protein.
It does whatever it does, and then the body recycles, breaks that chain of amino acids down into its component parts and recycles it.
Turns out that normal cellular prion protein likely has a half-life of maybe four to six hours.
So you're producing them relatively constantly.
Then there's the disease-associated form.
And all disease-associated prions start as the normal cellular prion.
So they're converted from one three-dimensional form To a different form, okay?
And this different form has these radically different characteristics.
One is heat resistance and other is UV light resistance.
I mentioned that the normal cellular prion protein has a half-life of maybe four to six hours.
The disease associated ones can persist in the environment for years and potentially up to decades.
So if a deer sheds infectious agent, this prion protein, and so from the time a deer is infected, it's probably around two years before it develops clinical signs of disease, goes downhill, loses its fear of humans, dramatic weight loss, all of those things.
That incubation period, you know, it's probably shedding infectious agent for the vast majority of that time period.
So it looks healthy, but it's able of transmitting disease.
The two deer that were positive on our farm, two bucks, two-and-a-half-year-old bucks, we had them tested, as you know, for the last several years we've been getting...
Initially we got our only bucks tested and then the last three or four years we've gotten all the deer tested.
They were two and a half year old bucks, looked perfectly healthy.
They tested positive and we tested in excess of 35 deer over the last, well more than that, more like 50. During the incubation period would they still test positive?
So it's probably between three and six months out when we can test an animal, test positive.
But it's likely shedding infectious agent at least at lower quantities prior to that point in time.
And so it's shedding infectious agent.
It's capable of transmitting disease.
Long before it looks clinically ill.
That's one of the real challenges with this disease from a management standpoint.
They look perfectly healthy, they act perfectly healthy, but they're starting to have that progressive neurological degeneration that we can only see very near the end of disease.
So, correct me if I'm wrong, but this seems like we could potentially be facing a ticking time bomb of many, many, many deer that are wandering around out there right now that look totally normal, that are spreading this stuff all over the place, and they're acting normal, they look perfectly healthy.
And then, obviously, with this multi-year incubation period, this could just cascade.
Started out, you know, we talked about being isolated disease.
It was picked up in Wisconsin at the end of 2001. As of today, CWD has now been picked up in 25 states in captive and or free-ranging populations in white-tailed deer, mule deer, elk, or moose.
Two Canadian provinces.
In addition, it was picked up in South Korea.
And that was real interesting.
It was in captive elk, and those elk still had Canadian ear tags in them.
So we pretty much know how CWD, you know, those elk didn't swim across the Pacific pond.
Most recently it was picked up two years ago in free-ranging reindeer in Norway and subsequent to that it was picked up in a small handful like three or four moose and a red deer in Norway and a single moose in Finland.
There's a real concern over in Norway with reindeer.
Okay, so reindeer are very gregarious.
You know, white-tailed deer, you know, caribou, reindeer.
So not unusual to see them in herds of hundreds of animals.
So very, very different than what we see with white-tailed deer, mule deer, elk, or moose.
We don't see those huge herds.
Well, with elk, you can in the wintertime.
But anyway, it's thought that this gregarious behavior might really facilitate transmission in reindeer, right?
So when it was picked up in reindeer, Norway said, you know, maybe we should do something.
It's an interesting story in that Norway's got experience with scrapie and sheep, and so they have a long history.
So when they picked up CWD and reindeer in Norway, the researchers over there Had witnessed our lack of success on this side of the pond over the course of the last 20 years.
They took it very, very seriously.
So they took kind of some harsh medicine.
They announced their plans that they were going to eliminate a herd unit.
They were going to kill every reindeer in an entire herd unit in Norway.
The idea is to eliminate the host population.
It's called stamping out.
And it works in a pen.
This is the first time it had been done realistically in a free-ranging population.
The whole idea is we don't have effective tools for management of disease.
They were very fearful of what would happen if this spread throughout that reindeer population and throughout other reindeer herds.
Five years, is that, with it being in the soil and dirt and from what I was reading, wood and everything else, is that, so at some point there becomes the prions diminish in population or they die out or whatever the Proper word, I mean, they're not living so they don't die, but they don't become viable anymore?
Yeah, five years is probably a pretty good, it's a guesstimate, okay, with regard to how long these prions remain viable in the environment and in the substrate.
So it's a good first guess.
And what they'll do then is slowly allow reindeer to repopulate.
And as they do, they'll be harvested periodically and every one of those will be tested.
So, I mean, it'll be a long-term experiment into, you know, successful management, and it'll also learn quite a bit about whether, how far along the environment was contaminated.
So another thing, they caught this disease very early.
So after killing off, you know, 2,400 reindeer, I think they had around 20 positives.
So very low prevalence, suggesting the disease was very, very new in this system.
So if you're going to be successful, With a disease where animals are shedding infectious agent out into the environment, it persists for years to decades, do it early.
If you're gonna get on it, detect it early, get on it fast, get on it hard.
Why the decision to let human beings consume them?
Well, at this point in time, we really don't have any evidence that humans can get CWD. Could that potentially, though, be an incubation period issue, just like it is with deer, maybe extended with humans?
Because you were talking about...
Was the correct pronunciation?
I was pronouncing it wrong.
No, no, no.
So that has a long incubation period in human beings, correct?
I want to talk about Kuru for a minute because every time I talk to this guy, I mean, I've learned a lot from him about all kinds of things and diseases, but yesterday we were talking about Kuru, and one of the things that was interesting to me about it is that these tribes, the women and children contracted it first.
As Kuru took off, it was one of the features as the researchers in the 1950s were looking at the population, Very few adult males had kuru, and it was more focused in the females and the children.
And so it came back to that ritualistic cannibalism, and it hit it right on the head.
The women and children got the internal organs, including the brain, that had the highest concentration of the prion protein.
The men, if they consumed anything, consumed the finer cuts of meat.
I guess I would, yeah, I'd have to agree with that.
There's other disease out there called epizootic hemorrhagic disease, EHD, and periodically you'll have significant outbreaks of this disease and in northern latitudes where the disease has not been present as often, You can see dramatic mortality.
80-90% of a herd can be killed in a single event.
But a very, you know, distinction between these diseases, you know, EHD is spread by midges.
A little black no-see-ums.
A bug.
It actually transmits the disease, the virus from animal A to animal B or from the environment to animal A, either one.
So while you have these pretty dramatic die-offs, as soon as the weather changes after the first frost, the first hard frost kills off the midges and within about two weeks the disease cycle is broken completely.
So it has significant impacts on a localized level periodically, but the disease cycle, there's a definite end to the disease cycle.
And isn't there some genetically engineered food plots that they're putting together now, different types of seed that inhibits midge growth and inhibits EHD? I'm not aware of that, but I wouldn't doubt it.
And I think there's also some stuff they're doing that bolsters the animal's immune system.
