Joe Rogan - Wildlife Biologist on Deadly Deer Disease!

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Doug Duren

3 appearances

Doug Duren is a passionate hunter, farmer, land manager and conservationist.

Bryan Richards

1 appearance

Bryan Richards is the CWD project leader for the U.S. Geological Survey's National Wildlife Health Center.

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Transcript

Brian Richards, your friend, a 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 Mediator television show. And this is a new thing that this chronic wasting disease was just, 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. Is this all correct and accurate, Brian? Well, you just started out about an hour's worth of conversation. So, yeah, just a little bit. I'm a wildlife biologist with the National Wildlife Health Center, US Geological Survey up in Madison, Wisconsin. And so one of the things that I spend a lot of time on is chronic wasting disease. I wouldn't say that makes me necessarily an expert, but I've gotten to know a lot of people that I would call experts over the years. So I've gained a little bit of knowledge. So I don't even, your statement there, we could start a number of different places. Yeah, this disease, it essentially, describe what it does to these animals and why it's such a major concern. It hasn't jumped to humans yet. That we're aware of. That we're aware of. But it is a possibility, a very real possibility. We can't rule it out at this point in time. Science is unable to rule it out. So, okay, that's a great place to start. 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 reasons, some rationale why this disease might be thought of as being important. The first we look at is, 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 north eastern 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. What does it do to the deer? It kills deer. Right, but how does it kill them? All right, so this is a member of a family of diseases called transmissible spongiform and encephalopathies, or TSEs. So big long words. Transmissible means it can go from animal A to animal B. Spongiform means looks like a sponge, and encephalopathy means disease of the brain. So you put it together, and so this disease results in holes in the brain, resulting in progressive neurological degeneration, followed by death. Okay, it's a death sentence. And there's no cure for it. It's not like you can capture the deer and give them some sort of medication. No cure for these diseases. The sweeter diseases, you know, there's members of the TSE group of diseases in humans. Most familiar is one called Creutzfeldt-Jakob's disease. So it's very similar to mad cow disease. They're in the same family. So it comes from prions? Well, I'd say prions. I don't know how to say it. I'll just read it. That's interesting. You know, there's a, it goes back and forth on whether it's prion or prion. Stan Proisner, who received a Nobel Laureate for his work on these diseases, coined the term prion. And in his first publication describing these diseases, he did a phonetic spelling, and it's prion. So other researchers, it's especially, you know, some from across the pond, say it's got to be prion. And the main reason that, you know, some of them I've talked to about that is that it irks Stan Proisner when he hears it called prion. Oh, so we'll say prion. So I'll say prion from now on. Now, this disease, which people know as mad cow disease, obviously is transmissible to humans. And that's one of the reasons why people are very scared that this could potentially jump from deer into humans. And correct me if I'm wrong, but it also is making its way into the actual plants that these animals eat. You're correct on both accounts. So with BSE, mad cow disease, that was an interesting disease where it resulted from, in essence, turning cows into cannibals. We were recycling. Which also exists in New Guinea, right? With cannibals, Jacob Kritsfeld. With Kuru, which is a human disease, TSE, likely started when one individual developed Kritsfeld-Yakob's disease, that individual died. And as is a practice, was the practice, in the Furee 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 port, you know, the bodies of their deceased. So when one individual died of probably some variant of Kritsfeld-Yakob's disease, then the causative agent, the prion protein, which is concentrated in the central nervous system and lymphatic systems of, you know, 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 the 1960s, 1960 or around there, it was realized that this cannibalistic behavior was likely the result, you know, or the 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 BSC 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 a butchered cattle, we would take all the awful OFFAL, you know, the high, 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, you know, 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. So at some point, turning, turning, turning cows into candles. Yeah. So at some point in time, a cow developed a TSC, a prion disease, whether it came from scrape, either TSC of sheep or a rose on its own is unknown. But that cow died, it was rendered into meat and bone meal. And this high protein feed was then fed out to hundreds to thousands. And correct me if I'm wrong with these prions, they can survive up to more than a thousand degree temperature. Yeah. Surviving is kind of a strange term, Joe, in that they're not alive to start with. It's a protein. They can persist. They cannot be inactivated. So yeah, you have to cook pretty hot. So it's not necessarily, these prions are not necessarily a living thing like a disease or a virus or a bacteria. Well, they're a disease causing agent, but they're 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, you know, 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. Okay, 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. Another 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. When you say persist in the environment, you mean in like on the ground, on leaves, on like how would they persist? Yeah, all of those things, Joe. 