They're supplementing some of the food with, I don't know what they're using, but it bolsters the animal's immune system and makes them less susceptible to it.
So when I learned about EHD and comparative diseases, chronic wasting diseases like none other, as it develops within the herd, as it develops within the animal, It just continues to grow.
So it'll start out as a very small problem.
There's some maps of how it developed or how it spread in southwest Wisconsin.
And we're on the front edge of it now.
Correct me if I'm wrong, Brian, but it's almost like the way it develops within the deer Taking that period of time before it becomes clinical and the deer dies, it's almost as if that's reflective of how it moves through the landscape.
It moves very slowly, but once it's there, it's there.
There have been instances where people that hunted deer later died of a prion disease, likely developed Creutzfeldt-Jakob's disease.
Was it the deer that gave it to them?
Well, there's no epidemiological evidence that this occurs at this point in time.
And we've hinted about some of the human health issues.
So there's a few things we can look at.
In areas where CWD is known to exist, Do we see higher mortality rates from Creutzfeldt-Jakob's disease, the prion disease of humans, than we do elsewhere?
The answer is no.
So from an epidemiological standpoint, there's no evidence that CWD has crossed over that species barrier into humans.
Now, we can take a look at a number of science experiments that have been conducted.
And at least in some of these studies, In experimental models, we have evidence that the CWD prion protein can cause human normal prions to convert to a disease-associated form.
But now these are models.
It's not quite the same as pumping CWD into the brain of a human patient and seeing what developed.
So the science suggests that there is a small Non-zero chance that CWD could become a human health issue.
There's also some of the more recent science that's been conducted suggests that this barrier, we call it the species barrier, and it really is a very robust barrier, one would think, that keeps CWD from crossing into human hosts.
That barrier may not be as tough as we think it is.
So, yeah, the idea of strains is really interesting.
With Scrapia, I mentioned that disease of sheep.
We recognize some 30 different strains and it's still all that same identical strand of amino acids and its shape.
That tertiary form must be slightly different and it manifests slightly differently in sheep.
So, now with CWD, there's at least two recognized strains that have been published in, you know, peer-reviewed literature.
There's probably more strains out there.
In fact, it's kind of interesting.
There was a paper done a couple years ago which looked at the actual architecture of this disease-associated prion protein.
And there's a portion of it that's referred to as a loop structure.
And it's just kind of, you know, if you take a rubber band or a piece of yarn or something and ball it up into a three-dimensional shape, there's a little loop hanging off the side of this disease-associated prion protein.
And in DEAR, in CWD, that loop is very, very rigid.
It's very inflexible, shall we say.
In humans, it is more of a flexible loop as opposed to the rigid loop.
And it's thought that this difference in that architecture is partially, you know, controls that species barrier.
So now it turns out mice, experimental laboratory mice, Their prion protein has the same structure as the human prion does.
So you cannot give CWD to a normal laboratory mouse.
They just don't get it.
And it's likely this difference, some of this difference in their prion structure.
This one cannot convert that one to a different form.
So some researchers in Alberta identified a strain of CWD which came from wild deer.
It's not something they engineered in the laboratory.
They have a strain from wild deer that does give mice CWD. So most of the strains out there mice can't give, but they discovered one that mice do get.
So, researchers from a few years ago, and lately I've seen it in the popular media, that hey, this difference in this loop structure is going to keep people from getting CWD. Well, all the assumptions that people can't get CWD are based on this idea that CWD is CWD and it will always be exactly the same thing.
But our experience with Scrapey strongly suggests that even though there's no DNA in these things, that they do change over time.
They morph over time into slightly different disease characteristics and etiologic agents.
You almost want to stick your head in the sand and just forget about it.
You know, besides the sort of things that, you know, your friend that we were talking about before, like I was doing on the farm, of, you know, managing deer in a particular way for a particular kind of deer, which might be contrary to the spread of the disease.
Well, geez, nobody wants to hear that I can't do what I want to do.
We're talking about management-wise, we're talking about my friend John Dudley's farm in Iowa, is that he only shoots the big mature males and he lets all the other deer grow to a very large size so he has a really healthy population of big deer on his farm.
So 15 years ago, or 16 years ago, when CWD was discovered, there were a lot of changes in hunting structure.
And there was an effort by the Department of Natural Resources to eradicate the disease in the core area south of the Wisconsin River, about 70 miles from us.
In 15 years, the disease has moved 70 miles north.
That effort that the DNR started became political.
And quite honestly, that many years ago, I would have likely been a little skeptical.
Well, I know I would have been skeptical.
You want me to do what?
They wanted to kill all the deer in a particular area.
That many years ago, had they come to my farm and said, we're going to kill all the deer here and all the neighboring deer, I would have had some real hard questions.
I have no idea how I would have reacted to it.
I continued to do buck management, and you were there when we were still doing that.
And we can talk about how bucks contribute to the spread of the disease and that sort of thing.
We see different prevalence or curves depending on the demographic faction of deer.
Adult males, the ones with the big antlers, the gears on the wall over there, tend to have higher prevalence, sometimes maybe two, three, four times as high as other segments of the population.
So, highest prevalence in adult males followed by adult females and then by juvenile animals.
So, it's likely behavioral reasons why we see that in adult males.
So, adult male deer, during the rut or breeding season, they greatly expand their home range.
They contact multiple female or family groups of females.
Earlier in the fall, especially with white-tailed deer, adult males tend to gather in these bachelor groups.
So there's a lot of social contact, grooming, things like that.
So because of their behavior, they contact more animals at different times of the year.
And this number of contacts, it's believed, is likely responsible for them becoming infected at a higher rate than other members out in the herd.
So now, if you are an adult male, Then you're in this group.
You also have a higher likelihood of being able to transmit disease to other animals because you're out there during breeding season, right?
Is there any evidence that any of these deer have transferred this to livestock or that it's gone into agriculture, to food sources, to corn and what have you that could be consumed by people even that are vegetarians?
So, with regard to transmission into cattle, it's basically the same situation as with humans.
No evidence that it has, but in an experimental sense, we can push it over that species barrier, okay?
Now, interesting you bring up plants because we have shown research that we've done at the National Wildlife Health Center has shown that if you grow some plant types in a slurry, a concentrate of prion protein, That those prions can be uptaken through the roots and deposited into stems and leaves.
Okay?
And so that's one possible mechanism.
A second is that so prions themselves, the disease-associated prions, tend to perform very tight chemical bonds with various surfaces.
I showed him a paper on the way out here yesterday where they bind to just about anything.
They bind to plants as well.
So that deer that's out there with CWD positive, shedding infectious agent out into the environment through its urine, through its saliva, through its feces.
So if a deer urinates, this deer with CWD urinates on plants, the prions have a tendency to bind to those plants, form a chemical bond.
It's not just dried on, it forms a chemical bond to the plant.
So a deer could eat those plants and that could be one of the possible transmission mechanisms.
So that's the second one.
The third one is speculated about and some folks have looked at and it has potential impacts for agricultural commodities.
So when CWD was You know, 20, 30 years ago was really, really rare.
It probably couldn't happen.
But now it's in 25 states, vast geographic areas.
We have, just south of where he lives, in adult males, nearly 50% prevalence.
So when you kill that big buck, take a coin out of your pocket, flip it in the air, and that's the odds that that deer has CWD. And when he says just south, it's 15 miles.
Okay, so take that amount times 20% or that amount, whatever percent have CWD, figure out how many times does the deer defecate or urinate on a daily basis, and that's a bunch.
And now think about the possibility that when you harvest those agricultural foodstuffs and roll it up into big bales, that you might have fecal material rolled up into those big bales.
Another thing that's very easy to do is cherry picking the literature that's out there.
We saw a real great example of this about a year ago.
Where there's a lot of letters to the editor being sent into newspapers in areas where CWD is.
And I think it's an attempt to change the conversation.
So they were very careful to use citations from peer-reviewed literature.
And one of the ones they used was they found that in Researchers in Wisconsin found that CWD was not having a significant effect on mortality rates when they studied the disease.
So this is a true statement taken directly from peer-reviewed science.
What they didn't identify was that when they studied that disease was between 2003 and 2007, 10, 12, you know, 11 years ago.
The next sentence in the paper was, our study can use as a baseline for comparison at a later point in time should disease change over time.
So you mentioned that exponential growth curve and how early on, back in 2003 to 2007, this area, disease prevalence was probably lower than 5%.
Now it's shot up in that curve and it's probably in that 25, 30, 30 plus percentage range.
So you're cherry-picking literature to make your arguments that even scientists say this is not having a big effect when they studied it.
Yeah, and it's also one of the reasons why they're so delicious.
They're so well-fed.
You know, they're so, you know, nutritionally balanced diets.
But the real, what terrifies me is this potential for a pandemic disease also comes with an incubation period.
And that we are looking potentially at, like, if you just objectively look with no hysteria and no hyperbole, you look at the history of diseases.
Diseases mutate, and many of them come from animals.
This is why swine flu and avian flu and all these different things have actually come from either farm animals or wild animals that have somehow or another managed to transmit diseases that have morphed and mutated and become diseases.
One switch one way or the other like you've observed or they've observed rather with mice and this could potentially infect human beings and spread across I mean the entire country like wildfire.
And the mule deer have an extended range in terms of, like, their migration.
That's one of the things that we've realized, I believe, over the last decade, right, is that mule deer travel far more, far longer, and far longer distances than we ever saw before.
The state of Minnesota, you know, they've got what appears to be a fairly recent CWD outbreak in the southeastern part of the state.
So their researchers are really trying to get ahead of this and figure out what could move this around.
So they went in and captured deer in an adjacent area, put radio telemetry collars on these to see, well, just how far do they go?
This was in an article just about a week ago, a popular media article, so it's not published yet, but they had a doe, a single doe, collared, that went 80 miles.
And it could be in, again, all these different plants, all these different berries.
People could be eating these berries, eating these plants, fruits, vegetables, all these different things, and they could be potentially consuming these prions.
Well, I think it's very clear that there's exposure.
And I talk with Doug quite a bit about the difference between exposure and disease transmission.
So it is certain that lots of humans are exposed to disease-associated prion protein from CWD and likely from plant materials as well.
Whether that will result in transmission of disease across that species barrier is an open question.
We absolutely cannot say it will.
We absolutely cannot say it will not.
It's an open question.
And one thing we can, though, identify very clearly is that the rate of exposure is increasing exponentially.
As disease has a larger geographic footprint and prevalence goes up, more and more hunters are, just by simple math, being exposed to that positive material.
So we're rolling the dice.
And when you do biological experiments, I mean, there's a certain likelihood that you'll see outcome A or outcome B. So if you keep rolling the dice enough times, you might see an alternative outcome.
When we talked about this when you were on with Ranella and I at the farm, meat eater podcast number 70, Brian, you put it as the chances are very small.
At this point that it can...
And this is what the CDC and the World Health Organization says as well.
The chances are very small, minuscule even, but they're not zero.
And I'm assuming that we continue to...
That continues to be the concern.
And I know you're talking a lot, Joe, about...
And I get it, because after all, humans.
But I've actually...
We've begun to focus more on the effect on the resource, on the deer.
I mean, I tested positive animals.
We properly disposed of the meat, which is a whole other line of discussion.
Well, I do grass-fed beef, and this is actually kind of interesting.
You were talking about the deer, the white-tailed deer, on our place, eating corn and beans and GMO corn, GMO beans, alfalfa, whatever they want to eat.
I control what my grass-fed beef eat.
I mean, you've met some of my cows.
The one says hello, by the way.
Tell ourselves I. Anyway, but it's very controlled.
Now, with the incubation period that you were discussing earlier, you're talking about a two-year incubation period with deer before they potentially show any effects.
So these animals would fall into that line between birth and slaughter, that that would be inside that incubation window for deer.
It could be potentially larger for cow, is that correct?
There's two primary mechanisms if we lump them together for how CWD moves.
One is deer to deer to deer to deer.
That slow, diffusive process of moving out on the landscape.
That's really hard to deal with.
The other one is this anthropogenic or human-assisted movement where humans are moving infectious material.
And that might be how it got from Colorado to Wisconsin in the first place.
It's highly unlikely that a mule deer or a white-tailed deer got up, woke up one morning in Colorado and decided to, you know, go 900 miles across the Mississippi River and settle in, you know, western Dane County.
And back in the day, my dad and a bunch of his buddies used to go out to Colorado, or Wyoming is actually where they went, and they hunted Elk and mule deer and they bring the whole damn thing back.
I mean, just what you did, right?
You put it on the back of the truck and off you went.
And then process that.
You can remember doing it in the garage in Cazenovia as a kid, you know, working there with knives.
This is a great thing.
Well, what do you do with the bones and the non-meat stuff when you're done?
Well, back in the day, it still happens.
We take it out and Put it in a bone pile, a coyote pile or something like that.
Southeastern states and some of the far western states haven't picked it up.
If you go to our website, you'll see a map there that shows the current known distribution of where the disease is.
So the other states really don't want it.
They don't want it bad.
So it makes sense, you know, to look at these anthropogenic factors, human assisted, identify the possible mechanisms, how humans could bring CWD to them, To you and stop them either with regulatory frameworks or with education.
Teaching hunters that it's a risk to move carcasses around is likely much more effective than just putting a rule in place that says you can't do it.
And there are Unscrupulous people who purchase deer from these high-fence operations and release them in the wild because they want big racks and Animals that like people don't know there are these high-fence operations I shouldn't call them high-fence operations because some of them are wild animals that are contained in a fence These are farms.