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. We'd call that, you know, a typhoid Mary syndrome. The two deer that we that were positive on our farm, two bucks, two and a half year old bucks, we're, we had them tested, as you know, we're, 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, perfectly looked perfectly healthy. And these are the first ones that you tested? That tested positive. We tested in excess of 35 deer over the last, well, more than that, probably more like 50. During the incubation period, would they still test positive? At some point, they will. At some point. So they could be spreading infectious agents without testing positive? Yes. Oh, fuck. So it's, 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 then, so it's shedding infectious agent, it's capable of transmitting disease. Okay. Long before it looks clinically ill. That's, 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, they're acting normal. They look perfectly healthy. And then obviously with this multi-year incubation period, this could just cascade. And I think we've seen evidence of that now. 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 been picked up in 25 states in captive and or free ranging populations in White Tildir, Mule Deer, Elk, or Moose. Two Canadian provinces. In addition, it was picked up in South Korea. And that was a 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. It's a real concern over in Norway with reindeer. Okay, so reindeer are very gregarious. You know, White Tildir, caribou reindeer. So not unusual to see them in herds of hundreds of animals. So very, very different than what we see with White Tildir, Mule Deer, Elk, or Moose. We don't see those huge herds with Elk you can in the wintertime. But anyway, it's thought that this gregarious behavior might really facilitate transmission in reindeer. So when it was picked up in reindeer, Norway said, you know, we maybe should do something. It's an interesting story. And Norway's got experience with Scrapie and sheep. And so they have a long history. Scrapie is the same as, well, it's the same family diseases and sheep. It's actually the first one that was described Scrapie we've known about since the early 1700s. A disease of domestic sheep. And it's called Scrapie because of the behavior these animals once they entered a clinical phase of disease display. And they seem like they itch bad. And so they'll go up defense posts and other objects and they will literally rub their hide off of their body. So that's the name Scrapie. And it's the same progressive neurological disorder followed by death. And you think about it. So as this disease creates vacuoles in the brain, it's killing off neurons. And so without those neurons firing, you fall into that progressive degeneration. And yet at some point, your body can no longer survive. And that's what's really spooky about how this thing kills. So anyway, go back to Norway. When they detected CWD. Right. Try to keep this a little bit closer to your You're very soft spoken. I can hear myself plenty. I know the promise of recording. Sorry. Okay, no worries. So when they picked up CWD and reindeer in Norway, the researchers over there had witnessed what we are 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's 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. And like Alaska, they have multiple herds like last year, I hunted caribou with Steve up in the 40 mile river area. And so they're very localized is probably not, but at least they have a range that they move through. So and in Norway, they have two or three different herds. Many more than that. So I don't know exactly how many herd units they have. You could isolate one of the herds. So the idea is before this gets to be any worse, before it gets any farther, let's take it out. So they had a hunting season, they allowed hunters to take as many as they could, which was a little over 1000 reindeer. Then they came in with government agents. But is there a concern that the hunters could eat something with CWD and then catch it? Well, that's always a concern. But we can talk about human health. Let me finish this with Norway in it. So they took literally took the bull by the horns, they decided to do what was very unpopular, what we have not been able to do in North America. They and so after the hunting season, government agents, sharpshooters took an additional 1400 reindeer. So they killed every reindeer in this herd unit, and they're going to keep it foul, allow no reindeer in there for a minimum of five years. So it says every bit of promise of being the first large scale success with dealing with this disease in a free ranging herd. Pretty different than what we've been able to accomplish over here.