They're farms that grow deer and they grow deer with special protein feed so they have enormous racks so you have these really Perverse examples of a deer.
And people look at that, and to someone who enjoys wild animals, you see those, and you're like, it's like a stripper with triple F tits.
It's like, what the fuck did you just do?
They don't look real.
They have like 80 points.
Instead of like an 8-point buck, which is very typical, or a 10-point buck, you're like, wow, look at that monster.
That's a natural animal that lives in the wild.
They have these things that they don't even look like deer.
It's genetics, age, and nutrition are really the key three there.
But now, a lot of places will identify these as genetically superior.
Well, that's kind of a misnomer.
When you get back to the definition of fitness, genetic fitness, there's only one measure of genetic fitness, and that's how well represented you are in the next generation.
Okay?
So let's take an example where we took one of these, you know, 80-point whatever, and let's release it out into the wild.
And during breeding season, it comes across a prime three-and-a-half or four-and-a-half-year-old eight-pointer.
You know, this physical specimen that you've witnessed them.
They're unbelievable.
So now, if you put those up against each other in a mortal battle, I know who I'm putting my money on.
So these animals, while they're bred very much like livestock for very specific characteristics, big antlers, these don't necessarily translate into something that would be more fit out in the wild.
There's an interesting example if you look to history.
It's an animal called the Irish elk.
Those things were incredible.
They're extinct now.
They were twice, three times the size of our normal elk, and their antlers were measured in feet instead of inches.
And so during their evolutionary time period, when they were on the face of the earth, it was when animals were larger, predators were larger.
These things got gargantuan.
Then they disappeared from the landscape.
And at least, you know, they offered author Stephen Jay Gould.
There you go.
Stephen Jay Gould has offered up that likely What occurred was a change in the habitat, that climate changed over time and that forests grew up.
If you're in the plains and you have antlers that are seven, eight feet wide, you can walk around.
But now when trees start to grow up, how can you survive when the world around you changed?
And you'd have to literally walk with your head turned sideways.
And Irish Alkaline extinct.
So there's a very real example of how a phenotypic characteristic, these mega antlers, really in the long term were not in the best interest of the species.
Yeah, and there's certain high fence operations that you can go online and they, you know, this is what, like, look, go back to that photo you just had with that guy standing there.
There's these places that have these animals and some people will take these animals and then they import them.
They purchase them, import them and then release them into the air quotes wild and then they'll hunt them and then they'll pretend that that's a wild animal that they shot.
Well, I think deer farms have been around for a long time.
There's, if you Google, you know, tame deer, you'll find some from the, you know, the late 1800s when photographs became possible of deer following people around.
So we've domesticated animals for a long, long time.
But as an industry, probably really came into vogue in, you know, maybe the 60s and 70s.
And more recently now it's grown, you know, that industry has grown exponentially.
I used to work for Texas Parks and Wildlife before I worked for USGS. And one of the things I did was I administered the deer breeding program for the state.
So when I started this, I didn't start the program, but when I came into that role...
But I don't want to place all the blame for CWD moving it around because there's other possibilities for how this disease moves around.
Doug hit on one of them, and that's the idea of carcass movement.
It hasn't been proven that this occurs, but it's certainly, when you look at it from a scientific standpoint, it's very easy to identify.
So if, you know, I butcher my own deer, so if I kill a deer that happens to have CWD, I butcher my own deer, I've got to do something with this stuff, okay?
You know, the meat component in a deer is probably around 30%, 35%, something like that.
So I've got a lot of other stuff.
Landfills, it turns out, are very loath to accept this material.
You know, it's almost taboo now.
Ooh, it might have CWD, so we don't want it at our landfill because the effluent might be pumped out onto a farmer's field and they could come back and, you know, they see it as a liability.
So, I've got my deer bones and offal, the rest of the material, and I drive to the dump, which is, you know, 25 miles away, and I say, no, we're not taking that.
Well, now what am I going to do with this stuff?
So, I could double bag it, you know, a little bit at a time and put it out in the trash, you know, Or maybe on the way home, I'm driving past a state-owned state park or a state natural area or a wildlife management area and I see a trail go down there.
And I drive down that trail and, hey, there's a pile of deer bones and deer heads here.
What kind of hygiene do we have with the carcasses?
And it is something that we're talking about a lot more in Wisconsin now.
And it's become an issue.
And one of the...
Interestingly, I'm in the County Deer Advisory Committee for Richland County.
And we...
It's a citizen group.
And we have some say in season structure and then how many antlerless permits there are.
There's a lot of things we don't have any say in, which is fine.
I'd rather leave it to the biologists.
But...
Because there are hunters involved, I'm happy to be one of them.
One of the things that happened in our spring hearings is that we had folks come in and say, you know, we're concerned about chronic wasting disease and we don't want to spread it on the landscape, but when we put the bones out on the curb, they aren't taking it.
On the Wisconsin DNR CWD website, there's a list of haulers who will take it.
And so one of the researchers at UW-Madison, his name's Joel Patterson, was looking at this issue 10 years ago to try and figure out, can it be safely done?
Turns out if you put about an 8-inch clay liner underneath one portion of your landfill, You can put all the deer and all the prions there that you want to.
And while the prions will then migrate down over time through the soil, when they come in contact with the clay particles, they bind.
And they don't go anywhere.
So it can be completely safely done.
So there's a way to dispose of these materials very, very safely.
But the thought of it, the risk associated with it, the liability, some landfill owners are just like, nah, we'd rather not.
And it is something I'd like to talk about a little bit.
When this all first happened 17 years ago, they were incinerating deer and it became a problem.
But there are landfills that are taking it and there are haulers who will take it.
They have dumpsters that they use specifically for it.
They're lined with heavy mill plastic.
They're very specific to deer bones.
But some haulers aren't doing it.
So I contacted the head of Solid Waste for the state of Wisconsin and asked, well, how is this?
I go on your website and I see some take it and some don't.
And her response was, we have no legislative authority to require them to take this.
So some are doing it voluntarily, and actually one solid waste hauler said to me, geez, we're putting a hell of a lot worse stuff in the landfills than some deer bones.
But it's simple hygiene.
So one of the efforts that we're working on in southwest Wisconsin right now Is to and it's a funding issue is to put place dumpsters in areas where You know like I'm volunteering to have one on my farm It's a question of who's gonna pay for it and if it comes down to it I'm gonna pay for the damn dumpster They're about $500 for a 20 yard dumpster.
So that then people can come by and put their bones in that dumpster and then they'll be properly disposed of because we have a hauler near us who's said we're willing to bring them there.
You know, to bring the dumpster there and then dispose of the bones properly, like they do at one of the lockers, one of the butcher shops that processes deer.
They have the setup, which is actually when I saw it, I was like, well, why aren't we doing that countywide in various places so that people aren't chucking them in the ditch?
I mean, otherwise, you're holding on to the damn bones until you find out whether the things...
If you're being...
Completely careful about the hygiene, which I've been trying to do.
Suddenly you've got a pile of bones in the old milk house down there until you find out whether it's positive or not.
And I'm literally keeping the deer bones separate so that when I find out that deer A was non-positive, well, okay, I can put those out or something like that.
So that's one of the things.
There's a difference between what we can...
There's natural spreading of the disease.
And then there's human, like, putting them on trucks and moving them around or taking the bones around.
I've been working with the DNR a little bit on this and we're in some discussions about two things.
One is Self-service kiosks to make getting your deer tested easier, where you essentially cut the head off the deer and leave it in a kiosk with some information about where it was.
They're fairly simple.
They've been doing this for a couple of years on an experimental basis.
But again, it becomes a budget issue.
So we're hoping that what we're going to be able to do is start something called adopt a kiosk, essentially, that hunters and people or sportsmen's groups will...
Gather those heads and then take them into the testing facility and therefore keep the budget money targeted at doing the actual testing.
Right next to that self-service kiosk really should be a dumpster that you can throw your deer bones into.
Whether you know whether it's positive or not.
Otherwise you are holding it.
The other thing that the DNR suggests that we do is if you kill the deer on your farm, leave the bones on your farm.
The last one is being transparent with your stakeholders, being open and communicative with them.
So with many diseases, we have good therapeutics.
We can treat some diseases.
CWD and other prion diseases, we have no therapeutics.
We have no treatments right now.
But people are certainly working towards it.
Now, it's likely, it's going to be very challenging to create a therapeutic, something that treats a prion disease, because treatment would then mean you would have to get past the blood-brain barrier.
And once you start this cascading interaction of normal prions to disease-associated prions in the central nervous system, it's going to be really, really challenging to stop that.
I mean, it's a roller coaster going awry by the time it gets up into the brain.
So then you're looking at preventative measures.
The idea of vaccines is number one.
And number two is looking at animals that through their genetic profile are resistant to disease.
And there's some advances on each front.
So we can talk about vaccines for a moment.
So people, individuals, scientists, research outfits have been trying to develop vaccines for TSEs, for prion diseases, for a long time.
Okay?
None have been successful.
There's no human prion disease vaccines.
There's nothing for BSE. There's nothing for scrapie, but there's research ongoing and there have been some advances.
There is a Canadian research group that had a vaccine candidate for CWD. They thought it looked very promising, so it went to a field production stage and they actually tried deploying this vaccine in a captive facility in Wyoming, a research facility.
It turned out that this vaccine was not ready for prime time.
And actually after giving this vaccine to some elk, giving a placebo to other elk, and then leaving him in a CWD contaminated facility, actually the vaccinated animals got CWD faster and at a higher rate than the non-vaccinated animals.
So if you have a vaccine that makes the average course of disease three years instead of two years or four years instead of two years, they still have CWD. Are there any deer farms that have 100% negative CWD deer in them?
Well, okay, so you're looking at the difference between a herd that is CWD-free, which means it likely hasn't been exposed to CWD, versus animals that are CWD-resistant through genetics.
So to date, we have not seen any deer that are genetically completely resistant.
There are different genotypes of the prion protein gene out there that do impact the length of disease and also seem to have some impact on how often the frequency that these animals get disease.
But even the genetically resistant deer do get CWD. And they transmit it.
They get it at a lower rate.
They likely transmit it.
They're likely shedding infectious agent.
So instead of that kind of garden variety two-year incubation period, it might be closer to a five-year incubation period.
So now, on the one hand, you're going, great, most deer die before they're five years old anyway, so this would be a good thing.
But on the downside, you're talking about a population of animals that have CWD with all these other side effects.
They're shedding infectious agent out into the environment, this, that, and the other, and cause a potential risk to human and other health impacts on the landscape.
So I'm not so certain that this is a success story.
Just like a vaccine, That results in a longer course of disease where deer can get CWD, but they die from something else.
A population of resistant animals that have a high prevalence of CWD. I guess I don't see that as a desirable endpoint because of the other consequences and potential repercussions of CWD. It would almost be more desirable if it killed them instantly.
And there's research going on in some of the conservative farms, the deer farms...
That they've identified genetic markers, ones that are not published in the literature yet, that are affording a higher degree of protection from disease.
But until it's published in the peer-reviewed literature and really tested, it's a speaking point until that point in time.
When it enters the central nervous system, it's a death sentence.
Okay?
So it's contagious, it's fatal, neurodegenerative disorder, it's got to be a horrible way to die.
So that's a pretty significant set of clinical signs or symptoms in an individual animal.
Now let's look at the geographic spread, rampant geographic spread.
So it has an ever-expanding geographic footprint.
In areas where it has been known the longest, we now have prevalence in a cohort of animals, adult males of around 50%, and in adult females around 30%.
Can you name any other disease of humans, fish, domestic livestock, dogs, wildlife, anything else that has that set of characteristics and that degree of penetrance into the population, and you go, meh, that's no big deal.
Yeah, but by doing that, by forcing these animals to have all the saliva excretion, this is a very effective means of transmitting this disease throughout the environment.
The set of characteristics of this whole disease where the protracted incubation period shedding infectious agents through bodily fluids for the majority of that incubation period The infectious agent persists in the environment for years out to decades.
I mean, if you wanted to stack the deck for a disease, you couldn't come up with a better set of characteristics.
Plus, they look perfectly healthy, so we have no idea that they're diseased until later on in the disease progression.
To date, there's no evidence that any canid, any member of the dog family, has ever developed any TSE. They never got BSE as far as we know.
No evidence that any canid has gotten CWD. Now that could be a real observation.
It could also be that we haven't done enough science on it.
But there's certainly exposure.
As opposed to cats, in the BSC situation, both great cats and domestic cats got a TSC, it was referred to as feline spongiform encephalopathy, and it was from consuming BSC-contaminated meat.
Now, with CWD in North America, again, we have no evidence that any mountain lion or any great cat or small cat has contracted CWD. In fact, it's very interesting.
In a research study in Wyoming that I was a part of, It turned out that the highest source of mortality for CWD-positive deer was mountain lion predation.
And so somebody's going, aha, CWD doesn't always kill deer.
Well, but it predisposes them.
So think about that progressive neurological degeneration and think about how mountain lions hunt.
They're ambush hunters.
So if you're a deer and you're not quite right, you know, I mean, this disease is developing in your brain, you're progressing progressive dementia.
It's not at the point where we are humanized, which really are very, very poor.
We can't see disease yet, but disease is progressing and an ambush predator can leverage that and take advantage of that in that weakness in the prey.
See, the same thing in Colorado.
Studies have identified that CWD-positive deer tend to get hit by cars more often than CWD-negative deer.
It's very logical.
So now let's extend that to wolves and ask the question, could wolves be a management tool for CWD? Okay.
Wolves are present in northern Wisconsin, a lot of other locations.
And at some point, wolves and CWD will meet.
So there's been mathematical models developed, which are...
There's a lot of assumptions built in those models, but it leaves it as an open question.
Could a large coursing predator...
Whose vision and senses are much more acute than ours, could they take advantage of this disease in earlier stages?
And so when disease meets geographically wolves, could wolves slow or maybe stop the progression of disease?
You could likely take all the predators you could find, wolves and mountain lions, and dump them You know, into Iowa County, just south of where Doug lives, and they likely would not be able to eliminate disease.
But as disease spreads geographically, at the inner base, could predators be an effective tool to slow or stop disease from spreading?
It's an interesting question, especially when states are contemplating more aggressive control measures, opening up hunting and trapping seasons to reduce population densities of wolves.
So we don't have good tools.
And I'll leave it an open question.
Do we want to take that potential tool and take it out of the toolbox?
And what about, okay, so a wolf, well, a coyote by us, you know, they're eating...
Deer die in our woods.
We found a dead one last time Steve was there and I was very suspicious of it being a CWD because it was a two and a half year old buck.
It was laying there and it turns out it was probably hit by a car, but it was fairly well consumed by coyotes by then.
And I cut the head off of it and sent it in and it came back non-positive.
What happens when that coyote, which is going to travel, well, they aren't traveling huge distances, but say he's eating a CWD-positive deer on the Dernan farm, and he's running over to Bunker Hill seven or eight miles away because they do that, and he takes that dump over there.
Yeah, that science has been done, and so it turns out if you take CWD-positive material, you put it in the front end of a coyote, It comes out the back end of a coyote and it's still capable.
It's still infectious.
There's still infectivity and it is capable of transmitting disease.
So that coyote, you have to ask, so he could eat CWD-positive material, he could poop it out X number of hours later and he might be a mile or two away.
Okay, so that's a fairly local geographic phenomenon.
They could be spreading infectious material.
Now you have to ask yourself more questions.
When they defecate on the landscape, is a deer likely to encounter and consume that material?
Well, maybe not now, but it might be fertilizer two years down the road for plants that the deer could eat.
I mean, I've seen bait piles where there's a pile of corn, there's a pile of apples.
Well, they're all eaten off the same pile.
You've got all these deer coming into that.
That's something we can do something about.
There are all these natural movements that we can't do anything about, but if we can slow the spread by stopping these unnatural gatherings of deer and these unnatural, you know, spreading of the disease, why wouldn't we do that?
Yeah, there's a few things, you know, you keep honing in on, you know, there's these anthropogenic factors, and then what can we do where disease is, truly is?
Yeah, the things you're talking about, the baiting and feeding.
Artificial congregations of animals.
Where TB is in Michigan, you can't bait and feed.
And in Wisconsin, some of the other states where CWD is, you can't bait and feed deer.
The idea is you're artificially congregating them.
So remember that single deer, we saw him up there on the screen, he was shedding copious amounts of saliva.
So if that deer goes up to a pile of corn on the ground, he's sharing, spreading infectious agent into that corn.
It can persist on that corn for a long, long time.
Healthy, naive, susceptible animal comes up and eats that corn or licks that mineral lick, and it's likely that that animal is ingesting viable infectious agent and can transmit disease.
The analogy there is daycare, okay?
If you want to get your kids sick, your three-year-old kids sick, what's the best place to do it?
Send them to daycare, okay?
Daycare is the analogy there is that pile of corn on the ground.
So if every child that ever goes to daycare is perfectly healthy, they're not little disease factories.
But we know that's not the case.
So they're a great place and schools are a great place to spread disease and then those kids come home and share it with you and then you can share it with others, right?
Same thing there.
So these artificial congregations, if all the deer are healthy, well then they can't be a place to transmit disease.
But we know that's not the case.
So it's one of those risk factors we can control.
But now you hit, Doug, you know, we get back to this area where disease is established.
Is there anything we can do?
And there's certainly things we can try, right?
We haven't exhausted the toolkit yet.
Mike Samuel at UW is now retired.
He looked at this from a mathematical perspective and he's trying to leverage the idea that adult males have higher prevalence.
So they are sinks for disease, they're gathering disease, and then they're shedders of disease as well.
So what if in our harvest regime, in hunting season, We focused on adult males.
We hammer the bucks because they're the ones most likely to have disease.
So we would lower prevalence in that we're reducing the proportion of the population with the highest prevalence of disease.
The idea is if you knock that segment down enough that you would interrupt disease transmission cycles and you could actually lower herd prevalence over time.
Now you still have the persistence in the environment, But, from a modeling basis, it works.
Alright, so now think about the deer hunter out there listening to me today, listening to this show today.
Oh, now they want us to go out and kill all the bucks.
So it's not going to be a very desirable, from a hunter's perspective, Tool.
So all the tools we have, you consider these like medicine for a disease.
I'm part of the County Deer Advisory Committee again.
We're giving more doe tags or antlerless tags because the other part of it, sure, we have a population, the bucks, that because they're sinks, as he said, and they're spreading the disease, And they're traveling more.
You know, a doe and her family tend to kind of stay in one area a little bit more, where the bucks have a bigger range.
But the other thing is population.
So one of the things that, for a couple of different reasons, I mean, you saw the number of deer that we have in our place.
In Richland County, we have in excess of 75 deer per square mile of habitat.
And I know there's places in the country that are higher than that.
But, you know, it's sort of...
It's a big population, and I have issue with it for a few different reasons.
One of them is disease.
The other one is that when I have too many deer, my little oak trees are getting, because they love those little oak trees, and they're getting chewed off, and I'm trying to do multiple things.
I'm not just trying to raise deer on our farm and on our woodlands.
So, you know, that...
That's one of the issues.
So there's this demographic issue that Mike Samuel had been working on, but then there's the population issue as well.
We're given four...
When I was a kid, when you bought a buck license, you and four other dudes would get together and then fill out this form and send it in in August to get what was called a party tag, and you could shoot one doe between four people because we had...
They were trying to manage the herd to have more deer.
Because again, when I was a kid, seeing deer was a big deal.
It's the exact opposite now.
So now you get a buck tag and you get four antlerless tags with every tag that you buy in our county.
And when you're controlling, because you don't have many deer, and you're managing to increase the deer herd, and you have a mentality out there that, well, I'm not going to shoot a doe because, you know, those are the...
And they're having two fawns, and this year, at least in my area, we're seeing a lot of does having three fawns.
I talk with folks in the state of Michigan, and they've got an issue, a relatively recent likely issue, with CWD. And there's user groups out there that are trying to advise the state on how to manage CWD. One of the groups is talking about, it's called antler point restrictions.
The idea is a yearling buck, 18 months old, has fairly small antlers.
And then as they get older, they typically get successively larger antlers.
So a group is out there right now as an active proponent of implementing antler point restrictions and promoting antlerless harvest at the same time as a disease management tool.
So as we noted, lowering the population In the areas that already have CWD. CWD is beneficial in that if we have a herd of 500 animals with 10% prevalence, that's 50 positives, versus a herd of 20 animals with 5%, which would be 1, and that's a dramatic difference.
The prevalence is the same, but we have fewer positives out there, right?
So lowering populations overall does make sense with regard to disease, okay?
But now, the other part of antler point restrictions is allowing males to get older.
And they argue that that will keep hunters engaged.
And if hunters are engaged, they'll shoot more does and keep the population down, and that'll be a good thing.
But, you know, we've already discussed how adult males tend to have the highest prevalence of CWD, okay?
And so now you're talking about promoting, pushing more males into these older age groups in an area where CWD is already known to exist.
And so from a biological perspective, from a numerical modeling perspective of disease, I fail to see how this can work.
So, will it keep hunters engaged?
That's a sociological question that I can't really address.
But from a purely biological, disease-driven process, promoting more older-aged animals, older-aged deer in a population with CWD, I cannot figure out how that could be beneficial.
I'm hoping that through this podcast this information becomes more digestible because I think that in order to get what you just laid out over two hours, in order for someone to get that by reading, it's like they're not going to do it.
Most hunters are just not going to do it.
So I have a feeling that Like what Ted Nugent had said, that his perspective is possibly way more prevalent than should be.
And because this information is not that digestible.
I think that there's, you know, I know you talked about it on Meat Eater episode...
70. 70. And then now today, this is going to reach a lot more people, and it's in a very digestible form, where they can just sit down and listen to it.
And hopefully we can get the word out on this in a way that it's not getting out now so people understand the consequences of this.
This is a real issue.
And this is not simply like, hey, we don't want to do this because this could negatively impact our hunting opportunities.
We might not have any hunting opportunities in 10 years or 20 years.
This literally could devastate the entire population of deer.
This is not a simple thing.
This is an incredibly complex thing with a terrible disease that is 100% fatal and is absolutely spreading.
Some of the take-home points I always think, and I get regularly asked by hunters, well, what can I do?
Well, what do hunters do?
They sit at deer camp and they shoot the crap around whatever, libations or whatever.
And they're going to talk about things like CWD and good.
So let those conversations be driven by fact and science as opposed to rumor and innuendo.
That's what we're doing here today, and that's why I think this public information is It's so important.
There's other things it can do.
Doug hit on a bunch of them.
Hunting is part of promoting a healthy deer herd.
Keep populations low.
Test your deer and manage those carcasses.
Don't leave them out on the landscape.
There's another category though of things that can be done You know, in deer camp, what's the easiest thing to do is blame the DNR for everything, the Department of Natural Resources, okay?
It's almost a sport to kick around at night and see who can insult the DNR the worst, right?
So with regard to disease, though, is that really an effective use of your time?
It might be fun, but it's likely not effective.
Because think of these state management agencies that deal with deer.
It might be the Agriculture Department or the Natural Resources Department.
They're very, very restricted in what they can do.
They operate within a legislative framework.
So if you really want to impact change in how a government agency goes about its business, should you talk to the local biologist or should you talk to the elected leader who establishes the legislative framework that that agency works underneath?
Social and political pressure forced the DNR to vacate their plans and their aggressive measures.
And even more recently, there was a court case.
The state of Missouri, the Missouri Department of Conservation, tried to implement some restrictions on the captive cervix industry to stop importation of live deer, seeing them as a risk factor.
The deer breeders sued the state.
It went through, you know, the court system, and it was decided by the Supreme Court in the state of Missouri about three weeks ago that, in fact, all deer represent wild deer.
And that the Department of Conservation was well within their constitutional and legislative authority to implement measures designed to protect the integrity and viability of that deer herd for future generations.
So the Supreme Court said, yes, Department of Conservation, you do have the right to restrict import of animals into captive cervid facilities to protect the integrity of the herd.
The legislative part of it is really important, and I can't put too fine a point on it.
Laws can be changed, and there's pressure to do that under a lot of different reasons.
I've been a part of changing some legislation that had to do with forestry, and I know how it's done.
And, you know, one of my favorite quotes from Elder Leopold is, ethical behavior is doing the right thing, even when no one's watching, and the wrong thing is legal.
So just because it's legal doesn't mean it's the right thing to do, and it doesn't mean it's the ethical thing to do.
Is there any potential to changing the limits, tag limits, or making them more widespread if they understand the issue with this and they understand that one of the main tools of handling this in a more effective manner and slowing the spread of this disease to the population of deer is reducing the population itself.
I mean, even these hunters would resist this because it would limit hunting opportunities.
This could potentially be a large tool in the toolbox of conservation and stopping the spread.
Well, it was vehemently opposed by a very noisy group of hunters, just like, and again, with my experience with working with the legislature, a small group of people making a hell of a lot of noise with a certain amount of money can change things.
It wasn't popular.
It was popular with me as, well, again, you hunted on my farm.
We shoot way more antlerless deer than we shoot bucks.
When earn a buck was in place, we'd have a stack of buck tags because we were shooting so many DOAs.
That was because it was politically or socially became a political issue.
It was rescinded.
And so now what we found in Richland County is we can give...
And the data shows that the first couple years of this aggressive management with Ernebuck Was actually forcing the population down, but it was very unpopular and so political pressure was applied and that tool was taken out of the toolbox, thrown on the ground immediately.
When you stop doing earn a buck and you stop having longer seasons, the population trends reversed and started going back up.
So it was easy to label, hey, the DNR failed.
Their effort to eliminate disease by having aggressive seasons failed.
Like Doug said, we don't know that because we stopped.
We pulled the plug on the tool.
Alberta, when CWD started really blossoming in Saskatchewan, Alberta was like, we don't want it.
And they found their first handful of cases right on the border between Alberta and Saskatchewan.
They raised the odds a little bit.
They started harvesting deer from an aerial platform called a helicopter.
A helicopter with government agents sharpshooting deer to try and basically eliminate deer in a buffer zone between Saskatchewan and Alberta, knock the diseased deer out and create a buffer zone where disease wasn't.
And the western states, you know, Montana, Colorado, Wyoming, where disease has been a long time, they're wildlife health professionals.
They have put together a set of uniform management recommendations for the western states, okay?
And they're promoting the things that we've been talking about, reducing those artificial congregations of animals, Implementing a harvest structure to focus on males.
Okay?
The male focused the social group with the highest prevalence.
And also kind of what I guess I would refer to as hotspot shooting.
When you see a new spark of disease out there on the landscape, Get on it.
Don't allow it to become established.
Your only chance to be successful to eliminate disease is very, very soon, before it gets established and starts spreading.
So now we're seeing in Wyoming and Colorado and Montana, they're actively talking.
They're talking to the media.
They're talking to their commissions.
And they're talking about implementing these regulatory structures, at least on an experimental basis, recognizing that doing nothing It's no longer an option.
And that's one of the things that was learned from the Wisconsin experiment, for lack of a better word, that our failure, I mean, you know, the analogy that I often use is, you know, we had this car, and it was, you know, a pretty decent car, this pretty decent model of how we were going to control the disease.
But, you know, they kind of let the oil go out of the car, and they ran it in the ditch and banged it around and then brought it up and said, damn, this Ford doesn't run worth a shit.
And you can't actively try to defeat something and then say it doesn't work.
You really have to let it, you know, of course.
And in Wisconsin, I hope that what's happening and what I can see is, you know, in the 15 years that I've learned about CWD, is that not only is there a lot being learned about the disease, but there's been a lot learned about how to manage it, both on a scientific level, but on a social level as well.
And I can tell you, man, if you don't have it, you don't want it.
You know, 15 years ago I felt, and there's so much more known now than there was 15 years ago.
You know, I feel like it's not too late in Wisconsin.
I mean, we can keep slowing it down and we can protect the rest of the state, but we've got a lot of work to do.
I think it takes information too because I don't think people are really aware of the extent of this disease or the danger of it or all the ramifications of it.
So I appreciate so much the opportunity to come out here and talk about it and Brian and Mike Samuel are going to come to Richland Center in September, which is the capital and county seat of Richland County, and we're going to do another presentation on chronic wasting disease, and we're advertising it widely, and more of that information has to get education is a big part of it.
I mean, I'm pretty not very savvy on social media and things like that.
I wasn't even sure what a podcast was when, you know, Stephen Rinawa, you know, asked me to come on and do Meat Eater.
And so we did that, and I understand now it's been downloaded like 650,000 times, which for a scientist, you know, I've been an author on a lot of peer-reviewed papers, and I can guarantee you they haven't been read You take a couple zeros off of there and that's probably the readership on those things.
So from an impact, being able to get a message out to people, this type of forum really, really is helpful.
And getting it down, like you say, down to a level that, you know, hunters can understand and digestible, I think is very, very important.
Because we talked about how misinformation, active misinformation to try and, you know, hey, it's not so bad.
Or look over here.
Don't look at this.
Look over there.
You know, these diversionary tactics are very, very successful.
They were very successful with tobacco.
They were successful with other scientific endeavors, you know, today.
But remember what the joy of hunting is, and the reason for it, and how important it is to make sure that that continues into the future.
There have been some folks who really you know sounded huge alarms about this and you know you talked about a little bit that 20 years from now it could you know could be well it might take a generation or two but it really could become that.
I want to be able to eat the meat and I want to know that in future generations you know 100 years from now and that farm is still there and it's still in the Durin name it's been in my family for 115 years I want to know that 100 years from now.
That my descendants and their friends and their family are going to be able to come there and still enjoy that.
And in order for that to happen, just like when I'm managing my oak trees, so that 100 years from now there's going to be those big oak trees there again.
100 years from now, we have to do what we need to do now in order for this Opportunity be there for the future.
In a place like Wisconsin, there's over 650,000 people that hunt deer.
They pump in excess of one billion dollars every year into the economy of the state of Wisconsin, surrounded by hunting.
If we put that on a national basis, there's millions of hunters and more billions of dollars spent.
It's not a small thing when you think about, you know, the economics of hunting, but the heritage of hunting is very, very important.
I mean, I've been hunting my whole life.
Now, I hunt primarily one county west of him.
And, you know, CWD is coming.
I'd say I'm sitting in my tree stand three years ago and CWD is in the next county over.
Two years ago, the first CWD positive deer in Crawford County, Wisconsin was detected less than two miles to the southwest of the tree that I'm sitting in.
Last year, CWD had been detected in a second deer in Crawford County, this time one mile to the northeast of where my tree stand is.
I find myself looking at deer differently.
I'm looking for those subtle cues of disease.
It's changing the experience.
I get calls pretty regularly from hunters who are like, you know, really?
I know because I'm on that deer advisory committee, a group of hunters came in who bought land south of us, you know, 20 miles south of us, in a significant portion.
And they're doing, they bought it to manage it for bigger bucks.
and population and all that they came into the County Deer Advisory Committee and talked to us about what they're doing they shot 43 deer on that property last year all of the bucks tested all the antler bucks tested positive for CWD about 25% of the does and some of the fawns so a doe fawn who has Who has CWD and she's going to be clinical and die in two
years.
She's never going to have fawns of her own.
That's a population issue.
But what I, you know, I hope those guys are listening.
What I applauded about them is what they've done is really worked.
With bringing in other people, and I'm going to do the same on our place, bringing in more people to hunt to take more deer and to do what they can to manage because they saw it.
Well, you know what?
They're not seeing big old bucks anymore because they're dead.
They're dying.
They're finding them, but they're finding them dead.
I talked a little bit about population impacts, driving populations down.
The other thing we would identify is changes in that demographic structure.
When you're hunting for the big antler deer, you're looking for animals that are four or five years old, mature or over-mature animals.
In an area where CWD is established at high prevalence levels, those animals are not going to exist or will be extremely, extremely rare.
They're rare now.
There's an example of a real large ranch out in Wyoming.
It was about 100,000 acres, and they managed historically exclusively for these over-mature mule deer, you know, the ones with the antlers, you know, like that, monstrous mule deer.
Even in the good times, they probably killed maybe three of them a year, something like that, on that vast acreage because, you know, there's a lot of sources of mortality.
They're not anymore because, you know, those deer aren't living that long.
Think about it, a math question, math quiz for Duren here.
So in this population with super high prevalence, So let's say at 18 months of age, yearling deer, let's say they have 20% prevalence, and we have that.
We've demonstrated that.
At 2.5, it's probably 30% prevalence.
At 3.5 and 4.5 and above, it's close to 40, 45, 50% prevalence.
So this is a two-year disease, right?
So half your prevalence dies every year.
So if you have 20% prevalence, Half of those deer are going to be dead the next year and half the year after that.
Okay, so over time, you would expect these cohorts to diminish.
So the math question is, in that population, how many five-year-old bucks are there?
He took people out, landowners out, hunters out, into these deer yards in the spring to show them how there was nothing to eat within reach of a deer on its hind feet.
And there were bodies of dead deer that had starved through the wintertime in order to demonstrate to them the consequences of mismanagement of deer herds.
So he was a real proponent of showing people the results of doing things the wrong way and education.
So I think, you know, it comes back.
It's what we're trying to do.
Not saying that, you know, we're Leopoldian or anything like that.
But education, getting information out, getting accurate information out is maybe one of the biggest things we can do.